mild. Decroix indeed claims that if a person suffering from

hydrophobia is kept in a dark room and perfectly quiet, no paroxysms appear. The malady is, however, none the less fatal.

DIAGNOSIS.--The diagnosis of rabies and hydrophobia is not usually difficult if the disease has progressed to its paroxysmal stage. The most pathognomonic features are the fact of a bite by a rabid animal and the evidence of lesions and an extraordinary irritability of the medulla oblongata, inducing severe reflex spasms of the muscles of deglutition and respiration under the influence of any peripheral irritation. The clonic nature of the spasms and the entire absence of trismus serve to distinguish it from tetanus. From pharyngeal anthrax and diphtheria attended with spasm it is diagnosed by the extreme exaltation of the special senses and the absence of any marked febrile reaction; from acute mania by the difficulty of breathing and deglutition, the more rapid heart-beats during {901} a paroxysm, and by the marked hyperæsthesia and exalted reflex susceptibility, as well as by the perfectly lucid intermissions; and from epilepsy, in that the latter is not associated with the same hyperæsthesia, that the paroxysm is not developed by noise, movement, attempts to swallow, sight of water, etc., that the spasms are more universal, and that they do not recur often, nor can they be roused by the causes immediately producing those of hydrophobia. Hysterical cases can usually be recognized by the imperfection of the symptoms; the subject, not knowing all the manifestations of hydrophobia, naturally fails to produce them.

The most difficult to distinguish from the genuine disease are those cases in which hydrophobia occurs as a disease of the imagination, the result of fear--the lyssophobia or hydrophobie non-rabique of the writers. In these there is always the history of a bite; the cicatrix even may have become the seat of congestive redness, itching, or neuralgic pains, and these, acting on a susceptible brain, develop a disease which is hardly distinguishable from true hydrophobia, and which is quite as fatal if left to run its course. These cases have usually less reflex susceptibility than genuine hydrophobia; the attack mostly occurs shortly after some conversation on the subject, and especially about the effects of the bites on others; and the victim is seen to have a nervous organization, and may even be known to have been subject to hysteria or other nervous disorder. At the same time, the concentration of the mind on this subject sometimes produces even structural changes in the medulla, and the reflex susceptibility in co-ordination with the other symptoms may be almost perfect. In a case reported a few years ago by Hammond the symptoms appeared perfectly characteristic, and at the necropsy circumscribed points of congestion were found near the roots of the vagus; yet the dog that bit this man was said to be alive and well, and in the absence of any successful inoculation from biter or bitten the case must be presumed to have been lyssophobia.

Many cases with a more favorable issue are recorded. Bellenger had a patient who had been bitten by his cat, and manifested violent paroxysms of hydrophobia, but was instantly cured by the sight of the animal in good health. Bouardel records that a man was bitten by his dog, which afterward disappeared. He was seized with severe hydrophobia, which continued for two days, when the lost dog was found and presented to him, and the symptoms disappeared. Trousseau speaks of a magistrate whose hand had been licked by his hound, which immediately after attacked a flock of sheep, so that many of them died of rabies. The master then manifested hydrophobia, but as death was deferred beyond the usual time, he concluded it was not genuine and recovered. Prof. Dick was called to visit a man who had been bitten by a favorite dog while suffering from distemper, had manifested severe hydrophobic symptoms, and had been given up by the attending physicians. He succeeded in convincing the subject that as the dog had had distemper, and as no two great diseases could coexist in the same system, it could not have had rabies. In spite of the false premises, this reasoning had the desired effect and the patient recovered. A few years ago a boy twelve years old in Ithaca, N.Y., was bitten by a dog supposed to be rabid, and in due time manifested hydrophobia, which advanced rapidly until he was having a violent paroxysm every half hour, and it was pronounced impossible for him to survive another day. At this time I saw him, observed that he {902} had a nervous organization, and was somewhat lacking in the hyperæsthesia of rabies, learned that he had recently been gorging himself with Christmas delicacies, and was now very costive; and, as there was no satisfactory history of the dog, I at once suspected lyssophobia. The friends and strangers who had come to condole with the parents and feast on the horror were excluded, and the boy's attention fully engaged in amusing pictures and conversation; the paroxysms were omitted, and in two hours the patient, overcome by weariness, went to sleep. Next morning he was still kept secluded and quiet, and two enthusiastic students took up the rôle of keeping his attention constantly engaged on whatever would interest him. The prima viæ was relieved by medicine, and under a course of tonics the boy quickly recruited, and at the end of a week went back to school.

In doubtful cases the test by inoculation may be tried. Inoculation with the saliva of a man suffering from hydrophobia is manifestly useless, since he must die before we can hope for the development of the disease. But in the case of a dog having bitten one or more people the inoculation of the virus on the brain of one or two other dogs would ensure the development of the affection in the course of one or two weeks, provided the first was rabid. The non-success of this operation when practised on two dogs would provide the best possible medicine for the diseased mind of the person bitten.

PATHOLOGICAL ANATOMY.--Post-mortem lesions are rather remarkable for their inconstancy than for their specific characters. Hardly a single lesion can be specified which may not be absent in particular cases, yet some are so characteristic that, when taken along with the symptoms during life, they very materially assist in diagnosing the disease. Of the pathological appearances common to man, dog, and other animals the following may be named: The body is greatly emaciated; the rigor mortis is normal or nearly so; decomposition usually sets in early; a white skin is livid, cyanotic, or petechial; the cicatrix is often hardly noticeable even after the animal has been shaved; the superficial veins, especially those of the neck and head, are filled with black inspissated blood; the external mucous membranes are of a dark livid hue, those of the mouth and nose being covered by a tenacious mucous or muco-purulent secretion (in dogs they are usually covered with earth or dust); the fauces, pharynx, and tonsils are usually of a dark livid hue, and sometimes swollen; in other cases the dark red hue and manifest swelling that obtained during life disappear after death; similar lesions are found in the larynx, and I have seen extensive erosions; the bronchial mucous membrane is reddened and coated with a muco-purulent secretion (and in dogs with earth and foreign bodies); the lungs are usually congested, often to the extent of showing death by asphyxia; the heart and large blood-vessels are filled with a black thick, venous blood, and the muscles, charged with the same blood, have a dark reddish-brown hue; the stomach is usually congested, sometimes to a port-wine hue, and is the seat of blood-extravasations and even erosions; this congestion is often present, though to a less degree, in the intestines; the mesenteric glands and those in the vicinity of the pharynx are not unfrequently enlarged and congested; a very constant feature is the entire absence of proper food in the stomach and of chyme in the small intestine; the liver is usually hyperæmic, {903} exuding on pressure the characteristic dark blood, and it may be the seat of some granular degeneration, but it usually retains its normal consistency; the spleen is normal; the kidneys are hyperæmic and leaden or bluish gray, and slightly cloudy on the surface (in dogs fatty degeneration of the inner cortical layer is common even in health); the urinary bladder is usually empty or contains a little turbid, yellowish, slightly albuminous urine, while the mucous membrane is often covered with dark reddish-brown petechial spots; the brain is usually hyperæmic, and, together with its membranes, slightly oedematous, yet the lesions are not constant either in kind or degree; the medulla oblongata usually shows a similar condition, and even minute points of acute congestion, but neither these nor the hyperæmia and oedema of the spinal cord can be found in every case.

Some conditions are especially pathognomonic in the dog. In nearly all cases of furious rabies the stomach is gorged with foreign bodies, such as hay, straw, wood, coal, leather, portions of textile fabrics, fæces, earth, sand, stones, pieces of iron, lead, etc., and the same materials are usually found in the small intestine, while the large intestines are empty. Portions of these foreign bodies are often found in the bronchia as well, giving rise to circumscribed lobular pneumonia. The significance of such matters when found in large amount in the stomach of a dog which has been given to biting or other symptom of rabies is very great, and if the stomach contains none of the natural food of the animal and the duodenum no chyme, it may be held pathognomonic of rabies. If, however, the materials are small in quantity and mingled with natural food, and if the duodenum contains chyme, the dog was probably not rabid. Dogs frequently chew and swallow fresh leaves of grass, and those in detention gnaw and swallow pieces of wood, cloth, horn, etc.; but these are used either as an emetic or a teething-ring, and virtually imply that digestion is not entirely abolished. Their presence, therefore, along with food does not indicate rabies.

PROPHYLAXIS.--In view of the almost or quite constantly fatal issue of rabies in man and animals, the main attention should be given to the question of prevention. As the disease is perhaps never in our time developed except as the result of contagion, we have the most perfect guarantee that by suitably devised measures it may be absolutely suppressed and excluded from any country. Even if we allow that a rare case is at long intervals developed spontaneously, it is none the less certain that the disease can be practically abolished, as nothing can be easier than to nip the disease in the bud in the locality where it first shows itself. Thus in Australia, Tasmania, and New Zealand rabies has not yet appeared, though prevailing in the same latitude and climate in both hemispheres. It reached Mauritius in 1813, and has prevailed uninterruptedly since, while in Bourbon, immediately adjacent and almost identical in geology, climate, flora, and fauna, it is still unknown. The same truth is told in the entire extinction of rabies in Berlin by the universal muzzling of dogs, as recorded above. The immunity lasted for nine years, during which muzzling was enforced. A more recent example of the same kind is found in Holland. In 1875 universal muzzling was made obligatory in all communes where rabid animals had been and in adjoining communes. From 1877 on the disease was unknown save on the borders of {904} Belgium and Prussia and in a very few dogs recently imported. Nearly all cases of hydrophobia in man and animals being due to bites by rabid members of the canine fraternity, a fundamental condition of all success in prevention is the prohibition of its diffusion by dogs. For this reason the following measures are requisite: 1st. All dogs should be registered and heavily taxed. The number of useless dogs kept in every community affords the greatest opportunity for the speedy diffusion of the rabid germ whenever that has been introduced. Whatever tends to reduce this number directly tends to the restriction and extinction of rabies. 2d. Every dog should be made to wear a collar with plate bearing the name and residence of his owner. All stray dogs without such badge should be summarily shot by the police. This will secure the payment of the taxes and the destruction of superfluous and dangerous dogs. 3d. In all cities and counties where rabies has existed within a year, and in the counties adjoining them, every dog should be muzzled except when securely shut up or tied. All dogs found at large without a muzzle should be promptly shot by the police. The objection to muzzles is satisfactorily met by the use of the wire muzzle, which impedes neither breathing nor drinking. 4th. Dogs and cats suspected or known to have been bitten by rabid animals should be at once destroyed, or if considered sufficiently valuable may be confined in a secure cage for six months under veterinary supervision. 5th. Dogs which have bitten and are supposed to be rabid should be similarly caged and placed under veterinary supervision. If rabid, the symptoms will be fully developed in a few days, whereas if destroyed at once the bitten party is liable to develop lyssophobia. 6th. Dogs imported from countries where hydrophobia is known to exist should be subjected to a period of quarantine of six months. 7th. Foxes, wolves, badgers, martens, skunks, must be indiscriminately destroyed in localities where they have become infected with rabies. 8th. The disinfection or burning of the kennels where rabid dogs have been is a natural corollary of the above.

Other measures less thorough and efficient are often advocated and resorted to, but should be discarded whenever it is possible to practise a method of absolute extermination. Among these may be named the flattening of the teeth, and especially of the canines, with a file, as advocated by Bourrel, and later by Fleming. While this is a measure of protection, it does not remove the desire to bite, nor the power of wounding the skin when that is delicate or tender. Another method is to hang a block of wood from the neck, so that it may impede the movements of the forelegs and prevent a rush and sudden attack. The futility of such a resort need hardly be remarked upon. The emasculation of dogs is another preventive measure advocated. The single advantage of this is that it does away with the host of suitors that follow a rutting bitch, and the mutual worrying and biting that ensue. But it is not yet proved that the disease is produced by privation of the generative act, while if it were it is still certain that cases of spontaneous rabies are extremely rare; that the rabid dog bites the castrated one as readily as the perfect male; that the emasculated one contracts rabies as readily as others when bitten, and that he communicates it no less persistently. Galtier's method of intravenous injection of the rabic saliva, which seems to have proved effectual in sheep and rabbits, utterly failed in the hands of Lussana and {905} Pasteur in dogs. Besides this objection, that it is useless for the animal which is beyond all comparison the main propagator of rabies, it has the serious disadvantages that its practice would necessitate the maintenance of a constant succession of cases of rabies, that great danger attends this production and handling of the virus, and the expense and risk of a general application of the measure must absolutely forbid it.

More recently Pasteur has found that the virus when transmitted through several monkeys in succession becomes so weak as to be harmless to the animal inoculated, and yet protects the animal against the more virulent poison. This fact he utilizes by inoculating this mitigated ape-virus on the brain of the animal just bitten, so as to render that refractory to the disease when the poison from the bitten wound shall reach it by its ordinary slow channel. At the time of writing, the method is being attempted on a man bitten by a mad dog.

Another precautionary measure which is always in place is the diffusion among dog-owners of correct information as to the premonitory symptoms of rabies, and the necessity for careful seclusion when any such symptoms are manifested.

TREATMENT OF BITES.--The treatment of bites by animals supposed to be rabid consists mainly in seeking the elimination of the poison or its destruction by caustic. The first object should be to prevent absorption of the poison. If the bite has been on a limb, a tourniquet should be instantly placed above it. A stout cord or handkerchief is always at hand, and may be tied around the limb and twisted with a piece of wood until circulation is arrested. Sucking the wound is usually effective in withdrawing the poison, and can convey no additional danger to the person bitten. If the patient cannot reach the wound with his own mouth, another may volunteer to suck it, though in these days of diseased teeth and gums the act is pregnant of danger. This may be largely obviated by alternately sucking and rinsing the mouth with a solution of carbolic acid, or, better, by applying such a solution to the wound before sucking, or finally by sucking through a tube. Cupping over the wound is highly commendable, though less effective than sucking. When cupping can be combined with wringing of the wound, there is an approximation to sucking. Cupping is especially valuable in wounds of the trunk, where a tourniquet cannot be applied. Intermittent squeezing and wringing of the part and steeping in warm water is an excellent resort when no better measure can be had. Cutting the wound open to its depth, while it may in certain cases be necessary to allow of the thorough application of a caustic, is objectionable as multiplying the points of infection and absorption. Drinking of liquids to excess temporarily retards absorption by overfilling the vascular system. Ammoniacal, alcoholic, and other stimulants are resorted to for the same purpose, being held to cause plenitude, not only by quantity, but by rarefying the animal fluids.

No such measures should, however, be allowed to delay for an instant the use of caustics. This is the one effectual means of destroying the poison, and the choice of caustic is of less consequence than its thorough application. The hot iron in the form of a skewer, nail, poker, or other available instrument, at a white heat, may be brought in contact with all parts of the wound to its utmost recesses.

Of chemical caustics, solid sticks of nitrate of silver, chloride of zinc, {906} and potassa, or the crystals of cupric or ferric sulphate, are to be preferred to the liquid forms (mineral acids, butter of antimony, etc.), because of the greater thoroughness with which they can be brought into contact with all parts of the wound. Lastly, the galvano-cautery may be used if within reach. If the liquid caustics are employed, they may be introduced into the depth of the wound by means of a pipette, a piece of porous wood, or a pledget of tow. For a great number of small wounds a bath of corrosive sublimate has been recommended.

In some cases the amputation of a badly-lacerated member or one with a compound fracture offers the only measure of protection.

But although nothing should be allowed to delay cauterization, yet the impossibility of an immediate application should not be accepted as a reason for its neglect at a later date. On the presumption that the virus is localized in the seat of inoculation until it has increased largely and is poured into the blood in sufficient quantity to subjugate the blood-globules to its influence, it is logical to excise the cicatrix and cauterize the wound, though days or even weeks have elapsed.

If it should be shown by further experiment that Galtier's intravenous injection of virulent saliva is harmless and protective to sheep, rabbits, and it may be other Herbivora, it would be logical to employ this in these animals just after they have been bitten, as there will be ample time to establish the systemic influence of the intravenous injection before the poison shall have accomplished its recrudescence in the cicatrix. The constantly fatal result of rabid bites in these animals would at least warrant such an attempt, the main precaution being that the liquid shall be most carefully preserved from contact with any of the tissues, including even the coats of the injected vein.

In addition to the local treatment of the sore, certain general medication has usually been resorted to, though its real value may well be questioned. Thus, the elimination of the poison has been sought by profuse perspiration induced by warm, Turkish, and Roman baths, and by the use of medicinal agents, sudorifics, sialogogues (mercury), laxatives, and diuretics (cantharides). The neutralization of the poison has been attempted by ammonia, the sulphites and hyposulphites, chlorine, etc. Besides these are used nerve-sedatives and tonics, such as venesection, belladonna, prussic acid, tartar emetic, sulphates of copper and zinc, arsenic, strychnia, etc.

What is probably of greater importance is a sound hygiene. Stimulating food eaten to excess is injurious alike to man and beast, and by inducing digestive disorder and cerebral congestion will tend at least to precipitate the attack. Costiveness or biliousness from sedentary habits and lack of exercise in the outer air and sunshine, exposure to intense heat or cold and over-exertion, are all to be guarded against.

Finally, psychical treatment is of the highest importance. Those about the person who has been bitten should preserve a calm, equable, and cheerful demeanor and avoid all allusion to the occurrence. The patient should be protected against all sources of excitement, and should not be allowed to see that he is an object of solicitude. If the matter is referred to incidentally, he should be impressed with a conviction of the efficacy of the treatment adopted.

THERAPEUTIC TREATMENT.--Almost every agent in the {907} Pharmacopoeia has been employed as a remedy for hydrophobia, but, up to the present, it must be acknowledged, with no measure of success. The agents supposed to be prophylactics are those also resorted to as therapeutic remedies. To these may be added the potent nerve-sedatives and anti-spasmodics--chloroform, chloral hydrate, ether, bromides of potassium, sodium, and ammonium, curare, Calabar bean, and the sialogogue diaphoretic pilocarpine.

Chloroform is one of the most appropriate, as it may be taken by inhalation, though with much excitement to the patient, and it at once relieves the oppressed breathing and pharyngeal and other spasms, while it acts as a cerebral sedative and anæsthetic; and if it cannot be held up as a curative agent, it at least secures euthanasia. Chloral given as an injection, so as to induce its soporific action, is equally soothing, though nothing more. Curare injected hypodermically overcomes the spasms, but does not usually, if ever, retard death. Three cases of hydrophobia in man treated in this way recovered, but we have no proof that even these exceptional cases were rabies. Pilocarpine has been used in a number of cases, but, with the exceptional case of a young man reported by Denis Dumont, all terminated fatally. The committee of the Paris Academy of Medicine reported in 1874 that in three experimental cases "it hastened death by the fits it brought on." Morphia is often of great value in calming the excitement and giving rest and sleep during the intervals of the paroxysms. Daturia and atropia, administered hypodermically, are somewhat less effectual. Inhalation of oxygen is said to arrest the convulsions and delirium, but not to retard death. Vaccine virus and the venom of the viper have each been tried, but with no good effect.

Of non-medicinal therapeutic measures the following are among the most promising: Perfect seclusion, quiet, and darkness serve to abate the hyperæsthesia, the painful acuteness of the senses, and the convulsive and delirious paroxysms. It can no longer be doubted that a very few cases of genuine rabies recover, but those that do so have almost all had special advantages in the way of quiet and seclusion, and few have had the excitement of medicinal treatment. Eight cases of the recovery of rabid dogs are reported by Menecier, Decroix, Laquerriere, Rey, Harold Leiney, and Pasteur. The two first were attested by successful inoculation on other animals; Decroix's second case was caused by inoculation with the saliva of a hydrophobous man; the next three had been bitten by dogs undoubtedly mad; while Pasteur's was inoculated with the brain-matter of a rabid cow. All in due time presented the characteristic symptoms of rabies, yet all recovered, without any record of medicinal treatment. Pasteur's case, when again inoculated, resisted the disease. A certain number of recoveries of men from pronounced hydrophobia under medicine and without it are on record, but in the absence of successful inoculations it is impossible to tell how many were cases of infecting rabies. The parallel between rabies and tetanus in the intensity of the reflex excitability would demand darkness and quiet as a sine quâ non of any rational treatment. Faradization has produced a temporary relief, but no permanent improvement. Warm baths, steam baths, and hot-air baths serve to abate excitability and spasm, and have been lauded as specific in hydrophobia, but have proved useless in the lower animals.

{908} Intravenous injection of warm water (two pints) in a hydrophobous man reduced the pulse from 150 to 86 and restored the power of deglutition. Life was prolonged for nine days, but in great agony, from the supervention of suppurative arthritis (Majendie). In another case the dread of water disappeared, but death ensued in fifty-four hours. In the hands of Youatt and Mayo it proved equally unsuccessful in dogs. A cold bath with submersion to unconsciousness is an old remedy now abandoned. Venesection to fainting, with or without mercury, mitigated the symptoms, but seemed to hasten paralysis and death. The excision and cauterization of the cicatrix, or the cutting of the nerves proceeding from it, has been useful in delaying, or even absolutely preventing, the paroxysms. When, therefore, the premonitory symptoms of hydrophobia have set in, and when an aura or shooting pain is felt proceeding from the seat of the wound toward the heart, one or other of these measures may serve to prevent the immediate occurrence of reflex convulsions. When the poison has actually invaded the brain, this can be looked on as a palliative measure only, but in the many cases of lyssophobia it may put an instant stop to the affection.

{909}

GLANDERS (EQUINIA GRAVIOR, FARCY).

BY JAMES LAW, F.R.C.V.S.

SYNONYMS.--_Greek_, [Greek: malis]. _Latin_, Malleus, Equinia Nasalis, E. Apostimatos, Farcinia. _French_, Morve, Farcin. _German_, Rotz, Lungenrotz, Hautrotz, Wurm, Hautwurm. _Italian_, Morva, Moccis, Cimurro. _Spanish_, Cimorro, Lamparones.

DEFINITION.--An infectious, bacteridian disease occurring in the horse, ass, or mule, and communicated by inoculation to various other animals, including man. It is usually ushered in by rigors, followed by articular pains, lameness, and the formation of a specific deposit in the lymphatic system of some part of the body, with a tendency to destructive degeneration and ulceration. In the form known as glanders these deposits and ulcers take place mainly in the nasal mucosa, in the lungs, and in adjacent glands, while in that known as farcy the deposits occur in the cutaneous and subcutaneous lymphatic plexuses and the dependent glands.

HISTORY AND GEOGRAPHICAL DISTRIBUTION.--Under the name of malis Aristotle describes a fatal disease of asses, supposed to have been identical with the malleus humidus of Vegetius Renatus and other writers of early Christian times, and with the cymoira of other early Roman writers. This malady was characterized by swelling of the submaxillary glands and discharge from nose and mouth. From the fourteenth century onward glanders is reported from different parts of Europe at frequent intervals; thus in 1320 in England (Rogers); in 1640 in Badajoz, brought by Portugese horses (Villalba); in 1686 at Treves (Eggerdes); again in 1776 in Southern France (Lafosse); in 1794 in Bavaria (Plank); in 1796 in Franconia (Laubender); and in 1798 in Piedmont (Toggia). At the beginning of the present century this affection was very widely prevalent in Great Britain, the chronic cases being habitually worked in stage-coaches, but of recent years, when it has been made criminal to expose or use a glandered horse, the malady has to a great extent disappeared. To-day glanders is almost coexistent with the distribution of the domesticated equine family, yet its prevalence bears a direct relation to the facilities for infection (horse-traffic, war, preservation of the diseased, confinement in close stables, ships, etc.), and some countries appear to be entirely free from the affection. Thus, Krabbe gives the yearly losses per 100,000 horses for the principal countries of Europe and Algiers as follows: Norway, 6; Denmark, 8.5; England, 14; Sweden, 57; Wurtenberg, 77; Prussia, 78; Saxony, 95; Belgium, 138; {910} France (army), 1130; Algeria (army), 1548. The losses in Prussia more than doubled after the Franco-German War; thus, in 1869-70 they were 966, and in 1873-74, 2058. In Bavaria they rose in the same period from 173 to 390 (Hahn). In Lisbon, Portugal, glanders was unknown for the thirty years preceding the Peninsular War, whereas after the war it proved a veritable scourge (Saunier). Charles Percivall, during an eight years' residence at Meerut and Cawnpore, Hindostan, saw not a single case of glanders, and so late as 1275, Fleming claims an entire immunity for India; yet in 1877 complaints were numerous of the very general prevalence of the disease in Upper India especially, while in 1879 the campaign in Afghanistan was seriously affected by its ravages. Climate appears to have little influence. The disease is virtually unknown in the island of Bornholm with 7000 horses, and in the Faroes and Iceland with 35,000, while it is quite frequent in Sweden. It is unknown in Australia, but is very prevalent in China, South Africa, Abyssinia, and Algiers, and but little known in Asia Minor, Arabia, and Egypt.

In the United States as in Europe the disease has mainly concentrated itself in the large cities in times of peace, and spread widely on the advent of war. It is alleged that it first entered Mexico in 1847 with the American cavalry, though with the horses kept in the open air it failed to gain a wide extension. The horses and mules drawn into the Union armies in 1861 brought infection with them, and soon the disease was most prevalent and destructive, not only in the ranks, but in every State in which the armies operated. John R. Page says the first case he saw in the Confederate army was a captured Federal troop-horse on the retreat from Manassas, and that the breaking down of the Confederate cavalry in the last two years of the war was mainly due to glanders. At the close of the war the sale of army horses distributed the infection widely through all the States, North as well as South. Every year in a country district in Western New York I see several cases of glanders, and occasionally a whole stud is carried off through an infected purchase. In other States the case is no better. In Pennsylvania, Ohio, Illinois, and Michigan cases are constantly seen in the country districts, and in the three last-named States five human victims have been reported within a short period. In Connecticut the same is true, and the disease made one human victim in Waterbury in 1879. In the large cities the case is still worse. Liautard of New York in 1878, in a single visit to one car-stable, condemned 8 horses, in another stable 18, and in a third, at two visits, 45, while a fourth had lost no fewer than 200 horses in the course of one year from glanders. In the Troy (N.Y.) car-stables the malady prevailed from 1875-77, most of the subjects suffering from chronic farcy, until in the latter year, by my advice, these propagators of contagion were destroyed. In Springfield, Mass., in 1879, the disease assumed such alarming proportions that it was vigorously suppressed by a city ordinance enjoining summary slaughter. These are but indications of what is happening all over the country, entailing losses of many hundreds of thousands yearly as well as an enormous risk to humanity.

The following table gives the number of cases occurring in the equine family in two of the principal countries of Europe in the last few years: {911}

Cases of Glanders in-- Great Britain. Germany. 1878 888 2753 1879 1367 1880 2048 1941 1881 1710 1774 1882 1389 1838

As both countries systematically suppress this disease through their veterinary sanitary officials, it cannot be doubted that the figures for America, if obtainable, would be relatively higher.

Glanders prevails especially in horses, asses, mules, and other solipedes, and is communicated by inoculation to all domestic animals except the genus Bovis. In the sheep and goat the receptivity is considerable, and the disease may prove fatal in fifteen days (Gerlach) or it may be delayed for seven weeks (Bollinger). The Carnivora (dogs, cats, lions, polar bears) contract the affection by eating diseased flesh, as do some rodents (prairie-dogs, rabbits, guinea-pigs, mice), and, by administration, solipedes. Swine contract the disease by inoculation (Gerlach, Spinola), though in these and in the dog the constitutional symptoms are usually slight and recovery may follow the local affection.

The susceptibility of man is doubtless less than that of the solipedes, judging from the few cases of glanders compared with the frequent exposures, yet when once established in the system it can hardly be said to be less malignant or fatal.

ETIOLOGY.--The one known cause of glanders is contagion, and the recent experiments of Capitan and Charrin in France and of Schütz and Löfler in Germany, demonstrating that the bacillus of the glanderous deposits is the one essential cause of the disease, effectually dispose of any claim of its spontaneous origin. Glanders can no longer be considered spontaneous, further than that its germ is now proved capable, like that of anthrax, of survival and multiplication out of the animal economy, so that infection may come from other objects than a sick animal; and it may even yet appear that the bacillus, living at times as a harmless saprophyte out of the animal body, may acquire deadly properties under certain conditions of the environment. At the same time, the most extensive acquaintance with glanders and the broadest generalizations from known facts do not warrant the assumption of the extension of the disease by the growth of the bacillus out of the living body, unless it be on the rarest possible occasions, while the soundness of extensive countries (Australia, New Zealand) for a century or more speaks strongly against any frequent development from a harmless saprophyte.

To the same effect speak the experiences of the English army. At the beginning of the century, under the teaching of Coleman, most cases were attributed to lack of stable care, and extensive experiments were made in the treatment of the disease, with the result of a very high mortality from this cause. Now, when contagion is looked on as the main or sole cause, and all suspected horses in the army are promptly destroyed, the disease is only seen in recently-purchased animals or after the inevitable exposures of a campaign.[1] In the French army the doctrine of the {912} non-contagiousness of chronic glanders led to a greater prevalence of this disease than in any other country of Europe. Prior to 1836 it was about 90 per 1000 per annum, whereas now, under the doctrine of contagion and a corresponding practice, glanders kills but 2 per 1000 per annum (Rossignol).

[Footnote 1: Wilkinson, _Jour. of Roy. Agr. Soc._, No. 50.]

But while the essential cause of glanders is the specific bacillus, an individual susceptibility is no less requisite to an attack. This may be innate or acquired. As we have seen, it varies according to the genus, being greatest in the solipede. But many solipedes show a strong power of resistance. Of 138 horses similarly exposed by cohabitation with glandered horses, but 29 (21 per cent.) suffered. Of 28 inoculated with glanders virus, but 9 (32 per cent.) succumbed (Lamirault, Bagge, Tscherning). The accessory causes which predispose the system to the reception of glanders may be included under one general term--low condition and ill health. Three of these causes, however, deserve especial mention: 1st. Impure and rebreathed air. Prior to 1836 the yearly losses per 1000 of the French army horses were from 180 to 197. At the date named the ventilation of the stables was greatly improved, and the mortality fell to 68 per 1000 per annum, one-half from glanders. Later improvements have reduced the 34 cases to 2. During the Italian War, in 1859, 10,000 of these horses were kept for nine months in open sheds, with but one case of glanders.[2] In the expedition to Quibéron during the Napoleonic wars, a cavalry contingent, believed to be healthy, shipped on new transports, encountered a storm, and had the hatches fastened down, so that several horses were suffocated. Among the survivors, landed at Southampton and placed in stables hitherto unchallenged, many soon developed glanders in its worst form. Similar results followed the English expeditions to Varna in 1854, and that to Abyssinia in 1867. In badly-ventilated mines and stables, especially cellar stables, glanders, once started, is always most virulent.

[Footnote 2: Larrey, _Hyg. des Hop. Mil._, 1862, p. 63.]

2d. Cold, damp, draughty stables greatly favor the progress of glanders. Leblanc reports the case of a stud of 240 horses that had had no glanders for eight years, but which lost half their number in three months after removal into a new stable, very lofty, but dark and damp, and subject to cold draughts. It is worthy of notice that they had also been subjected to double work, and were consequently emaciated, but there was not known to be any unusual exposure to contagion. In a Boston street-car stable, where glanders had long prevailed, Thayer cut it short by destroying the infected animals and by improving the ventilation by windows hung at the bottom and opening inward, so that the air entered in an upward direction, and cold draughts on the horses were avoided.

3d. Debility from ill-health, low feeding, or overwork.--The nervous and nutritive debility consequent on chronic disease, overwork, and exhaustion lessens the power of resistance to specific poisons, but in such circumstances there is always the added predisposition of an excess of waste material in the blood, a specially abundant food for the disease-germ. So notorious is this that it used to be held that the specific poison of glanders was generated in connection with the excess of creatine, creatinine, and lactic acid resulting from muscular action. Of the effect of {913} low diet we have a striking example, furnished by Bouley, of a stud of 120 horses, 60 of which were attacked within a year after they had been placed on a food insufficient to repair the body-waste, and from which the disease disappeared after the slaughter of the infected and improvement of the ration. So long as glandered horses were preserved for work, the then nearly ubiquitous germ attacked nearly all that were run down by chronic diseases; hence glanders was looked upon as the natural winding up of exhausting diseases in the horse, as tuberculosis was thought to be in the human subject. Modern discovery shows that without the germ all such debilitating causes are impotent, but it can never disprove the great potency of these in laying the system open to attack, nor the value of vigorous health and sound hygiene in fortifying the system against it.

The channel of infection manifestly varies in different cases. In direct inoculations the morbid process develops first at the point of insertion, and secondly in the nearest lymphatic glands and internal organs. When contracted in the ordinary way, the lesions are usually first seen in the posterior nasal passages, the larynx or the lungs, or in the superficial lymphatics, especially of the hind limbs. This susceptibility of the deeper portions of the air-passages seems to imply that the bacillus, borne on the air, is lodged on different parts of the respiratory mucous membrane, and first sets up the morbid process in the thinnest or most susceptible portion. That it can be thus borne on the air is shown by the experiments of Viborg and Gerlach, who separately collected the particulate elements from the exhalations of glandered horses and successfully inoculated them. That the virus is not usually carried far on the air in a virulent form is attested by the many instances in which horses have stood for months in the same stable with a glandered animal without becoming infected. That infection may also take place through the ingestion of infected matters is undoubted, as glanderous products mixed with food, or even made into balls and enclosed in paper and administered to horses in this form, have produced the disease. The virulence is said to be lost by passing through the digestive canal of man (Decroix), dog, pig, and fowl (Renault), but even to Carnivora the infection may be conveyed in the food.

While the virus is concentrated in the material of the special glanderous deposits and the discharges from these, yet no part of the body can be considered as free from the poison. Viborg, Coleman, Hering, and Chauveau have communicated the disease by transfusion of blood from a glandered horse to a healthy one; hence every vascular organ must be liable to infect. The secretions of the diseased body (tears, saliva, mucus, sweat, urine, and milk) have each been successfully inoculated, and the conveyance of the disease to the foetus in utero and to the female by coition imply that even the generative secretions are virulent. Failures to convey the disease by inoculation with the blood and secretions have often occurred, however, and they must be held as less virulent than the products of the local disease-processes.

The claims that inoculation with pus, ichor, and other irritants have produced glanders must be entirely discredited. The deposits and ulcers in the lungs and elsewhere resulting from such inoculations have been either septicæmia, mistaken for glanders in the earlier days of pathological anatomy; or the septic and other inflammations set up by these {914} inoculations have merely served as fertile spots for the planting and growth of the glanders bacillus accidentally present, and which to a healthy system might have proved harmless.

In 1882, Chauveau had demonstrated the particulate nature of the glander germ by his unsuccessful inoculations with the liquids filtered from dilutions of pus taken from a pulmonary glanderous ulcer. The filtrate and the liquid mixture formed by mixing the pus with five hundred times its own weight of water retained their virulence undiminished. In 1868, Christol and Kiener discovered in glanderous products a bacillus which they figured as made up of a chain of nearly globular elements apparently enclosed in a common sheath. In 1881-82, Bouchard, Capitan, and Charrin cultivated these microphytes in a neutralized extract of meat through five successive cultures, using in each case a milligramme of the previous culture, or less than 1/1000 part of the culture-liquid. Counting that the milligramme of pus would give to each centigramme of the first culture-liquid 1,000,000,000 bacilli, it follows that the second culture would, on the principle of dilution, contain 1,000,000, the third 1000, the fourth 1, while for the fifth it was as 999 to 1 that it would receive nothing unless the germ were multiplied in the culture-liquid. Inoculation of a cat with this fifth culture, started originally from a nasal ulcer of a glandered horse, led to a fatal result in twenty-five days, with suppurating tumor of the left testicle and inguinal glands. The products of the first cat were inoculated on a second, those of the last on a third, those of the third on a guinea-pig, and those of the guinea-pig on an ass, producing in every case specific lesions of glanders, including miliary nodules and abscesses, and death respectively on the following days: 16, 7, 31, and 10.

In September, 1882, and the two succeeding months, a similar course of experiments was conducted by Schütz and Löfler at Berlin. The virulent matter used for starting the culture was procured from a pulmonary deposit and spleen of a glandered horse; the cultivation was continued through eight successive culture-fluids. One horse was successfully inoculated with the product of the eighth culture, and a second with both the fifth and eighth. The first died on the fifty-eighth day, and the second, now very weak, was sacrificed on the fifty-ninth. Both showed the most extensive lesions of glanders alike in the skin, the lymphatic glands, the pituitary and laryngeal mucous membrane, and the lungs. To demonstrate the bacillus they take a thin layer of the infecting liquid on a cover glass, dry it, stain with methyl violet, wash with dilute acetic acid, dehydrated by absolute alcohol, and clear by oil of cedar. Like other pathogenic microphytes this may be preserved for months or years if thoroughly dried, but in the moist condition it is easily destroyed by heat (133° F.; Viborg, Hofacker, Renault), chlorine, and the disinfectant chlorides and sulphites.

SYMPTOMS.--Acute nasal glanders in horses has a period of incubation lasting from three to five days in inoculated cases. Where in infected subjects the incubation appears to have extended over months or a year, there have usually (or always) been deposits in internal organs which passed without recognition until the lesions appeared in the nose. At the outset there is fever, which appears before any local lesions are recognizable, even post-mortem (Chauveau), and soon with languor, {915} and loss of appetite, there is a serous nasal discharge, often from one side only. By the sixth day this has become yellowish, the margin of the nostril is often swollen, and upon the pituitary membrane may be detected elevations of various sizes of a general yellowish tinge, dotted with minute red points and surrounded by a bright-red or purple and slightly elevated areola. These may be simple, pea-like nodules or more or less extensive patches, which in certain cases extend over nearly the whole pituitary membrane. At the same time the submaxillary lymphatic glands on the same side become the seat of a hard nodular painless enlargement, feeling like a conglomerate mass of peas, and often showing a tendency to become more closely adherent to some adjacent part (bone, skin, base of tongue); but they only ulcerate exceptionally. Extensive hot, painful engorgements also often appear on other parts of the body, and if on the limbs or joints cause lameness. Soon the swellings on the mucosa become eroded and are gradually destroyed, forming large unhealthy, chancrous-looking ulcers, tending to become confluent and to eat deeply through the mucosa into the subjacent tissues. These are mostly reddish gray or yellowish gray, with raised ragged red or yellowish-red margins. They bleed readily, and may be black from hemorrhage, or greenish or of some other shade from decomposition. The discharge is always somewhat glutinous and sticky, but it may vary in color from simple white to yellowish, greenish, brownish, or red, according to the destruction of tissue, the septic changes, or the effusion of blood.

By the sixth to the fifteenth day the acme has been reached. The alæ of the nostrils are glued together by the drying discharge, and this, with the general swelling of the nasal passages, renders the breathing snuffling and difficult. The lymphatics on the side of the face are usually inflamed and corded, and the same is true of the cutaneous lymphatics of the hind limbs of some other part of the body (farcy). Death usually ensues from suffocation, preceded by the most painful dyspnoea.

Chronic glanders in horses often sets in insidiously, but frequently also it first shows itself by constitutional disturbance, which gradually subsides as the local lesions are formed. Among frequent premonitory symptoms may be mentioned intermittent or continued lameness, oedema of one or more limbs, infiltration of the testicle, cough, and bleeding from the nose. The general health may appear good, and if in good hygienic condition the digestion and nutrition may be sufficient, the body plump, and the skin shining; but there is usually some dulness of the eye, dryness of the coat, lack of endurance, and a tendency to sweat easily and to run down rapidly under hard work or debilitating conditions. The discharge, at first clear, becomes turbid, grayish, sticky, and purulent, tending to agglutinate the hairs and edges of the alæ nasi, and is expelled by snorting in masses. The nasal mucosa, and especially over the septum, is the seat of the peculiar elevations, ulcers, and firm white, condensed deposits resembling cicatrices, usually low enough down to be seen or felt. The submaxillary lymphatic glands are the seat of the nodular enlargement described in acute glanders, and, as in that affection, there may be pulmonary or skin deposits shown by cough or oedema, with swelling and cording of the cutaneous lymphatics with nodules and ulcers.

These cases often maintain this indolent type for years, spreading the {916} infection widely, but they tend sooner or later to develop the acute type, especially under some debilitating conditions.

When the mucous membrane of the larynx and bronchi is first attacked the nasal lesions may be delayed for a time, but the cough, the variously colored tenacious expectoration, the excessive tenderness of the larynx, and the nodular enlargement of the adjacent lymphatic glands, with the general ill-condition, suggest that which is later confirmed by the specific lesions in nose and skin.

When the affection is confined to the bronchia and pulmonary parenchyma, there are the usual signs of bronchitis, disturbed breathing, with hard, soft, mucous, or dry husky cough, and blowing, mucous or sibilant râle, at points crepitation, and at others some diminution of murmur and resonance. The breath is mawkish or fetid, and expectoration more or less sticky and charged with bacilli; but all these symptoms are at times equivocal, and inoculation alone can attest the true nature of the disease. This should be practised by preference on a donkey or an old horse in poor condition but with general good health. Then the disease shows itself in the acute form in six days. If solipedes are not available, rabbits or guinea-pigs may be used for inoculation.

In acute cutaneous glanders or farcy, premonitory symptoms resemble those of ordinary acute glanders, which indeed is usually present as well, and always supervenes before farcy terminates in death. The local lesions consist in inflammation of the lymphatic vessels, which become like firm cords, the appearance at intervals along these cords of rounded glanderous nodules varying in size from a pea to a hickory-nut, and with a marked tendency to ulceration and the formation of hot, painful oedematous swellings. The swelling of the lymphatics appears by preference in the lower part of a hind limb, and the first nodules may be near the fetlock or tarsus. The ulcers forming about the sixth day have a yellowish-white appearance with red points and raised irregular borders, and the discharge is grumous and viscous, with a yellowish or reddish tinge. The disease extends toward the body, the upper air-passages become involved, and death speedily follows.

Chronic cutaneous glanders, chronic farcy, usually begins by a local swelling, mostly of the fetlock, in the midst of which a careful examination detects a small glanderous nodule. This tardily softens, ulcerates, and discharges the characteristic ichor, the lymphatics leading up from it become thick and rigid (corded), and new nodules appear. Though very indolent, these finally tend to ulcerate, and in time oedematous swellings appear in the vicinity or at distant parts of the body, with nodules at intervals. This will go on for months, or even for years, and recoveries occasionally take place, while in other cases, and especially when the conditions of life are bad, acute glanders supervene.

MORBID ANATOMY.--The lesions consist essentially in a cellular growth in the connective tissue, determined by the presence of the specific poison, and in destructive changes in the elements of such growth--softening, fatty degeneration, ulceration, and discharge. In certain cases of nasal glanders at the earliest stage there is merely an increased proliferation of the mucous corpuscles, which become more granular or purulent. Soon, however, the fibro-vascular layer is involved, the affected part being the seat of dark bluish congestion, and {917} of the proliferation of small rounded lymphoid cells, comparable to those of the early stage of tubercle, and enclosed in more or less dense fibrous areolæ. The common nasal nodule or patch has a soft velvety surface, dirty gray or grayish yellow, and the lymphoid cells are so circumscribed in nests that when soaked in water the cells are washed out and the fibrous reticulum is left hollowed out like a honeycomb. In this fibrous reticulum are many spindle-shaped and a few rounded cells. Its vascularity is easily demonstrated by injection. The centre of each nest is the palest part of the mass, and unless stained by extravasation it contrasts with the reddish areola. These islets of lymphoid cells, at first isolated and each the size of a pin's head, may enlarge and become confluent, forming the larger nodules. With this increase the centre of each becomes turbid, and the cells are found to have become granular and fatty, and to have in part broken up into a granular débris. This characterizes the period of ulceration, and erosions and ulcers follow in ratio with the extent of the neoplasm and the rapidity of its growth. If the growth is tardy, the ulcer, with irregular eroded and everted edges, may remain for some time stationary or even recede, while if rapid, new tubercles form around the margin of the first, and by the disintegration of their elements the ulcer is continuously extended. The lesions are especially common on the septum nasi and turbinated bones. Similar lesions may be found in the nasal sinuses or larynx.

The nodules found in the lungs strongly resemble miliary tubercles, but are usually less numerous. As in the nose, they have a punctiform, central, grayish, turbid portion, encircled by a more translucent ring, surrounded in its turn by a vascular area. They are also composed of the same granular rounded cells, though they may, especially in the chronic forms, have undergone caseous, fibrous, or calcareous degeneration. The acute tubercles are often surrounded by circumscribed pneumonia with considerable exudation. They are distinguished from genuine tubercle by their vascularity and by the absence of giant-cells.

The cutaneous deposits are composed of the same histological products imbedded in the dermis or in the subcutaneous connective tissue, and extending in some cases deeply between the muscles, with no clear line of demarcation from the sound tissue. Not only the chains of nodules (farcy-buds), but the connecting lymphatic trunks, are the seat of the characteristic cellular product, and in chronic cases there is the enlargement of the adjacent lymphatic glands as well. In these there is a special tendency to early disintegration and ulceration.

In the diffuse glanderous swellings (infiltrated glanders, inflammatory glanders) the affected tissues are the seat of an inflammatory process with profuse exudation throughout, while in the interstices of the connective tissue are numerous granular glander-cells. The same tendency to necrobiosis is shown as in the other forms of glanderous neoplasms, and such diffuse swellings become the seats of very extensive, deep, and irregular ulcers, or frequently of fibroid growth and induration, forming the so-called cicatricial deposits. These are hard, firm, and resistant, and histologically consist of a dense fibrous stroma interspersed with the spindle-shaped cells. They are especially common in chronic cases, and such an appearance on the nasal mucous membrane is always suspicious, as this dense fibroid appearance rarely follows a simple traumatic lesion.

{918} Diffuse glanderous infiltrations in the nose may implicate the entire mucosa of one or both nasal chambers, and the ulcers are liable to be greater than from the nodular form of the disease. They are also especially associated with thrombosis of the veins, which occurs to a less extent in the nodular form and conduces to the dark-blue tint of the mucosa.

Glanderous infiltration of the lungs is inflammatory in its nature (pneumonia malleosa), attacking an area of two or three inches in diameter at or near the margin of the lungs, and proceeds to caseous necrobiosis, suppuration, calcification, or fibroid induration. In the skin such infiltrations also frequently terminate in induration, while ulceration and abscess tend to appear when the proliferation of glander-cells is most abundant (farcy-buds).

The glander-nodules are not uncommon in muscles, intermuscular connective tissue, spleen, liver, kidneys, and testicles. Leukæmia is also a constant feature, the irritation of the lymphatic glands manifestly stimulating the production of the lymph-cells.

DIAGNOSIS.--The diagnosis of glanders usually rests on the viscid nature of the discharge, the painless nodular swelling of the submaxillary glands and the indisposition to suppurate, the characteristic appearance of the nodules, elevations, ulcers, and indurations of the nasal mucosa, and the presence of the specific bacillus. The diagnosis of farcy rests mainly on the nature of the nodules and corded lymphatics, of the ulcers and their discharges, on the extension of the affection toward the trunk, and the tendency to implicate the respiratory organs. Usually, there are several victims, the earlier ones chronic cases, the later ones acute, or there is a history or presumption of exposure. Yet in many cases, and especially in the more chronic internal forms (laryngeal, pulmonary, etc.), the diagnosis is difficult, and inoculation of a horse, goat, sheep, or rabbit may be the only available means of reaching a decision. Auto-inoculations are unreliable, as parts not yet the seat of active disease will often resist inoculation.

PROGNOSIS.--This is always unfavorable. The constancy of internal deposits and the viability of the germ in such products render it impossible to eliminate the poison from the system in the great majority of cases. In external glanders only is there any reasonably good hope, and even this is confined to the chronic cases. In stating this much, it is not denied that recoveries even of chronic nasal glanders do occur, yet these are few, and the majority of those that do apparently recover usually succumb as soon as they are subjected to hard work or specially trying conditions of life, so that but little faith can be placed in most of the alleged recoveries.

TREATMENT.--Considering the great danger of multiplying and preserving the germs of a disease so fatal alike to man and beast, the treatment of glanders is never commendable. The danger is least in the case of chronic farcy, not only because the processes are less active, but because the virus is not being thrown out and diffused with the tidal air of respiration, sneezing, and coughing. The unbroken farcy-buds and swollen lymphatics may be actively treated by compound iodine ointment, and the ulcerous nodules freely cauterized with corrosive sublimate, biniodide of mercury, chloride of zinc, sulphate of copper, or iodized {919} phenol. Local inflammations may demand fomentations and astringent antiseptic lotions. Meanwhile, the system must be supported by a tonic regimen and medication, abundance of pure air, a liberal and wholesome diet, and the maintenance of the various bodily functions in a healthy condition. Of medicinal agents the most pronounced tonics have the best reputation--sulphate of copper and iron, biniodide of copper, arsenic, and, above all, arsenite of strychnia. Next to these the sulphites rank, and a combination of the two last named is perhaps to be preferred.

PREVENTION.--The glandered horses and all animals attacked with acute or obstinate farcy should be destroyed and their bodies be burned or deeply buried. Every State should legally interdict the use of a glandered horse or his exposure in any public or other place where infection is likely to reach other animals by contact or through fodder, litter, stable utensils, or any other objects employed about animals. No less imperative should be the perfect disinfection of all stables, harness, and other objects with which glandered animals have come in contact. The value of such measures is sufficiently attested by what has been stated above as to the prevalence of this disease in the French army so long as the doctrines of non-contagion dominated in its management, and the comparative disappearance of the disease so soon as a change of theory and method had been inaugurated; the absence of the disease in the English army, where the doctrine of contagion and its extinction has long prevailed; and the entire absence of the disease from Australia, New Zealand, etc., into which it has never been imported, though prevailing in a corresponding latitude and climate at the Cape of Good Hope.

Glanders in Man.

Up to 1812 the communication of glanders to man failed to be recognized. Then Lorin, a French surgeon, published a case of the kind in which inflammation of the hand was induced by inoculation from a horse suffering from farcy, and Waldinger and Weith drew attention to the dangers of infection about the same time. In 1821, Muscroft in England and Schilling in Germany simultaneously reported cases of infection from the horse in which the true symptoms of glanders in man were recognized. Rust, Sedow, and Weiss soon followed with additional cases; then Forozzi (1822), Seidler (1823), Wolff, Grossheim, Eck, Brunslow, Lesser, Travers (1826), Kries, Grubb, Brown (1829), Neumann (1830), Vogeli (1831), Alexander (1832), and Elliotson (1833). Though the disease was now well recognized, yet its nature has been elucidated by a series of later writers, including especially Rayer, Tardieu, Virchow, Leisering, Gerlach, and Korányi.

ETIOLOGY.--Man is rarely infected from any other source than the horse. In a very few instances the contagion has been derived from infected men. The modes of infection, immediate and mediate, are the main points to notice in this connection. Those employed about horses are usually infected by direct contact of the poisonous discharges, blood, or tissues with abrasions on the skin or mucous membranes. The inoculation received in giving medicine, examining the nose, performing operations with effusion of blood, dressing cutaneous ulcers, slaughtering, {920} skinning, making a necropsy, burying, etc., is not uncommon. Again, direct infection is sustained through snorting of the horse, so that particles of the virulent discharge are lodged on the mucous membrane of the eye or nose. Closely allied to this is infection by inhaling the exhalations of glandered horses, and this doubtless accounts for some few cases which have been recorded as communicated through the unbroken skin. The bite of the glandered horse is a rare means of infection. From infection by eating glandered animals man is usually saved by the cooking of his food and by his inherent power of resistance, yet with instances of this kind on record, as recorded by Ringheim, and the well-known conveyance of the disease to animals in this way, it would be folly to ignore the risk to man from eating the flesh of glandered horses, sheep, goats, and rabbits.

Among the mediate forms of contagion may be named drinking from the same pail or trough after a glandered horse, using a knife that has been employed to open a glanderous abscess, wiping a wound with an infected blanket or handkerchief, handling infected harness, wagon-pole, or manger with wounded hands, sleeping over glandered horses or in a stall or on litter previously used by such horses.

Conveyance of glanders from man to man has taken place through using or handling the same dishes, towels, or handkerchiefs, through dressing the wounds, or, as in the case of the veterinarian Gerard, through making an autopsy of a victim of the disease.

Fortunately, the susceptibility of man is slight, but few out of the multitudes handling glandered horses becoming infected. It is essentially an industrial disease, 114 cases being distributed as follows among the different occupations: hostlers, 42; farmers and horse-owners, 19; horse-butchers, 13; coachmen and drivers, 11; veterinary surgeons and students, 10; soldiers, 5; surgeons, 4; gardeners, 3; horse-dealers, 2; policemen, shepherds, blacksmiths, employés at veterinary school, and washerwomen, 1 of each.

A condition of ill-health doubtless predisposes to this as to other invasions of infectious disease, yet men in apparently the most vigorous health have succumbed to the poison.

SYMPTOMS.--The incubation of acute glanders in inoculated cases usually varies from one to four days. In cases in which the mode of entrance is not so manifest it may apparently extend over one, two, or even three weeks. If the disease has occurred by external inoculation, the seat of the wound shows the first symptoms, consisting of tense swelling, pain, and a dark or yellowish erysipelatoid redness, while the edges of the wound are puffy and everted, the matter escaping is sanious, and the surrounding lymphatics are swollen and red and the lymphatic glands enlarged and tender. After a few days constitutional disorder sets in--languor, extreme weakness and prostration, aching in the limbs (muscles and joints) and in the head, rigors alternating with fever or a continued fever after the first violent chill, and in some cases nausea, vomiting, and even diarrhoea. In cases not resulting from external inoculation the febrile symptoms are the earliest to be noticed, and the muscular and articular pains may be at first mistaken for acute rheumatism. In other cases, in which the gastric and intestinal disorders are the most prominent and the prostration and weariness extreme, the symptoms at first strongly {921} suggest typhoid fever. Soon, however, with a sense of formication a local yellowish or livid erysipelatoid inflammation appears, by preference on the softer parts of the face, the nose, eyelids, cheeks, or on one of the principal joints, the shoulder, elbow, or knee. In the midst of the phlegmonous swelling, or even antecedent to it, there appear small firm red spots or nodules, sometimes as small as those of variola, at others like a pea or as large as a walnut or larger. These gradually blanch in the centre, soften, and change into pustules or abscesses, and, bursting, discharge a slimy, thick, sanguineous pus, often emitting a mawkish or fetid odor. The sores thus formed are ulcerous and unhealthy, with puffy, ragged, everted borders and a grayish or yellowish red base, which often extends deeply between the muscles and exposes tendons and bones. When several deposits of this kind are closely aggregated, they tend to combine in one slough, which may involve a great extent of tissue. In all cases there are the swollen, reddened, tender condition of the connecting lymphatics and the tumefaction of the lymphatic glands. At times the deposits and abscesses are deeply seated in the interstices of the muscles, and at other times the joints are enlarged by exudation.

In nearly one-half of the cases glanders supervenes on the cutaneous symptoms. At first a viscid, whitish nasal catarrh appears from one or both nostrils, mixed with striæ of blood; then upon the pituitary membrane appear ulcers like those already described in the horse; the same form on the buccal, pharyngeal, and laryngeal mucous membranes, and by physical examination they may even be found to have invaded the lungs. The margins of the nostrils become adherent through the drying of the tenacious mucus; the meati are blocked or narrowed by the swelling of the mucosa, the detachment of sloughs, and the accumulation of the discharges; the breathing becomes snuffling and difficult; the voice altered or lost; the cough weak, with a mucous and bloody expectoration, and the breath offensively fetid. The submaxillary lymphatic glands are inflamed and enlarged, and may even go on to suppuration and ulceration. The conjunctiva is usually involved, and at times the specific formation and ulceration extend to the stomach and intestines, and nausea, vomiting, indigestion, irregularity of the bowels, and fetid diarrhoea ensue. There is complete anorexia, but thirst is ardent, especially with diarrhoea. With the advance of the disease dyspnoea supervenes, and nervous disorder is shown by the extreme weakness, anxiety, sleeplessness, troubled dreams, nocturnal delirium, dilated pupils, and even coma. The temperature, though at first unaltered, may later rise to 104° F., and the pulse to 110 to 120 beats per minute. The diagnosis is confirmed by detection of the bacillus in the discharges, and, above all, in the liquids of freshly-opened pustules (Wassilieff).

The duration of acute glanders in man may be no more than three days, though usually it is protracted to fourteen or twenty-one, and exceptionally to twenty-nine days. The almost constant termination of this form of the disease is in death.

Chronic glanders occasionally appears in man, and is in most respects the counterpart of that of the horse. The morbid process shows itself in the integumental or other tissues of the body, and only attacks the nose and air-passages later, when the constitutional symptoms become more intense. The general malaise, languor, prostration, aching of {922} limbs and joints, and inappetence are usually present, complicated by a local swelling in the seat of inoculation (face, hands, etc.), with small nodules progressing to pustules, congestion of the lymphatics, and swelling of the lymphatic glands. These lesions may subside even before suppuration, and the disease is manifested for a week or two only by a general feeling of weariness and ill-health; but sooner or later the local symptoms reappear in the same or another seat, and the neoplasms, though indolent for an indefinite length of time, finally degenerate, soften, burst, and form ulcers. These ulcers have the general characters already described--a livid grayish or yellowish hue, with red, puffy, irregular edges, and a viscid greenish, yellowish, dirty white, or bloody discharge. They tend to increase, or they may appear to heal by the peculiar firm cicatricial formation, but on the swollen margins new deposits, abscesses, and ulcers tend continually to form. Sometimes these are of considerable size and seated deeply among the muscles, but when opened they show the same unhealthy serous or bloody pus, and manifest a tendency to extension rather than to healing. When the disease extends to the respiratory organs, often two or three months after the onset, there is cough and sore throat, blocking of the nose by the tenacious discharges and swollen mucosa, and in the pharynx, fauces, and nose the characteristic ulcer may be detected. The attendant constitutional symptoms are also much more marked--indigestion, nausea, vomiting, diarrhoea, rigors, profuse perspiration, high temperature, excited breathing and pulse, a yellowish or earthy hue of the skin, rapid emaciation, and great prostration. Though great emaciation, debility, and hectic ensue on the indolent chronic processes, yet the disease usually assumes all the characters of the acute type before terminating fatally.

In cases that recover the fever diminishes, exacerbations cease, ulcers granulate and cicatrize, vesicles dry up, the nodules and enlarged glands diminish, the erysipelatoid swellings of skin and nose subside, and a very tardy and imperfect convalescence is established.

The duration of chronic glanders, nasal or cutaneous (farcy), is exceedingly indefinite, varying from three months to ten or eleven years. One of the most protracted cases is that recorded by Bollinger of a veterinarian who, after an eleven years' illness, recovered with cicatricial contraction of the nose and larynx and a decided cachectic appearance.

MORBID ANATOMY.--Besides the lesions above mentioned as occurring in the skin and mucous membranes of the nose, mouth, and pharynx, the frontal sinuses, the larynx, and less frequently the lungs, are the seats of the specific glanderous processes. In the lungs there are then the nodules, hard, caseous, or purulent according to their age, and varying in size from a millet-seed and pea upward to the involving of the greater part of a lobe. Beneath the pleuræ may be seen ecchymoses, hard, fibrous nodules, and yellow elevations, which on being incised furnish grumous pus. The spleen is usually enlarged, gorged with blood, gray or black, and is the seat of suppuration. The liver is enlarged, softened, and may be the seat of glanderous processes, with ulcers in the bile-duct or gall-bladder. The joints, like other serous cavities, become the seat of specific suppuration. The bones are often implicated in adjacent deposits, especially in the face, cranium, and hands, so that the compact tissue may become reduced to the merest shell, while the medulla and periosteum {923} abound in the specific products. The cerebral meninges and brain-tissue are frequently the seat of specific growths and minute abscesses. It is noticeable that the enlargement of the lymphatic glands is usually less than it is in the horse, though they are never entirely free from lesions. Indeed, the tendency in man to the formation of considerable glanderous neoplasms is much less than in the solipede.

The microscopy of the lesions is essentially the same as in the horse. O. Wyss describes the cutaneous nodules as formed by a great proliferation of round cells (like pus-cells) in the upper layer of the corium just beneath the papillary layer. In a more advanced stage the corium and papillæ are filled with pus-cells, and, becoming disorganized, give rise to the formation of pustules and small abscesses. Lagrange describes in a chronic ulcer of the palm, a layer about 2 mm. in thickness of embryonic cells closely packed with an amorphous intercellular substance. The nuclei appeared larger than in ordinary ulcers or tubercles. Extending into this layer were capillary vessels packed with red globules and with blind extremities, or in some instances minute ruptures and hemorrhages. Beneath this superficial cellular layer was a stratum of striated muscle, especially noticeable for the excess of condensed connective tissue making up the intermuscular septa, and the great multiplication of nuclei with large, clearly-defined nucleoli, not only inside the sarcolemma, but also between the fibrillæ and separating them widely. At some points the muscular tissue had undergone a vitreous degeneration, while at others were many fusiform cells. At one point, where the ulcer extended to the phalanx, the compact layer of the bone was attenuated to the thinnest shell and perforated, so that the medulla was continuous with the ulcer. The medulla contained a great number of white globules, medulla-cells, and minute embryonic nuclei. The vessels were remarkable by the extensive fibroid thickening of their coats. On section of the ulcer many orifices stood widely open because of the rigidity of their walls. The internal coat was plicated, as if too large for the lumen. The external fibrous layers were at points abundantly interspersed with, and even replaced by, groups of embryonic cells, the active proliferation of which meant the destruction of the perivascular fibrous layer. These embryonic cells even invaded the lumen of the vessel and partly blocked it, so that the remnant of the tube remained as the centre of a disintegrating mass, or later a caseous or purulent focus.

DIAGNOSIS.--Acute glanders, when well developed, is unmistakable. The presence on or near the skin of the characteristic nodules, pustules, phlyctenæ, and ulcers, the oedema or erysipelatoid condition of the adjacent skin, the redness of the lymphatics, the presence of the neoplasms and ulcers in the nose, and the sticky, fetid, variously colored nasal discharge, with the acute fever, prostration, and pains in the limbs and joints, make a tout ensemble that is pathognomonic. In the initial stage only it may be confounded with rheumatism, but the arthritic pains are not usually attended by the same amount of redness and swelling of the joints, the prostration is far more profound, and there are in most cases an irritable, unhealthy-looking wound and a history of exposure to infection from glandered horses.

In chronic glanders, and especially in the external form (farcy), the diagnosis is often more difficult. From pyæmia and septicæmia it is {924} usually to be distinguished by the comparative absence or the slightness of the chills, by the less healthy character of the pus, and by the implication of the nasal mucosa, the larynx, and lungs. When the nose, larynx, or lungs are but slightly affected, there may be a strong resemblance to syphilis or miliary tuberculosis, but a close attention to the character of the lesions, the absence of any concomitant history or symptoms of syphilis, and deductions drawn from the occupation of the patient and the presumptive exposure, will greatly assist in reaching a diagnosis.

The detection of the bacillus is not conclusive, as in tuberculosis and some forms of septicæmia there are similar organisms, agreeing with the microbe of glanders even in the matter of size. In cases of doubt a little delay will usually allow the development of new and more characteristic symptoms.

The final resort, however, is to inoculation. Auto-inoculation, as practised by Poland, is rarely satisfactory, as the system has acquired a partial tolerance of the disease and local lesions are not so certainly developed as in the healthy subject (St. Cyr). Inoculation on a healthy goat, sheep, or rabbit can always be availed of, and if practised on more than one subject can be relied upon, as the virus loses nothing of its power in passing through the human system, but usually determines an acute form of the disease in the animal inoculated.

PROGNOSIS.--Acute glanders is almost constantly fatal to man. Of chronic cases, and especially the external form (farcy), from one-third to one-half of the subjects recover. When both internal and external (farcy--glanders), the issue is usually fatal. Kütner claims that cases caused by external inoculation are more favorable than those caused by the inhaled poison. This accords with the general principle, that a poison viable in the comparatively vitiated air of the lungs or on the surface of the intestinal canal is better fitted by its habit of life for survival in the blood and plasma, and is consequently more redoubtable. The greater the duration of the disease in any particular case, the more favorable is the prognosis.

TREATMENT.--In the treatment of glanders in man the same principles must guide as in animals. In external, inoculated cases the wounded tissues should be early destroyed by potent caustics--fuming nitric acid, corrosive sublimate, iodized phenol, chlorine, sulphate of copper, carbolic acid, or the hot iron. The erysipelatoid swellings may be treated by leeching, followed by solutions of carbolic acid, iodine, or chlorine-water, by ice, and internally by laxatives and iodide of potassium. The first two antiseptics may be freely used by hypodermic injection. Abscesses and tumors should be laid open and cauterized as above, and then treated by weaker solutions of the same agents. Nasal ulcers may be treated by insufflation of iodoform and injections of creasote, carbolic acid, nitrate of silver, or permanganate of potash solutions. Of the greatest importance is a general tonic and stimulating regimen. A nutritious diet (including beef-tea), abundance of pure air, alcoholic stimulants, quinia, tincture of the chloride of iron, and, above all, arseniate of strychnia, have been used with advantage. Various anti-ferments, such as the bisulphites in full doses, carbolic acid, and iodide of potassium, have apparently proved beneficial, and deserve a further trial. As in the horse, a great {925} variety of other agents, mostly of a tonic nature, have been employed, but with very variable results.

PREVENTION.--The first step toward the prevention of glanders in man is the systematic restriction and extinction of the affection in animals. This has been already sufficiently referred to above. Further measures of prophylaxis embrace the following: the avoidance of contact with glandered and suspected horses by all persons having any wounds, abrasions, or ulcers on their skins; the cauterization with nitrate of silver of all such sores on persons necessarily brought in contact with glandered or suspected animals or their products; the general diffusion of information as to the danger from glandered animals; washing of hands and face in a solution of carbolic acid or chloride of lime after handling infected or suspected animals or their carcases or products; the thorough disinfection or destruction (preferably by fire) of harness, clothing, racks, mangers, wagon-poles, buckets, troughs, brushes, combs, litter, and fodder that have been exposed to infection; and, finally, the exclusion from the markets of all meat derived from suspected or infected animals. It is generally held that the flesh of the horse alone demands inspection, but with the known susceptibility of sheep, goats, and rabbits it can easily be conceived how the infection may reach man through his food, though horse-flesh is never consumed. That glanders has never been recognized as arising from the consumption of diseased sheep or rabbits does not prove that it has never reached man by this channel, any more than the absence of all recognition of the infection of man from the horse would prove the non-occurrence of such infection until the beginning of the present century. The knowledge that the animals used for food in this country are liable to contract and convey this disease is an additional reason for the systematic and universal suppression of the disease among the equine population.

{926}

ANTHRAX (MALIGNANT PUSTULE).

BY JAMES LAW, F.R.C.V.S.

SYNONYMS.--_Latin_, Ignis Sacer, Anthrax Epizoöticus, Pustula Maligna, Pustula Pestifera, Erysipelas Carbunculosum, Carbunculo Contagioso, Glossanthrax, Angina Carbunculosa, Anthrax Hæmorrhoidalis, Mycosis Intestinalis, Apoplexia Splenitis, etc. _English_, Black Erysipelas, Malignant Vesicle, Anthrax Fever, Splenic Apoplexy, Splenic Fever, Inflammatory Fever, Carbuncular Fever, Black Quarter, Blood-Striking, Bloody Murrain, Blain, etc. _French_, Pustule maligne, Charbon, Fièvre putride, Typhohémie, Pélohémie, Mal de Rate, Splenite Gangréneusé, etc. _German_, Karbunkelkrankheit, Contagiose Karbunkel, Milzbrand, Milzseuche, Milzbrandfieber, Brandbeulenseuche, Rothlauf, etc. _Russian_, Jaswa (boil-plague). _Italian_, Antrace. _Spanish_, Carbunculo, Lobado. _Swedish_, Boskapssjukan. _Mexican_, Calentura del piojo.

DEFINITION.--Anthrax is an acute, infectious, bacteridian disease, occurring mostly in the Herbivora and Omnivora, but communicable to other mammals (including man), to birds, and even fishes. Its local manifestations are exceedingly varied in kind, but the malady is characterized by the presence in the tissues or blood, or both, of specific spherical and linear bacteria (micrococcus and bacillus anthracis), leading to arrest of hæmatosis, to disintegration of the blood-globules, to sanguineous engorgement of the spleen, to capillary embolism, and to a spreading gangrenous inflammation.

HISTORY AND GEOGRAPHICAL DISTRIBUTION.--While ancient history is not clear as to the specific diseases of animals, yet there is the strongest presumption that nearly all great plagues that attacked indiscriminately animals and man were of this nature. Thus, the plague of murrain, with boils and blains breaking out on man and beast, in the days of Moses, was probably of this kind (Gen. ix. 3.); also that which at the siege of Troy extended from animals to man, and many later epizoötics in all parts of the world. No infectious disease of man and animals, with the single exception of tuberculosis, has been more widely diffused, and none can be considered as more cosmopolitan. Heusinger, in his classic work on _Milzbrandkrankheit_, traces the ravages of the disease from the highest to the lowest latitudes in the northern and southern hemispheres and in the Old World and the New. He adduces outbreaks in Siberia, Astrakan, Lapland, and Finland, in Russia, Prussia, Poland, Silesia, Bavaria, Holland, Belgium, France, Spain, Portugal, Italy, Switzerland, Austria, Hungary, Greece, Turkey, Egypt, East and West Indies, {927} North and South America, etc. We can now add all the great English, French, and other European colonies not included in the above (South Africa, Australia, New Zealand, Algeria, etc.), together with China and Japan. We find, moreover, that the disease is always most prevalent where agriculture is in its most primitive condition, so that there can be little doubt of the prevalence of the affection in the less-civilized countries as well. But while the disease is prevalent in all parts of the world, its ravages are largely subordinate to the nature of the soil. Wherever this is close, impervious, marshy, or charged with an excess of organic matters, the gaseous emanations of which drive out most of the oxygen, the anthrax-germs, once introduced, tend to be preserved indefinitely. Thus, in drying up basins with no natural drainage, on lake and river margins, on deltas, in forests, in mucky, mossy, or peaty soils, and on those that are habitually over-manured, the germs of anthrax are especially liable to be perpetuated. It has long been noticed that herbivorous animals are the most susceptible to anthrax, while the purely carnivorous, and to a less extent the omnivorous, have relatively a far higher resisting power. That the immunity is largely due to the food is manifest from the experiments of Feser on rats. Those fed on vegetable aliment contracted anthrax readily from inoculation, while those kept on an exclusive diet of flesh successfully resisted. The same rats that escaped while on a flesh diet were afterward placed on a vegetable diet, and then perished after inoculation.[1] Davaine found the same to be true of foxes kept on meat and vegetables respectively, and inoculated with the virulent blood of the allied disease, septicæmia. He found, moreover, that guinea-pigs were much more susceptible to anthrax than rabbits. One-thousandth of a drop of virulent anthrax blood invariably killed the guinea-pig, while it left the rabbit unharmed.[2] Klein has never found a rabbit insusceptible. It has recently been claimed that pigs are insusceptible, but I have known of many instances in which the offal of anthrax cattle, when devoured by pigs, has determined fatal anthrax in the latter. Chickens too prove much less susceptible to anthrax than the Herbivora. Inoculations made by Cohn and others proved invariably unsuccessful, while Pasteur has showed that they can be infected easily after the body has been cooled by partial immersion in cold water.[3] Pasteur attributes this immunity to their normally high temperature, yet rabbits, sheep, pigs, wolves, and foxes, though maintaining a correspondingly high temperature, are still subject to anthrax. Even the herbivorous mammal suffering from acute anthrax fever has its temperature raised to that of the chicken, yet the disease progresses none the less surely to a fatal result. Again, anthrax liquids inoculated under the skin of a fox proved harmless, while if thrown into the warmer peritoneal cavity they proved fatal. It may well be suspected that the relative insusceptibility of chickens is in part due to the large amount of animal food consumed by them, and that the chilling process increases the receptivity by deranging sanguinification and nutrition.

[Footnote 1: _Wochenschrift f. Thierheilkunde und Thiersucht_, Nos. 24 and 25, 1879.]

[Footnote 2: _Rec. de Med. Vet._, Mar. 15, 1879.]

[Footnote 3: _Ibid._, Mar. 15, 1880.]

The insusceptibility to anthrax is often characteristic of certain individuals or families or of the animals living in a particular district. Thus, Chauveau found that some French sheep, and nearly all Algerian ones, {928} resisted inoculation with a moderate amount of anthrax virus, while the introduction of a maximum amount proved fatal to these as to others. In the same way, it is often noticed that animals living in an anthrax region escape the evil effects of the poison, while strange animals brought in either fall ready victims or for a time do badly until they have become habituated to the locality. In view of the subsequent protective effect on the system of a first and non-fatal attack of anthrax, it is probable that all these examples of immunity in the Herbivora depend on a previous mild attack of the same disease or on the extinction of the more susceptible races. Even in the case of the animals that do badly on first coming into an anthrax district, and recover better health with immunity later, we may well infer that a mild form of the anthrax infection has been passed through.

ETIOLOGY.--The one essential cause of anthrax is the introduction into the system of a specific bacteridian germ (bacillus anthracis or its spores). This is not, as a rule, carried far on the atmosphere, but demands for its propagation contagion, immediate or mediate. Unless, therefore, it meets in the soil the conditions necessary to the preservation and propagation of the germ, it is transmitted with some uncertainty from animal to animal, and thus the disease does not spread widely and rapidly, like an ordinary plague, but tends to become localized in particular districts as an enzoötic.

But its dangers are none the less real nor its existence less to be dreaded. In predisposed localities, where the disease-germ has gained a footing, the animal mortality may exceed that caused by the great plagues, while the risk to human beings is incomparably greater than from any other acute infectious disease of the lower animals. Thus, in San Domingo, in 1770, 15,000 people perished in six weeks from eating the carcases of anthrax animals, and the mortality was only arrested when the meat was legally interdicted. In the worst anthrax years on some of the Siberian steppes as many as one-fourth of the whole human population suffer from the malady. The prevalence and death-rate, however, vary greatly in different localities and seasons. Sometimes only one or two solitary cases of the affection are observed; at other times the disease becomes moderately prevalent, but a lack of virulence in the poison or a previously acquired insusceptibility of the individual protects the great majority of the animals exposed, while at others, still, the poison attacks nearly all exposed to its contagion.

The animal products that mainly convey the disease are the blood, the liquid exudations, portions of the diseased carcase, and the bowel dejections. The virus is most potent when derived from an animal still living or only recently dead, yet under certain conditions (with spore-formation) it may long retain its virulence under the most extreme changes of climate, temperature, dryness, and humidity. Russian hides tanned in England or America frequently convey anthrax, which is known especially as a tanner's malady, and wool and hair sent from Buenos Ayres have repeatedly produced malignant pustule (woolsorter's disease) in Britain and the United States. The preserved scabs of malignant pustule have been often successfully inoculated on the lower animals, so that, like other forms of poison, this seems to be preserved indefinitely by desiccation.

The simple contact of the virus with the slightest abrasion will suffice {929} to convey the disease. It has often been communicated where no lesion of the epidermis could be found, yet the presumption is that even in such cases the cuticle had been in some way wounded. Eating the flesh of animals killed while suffering from anthrax has often conveyed the disease. In an outbreak in Swineshead, Lincolnshire, England, in 1863, I found a dog and a number of swine suffering from eating the bodies of dead bullocks. In 1864 an East Lothian (Scotland) farmer fed his pigs with the offal of a slaughtered anthrax bullock, and lost nearly the whole herd. The carcase of the bullock had been sent to market. About 1860 cattle, and even horses, died yearly on a swampy meadow at Brighton, Mass. On one occasion the owner, John Zoller, fed the offal of a dead bullock to his pigs, which were speedily attacked with anthrax, and as speedily killed to save their bacon (Dr. Thayer). Even when cooked the flesh is not always safe. Of this we have the undoubted case in San Domingo above noticed, the alleged death of 60,000 people in the vicinity of Naples from the same cause in 1617 (Kircher), and the thousands that die on the Russian steppes every anthrax year from eating the sick horses (Rawitch). But in all these, and in the ever-recurring cases in which families suffer from eating anthrax meat, there is the possibility, if not the probability, of the contamination of the meat subsequently to cooking by the knives, forks, tables, and dishes used. The San Domingo slaves had few appliances for cleanliness, much less disinfection, and the Tartars eat their meat from the same board on which it has been chopped up raw.

In accurate experiments it has been found that the bacilli are destroyed by a temperature of 145° F. maintained for five minutes, but the spores are capable of surviving the boiling temperature for five or even ten minutes. The varying power of resistance may be compared to that of the green stalk of the pea and the dry flinty seed. The first is destroyed by a very moderate heat, while the second will sprout after having had boiling water poured over it. The resisting bacillus-spores are never found in the living animal, but may be developed in the blood and tissues after death, and may account for the occasional extraordinary viability of the poison when exposed to a boiling temperature.

Milk, though often used with impunity, conveyed the disease when inoculated by Bollinger, and the same was true of the vaginal mucus. Innocent in the early stages of the disease while the germs are still localized, they become virulent after the bacilli swarm into the blood.

Healthy men and animals often carry the poison, though themselves insusceptible. The question of its conveyance by insects has been much debated, but the constant occurrence of malignant pustule on the uncovered parts of the body goes far to settle the question. Bourgeois long ago noticed that it was most frequent on the face, hands, neck, and arms, and rare on the trunk. In sixty cases recorded by A. W. Bell of Brooklyn, all occurred on the face except two on the hands, one on the wrist, and one on the forearm. The bite of a fly or mosquito had in many of these cases proved the starting-point of the malady. Bollinger has shown the presence of the bacillus in the stomach of such flies as fed on flesh and blood (horse-flies, bluebottles, etc.), and, together with Raimbert and Davaine, has produced anthrax by inoculations with the stomachs, legs, and proboscides of these insects.

{930} Surgical instruments occasionally convey anthrax. At Cockburnspath, East Lothian, Scotland, a yearling heifer contracted anthrax, and the whole herd was bled, commencing with the sick one. Next morning seven were found dead, the disease in each case extending around the fleam-wound. At Brunt, in the same county, a shepherd skinned an anthrax bullock, and after washing and taking a turn among his sheep, on the same day castrated several litters of pigs, all of which perished. In St. Lawrence Co., N.Y., in 1870, a surgeon inoculated himself while opening a vesicle on the hand of a farmer.

Harness, stables, stable utensils, vehicles, fodder, and litter are frequent bearers of contagion. At Geneseo, N.Y., in 1877, three horses and a cat died in midwinter after licking the blood from a stone-boat which had conveyed the skin of an anthrax bullock to market. Green fodder or hay harvested from ground formerly occupied by anthrax victims or from their graves often convey the poison, but probably only by the adherent earth and dust containing the anthrax-germ.

That the anthrax bacillus and its spores may be long preserved in earth is abundantly proved. At Avon, N.Y., nine months after any cases of the disease, the liquid leaking out on the river-bank near to the grave of a victim of the year before was licked by six cattle, and in two days they all perished. On the same pasture victims were seized yearly for seven years, but with a rigid seclusion of these, their products, and their graves the malady has finally disappeared. The persistent deadly effect of some soils on animal life, apart from the presence of the carcases, seems to show that in certain soils we find the normal home of the anthrax bacillus, while the migration into the animal economy is but an accident of its existence. The soils that are especially subject to anthrax are the dense clays, the limestones, and the rich alluvials. Among the essential conditions are the exclusion of oxygen, excepting a limited amount bearing some relation to what is found in the animal fluids, and the abundance of some alkaline agent (lime, potash, soda, ammonia), so that the earth is either neutral or only very slightly alkaline or acid. An acid vegetable infusion is inimical to the germ, which soon disappears from such a medium. The requisite paucity of air is found in all the dense, less pervious soils (clays, etc.), in soils habitually waterlogged (swamps, deltas, river-bottoms, low meadows, natural basins, drying lakes and ponds), and in soils rich in decomposing organic matter (peat, alluvial, over-manured). The antacid is often found present as lime or potash, or is constantly being produced in the form of ammonia, etc. by organic decomposition. Such places are known to farmers as "dead lots," because no stock will live on them. The bacillus in the buried carcase does not produce spores (Bollinger), though it may in the soil at any temperature between 59° and 110° F. In the graves, therefore, at a lower temperature, the poison can only be preserved by a continuous generation of the bacillus.

Pasteur, who successfully inoculated the casts of earth-worms taken from anthrax graves, attributes to these an important rôle in bringing the germs to the surface. A more important agent, however, is probably the rise and fall of water in the soil. By this means the bacilli and spores are washed up toward the surface, and when the superficial layers dry out they are easily carried by the winds. Hence it is that anthrax is usually prevalent in late summer and when the soil is dried and heated to its {931} greatest depth. Thus it is, too, that wet seasons followed by specially dry and hot ones are, above all, productive of anthrax in herds. Wet seasons fulfil the further purpose of carrying off the germs into rivers and depositing them on the banks or on inundated meadows, where after the subsidence of the flood the disease appears, for the first time perhaps.

There is, however, good reason to believe that the effect of a warm season is not confined to its influence on the soil and its germs. The high temperature deranges the vital functions of the animal economy, and, inducing a febrile disturbance, lessens the power of resistance to the anthrax virus, just as the cooling of the warm-blooded bird lays it open to infection. On this account, and because of the frequently recurring electric storms, the hot dry season is especially the season of anthrax. The hottest, driest autumns of Siberia always coincide with the anthrax years, and in the last fifteen years in the United States I have noticed the wide extension of anthrax whenever the season has been unusually hot and dry. In Corsica the herdsmen confidently pasture their stock in the close still valleys throughout spring and early summer, but whenever the surface soil is dried out they make all haste to remove it to the hills, well knowing that delay means devastation and ruin.

Plethora is undoubtedly an important predisposing cause of anthrax, and so is the alternation of cold nights with hot days. The febrile condition induced in the animal economy is perhaps the main factor at work in each case. Finally, youth is on the whole more liable than age, but whether because of the greater receptivity of the growing system and its tissues, or because it has not yet acquired some immunity by exposure to the milder effects of the poison, is not certainly determined. Sex is without influence.

It is not a little remarkable that the bacillus germ has not yet been found in the placental liquids nor foetal blood of sheep, goats, or rabbits, though swarming in that of the mother. Bollinger attributes this to the action of the placenta as a "physiological filter"--a conclusion seemingly at variance with the passage of the bacillus through all the other animal membranes, including those lining the mammary glands and the vagina. Two other possible explanations remain: first, that the secretions of the uterine glands are inimical to the bacillus; and, second, that the foetus, being in some sense a carnivorous animal, possesses the immunity characteristic of Carnivora. Bacilli have recently been found in the foetal guinea-pig.

The bacillus anthracis was first observed by Pollender and Branel in 1849 (Birch-Hirschfeld), but it was only publicly claimed as the cause of the disease in 1855 by Davaine. Branel discarded Davaine's theory, because blood in which he had failed to find bacillus produced anthrax with bacillus in the blood of two foals inoculated. Later observations by Bollinger and others have shown that cultures of bacillus can always be made from such infecting blood, and that in most cases the presence in the infecting blood of spherical bacteria can be demonstrated by the microscope. That the bacillus is the true pathogenic element is proved by the following facts: 1st. That the bacillus is the only ectogenous, particulate, organized structure constantly found in the anthrax blood and fluids; in cases in which it is apparently absent cultures show its actual presence. 2d. After cultivation in pork or beef infusion to the {932} hundredth generation the virulence is unimpaired, though it must be assumed that all non-organized poisons derived from the infected animal body must have been diluted or decomposed to extinction. 3d. That filtration of the anthrax liquids through a plaster or other efficient filter renders the filtrate innocuous, while the solids retained in the filter remain infecting (Chauveau, Bert, Toussaint). 4th. That the clear filtrate injected to excess killed by virtue of its contained chemical products in twelve hours, while the solids filtered out and containing the bacillus or its spores only killed after thirty hours.[4] 5th. Anthrax blood from the living animal or one just dead, and destitute of spores, when subjected to compressed oxygen (50 atmospheres), is non-infecting (Bert). 6th. The same anthrax liquid, destitute of spores, after boiling is completely innocuous. 7th. The same liquid, if kept in a closed tube apart from oxygen for eight days, shows the bacilli broken down by granular degeneration, and proves absolutely harmless when inoculated in small quantity. 8th. The same sporeless anthrax fluid when treated with absolute alcohol loses its virulence. 9th. The anthrax liquid which has been cultivated with free access of air in a temperature varying from 25° C. (77° F.) (Klein, Löffler) to 41° C. (105.5° F.) forms spores, and then remains infecting, though it may have been subjected to compressed oxygen, boiling for several minutes, absolute alcohol, dilution with water, putrefaction, or the exclusion of oxygen.

[Footnote 4: Bert, _Compt. Rend. de la Société Biol._, p. 355, 1879.]

The bacillus anthracis, as found in the blood and animal fluids, is in the form of fine rods, straight (rarely bent or angular), motionless, and 0.007 to 0.012 Mm. in length. Smaller forms are seen to be minute ovoid or oblong bodies, and the smallest absolutely spherical (micrococcus); but in all cases, as seen under the highest powers of the microscope, they have clear-cut, even margins, linear or curved, which easily distinguish them from the irregular normal granules of the blood and tissues. Under the highest powers of the microscope the bacillus is seen to be made up of a series of oblong (Koch) or cubical (Klein) cells enclosed in one common sheath. This is rendered more manifest if they are first swollen by the addition of water. The motionless form of the anthrax bacillus is of especial value in distinguishing it from the motile bacteria of putrefaction (saprophytes).

Within the living animal body the development never goes aside from these forms. The growth appears limited to micrococcus and bacillus rods, while spores or bacillus threads are never found. This finds its counterpart in the micrococcus poisoning caused by the inoculation with the spores of common moulds (Grawitz); and in septicæmia also micrococcus and bacillus forms only are found, the filamentous never.

When grown in organic infusions out of the animal body the anthrax-germ develops from micrococcus or bacillus into a long, branching, filamentous product, which in the presence of oxygen develops into spores. Apart from oxygen or when the proper nourishment of the bacillus is exhausted the protoplasmic elements within the filamentous sheath undergo granular degeneration, and finally the empty envelope disintegrates and disappears. The spores appear at intervals in the protoplasm of the filament as clear, brightly refrangent bodies, at first spheroidal, afterward larger and oblong. Unlike the micrococcus and bacillus, {933} they do not stain. Under favorable circumstances the primary cell is capable of forming one, or if extra long, two spores (Koch, Klein). Cossar-Ewart claims to have seen the formation of motile flagellate organisms aggregating themselves into zooglæa masses, but as these were not found in the carefully-conducted cultures of Koch and Klein, they are supposed to have been aërial microphytes accidentally introduced.

The great tenacity of life in the spores in heat and cold, dryness and wet, excluded from air and under several atmospheres of oxygen, in the midst of putrefaction and in pure watery fluids, well accounts for the persistence of infection in buildings and localities where the poison has gained a foothold. In order to their destruction in a natural manner it seems necessary that they should germinate and develop into the anthrax micrococcus, bacillus, or mycelium. This germination may take place in the presence of moisture, oxygen, and suitable nourishment, whether in the soil, the animal body, or elsewhere, and then the exhaustion of the aliment, the exclusion of the oxygen by putrefaction, the submergence in a medium unfavorable to development, or exposure to a very high temperature, may suddenly destroy the poison.

There is reason to believe that a too free exposure to oxygen proves destructive to the virulence, if not to the life, of the poison, and thus in all porous, well-drained soils the anthrax poison, even when introduced from without and concentrated by the death and burial of many victims, soon disappears. This feature, which is common to many zymotic diseases the germs of which live and multiply outside the animal body (typhoid, yellow fever, tuberculosis, swine plague, chicken cholera, diphtheria, etc.), offers countenance to the claims of Buchner that he had by prolonged culture, in the presence of air, metamorphosed the bacillus anthracis into a harmless mycrophyte, and that, conversely, by continuous cultivation under the surface of a suitable beef infusion he had changed the harmless bacillus subtilis of hay into the deadly bacillus anthracis. Koch, Klein, and others have discredited Buchner's results, on the ground that he had not, in their opinion, taken due precautions against impure cultures, and that his alleged transitions took place too abruptly; yet further observation must determine whether he has been condemned too hastily. The diminished virulence of Pasteur's attenuated virus, which is unaffected by the next subsequent culture or by the formation of spores, shows plainly enough that the bacillus anthracis is capable of physiological changes under the influence of varying conditions of growth, and that such changes are not at once undone by a return of the former conditions.

How anthrax-germs enter the body is partly known and partly conjectured. Direct inoculation on a sore by contact, by insects, by harness, by accidents, etc. is an undoubted method. The sound cuticle is probably an efficient barrier, since bacteria habitually inhabit, without hurt, the surface and gland-ducts of the skin; yet the entrance of these saprophytes through the shell and membranes of the egg leaves a doubt as to the efficiency of the cuticular obstacle. The mucous membranes are manifestly frequently penetrated by the parasite. Hence the local affections in the mouth and throat (glossanthrax, anthrax angina) and in the lungs (pulmonary anthrax). Cohn claims that the gastric juice of Carnivora especially is destructive to the anthrax poison, yet the constant recurrence of intestinal anthrax (mycosis) seems to imply that the germs often escape destruction {934} in the stomach. Pasteur supposes that anthrax-infected food is only injurious when there are inoculable sores in the mouth or pharynx, but it seems as if in that case the disease would be first shown at these points and in the nearest lymphatic glands rather than in the bowels, the rule for the inoculated anthrax being to develop first in the tissues and thence to reach the blood-vessels through the lymphatics.

The anthrax poison expends its fatal energy especially on the blood and blood-vessels. The bacilli in the blood use up the available oxygen, so that the circulating liquid becomes venous, dark, and unfitted for the maintenance of the normal functions of life. What is even worse, the ability of the blood to absorb oxygen is greatly impaired. In men and dogs suffering from anthrax the consumption of oxygen was found to be reduced in one instance even by two-thirds, probably in part by reason of the action of the chemical products of the bacillus. A third condition constantly found is embolism of the capillaries by the bacillus and the occurrence of local gangrene.

SYMPTOMS.--Anthrax shows itself in three principal forms: 1st, the apoplectiform; 2d, anthrax fever without local external lesions; and 3d, external localized anthrax. The two last forms correspond in the main to the acute and subacute forms.

The period of incubation varies according to the dose of the poison and the receptivity of the animal. In some cases infection is at once followed by illness. In these it is probably the chemical products that produce the first effect, while the disease caused by the propagation of the bacillus appears later should the animal survive. Such incubation is shortest for the smaller animals (mice, rabbits, guinea-pigs, cats), in which illness usually sets in in from twenty-four to forty-eight hours. In sheep and goats incubation may be extended to three or four days, while in horses and cattle it may last a day longer.

The apoplectiform type attacks animals which a few minutes before seemed in fine health, appetite, and spirits, striking them down as if by lightning, and the victims struggle convulsively for some minutes, expel blood perhaps by the nose or anus, and expire. In the less suddenly fatal cases there may be muscular trembling, unsteady gait, excited breathing, accelerated pulse, tumultuous heart's action, bleeding from some natural orifice, and death in from one to several hours. Occurring as these cases often do in summer, the sudden death is probably hastened by insolation.

In anthrax fever or acute internal anthrax there is loss of appetite, and, in ruminants, of rumination, suppression of milk, dulness, languor, staring coat, or even a rigor, and thirst. Then follows the hot stage, in which the temperature may rise to 106° or 107° F.; there are acceleration of pulse and breathing, petechiæ or a brown or yellowish tinge of the mucous membranes and white parts of the skin, tenderness of the spine, often jerking or clonic spasms of the muscles of the extremities, and much prostration and weakness, the patient hanging back on the halter, leaning against a wall, or swaying when made to move. The feces are usually more or less mingled with blood-clots, or may be at once liquid and bloody. Bloody urine and the discharge of blood from other natural channels are frequent. Some cases are manifestly delirious, and in others the skin crackles on being handled. Remissions are not uncommon, {935} during which the animal remains dull and prostrate. As the disease advances and the blood is robbed of its oxygen, the temperature descends below the natural standard, great weakness and stupor set in, the pupils are widely dilated, and death from asphyxia occurs in one or two days from the onset.

In localized external anthrax the local swellings may be first seen. There are usually some tenderness of the skin, erection of the hair, and the formation of a little nodule, like a hazel-nut or walnut, adherent to the deeper parts of the skin, firm and comparatively painless even when cut. Sometimes the swelling is diffuse, with a dropsical or erysipelatoid aspect, and crackles like parchment when handled. Whether the affection attacks the tongue, the throat, or some part of the head, body, or limbs, the tendency is to gangrene of the part, and, if the subject survives long enough, to an extensive sloughing and unhealthy sore. The sloughs and sores have either a black sanguineous appearance or they are lardaceous and intermixed with streaks of dark red. If fever is not present at the outset, it sets in early, and passes through the same stages as in the acute internal anthrax, the animals being suddenly plunged in prostration and stupor, with dusky yellow or blood-stained mucous membranes, dyspnoea, dilated pupils, convulsions, and death. On the mucous membranes (gloss-anthrax, anthrax angina) the engorgement is usually complicated with bullæ with red or yellow contents, and which on bursting leave unsightly gangrenous ulcers. In all such cases the morbid liquids of the swellings teem with bacilli.

MORBID ANATOMY.--The most characteristic changes are usually met with in the blood. This is black, thick, tarry, uncoagulable or coagulates only in loose diffluent clots, which are redissolved before squeezing out the serum; the fibrin is diminished (often by two-thirds), the red globules are not adherent in rouleaux, and are crenated and broken down and the hæmatin diffused through the liquid, so that it stains the hands or paper deeply; the white globules are increased, probably by reason of the early irritation of the lymphatic glands and spleen by the poison; and it reddens slowly and but slightly on exposure to the air, and speedily passes into decomposition. The blood can scarcely be made to flow in a full stream, but often trickles down the hair and skin by reason of its thick, consistent character. The microphytes above described are usually found in the blood, and always in the affected tissues if examined just after death.

Next to the blood, the spleen presents the most constant lesions, being enlarged (by one-third, one-half, or to double, triple or quadruple its normal size) and gorged with blood (sometimes even to rupture). The lymphatic glands, and especially those adjoining the local anthrax swellings of the tissues, are always enlarged, marked with petechiæ, friable, easily reduced to a pulp, and swarming with bacilli and micrococci. Next to the glands of the affected parts the central ones, the axillary, prepectoral, thoracic, sublumbar, and abdominal, are the most constantly affected. The lymph is reddish and opaque.

Decomposition sets in early, and the resulting gases cause a puffy, emphysematous condition of the connective tissue. The fat and other white tissues are dusky brown or yellow, and petechiated; the muscles are soft, flabby, and dark red or brown, with occasional blood {936} extravasations; the blood-vessels, especially the veins, and the right heart are gorged with black, uncoagulable blood, and have their inner coats blood-stained. The serous membranes present numerous petechiæ, and contain more or less of a reddish serum. The intestines, and sometimes the stomach, are dark red throughout, marked by petechiæ, and are often the seat of thickening from sanguineous or transparent colloid infiltration. The lesions are especially extensive on the small intestines and rectum. The vagina and womb are also the frequent seats of sanguineous infiltration. The liver and kidneys are enlarged, congested, softened, and friable, and the ganglia of the sympathetic are enlarged, congested, and softened. The swellings are of two kinds, sanguineous and colloid. The former, when cut into, present one or more loose clots of black blood or a grumous mass of blood-elements, separating the tissues and often mixed with fetid gases. The colloid exudations are glairy, semi-solid, jelly-like masses, infiltrating the tissues. The tissues affected and the skin covering them are the seat of bacterial embolism and gangrene, and there is no tendency to suppuration. These products swarm with the specific microphytæ.

DIAGNOSIS.--The differential diagnosis of anthrax from other affections due to the propagation of microzymes in the system is not always easy--so much so that a variety of bacteridian and allied diseases (septicæmia in its various forms, erysipelas, swine plague, chicken cholera, poisoning by the micrococci of fungi, black quarter from bacteria, milk sickness, and Texas fever) have been erroneously confounded with this affection. These all show the same dusky or cyanosed mucous membranes, disintegrating blood-globules, loose blood-clots, petechiæ, blood-extravasations, sudden and great prostration, and enlargement and congestion of the lymphatic glands or spleen. In some of these the duration of incubation (in swine plague six to fourteen days and in Texas fever one month) serves to distinguish, while in the majority the microzyme is globular (Texas fever, micrococcus of fungi-poisoning, chicken cholera); in swine plague the cocci are arranged in pairs; in black quarter the microbe is a refrangent ovoid, single or in chains of two or three and a motile linear body with a refrangent nucleus in one end; and in milk sickness the germ is a spirillum. The germs are far more likely to be detected in the local lesions and lymphatic glands than in the blood. The specific nature of the symptoms and lesions can usually be relied on, but in cases of doubt the inoculation of a small animal (rabbit, guinea-pig, sheep) will be a material guide.

PROGNOSIS.--True anthrax leads to a very high mortality. The apoplectiform cases are fatal almost without exception; the acute cases of anthrax fever in many outbreaks perish to the extent of 75 or 80 per cent., and the more tardy ones to the number of 50 per cent. In a general outbreak the earlier cases are usually the most fatal, while later, when the less susceptible animals are attacked, the mortality is often decreased. Again, the mortality is often at once arrested by the emigration of the herd to a more healthy soil, a large proportion of those already attacked recovering.

PROPHYLAXIS.--In prophylaxis the soil demands the first attention. If this is damp and calcareous or rich in organic matter, the remainder of the herd should be at once removed to a drier and more porous soil, where the germ is less likely to be preserved and increased. In an {937} enzoötic in Livingston County, N.Y., in 1875, 40 bullocks out of 200 had perished in ten days, yet after removal to an adjacent dry pasture and the use of antiseptics with the food and water the attacks abruptly ceased and 48 out of 50 head already sick recovered. The drainage of anthrax soils leads to a steady reduction of the poison, favoring as it does the germination of the spores and the destruction or modification of the germ. When drainage is impossible, the mortality may be reduced by driving the stock to drier grounds during the hot, dry season, by stabling them morning and night when the dews are on the grass, also in wet times, when they are likely to pull up the plants by the roots, or, better still, by cutting the fodder and soiling the stock in stables or yards. Yet in all these cases the germs will at intervals find access to the animals in the green food or hay, so that badly infected soils must be secluded from live-stock, and either be abandoned or devoted to other cultures. A point of the very first importance is the safe disposal of the products and carcases of the sick. These should be thoroughly burned, or, failing this, deeply buried (4 feet) and the graves covered with coal tar and fenced in from all other stock for from five to ten years. Contaminated litter and fodder should share the same fate. Stables and yards where the sick have been, and all vehicles and implements used for them or their products, should be thoroughly disinfected. In the epizoötic in Livingston County, above referred to, these measures seem to have eradicated the disease in the course of six years, though the land was neither drained nor subjected to cultivation, and the dangerous meadows are now again pastured with impunity.

In the case of sick animals the greatest care is requisite to keep them from common drinking- or feeding-troughs; to exclude all other animals, even the smaller quadrupeds and birds, which may become the bearers of the poison; to avoid the chance of the drainage of infected excreta into other yards and pastures, and to carefully disinfect and guard the human attendants against contamination. The sale of animals out of an infected herd, and, above all, for the meat-market, and the use of the milk or other products of such animals, until attested sound, are highly reprehensible.

Finally, there are the different methods of protecting the system by inoculation with modified virus. The first of these is that of Burdon-Sanderson, Dugnid, and Greenfield, who in 1878 and 1879 inoculated six cattle with the blood of guinea-pigs dead of anthrax, all of which survived except an old, emaciated, worn-out, and pregnant cow, and all the survivors would only afterward contract anthrax in a mild form. The anthrax blood of the guinea-pig inoculated on the sheep proved fatal. The second mode is that of Pasteur, who cultivated the anthrax-germ artificially in flasks of meat-infusion, and after the nourishment in the latter had been used up left the bacilli to degenerate until their virulence had been so far decreased that the liquid could be safely inoculated on animals, so as to produce a mild anthrax infection and thereafter secure immunity from this poison. For all the larger domestic animals he found that the eighth day of the culture sufficed, provided there had been no formation of spores; and the method has now been applied on many scores of thousands of domestic animals. Klein, however, has found that cultures in pork-broth of the same age are invariably fatal to rodents, {938} and that a guinea-pig which survived inoculation with culture a month old did not possess immunity against fresh virus. The third method, that of Toussaint, consists in heating the fresh virus, so as to lessen its activity, and then inoculating it on the animals to be protected. He found that a temperature of 55° C. (131° F.) maintained for one hour rendered the virus non-fatal, without impairing its prophylactic powers on animals inoculated. In spite of a partial failure at Alfort from insufficient heating of the virus, the method has now been firmly established as at once easy and effective.

The great value of these discoveries can hardly be overestimated, yet it is to be feared that the éclat of their reception has led to a far too general adoption of the methods. No one of the methods professes to destroy the life of the bacillus nor to impair its power of self-propagation. The bacillus, therefore, is likely to be planted in the localities where it is being employed, and, if the soil is favorable, to be perpetuated there. It follows also, from the susceptibility of the bacillus to change under varying conditions of life, that the modification impressed on it by the methods of Pasteur and Toussaint may be reversed under a reverse state of the environment, and that the harmless virus sown by our inoculators may in favorable soils produce the more deadly types. The methods secure the safety of the individual herd inoculated, at the expense of planting in the pasture a seed most perilous to all future uninoculated herds that may roam there. The only place for such protective inoculations is on pastures already charged with the anthrax bacillus, and from which that cannot be eradicated. On the dry, healthful soils where the bacillus cannot survive the inoculation is useless, while on the dense, damp, rich soils favorable to its preservation, but as yet uninfected or nearly so, this inoculation is but sowing deadly seed to secure a very temporary and questionable advantage.

TREATMENT.--Bloodletting and laxatives have been largely used in the treatment of anthrax, though both are mostly useless in acute cases, their possible good effects being anticipated by the early death. When of service at all, it is probably mainly in reducing that plethora which serves often to enhance the virulence and severity of the malady. Apart from these, the agents resorted to are more or less of an antiseptic nature, and probably exert their action mainly on the bacilli undergoing development near the surface of the skin or intestinal mucous membrane. In extensive outbreaks I have had the best results with the administration thrice daily of carbolic acid, nitro-muriatic acid, or bichromate of potassium, and hypodermically of iodide of potassium and sulphate of quinia. Alcoholic stimulants, chlorate of potassium, and muriate of iron are equally indicated, especially when the period of prostration has set in. If the local anthrax can be detected when there is as yet but a hard nodule, there should be no hesitation in cauterizing it to its depth and treating the resulting sore and surrounding parts with tincture of iodine or iodized phenol. After crucial incision the nodule may be treated with powerful caustics (potassa, nitric acid, chloride of zinc), to be followed by iodized phenol, with or without poultices or fomentations.

{939} Anthrax in Man (Malignant Pustule or Vesicle, Anthrax Intestinalis, Mycosis Intestinalis).

Fournier in 1769 first traced the communicated anthrax of man to the consumption of the flesh of diseased animals and the handling of their wool. Until quite recently, however, the form which originated as a local external affection was the only type recognized, while internal anthrax was confounded with a multitude of other affections.

ETIOLOGY.--That anthrax in man is almost invariably derived from the lower animals by infection is now undoubted, while for the direct infection of man, as of animals, by the germs propagated in the soil, there is no absolute proof. The latter mode of propagation has only been recognized in the Herbivora, which are so much more exposed to contamination from the soil; yet, abstractly, there is no reason to suppose that man is less susceptible to the earth-grown bacillus than to that produced in the animal, if only he were as frequently exposed to its infection. The spontaneous development of anthrax apart from the pre-existent bacillus in animals or soil is a chimera. The principal modes of infection may be considered as direct and mediate. Among the direct are included infection from handling the sick animals, their carcases, their wool, hair, bristles, hides, fat, and guts; the inoculation of physicians, surgeons, and nurses from their patients; and the infection of men by the meat, milk, and cheese eaten. As attested modes of mediate infection may be cited the inoculation by insects (mosquitoes, bluebottles, and other bloodsuckers), and the introduction by water into which anthrax products have drained or been washed; there are also hypothetical cases in which anthrax-germs from the earth have entered the system in the air, drink, or food (raw vegetables). The direct inoculations are especially common in certain classes (shepherds, farmers, butchers, knackers, tanners, veterinarians, and workers in hides, hoofs, glue-factories, fat-rendering works, in hair, wool, bristles, and catgut, and in felting and paper-making). In such cases the disease usually begins as a local one, and occurs on uncovered portions of the body. Three such cases occurred in 1875 on one farm at Avon, N.Y., where the victims had assisted in burying forty dead cattle, and a number of other similar instances can be adduced in different parts of the same State, in one of which a physician was accidentally inoculated in dressing a farmer's hand. Physicians whose practice includes large tanneries become very familiar with the disease and recognize it very readily.

Infection through food is much less frequent in men than in animals, the process of cooking combining with the action of the gastric juice in destroying the poison. Yet it is by no means unknown. The records above given of infection in St. Domingo, Naples, and the Russian steppes can be easily supplemented. Dr. Keith of Aberdeen, Scotland, records the case of a family that suffered, two of them fatally, after partaking of broth and meat which had been boiled for hours, one member of the family (a vegetarian) having alone escaped. Infection through milk, butter, and cheese is less common, the gravity of the disease in animals leading to an early suppression of the mammary secretion. In all such cases the infection enters through sores in the mouth or from the bowels.

Those cases in which the bacillus enters the system with the inspired {940} air are probably the least numerous. Yet the germ may reach the lungs in fine dust, and then find in the delicate respiratory mucous membrane the most accessible of all channels into the system.

The proportion of men affected is much greater than that of women and children, doubtless by reason of their greater exposure to infection, and, as in the lower animals, the summer months are most productive of anthrax. The susceptibility of the human race appears to be less than that of the Herbivora, and doubtless varies, as in these animals, with the nature of the food. It is at least temporarily exhausted by a first attack, though in exceptional cases and under a strong dose of the poison a man may be affected a second time.

SYMPTOMS.--Symptoms usually set in within twenty-four hours after inoculation of the poison, though it is alleged that the incubation may be extended to twelve or fourteen days. Itching draws attention to a small red spot like a mosquito bite, but with a black central point. This speedily increases to a small rounded swelling (papule), and in fifteen hours is surmounted by a minute vesicle with dark-red or bluish contents. From the size of a millet-seed this increases to that of a pea, and in thirty hours bursts spontaneously or under friction and forms a dark-red, indurated, comparatively painless nodule (parent nucleus, Virchow). The adjacent skin shows a swollen areola livid and red, on which there appear vesicles similar to the first, which pass through the same stages, burst, and leave a livid, hard, or doughy gangrenous surface. By this time the surrounding skin is red, shining, and puffy, and the disease continues to spread by the same method of extension. The diseased part now becomes the centre of an oedematous swelling which may invade the entire arm, face, or neck, and is attended with more or less constitutional symptoms. The affected part may be cold or hot, and it may show the red lines of lymphangitis and the swelling of the adjacent lymphatic glands.

The pyrexia, at first slight, often reaches a high grade, attended with occasional chilliness, pains in the back and loins, great prostration, languor, dulness, and even delirium, with cold sweats, anxiety, dyspnoea, and at times muscular spasms. As in beasts, there are the dusky skin and mucous membranes, petechiæ, and cyanosis, and in bad cases there may be sudden collapse and death. The symptoms vary much, however, according to the extent of the local lesion, to the amount of poisonous chemical products thrown into the blood, to the degree of the invasion of the blood by the bacillus, and to the complication (not infrequent) of the affection with septicæmia. In the very mildest cases the affection never proceeds beyond a local slough, the size of a quarter or half dollar, the germs do not enter the blood in sufficient numbers to survive, the constitutional symptoms are few or absent, and the sore heals by granulation.

The disease usually lasts from six to ten days, and for the first forty-eight hours the symptoms are generally purely local.

Malignant anthrax oedema (oedeme maligne) was first observed by Bourgeois as occurring in the eyelid, and has since been recognized in other parts of the body (arm, forearm, head). It differs mainly from malignant pustule in the absence of the preliminary vesicle, of the hard nodule (parent nucleus), and of the early circumscribed gangrene. It has this further peculiarity, that the local disease often appears as a {941} sequel rather than a precursor of the constitutional disturbance. It corresponds in the main to the diffuse erysipelatoid anthrax of the lower animals, and has been attributed to the anthrax poison introduced by inhalation. It has been observed to follow eating of anthrax flesh (Leube, Müller). Inasmuch as the active disease is often delayed a week or ten days after exposure to infection, it may reasonably be supposed that the bacillus has been imprisoned on the mucous membrane, or, entering the blood in small quantity only, has been held in check by the antagonism of the blood-globules until some elements, escaping into the connective tissue, have started the local disease. The symptoms are usually first languor, sleeplessness, restlessness, with some sense of chill, debility, and headache, and finally, after a few days, the formation of the specific oedema at one point or more. This has a pale, semi-translucent, slightly yellowish or greenish aspect, pits on pressure nearly equally at all points, and tends to a rapid extension, with concomitant aggravation of the constitutional symptoms, and in many cases nausea and vomiting. Gangrene sets in--not progressively, as in malignant pustule, but simultaneously over a more extensive surface--and is followed by great prostration, stupor, dyspnoea, cyanosis, collapse, and death.

Anthrax intestinalis may be looked upon as the counterpart of the internal anthrax or anthrax fever of animals, described above. As in animals, the constitutional symptoms may result early in a fatal issue, with scarcely any local lesion save in the blood and spleen (Carganico, Leube, Müller, Winkler, Lorinser). As in animals too, the sanguineous engorgement of the spleen and the intestinal anthrax are often complicated by external anthrax oedema or malignant pustule (Heussinger, Virchow, Buhl, Waldeyer, etc.). In this form pyrexia and other constitutional disturbances are first seen. There is a general feeling of languor and depression, with some chilliness, fever, pains in the limbs, back, and head, vertigo, and ringing in the ears. Even at this early stage there is noticed a dusky hue of the skin and visible mucous membranes, which goes on increasing to a brown or yellow tinge, to petechiæ, or, with the supervention of dyspnoea, to cyanosis. Digestive derangement is early shown in abdominal pain, nausea, vomiting, tenderness, some swelling, and finally diarrhoea, often bloody and sometimes profuse and exhausting. In acute cases the symptoms become rapidly worse, and then follow discharge from the mouth and nose of uncoagulable blood, dyspnoea, cyanosis, small pulse, dilated pupils, great anxiety or drowsiness, and stupor, or there may be tonic spasms of the trunk or extremities. Death usually results from asphyxia or collapse, as in animals. These cases are almost invariably fatal within a period of thirty-six hours, though some linger six or seven days.

Allied to the intestinal anthrax is anthrax angina, a not unknown occurrence in man. This begins as a bad sore throat, with an especially dark-red hue of the pharyngeal mucous membrane. As it advances the shade becomes increasingly darker, the power of deglutition is lost, serous phlyctenæ with gangrene and deep ulceration set in, but without any tendency to the formation of false membrane as in diphtheria. There are early superadded the constitutional symptoms above described, and the patient dies in a state of collapse or asphyxia.

MORBID ANATOMY.--The lesions closely agree with those already {942} described for animals in general. The blood presents the same dark-red or black, tarry, incoagulable, or only slightly coagulable condition in the worst cases, yet this is less constant in man, as the bacteria are less constant or numerous in the blood, in keeping with the more prolonged localization of the external anthrax in man, and the more pronounced antagonism between the blood and the bacillus which results from feeding exclusively or largely on flesh. The red globules do not tend to adhere together, and the white globules are in excess and very granular. The spleen is less extensively enlarged than in animals, but is highly charged with blood, bacilli, and micrococci. The lymphatic glands too are enlarged, hyperæmic, cloudy, hemorrhagic at points, of a dark grayish, deep red, or blackish color, and highly charged with the bacillus. The surface of the skin and mucous membranes (mouth) presents hemorrhagic spots and patches, with serous vesicles and eschars. The malignant pustule when cut into presents a central slough and a surrounding hard indurated mass, both of a dark blood-red, with similar prolongations downward into the adipose tissue, and around all the characteristic oedematous infiltration, often streaked with blood. The bacillus is found in tufts or dense groups at intervals in the rete mucosum, the dermis, and the subcutaneous connective tissue. The serous membranes present the same general lesions as in animals. The walls of the stomach and bowels are the seat of cloudy red infiltration, with at intervals small hemorrhagic foci, and on the mucous surface distinct sloughs. Jelly-like exudations are also found in these membranes in the mesentery and in the retro-peritoneal tissue. The liver and kidneys are usually congested or are infiltrated with an oedematous exudate, and in these, as in all the local anthrax lesions, the characteristic bacilli are found.

DIAGNOSIS.--Malignant pustule is distinguished by its commencing from a minute red point with dark centre, and by its progressive extension from this point by a dark-red, puffy, and vesicular areola, with steadily advancing induration and gangrene. The bites of insects have a yellowish central point with red areola. A boil lacks the dark centre and the rapidly rising elevated red areola. Carbuncles and plague-boils tend to appear on clothed parts of the body, respectively on the back of the neck and shoulders and on the trunk and extremities. In carbuncle several boils rise and burst simultaneously, though they may finally slough into one sore, while in anthrax the extension is from one point. The plague-boil is usually multiple and much more painful than anthrax. The glanderous nodule is usually multiple, situated at intervals on the course of a lymphatic, the intervening portion of which is inflamed, hard, and cord-like. It is also usually associated with the specific glairy discharge from the nose, the nasal ulcers and nodules, and the enlarged painless, nodular, and indolent submaxillary lymphatic glands. As a last resort the detection of the bacillus in the indurated nucleus and the inoculability of the disease on the lower animals (rabbit, guinea-pig), may be appealed to.

Malignant anthrax oedema is less easily recognized, but may be inferred from the sudden swelling with a dusky yellow or greenish hue and a tendency to vesiculation and gangrene, the whole preceded and attended by the constitutional symptoms of anthrax, and, above all, from the presence of the bacillus in the exudate.

{943} In both of these forms much may be deduced from the known liability of the district to anthrax, from the occupation of the subject as being exposed to infection (worker in hair, wool, bristles, hides, catgut, etc.), or from his having eaten meat which was open to suspicion.

Internal anthrax is less certainly diagnosed because of the absence of local symptoms until the constitutional disorder is well advanced. Yet the reasonable suspicion of infection and the sudden and violent eruption of the disease (headache, nausea, vomiting, bloody diarrhoea, extreme anxiety, debility, dyspnoea, cyanosis, convulsions, collapse, with petechiæ, and local discharges of diffluent blood) serve to identify it. The bacillus is not always to be detected in the blood under the microscope, but its presence can usually be demonstrated by inoculation.

PROGNOSIS.--The prognosis of malignant pustule energetically treated in its early stages is good. The disease is as yet a local one, and the germs can be extinguished by local treatment. In anthrax districts, where the disease is feared and early recognized, the mortality may be from 5 per cent. (Nicolai) to 9 per cent. (Lengyel, Koranyi). Even this mortality is mainly due to delay in treatment. In districts, on the other hand, where the malady is infrequent, and where efficient measures are applied too late, the mortality is often 30, 40, or even 50 per cent. After internal infection, and where local symptoms only appear after general infection, the case is very hopeless.

PROPHYLAXIS AND TREATMENT.--The prophylaxis of anthrax in man is to a large extent identical with that for animals. All considerations as regards soil, culture, drainage, sick and dead stock, cremation, burial, disinfection, etc. have a most important if only a secondary bearing on the protection of man. Still more important is the free use of carbolic acid, chloride of lime, or tincture of iodine for the hands of those dressing unhealthy sores in animals or handling suspicious cases of sickness or cadavers, and of those working in hides, wool, hair, horns, hoofs, guts, etc. Similarly, all products of animals with anthrax should be withheld from general use.

In external anthrax of man, before the system has been contaminated, the thorough destruction by caustic of the diseased part with its contained poison is most effectual. Where there is as yet but the preliminary papule it may be incised and thoroughly destroyed by a stick of chloride of zinc, caustic potassa, or nitrate of silver, or, if more convenient, by fuming nitric acid, muriatic or sulphuric acid, or, perhaps preferably to all others, iodized phenol. Should the parent nucleus have already formed, it should be excised with the knife or deeply incised in a crucial direction, and then thoroughly cauterized with one of the more potent escharotics (caustic potassa, strong nitric acid) or with the iodized phenol. The latter agent may be further applied on the sound skin adjacent, especially if there is the slightest swelling or redness. Should the peripheral oedema persist or reappear after the cauterization, the latter should be repeated until this tendency is overcome. Hypodermic injections of a solution of iodine and iodide of potassium may be made into the entire swelling. After the caustic has done its work the eschar may be softened and its separation favored by a warm poultice containing a small amount of carbolic acid or iodized phenol. This treatment is often highly beneficial, even after constitutional symptoms have set in, by arresting the {944} propagation of the bacillus and checking its introduction and that of its chemical products into the circulation.

Constitutional treatment is not to be forgotten. Carbolic acid may be profitably given to the extent of fifteen drops daily, iodide of potassium ten to twenty grains thrice a day, and sulphate of quinia ten grains at the same intervals. The strength should be sustained by iron (tincture of the chloride) and wine or other alcoholic beverage, both being, like the agents already named, calculated to retard if not to limit the propagation of the bacillus. The diet throughout should be nutritious and easily digested.

When a person is known to have eaten anthrax meat an emetic will be indicated, followed by a smart oleaginous purgative combined with five drops of carbolic acid, and subsequently by the constitutional treatment above recommended. In case of extensive anthrax oedema, incisions may be made into the part as far as the yellow exudate extends, and a poultice containing carbolic acid may be applied. Or, preferably, the swelling may be freely injected with a weak solution of iodized phenol (1:100 water), and then painted with the same agent or with tincture of iodine.

{945}

PYÆMIA AND SEPTICÆMIA.

BY B. A. WATSON, M.D.

HISTORY.--There is little to be learned from existing literature of the views which were maintained by the ancients, prior to the birth of Christ, in regard to the morbid conditions now designated pyæmia and septicæmia; although it is certain they were recognized by the "Father of Medicine," who reports a well-marked case of puerperal fever terminating fatally on the twentieth day of the disease, and also a case in which death was unquestionably caused by septic poisoning, as is clearly shown in the following:[1] "Criton, in Thasno, while still on foot and going about, was seized with a violent pain in the great toe; he took to his bed the same day, had rigors and nausea, recovered his heat slightly; at night was delirious. On the second, swelling of the whole foot, and about the ankle, erythema with distension and small bullæ (phlyctænæ); acute fever; he became furiously deranged; alvine discharges, bilious, unmixed, and rather frequent. He died on the second day from commencement." Additional confirmation of the fact that Hippocrates was familiar with the phenomena of these diseases may be found in his dissertation on empyema and fevers. Prof. C. Heuter says, under the head of septic fever,[2] "Hippocrates and Celsus observed the fever in cases of injuries which proved so dangerous that this danger could not have originated from the inflammation or from the wound alone." Jacotius, a commentator of Hippocrates, has even mentioned putrid fevers, the same as Adrianus Spigelius, who spoke of fevers which arise from putrefaction; but both authors, as well as their followers, did not discriminate between septicæmia arising from the putrescence of wounds and pyæmia. In the mean time both varieties were regarded as intermittent fever.

[Footnote 1: _Works of Hippocrates_, trans. by Adams, vol. i. p. 377.]

[Footnote 2: Pitha und Billroth, _Handbuch der Chirurgie_, 1 Band, 2 Abth., 1 Heft, 1 Liefg., S. 6.]

"Aretæus lived during the middle of the second century of the Christian era. In his remarks on pneumonia he observes that the subjects of this disease die mostly on the seventh day. 'In certain cases,' he says, 'much pus is formed in the lungs, or there is a metastasis from the side if a greater symptom of convalescence be at hand. But if, indeed, the matter be translated from the side to the intestine or bladder, the patients immediately recover from the peripneumony.' He speaks of a metastasis to the kidneys and bladder being peculiarly favorable in empyema. He ascribes suppuration of the liver to intemperance and protracted disease, {946} especially dysentery and colliquative wasting. The symptoms described by him resemble those of chronic pyæmia."[3]

[Footnote 3: Braidwood on _Pyæmia_, p. 2.]

Galen and some of the other ancient physicians recognized the existence of septic poisoning, as is shown by the opinions expressed on the subject of putrid fevers. According to Galen, putrid fevers may either arise from the conversion of ephemerals, or originally from putrefaction of the fluids within the vessels.

Aetius states that they arise from constriction of the skin or viscidity of the humors, whereby the perspiration is stopped, and the quantity of vital heat so altered as to give rise to putrefaction, first of the fluids, and afterward of the fat and solid parts. When these corrupted fluids are contained within the vessels they occasion synochous fevers, but when distributed over the body they give rise to intermittents. Synesius and Constantinus Africanus give a similar account. Alexander gives an interesting and ingenious disquisition on the origin and nature of putrid fevers, one of the most common causes of which he holds to be the conversion of ephemeral fevers, and the inseparable symptoms being want of concoction in the urine and quickness of the pulse with systoles. This is the account of them given by most of the other authorities, both Greek and Arabian, so that we need not enter into any circumstantial exposition of their views. We shall merely give the brief account of those furnished by Palladius. There are, he says, two kinds of synochous fevers, the one being occasioned by effervescence, and the other by putrefaction of the blood; of these the latter are the more protracted and dangerous. In them the pulse is contracted, the heat pungent, and the urine white and putrid.[4]

[Footnote 4: Paulus Ægineta, trans. by Adams, vol. i. p. 236 (Sydenham Soc., 1844).]

A new era in the literature of this subject dawned during the sixteenth century. Ambrose Paré and Bartholomew Maggi each published a work in which they pointed out the old errors and announced new truths. Paré's _Treatise on Gunshot Wounds_ was published in Paris in 1551, while Maggi's treatise appeared a year later at Bologna. Paré gained his first experience in the treatment of gunshot wounds in 1536, which is described as follows: "The storming of the small mountain-fortress Villane, near Susa, probably gave him for the first time full occupation, and he followed in all things the example of older colleagues. Like them, although hesitatingly, he poured into the gunshot wounds boiling oil of elder to destroy the poison, but the oil fell short, and then he was compelled to dress the other wounded men with an ointment of oil of roses and turpentine. Fearing that the latter would soon become victims of the wound-poison, he passed a sleepless night, got up early to see the ill consequences, but was greatly surprised to find those that he had half given up free from pain and without inflammation or swelling, while those who had been treated with boiling oil lay in a state of fever, with great pain and much swelling. He therefore determined, as he tells us, never again to burn the poor subjects of gunshot wounds so cruelly."[5] It will be seen that Paré's treatise on gunshot wounds was published fifteen years after this impressive experience at the fortress of Villane. In this work he sought to correct the prevailing idea that {947} gunshot wounds were poisonous, and was ably supported in his effort by Bartholomew Maggi; but it required all the respect which Paré enjoyed in riper years to gradually obtain consideration for the new view. The idea that gunshot wounds were poisonous is supposed to have originated in the fact that in every war there are cases of acute sepsis, developed after the infliction of these injuries, which agree in all their essential points with the results of the bites of poisonous snakes. We are even informed that during the late Franco-Prussian War there were cases which even excited suspicion among the laymen that the enemy had used poisoned missiles.

[Footnote 5: _German Clinical Lectures_, 2d series (New Sydenham Soc., 1877), p. 65 _et seq._]

The nature of the error which Paré and Maggi endeavored to correct is shown by the declaration made by Johannes de Vigo at the commencement of the sixteenth century, who expressed in dogmatic form the views then firmly held by physicians. "A gunshot wound is a contused wound, he says, for the bullet is round; it is burnt, for the bullet is heated; it is poisoned, for the powder is poisonous. The poisoning is the essential condition; therefore the treatment must be directed above all to counteract this."

The next step was that a poisonous substance may develop itself or settle in the wound, and especially in gunshot wounds--a substance which has nothing to do with powder or lead. Paré himself adopted this view. When he took part in the siege of Rouen many wounds sloughed and had a cadaverous smell, and on opening the bodies of those who died numerous collections of pus were found in different parts full of greenish ill-smelling ichor. Besiegers and besieged believed themselves to be wounded with poisoned bullets. Paré looked for the cause in a deterioration of the air by the large quantity of decomposing substances, and he appears to have assumed, as is done at this day, a direct action of the so-called deteriorated air upon the wound itself.

The evil influence of air vitiated by the products of decomposition, not upon wounds only, but upon the organism generally, has never been lost sight of by physicians since that time. That rotten straw, decomposing bodies of men and animals, surfaces saturated with excrement, and overcrowding of badly-ventilated hospitals give rise to infectious fevers and unhealthy state of wounds is not a result of modern observation only. That it was a question of the processes of fermentation which became communicated to the body by means of the exciters of fermentation contained in the air was a view frequently adopted. "To quote one only out of many; John Pringle, in his _Observations on the Diseases of the Army_, published in 1775, devotes a chapter especially to 'Diseases resulting from Bad Air,' and his forty-eight experiments on septic and antiseptic substances contain numerous hints at attempts resembling those made at the present day to determine the antiseptic power of certain things. No advance was made, however, beyond vague surmises concerning the nature of the exciters of putrefaction, and they were for the most part looked for amongst the volatile, ill-smelling products of decomposition, and were believed to be extremely subtle gaseous matters."[6]

[Footnote 6: _German Clinical Lectures_, Second Series (New Sydenham Soc., 1877), p. 67 _et seq._]

Ambrose Paré (1582) first taught that secondary abscesses in surgical cases, "which he had observed in the spleen, lungs, liver, and other viscera, were due to a changed condition of the fluids produced by some {948} unknown alteration in the atmosphere and determining a purulent diathesis."[7] The following quotations force the conclusion that in the early history of medicine there was supposed to be some important relation between wounds of the head and multiple abscesses. "Nicholas Massa (1553) mentions a case of abscess of the left lung, following an injury of the head."[8] "Valsalva (1707) was induced by his own observation to say that the viscera of the thorax were sometimes affected in wounds of the head." "Desault (1794) considered abscesses of the liver to be a very frequent sequence of head injuries."[9] The fact that wounds of the head were frequently followed by abscesses of the lungs, liver, and other organs probably led to the opinion expressed by Desault, Barthez, Brodie, W. Phillips, Copeland, and others, that the disease had its origin in a nervous agency.[10] "Bertrandi and Audouille (1819) sought for a mechanical explanation of the occurrence of hepatic abscesses after head injuries and in cases of apoplexy." Morgagni (1740) somewhat obscurely hinted at the doctrine of the reabsorption of pus--a doctrine which was afterward elaborated by Quesnay in 1819. Morgagni, after quoting a great number of instances of wounds of the head followed by visceral abscesses, opposes the idea of a mechanical transportation of pus thither, and states that abscesses are not confined to the liver and that they may follow wounds and ulcers of other parts besides the head. He ascribes their formation to particles of pus (not always deposited in the form of pus) resulting from the softening and suppuration of small tubercles, which, having been mixed with the blood and disseminated, are arrested in some of the narrow passages, perhaps of the lymphatic glands, and by obstructing and irritating these, as happens in the production of venereal buboes, and by retaining the humors therein, distend them and give origin to the generation of a much more copious pus than what is carried thither; and by this means, he says, we may also conceive how it is that much more pus is frequently formed in the viscera and cavities of the bodies than a small wound could have produced.[11]

[Footnote 7: Braidwood on _Pyæmia_, p. 2 _et seq._]

[Footnote 8: _Ibid._, p. 2.]

[Footnote 9: _Ibid._, p. 3.]

[Footnote 10: _Ibid._, p. 10.]

[Footnote 11: _Ibid._, p. 3 _et seq._]

Cheston (1766) believed that the translation of matter from one point to another was a frequent occurrence after amputations of the larger limbs. John Hunter (1793), and after him Velpeau, demonstrated the existence of pus in the blood. Hunter believed that the pus was derived from the interior of the inflamed veins. He described three forms of inflammation of these vessels--viz. adhesive, suppurative, and ulcerative. Pyæmia he considered to be an aggravated form of phlebitis. Arnott (1829) concluded from his observations--1, That death does not result from the extension of the inflammation of the veins to the heart; 2, that the dangerous consequences of phlebitis have no direct relation to the extent of the vein which is inflamed; and, 3, that the presence of pus in the veins, though the principal, is not the sole, cause of the secondary affection. He accordingly opposes the idea of Abernethy, Carmichael, and others that the constitutional affection is owing to the extension of the inflammation to the heart. The publication of Arnott's and Dance's treatises led to the general opinion being held in England and in France that phlebitis and purulent infection were identical affections, or, at least, that the latter was invariably caused by the former.[12]

[Footnote 12: _Ibid._, p. 14.]

{949} Cruveilhier (1829), admitting the doctrine of the formation of secondary abscesses being due to capillary phlebitis, further laid down an axiom, since proved untenable, that the foreign body introduced into the veins, whose elimination by the emunctories is impossible, will produce visceral abscesses similar to those which occur after wounds and operations, and that these abscesses are the result of capillary phlebitis of those viscera.[13]

[Footnote 13: Braidwood on _Pyæmia_, p. 14 _et seq._]

During the early part of the present century it was generally admitted by the best authorities that the symptoms and lesions in pyæmia were entirely due to the presence of pus in the blood, but whether absorbed from the wound or developed by an inflammation of the veins was at that time a disputed question.

Haller made the first experiments on animals with putrefying substances in the latter part of the eighteenth century, and was convinced that nothing destroys the animal fluids more powerfully than putrefaction. Gaspard (1822) published a complete work based upon his experimental research in regard to the action of putrefying substances on living organisms. He, having produced septic infection in animals by injecting into their blood pus or other putrefying substances, thus prepared the way for other experimenters, by whom he was quickly followed. Ernst R. Virchow repeated the experiments of Gaspard, and discriminated with greater precision between the surgical diseases--septicæmia with its sharply-defined group of symptoms, the opposite of pyæmia. Furthermore, "he showed that the changes in the veins which had been regarded as due to phlebitis were caused by the coagulation of the blood and by subsequent degenerative changes in the thrombi thus formed; that the infarctions and abscesses seen in the viscera were due to emboli which had become detached from softened thrombi; that, as the white blood-globules and pus-globules were identical in appearance, they could not be distinguished; and that it was improbable that pus-globules made their way into the blood."[14]

[Footnote 14: _The International Encyclopædia of Surgery_, ed. by Ashhurst, vol. i. p. 204.]

Panum (1855) conducted a series of important experiments, and endeavored to separate the infectious substance and determine its real nature. He concludes that the real poison is not identical with any of the chemical combinations or any of the single substances which have until now been isolated by chemical analysis from the products of nitrogenous decomposition, but adds that it is probably a concealed ferment belonging to the so-called extractive matters--carbonate of ammonium, leucin, tyrosin, fatty acids, acetic acid, etc. Furthermore, that the putrid poison is stable, fixed, and non-volatile; that it is neither decomposed by boiling nor by evaporation to dryness; that it is insoluble in absolute alcohol, but soluble in water; that the albuminous substances found in putrefying liquids become venomous only because they are impregnated with the septic poison; and that washing these substances in a large quantity of water renders them innocuous; and that the energy of these putrid poisons can only be compared to the venom of serpents, curare, and other vegetable alkaloids.

The prize offered by the Faculty of Medicine at Munich for the best essay on the action of putrefying substances in the animal organism was awarded to Hemmer in 1866. His essay was distinguished for its {950} accurate delineation of the pertaining literature and for the number of experiments reported, while his conclusions bear a striking resemblance to those of Panum.

Bergmann in 1868 sought to determine the poisonous element contained in decomposing animal substances, and for this purpose chemically treated putrid fluids, hoping to find the agent that would excite all symptoms of septic poisoning. He obtained a body of this nature from decomposing yeast, which he called sepsin, although we have no proof that either he or any one else has ever found the same in pus or any decomposing animal matters; and even if it had been found in these, it would then become necessary to demonstrate the fact that no other substance contained in the putrefying liquids could produce septic poisoning. Many other experiments, similar to those which have just been mentioned, were made in the mean while by Magendie, Stich, Billroth and Hufschmidt, O. Weber, Duprey, Learet, Urfrey, Saltzman, Fischer, Frese, Muller, and others. Bergmann had extracted the sepsin from yeast, but Schmidt and Petersen (1869) were able to obtain it from putrefied blood. In 1869, Zuelzer and Sonnenschein claimed, on the contrary, to have separated a new, unnamed septic alkaloid, which was not the sepsin, and the action of which resembled that of atropine and hyoscyamine. Nevertheless, the separation of the sepsin or of the alkaloid of Zuelzer seemed to demand a talent in the manipulator which is not possessed by everybody, and rare are the chemists who possess it--so rare that these substances are not yet either officinally recognized or classified. The attention of the medical profession had now become thoroughly fixed on the chemical character and the physiological action of these newly-discovered substances. It is therefore only natural that we should find during the next few months that the medical societies were much occupied with discussions on these subjects, although no important progress seems to have been made.

Political events now gave a new direction to thought, and the Franco-Prussian War filled the hospitals of both nations with wounded in which there was opened a grand field for the practical study of purulent infection in all its various forms. Humanity now demanded the best efforts of the medical profession. Neither the mechanical nor chemical theories had ever yielded practically any beneficial results; consequently, something better was demanded in this emergency. It was during this important epoch that the germ theory began to assume form and to attract some general attention in the medical profession, although Schroeder and Dusch had shown in 1854 that the filtration of the air through cotton was sufficient to prevent the putrefaction of albuminous substances which had been previously boiled. Pasteur also demonstrated the existence of germs in the air in 1863, and likewise showed their agency in the process of fermentation.

Lister began the antiseptic treatment of compound fractures in 1865, although he did not publish his report until 1867. The cotton-wadding treatment of wounds, which is based on the fact that the air passed through cotton is freed by it from all germs, was first employed by Alphonse Guérin, who refers to it in the following language: "In the latter part of 1870 I had the idea that the cause of purulent infection existed in the germs or ferments which Pasteur had discovered in the air. It was at the end of the war; all the cases of {951} amputation had succumbed to the purulent infection, and not a single large wound escaped the scourge. The studies which I had made from the month of September to the end of December in 1870 had confirmed me in the opinion that purulent infection is neither due to phlebitis nor to the absorption of pus. I believed more firmly than ever that the miasms emanating from the pus of the wounds were the real cause of this frightful malady to which I had been compelled to see the wounded succumb, whether they were treated with charpie or cerate, whether with the lotions of alcohol or of carbolic acid applied several times a day, and which was soaked up by the linen which remained in contact with the wounds. But this miasmatic theory remained, nevertheless, useless, since from 1847, when I professed it, the cases of amputation in my service succumbed to purulent infection in about the same proportion as those who were cared for by my partisan colleagues did from the absorption of pus or the inflammation of the veins. In my despair, seeking constantly a means to prevent this terrible complication of wounds, I had thought of the miasm of which I had admitted the existence, because I was not otherwise able to explain the production of the purulent infection, and which was not only known to me by its deleterious influence, but which appeared to consist of living corpuscles of the nature of those that Pasteur had seen in the air; and then the history of the miasmatic poison possessed for me a new clearness. So, said I then, the miasms are the ferments. I am able to protect the wounded against their fatal influence by filtering the air, as Pasteur had done, while maintaining, in opposition to Pouchet of Rouen, that there is no spontaneous generation. I thought then of the cotton-wadding treatment, and had the satisfaction of seeing my anticipation realized. It was from this time that dates in reality the theory of germs or of ferments as a cause of purulent infection."[15]

[Footnote 15: _Nouveau Dictionnaire de Médicine et de Chirurgie pratiques_, t. xxx. p. 265.]

A series of important experiments were made in 1872 by Coze and Feltz, which consisted in injecting into the jugular vein and the subcutaneous cellular tissue putrid liquids; and they record, among other interesting results observed by them, that the blood of the animal thus destroyed always contained infusoria. These experiments have been repeated and their results confirmed by several observers, and in particular by Davine in 1872.

Another series of experiments were made by Behier and Lionville, which absolutely confirmed those of Coze and Feltz; they likewise found in the blood rounded and rod-shaped corpuscles possessed of movements more or less energetic. Vulpian also confirmed the results obtained by Davine and Behier. He says: "It will not do to deny to the immovable or movable vibriones and corpuscles found by Coze, Behier, and Davine a very important rôle, because they are not the essential contagion of the poisonous blood; it is at least necessary that they should be there in order to produce the alterations which have occurred in this fluid." Chauveau has experimented extensively, and likewise admits the action of the septic vibriones of Pasteur.

Pasteur has made known the result of his investigation in communications to the Academy of Medicine in 1877, 1878, and 1879. There exist, according to him, two principal vibriones--the pyogenic, or the {952} producer of pus, and the septic, the producer of the properly so-called septicæmia. But the latter is not a unique disease, and, as we have seen from the outset, there are confounded under this name different states, light or grave, corresponding with as many forms of vibriones.

The questions of greatest practical importance in regard to this whole group of diseases seem to us to be, as expressed by Dr. Budd, where and how the specific poisons which cause them breed and multiply; and all who have closely followed the scientific investigations bearing on these points which Prof. Tyndall has conducted during the past few years, and who have repeated even a portion of his experiments, cannot fail to be powerfully impressed with the value of the views which he embodied in his work entitled _Floating Matter of the Air_.

NOMENCLATURE.--The want of a systematic classification of the various morbid conditions arising from septic infection has long embarrassed alike authors and students, and even at the present time the vague manner in which the terms pyæmia and septicæmia are used leads to much confusion. The Pathological Society of London appointed, in 1869, a committee to investigate the nature and causes of those infectious diseases known as pyæmia, septicæmia, and purulent infection. This committee, having spent ten years in the study of these affections in connection with nearly all the large hospitals of London, report the following: "Summary.--It would seem, from a careful study of all the cases here collected, that it is probable that the diseases commonly known clinically as pyæmia and septicæmia may be grouped as follows: 1. Septic intoxication.--The effects of poisoning by the chemical products of putrefaction. A non-infective disease. 2. Septic infection.--A general infective process arising from the introduction of some peculiar constituent of putrid matter into the blood-stream. It is supposed by some to be due to the multiplication of living organisms in the blood, and by others to the effect of a non-organized ferment. It terminates fatally without secondary inflammations. 3. Pyæmia (for want of a better name).--An infective process probably, similar in nature to septic infection, but differing from it by giving rise to local inflammation and suppurations, often complicated by thrombosis and embolism, probably due to the blood condition. 4. Thrombosis with softening and decomposition of the thrombus and embolism, causing local abscesses in the viscera wherever the septic emboli lodge, but without the development of any general infective process. 5. Various combinations of one or more of the foregoing conditions in the same subject. 6. Infective periostitis or acute necrosis. 7. Infective endocarditis or ulcerative endocarditis. 8. Infective myositis. 9. A group of obscure cases in which it is impossible to form any idea as to the exact nature, often called spontaneous septicæmia or pyæmia."[16]

[Footnote 16: _Trans. Pathological Soc. of London_, vol. xxx. p. 38.]

It will be observed that the earlier writers on medicine, although aware of the existence of septic diseases, wholly failed to discriminate between pyæmia and septicæmia until 1848, and even since that date these terms have been only partially adopted by authors, by whom frequently the meaning of the same word has been so modified as to refer to essentially different conditions. Custom having fully sanctioned the use of these terms, it is now thought that a separate consideration of their {953} nomenclature may be advantageous, and consequently we shall pursue this course.

NOMENCLATURE OF PYÆMIA.--In Dunglison's _Medical Dictionary_ the definition given to pyæmia is, "Pyohæmia," and the latter word is defined as follows: "Pyohæmia, Pyæmia, Pyohémie (F.), from _pyo_, and [Greek: haema], 'blood;' alteration of the blood by pus, giving occasion to the diathesis seu infectio purulentia."

The committee appointed by the Pathological Society of London in 1869 report on this subject as follows: "The most common definition of pyæmia is, no doubt, that adopted by the College of Physicians in the nomenclature of diseases. It is as follows: 'A febrile affection resulting in the formation of abscesses in the viscera and other parts.'"

Birch-Hirschfeld includes under the name pyæmia "all cases in which any general infective process is set up as a secondary consequence of a wound."[17] Virchow has proposed the name ichorrhæmia. O. Weber uses the name embolhæmia for the condition in which emboli are found in the blood. Hueter in pure cases of purulent infection without metastasis calls the disease pyohæmia simplex; in cases with metastasis, pyohæmia multiplex; and when complicated with septicæmia he designates it as septo-pyohæmia. The term hospitalism has been applied to this disease by Erichsen and Sir James Y. Simpson, and the former remarks that "the term pyæmia is used in a very wide and elastic manner, and by many is made to include various forms of blood-poisoning."[18] Billroth says: "Pyæmia is a disease which we believe to arise from the taking up of pus, or of the constituent parts of pus, into the blood." Koch employs the term pyæmia merely to denote a general affection accompanied by metastatic inflammation and suppuration.

[Footnote 17: _Trans. Pathological Soc. of London_, vol. xxx. p. 22.]

[Footnote 18: _On Hospitalism_, p. 73.]

The French definition and nomenclature of pyæmia, according to Guérin, is as follows: "Purulent infection, or pyohæmia, purulent fever, surgical typhus." The purulent infection is a poisoning of the blood, which terminates by the formation of multiple abscesses, which have been improperly known under the name of metastatic abscesses.

From 1820 to 1870 surgeons admitted that these abscesses were the result of a phlebitis having its origin in a wound exposed to the air. Therefore, this disease was variously designated under the name of phlebitis, pyohæmia, or purulent infection. Tessier called it purulent diathesis; "in 1847, I compared it to the typhus, and, as the poison is absorbed from the surface of the wound in the purulent infection, I gave it the name of surgical typhus or purulent fever."[19]

[Footnote 19: _Nouveau Dict. de Méd. et de Chir. pratiques_, t. xxx. p. 222.]

Having given enough on this subject to answer our purpose, we will consider the nomenclature of another septic complication.

NOMENCLATURE OF SEPTICÆMIA. The term septicæmia was first employed by Piorry, and was applied for a considerable time to all those diseases in which the blood was submitted to a septic influence. Therefore, the term was made applicable to the morbid conditions existing in anthrax, glanders, typhus and typhoid fevers, variola, and also all forms of purulent and putrid infections. Guérin now adds: "Fortunately, for several years the most competent authors seem to have wished to {954} reserve the name of septicæmia for what surgeons call putrid infection, and for the morbid state that the experimenters produce by the injection of putrid material into healthy animal tissues; it is consequently the experimental septicæmia which we aim at first and foremost."[20]

[Footnote 20: _Nouveau Dict. de Méd. et de Chir. pratiques_, t. xxx.]

Dunglison defines septicæmia with a single word, septæmia. The same authority gives the following derivation and definition to septæmia: "From [Greek: sêptos], 'rotten,' and [Greek: haema], 'blood.' A morbid condition of the blood produced by septic or putrid matters."

Sanderson says: "What I mean by septicæmia is a constitutional disorder of limited duration, produced by the entrance into the blood-stream of a certain quantity of septic material. It must, therefore, be regarded less as a disease than as a complication, differing from pyæmia not only in the fact that it has no necessary connection with any local process, either primary or secondary, but also in the important particular that it has no development."[21]

[Footnote 21: _British Medical Journal_, Dec. 22, 1877.]

Both Davine and Koch designate as septicæmic all cases of general infection from wounds in which no metastatic changes occur. "Birch-Hirschfeld limits the term septicæmia much in the same way as Sanderson. He describes as septicæmia those cases in which the disease results merely from the absorption of the products of putrefaction, and regards it merely as a process of poisoning, such as might arise from the injection of any other noxious chemical substance into the blood. Pyæmia, on the other hand, he considers a truly infective process, probably due to the entrance of specific organisms into the body. He would therefore include many of the cases described by Koch as septicæmia under pyæmia."[22]

[Footnote 22: _Trans. Pathological Soc. of London_, vol. xxx. p. 9.]

Billroth defines septicæmia as an "acute general affection which arises from the taking up of various kinds of putrid substances into the blood, and it is believed that these putrid substances so change the quality of the blood that it can no longer fulfil its physiological functions."[23]

[Footnote 23: _Lectures on Surgical Pathology and Therapeutics_ (trans. from 8th ed.), vol. ii. p. 41.]

Heuter defines septicæmia as a fever caused by the entrance into the circulation of the products of putrefaction from local centres of decomposition. He draws no clear distinction between an infective and a non-infective form, but the affection he describes as pyæmia simplex or pyæmia without metastasis seems to include many cases which Davine, Koch, and others would include under septicæmia.[24]

[Footnote 24: _Trans. Path. Soc. of London_, vol. xxx. p. 9, 1879.]

Having before us the views of some of the prominent authors who have written upon the nomenclature of pyæmia and septicæmia, we observe that the use of these terms is based either on known or imaginary morbid conditions of the body, more especially of the blood. It therefore seems that the first step toward determining the proper limit within which these terms can be employed consists in learning their accurate meaning, which is fortunately clearly shown by their derivation. The next step consists in the application of these terms to the morbid conditions which are described more or less completely by these words. It may be here added that there will be frequently required for a full and definite expression certain modifying words, and consequently we may {955} properly employ such phrases as puerperal septicæmia, spontaneous pyæmia, etc.

Having carefully examined the terms employed by various authors in connection with the morbid changes which are known to occur in certain cases of septic contamination, we give our preference to the following nomenclature: Septicæmia, septo-pyæmia, pyæmia simplex, and pyæmia multiplex.

The term septo-pyæmia is applied to a morbid condition possessing certain peculiarities of both septicæmia and pyæmia, and it is supposed to arise from the absorption of both poisons; the term pyæmia simplex is applied to a pyæmic condition in which there is no metastasis; while the name pyæmia multiplex is given to that form of disease which is characterized by the existence of metastatic abscesses. It may be well to add here that this nomenclature is not intended to cover all cases of septic poisoning, but to be applied to those cases only in which the morbid changes give to the terms a certain degree of appropriateness.

Septic poisoning may be justly regarded as a single chain composed of many links. Take, for example, a case of amputation of the thigh, followed within a few hours by traumatic fever, later by septicæmia; afterward there may be developed secondary fever; formation of ichorous pus, with absorption and its concomitants; pyæmia, accompanied by embolism, thrombosis, abscess in the lungs, liver, etc. To these may also occasionally be added phlebitis and inflammation of the joints, terminating speedily in suppuration. This chain may in this case be further lengthened or varied with traumatic erysipelas or with hospital gangrene. In fact, the variations in these cases are very numerous, and all these conditions, together with many others, are due to septic blood-poisoning.

ETIOLOGY OF PYÆMIA.--Four theories have been advanced at different times to explain the etiology of pyæmia, and they have been designated as follows: the mechanical, the nervous, the chemical, and the germ theories respectively; and their action is based on the following hypotheses: 1, that pus enters the blood, circulates in it, and acts as a poison; 2, that an irritation is excited in certain visceral organs in sympathy with inflammation of the fibrous membranes of the cranium or the bones of the upper or lower extremity, and there is thus produced a metastasis to these organs of an ichorous miasm or of a fluid which is more or less acrid; 3, that a chemical poison is generated from the pus in the wound, and when it is absorbed produces pyæmic manifestations; 4, that the putrefaction of pus in wounds is caused by a microscopic organism which enters the circulation and produces pyæmia.

The first hypothesis was somewhat modified, as we have already mentioned, by John Hunter and others, who advanced the idea that pyæmia consisted essentially of a phlebitis, and that the pus found in the circulation had its origin within the veins. However, it has since been shown conclusively that pyæmia cannot be produced by the injection of healthy pus into the cellular tissue or veins. This fact having been generally admitted by the profession, it is thought unnecessary to adduce here either the experiments or the arguments which have been accepted as conclusive on this important point. It is not even necessary to bring forward the disputed question of the possibility of the entrance of pus into the blood, since laudable pus does not produce pyæmia. In fact, we have reached a point in the {956} progress of medicine when the discussion of either the first or second hypothesis ceases to be interesting to medical men. Consequently, our chief interest in the study of the etiology of pyæmia centres in the third and fourth hypotheses; and we believe that it may be safely asserted that the origin of this disease has been fully demonstrated by an almost unlimited number of experiments.

The injection of pus into living animals produces local, remote, and constitutional symptoms. The character of these symptoms depends principally on the kind of pus, laudable or ichorous, the quantity injected, and the site of the injection. It will be readily perceived that in cases where the pus is thrown directly into a vein the local symptoms would be unimportant, while the danger of remote trouble--metastatic abscesses in the lungs, liver, etc.--would be very great; but should the injection be made into the connective tissue, then the relations would be reversed. Constitutional symptoms may exist in both cases, but will differ in character and degree.

In regard to the character of the pus, and its agency in the production of this disease, Billroth says: "The old view, that pyæmia is only induced when decomposed pus (ichor) is reabsorbed, is entirely erroneous. There are cases where decomposed, putrid pus enters the blood, and which present a combination of the symptoms of septicæmia and pyæmia (septo-pyæmia of Hueter)."[25] Dupuytren failed to produce metastasis by injections of pus into the veins of dogs; these results were confirmed by Boyer, who only obtained metastasis when he used ichorous pus in his experiments. The same results are recorded in the works of Günther and Sedillot, based on numerous experiments. Beck made fourteen experiments very carefully, but did not succeed in producing metastasis in a single case. The same results are recorded by a commission of the Physiological Society of Edinburgh. O. Weber has recently shown by extended experiments that carefully filtered pus will not produce metastatic abscesses in the lungs. Therefore, it may be considered as proved that fluid pus injected into the veins of an animal produces no metastatic points of inflammation.

[Footnote 25: _Surgical Pathology_, p. 344.]

It should not be supposed, however, that because injection of fresh (non-ichorous) pus failed to produce metastatic abscesses, it was therefore without results, as the earlier experimenters thought. Billroth and O. Weber have shown by their recent experiments that these injections are uniformly followed by fever, and, if subcutaneous, by abscess; and further, that injections of fresh pus produce even a higher temperature than do those of ichorous pus; but the pus taken from cold abscesses has apparently very slight effect. The fresh non-ichorous dried pus was found to possess in a similar degree the power to excite inflammation and suppuration; even the removal of the albumen did not change its character or power. It will be observed that these injections caused not only local inflammations, but severe constitutional symptoms, as high temperature, etc. Experiments have thus far completely failed to show the agent that excites the inflammation, although it is generally admitted that it at least exists in the molecular bodies.

Virchow and Panum have shown conclusively by their experiments on living animals that the introduction of foreign bodies into the {957} veins--as powdered coal, wax balls, and quicksilver--fail in all cases to produce metastatic abscesses in the visceral organs or symptoms of pyæmia. These foreign bodies were frequently found blocking up the terminal branches of the pulmonary artery, in some cases encapsulated, frequently resembling miliary tubercles, and occasionally surrounded by evidences of slight local inflammation, but in every instance without suppuration. The same experimenters, however, observed that the introduction of ichorous pus and decomposing animal tissue into the veins was attended with the formation of metastatic abscesses and other symptoms of pyæmia. They therefore conclude that the introduction of putrid animal substances into the veins, and the further transport of the same to the branches of the pulmonary artery, produce metastatic abscesses, and that the origin of these deposits is independent of the mere stopping up of the branches of this artery.

The occlusion of the blood-vessels in this diseased condition is a subject which has given rise to much discussion. Some of the earlier writers supposed this phenomenon constituted the disease pyæmia, while others believed it to be the essential cause. Roser says: "But the thrombus is, as can be easily proved, not the cause, but only a symptom, of pyæmia. If a surgical patient--_e.g._ one suffering with an injury of the head--is attacked by inflammation, and occlusion of a large vein, as of the common iliac vein, for instance, then there are three different theories for the inflammation of the occluded vessel--viz. Hunter's, Rokitansky's, and Virchow's. According to the old Hunterian phlebitic theory, the coagulation of the blood should be the result of the inflammation of the vein. On account of the circumstances under which the coagulation of the blood in the vein has occurred, one might suppose that the cause must be the oozing of coagulable exudation from the inflamed wall of the vein, but pathological dissections, especially Rokitansky's, would not accord with it. Large veins were found plugged up without the existence of corresponding indications of inflammation, and perfectly clear indications were often present that occlusion had preceded the inflammation. Consequently, the occlusion of the vein was the primary condition, and this must be explained in some other way than by its inflammation. Rokitansky in his theory recognized an independent disease of the blood. Yet it does not appear, on examination of the morbid conditions, that this theory can account for them. If it is recognized as correct that a primary disease of the blood is to be admitted, yet the coagulation of the blood in a large vein has not been traced back to it. It remained wholly unexplained why a single vein, especially one so large and strong as the common iliac, should become the seat of the local coagulation. The necessity of finding a local basis for the local coagulation could not be denied. For that reason it was greeted as a highly desirable advance when Virchow pointed out that the occlusion of such large veins could be dependent on the coagulation of the blood in the concave spaces behind the valves of the veins, or through the coagulation in the small branches--_e.g._ the hypogastric veins, which is gradually carried forward until it reaches the common iliac, and by continual increase this vein may also be filled up. At the same time, it was demonstrated that not infrequently, much oftener than {958} was formerly supposed, the coagulated masses of blood are broken up and carried farther on in the circulation, in this manner producing occlusion of the pulmonary artery or its branches."[26]

[Footnote 26: _Archiv der Heilkunde_, Erst. Jahrg., Erst. Heft, S. 4.]

The examination of this subject finally brings Roser to this conclusion: "Contamination of the blood is essentially the primary cause of pyæmia; thrombosis is only a result of this morbid contamination, and cannot, therefore, be regarded as the cause of pyæmia, but only as an apparent part, as one of the symptoms of the same."[27] The opinion here expressed by Roser I believe to be the one generally entertained by the profession at this time.

[Footnote 27: _Ibid._, S. 43.]

In cases of pyæmia there are recognized two principal sources of contamination of the blood--viz. the wound itself, and the vitiated condition of the atmosphere surrounding the patient--contamination, in the first place, directly from the wound through the blood-vessels; and in the second, by the passage of disease-germs or of the poisonous elements into the blood along the respiratory tract. E. Wagner says: "The latest examinations in regard to the vegetable parasites have made it very probable not only that these are the active agents, but also--what has been clinically quite generally accepted--that septicæmia and pyæmia owe their origin to different plants (the first to rod bacteria, the latter to globular bacteria); and, finally, that both may combine."[28] These germs may be generated in the wound or be received into it from the surrounding atmosphere. The character of the wound and the conditions surrounding the patient thus become important subjects for the consideration of the surgeon.

[Footnote 28: _Manual of General Pathology_, p. 593.]

It has been observed, and is now generally admitted, that wounds complicated with a fracture of the long bones of the extremities, opening large medullary cavities and accompanied by extensive laceration of the soft parts, always increase the danger of blood-poisoning. This fact may be more thoroughly understood by a brief consideration of the condition of the parts. Frequently in open fractures large quantities of pus constantly remain in contact with the surface of the wound, while detached fragments of bone, which become speedily necrosed, move about with every motion of the injured limb, lacerating more or less the surrounding tissues, and thus exciting inflammation and suppuration. The periosteum becomes inflamed; a widespread suppurative periostitis is the result; necrosis of the bone from insufficient nutrition follows, while mechanical pressure on the pus aids in its absorption. The medulla frequently takes on suppurative inflammation, and here the surgeon fails to receive prompt warning of danger; slowly the suppuration progresses, without pain or other symptoms unless the disease has extended to the other tissues; the medullary cavity at the fractured end of the bone may be completely or partially occluded by a new osseous formation; and in such cases the absorption of pus by the comparatively large venous vessels of this cavity is greatly facilitated.

The soft parts may also be the seat of dangerous trouble. The same force that produced the wound and fracture may have also contused the soft parts, destroying in a greater or less degree their nutrition, thus giving rise to gangrenous sloughs, or in other cases to the formation of abscesses, etc. I will also call attention to the fact that the laudable pus {959} in these cases is most favorably situated for a rapid change into that commonly called ichorous. The heat of the parts and the contact of the pus with the atmosphere will not fail to effect its rapid decomposition.

ETIOLOGY OF SPONTANEOUS PYÆMIA.--It is unquestionable that cases of true pyæmia have been observed in which the etiology was not traceable to a wound; and it is equally certain that this failure to discover such a source of contamination in the majority of cases is no proof that it did not exist. When it is remembered that a large portion of the alimentary canal, the respiratory and the genito-urinary tracts, are so situated that the existence of a contaminating wound might be absolutely undiscoverable, we are compelled to admit the possibility of a local centre of contamination in all these cases. But the question may be asked here with propriety, "Is fatal pyæmia, independent of a wound, ever produced by breathing vitiated air?" The answers to this question must generally be a negative, although it is certainly true that poisoning of the blood does take place to a certain degree, as is abundantly shown by the different symptoms arising in patients thus exposed who are not suffering with wounds. It is said that dogs exposed in this way are found to rapidly emaciate and suffer from severe and constant diarrhoea. The various symptoms arising in patients confined in overcrowded and pus-infected wards, among which may be mentioned loss of appetite, with diarrhoea and emaciation, are too well known to require an enumeration here. Therefore it appears highly probable that living in and breathing a vitiated atmosphere may act as a strongly predisposing cause, only requiring a slight scratch or abrasion of the skin, in which the infection may be said to act as an exciting cause of pyæmia.

In reference to such complications the following questions are asked by Roser: "Is it a specific deleterious material, a miasmatic or contagious disease-poison, or, as it is generally expressed, a zymotic agent? Must we regard each particular typhus-like fever, with its remarkable changes of blood, with its various localizations in all the organs and membranes, with its chills, furred tongue, petechiæ, delirium, etc., as we regard typhus, scarlatina, variola, etc.? or, as Virchow teaches us, is this pyæmia, so greatly feared by all surgeons, only an ontological idea? Is the word pyæmia only a general name for three different conditions--viz. leucocythæmia, thrombosis, and embolism, or ichorrhæmia and septicæmia? or are there, as many have supposed, two ways in which pyæmia may originate? Is there one primary miasmatic pyæmia analogous to the other epidemic, so-called zymotic diseases? and again, a secondary pyæmia arising from suppurative inflammation, wherein the poison is formed in the patient's own body, which is infected by a single organ?"[29]

[Footnote 29: _Loc. cit._, S. 39.]

That this disease is caused by a specific deleterious material in the large majority of cases is no longer a question for discussion. The only question to consider is, whether it always arises from the same cause. Is it possible for pyæmia to originate spontaneously? Are there any cases of sporadic origin, or are they always due to endemic or contagious influences? No definite answer can be given to these questions, although, undeniably, the weight of the argument is strongly opposed to a sporadic origin. The term miasmatic, as {960} used by Roser, probably refers to the vitiated condition of the atmosphere, as seen in the overcrowded surgical and obstetrical wards of hospitals. In no other sense can the word be appropriately used in connection with the subject of pyæmia. It is true, pyæmic diseases are found to prevail at certain seasons and in certain localities much more extensively than under other circumstances. The same, however, is true of cholera, typhus fever, scarlatina, variola, and other contagious diseases. That pyæmia is contagious has been frequently demonstrated. I therefore conclude that the prevalence and spread of this disease must be explained by the same rules as are applied to the existence and propagation of these allied affections.

This inquiry into the etiology of pyæmia brings before us again the four hypotheses which have been given in explanation of the same number of theories. The first and second have been already abandoned by the medical profession, after it was satisfactorily demonstrated that they were based on false theories, and consequently there remain for our consideration only the third and fourth.

The third hypothesis assumes that a chemical poison is developed in the wound-secretions, which when absorbed produces pyæmia. An examination of the subject does not justify us in asserting that this proposition has been proved, although it is certain that the results of experimental inquiry demand for it a more extended investigation. In all the analyses which have thus far been made the investigators have entirely failed to give us an adequate knowledge of this poison, and not a word has ever been said in regard to the agency by which it is produced, although it is universally admitted to have been only obtained from decomposing animal substances. It is therefore pertinent to the continuation of this inquiry to ask, By what agency is the putrefaction of animal substances produced? It has now been fully shown that there can be but one answer given to this question--viz. the putrefaction of albuminoid substances can only be effected by living organisms. We therefore conclude that the fourth hypothesis brings us at least one step nearer the correct explanation of the etiology of pyæmia than the third, since we justly assume that if there is a chemical poison in decomposing albuminoid substances, it is produced through the agency of living organisms.

ETIOLOGY OF SEPTICÆMIA.--The first question which arises in the discussion of the etiology of this morbid condition is entirely dependent on the scope which we give to the word septicæmia. Sternberg says: "The view which is entertained by high authorities, upon clinical and experimental evidence, is that there are two forms of septicæmia--the one a septic toxæmia due to the effects of a chemical poison or poisons evolved during the putrefactive decomposition of certain organic substances, especially of nitrogenous animal products; the other an infective disease produced by the rapid multiplication in the body of the infected animal of a parasitic organism. The best-studied and most widely known form of septicæmia, due to the presence of a parasitic organism, is the disease known as anthrax--charbon of the French, milzbrand of the Germans--but several other varieties are now well established, in which similar symptoms and pathological results are produced by organisms morphologically different from the bacillus anthracis. Among these may {961} be mentioned the form of septicæmia in the mouse, so well studied by Koch, which is due to a minute bacillus, and the form of septicæmia in the rabbit, produced by the subcutaneous injections of human saliva, due to micrococci, which has been studied by Pasteur, Vulpian, and myself independently."[30]

[Footnote 30: _Amer. Jour. Med. Sci._, July, 1882, p. 70.]

The terms septic toxæmia and septic intoxication are applied indiscriminately to the same disease, and the committee appointed by the London Pathological Society to investigate the nature and cause of those infectious diseases known as septicæmia, etc. further report that "ordinary wound-fever is merely septic intoxication in a very mild form, and it is only necessary for the dose absorbed to be sufficient in quantity for fatal consequences to ensue. Septic intoxication is, therefore, of the commonest possible occurrence as a complication of severe surgical injuries, but it is in so mild a form as to bear but little resemblance to that experimentally produced on animals."[31] The question which now arises is, Shall septic intoxication be classified with septicæmia?

[Footnote 31: _Trans. Pathological Soc. of London_, vol. xxx. p. 14.]

We have been long accustomed to speak of this complication as a surgical or traumatic fever; and consequently any change in this classification must necessarily lead to confusion. Furthermore, it is now generally supposed there is much difference in the etiology of these morbid conditions. It is claimed that septic intoxication arises from the absorption of a chemical poison evolved through the agency of living organisms during the process of putrefaction in a wound, and that the conditions are unfavorable for their development within the blood or tissues of a living animal; but in true septicæmia the organisms are developed in the wound during putrefaction, and then find their way into the blood and tissues of the body, where they rapidly multiply. Consequently, the former condition tends to a rapid recovery--unless the quantity of poison primarily admitted to the system has been excessive--while the latter tends to a fatal termination.

Septic intoxication is regarded as a non-infective disease, and true septicæmia as an infective malady. The only etiological similarity between these morbid conditions is found in the fact that they take their origin in putrefaction, which is effected by the action of different organisms possessing marked morphological differences and requiring essentially different surroundings for the maintenance of life and reproduction. Thus, it is supposed that in cases of septic intoxication the organism by which putrefaction is caused in the wound-secretions can only live in the open air, and that its life is commonly only of a few hours' duration. The brevity of bacterial action in this instance may be due to a failure of the absorptive power or to a changed condition in the wound-fluids, rendering them unfit to support the organism.

It is now a well-recognized fact that all septic absorption ends so soon as the wound-surfaces are covered with healthy granulations, but that septic absorption, which produces septic intoxication, is most commonly of a much shorter duration, and, consequently, that the wound complication, which I prefer to designate traumatic fever, is essentially an acute disease, and can only be lengthened out by unusually favorable circumstances for the continuance of the absorption of the poison by which it is produced. {962} The severity and danger of the disease will necessarily depend on the amount of poison absorbed and the resisting power of the patient; but since there is no multiplication of the materies morbi within the body, a rapid elimination by the natural emunctories may be reasonably expected under favorable circumstances.

It should be observed here that the etiology of septicæmia differs from that of traumatic fever, since the organisms in the former condition are first formed in the wound-secretions, but quickly enter the body, where they rapidly multiply; consequently, Chauvel has defined surgical septicæmia as follows: "The particular intoxication which results from the penetration and multiplication in the body of a specific microbe designated by Pasteur under the name of septic vibrio." The bacterial origin of this disease is now generally accepted, and the only question in the professional mind seems to be whether the organisms are the direct or indirect cause of the malady.

There are also some other interesting questions which have arisen in connection with the study of this subject, and are thought to be of sufficient importance to merit mention here. It has long been known that dissecting wounds are most dangerous when made while examining the body very soon after the death of the subject. Recent observations seem to justify the conclusion that the greatest activity of the septic agent is often, if not always, attained before the odor of putrefaction has become fairly perceptible; and even before this odor has reached its maximum degree of offensiveness the danger from septic poisoning has generally disappeared. In some cases septic intoxication is promptly followed by a slight inflammation in and about the wound, which may entirely disappear within a few hours, but only to reappear after a lapse of eight to fifteen days, with the first vigorous physical exercise of the patient. Two cases of this kind have recently come under my observation. In both instances the wounds were located in the hands, and the exercise which developed the septicæmia consisted in rowing a boat, and while thus engaged the local symptoms reappeared with such severity as to cause the patients to quickly discontinue the labor. The reappearance of the local inflammation in both these instances was quickly followed by a rigor and the rapid development of other constitutional symptoms, although prior to the recurrence there was no pus, nor even marked inflammatory action, in any part of the hands.

Professional attention was first called to the above-stated facts by Panum in 1855, who discovered that the maximum toxic action of putrid substances is generally developed during the first hours of bodily activity. In this stage of incubation in cases of surgical septicæmia, if we admit the bodily action as an etiological factor, we observe a striking resemblance to one of the leading characteristics of all the infectious diseases, which unquestionably depend on some sort of septic poison. Furthermore, this analogy becomes most striking if we contrast the effects arising from dissecting wounds with those of the bites of poisonous serpents and rabid animals.

Further investigation is required to settle the perplexing questions of etiological and pathological differences in these allied morbid conditions, for although much has been accomplished during the last two decades, still much more remains to be done. It has only recently been discovered {963} that the septic material in septicæmia is absorbed by the lymphatics, while in pyæmia the poison enters the body through the veins.

ETIOLOGY OF SEPTO-PYÆMIA.--It is now generally admitted that remittent fever and typhoid may be associated, and this morbid condition is commonly designated by the term typho-malarial fever. The etiology is unquestionably dependent upon the action of the two distinct and entirely dissimilar poisons. Scarlatina is likewise frequently complicated by diphtheria, and here we have the combined action of two poisons, each commonly designated as septic and supposed by many physicians to be similar.

In a like manner, it is believed that septicæmia and pyæmia may be associated, and take their origin in dual poisons; but since the etiology of both these morbid conditions has been already described, it is not deemed necessary to dwell longer on septo-pyæmia under this division of our subject.

PATHOLOGY OF PYÆMIA.--The study of the pathology of pyæmia is advanced by adopting the following classification, which is based on recognized post-mortem lesions. The pathological appearances in these forms of the disease differ widely, although the clinical symptoms are often similar. In pyæmia simplex the pathological conditions are essentially more negative. This variety of the disease can only destroy life by the height and duration of the fever which is maintained in connection with the continued existence of ichorous pus. There is found, as an essential basis of this form of disease, extensive suppuration in the subcutaneous tissues.

The arguments in favor of the admission of pus-corpuscles into the blood are as follows: 1. The blood in pyæmia is known to contain more white granular spherical bodies than are normal. The question has been raised, Are they pus-cells or white blood-corpuscles? The answer is difficult, and has not yet been attained. Virchow, in the mean time, has proved that we cannot differentiate, morphologically, between the blood- and pus-corpuscles. 2. Cohnheim has demonstrated the existence of the wandering corpuscles in cases of inflammation. Therefore it appears probable that in cases of pyæmia the blood may contain the pus-corpuscles, but further investigation is needed to establish this fact. However, the establishment of this point would still leave the more important undetermined.

There are often important changes observed in the blood of patients dead of pyæmia, to which I now desire to direct attention. The red corpuscles of the blood, even in the early stage of the disease, in many cases show signs of disintegrating into molecules, and are observed to be accumulated in masses without showing the slightest tendency to form rouleaux. There is a steady increase in the number of pus- or white corpuscles in the blood of pyæmic patients during the whole course of the disease in fatal cases. The condition of the red corpuscles, already mentioned, becomes more and more marked toward the fatal termination.

In all cases of pyæmia multiplex the increased coagulability of the blood may be observed in the early stages of the disease, and steadily increases as the disease progresses.

In pyæmia simplex this condition is less marked, although generally present, "while we know septicæmia diminishes or destroys the {964} coagulability of the blood. Hereby the possibility is given, at least on the cadaver, to differentiate between pyæmia simplex and septicæmia, although cases occur of the more fatal septic infection in which the post-mortem condition is a complete or almost complete negative. Therefore, in these cases the differential diagnosis on the cadaver must be limited to this, that we are able to demonstrate the existence of a purulent or ichorous deposit." It will be readily observed that the difference in diagnosis mentioned above relates to pyæmia and septicæmia, and not to the different varieties of the former disease.

The following facts should be constantly kept in mind by the surgeon to enable him to differentiate between the two forms of pyæmia: In pure cases of purulent infection, without metastasis, the disease is called pyæmia simplex, and in cases with metastasis, pyæmia multiplex. The various conditions on which the metastasis may depend are shown by Hueter, who says: "The metastatic abscesses of pyæmia multiplex met with in the lungs, liver, spleen, and other internal organs are regarded, with the greatest probability, as a result of the embolic process. The metastatic inflammation of the serous membranes, of the cellular tissues, and of the parotid glands, and probably also a few metastatic inflammations of the internal organs, are at present supposed to arise from a general inflammatory diathesis."[32] It has already been shown by numerous experiments on animals that metastatic abscesses in the lungs, liver, and other visceral organs only arise after the introduction of ichorous pus, while healthy pus has uniformly failed to produce these results.

[Footnote 33: Billroth's _Handbuch der Chirurgie_, S. 88.]

It now remains to be shown how the introduction of ichorous pus acts in the production of pyæmia multiplex. The ichorous pus, having found its way into the venous circulation, gives rise to the formation of thrombi in the veins; these clots become more or less broken up, and are carried forward by the blood to the right auricle; from this auricle to the right ventricle; from this ventricle to the pulmonary artery, and through its ramifications to every part of the lungs. In the minute ramifications of this vessel are found wedge-shaped clots of various sizes in different conditions, some softened and others still firm. The possibility of these clots ever passing through the lungs, and afterward being arrested in other visceral organs, has been demonstrated on animals. It has been shown that fine particles of foreign matter injected into the veins have passed through the lungs and subsequently lodged in the liver. This theory enables us to account, upon a mechanical basis, for the existence of the metastatic abscesses in the liver which have apparently originated as the result of primary infection.

In other cases these abscesses are supposed to arise from secondary infection. Thus, ichorous pus, having found its way into the venous circulation, produces primarily venous thrombi, which, as in other instances, break up, the clots being carried in the same manner into the terminal branches of the pulmonary artery, where they are designated as emboli. The first action of the emboli is the mechanical closure of these vessels, thus depriving the surrounding parts of nutrition to a greater or less extent. It will be proper now to recall the fact that the composition of these emboli is such as to favor rapid suppuration; this commonly commences {965} in the clot and surrounding tissues, having been preceded by a brief stage of congestion and inflammation. There is also occasionally found around these points more or less extravasation. The metastatic abscess thus formed in the lungs is favorably situated for the production of secondary infection. From this abscess thrombi arise in the pulmonary veins, which become disintegrated, and are carried to the auricle, thence to the left ventricle, and finally through the aorta, and find lodgment in the terminal branches of the arteries of the various organs, where they produce the characteristic lesions.

The organs which most frequently become the seat of this secondary infection are the liver, spleen, kidneys, brain, and eyes.

Let us now briefly examine this mechanical theory. Do metastatic abscesses arise from a single cause or from a combination of causes? I am inclined to the opinion that the proximal cause of metastatic abscesses in the visceral organs is the existence of emboli in the terminal branches. The vitiated atmosphere surrounding the patient, the existence of a wound, and the formation of ichorous pus are conditions which should not be lost sight of. These are the elements acting on the blood, producing in it morbid changes, and may therefore be regarded as predisposing causes. The morbid conditions of the blood, the increased number of white blood-corpuscles (possibly pus), the disintegration and other changes in the red corpuscles, may be regarded as the exciting causes of metastatic abscesses. It is thus readily observed that emboli may form in the lungs and liver at the same time, or the origin of those in the lungs may precede the formation in other organs.

Is the formation of emboli in the terminal branches of arteries always dependent on the disintegration of thrombi? The answer to this question must, I think, be a negative, although in surgical practice it rarely happens that the emboli take their origin from any other cause. In the large majority of cases, unquestionably, the thrombi primarily exist in the vicinity of the wound in which ichorous pus is generated; but it not infrequently happens during the process of disintegration that broken-up clots are carried forward by the current of blood, receiving accretions on the way, until finally they fill a large venous trunk. In confirmation of these facts relating to the primary origin of thrombi, it is said to have been observed in epidemics of puerperal fever, which were complicated with metastatic abscesses of the visceral organs, that the thrombi occurred in the pelvic veins. In case of wounds of the lower extremity the clot is frequently found in the common iliac vein, although probably it should always be regarded as a secondary formation. In rare cases the only thrombi discovered at the autopsy are found situated far away from the injury.

Observation fully establishes the fact that, after death from pyæmia, pathological changes are much more frequently met with in the lungs than in any of the other organs. This certainly strengthens the embolic theory. Billroth mentions eighty-three cases of true pyæmia multiplex, in which the metastatic abscesses occurred as follows: seventy-five times in the lungs, seventeen times in the spleen, eight times in the liver, and four times in the kidneys. Sedillot remarks that in one hundred cases of pyæmia we find the lungs affected in ninety-nine, the liver and spleen in eight, the muscles in seven, and the heart and peripheric {966} cellular tissue in five cases. The brain and kidneys are comparatively seldom involved.

The theory previously mentioned as the embolic relates to the aggregation of fibrin into clots; but another theory has been recently advanced by E. Wagner, who found in many cases the capillaries in the lungs filled with fat, and was inclined, from the direction it extended in these vessels, to explain a certain number of the pyæmic cases by the fat emboli; but it has been shown that the existence of the fat emboli in pyæmia is purely accidental and possesses no significance. Pyæmia multiplex very frequently occurs without fat emboli, and vice versâ; either process may complicate the other, and so the fat emboli may acquire special importance by obstructing the respiration, and probably also in their way the embolic fat may serve as a carrier of putrid material.

MORBID ANATOMY.--The external appearance of the body varies greatly. The skin, in those cases in which the patient was jaundiced before death, will be found in every part of the body to be of a dark orange or dirty icteric tinge, but in other cases it may present a pale or anæmic appearance. There are also sometimes found circumscribed ecchymoses or purpuric patches, while the edges of ulcers or open wounds are generally of a blackish or dirty yellow color. The lips and finger-nails present a livid appearance; epithelial defects are observed in the cornea, but these had their origin there before the death of the patient.

The eyes in some cases are sunken deeply in their sockets, and where the disease has been protracted there is often very great emaciation. Rigor mortis is commonly well marked after a few hours. When death occurs from puerperal pyæmia there are generally found some indications of the recent parturition, although the principal lacerations or injuries may be confined to the womb. All fluids disappear from external wounds before the death of the patient, and they remain dry afterward.

In some cases the cellular tissue is the seat of diffuse suppuration. The pus formed is thin, fetid, and unhealthy. This suppuration is limited to certain parts of the body, as an injured extremity, or, as frequently happens, it may be found on the trunk and limbs at the same time. The pus in this form of suppuration is exceedingly apt to burrow, on account of the peculiarities of the tissue in which it occurs, and also the condition of the surrounding structures, especially the relaxed and flabby condition of the skin. These abscesses in some instances are superficial, in others deep-seated.

There are few changes which occur in the muscles, and these are not uniform or constant. They are occasionally the seat of abscesses, which have been observed in the heart, tongue, and other organs. The muscles may be of a light-brown or greenish color when they have been covered a considerable time with pus, and are sometimes softened and pultaceous. Suppuration may also take place beneath the fascia of the tendons.

The brain and its membranes are frequently found in a perfectly healthy state after death from pyæmia, although when the diseased process has extended during the life of the patient to the lungs and pleura, giving rise to great dyspnoea, there will generally be observed some congestion of the membranes, an increased quantity of fluid in the brain-substance and ventricles, and also an increased fulness of the meningeal veins and sinuses. Occasionally there have been observed suppurative {967} meningitis, blood extravasations on the surface of the brain, lymph-deposits on the membranes, softening of the cerebral tissues, and circumscribed abscesses in the substance of the brain, which in some cases have been traceable to embolism of its vessels. The changes in the spinal cord and its membranes are probably similar to those found in the brain, but these parts appear to have been rarely examined.

Virchow found emboli of the retinal and choroidal vessels. Heiberg found these vessels occluded with colonies of micrococci. There have also been observed opacity of the cornea, sloughing of the conjunctival epithelium, suppurative infiltration into the periphery of the vitreous body, and deposits of pus in Petit's canal and in the anterior and posterior chambers. Pyæmic ophthalmia has been observed somewhat frequently in puerperal cases, especially when preceded by endocarditis, with deposits on the semilunar or mitral valves. In surgical cases it is rarely seen.

Toynbee "relates several cases of purulent infection following suppuration of the ear. Cases of disease in the mastoid cells terminate fatally, he says, from two different causes: first, from purulent infection, arising from the introduction of pus into the circulation through the lateral sinus; second, from disease of the cerebellum or its membranes. Cases of purulent infection, he further remarks, have not been met with where the disease occurs in the tympanic cavity."[34]

[Footnote 34: Braidwood on _Pyæmia_, pp. 168, 169.]

Numerous lesions of the osseous system have been noted in pyæmia, probably from the fact that this disease results very frequently in cases of bone-lesions, but these changes have very little diagnostic importance. The following have been observed: thickening or infiltration of the periosteum, which may be found to separate readily from the bone after the death of the patient, or there may be pus found between the periosteum and the bone. In the bone-structure there were found caries and necrosis, "while in other cases the whole thickness of the compact tissue is perforated in a honeycomb-like manner by minute cavities filled with thickish pus or caseous matter of a pinkish-white color."[35] "To sum up, the chief morbid alterations met with in the bones are congestion, dilatation of the Haversian canals and cancellated tissue, tending to abscess formation, and the excavation of the cavities by the unhealthy pus."[36]

[Footnote 35: _Ibid._, p. 192.]

[Footnote 36: _Ibid._, p. 194.]

The pathological lesions of the joints commence with marked congestion of the synovial membranes and increase in the synovial fluids, and afterward the fluid is mixed with pus; these conditions are followed by erosion of the cartilage and ligaments, the former thus becoming separated from the bone. Both the small and large joints are occasionally the seat of morbid changes.

The parotid gland is occasionally the seat of a secondary inflammation during the progress of pyæmia, and this may endanger life by interfering with respiration and deglutition. The lymphatic glands are only secondarily affected, and even this takes place very rarely. The changes in the glandular system, when observed, are similar to those which happen in other tissues of the body--viz. congestion, inflammation, and suppuration.

The arteries are usually found empty after death from this disease, and the coats are sometimes apparently thickened. The veins, on the contrary, are commonly found filled, or even distended, with firm fibrinous clots. They are sometimes also found inflamed or altered, although more {968} commonly healthy. The distended condition of the veins gives rise to the cord-like feeling often mentioned by different observers. In some cases of phlebitis there may be pus deposited between the coats of these veins. The most important pathological changes are found in the blood. These changes occur early in the disease, become more marked toward its fatal termination, and may be always studied after death. It is generally admitted that pus is frequently found in the blood of these patients; but it has been shown by numerous experiments that healthy pus never produces the pathological changes which characterize this disease. Pyæmia is only produced by the presence in the blood of ichorous pus or some other decomposing animal substance, or some material having its origin in the decomposition of the same, and no decomposition in these substances is ever effected except through the agency of living organisms. It therefore follows that the discovery of living organisms in the blood of those sick and dead of this disease has given a renewed interest to the study of its pathology. The recent investigations made by Pasteur, Koch, Birch-Hirschfeld, and the London Pathological Society show conclusively that in all cases of pyæmia and septicæmia organisms are present in the blood during the entire course of the disease, and that in the former there is found the globular, and in the latter the rod bacteria. It has further been observed in each morbid condition that the severity of the disease is always increased in proportion to the increase of the organisms in the blood, and that the bacteria found within the body are of the same species as those in the wound from which they have gained admission. The micrococci found in the blood of pyæmic patients are surrounded by the decomposed products of the red and white corpuscles, which appear in the blood-plasma in the form of pale granular bodies. There is likewise in this disease an increased coagulability of the blood, and it steadily increases as the disease progresses. In this condition there may be found in the blood-vessels both thrombi and emboli. The thrombi are occasionally observed as firm fibrinous clots, but they may be likewise found in the rapidly fatal cases to have undergone suppurative changes. These changes begin in the centre of the clots, which often contain true pus or a greenish or puriform fluid.

The pericardium may contain a small amount of serum tinged with blood, but it is seldom covered with recent lymph. Both the lung-tissue and pleuræ are commonly inflamed in this disease. The costal and visceral layers may be agglutinated by old adhesions, but are more commonly united together by recently formed lymph. The pleural cavities often contain some opaque, muddy, sero-purulent fluid, mixed with blood and having masses of lymph floating in it.

The lungs are more frequently the seat of metastatic abscesses and other morbid changes in pyæmia multiplex than any other organs of the body. There may be found emboli in the branches of the pulmonary veins, and in the lung-tissue metastatic abscesses surrounded with capillary congestion and other evidences of inflammation; "The smaller vessels, trying to overcome this afflux of blood, may produce ecchymosis or extravasation beneath the lining membrane of the air-vesicles, but the minute capillary congestions are generally observed as red points studded over the pulmonary surface, which by and by exhibit yellowish-white or bluish-white centres. While one part, generally the lower half of the {969} lung, is thus hepatized, solid, and of a dark greenish color, the remainder of the lung is emphysematous and more or less oedematous. A section of the former presents the same appearance as is observed in the lungs of pneumonic patients. Whether these incipient abscesses are developed from the minute points of congestion before mentioned, by the breaking down of the thrombic clots in their centres, or whether the pus is developed out of the serum exuded by the walls of the engorged capillaries, cannot be easily determined, and has as yet not been decided. These secondary abscesses vary in size from that of a hemp-seed to that of a hen's egg."[37] These are generally situated on the periphery of the lungs and in the lower lobe, although in some cases they are found imbedded deeply in the pulmonary tissue. The contents of these abscesses are similar to those found in other parts of the body in this disease. The bronchial mucous membrane is commonly of a bright pink color, while its secretion is increased in quantity, and may be clear and frothy. These changes are the result of acute bronchial catarrh. Lobular pneumonia has been frequently observed as a complication of pyæmia, and is supposed by some authors to be caused by the vitiated condition of the blood; but probably it is more frequently occasioned by infarctions and embolic abscesses, which have been previously mentioned in this connection.

[Footnote 37: Braidwood, _op. cit._, p. 173 _et seq._]

Billroth and Sedillot observed pathological lesions involving a solution of continuity in the spleen, liver, and kidneys, in the order in which they are mentioned; other authors, however, assert that the liver, next to the lungs, is the most frequent seat of purulent deposits. Enlargement of the spleen is frequently met with in cases of pyæmia multiplex. The metastatic abscesses found in the spleen and kidneys are much smaller than those found in the lungs and liver, but in other respects are of a similar character. The capillary congestion and the accompanying infarctions require no special attention here. The liver, like the spleen, is sometimes enlarged, and at other times is found to have undergone fatty degeneration to a greater or less degree; in which condition its tissues are generally soft and friable. Abscesses in the liver are so much like those in the lungs as to need no separate description. The same may be said of other pathological changes found in this organ in pyæmia multiplex. The abscesses found in the kidneys vary from the size of a hemp-seed to that of a bean, and are surrounded by the usual zone, marking more or less definitely the extent of the inflammation. The capsule is generally healthy. There are also, in very rare cases of this disease, abscesses found in the stomach and intestines, involving the thickness of the mucous membrane; and it is further supposed that these abscesses may be found occasionally on any portion of the mucous membrane lining the alimentary canal. Post-mortem examinations in pyæmia multiplex have established the fact that there is no organ in the body that may not become the seat of pathological lesions in this disease; but there is unquestionably a vast difference in the relative frequency of these changes in the various organs. In some instances of this disease peritonitis is developed, with its concomitant changes in this membrane and the abdominal fluid, which is generally increased in quantity and sometimes slightly tinged with blood, but more frequently remains clear. {970} This inflammation is commonly dependent on an extension of the inflammatory process from a metastatic abscess, which may be situated near the periphery of some organ covered with peritoneum, although it is claimed that pleuritis occasionally occurs in connection with pyæmia independent of metastatic abscesses in the lungs.

The careful study of the pathology of pyæmia multiplex renders it exceedingly probable that the immediate agency in the production of all these lesions is the presence in the blood of a particular species of living organism, and that all the morbid changes which occur in the visceral organs are secondary to those which take place in the blood, but that the former are only dependent on the latter in a minor degree. The pathological changes effected by these organisms seem to be as follows, and to occur in the following order: viz. disorganization of the blood, especially a destruction of the red and white blood-corpuscles; the formation of granular bodies around the organisms out of this débris; the production of an increased coagulability of the blood; the lodgment in the blood-vessels of these granular bodies, which are increased in size by a deposit of fibrin; these obstructions occur most frequently in minute ramifications of the pulmonary arteries; nutrition is effected locally by these infarctions, and generally by the vitiated condition of the blood, which enables the organisms under these favorable circumstances to penetrate the adjacent tissues and produce the metastatic abscesses and other accompanying lesions.

The pathological changes in pyæmia simplex are of the same kind as those which have just been described as characterizing pyæmia multiplex, with the exception of the metastatic abscesses, which are always absent. Furthermore, the disease in both instances is believed to have its origin from the same causes, and the dissimilarities in the pathological lesions are equally susceptible of a rational explanation, as are those of scarlatina simplex and scarlatina maligna.

There were reported by the committee of the London Pathological Society some interesting details pertaining to this form of pyæmia. Their report shows that among the one hundred and fifty-five cases classed as pyæmia there were twenty-four cases without visceral abscesses; and furthermore it shows that in twenty-three of these cases there was no suppuration, although local inflammations affected many of the different tissues, since these patients suffered with arthritis, cellulitis, pleuritis, meningitis, pericarditis, and carditis. It is also added that "the post-mortem appearances, in addition to the local secondary inflammation before noted, were in many cases those changes common to all forms of blood poisoning. Out of the twenty-four cases, the following are noted: Swollen spleen, nine times; congestion of the lungs, ten times; swollen liver, six times; cloudy swelling of the kidney, fourteen times."[38]

[Footnote 38: _Trans. London Pathological Soc._, vol. xxx. p. 26.]

In this form of pyæmia it has been supposed by some authors that the materies morbi occasionally produces death before the metastatic abscesses have had time to develop, but this is not always the case. The same committee report on the above-mentioned twenty-four cases, on this point, as follows: "The duration of the cases before the fatal termination was very various. It is tolerably accurately recorded in eighteen cases: of these five died in the first week, five in the second, {971} four in the third, and the remaining four survived to the thirtieth, forty-ninth, fifty-second, and sixty-second days."[39]

[Footnote 39: _Trans. London Pathological Soc._, p. 25 _et seq._]

The pathology of pyæmia multiplex having been already fully described, and since the only essential difference in these morbid conditions consists in the complete absence of the metastatic abscesses in cases of pyæmia simplex, it is therefore thought unnecessary to dwell here longer on this subject.

The morbid anatomy of septicæmia has been carefully studied of late, and it is now known that the most characteristic lesions are found in the blood and the alimentary canal.

As a manifestation of the general poisoning of the blood, it might be expected that putrefaction would follow rapidly after the death of the patient. In fact, Davine defines septicæmia as "putrefaction of a living body." Observation has now thoroughly confirmed that which was formerly an anticipation. Panum, Hemmer, and Bergmann have each called attention to the fact that rapid decomposition follows the death of all animals in which septicæmia has been produced for experimental purposes. It has also been observed that putrefaction in the human cadaver begins much sooner, and progresses much more rapidly, under similar circumstances, when the death has been produced by this disease than when it has occurred from any other cause. Furthermore, this rapid decomposition is not limited to the internal organs, but may be frequently strongly marked on the surface of the body after the lapse of twelve hours, although it has been kept in a comparatively dry and cool atmosphere. In those cases where the septicæmia has originated in an external wound it has been uniformly observed that putrefaction goes on most rapidly in the vicinity of the wound after the death of the patient.

In every case of fatal septicæmia the post-mortem examination will show that the coagulability of the blood has been diminished or destroyed. In fact, it has been abundantly shown that in all cases of true septicæmia the coagulability of the blood is more or less diminished. The few imperfect clots of blood found after death are of a deep-black color. The putrefaction of the soft tissues is greatly hastened by the presence of this blood; and, consequently, this process goes on most rapidly in the most dependent portions of the body, especially along the course of the large veins. The septicæmic blood possesses a peculiar putrefactive odor, and it is occasionally found to be acid in its reaction, according to Vogel and Scherer, making it highly probable that it will end in the formation of the carbonate of ammonium. The chemical examinations of septicæmic blood which have heretofore been made have completely failed to give satisfactory results in regard either to the existence or nature of the materies morbi in this disease, although, without doubt, there has occasionally been found, principally in the blood of those who have died of acute septic intoxication, a poisonous substance, which Bergmann designated sepsin. Microscopic examinations have shown that in the blood and also in various organs of those who have died of septicæmia there are always present, under these circumstances, a large number of the rod bacteria; in fact, they are more numerous than after death from any other infectious disease. Furthermore, they are found in the blood, lymph-glands, and cellular tissues during the whole course of the disease.

{972} There are no pathological changes in the central nervous system which arise directly from septicæmia, although in some cases, when there has been some cardiac complication or very severe dyspnoea from any cause immediately prior to the death of the patient, there may be found hyperæmia of the membranes of the cerebro-spinal axis. The brain and spinal cord remain unchanged.

The endo- and pericardium occasionally present a somewhat mottled appearance resembling ecchymosis, which is evidently a deposit from the blood, and may be washed off with water. The inner surface of the ventricles presents a similar appearance from the same cause. In addition to those changes which have been mentioned there are occasionally found some slight traces of an inflammatory process in these parts; but it never extends to the formation of pus or ulceration, which frequently happens in cases of pyæmia. The quantity of pericardial fluid is sometimes increased in septicæmia, and is generally somewhat thickened, cloudy, and slightly tinged with blood. The changes in the pleural surfaces are the same as those which have been noted in the pericardium, but any increase of the fluid within the pleural sacs is an exception to the general law, and is very rarely seen. The lungs are generally found slightly congested, but there may be some ecchymosis in exceptional cases. Pus is never found in the lungs or within the pleural cavities in pure unmixed septicæmia. The pathological changes in the liver resemble those in the lungs. This organ is commonly found in a state of passive congestion, while the color of its tissues is slightly darkened. The congestion of the kidneys and spleen in this disease is much more marked than that of the lungs and liver. The parenchymatous tissue of the kidneys is commonly found in an oedematous condition, and the tubuli uriniferi are more or less affected by a catarrhal inflammation, which is manifested by the exfoliation of granular epithelium. The same catarrhal condition, but in a milder form, is found to affect the mucous membrane of the bladder. In females the ovaries, uterus, and vagina are in a state of hyperæmia, with more or less catarrhal inflammation of the latter organ. Septicæmia invariably causes pregnant females to abort. There is commonly softening of the spleen. The alimentary canal is almost constantly affected by acute intestinal catarrh, with enlargement of the intestinal follicles and mesenteric glands, while there are frequently hemorrhages from the serous and mucous membranes. The various muscles of the body and the extremities are found to be of a dark brownish-red after the death of the patient, instead of possessing their natural pale-red color. It may now be stated, finally, that the pathological changes in septicæmia are less marked than those of pyæmia multiplex.

The semiology, etiology, and pathology of septo-pyæmia consist in a blending, in different degrees, of the essential parts of pyæmia and septicæmia; and since the pathology of both these diseases has been presented separately, it is deemed unnecessary to enter into a consideration of this combination.

SYMPTOMS OF PYÆMIA.--Pyæmia very rarely, if ever, develops except in connection with an open suppurating wound, and consequently it must generally be regarded as a wound complication or as a secondary diseased condition. Those open wounds are unquestionably the most favorably situated for the development of this disease which involve the medullary {973} cavities of the long bones, owing to the liability of unhealthy suppuration, the difficulty of complete drainage, and the favorable anatomical conditions for absorption.

Every form of pyæmia is frequently preceded by a distinctly marked prodromal stage, which varies in duration from four days to two weeks. In fact, the ordinary precursor of this disease, in all those cases in which the bones are involved, is an attack of osteo-myelitis; but in other cases the patient often complains of malaise, giddiness, headache, pain in the limbs, weakness, and loss of appetite, while the experienced surgeon will be deeply impressed with the patient's rapid emaciation and cadaverous face. These symptoms are soon followed by jaundiced skin, etc. The commencement of an attack of pyæmia is commonly manifested by a chill. The importance which will naturally be attached to this phenomenon in connection with an open wound must depend to a certain degree on the circumstances attending its occurrence; and therefore the following question will present itself: Is the chill associated with suppuration? A negative answer to this question, based on the fact that insufficient time has elapsed since the occurrence of the injury to render suppuration possible, can never fail to be a source of satisfaction to the surgeon, whose experience has taught him to dread pyæmia.

Billroth has observed in 83 cases of true pyæmia multiplex that 62 commenced with a chill, and 21 without; in 81 cases of septicæmia and simple pyæmia 24 commenced with a chill and 57 without. The number of chills in each individual patient occurred according to the following table:

Number of patients 19 21 14 15 9 5 2 3 4 1 1 1 Number of chills 1 2 3 4 5 6 7 8 9 10 13 14

In one patient during three weeks sixteen chills were observed, and probably the longer the duration of the disease the greater is the number of chills. Still, there are chronic cases with a single chill, and acute cases with many. It rarely occurs that a patient has more than one chill in twenty-four hours. Billroth noticed among his patients only sixteen who had two chills, and only six who each had three chills, in one day. The experience that fewer chills occur during the evening and night than in the morning and afternoon has been confirmed by statistics. Among 287 chills, 220 occurred from 8 A.M. to 8 P.M., while during the night, from 8 P.M. to 8 A.M., only 67 were observed. By this arbitrary division of the twenty-four hours Billroth desired to take into consideration the daily exacerbation in connection with the usual daily irritation of the wound, the bandaging, and other manipulations. He saw, for example, a chill occur three times from the introduction of a sound, and twenty times after the opening of an abscess. The time which elapsed from the first injury to the first chill is shown in the following table:

First chill began, times 14 19 15 9 4 3 2 4 Length of time after injury, in weeks 1 2 3 4 5 6 7 8

Patients who had fever before the operation were more inclined to early chills than recently-injured healthy individuals. Billroth's experience was to have only the first chill before the end of the first week. It may be further stated that nervous, irritable patients suffer much more {974} frequently from chills than those of a phlegmatic temperament. This fact has given rise to the opinion that the absorption of pus acts especially on the central nervous system.

The chills in pyæmia are supposed by Billroth to be associated with inflammation, and he says: "It must be mentioned, as a matter of observation, that chills occur almost exclusively in the commencement of an acute inflammation, and are intermittent only in intermittent fever and reabsorption of pus, while they do not occur in acute septicæmia."[40] But the fever in pyæmia rarely intermits entirely; it is generally lower, however, in the morning than in the afternoon. This symptom is even more important than the rigors in enabling the surgeon to make a correct diagnosis. Let it, however, be remembered that the temperature frequently becomes very high within a few hours after the receipt of an injury or the performance of a surgical operation; that this high temperature may be due to septic absorption, and that this diseased condition is what we designate as septicæmia. Another condition, less marked, with an elevated but somewhat lower temperature, is usually spoken of as traumatic fever. In this condition the fever may gradually increase for a few days, and then disappear.

[Footnote 40: _Surgical Pathology_, p. 344.]

One important peculiarity of the temperature in pyæmia are the sudden and great changes; thus, at one hour the temperature may be slightly raised above the normal, and at the next the thermometer may mark 105° F. These sudden changes of temperature are of frequent occurrence, are not observed to the same extent in any other disease, and therefore supply a very important diagnostic indication. It is impossible to know, or even to anticipate with any degree of certainty, when the highest temperature will exist; consequently, Billroth and other writers have suggested the desirability of having a thermometer constantly kept in a position to indicate every change in the heat of the body, and a careful attendant to note the same; but, thus far, I am not aware that this has been attempted, probably on account of the inconvenience to the patient and the additional labor in nursing it would entail. It has been further observed that during the existence of a chill the temperature continues to steadily increase, and the maximum seen during the whole course of the disease is attained during the hot stage which immediately follows the rigors. "This condition is followed by profuse cold perspirations. The perspirations which accompany this disease are most profuse, like those of advanced phthisis. They never precede the rigors, but may occur independently of them. They are either continuous in their duration, or exhibit more or less distinct exacerbations. They are occasionally accompanied by sudamina, and they do not abate with the use of any known remedy.... Occasionally perspiration is scanty; but before death a cold clammy sweat and a tawny discoloration of the skin occur."[41]

[Footnote 41: Braidwood, _op. cit._, p. 112.]

Besides the sudamina there are frequently observed on the skin vesicles, pustules, and boils, purpuric patches, and various discolorations. There is frequently observed to arise in the neighborhood of the wound a reddish erythematous blush, which soon extends to the whole limb, and commonly begins to disappear in the early part of the second week. This recently occurred to a patient under my care, and was speedily followed by an abscess of the knee-joint. The wound was situated at the hip-joint, {975} and the first change in the color of the integument took place around its lips. The redness extended rapidly downward until it covered the foot, and even the toes; but the extension upward was slight, not much above the nates, on which there was situated at the time a bed-sore. It observed the same order in passing off as in coming on--_i.e._ where it first made its appearance it first disappeared. The superficial veins leading from the wound were inflamed and cord-like. This condition of the integument and the abscess of the knee-joint were followed by diarrhoea, on which medicines had no beneficial effect. It continued, with occasional vomiting, until the death of the patient.

The pulse in pyæmia may be nearly normal as regards frequency, while at other times very rapid. It has been remarked in some cases that the pulse seldom rose above 90 per minute until near death. The pulse, although only moderately accelerated at the commencement of the disease, always becomes more rapid, quick, feeble, and irregular toward the termination of the unfavorable cases, while in cases of recovery it returns gradually to the normal standard.

In all cases in which the blood has been examined during the progress of pyæmia the examiners have agreed in regard to its extreme coagulability, the diminution of the number of red corpuscles, and the increase of the granular spherical bodies. The red corpuscles, even in the earlier stages of the disease, show evident indications of disintegrating; and these become more and more marked as the disease progresses, while there is a steady increase in the number of pus- or possibly of white blood-corpuscles. Epistaxis occasionally occurs, and also venous oozing from the wound.

The condition of the tongue in pyæmia may be regarded as an important symptom, indicating the state of the alimentary canal--not, however, during the prodromal stage, but after the disease has progressed a few days. It is then observed that the tongue has become peculiarly smooth, dry, and often excessively red. This smoothness is caused by the collapse of the papillæ, and the dryness by a diminished secretion. The organ now frequently appears as if covered with a thin layer of collodion which had been caused to dry on the surface, so as to present a glazed look. Again, the tongue may be covered with brown crusts and the teeth with sordes. These brown crusts and sordes are usually seen in advanced cases, following the first condition described. Much importance is attached to these brown crusts by many experienced surgeons, and although there may be very marked improvement in all other symptoms, still they insist on a very guarded prognosis until the tongue has assumed a healthy appearance. Aphthæ on various parts of the mouth and pharynx are frequently present in the more chronic cases, but are usually absent in acute cases. Herpes of the lips sometimes occurs in the commencement of the disease.

Vomiting is comparatively rare, but there is, even in the early stages, a complete failure of the appetite, with great thirst. Singultus is rarely present in genuine pyæmia, but frequently so in septicæmia, and occasionally in septo-pyæmia. Diarrhoea is not so frequent or the stools so copious in pyæmia as in septicæmia. Billroth observed in one hundred and eighty cases of pyæmia thirty-two cases of diarrhoea. It is impossible to determine whether those cases in which the diarrhoea {976} occurred were pure or mixed pyæmia. The stools are often of a pappy consistence, and passed involuntarily in bed. There are, however, severe cases of pyæmia with high fever, and accompanied by obstinate constipation.

Examination of the heart may, in rare cases, show the existence of pericarditis, although usually the only indications of disease are the too feeble sounds. Auscultation and percussion of the lungs may yield unsatisfactory results when the metastatic abscesses are small and scattered, for the same reason as in miliary tuberculosis. The large deposits in the lungs are by these means readily determined. There may be a sensation of suffocation, the pneumonic sputa, the friction sound of pleurisy, or the signs of pleuritic effusion; and the existence of these symptoms or signs would naturally aid in the diagnosis of metastatic abscesses.

Enlargement of the liver and spleen may be determined before death, and in connection with other symptoms would aid in diagnosing deposits in these organs.

The urine in the first stage of this disease is scanty, high-colored, contains a large amount of salts, and is of a high specific gravity. Epithelial, fibrinous, and blood casts, and also albumen, are occasionally found in it during the course of the disease. Billroth mentions a case in which there was complete suppression, with uræmia.

In many cases of pyæmia suppuration of the joints, one after another, takes place with great rapidity and with comparatively little pain, but occasionally some swelling, redness, etc. are present. In most cases these suppurations are easily diagnosed. Instead of suppuration taking place in the joints, there are cases in which it occurs in the cellular tissue; and I have recently seen a case where abscess after abscess formed with such rapidity that within a single week the patient was literally covered with abscesses from the crown of his head to the soles of his feet.

Delirium generally exists during some stage of the disease, more frequently the last, and is then mild in its character, although active delirium has been observed in the first stage. Patients are low-spirited and very apprehensive of death. The face at the beginning of the attack may be flushed or pallid, but toward the end it always becomes careworn and haggard. The breath occasionally has a sweetish or purulent odor.

The changes in the wound are in some cases very marked, even in the first stage of the disease. The suppuration, which has been previously free and healthy, may be suddenly checked, the wound becoming dry. The discharge, if it continues, becomes scanty, thin, ichorous, or greenish. The granulations, if previously healthy, may soon slough. These changes may not always appear in the first stage, but should they not then take place they may be expected later in the disease.

SYMPTOMS OF SEPTICÆMIA.--These are commonly developed within twenty-four hours after the receipt of an injury or the performance of a surgical operation, and they may be sketched as follows: Frequent pulse; tongue, lips, and throat dry; skin hot and the temperature of the body high. The patient replies accurately to questions, but with some hesitation. He is much inclined to sleep, has entirely failed to take nourishment, drinks frequently when aroused from his lethargic condition, and has vomited everything taken into his stomach since the receipt of the injury or the performance of the operation. If {977} the dressings are now removed from the wound, the foul odor of putrefaction greets the attendants. In cases of amputation-wounds considerable discoloration of the flaps may be observed, the edges being blackened. Above these blackened edges the integument is reddened and slightly oedematous. The wound having been closed with sutures, which are now removed, there escapes a few drachms--possibly ounces--of highly offensive fluid, the decomposed remains of blood, etc. A further examination of the flaps on their inner surfaces show that their capillary circulation has ceased. The tissues, instead of presenting a life-like appearance, are now of a very dark color and occasionally mottled with dull grayish spots, although the movements of the ligature at the point where it embraces the femoral artery, for example, show that the blood still rushes against the artificial boundary.

Let us now leave our patient, without further comment, for the next forty-eight hours, when we will resume the examination. We now find the same dryness of the mouth that was previously noticed; the pulse is more frequent, and has become very feeble; he complains of much thirst, has vomited frequently, and has taken very little nourishment, and that only at the earnest solicitations of the attendants. The temperature is higher than at the former examination, and has been steadily increasing; in the morning it is lower, however, than in the evening of the same day. The patient is lethargic, and is suffering with a profuse diarrhoea. The odor of the stools is highly offensive; they are properly described as rice-water evacuations. The abdomen is tympanitic; the body bathed in perspiration; the respirations rapid; the urine scanty, high-colored, and contains albumen. The examination of the stump shows that gangrene has extended rapidly, involving not only the flap, but a portion of the adjacent tissues. The stench arising from the wound is almost stifling. The decomposing fluids are continually forming. That portion of the thigh not already gangrenous is now very oedematous, and the integument covering it is much discolored, being of a dark, icteric, or reddened hue.

We now allow twenty-four hours to elapse, and then make our final examination. The patient's tongue is more moist; the body still bathed in perspiration; the eyes dull; the conjunctivæ icteric, and the same hue extends to the body, though in a less marked degree; the pulse has become very frequent, feeble, and not easily counted; the temperature is below normal. Singultus is now present, and has been so during the last twenty-four hours. Bronchial symptoms, combined with marked oedema of the right lung, have appeared; the diarrhoea continues the same; the gangrene is still extending.

It must be admitted that the report here offered shows only the symptoms that are found in a single class of cases. The symptoms vary greatly in different cases, but they are especially marked in the acute sepsis mentioned by Massanneuve under the head of _gangrène foudroyante_. In these cases there appears, immediately after the receipt of an injury, enormous oedema about the wound, which extends rapidly in every possible direction, followed by the death of the patient within a few hours unless prompt measures are adopted. The puncture of the cellular tissue or of the blood-vessels involved in the oedema prior to the death of the patient gives rise to the escape of a highly offensive gas. Roser mentions a case of this disease in which he promptly amputated {978} the limb of the patient through the healthy parts, without even waiting for the administration of an anæsthetic, and his patient recovered.

The symptoms of septicæmia must necessarily depend greatly on the condition of the patient and the amount of septic material introduced, but it is not deemed necessary to dwell longer on this subject.

DIAGNOSIS.--It is thought that a brief presentation of the etiological, pathological, and semiological differences may be advantageous to busy physicians who desire to obtain, with the least expenditure of time, an accurate knowledge of the chief points of distinction between these morbid conditions. This effort at differentiation is merely intended to place the most important characteristics in marked contrast; and consequently it should be remembered that it is not our intention to give here the complete etiology, pathology, or semiology of either of these morbid states, but only their essential differences. Furthermore, it is thought that the following arrangement will facilitate the object which we desire to accomplish:

ETIOLOGY. PYÆMIA. | SEPTICÆMIA. 1. Pyæmia generally commences | 1. Septicæmia generally commences with the putrefaction in an | with the putrefaction in an open wound of the secondary | open wound of the primary wound-fluids--pus, etc.--in | wound-fluids--blood, serum, which there are developed | etc.--in which there are globular bacteria, which enter| developed rod bacteria, which the blood and certain tissues | enter the blood and certain of the body, where they | tissues of the body, where multiply and produce | they multiply and produce constitutional disturbances. | constitutional disturbances. 2. Pyæmia is commonly preceded by| 2. Septicæmia is commonly a some local inflammatory | primary wound-complication, wound-complication, such as | which is generally developed suppurative periostitis, | within forty-eight hours after osteo-myelitis, etc., and is | the receipt of the injury. rarely developed before the | end of the second week after | the receipt of the injury. |

PATHOLOGY. 1. Increased coagulability of the| 1. Diminished coagulability of blood. | the blood. 2. There are metastatic abscesses| 2. Complete absence of purulent in various parts of the body, | or ichorous deposits in all especially in the lungs, | cases of unmixed septicæmia. liver, and kidneys: serous | Post-mortem appearances may be cavities frequently contain | completely negative, with the sero-purulent deposits; | exception of the condition of similar deposits are often | the blood, although there is found in the joints; abscesses| often some oedema of the in the cellular tissue; and | lungs. also abundant evidence of the | existence during the life of | the patient of pyæmic endo- | and pericarditis. |

SEMIOLOGY. 1. Pyæmia commonly commences with| 1. Septicæmia commonly commences a chill. | without a chill. 2. Fever variable, but rarely | 2. Fever steadily increases, but entirely intermits. | is lower in the morning. 3. Sudden and great changes in | 3. The temperature is high at the temperature, followed by | beginning of the disease, profuse perspiration. | increases until near the fatal | termination, when it falls | below the normal. The skin is | moist, but without profuse | sweatings. {979} 4. Pulse variable; toward the | 4. Pulse rapid, and gradually fatal end rapid, feeble, and | increases in frequency toward irregular. | the fatal end. 5. Facies at the beginning | 5. Facies expressive of a dull, flushed or pallid, toward the | listless condition throughout end careworn. | the whole course of the | disease. 6. Tongue smooth, dry, and | 6. Tongue, lips, and throat dry excessively red, later | at the commencement, toward brown-coated, and even the | the end moist. Thirst is teeth coated with sordes. | marked. 7. Diarrhoea with stools of a | 7. Rice-water evacuations, very pappy consistence. | offensive; obstinate vomiting. 8. Epistaxis. | 8. Epistaxis rarely occurs. 9. Mild delirium toward the fatal| 9. A lethargic condition from the end. | beginning, increasing toward | the fatal end. 10. Aphthæ in the mouth and |10. Icteric hue of conjunctivæ; throat, sudamina, vesicles, | singultus often present. pustules, and purpuric | patches. |

The differences in the local manifestations occurring in and around the wound, during the progress of these diseases, may be summed up as follows:

At the commencement of this | The odor of putrefaction is disease the suppuration is | commonly very marked within commonly checked, the wound | twenty-four hours after the becoming dry, and if a discharge | receipt of the injury, the continues, it becomes scanty, | integument slightly reddened thin, ichorous, greenish, etc. | about the wound, and the The granulations, when previously| surrounding parts somewhat healthy, soon slough, and venous | oedematous. The wound-tissues oozing sometimes takes place. | soon assume a dark-brown color, There occasionally appears in the| and are occasionally mottled later stages of this disease | with dull grayish spots, while around the wound a reddish | the edges of the wound are at erythematous blush, which soon | the same time blackened, extends over the whole limb. | although the movements of the | ligature, when arteries have | been tied, show us that the | blood still rushes against its | artificial boundary.

TREATMENT.--It must be admitted that the management of either pyæmia or septicæmia, when fully developed, is always unsatisfactory, and generally unsuccessful; consequently, the success which has attended the use of the prophylactic measures employed in connection with the treatment of wounds during the last ten years has given much satisfaction to the medical profession. The committee of the London Pathological Society reports as follows on this subject: "The accumulation of septic matter in the uterus after labor, in contact with the raw surface left by the separation of the placenta, would also present the conditions favorable to acute septic intoxication. In the present day, when the necessity of thorough drainage of wounds is so thoroughly understood, and the means at the surgeon's command for carrying it out are so efficient, it can only be under peculiar circumstances that a sufficient quantity of putrid serum or pus to yield the fatal dose of the septic poison is allowed to accumulate in the wound. Moreover, the antiseptic treatment of wounds, now so largely adopted, by preventing decomposition of course renders septic intoxication impossible. Ovariotomy would seem to furnish conditions most favorable to septic intoxication, and a large proportion of the deaths occurring in the first forty-eight hours {980} have always been attributed to it. The proportion of fatal cases from this cause has, however, of late been greatly diminished by drainage, and more especially by the employment of the antiseptic treatment."[42]

[Footnote 42: _Trans. Path. Soc. of London_, vol. xxx. p. 15.]

We cannot repeat too frequently or too emphatically the fact that the treatment of pyæmia and septicæmia, when fully developed, is almost invariably unsuccessful, and that consequently he who desires to save the greatest number of lives must make every exertion and use all available means to prevent their development--a task which fortunately has now been brought within the scope of possibility in the large majority of cases. Every surgeon will readily admit that, were it possible to secure union by first intention in all cases of wounds, then it would be impossible for either septicæmia or pyæmia to occur in surgical practice. Therefore, it follows that the character of the wound, the method of operation, the surroundings of the patient, the character of the treatment, become proper points to consider in this division of the subject. The character of the wound and its relations to pyæmia and septicæmia have already been briefly referred to under the etiology of these diseases. The various methods of operating, with their respective advantages and disadvantages, are of course not suitable topics for discussion in this work.

The surroundings of the patient form a subject of vast importance in a prophylactic view, and should never be lost sight of in the construction of hospitals. I desire here to express my firm conviction that surgical pyæmia is essentially and almost wholly a hospital disease. The question of surroundings for the patient presents to my mind the following demands as a sine quâ non for obtaining the best possible results in surgery: (1) Absolute cleanliness. This demand should be strictly enforced in regard to the wound, the patient's body, the bedding, and everything else, including nurses and instruments. (2) Absolute purity of the atmosphere. (3) Moderate and equable temperature, containing a proper amount of moisture. (4) Proper quantity of nutritious and easily digestible food, with suitable drinks, etc. (5) Cheerful and pleasant surroundings, especially in companions, nurses, and other attendants. It may be objected to these conditions that they can never be obtained. I must confess that perfection in every detail cannot always be attained, but I am thoroughly convinced that he who makes a determined effort in this direction will succeed far better than that person who is constantly looking about for some excuse for negligence.

The question of treatment brings up the entire subject of antiseptics. The favorite remedies of this class are carbolic and salicylic acids, permanganate of potassium, chloride of zinc, bichloride of mercury, and liquor sodæ chlorinatæ. There is no doubt that good results may be obtained with any of these remedies. The surgeon should never forget that he uses medicines merely as agents to enable him to accomplish certain objects; and, keeping this in mind, he need very seldom fail with his antiseptic when the object is to prevent putrefaction in an open wound. Therefore it appears certain that each method of treatment may possess special advantages in particular cases, and probably the same may be said of the antiseptic itself. The importance of this subject may be more fully appreciated when it is remembered that it is generally admitted by the best surgical authorities {981} that more lives are lost from septic infection than from all other causes combined during a war. The further consideration of this subject may be arranged for convenience under the heads of local and general treatment.

The local treatment of the wound should, if possible, be of such a character as to prevent the absorption of either putrid substances or pus. It therefore becomes highly important, in cases of amputation and other operations, that all tissues injured to such a degree as to be likely to excite either putrefaction, irritation, or inflammation should be removed. The same care is necessary in removing all foreign bodies from the wound in cases where no operation is to be performed. The amputation of the injured limb may be necessary to prevent the development of these diseases, or it may be resorted to in certain rare cases after the origin of pyæmic symptoms; however, in the latter instance great care should be taken to remove all the tissues already infiltrated with serum, otherwise nothing will be gained. The use of the surgeon's knife at the proper time may be the best prophylactic against both pyæmia and septicæmia, but it should be directed by an intelligent mind and the instrument guided by a practiced hand. Again, it is found that opening a large medullary cavity may be attended with danger to the patient. This fact teaches us an obvious lesson.

The wound existing or the operation having been performed, the surgeon now turns his attention to the prevention of putrefaction and inflammation. The first source of danger requiring attention from the surgeon is the fluid escaping from the wounded surface. Do not allow it to undergo putrefaction in contact with the wound. It should not be forgotten that pyæmia is an infectious disease, having its origin in a local nidus, an open wound, in which putrefaction of pus or other wound-fluid is taking place. The question of amputation, or of the extirpation of the parts for the relief of this disease, should only be entertained when the surgeon is confident that he can remove the whole of the infiltrated tissues. In other words, the performance of these operations after the disease has become constitutional can never be advantageous to the patient. Even in those cases where infiltration is limited to the lymphatics, unless all these glands so affected are removed the operation will be unsuccessful. It has been further recommended in the treatment of this disease, in order to prevent the formation of metastatic abscesses, to ligate the veins in which thrombi have formed or may be reasonably expected to form, at some convenient point between the heart and these obstructed points. The value of this proceeding has never been fully determined, and may be reasonably questioned. The formation of metastatic abscesses in various parts of the body within the reach of the surgeon's scalpel demands his attention; and we have been taught by experience that they should be speedily opened, which generally lowers the temperature and diminishes the danger from septic absorption. In the performance of this operation Lister's antiseptic system of wound-treatment should be strictly adhered to, since it unquestionably gives the best results which can be obtained under the circumstances. When the metastatic inflammation which occasionally appears in the thyroid and parotid glands during the course of this disease terminates in the formation of pus, this should be speedily evacuated. This prompt action is often required, particularly for the relief of the grave symptoms which are apt {982} to arise in connection with respiration and deglutition. The accumulation of pus within the joints in pyæmic cases should, it is now thought, be treated in the same manner as abscesses in the cellular tissues--_i.e._ the articulations should be opened and thoroughly disinfected, and afterward kept in a perfectly aseptic condition, and also rendered absolutely immovable during the treatment.

Having directed attention to the more important local measures, we may now briefly enter on the consideration of some of the constitutional remedies. In the general treatment of pyæmia there have been recommended at various times a great variety of drugs, but the general want of success attending their use leaves comparatively few to be mentioned here. The mineral acids are still employed, and are found to be at least agreeable drinks, and as such can be still recommended. The sulphites of magnesium, sodium, potassium, and lime were recommended by Giovanni Polli for the treatment of typhus fever, scarlet fever, small-pox, septicæmia, and pyæmia. He further suggested that the medicine should be given until the whole quantity taken bore to the weight of the patient's body the proportion of 1 to 1000. The experiments made on animals with these salts seem to confirm their value in the treatment of septic diseases. It is certainly true that animals treated with these salts are not so easily affected by septic poison as those which have not received this treatment. Further, it has been shown that putrid substances when mixed with either permanganate of potassium or the sulphite of sodium, and then injected, are harmless, although the same quantity of putrid matter injected without either of these salts destroys life.

Brandy and other alcoholic stimulants have been strongly recommended on account of their well-known antiseptic properties. The sulphate of quinia is certainly, in most cases of pyæmia, a valuable agent. In large doses it enables the surgeon to reduce the temperature of the patient, and in smaller doses it frequently serves a valuable purpose as a tonic. It has also considerable value as an antiseptic.

Lattin has recommended the use of large doses of ergotine in infectious fevers, but this substance, when employed in the treatment of pyæmia, should be given in the formative stage of the disease. The use of drastic cathartics should be avoided, as should that of sudorifics, on account of their prostrating effects. In some cases hypnotics may be required to secure sleep.

Tonics are always more or less useful. The free use of stimulants and nutritious food is also indicated. Brandy, wine, and whiskey may be advantageously used as stimulants. Musk, ammonia, and camphor are occasionally required. However, it should not be forgotten that in cases where the disease has become fully developed the usual termination is death, few recoveries being recorded. In the early stages of this affection, by the removal of the patient from an overcrowded hospital ward to some place where pure air and proper hygienic arrangements can be obtained, recovery may take place, but under other circumstances the prognosis is exceedingly grave.

The treatment of septicæmia in most particulars is the same as that of pyæmia. The first effort should be to prevent the development of the disease, and the second to care for the patient in cases where the affection has already developed. It is not, of course, in our power to limit or in any way {983} regulate the primary injury, for we are obliged to take the patient as he is. The amount of injury to living tissue may be great or small. The question of an operation, the character of the same, and the subsequent management must be determined in accordance with the circumstances of each particular case.

The primary death of the parts is generally due chiefly to the injury itself; the secondary, frequently to bad surgical management. Let us now take a case in which the primary injury has been severe, greatly diminishing, but not destroying, the circulation in the injured parts. Here the immediate application of ice would be injurious, but a warm application might assist nature. It is humiliating to the profession that we are obliged even at this date to admit that the treatment of septicæmia is largely symptomatic. The profuse choleraic diarrhoea which generally accompanies this disease may be regarded as an effort of nature to eliminate the septic poison; but, nevertheless, it is so prostrating in its effects that it requires to be controlled with properly selected astringents, and these remedies may be still further aided by the use of stimulants and tonics.

The treatment of septicæmia may be summarized as follows: (1) A strict adherence to the five rules given under the head of the prophylactic treatment of pyæmia. (2) The avoidance of all putrefaction in contact with the wound, especially prior to the development of sufficient granulations to completely cover its surface. This object is to be accomplished by the removal of all necrotic tissues, the avoidance of putrescent fluids by cleanliness, and the proper use of antiseptic agents. (3) Free use of the alkaline sulphites and hyposulphites. These drugs should be used in all cases where there is reason to anticipate the development of septic diseases, as soon after the receipt of the injury as practicable, but should not be neglected even after the disease has become fully developed. (4) Sulphate of quinia should be used in all cases where the temperature is above 100° F., and its persistent use in large doses may be necessary to prevent the fever from rising still higher. It will be remembered in this connection that experience has taught us that "a temperature of 108.5° F. is the limit beyond which life can no longer exist,"[43] and even a much lower temperature is not without dangers. "The essential danger of fever in acute diseases consists, then, in the deleterious influence of a high temperature on the tissues."[44]

[Footnote 43: Liebermeister, _New Sydenham Soc. Trans._, vol. lxvi. p. 278.]

[Footnote 44: _Ibid._, p. 280.]

The treatment of puerperal septicæmia, although requiring the application of the same principles as any other form of this disease, may be briefly described as follows: The womb should be maintained in a firmly-contracted state by the proper use of ergot, even as a prophylactic measure, and also during the whole course of the disease; the uterus and vagina should be kept in an aseptic condition by the efficient use of antiseptics; sulphate of quinia should be given in large doses, and repeated as often as may be necessary in order to lower the temperature; and morphia or some form of opium should be employed for the relief of the pain.

{984}

PUERPERAL FEVER.

BY WILLIAM T. LUSK, M.D.

DEFINITION.--Puerperal fever is an infectious disease, due, as a rule, to the septic inoculation of the wounds which result from the separation of the decidua and the passage of the child through the genital canal in the act of parturition.

To maintain this definition it is, however, necessary to group by themselves cases of childbed fever dependent upon causes which are operative in the non-puerperal condition, though the latter imparts to these causes oftentimes an exceptional activity and virulence. In this category are to be placed especially scarlatina, typhus, typhoid, and malarial fevers. It is to be borne in mind that the zymotic fevers may provoke in the puerperal woman the same inflammatory lesions commonly associated with puerperal fever.[1] This is in accordance with the well-known surgical experience that a febrile paroxysm from any cause exerts an unfavorable influence upon a wounded surface.

[Footnote 1: Hervieux, _Traité clinique et pratique des maladies puerperales_, pp. 1073 _et seq._]

Like all brief statements, the writer is well aware that the foregoing definition is necessarily imperfect, and stands in need of further limitations to meet the requirements of exactness. Exceptions, however, either apparent or real, will be noted hereafter in their proper connections.

FREQUENCY.--In a careful search through the records preserved by the Health Department of New York City, I found that from 1868 to 1875 inclusive the total number of deaths for nine years was 248,533. Of these, 3342 were from diseases complicating pregnancy, from the accidents of child-bearing, or from diseases of the puerperal state; or, in other words, 1:75 of all the deaths occurring during that period was the result of the performance of what we are in the habit of regarding as a physiological function.

The deaths from miscarriage, from shock, from prolonged labor, from instrumental delivery, from convulsions, from hemorrhage, from rupture of the uterus, and from extra-uterine pregnancy, and deaths from eruptive fevers, from phthisis, and from inflammatory non-puerperal affections complicating childbirth, made a total of 1395, or about 42 per cent. of the entire number. The remaining 1947 cases, variously reported as puerperal fever, puerperal peritonitis, metro-peritonitis, phlebitis, phlegmasia dolens, pyæmia, and septicæmia, represent the very serious sacrifice of life resulting from inflammatory processes which have their starting-point in the generative apparatus. If we apply the general term, puerperal fever, to this class of cases, it will be seen that the malady is the cause of nearly one {985} one-hundred-and-twenty-seventh of all the deaths occurring in the city. The actual number of births for the nine years in question was roughly estimated at 284,000[2]--an estimate erring upon the side of liberality. The total number of deaths to the entire number of confinements was, then, at least in the proportion of 1:85, or, from puerperal fever alone, in the proportion of 1:146. Garrigues[3] examined the records of the various city institutions during the period in question, and from them estimated the number of births which took place in hospitals at 10,572. The recorded deaths were 420. Deducting these from the totals given above, the general death-rate in civil practice from puerperal causes in New York City was in the proportion of 1:94. Max Boehr[4] in his now-famous statistics reckons that one-thirtieth of all married women in Prussia die in childbed. The Puerperal Fever Commission[5] appointed by the Berlin Society of Obstetrics and Gynæcology arrived at the conclusion that from 10-15 per cent. of the deaths occurring in women during the period of sexual activity were due to childbed fever, and that this disease destroyed nearly as many lives as small-pox or cholera. But puerperal fever differs from either small-pox or cholera in that the latter presses largely upon the aged and the very young, while the former gathers its victims exclusively from a selected class--viz. from women in adult life, the mothers of families, whose loss, as a rule, is a public as well as a private calamity.

[Footnote 2: This estimate was based upon the assumption that the natural birth-rate is 33 to the 1000--a proportion believed by the statisticians of the Board of Health to be approximatively correct, though probably somewhat in excess of the reality. P. Osterloh has recently stated that my statistics were computed in so arbitrary a manner as to render deductions from them valueless. In this, however, he is mistaken. The most conscientious care was taken in their preparation; wherever the possibility of error existed the fact was distinctly indicated, and all calculations were made in such a way that whatever corrections might be required would strengthen the conclusions.]

[Footnote 3: "On Lying-in Institutions," _Trans. Am. Gyn. Soc._, vol. ii., 1878.]

[Footnote 4: "Untersuchungen über die Haüfigkeit des Todes im Wochenbett in Preussen," _Zeitschr. f. Geburtsk. und Gynaek._, vol. iii. p. 82.]

[Footnote 5: _Zeitschr. f. Geburtsk. und Gynaek._, vol. iii. p. 1.]

For those who regard statistics with habitual distrust it may perhaps be well to state that the foregoing frightful picture is no exaggeration, but is less sombre than the actual truth.

Before proceeding to consider the nature of puerperal fever it is desirable to first recall the anatomical lesions with which it is associated. These, it will be found, are for the most part inflammatory processes having their starting-point in injuries of the genital passage produced by parturition, complicated in many cases by septic changes in the blood, by secondary degeneration of parenchymatous organs, and at times by phlegmonous and erysipelatous affections in remote as well as in the adjacent serous and cutaneous tissues.

MORBID ANATOMY.--The primary lesions connected with puerperal fever are so various that the student will find it convenient to classify them according as they are situated in the mucous membrane of the utero-vaginal canal, the parenchyma of the uterus, the pelvic cellular tissue, the peritoneum, the lymphatics, or the veins. Not, indeed, that such an arrangement is strictly in accordance with clinical experience--as a rule, the inflammatory processes are rarely limited to a single tissue--but because the prognosis and treatment {986} are determined in great measure by the tissue-system which is predominantly affected. The significance of puerperal inflammations, wherever seated, likewise depends upon whether they are local and circumscribed or whether they present a spreading character.

Personally, I have found the following classification of Spiegelberg[6] of great utility as a means of keeping in mind the principal points to which inquiry should be directed in estimating the significance of the febrile conditions of childbed:

1. Inflammation of the Genital Mucous Membrane.--Endocolpitis and endometritis.

_a_. Superficial.

_b_. Ulcerative (diphtheritic).

2. Inflammation of the Uterine Parenchyma, and of the Subserous and Pelvic Cellular Tissue.

_a_. Exudation circumscribed.

_b_. Phlegmonous, diffused; with lymphangitis and pyæmia (lymphatic form of peritonitis).

3. Inflammation of the Peritoneum covering the Uterus and its Appendages.--Pelvic peritonitis and diffused peritonitis.

4. Phlebitis Uterina and Para-uterina, with formation of thrombi, embolism, and pyæmia.

5. Pure Septicæmia.--Putrid absorption.

[Footnote 6: "Ueber das Wesen des Puerperalfiebers," _Volkmann's Samml. klin. Vortr._, No. 3.]

ENDOCOLPITIS AND ENDOMETRITIS.--In the superficial, catarrhal form of inflammation the mucous membrane of the vagina is swollen and hyperæmic, the papillæ are enlarged, and the discharge is profuse; in the vaginal portion of the cervix the labia uterina are oedematous and covered with granulations which bleed at the slightest touch; in the cavity of the body there are increased transudation of serum and abundant pus-formation. The deep structures of the uterus are usually not affected. Sometimes the inflammation extends to the tubes--_salpingitis_--or, passing outward through the fimbriated extremities, it may spread over the adjacent peritoneum.

The small wounds at the vaginal orifice are at times converted into ulcers with tumefied borders. These so-called puerperal ulcers are covered with a greenish-yellow layer. They are associated usually with oedematous swelling of the labia. Under favorable sanitary conditions the deposit, which consists in the main of pus-cells, clears away and the surface heals by granulation. The ulcerative form of inflammation is very rare outside of crowded hospitals.

Diphtheritic ulcers are situated with greatest frequency in the neighborhood of the posterior commissure or around the vaginal orifice. In rarer instances they are found upon the anterior wall and in the fornix of the vagina, in the cervix, and upon the site of the placenta. The borders are red and jagged; the base is covered with a yellowish-gray, shreddy membrane; the secretion is purulent, alkaline, and fetid; and the adjacent tissues are oedematous. From the vulva they may extend to the perineum or pursue a serpiginous course down the thighs. In the uterus and about the cervix they vary as regards size, and are either of a rounded shape or form narrow bands. The intervening portions of tissue which have not undergone destructive changes swell and stand out in strong {987} relief. Where the entire inner surface has become necrosed, it is often covered with a smeary, chocolate-brown mass which, when washed away with a stream of water, leaves exposed either the deepest layer of the mucous membrane or the underlying muscular structures.

The difference between the superficial ulcerations of the genital canal and the diphtheritic form involving destruction of the deeper tissues is due to the presence in the latter of minute organisms termed micrococci, the relations of which to puerperal infection will be considered in a subsequent division.

METRITIS AND PARAMETRITIS.--In ulcerative endometritis, and even in the extreme catarrhal form, the parenchyma of the uterus likewise becomes involved. The changes which are designated under the term metritis consist in the first place of oedematous infiltration of the tissues. As a consequence, the organ contracts imperfectly and becomes soft and flabby, so that sometimes, upon post-mortem examination, it bears the imprint of the intestines.

In diphtheritic endometritis the gangrenous process may attack the muscular tissue, and give rise to losses of muscular substance--a condition known as necrotic endometritis or putrescence of the uterus.

Inflammatory changes are rarely lacking in the intermuscular connective tissue, which exhibits in places serous or gelatinous infiltration, with afterward pus formation, and with here and there small abscesses. The sero-purulent infiltration of the connective tissue is specially marked beneath the peritoneal covering of the uterus either behind or along the sides at the attachment of the broad ligaments. In the same situations the lymphatics, which normally are barely perceptible to the naked eye, are sometimes enlarged to the size of a quill, and are characterized by varicose dilatations occurring singly or presenting a beaded arrangement. In the substance of the uterus the dilated vessels are liable to be mistaken for small abscesses. The pus-like substance contained in the lymphatics is composed of pus-cells and of micrococci. From the cellular tissue surrounding the vagina, or that beneath the peritoneal covering of the uterus, the inflammation may spread by contiguity of tissue between the folds of the broad ligament, and thence pass upward to the iliac fossæ. Usually the process is unilateral. After the inflammation has crossed the linea terminalis it may take a forward direction above the sheath of the ilio-psoas muscle to Poupart's ligament, or it may creep upward, following the course, according to the side affected, of the ascending or descending colon, to the region of the kidney. It is rare for inflammation of the cellular tissue to travel around the bladder to the front. In such cases it pursues its course between the walls of the bladder and the uterus, and along the round ligament to the inguinal canal. In a few cases the cellulitis mounts above Poupart's ligament, between the peritoneum and the abdominal wall.

The course of the inflammation is not simply fortuitous, but follows prearranged pathways in the connective tissue. König[7] and Schlesinger[8] have shown that when air, water, or liquefied glue is forced into the cellular tissue between the broad ligaments the injected mass has a tendency to invade the iliac fossæ. In Schlesinger's experiments, if the canula of the syringe was inserted into the anterior layer of the broad ligament, {988} the glue spread between the folds to the abdominal end of the Fallopian tube; thence, following the track of the vessels, it passed to the linea terminalis; and finally mounted upward along the colon or swept forward to Poupart's ligament until the advance was stopped at the outer border of the round ligament. If the injection was made to the side of the cervix through the posterior layer at the junction of the cervix and the body, the posterior layer gradually bulged out, the peritoneum was lifted from the side wall of the pelvis, and the glue passed beyond the vessels to reach the iliac fossa. If the injection was made to the side of the cervix through the anterior layer, the glue passed between the bladder and the uterus, and forward along the round ligament to the inguinal canal, while another portion of the fluid passed between the layers of the broad ligament, and reached the peritoneal covering of the side walls behind the round ligament. If the injection was made in the median line in a peritoneal fold of Douglas's cul-de-sac, the fluid travelled forward upon one side along the round ligament and thence to the posterior wall of the bladder.

[Footnote 7: _Arch. der Heilkunde_, 3 Jahrg., 1862.]

[Footnote 8: _Gynaekologische Studien_, No. 1.]

The term parametritis, introduced into use by Virchow, is, properly speaking, limited to inflammation of the connective tissue immediately adjacent to the uterus, the older one of pelvic cellulitis furnishing a more comprehensive designation for cases where, as a consequence of a progressive advance from the point of departure in the genital canal, the remoter regions have likewise been invaded. Connective-tissue inflammation presents, as the first essential characteristic, an acute oedema, the fluid which fills the gaps and interspaces consisting of transuded serum rendered opaque by the presence of pus-cells or possessing a gelatinous character. In the mild, uncomplicated cases the oedema disappears rapidly. Where the cell-collections are of moderate extent the entire process may vanish without leaving a trace of its existence. If the cell-elements, on the other hand, are present in great abundance, they, as a rule, first undergo fatty degeneration, and, after the absorption of the fluid portion, form a hard tumor composed of a fine granular detritus, which under favorable circumstances likewise after a few weeks becomes absorbed. In rare cases abscess-formation in the tumor results.

In the cellulitis resulting from septic infection, especially in cases complicated by diphtheritis, the tissues seem as if soaked with dirty serum, and contain scattered yellowish deposits, which soon present, even to the naked eye, the appearance of pus-collections. This sero-purulent oedema is always associated with lymphangitis, the lymphatic vessels possessing varicose dilatations and beaded arrangements similar to those already described in the uterine tissue. The foregoing changes are most distinct in the firm connective tissue adjacent to the uterus and at the hilum of the ovary, while they are less clearly traced in the looser structure of the broad ligament (Spiegelberg).

In favorable cases the inflammation is circumscribed, or at least is limited, by the nearest lymphatic glands. In cases of intense infection it spreads rapidly, and justifies the title bestowed upon it by Virchow of parametritic malignant erysipelas.

PELVIC AND DIFFUSED PERITONITIS.--Inflammation of the pelvic peritoneum may result from severe attacks of catarrhal endometritis, the inflammatory process either traversing the uterine tissue or passing {989} through the Fallopian tubes to the adjacent serous membrane; or it may proceed, secondarily, from the stretching and irritation occasioned by an associated parametritis.

As a rule, pelvic peritonitis is not attended with much exudation. The latter is situated upon the folds of the peritoneum limiting the cul-de-sac of Douglas, upon the ovaries, and upon the broad ligaments. In favorable cases it consists of fibrinous flakes and fluid pus. If the latter is abundant, it may become encysted by the formation of adhesions between the pelvic organs.

General peritonitis may result from the extension of a pelvic peritonitis, or from the transport of poison through the lymphatics into the peritoneal sac. In the first case the entire peritoneum is injected, and the contents of the abdominal cavity are loosely bound together by pseudo-membranes, composed of pus and coagulated fibrine. The intestines are at the same time distended and the diaphragm is pushed upward. In the so-called peritonitis lymphatica the inflammatory symptoms are at the outset lacking. The abdominal cavity is found filled with a thin, stinking, greenish or brownish fluid composed of serum and micrococci. The intestines are lax and oedematous, and the muscular structures are paralyzed, with resulting tympanitic distension. The peritoneal covering of the intestines is devoid of lustre, and covered with injected patches, or is stained of a dark-brown color. Death often ensues before the occurrence of exudation.

Septic forms of pelvic inflammation are often associated with oöphoritis, the dilated lymphatics either extending to the substance of the ovaries, where they may lead to the production of small abscesses, or, as a result of blood-dissolution, the organs become soft, pulpy, and infiltrated with discolored serum, and present hemorrhagic spots distributed over the surface.

PHLEBITIS AND PHLEBO-THROMBOSIS.--The formation of thrombi in the uterine and pelvic veins is sufficiently common during the puerperal period. The coagulation may result from compression or from enfeeblement of the circulation. A predisposition to its occurrence is created by relaxation of the uterine tissue. A normal thrombus is in itself harmless. In time it becomes organized, and the occluded vessel is converted into a connective-tissue cord, or a channel may form through it which permits the passage of the blood-stream. When, however, pus or septic matters obtain access to a thrombus, it undergoes rapid disintegration, and the particles get swept away into the circulation until arrested in the ramifications of the pulmonary artery. Wherever these poisoned emboli happen to lodge inflammation is set up in the adjacent tissues, and abscesses result (pyæmia multiplex). Sometimes countless collections of pus may form in the lungs. Less commonly abscesses are found in the liver or spleen, originating either from emboli which have already made the pulmonary circuit or from thrombi in the pulmonary veins.

Inflammation of the veins (phlebitis) sometimes occurs when the vessels have to traverse tissues in or near the uterus infiltrated with purulent or septic materials. The endothelium then undergoes proliferation, and thrombosis is produced. Phlebitic thrombi do not necessarily break down, and may in that case act as a barrier to the progression of septic germs into the circulation (Spiegelberg). As a rule, however, {990} under the influence of inflammation and infection, they become converted into puriform masses.

The thrombi grow by accretion in the direction of the heart. They may extend from the uterus through the internal spermatic, or through the hypogastric and common iliac veins, to the vena cava. Sometimes the thrombus may be traced back to the placental site.

SEPTICÆMIA.--From these local conditions, sooner or later, secondary affections develop in distant organs. The general affection is, in great part at least, likewise of local origin. Sometimes, however, where the poison, which enters the system through the lymphatics and veins, is very active and abundant, death may follow from acute septicæmia before the changes in the sexual organs have had time to develop. The fatal result in these cases is probably due to paralysis of the heart. After death post-mortem decomposition rapidly sets in, the blood is sticky, and swelling is found in the various parenchymatous organs.

The secondary affections consist in the metastatic abscesses already noticed as produced by infected emboli, in circumscribed purulent collections due to the conveyance of septic materials into the blood-current through the lymphatics, in ulcerative endocarditis, in inflammations of the pleura, the pericardium, and the meninges, and in purulent inflammation of the joints.

A study of the nature of puerperal fever will best show how intimately these seemingly distinct processes are linked together.

EARLIER VIEWS CONCERNING THE NATURE OF PUERPERAL FEVER.[9]--According to the teachings of Hippocrates, Galen, and Avicenna, of Ambrose Paré, of Sydenham, and of Smellie, the fevers of puerperal women were attributable to the suppression of the lochia. For twenty centuries this doctrine was accepted almost without dispute, the best clinical observers confounding a symptom which is often lacking with the cause of the disease itself.

[Footnote 9: For data given, and for a great variety of historical information, vide Hervieux, _Traité clinique et pratique des maladies puerperales_.]

In 1686, Puzos[10] taught that milk, circulating in the blood, is attracted to the uterus during pregnancy and to the breasts after confinement, but that milk metastases may form in other parts, and produce the symptoms of malignant or intermittent fever. In 1746, A. de Jussieu, Col de Villars, and Fontaine advanced in support of this theory the fact that they had found, on opening the abdomen in women who had died from an epidemic which raged that year in Paris, a free lactescent fluid in the lower portion of the abdominal cavity and clotted milk adherent to the intestines. This doctrine, which seemed to be based upon, and to accord with, observation, found many adherents in France. It lost ground, however, when, in 1801, Bichat pointed out the true nature of the abdominal effusions of women who had died in childbed, and demonstrated that they were to be found likewise in peritoneal inflammations occurring in men and in non-puerperal women.

[Footnote 10: _Premier Mémoire sur les Dépôts lacteux_.]

While, during the second half of the eighteenth century, the doctrine of milk metastasis held full sway in France, in England and Germany the dominant leaders in medicine referred the causes of puerperal fevers to inflammations of the womb and of the peritoneum. With the advances made in pathological anatomy in the beginning of the present {991} century, France taking the lead, stress was likewise laid upon inflammations of the veins and of the lymphatics. The vitality of the doctrine of local inflammations is well shown by the records kept by the Health Board of this city, where a large proportion of the deaths returned from childbed fever are entered under the head of metritis, of peritonitis, of metro-peritonitis, and of puerperal phlebitis.

In opposition to the doctrines of the so-called localists, the theory that puerperal fever is an essential fever, and as much a distinct disease as typhus fever, typhoid fever, or relapsing fever, has been strenuously advocated by some of the most distinguished clinical teachers who have devoted their attention to obstetrical science.

Fordyce Barker, the most recent exponent of the essentiality of puerperal fever, in his classical work upon the _Puerperal Diseases_, states the arguments against the local origin of the diseases as follows: 1st, that puerperal fever has no characteristic lesions; 2d, that the lesions which do exist are often not sufficient to influence the progress of the disease or to explain the cause of death; 3d, that there may be inflammation, even to an intense degree, of any of the organs in which the principal lesions of puerperal fever are found, and yet the disease will lack some of the essential characteristics of puerperal fever; 4th, that the lesions are essentially different from spontaneous or idiopathic inflammations of the tissues where these lesions are found; 5th, that puerperal fever is often communicable from one patient to another through the medium of a third party, and that this is not the fact in regard to simple inflammations in puerperal women.

However, neither Barker, nor those who entertain views similar to his, question the local origin of many febrile affections in childbed, but claim that purely local inflammations have each their characteristic symptoms, which differ from those of true puerperal fever, that puerperal fever is a zymotic disease of unknown origin, and that local lesions, where they coexist, are not the primary source of trouble, but are secondary to changes in the blood.

In 1850, James Y. Simpson[11] published a short paper "On the Analogy between Puerperal and Surgical Fever." This article may well be regarded as the foundation of the modern doctrine concerning puerperal fever, and is well worthy of perusal at the present day; for, though in the then existing state of pathology many of the links were wanting which have since raised the argument to nearly a mathematical demonstration, the paper furnishes a brilliant example of the scientific foresight which is able to discern the truth even where the evidence lacks completeness.

[Footnote 11: _Edinburgh Medical Journal_.]

In 1847, Semmelweis, who was at that time clinical assistant to the Lying-in Hospital at Vienna, made the startling assertion that "puerperal patients were chiefly attacked with puerperal fever when they had been examined by the physicians who were fresh from contact with the poisons engendered by cadaveric decay; that fever ensued in the practice of those who after post-mortem examination washed their hands in the usual manner, whereas no fever or but few cases of disease followed when the examiner had previously washed his hands in a solution of chloride of lime." In the face of insult, ridicule, and abuse Semmelweis {992} maintained this position for years, almost unaided, with fanatical persistency. It was easy for his opponents, for the most part managers of the great lying-in asylums, to show from clinical experiences the weakness of so one-sided a theory. But the employment of the equivocal demonstration _falsus in uno, falsus in omnibus_, served only as a temporary defence against the laxity which prevailed in hospital management only a quarter of a century ago. Though Semmelweis died with no other reward than the scorn of his contemporaries, it is impossible at the present day to so much as contemplate the abuses he attacked without a shudder.

In 1860, Semmelweis published the result of his ripened experience in a treatise entitled _Die Aetiologie der Begriff und die Prophylaxis des Kindbett fiebers_, in which, abandoning his earlier exclusive position, he maintained that puerperal fever arises from the absorption of putrid animal substances, which produce first alterations in the blood, and secondly exudations. He distinguished between cases in which the infection was introduced from some external source, and which he believed to be the most frequent variety, and those where the poison was generated in the system. The sources from which the infection is derived he believed to be--1st, from the dead body, regardless of age, sex, or disease, no matter whether the latter is of puerperal or non-puerperal origin, the virulence depending upon the stage of decomposition; 2d, diseased persons, whose malady is associated with decomposition of animal tissue, no matter whether the affected person suffers from childbed fever or not, the decomposing matter alone furnishing the product from which infection is derived; 3d, physiological animal substances in the process of decomposition. As carriers of infection he regarded the fingers and hands of the physician, midwife, or nurse, sponges, instruments, soiled clothing, the atmosphere, and, in brief, anything which, after being defiled with decomposing animal matter, was brought into contact with the genitals of a woman during or subsequent to parturition. Absorption takes place from the inner surface of the uterus or from traumata in the genital canal. Infection seldom occurs in pregnancy, because of the closure of the os internum, the absence of wounded surfaces, and because of the rarity with which examinations are made; during dilatation infection is common, but exceptional during the period of expulsion, because the inner uterine surface is at that time rendered inaccessible by the advance of the child; in the placental and puerperal period infection occurs from utensils and instruments, but chiefly through the access of atmospheric air when the latter is loaded with decomposing organic matter. In rare instances auto-infection may result from spontaneous decomposition of the lochia, of bits of decidua, of coagula of blood, of necrosed tissue, or in consequence of severe instrumental labors. In a word, puerperal fever was according to Semmelweis no new specific disease, but a variety of pyæmia.

I have been thus particular in giving prominence to the labors of Semmelweis partly from justice to a man who was hated and despised in his lifetime, and partly because I believe that few outside of Germany are really cognizant of the immense service he rendered to humanity, or that to him is really due a large part of what is now current doctrine concerning the nature and prophylaxis of puerperal fever.

THE NATURE OF PUERPERAL FEVER AS REGARDED FROM THE {993} STANDPOINT OF MODERN INVESTIGATION.--The older beliefs in the suppression of the lochia and the metastases of milk have long since been relegated to the domain of old nurses' lore, and do not call for serious discussion. The localist theory, that puerperal fever is a metritis, a peritonitis, a phlebitis, or an inflammation of the lymphatics, is, as mortuary records show, still adhered to by many practitioners, and, as we have seen, is justified by the fact that puerperal fever is, with rare exceptions, associated at some period of its progress with certain inflammatory processes which have their starting-point in the generative apparatus. But the localist theory leaves out of view the existence of blood-poisoning, and yet the coexistence of a blood-poison with the local lesions is an essential feature of puerperal fever. It was this defect which gave to the advocates of the specificity of puerperal fever their real importance. The outcome of modern investigation tends, however, to prove that the puerperal poison is of a septic nature, and that the usual points of introduction of the poison are the lesions of the parturient canal. This does not, indeed, exclude other points of entry, for clinical experience renders it probable that, under certain conditions, the poison may be primarily introduced into the blood through the respiratory and digestive organs. Puerperal fever is really a surgical fever, modified, however, by the peculiar physiological conditions which belong to the puerperal state. The argument against its septic origin is based chiefly upon mistaken ideas concerning the nature of septicæmia. So long as the symptoms of the latter were derived for the most part from the effects observed as a consequence of injecting putrid materials into the veins of dogs, a confusion arose from the fact that the results obtained were commonly those of putrid intoxication, and not those of true septicæmia. Under such circumstances it was not difficult to formulate definitions of septicæmia which could be shown to be at variance with the phenomena which ordinarily exist in puerperal fever.

The argument that the infectious diseases of childbed are of a septic nature can best be understood by presenting the proofs in their orderly sequence.

1st. _It is demonstrable that septic poisons are capable of producing the lesions ordinarily associated with puerperal fever._ Thus, it is a matter of ordinary experience that the retention of a small bit of the membranes within the uterus will produce fetid lochia, and, as the result of infection, a febrile condition, which, as a rule, subsides with the expulsion of the offending body and the use of disinfectant washes. A virulent form of fever is not unfrequently occasioned by retained coagula or placental débris which have undergone decomposition. I was once sent for to see a puerperal patient suffering from fever on the fourth day following her confinement. On entering the room I found the stench intolerable; turning down the sheets, I discovered that the patient was lying in a decomposing mass, and learned that her doctor had forbidden, after the birth of her child, the removal of the soiled linen and blankets. The patient died in the third week from pyæmia multiplex.

Haussmann[12] reported a case of auto-infection in the rabbit which terminated fatally. A portion of the membrane, retained in the left cornu, {994} led to diphtheritic losses of substance in the lower portion of the vagina, to hemorrhagic enteritis, and to peritonitis. The same author produced death from septicæmia by injecting into the gravid uterus of one rabbit serum from the abdomen of another which had died from infection. The post-mortem examination showed the muscles filled with granules and the peritoneum injected, but no fibrino-purulent exudation. Injections into the uterus of pus from the abdomen of a woman who had died from infectious puerperal disease produced no effect upon rabbits two weeks gravid, while in the second half of pregnancy premature delivery and death occurred, in one case in one and a half, in another in two and a half, days. In the animal which died in thirty-six hours there was commencing perimetritis and peritonitis, while in the one that died after the lapse of sixty hours the abdomen was found to contain fibrine and pus.[13] D'Espine injected into the uterus of a rabbit which had just produced her young pus from the abdomen of a woman who had died from puerperal disease two days before. This was subsequently followed by other injections of fetid fluids during the four days following. On the twelfth day the animal died. The autopsy revealed peritonitis, most marked in the pelvic cavity, inflammatory alterations in the vagina, uterus, and tubes, small abscesses in the body of the uterus, softened clots in the veins of the broad ligaments, and infarctions of the liver.[14] Schüller found that subcutaneous injections of septic material in female animals during pregnancy produced a diphtheritic ulcerative process on the uterine surface, which determined the separation of the placenta; diphtheritic patches, likewise, were found in the cornua of the uterus.[15]

[Footnote 12: "Entstehung der übertragbaren Krankheiten des Wochenbettes," _Beitr. zur Geburtsk. und Gynaek._, Bd. iii. Heft 3, p. 345.]

[Footnote 13: _Contribution à l'étude de la septicémie puerpérale_, Paris, 1873, p. 28.]

[Footnote 14: _Ibid._, p. 394.]

[Footnote 15: "Experimentelle Beiträge zum Studium der septischen Infection," _Deutsch. Zeitschr. für Chir._, Bd. vi. p. 141.]

Thus we find that in the human subject and in experiments made upon animals septic poisons introduced into the system following or near delivery produce lesions similar to those found in puerperal fever. As a further coincidence, we notice that, as in puerperal fever, the lesions from direct septic poisoning have nothing characteristic about them, producing in one case pyæmia, in another partial peritonitis, in another general peritonitis, in another diphtheritis, while in others the lesions are comparatively trivial, these differences being due to variable facta, such as the qualities of the septic poisons, the points of entry into the organism, and the resistance offered by the invaded tissues.

2d. _Septicæmia is a disease characterized by the invariable presence in the organism infected of minute bodies generally termed bacteria._[16]

[Footnote 16: In 1865, Mayrhofer (_Mon. Schr. f. Geburtsk._, vol. xxv., p. 112, 1865), at that time clinical assistant to the Lying-in Service of Braun in Vienna, stimulated by the researches of Pasteur, maintained that septic endometritis was the result of putrid fermentation within the uterine cavity, and drew attention to the vibrios--a term which he applied to the round as well as to the rod-like bacteria--as the source, and not the product, of putrefaction. He claimed that while in puerperal processes vibrios are always present, in healthy women they never occur before the second, third, or fourth day, and not always even then. The chief progress that has been made as regards our knowledge of puerperal fever in the last ten years has been in the direction of strengthening Mayrhofer's argument by careful experiment, and by defining the action of microscopic fungi in the production of septic morbid processes.]

Until very recently the whole subject of septicæmia has been in a state of wellnigh hopeless confusion. From Gaspard and Panum, through a long list of experimenters, hardly any two arrived at precisely similar {995} results. Something like an approach to order has, however, been produced since it has begun to be understood that the effects produced by septic fluids vary with the quality of the poison and the method of experimentation, and that to obtain identity in the result there must be identity in all the conditions. Thus, Samuel has shown that the same organic substance produces different effects at different stages of decomposition; again, that the enteritis which is commonly quoted as characteristic of septic poisoning occurs, as a rule, in animals when the septic fluid is injected directly into the blood, and is rare when it finds its way into the circulation through the lymphatics, as is the case usually in clinical experiences.[17] There is one experimental point of extreme practical importance too in connection with puerperal septicæmia--viz. that if the injection of a septic fluid be made directly into a vessel, toxic effects speedily follow, but are transitory, unless the amount of the fluid be large, or its virulence exceptional, or the animal very young;[18] whereas very small amounts injected subcutaneously, by developing rapidly-spreading phlegmonous inflammation, resembling malignant erysipelas in man, are capable, after a period of incubation, of producing fatal results; or they may, if injected into a shut cavity or underneath a fascia, lead to the development of an inflammation of an ichorous character. In other words, the eliminating organs suffice, under ordinary conditions, to remove from the blood the same amount of septic fluid which would prove fatal if injected into the tissues.[19] To produce similar results the injections into the blood need to be repeated at intervals. This experience leads us to the conclusion that in the tissues septic poison possesses the capacity of self-multiplication, and that in the local inflammation set up a reservoir is formed from which poison is continuously poured into the circulation.

[Footnote 17: _Loc. cit._, p. 349.]

[Footnote 18: "Traube und Gescheidlen, Versüche über Faülniss und den Widerstand des lebender Organismus," _Schles. Ges. f. vaterländische Cultur_, Feb. 13, 1874.]

[Footnote 19: In some instances in which absorption from the tissues is very rapid the effects of subcutaneous injections may be similar to those produced by injections made directly into the circulation, and the local lesion be insignificant.]

This capacity of self-multiplication which septic fluids possess has recently been found to be coincident with the presence of certain parasitic bodies, generically termed bacteria. All carefully-made experiments serve to show that if a septic fluid be deprived of these organic bodies by boiling or filtration while it continues capable of producing inflammation, the inflammation is usually of diminished intensity and remains local in its character;[20] whereas the bacteria retained upon the filter possess all the virulent properties of the original fluid.[21] This does not alone necessarily prove that the virus resides in the bacteria, for it does not exclude the possibility that both the virus and the bacteria remain upon the filter.

[Footnote 20: In filtration through porous earthenware cylinders the filtrate possesses no phlogogenic properties.]

[Footnote 21: Tiegel, _Correspondenzblatt für Schweizer Aertze_, 1871, S. 1275; Klebs, _Archiv für exp. Pathol. und Pharmakol._, Bd. i. Heft. 1, S. 35.]

So far, attempts at isolating the microspores of septicæmia and cultivating them separately in vehicles composed of water holding in solution inorganic constituents, or sterilized fluids containing organic matters, or of the semi-solid gelatinous substances recommended by Koch, have been only partially successful in proving them to be the sole source of {996} infection. Some earlier experiments of Tiegel and Klebs[22] were attended with positive results, and more recently confirmatory evidence has been furnished by Pasteur and Doléris.[23] Hiller, rarely quoted now, arrived at different conclusions. He found that bacteria washed in pure water were innocuous.[24] But pure water had long before been proven by observers to be inimical to the well-being of the organisms in question. Schüller says that Hiller's experiments prove apparently that while a putrid fluid may be in the highest degree poisonous, its component parts--viz. either the fluid or the bacteria singly--are neither deadly nor poisonous.[25] The fact is, that isolation experiments are subject to what has hitherto been in most experiments an unavoidable source of error. As Davaine noted early in his observations, the physiological action of bacteria is very dependent on the constitution of the medium in which they are developed, which is in entire harmony with what is known of organisms much higher in the scale. "Many plants," says Burdon-Sanderson,[26] "containing active principles, become inert when transplanted from an appropriate soil." Bucholtz, in a series of experiments designed to test the influence of antiseptics upon the vitality of bacteria, found not only a difference between those taken directly from the infusion and those cultivated in artificial fluids, but between bacteria derived from the same source and cultivated in modifications of the nutrient medium.[27] Then, too, it is not always safe to transfer to the human species the results of experiments made upon the lower animals. Indeed, among animals, not only in different species, but in varieties of the same species, differences in the susceptibility to septicæmic poisons are found ranging from gradations as to the intensity of the effect produced to absolute immunity. In anthrax, a disease analogous to the one in question, the bacterial origin has been established beyond dispute by the inoculation of isolated bacilli, which multiply in the blood and permeate in enormous numbers the lungs, liver, kidneys, spleen, and glandular structures. If the same unequivocal testimony has as yet not been obtained from isolation experiments as regards septicæmia, it is reasonable to suppose that this is due to the defects in the technique, for which it is presumable the ingenuity of investigators will in future find the remedy.

[Footnote 22: _Archiv für exp. Pathologie und Pharmakologie_, "Beiträge zur Kenntniss der Pathogenen Schistomyceten," Band iv. Heft 3, S. 241 und ff.; Tiegel, _loc. cit._]

[Footnote 23: In this connection may be mentioned some very interesting experiments by Dr. George Gaffky (_Experimentellen Erzengte Septicæmie, Mittheilungen aus den Kaiserlich, Gesundh. Amte_), in which micrococci from the blood of septicæmic mice were successfully cultivated in a gelatine preparation, and produced, when inoculated in small quantities, the symptoms identical with those obtained by inoculating the blood itself.]

[Footnote 24: "Exp. Beiträge zur Lehre von der organisirte Natur der Contagion und von der Faülniss," _Archiv für klinische Chirurgie_, Bd. xvii. Heft 4, S. 669 u. ff.]

[Footnote 25: "Exp. Beiträge zum Studium der septischen Infection," _Deutsche Zeitschrift für Chirurgie_, Bd. vi. S. 162.]

[Footnote 26: "Lectures on the Relations of Bacteria to Disease," _British Med. Journal_, March 27, 1875. See also Klebs, "Beiträge zur Kenntniss der Pathogenen Schistomyceten," _Arch. für Pathol. und Pharmakol._, Bd. iii. S. 321.]

[Footnote 27: "Antiseptica und Bacterien," _Arch. f. exp. Pathol. und Pharmakol._, Bd. iv., Heft 1 und 2.]

It is, however, from the constant presence of the bacteria in infected wounds, and their distribution through the tissues, that the argument in favor of connecting septic symptoms with the bacteria has been mainly deduced. Here the ground is sufficiently solid, and, judged by ordinary laws of scientific evidence, the pathological importance of the microspores {997} may be regarded as established. To be sure, we find them in tongue-scrapings of healthy individuals, but tongue-scrapings are poisonous if injected into the tissues. That they do not ordinarily prove so in the mouth is no more singular than that woorari can be swallowed with impunity. Tiegel[28] has endeavored to show that round bacteria are found normally in the internal organs of the body; but Koch[29] states that he has on many occasions examined normal blood and normal tissues by means which prevented the possibility of overlooking bacteria, or of confounding them with granular masses of equal size, and that he has never in a single instance found organisms.

[Footnote 28: _Arch. f. Path. Anat. u. Physiol. u. f. klin. Med._, vol. lx. p. 453.]

[Footnote 29: On _Traumatic Infective Diseases_, New Sydenham Soc. publication p. 15.]

It is stated that bacteria are sometimes absent from the blood withdrawn during life in septic diseases. As, however, their constant presence has been confirmed in the vessels and glomeruli of the kidneys, it is fair to assume that those organs, acting as filters, must have received the colonies observed in them from the general circulation.

The difficulty of obtaining bacteria from the blood in many cases during life in septic diseases does not, however, as was once supposed, invalidate the theory of their pathogenic importance. Septicæmia is at present employed as a collective term for a number of processes which may occur singly or in combination with one another. When a relatively large quantity of a putrid fluid is injected into the veins of an animal, death follows from the action of a chemical poison (sepsin). The blood during life rarely displays the presence of bacteria, the latter disappearing in the circulation. In animals thus poisoned blood does not possess infectious properties. This form is termed putrid intoxication. That the poison in these cases is, however, produced by the bacteria is shown by experiments of Gutmann,[30] who demonstrated that bacteria from a drop of putrid blood cultivated in Cohn's solution developed in the fluid a poison which, when injected into the veins of dogs, occasioned death with all the symptoms of putrid intoxication. Still more conclusive were the experiments of Koch. This observer injected four drops of putrid blood beneath the skin of mice. The latter died in from four to eight hours. There were no bacteria in the blood, and the blood was not infectious. When, however, a single drop was injected, the mice often remained unaffected, but in a third of the cases they became ill after twenty-four hours, death occurring in from forty to sixty hours. The blood during life communicated the same disease to other mice, and bacilli were always present in large numbers. In these cases the dissolved poison in the fluid injected was too small in amount to destroy life, and death resulted only after a period of incubation as a consequence of the multiplication of bacilli in the blood and in the tissues.

[Footnote 30: Vide Semmer, "Putride Intoxication," etc., _Virchow's Arch._, vol. lxxxi. p. 109.]

In another class of cases Koch experimented, not with putrid blood, but with a fluid produced by macerating a piece of mouse-skin in distilled water. Of this he injected a syringeful into the back of a rabbit. The result was peritonitis, swelling of the spleen, gray wedge-shaped patches in the liver, and in the lungs were found dark-red patches the size of a pea, devoid of air--all appearances in harmony with what is designated as pyæmia. Oval micrococci were found in great numbers {998} everywhere throughout the body. But the point of special interest in the present connection is the fact that wherever these micrococci come in contact with the red blood-corpuscles the latter stick together and become arrested in the minute capillary network. The thrombi thus formed are further enlarged by the deposition of micrococci, which multiply, block up individual capillary loops, and invade contiguous tissues. In the blood-current itself, however, the micrococci do not increase in numbers, and cannot always be found in the circulation upon a single examination, but Doléris[31] assures us that in puerperal fever by repeated trials, especially after a chill, he has never failed to demonstrate their presence.

[Footnote 31: _La Fievre Puerperale, etc._, p. 120.]

As to the exact manner in which these minute bodies exercise their pernicious influence, whether they operate mechanically, or whether they produce a virus in the process of nutritive activity, or whether, as is probable, both suppositions are correct, must be decided by future investigations. It is enough for us to note that the connection between sepsis and bacteria is intimate and vital.

3d. _Pathogenic bacteria are invariably associated with puerperal fever, and to them the infectious qualities of the disease are due._ I have been explicit regarding the evidence concerning bacteria in septic diseases, because it places the question of the infectious group of puerperal fever cases in the following position: Experiences occurring clinically, as well as those produced upon animals, teach us that certain lesions and symptoms, similar to those we are accustomed to regard as characteristic of puerperal fever, results from septic poisoning. In a large class of cases, however, the connection between childbed fever and sepsis has been deduced rather from analogy than direct proof. For those who chose to regard such as due to a specific poison peculiar to the puerperal state there was really no objection. If, however, bacteria are characteristic of septic poisoning, the question presents itself in a different light, and we have to inquire whether, in the less obvious cases, bacteria are present in puerperal fever in the proportions and groupings that we find them in other diseases due to putrid infection. Now, it is precisely proof of this nature that has recently been abundantly rendered.

Waldeyer,[32] Orth,[33] Heiberg,[34] and Von Recklinghausen[35] found the tissues and lymphatics of the parametria filled with pus-like masses, which consisted, in addition to pus-cells, chiefly of bacteria. Bacteria swarmed in the fluid of the peritoneal cavity. In one case examined by Waldeyer six hours after death, while the body was still warm, the peritoneal exudation was like an emulsion, and furnished an abundant deposit which consisted almost entirely of bacteria. Orth injected ten minims of peritoneal fluid from a woman dead of puerperal fever into the abdomen of a rabbit. As the animal was dying he broke up the medulla oblongata, and found in the peritoneal fluid enormous quantities of these {999} organisms. In puerperal fever round bacteria have been likewise found, though in less quantities, in the lymphatics of the diaphragm and in the fluids of the pleura, the pericardium, and the ventricles of the brain. In post-mortem examinations of fresh subjects the serous fluids, withdrawn under proper precautions, do not contain round bacteria except in cases of septic infection.[36] Orth found in the purulent contents of the vessels of the funis, in children who died of sepsis, precisely the same formations as existed in the exudations of the mother.

[Footnote 32: "Ueber das Verkommen von Bacterien bei der diphtheritischen Form des puerperal Fiebers," _Archiv für Gynaekologie_, vol. iii. p. 293.]

[Footnote 33: "Untersuchungen über puerperal Fieber," _Virchow's Archiv_, vol. lviii. p. 437.]

[Footnote 34: _Die puerperalen und pyæmischen Processe_, Leipzig, 1873.]

[Footnote 35: For the views of Von Recklinghausen I am indebted to his pupil Steurer. Vide the writer's paper on "The Nature, Origin, and Prevention of Puerperal Fever," _Trans. of the International Med. Congress_, Phila., 1876.]

[Footnote 36: Klebs, "Beiträge zur Kenntniss der Pathogenen Schistomyceten," _Archiv für exp. Pathol. und Pharmakol._, vol. iv. p. 441 _et seq._]

Doléris, in a remarkable essay already referred to, published in 1880,[37] furnishes not only conclusive evidence of the presence of bacteria in the various tissues and serous cavities of women dying of puerperal fever, but has added the evidence of their pathogenic character by cultivating them apart in sterilized fluids, and by reproducing in animals, by means of subcutaneous injections of the isolated bacteria, the infarctions, the blood-changes, and the suppurative processes of the original disease.

[Footnote 37: _La Fievre Puerperale et les Organismes Inférieurs._]

So far, the generic term bacteria has been employed to indicate the disease-germs which are the active agents of infection in puerperal fever. It is not, however, intended to assume that the germs of septic processes are all identical, or that they all produce precisely the same pathological conditions. Koch, indeed, maintains that a distinct specific bacterial form is found in such closely-allied affections as pyæmia, septicæmia, gangrene, and erysipelas, the different forms possessing, however, this link in common--viz. that they are alike generated in putrefying media. Singularly enough, the bacterium termo and the bacterium commune--to which the fetidity of matters undergoing putrefaction is due--are in themselves harmless. They are rapidly destroyed in the circulation, and are not inoculable. Fetid discharges from wounds are not therefore necessarily dangerous. The putrid odor serves a useful purpose, as it gives warning of the existence of conditions which favor the development of life-destroying organisms; but the latter may develop without the concurrence of the forms which give rise to putrefaction--a fact of considerable importance in view of the common belief that septic infection is excluded by the absence of fetid odors.

In puerperal fever Doléris found the prevailing pathogenic organisms consisted of bacilli or rods, and micrococci or round bacteria in the varieties of micrococci, simple points; diplococci, double points; and chains or wreaths. The bacilli he regarded as the source of acute, rapid septicæmia, while pus-production was associated with the multiplication of the round bacteria, and especially of the diplococci.

4th. _The presence of germs in puerperal fever serves not only to fix cases hitherto doubtful in the category of septic diseases, but affords the most satisfactory explanation of the protean phenomena of puerperal fever itself._

We have seen, from both Koch's and Gutmann's experiments upon animals, that death may occur independently of bacteria by the rapid absorption of a chemical poison developed in a putrefying fluid. Clinical experiences, such as the speedy death sometimes observed when retained coagula or portions of placenta undergo decomposition within the uterine cavity, renders it probable that similar cases of putrid intoxication are {1000} not unknown in puerperal women, though, so far, the anatomical demonstration of the fact has not been furnished.

In cases, however, where puerperal fever has a distinct period of incubation, and progresses step by step to the fatal ending, bacteria are always found invading the tissues of the genital canal. In rare cases they pass by the Fallopian tube to the peritoneal cavity and excite salpingitis and peritonitis. More commonly from local lesions they enter the canalicular spaces of the connective tissue forming the framework of the genital canal, which is continuous with the subperitoneal connective tissue of the pelvis. From the canalicular space they enter the lymphatics. Cellulitis is excited by their presence, and the lymphatic glands become inflamed and enlarged. In pernicious forms they produce a sero-purulent oedema, which spreads rapidly with a wave-like progress after the manner of erysipelas; or in milder cases the progress of the disease-germs is arrested by the lymphatic glands or the resistance offered by the tissues themselves, and the ordinary circumscribed phlegmon is produced. By the lymphatics which accompany the vessels of the Fallopian tubes they reach the ovaries (puerperal ovaritis), and by the broad ligaments they pass to subperitoneal tissues of the iliac and lumbar regions. Through the same system they are conveyed to the great serous cavities of the body. In the peritoneum they give rise, unless death occurs too speedily, to pyæmic peritonitis, which, unlike the traumatic form, is attended with but little pain, and for which the claim has been set up that it is peculiar to puerperal fever. The wide stomata upon the abdominal surface of the diaphragm allows the facile entrance of the organisms into its lymphatics. Waldeyer found in diaphragmitis the lymphatics of the diaphragm filled with bacteria. And thus, following the lymphatic system, if we only admit that bacteria are the active agents of sepsis, the frequency, in severe types of puerperal fever, of inflammation of the serous membranes of the peritoneum, the pleuræ, the pericardium, the meninges, and the joints finds an easy explanation. Nor is it altogether accident which determines in different cases the precise serous membranes which are affected. The widespread ramifications of the lymphatic system would naturally give rise to eccentric inflammations in place of those following the apparent continuity of tissues.

The ductus thoracicus is the principal channel through which the bacteria enter the blood. It is possible that they may further obtain access into the circulation through the radicles which furnish the communications between the capillaries and the lymphatics. We have seen that bacteria are found with difficulty in the blood during life. A few hours after death they swarm in that fluid. That they do, however, enter the general circulation during life is incontestable. Steurer writes: "As the kidneys are the great filters of the human system, I never neglected to examine them, and almost invariably found micrococci filling the arterioles and glomeruli." This is in correspondence with what occurs in other septic diseases, and accounts for the albuminuria and interstitial nephritis which often supervene in the advanced stages.

The action of the bacilli upon the blood differs materially from that of the round bacteria. So soon as the latter come in contact with the red corpuscles, the corpuscles stick together and form larger or smaller clots in the blood. They then are no longer able to pass through the minute {1001} capillary networks, but are arrested in the larger or smaller vessels (Koch). The micrococci in the resulting infarctions multiply, and migrate into the vessels and cellular tissue of the neighborhood. Thus fresh foci of infection are formed. Or by their destructive action they may, when situated near the serous surfaces, penetrate into the serous cavities, and in this way indirectly occasion peritonitis, pleurisy, meningitis, and purulent inflammations of the joints. When the micrococci enter directly into the circulation, they sometimes, in passing through the heart, adhere to the endocardium and the valves, where they cause exudation and ulceration, and give rise to the so-called endocarditis ulcerosa puerperalis.[38] The red globules of the blood undergo changes of shape, assume a stellate aspect, and rapidly disappear. The white globules are greatly increased in numbers, and the blood itself becomes nearly colorless. A certain amount of light is thrown upon these blood-changes by Doléris, who added micrococci to the fresh blood of a frog and watched the ensuing changes under the microscope. The micrococci could be seen in the act of penetrating the red globules, which thereupon lost their color and became shrunken, and, following the discharge of the organisms, which meantime had multiplied in an astonishing manner, little or nothing of the original globules remained.

[Footnote 38: Heiberg, _Die puerperalen und pyæmischen Processe_, Leipzig, 1873, pp. 22 and 34, with references to cases reported by Wiege and Eberth.]

In the bacillar form of septicæmia the blood is dark and has a semi-gelatinous appearance, compared by French writers to partially-cooked gooseberry jelly. The red globules, though they exhibit the various stages of deformation, are not diminished in number. The disease is further characterized by ecchymoses and minute apoplectic effusions, and by the absence of pus-formation. In the artificial septicæmia produced by Koch in mice by means of bacilli the rod-like organisms were found to enter the white corpuscles and to compass their destruction. They did not cause the red globules to adhere together, and there was no clogging of the capillary circulation. All the principal structures of the animals subjected to experiment were infiltrated with bacilli. The distribution of the latter was apparently accomplished by the blood-vessels, and not by the lymphatics, the bacilli probably effecting their entrance into the vessels by virtue of their penetrative power, in place of traversing preformed pathways. Possibly it is this action of the bacilli which causes the weakening of the vessel-walls, as evidenced by the large number of red corpuscles which pass out from them.

In puerperal fever it is rare to find either round bacteria or bacilli acting singly as the agent of infection. As a rule, both forms exist together in varying proportions, the predominant form, however, determining in general the character of the symptoms.

Thrombosis of the veins may be a physiological phenomenon, or may be due to an alteration of the blood, to weakness of the heart, or to local influences. So long as the clot remains firm its influence is limited to disturbances of the circulation. The pyæmic symptoms--viz. suppuration of the coagulum, the separation of emboli, and the formation of metastatic abscesses--are always dependent upon the presence of round bacteria. In phlebitis the latter are found in the endothelium and in the sheaths of the veins. The inflammation of the veins is followed by {1002} thrombosis. According to Doléris, micrococci derived from the blood are deposited upon the central extremities of the clots; beyond these dépôts a fresh inflammation is set up, followed by fibrinous coagulation. Thus the micrococci become imprisoned between two plugs. The same process may be repeated until a series of abscesses are formed. For a time no mischief may ensue. Finally, however, the resistance of the outworks is overcome, an embolus becomes detached, and an infectious abscess is opened into the blood--an event which is announced by an intense chill and the familiar systemic derangement.

In septic diseases death takes place from apnoea, partly from the inability of the blood-corpuscles to carry oxygen to the tissues, and partly from paralysis of the nerve-centres.[39]

[Footnote 39: Schüller, "Exp. Beiträge zur Studium der Septischen Infection," _Deutsche Zeitschr. f. Chir._, vol. vi. p. 149 _et seq._]

In hospital epidemics of puerperal fever diphtheritic patches situated upon the lesions of the vulva and in the course of the utero-vaginal canal are sometimes observed. Steurer found these patches were always associated with loss of substance, and were composed of disintegrated fibrin, white and red blood-globules, and colonies of round bacteria in great abundance. Morphologically, these so-called diphtheritic patches are identical with those which appear in the throat. Pallen[40] has reported an instance of the simultaneous occurrence of puerperal diphtheritis in the mother and throat diphtheritis in the two-weeks' old child. In lying-in hospitals it is the genital organs, as the locus resistentiæ minoris, and not the throat, which are the usual points of attack.

[Footnote 40: _Trans. N.Y. Obst. Soc._, 1876-78, p. 78.]

The question as to the extent to which erysipelas and puerperal fever are cognate diseases is in a fair way to be solved by recent investigation. Orth took the contents of a vesicle from an erysipelatous patient which contained bacteria in great abundance, and employed the same for injections under the skin of rabbits. In this way he succeeded in producing in these animals a species of erysipelas malignum. In the subcutaneous oedema and affected portions of the skin he found enormous masses of bacteria, so far exceeding in quantity the amount introduced as to prove an abundant new production.[41] Samuel produced similar results by the injection of ordinary putrid fluids containing round bacteria. An affection resembling simple erysipelas he obtained most frequently by the application of fluid to a wound torn open after the second or third day.[42] Lukomski found that erysipelas could be produced by fluid containing micrococci even when putrefaction did not exist. The contents of erysipelatous vesicles containing no micrococci excited no morbid manifestations. Where the erysipelatous process was fresh and progressing micrococci were found in great abundance in the lymphatics and canalicular spaces. Where the process was retrogressive, there were no micrococci to be found, even in cases in which inflammation existed to an intense degree.[43] Doléris submitted to the culture-process of Pasteur fluid obtained from vesicles which developed in the course of facial erysipelas in a man of forty years. Micrococci in chains were found in the liquids employed identical with those he had discovered in puerperal fever. In many cases I have seen an erysipelatous inflammation start from a puerperal diphtheritic ulcer {1003} upon the introitus vaginæ, and extend outward over the buttocks, the thighs, and the lower portion of the abdomen.

[Footnote 41: "Untersuchungen über Erysipel.," _Arch. für exp. Pathol. und Pharmakol._, Bd. i. S. 81.]

[Footnote 42: _Arch. für exp. Path. und Pharmak._, Bd. i. S. 335, u. ff.]

[Footnote 43: "Untersuchungen über Erysipel.," _Virchow's Archiv_, Bd. lx. S. 430.]

Virchow[44] has so far given in his adhesion to the new school as to say: "Especially in this connection are to be mentioned the diphtheritic process and the erysipelatous, especially erysipelas malignum. The granular deposit in diphtheritically affected tissues, of which I formerly spoke, has more and more proven to be of a parasitic character. What we formerly regarded as simple, organic granules, as infiltration or exudation, has since proven to be a dense aggregation of micro-organisms which penetrate into the tissues and cells to compass their destruction."

[Footnote 44: _Die Fortschritte der Krieg's Heilkunde_, Berlin, 1874.]

Thus we find in surgical fever, in puerperal fever, in diphtheria, and in erysipelas the presence of a common element which links them together, and which establishes the relationship which has long been recognized as existing between these various processes.

4th. _The differences between surgical and puerperal septicæmia are due to differences partly structural and partly physiological in the wounded surfaces exposed to septic contamination._

A certain amount of misapprehension has arisen from the circumstance that along with many coincidences in the symptoms of puerperal and surgical fever there are observable differences which, from a purely clinical point of view, would justify a separate classification of the two affections. It will not do, however, to ignore the fact that the conditions which prevail in the parturient canal subsequent to labor have no strict analogue in the lesions which the surgeon is called upon to treat, and that therefore a complete identity as to all the clinical features of puerperal and surgical fever would hardly be within the range of possibility.

In the puerperal state it is necessary to take into account the blood-changes induced by pregnancy, the effects of shock and exhaustion in protracted labors, the frequency of hemorrhage, the deep situation of puerperal wounds, the presence of clots, decidua, and dead tissue in a state of disintegration or decomposition, the ease with which deleterious matters are absorbed by the wide lymphatic interspaces, the serous infiltration of the pelvic tissues, the exaggerated size of the lymphatics and veins, and the proximity of the peritoneal cavity.

Samuel,[45] in speaking of the immunities and dispositions to septic poisoning, says: "The statistical frequency of septic puerperal disease is due to the length of the parturient canal, to the fact that through this long passage there must pass all the pathological and physiological excretions, and to the soiling of these parts with fingers, instruments, and secretions which have become the bearers of sepsis." He found, on the other hand, that it was extremely difficult to produce a progressive ichorous condition by daily painting an open stump with a septic fluid,[46] though the same was readily obtained when an infinitesimal quantity of septic fluid was injected underneath a fascia.

[Footnote 45: "Ueber die Wirkung des Faülniss Process auf den lebenden Organismus," _Arch. f. exp. Pathologie_, vol. i. p. 343.]

[Footnote 46: _Loc. cit._, p. 339.]

5th. _In the present state of our scientific knowledge it is necessary to admit that there is a limited number of febrile and inflammatory disturbances occurring in puerperal women, the bacterial origin of which may be fairly questioned._ As illustrations of this class may be {1004} mentioned: 1. Cases of catarrhal endometritis due to errors of diet and exposure. Indeed, I have frequently, in hospital practice, been able to trace severe cases of cellulitis, pelvic peritonitis, and general peritonitis occurring in the winter season to the patient getting out of bed dripping with perspiration, and clad only in a night-dress, and going thus barefooted over a cold, uncarpeted floor to the water-closet. 2. Cases of puerperal disorders proceeding from emotional causes, the nervous system furnishing the first impulse to the disturbed action. 3. Cases of excessive vulnerability in non-pregnant women; individuals are sometimes found so susceptible that a parametritis follows a simple application of the tincture of iodine to the cervix. 4. Cases of pelvic peritonitis starting from old intra-peritoneal adhesions. 5. Cases of peritonitis and retro-peritoneal inflammations secondary to ulcerative processes in the cæcum or the descending colon. This condition is apt to be masked during pregnancy, but starts into activity during childbed as a consequence of fecal accumulation or of excessive purgation.

It is by no means easy to decide as to the precise nature of local inflammations following lacerations of the cervix and the bruising or crushing of the soft parts in long or instrumental labors. The marvellous absence of heat, pain, redness, and swelling in wounds treated in strict accordance with the principles of Lister, the very slight reaction when the atmosphere is pure, and the severity of these symptoms in overcrowded hospitals, tend indeed to strengthen the belief that even the simplest inflammations proceeding from wounds owe their origin in great part to septic germs. But, on the other hand, in hospital practice it is not uncommon to observe puerperal inflammations and febrile conditions which possess this distinctive peculiarity--that they in no wise visibly affect the health of puerperal patients in their vicinity. The symptoms of blood-poisoning too are either absent or present to a subordinate extent. Probably the difficulty is best solved by assuming with Genzmer and Volkmann[47] that there is such a thing as an aseptic surgical fever due to the absorption of the products of physiological tissue-changes at the seat of injury. In surgical cases, even where the precautions of Listerism have been faultlessly observed, febrile movements of considerable intensity, but of no prognostic signification, are of frequent occurrence. While in puerperal women we can never exclude the possibility of the septic infection of puerperal wounds, it is in accordance with clinical experience to assume that a high fever belonging to the aseptic class may coincide with a septic process of insignificant proportions.

[Footnote 47: Genzmer and Volkmann, "Ueber septisches und aseptisches Wundfieber," _Samml. klin. Vorträge_, No. 121.]

GENERAL SYMPTOMS.--As in other infectious diseases, there is, from the time of the entry of the poison into the system up to the outbreak of fever, a distinct period of incubation. The first febrile symptoms usually occur within three days of the birth of the child. An attack coming on a few hours after childbirth is indicative of infection during or previous to labor. The third day is the one upon which ordinarily the beginning of the fever is to be anticipated. After the fifth day an attack is rare, and at the end of a week patients may be regarded as having reached the point of safety. Apparent exceptions to this rule are probably referable to cases of mild parametritis, in which the initial {1005} fever and the pain were insufficient to attract attention to the existence of local inflammation.

The symptoms of puerperal fever vary with the character of the local affections and with the extent to which the general system participates in the disturbed action. The different groups of puerperal processes possess the following pathognomonic symptoms--viz. increased temperature, enlargement of the spleen, disturbed involution, and sensitiveness of the uterus upon pressure (Braun).

In most cases the fever is ushered in by chilly sensations or by a well-defined chill. This symptom, however, does not possess much prognostic importance. A chill is significant of a sudden change between the temperature of the skin and that of the surrounding medium. It may, therefore, be absent in pernicious forms of fever, provided only that the temperature changes are inaugurated slowly, whereas it may follow a trifling increase of the body-heat if, as sometimes happens in sleep, the moist skin is exposed to cool currents of air. Repeated chills indicate phlebitis and pyæmia.

In order to grasp the many symptoms of puerperal fever, it is necessary to keep separately in mind the clinical features of each of the local processes, although in fact the latter rarely occur singly, but to a greater or less extent in combination with others.

The symptoms of ENDOMETRITIS AND ENDOCOLPITIS.--The uncomplicated catarrhal inflammation of the uterus and vagina is the most frequent and the mildest of the diseases of childbed. In endometritis the uterus is large, flabby, and sensitive upon pressure; the after-pains are often unusually severe, involution is retarded, and the lochia become fetid, remain sanguinolent for a longer period than usual, and at the outset may be temporarily suspended. Sometimes the large intestine is distended with flatus. In endocolpitis the vaginal discharge is thin and purulent, the patient experiences pain and burning in the acts of defecation and urination, and, where the wounds of the vulva and vagina assume an ulcerative character, there is often found at the same time inflammatory oedema of the labia.

The fever in these cases is ushered in frequently, but not always, by chilly feelings, and the temperature reaches its height usually upon the evening of the third or fourth day, is remittent, almost intermittent in character, and rarely exceeds 102° to 103° F. In mild forms the occurrence of the fever is often overlooked or is referred to disturbance produced by the secretion of the milk. In severer attacks the febrile symptoms may continue from three to seven days. At the end of a week the swelling of the labia subsides, the discharge becomes thick, and ulcers, if present, begin to assume a healthy granulating appearance.

In diphtheritic ulcerations, and in endometritis due to decomposing remains of the ovum, the load condition is often complicated by the invasion of the neighboring tissues.

The symptoms of PARAMETRITIS and PERIMETRITIS (Pelvic peritonitis[48]).--The symptoms of these two affections, as would be naturally {1006} expected from the proximity of the peritoneum to the pelvic connective tissue, for the most part overlap. It must be very rare for one form to occur entirely independent of the other. For this reason it will be found convenient to consider first the symptoms common to both morbid processes, and subsequently to direct attention to what are believed to be points of distinction between them.

[Footnote 48: The following clinical history, together with the statistical details, is borrowed in great part from the description of Olshausen ("Ueber puerperale Parametritis und Perimetritis," _Volkmann's Samml. klin. Vortr._, No. 28), the exactitude of which I have had abundant opportunity to verify.]

During the period of incubation there are usually no prodromic symptoms. Elevations of temperature in the course of the first twelve hours following labor are equally frequent under perfectly normal conditions. Suspicious symptoms are disturbed sleep, excessively painful after-pains, and a pulse of 80 to 90.

The beginning of the fever occurs in 90 per cent. within the first four days of childbed; most frequently upon the second or third day, and taking place upon the fourth day in scarcely 12 to 15 per cent. of the cases. If five days have elapsed without fever, the period of danger, with very rare exceptions, may be regarded as having passed.

At the outset the fever, especially in perimetritis, is ushered in by chilly sensations or by an intense chill. The temperature rises rapidly, though the highest point is usually not reached before the second, and in rare cases not before the third, day. In most cases the heat in the axilla exceeds 103°, and may even mount up to 105°. The decline occurs gradually, the fever ending in 70 per cent. in the course of a week, in 20 per cent. in two weeks, and only in 10 per cent. extending beyond that period. Protracted cases indicate abscess formation.

The fever does not, however, always pursue a regular course. In place of progressively declining until the termination is reached, the high temperature of the second day may be attained upon one or more occasions. The morning remissions are at first slight, but become marked as the disease approaches its close. In cases of long duration the morning hours are often free from fever, a circumstance calculated to mislead a physician who sees his patient but once a day. A pulse of 80 to 90 beats, a disturbed sleep, lack of appetite, and sensitiveness to pressure upon the sides of the uterus are, however, symptoms which should serve as a warning of some disturbing cause, and should lead the physician to renew his visit in the latter part of the day.

If, from a mistaken notion that the morbid process has come to an end, the patient is allowed prematurely to resume her household duties, the pains across the abdomen and along the hip and thigh return, and an examination reveals the existence of exudation in the pelvic cavity or upon an iliac fossa.

Errors of this kind are most frequent in cases of parametritis associated with slight peritoneal inflammation, as the local pain is then insignificant, and the initial chill, happening on the third or fourth day, is apt to be ascribed to engorgement of the breasts.

Relapses after the complete disappearance of febrile disturbance occur in 15 to 20 per cent. They are usually shorter, but sometimes more obstinate, than the original attack. As a rare exception may be mentioned cases with evening remissions and morning exacerbations.

In circumscribed pelvic inflammations the pulse rarely exceeds 120 beats to the minute. A pulse of 140, of more than half a day's duration, betokens severe septic complications, and is therefore of evil omen. In {1007} some cases the slow pulse observed after labor makes its influence felt in the first day or two of the fever, so that the curious phenomenon may be witnessed of a temperature of 104° coinciding for a time with a pulse ranging between 50 and 70 beats to the minute.

As regards other symptoms, headache and sleeplessness are rarely absent. Profuse sweating follows the first febrile attack, and frequently recurs during the course of the disease.

Pain is present at the onset in the majority of cases, and is then usually most violent. The spontaneous pain, which is due to the affection of the peritoneum, subsides in great part in the course of one or two days, but the sides of the uterus remain sensitive to pressure. In the rare cases of pure parametritis, however, this symptom may be absent altogether. The pain, like that from the inflammation of serous membranes, is of a lancinating character. Sometimes it is associated only with the contractions of the uterus. After-pains occurring under unusual circumstances, as in primiparæ or after the third day, are to be regarded with suspicion.

Vomiting occurs occasionally, but is comparatively rare unless the peritonitis becomes diffused and spreads to the region of the stomach. The appetite is lost, and only returns, as a rule, with the departure of the fever. The tongue is coated and moist, and constipation is common. In other cases there is diarrhoea with rumbling in the bowels, but without pain or tenesmus. The urinary secretion is rarely interfered with, and when this is the case it indicates the extension of the inflammation to the peritoneum covering the bladder.

Most cases of perimetritis and parametritis terminate in five or ten days, the fever and other symptoms gradually subsiding. When, as may happen in exceptional instances, the temperature falls suddenly from a high degree to one below the normal level, the body grows icy cold, the pulse becomes small and irregular, and symptoms of collapse develop. But in twelve to twenty-four hours the symptoms of collapse subside, and the disease reaches its end with a disappearance of the alarming manifestations.

If the fever subsides within a week exudation is somewhat rare. Its continuance beyond that date should lead to a careful exploration of the pelvic organs. The exudation is usually demonstrable in the course of the second week or at the beginning of the third week. It is recognized, according to its location, by external or by internal examination, or, where the deposit is considerable, by both methods. In most cases the deposit is extra-peritoneal, and is situated between the folds of the broad ligament, above and to the sides of the vaginal cul-de-sac. It has generally a rounded form, though with less convexity than fibrous and ovarian tumors. Sometimes, however, the tumor is flat below, like a board. It seldom exceeds in size that of a large apple. In fresh exudations the sensation produced is often that of a hard tumor surrounded by a softer layer, due to continued succulence of the soft parts. In a few weeks they may reach or exceed the hardness of a fibroid tumor. The older the tumor, unless suppuration sets in, the less sensitive it becomes. Often the exudation extends to the pelvic walls. The uterus, as a rule, is fixed, and in cases of large tumors becomes pushed toward the opposite side, while as a consequence of later shrinkage the fundus may be drawn permanently toward the affected side.

{1008} The cul-de-sac of the vagina is rendered broader and flatter by the pressure of the deposit, or, when the tumor is deep enough, the vaginal surface may be rendered convex. Behind the uterus the exudation is as it were flattened antero-posteriorly, and in some cases it may be felt in the form of rigid bands between the posterior ligaments which enclose the cul-de-sac of Douglas. The ante-uterine tumors have a spherical shape and depress the vagina anteriorly.

Tumors situated in the iliac fossa have a more or less convex form, and may be of such considerable size that the swelling may be recognized by the eye through the abdominal walls. As the exudation between the broad ligaments may in these cases have been slight from the beginning, or may have subsequently disappeared by absorption, the iliac tumors have often apparently a spontaneous origin.

Sometimes the uterus is surrounded by exudation, and the entire pelvis appears as though it were a mould filled with a solid mass. The fornix is then often pressed downward, and irregular rounded masses are to be felt through the vaginal walls.

The recognition of parametritic tumors through the abdominal coverings is possible when they are situated above Poupart's ligament, in the upper portion of the broad ligaments, and in the iliac fossæ.

The pain and the functional disturbances in the pelvic organs depend upon the size and situation of these inflammatory deposits. Of the functional troubles may be mentioned frequent and painful micturition, obstinate constipation and difficult defecation, contractures of the ilio-psoas muscles when the exudation is seated beneath the sheath or between the muscle and the pelvic bones, disturbances of motility in the abductor muscles, paresis of the lower extremities, and radiating pains in the upper portion of the thigh and in the renal and lumbar regions, produced by pressure upon the obturator, the crural, the cutaneous, and the sciatic nerves.

So long as fever is present the exudation rarely diminishes. If absorption takes place in one point, growth almost certainly follows in some other direction. When, however, the apyretic period is reached, the exudation, as a rule, disappears rapidly, so that often in the course of six weeks no trace of its existence remains. In a smaller number the solid mass may persist for months or even years.

After the fever has departed the patient usually feels well. The sleep and appetite return, the night-sweats disappear, the pulse often falls to 50 or 60 beats, and the temperature is in many cases for a time subnormal in character.

Where the fever persists for from five to six weeks there is always a suspicion of abscess formation. With the exception of afternoon fever and night-sweats the patient may feel very comfortable. Then the exudation becomes sensitive, the spontaneous pains recur, sleep is lost, and locomotion, defecation, and urination occasion acute suffering. The fever becomes violent, chills announce the presence of pus, and finally, about the seventieth or eightieth day, perforation of the abscess takes place. The usual seat at which the pus is discharged is just above Poupart's ligament; next in frequency perforation takes place into the colon, and in rare instances into the bladder, the uterus, and vagina. Fortunately, of very rare occurrence is the discharge of pus into the peritoneal cavity, which is {1009} naturally followed by acute peritonitis. Another likewise unfrequent but most dangerous accident is the septic infection of the abscess--an occurrence referred to by Olshausen to the diffusion of intestinal gases through the walls of the tumor.

In suppuration of parametritic exudations the pus commonly forms in small scattered collections, and rarely gives rise to large abscesses.

Although parametritis and perimetritis are usually found associated together, there are always cases in which the one form of inflammation so far predominates over the other as to justify an attempt to establish a clinical distinction between them.

In the beginning of the attack, sharp pain, high fever, and tympanitic distension of the lower abdomen are symptomatic of inflammation in the pelvic peritoneum. Whether the cellular tissue is simultaneously implicated can only be determined by a digital examination after the abdominal sensitiveness has subsided. The absence of the objective signs of cellulitis would then contribute to prove that the case had been one in which the peritoneum had been in the main affected. On the other hand, moderate fever, pain elicited only on pressure, and tympanitic distension confined to the colon, coinciding with exudation between the folds of the broad ligament, would be indicative of a nearly pure cellulitis.

A palpable exudation is by no means the necessary product of peritoneal inflammation. Indeed, in many cases, the distinctive symptoms of the latter may be present for from four to eight days, and may then subside without leaving a trace of its existence at the pelvic brim.

The demonstration of a fluid effusion by noting the change of level upon shifting the position of the patient is rarely possible, either because the quantity is too small or because it quickly becomes confined by pseudo-membranous adhesions between the intestines.

Bandl[49] mentions as a sign of local peritonitis, sometimes noticeable, a number of resistant points or tumors near the pelvic brim or above one of the iliac fossæ, due to a matting together of the intestines or to their adhesion to the uterine appendages. They are distinguished from solid tumors by their emitting a tympanitic sound upon percussion and by their changing position in consequence of an accumulation of urine in the bladder or of feces or gases in the bowels. Again, all tumors may be reckoned as intra-peritoneal which very rapidly form behind or to the side of the uterus from enclosed exudation-products, and which at the same time rise far above the level of the pelvic brim. If, however, they start from the cul-de-sac of Douglas, and do not much exceed the linea terminalis, or if they occupy an iliac fossa, it becomes very difficult to decide whether they are of intra- or extra-peritoneal origin. The peritoneal exudation, however, long remains soft and fluctuating. It arises, as a rule, behind the uterus, and does not exhibit a tendency to spread to the sides or to the anterior or posterior pelvic walls.

[Footnote 49: _Handbuch der Frauenkrankheiten_, red. Von Billroth, 5te Abschnitt, p. --.]

Still more difficult is it to decide as to the seat of exudations met with beneath the abdominal walls. When diffused and continuous with a pelvic deposit the diagnosis is uncertain. It is only safe to assume the peritoneal origin of extravasations of a rounded form, of a fluctuating consistence, and when they are situated high up and are disconnected from exudation at the pelvic brim. An opening of the abscess through the {1010} navel would indicate a peritoneal source, while the discharge through the abdominal parietes would point to a seat in the connective tissue.

After the perforation of an abscess the fever and pain subside; the wound, if external, either closes in the course of one or two weeks, or fistulas form which become the source of protracted suppuration.

In psoas abscesses the exudation extends beneath the sheath of the muscle or between the iliacus and the bone. In puerperal patients they proceed from an inflammation originating in the broad ligament. They are situated too deep to be easily palpated. The pains they occasion are referred rather to the hip or knee than to the abdomen. The contracture of the psoas muscle furnishes a diagnostic sign which distinguishes this form from the superficial abscesses of the iliac fossæ. The pus eventually is discharged beneath Poupart's ligament, in the lower portion of the inguinal fossa, at some point upon the crest of the ilium, or exceptionally along the thigh. Often the discharge is maintained for months.

The symptoms of GENERAL PERITONITIS.--This form generally begins with the usual symptoms of pelvic inflammation, but the tenderness, which at first was limited to the side of the uterus, gradually spreads over the entire abdomen. The abdominal pain is of a tearing, lancinating, sometimes colicky character. It is increased by the slightest bodily movement, by jarring of the bed, or even by the weight of the bed-clothes.

As a consequence of the peritoneal inflammation and of the accompanying exudation, the muscular walls of the bowels become paralyzed, and tympanitic distension results from the accumulation of gases. In the dependent portions of the peritoneal cavity it is often possible to demonstrate by percussion the presence of fluid exudation, though distinct fluctuation is rarely to be made out. The size of the abdomen is due much more to the tympanites than to the amount of effusion. Sometimes the liver, with the diaphragm, is pushed by the swollen bowels to the level of the fourth or third rib, and exercises such a degree of compression upon the posterior portion of the lungs as to place the patient in danger of suffocation. The respirations are jerky and attended with a moaning sound.

The loss of muscular power in the intestines permits the contents of the middle portion to pass unchecked toward the duodenum, and thence, upon accidental contractions of the abdomen, they may pass to the stomach and be ejected by vomiting. The first vomited matter has a dark-green color, and that ejected afterward presents the color of intestinal matter. Constipation at the outset may be subsequently followed by colliquative diarrhoea.

The fever begins, as a rule, though not always, with an intense chill, the temperature rises to 104°, and the pulse becomes small, hard, and resistant. Its frequency rapidly increases, varying from 120 to 160 beats to the minute. The skin is sometimes dry, sometimes dripping with perspiration. In fatal cases, as the end approaches, the temperature frequently falls, while the pulse becomes more rapid, the face assumes a pinched, anxious expression, sweat gathers upon the forehead, the extremities grow icy cold, and the patient dies in collapse. The duration of peritonitis averages not more than from four to six days.

In cases of recovery the pulse improves, the vomiting ceases, and the tympanites disappears. The diffuse exudation then becomes converted {1011} into circumscribed tumors, which on palpation are felt on the side of the pelvis and extending upward to the level of the umbilicus. Upon internal examination the uterus is often found depressed by the weight of the fluid, which likewise may bulge the cul-de-sac of Douglas into the pelvic cavity. Sometimes the exudation may become encysted above the pelvis and leave the contents of the latter free. In still other cases the uterus may become attached high up to the abdominal walls, so that the vaginal portion disappears and the os is reached with difficulty.

The peritoneal exudation may, as in pelvic inflammations, become absorbed and disappear. When, however, it is surrounded by loops of intestines it is apt to undergo purulent and septic changes, and the abscesses may then become discolored and filled with stinking gases. The patient, whose previous improvement has been watched with delight, now loses appetite, the pulse becomes frequent, the strength fails, and death may follow from septic fever or from rupture of abscess into the abdominal cavity.

In the pyæmic form--a still more deadly variety of peritonitis--the symptoms differ materially from those which have been recounted. As, however, it constitutes only a single one of the pathological changes connected with the poisoning of the blood through the lymphatic system, its consideration belongs properly to the study of the septic infection.

The symptoms of SEPTICÆMIA LYMPHATICA.--The symptoms of blood-poisoning in the infectious diseases of childbed vary to a considerable extent according to the channel through which the septic germs enter the general circulation. In the murderous epidemics which prevail in lying-in hospitals the lymphatics are, as a rule, the vessels primarily invaded. It is to this form that the cases already described belong, where, with diphtheritic patches upon the utero-vaginal canal and sero-purulent oedema of the parametrium, there are associated pyæmic peritonitis and deformation of the blood-corpuscles; or where, following the migrations of the round bacteria, the serous cavities become successively involved, septic vegetations gather upon the heart, and the glomeruli of the kidneys become choked with micrococci. The lymphatic form of septicæmia develops soon after labor, and is always ushered in by a chill. The temperature rises to 104° or even higher, and the pulse is thin and frequent. The abdomen swells rapidly, without being especially painful. Indeed, painless distension of the intestines is one of the characteristics of an acute invasion of the lymphatics. Peritoneal effusion is absent in cases which run a rapid course, and is distinctly recognizable only in a peritonitis of long continuance. The effusion is not so much due to exudation as to a transudation of serum with which micrococci are commingled. At the same time the tongue is moist, but slightly coated, and at times quite clean. Sometimes there is diarrhoea due to catarrh or to a diphtheritic affection of the colon. When the bowels have been constipated the administration of a purgative may provoke discharges which it may be found difficult to arrest. The skin is bathed in perspiration. At the beginning and during the course of the disease bleeding at the nose is of not infrequent occurrence.

Toward the end the pulse runs up to 140 to 160 beats, while in many cases the temperature falls. Immediately after death the heat of the body may for a short time exceed the highest point reached during life. The {1012} respirations are superficial and jerky. In many instances the face, the neck, and the fingers are blue from defective oxygenation of the blood. At the same time the skin becomes clammy and the extremities cold.

The sensorium, in cases which run a rapid course, is usually affected at an early period. The patients appear somnolent, are restless in bed, have light delirium, and respond only when spoken to loudly. As a rule, they make but little complaint, and, were it not for the dyspnoea, would have nothing to disturb their sense of comfort. Very few, even as death approaches, have any idea of the danger that threatens them. Now and then, in place of stupor, great restlessness, and even a maniacal condition, is developed. Albumen is usually found in the urine.

Pleurisy, so frequently associated with lymphatic septicæmia, is frequently double, more rarely single, and begins, as a rule, with sharp pain in the side and an aggravation of the previous dyspnoea. Pericarditis is less frequent, and occurs usually without symptoms toward the close of life. The joint affections are characterized by redness and swelling, and by pain, which is sometimes so great that touching the inflamed part suffices to arouse the patient from sopor. Sometimes fluctuation is felt, but death occurs before perforation and discharge of the pus.

The most frequent ending is death, which follows in from two to twenty-one days, and, as a rule, between four and seven days. Recovery is, however, possible.

The symptoms of SEPTICÆMIA VENOSA (phlebitis uterina, pyæmia metastatica).--The putrid infection of a thrombus at the placental site may take place within twenty-four to forty-eight hours after labor. Usually, however, the approach is insidious, and the disease develops from an apparently insignificant endometritis or parametritis; or the patient, with the exception perhaps of a tired feeling, of slight chilly sensations, and of profuse perspiration, may not have been conscious of any indisposition for days preceding the attack, or even until the first getting up from childbed. The initial chill in typical cases is characterized by its violence and duration. In some cases it may last for hours. It is accompanied and followed by high temperature, the febrile attack ending with profuse perspiration as in intermittent fever, with which it is apt to be confounded. The fall in temperature often assumes the form of a prolonged remission.

In many cases the pulse rises and falls with the variations in the body heat, while in others it remains permanently above the average. A frequent pulse is always a suspicious symptom in childbed, even where the other symptoms are apparently normal.

Erratic chills announce the lodgment of emboli in distant organs. With the formation of metastatic abscesses in the lungs and other parenchymatous organs the typical character of the disease changes. In place of chills occurring at irregular intervals, followed by remissions and periods of apparent improvement, the fever is continuous, the pulse becomes small and rapid, while sopor, slight delirium, a dry skin, a dry, brown, cracked tongue, and a moderately tympanitic abdomen, give the case the appearance of one of typhus fever.

Peritonitis is present in hardly one-third of the cases. The abdomen is therefore flat and soft, and often is not sensitive upon pressure. Icterus, due to disintegration of the blood-corpuscles, is an ominous symptom.

Death usually occurs in the second or third week. In the {1013} typhus-like cases, however, it may follow the first attack speedily. Recovery is possible where the organs secondarily affected are not of too great importance.

A combination of the lymphatic and venous forms of septicæmia is not uncommon in cases running a protracted course.

The symptoms of PURE SEPTICÆMIA.--Under the title of pure septicæmia should be placed cases in which the absorption of putrid materials into the blood gives rise to symptoms of intense blood-poisoning without the development of local lesions. A common example of this form is met with in the fever which results from the presence in the uterus of decomposing coagula or portions of retained ovum, the fever subsiding with the removal of the disturbing cause. In like manner we sometimes meet with cases of intense septic poisoning followed by speedy death, in which the post-mortem examination reveals only changes in the blood and softening of the parenchymatous organs. The symptoms are often similar to those produced by the injection of putrid materials containing rod-like bacteria into the vessels of animals. As the long bacteria do not possess the capacity of self-reproduction in the blood, to produce fatal results the quantity of putrid fluid injected must be large or be frequently repeated. This form is said not to be inoculable.

CAUSES.--The effects of a poisoned state of the atmosphere as a cause of puerperal fever is best observed in the so-called nosocomial malaria of hospitals. In days gone by, before I had learned by experience that the safe conduct of a lying-in service depends upon the fastidious exclusion of every source of contamination, I had frequent occasion to witness febrile outbreaks among puerperal women in the Bellevue Hospital, which were instantly arrested by the simple transfer of the inmates of the affected ward to a wholesome locality, though no changes were simultaneously made in either the personnel or the utensils of the service. In these instances it seems fair to assume that the previous unhealthy condition was not due to the direct transfer of an inoculable matter from patient to patient by the attendants, but by something residing in the air of the vacated apartment. In the inquiry as to the production of this condition it can be assumed that it is not caused by aggregation alone. The medical wards of Bellevue, always crowded, have often furnished in times of need safe receptacles for puerperal patients. It is certainly not due to the presence of the ordinary constituents of the atmosphere. We must therefore look for some additional element capable of unfavorably affecting the economy. What this element really is, is demonstrated by a familiar clinical experience. When the disturbance produced by nosocomial malaria is not at an early stage arrested by change of locality, the secretions of patients affected become inoculable. Then the epidemic spreads rapidly, and assumes continuously a more and more severe type. If during an epidemic the external genitals be carefully watched, now and then diphtheritic patches will be noticed to form upon them. At first these patches may disappear or yield readily to treatment. When an epidemic has assumed a pestilential form the patches, which may in isolated cases make their appearance at any time in a hospital, are rarely absent in fatal cases. The composition of the patches tells the tale of what it is in the atmosphere which accomplishes the charnel-house work. Favoring conditions have led to the multiplication of disease-germs {1014} in the air, and have fitted them to become the active producers of disease.

In a patient dying in the early stages of an epidemic there may be no diphtheritic manifestations, though the tissues and secretions are filled with bacteria. As, however, the epidemic gains headway, the lesions of the generative apparatus, and especially of the external organs, which are most exposed to air, become covered with patches which swarm with micrococci. Under the conditions named it is certainly more in accord with ordinary scientific reasoning to conclude that the micrococci play an important part in the production of puerperal fever than that the puerperal fever produces the micrococci.

To be sure, bacteria or their spores are always present in the air, and it may be fairly asked how patients are ever spared from their perverse industry. The answer is, that the effect produced by the atmosphere of a hospital is dependent partly upon the quantity, and partly upon the quality, of the suspended germs. Floating spores, when sparsely distributed, rarely possess the power of invading a healthy organism. In the inauguration of an epidemic the first patient severely attacked is usually one whose powers of resistance are broken down by prolonged labor, by hemorrhage, by poverty, or some other condition leading to impaired vitality.

Puerperal-fever epidemics due to contamination of the atmosphere, and not to direct contagion, do not at once reach the maximum of intensity. At first the temperature tables indicate the prevalence of milk fever; next follow cases closely resembling those of mild paludal poisoning; and, finally, if these warnings are unheeded and reliance is placed upon antiperiodic remedies rather than upon prompt closure of the threatened ward, the pestilence develops. In the conduct of lying-in hospitals it should never be forgotten that with the multiplication of the septic germs the danger increases.

At the same time, the quality of the agents which pervade the air where hospital patients are confined is an important element in the genesis of febrile outbreaks. The bacterium termo, which causes putrefaction, is not in itself, as we have already mentioned, a source of danger. A stinking odor is not necessarily incompatible with a low mortality-rate. The importance of the common forms of bacteria, according to Pasteur, results from the fact that by their power to consume oxygen they pave the way for the active development of the pernicious germs, nearly all of which thrive only in media in which that element has been materially diminished. Again, there is reason to believe that the same germs are not[50] always equally active for evil. Gravitz claims that the ordinary varieties of aspergillus and penicillium found everywhere on the surface of the ground, on moistened walls, on food of every variety, on decaying leaves and fruit, and whose spores are universally present in the purest air, can by a succession of cultures be gradually brought to flourish in a warm alkaline fluid, and that they then acquire the capacity to penetrate living tissues, to proliferate in them, to excite local necroses, and to cause death in the course of three days. The resistance of micrococci to carbolic and salicylic acids is found experimentally to depend in a measure upon the {1015} nature of the vehicle in which they are cultivated (Buchholz). The action of septic fluids varies too with the age of the infusions, with the materials employed, and with the conditions under which the poison-germs are generated.

[Footnote 50: Gravitz, "Ueber Schimmel vegetationen im thierischen organismus," _Virch. Arch._, vol. lxxxi, p. 355.]

Micrococci multiply in hospitals when organic materials favorable to their growth are present in sufficient quantities. Perrin, Quenquand and others have shown that the hospital wards in Paris, especially those upon the surgical and maternity divisions, contain an infinite number of vibrios, bacteria, and all the coccus forms (Charpentier). Robin[51] has demonstrated the existence of albuminoid matters in water condensed upon vessels containing freezing mixtures and placed in overcrowded wards of hospitals. When the results of crowding become manifest, these albuminoid matters not only impart a fetid odor and putrefy with great rapidity, but rapidly impart putrefaction to healthy muscle and normal blood with which they are brought into contact. Pasteur was able by the microscopic examination of the lochia from patients in the services of Hervieux and Lucas-Champonnière to predict, from the character of the contained organisms, an impending attack of fever in advance of the slightest symptom betokening danger.

[Footnote 51: _Leçons sur les Humeurs_, Paris, 1867, p. 195.]

It is unquestionably the lochial discharge which makes it such a difficult task to keep a maternity ward in a healthful condition. Putrid blood has been found to be the most favorable material for septic experiments. It was noticeable in Bellevue Hospital that febrile outbreaks always arose in, and were usually confined to, the ward in the hospital which, by a bad arrangement, was assigned to patients for the first four or five days following confinement--_i.e._ during the period of the lochia cruenta. As puerperal fever is rare after the fifth day, this at first sight would seem natural. But if a patient was transferred directly after confinement, during one of these unhealthy periods, to the ward containing the patients who had passed the first five days, but had not completed the ten days, she would escape the fever. It was always the same ward that required to be disinfected. In a communicating apartment all the confinements took place, and at all times, therefore, the conditions were present for loading the atmosphere with the products of decomposing blood. In the summer months, so long as the windows were open and the air was diluted by the continuous passage of fresh currents, the patients enjoyed immunity from nosocomial malaria. In the autumn, so soon as it became necessary to close the windows partially on account of the cool nights, it was not uncommon for the more trivial disturbances, such as so-called milk fever, the hospital pulse, and catarrhal affections of the genitalia, to manifest themselves. Through the months of February, March, and April the mortality was usually greatest. During the winter months there was, as a rule, crowding of patients, insufficient ventilation, stagnation of the air, and the rapid accumulation of disease-germs. That the later winter months should prove the most perilous is in accordance not only with the theory of continuous accumulation, but with the experimental fact that weeks sometimes elapse before a decomposing substance acquires the highest degree of virulence.

Apart from the nosocomial malaria of hospitals, there is reason to believe in the influence at times of certain general widespread atmospheric {1016} states which affect the entire community. In the year 1871 the mortality from childbed in New York was 399; in 1872, 503; in 1873, 431; in 1874, 439; and in 1875, 420. Now, the excess in the deaths for 1872 was due wholly to an increase in the cases of metria, those from ordinary accidents remaining nearly the same as in the preceding years. The disease certainly did not extend into the city from the hospitals serving as foci, for the mortality at Bellevue Hospital was hardly more than half the usual average. There was no especial mortality that year from either diphtheria, erysipelas, or scarlatina, but the aggregate mortality was the largest known in the history of the city. There are no positive data connecting the civil deaths from puerperal fever in 1872 with parasiticism, but the prevalence of epizoötics, of epidemic catarrhal affections, of peculiarly fatal forms of pneumonia and other diseases which are now attributed to the presence of minute organisms in the atmosphere, renders such a source highly probable.

It is proper to say here that, though the argument is very strong in favor of regarding the genitalia of puerperal women as the exclusive point of entry of infectious materials into the system, it seems impossible at the present time to make all the facts coincide with such a theory. I have the records of a number of cases occurring during an epidemic of puerperal fever in which patients were either attacked with fever previous to parturition, or in whose cases the unusual length of labor, the frequency of post-partum hemorrhage, and the imperfect contraction of the uterus immediately after confinement were signs of some abnormal influence exercised upon the economy at an early period of labor previous to the existence of traumatism. That deleterious materials may find other channels for entering the system than a wounded surface is evidenced by the cachectic condition not unfrequently produced in physicians by too assiduous attendance in dissecting-rooms and places in which _post-mortem_ examinations are conducted. One severe and rapidly fatal case of puerperal fever which occurred in Bellevue Hospital I find it impossible to attribute to any other cause than that the woman for five months previous to her confinement served as a helper in a lying-in ward. The post-mortem examination disclosed no special local lesions, but her symptoms were those of intense septicæmia. French writers report instances of toxæmic conditions developing in young midwives during puerperal-fever epidemics. While we are not prepared to go as far as Tarnier, who says, "It is probable that the lungs, by their extent and activity, offer conditions most favorable to absorption, and that often, if not always, it is by them that poisoning occurs," it does not yet seem time to give up the idea that under exceptional circumstances the respiratory and the digestive tracts may allow the passage of materials of a septic character.

Another and frequent source of puerperal fever is by direct inoculation. Any material of a septic character, introduced into the genital passages of a woman during or after confinement, may produce a general infection of the system. But the point upon which I wish especially to dwell is that it is possible to trace epidemics of puerperal fever directly to the carrying of puerperal poison from patient to patient through the medium of attendants. In such cases changes in wards and the most rigid sanitary precautions avail but little, so long as the affected personnel is continued {1017} in charge. Unless this fact is fully recognized, all the cleverest devices in hospital construction will fail to prevent the occurrence of disasters. In theory, the doctrine of the contagiousness of puerperal fever has ceased to be the subject of dispute; and yet no longer than thirty years ago it was combated as a pernicious heresy by both Meigs and Hodge of Philadelphia, at that time regarded as the best authorities upon obstetrical questions in this country. Hodge, addressing his students, said: "The result of the whole discussion will, I trust, serve not only to exalt your views of the value and dignity of our profession, but to divest your minds of the overpowering dread that you can ever become, especially in women under the extremely interesting circumstances of gestation and parturition, the ministers of evil--that you can ever convey, in any possible manner, a horrible virus so destructive in its effects and so mysterious in its operations as that attributed to puerperal fever;" and Meigs, in his letters to students, writes: "I prefer to attribute them to accident or to Providence, of which I can form a conception, rather than to a contagion of which I cannot form any clear idea, at least as to this particular malady." Contrasted with these rhetorical utterances, in an essay published in 1843 by Prof. Oliver Wendell Holmes, entitled _Puerperal Fever as a Private Pestilence_, the opposing testimony in favor of contagion was presented with equal literary and scientific skill. The evidence was complete and conclusive, and has exercised a most beneficial influence upon the practice of midwifery in America. With his many claims to our admiration and esteem there is probably no title which Prof. Holmes wears with greater pride than that of pioneer in a movement that has done so much to prevent the slaughter of innocent women and the wrecking of happy homes.

Thanks to changed theoretical views, physicians seem now rarely to be the carriers of contagion. At least, in studying the records of New York City for nine years, I find that the occurrence of two deaths from puerperal disease, following one another so closely as to lead to the suspicion of inoculation, occurred to thirty physicians; a sequence of three cases occurred in the practice of three physicians: one physician lost three cases, and afterward two, in succession; one physician had once two deaths, once three deaths, and twice four deaths, following one another; finally, a physician reported once a loss of two cases near together, then of six patients in six months and then of six patients in six weeks. Thus in the practice of more than twelve hundred physicians in nine years I find, excluding cases occurring in hospitals, that the experience of thirty-six only lends color to the idea that puerperal fever is due to criminal neglect on the part of the medical profession. Undoubtedly in many of these cases, too, the responsibility is only apparent, as when a practitioner has, for example, had the misfortune to lose in one week a woman from puerperal convulsions, and another in the following week from placental hemorrhage. Singularly enough, not one of the sequences mentioned occurred in the practice of a physician connected with a lying-in hospital. In face of the charge that the physicians holding obstetrical appointments in public institutions are active disseminators of puerperal fever through populous communities, I find that the total loss from all puerperal causes, occurring in the private practice of ten physicians intimately associated with such institutions, numbered during the nine years but twenty-one cases. Of these, thirteen were the result of ordinary {1018} accidents, and only eight cases of metria proper, of which one was developed before the physician was called in attendance; whereas a single physician, holding no hospital appointment, lost during the same time twenty-seven cases, of which twenty-one were cases of metria.

There is, however, a survival of the older ideas, chiefly to be seen among the laity, in propositions to secure absolute immunity from puerperal fever in hospital patients by confining them in wooden structures or by conducting births under carbolic acid spray.

I have been interested in endeavoring to ascertain how far experience corresponds with Semmelweis's original theory that puerperal fever owes its origin to poisonous materials obtained from dissecting-rooms and introduced into the genital canal by the hands of physicians attending cases of labor. With this view I have made personal application to a number of gentlemen who have engaged in midwifery practice while performing the functions of demonstrators of anatomy in our medical schools. H. B. Sands, of the College of Physicians and Surgeons, reports that in the five years during which he held the office of demonstrator he attended about sixty cases of labor. All did well. He lost his first patient, from childbed, a short time after he had resigned his position in the dissecting-room. J. W. Wright, the present professor of surgery in the Medical Department of the New York University, who held for one year the position of demonstrator in the Woman's College, writes me that "during the year I attended one hundred and four cases, including twenty-two forceps cases, two of craniotomy, two of podalic version, and four of breech presentation. Of this number I lost two cases, one from phlegmasia dolens complicating uræmia, from both of which troubles the patient had suffered during her previous labor, and one from double pneumonia, the result of unusual exposure following confinement. Out of these one hundred and four cases I can recall but three or four cases of metritis, and those of a mild character; I have never thought they had any special connection with my duties in the dissecting-room. I may add that for ten years I have attended a pretty large number of confinements each year, and that during the whole of this time I have been in the habit of making autopsies as occasion has offered, and of handling and examining pathological specimens both in and out of the dissecting-room, notwithstanding which my death-record among this class of cases has been unusually low." Samuel B. Ward, formerly demonstrator at the Woman's College, at present professor of surgery in the Medical School at Albany, writes: "While I was daily in the dissecting-room during the winter sessions of the school from 1868 to 1872, I attended thirty-two confinements, of which I have notes. All of the patients recovered, nor did any of them suffer from any complication that could be traced to infection." It is familiarly known that after Semmelweis had introduced the practice, among the physicians attending patients at the large lying-in hospital in Vienna, of washing the hands in a solution of chloride of lime, there was a great diminution in the mortality which prevailed, notwithstanding which G. Braun reports, however, that in 1857, in the month of July, in two hundred and forty-five deliveries there were seventeen deaths. The following month Klein gave orders to suspend the use of disinfectants. By chance, in August there were only six deaths out of two {1019} hundred and fifty confinements, and in September, of two hundred and seventy-five patients, none died. From 1857 to 1860 the mortality was slight, though disinfectants were not used, while during the three following years, in spite of the systematic and persistent employment of these agents, the death-rate once more assumed formidable proportions.[52]

[Footnote 52: Braun, _Rückblicke auf die Gesundheits Verhältnisse unter den Wöchnerinnen_, u. s. w., S. 32, 33.]

Of course I do not wish to underrate the importance of Semmelweis's labors. There is no question but that it is a perilous experiment to pass from the dissecting-room to a patient in labor without employing rigorous measures to disinfect the hands and all parts of the person brought into contact with the dead body. But it is well to call attention to the fact that puerperal fever is not due to any single, simple cause, nor can be effectually guarded against by a single precaution; and, again, that an infectious poison does not of necessity exist in every cadaver examined. Hausmann found that injections into the vagina of gravid rabbits, in the latter half of pregnancy, of serum from the corpse of a person who had not died of septicæmia produced no fatal results, while rapid death resulted from injections, under the same conditions, of pus from the abdomen of a woman who had died from puerperal infectious disease.[53]

[Footnote 53: "Untersuchungen und Versuche über die Entstehung der übertragbaren Krankheiten des Wochenbettes," _Beitr. zur Geb. und Gynaek._, Bd. iii, Heft 3, S. 374.]

Barnes and other English writers lay considerable stress upon cases of puerperal fever due neither to contagion nor to atmospheric conditions, but to the poisoning of the patient by her own secretions. There is justification for this view in the fact that even normal lochia contain bacteria, and when inoculated into animals produce in them affections of an ichorrhæmic and septicæmic nature. When death takes place the tissues of animals thus treated are found to be filled with round bacteria. Furthermore, the disease artificially produced is in itself infectious, and can be continuously propagated in other animals. But it may be asked, "Does not this admission cut both ways? How is it possible, if even normal lochia possess virulent qualities, that childbed is ever unattended by accessions of fever?" To this we can only answer that the reasons for immunity in ordinary cases are only known in part. Karewski[54] and other experimental investigators have shown that the virulence of the lochia increases proportionately to the number of days that have transpired since the birth of the child, and that during the first three days the lochia are comparatively harmless. Meantime, the retraction of the uterus, the closure of the sinuses, and the formation upon the wounded surfaces of protecting granulations, all act as natural barriers to the penetration of poison-germs. But, aside from these reasons, there is undoubtedly an unknown quantity calling for further investigation, which, in the absence of positive knowledge, we are content to term the predisposition of the individual patient. The vagina after childbirth possesses all the conditions most favorable for the production of putrefaction--viz. the access of air, fostering warmth, and stagnating fluids charged with dead tissue. It is probable that the first of these needful conditions is, in normal labors, happily wanting in the uterine cavity. In these days of intra-uterine medication it is well to {1020} bear in mind the relatively greater frequency of infection through vaginal and cervical wounds, as compared with that which takes place through the denuded intra-uterine surface. The term auto-infection may, with propriety, be employed as a distinctive appellation to designate those attacks of fever which, in the absence of any demonstrable cause, occur in the early days of childbed, and which there, quoad vitam, pursue a favorable course, and to cases of so-called late infection--_i.e._ where, after the fifth day, the accidental opening of a healing wound permits the tardy absorption of poisonous secretions; but with the reserve that the primary cause is, in point of fact, atmospheric, and the predisposing condition the susceptibility of the individual. Cases of auto-infection are in this country extremely rare, if not unknown altogether, in salubrious or rural districts.

[Footnote 54: "Experimentelle Untersuchungen ueber die Einwirkungen puerperaler secrete auf den thierischen organismus," _Zeitschr. f. Geb. und Gynaek._, Bd. vii, 2te Th., S. 331.]

On another occasion I have shown that in New York City the death-rate from puerperal fever is nearly twice as great during the six months from December to May, inclusive, as from June to November. The greatest mortality occurred in February and March, comprising rather more than one-fourth the entire amount. The smallest number of deaths occurred in September and October, in which months but one-thirteenth of the entire number took place.

That puerperal fever, in its harvest of death, does not spare the wealthy and well-to-do classes is too familiar a truth to be worthy of discussion. That, however, the wealthy do enjoy special immunities as compared with the less-favored members of society, I have shown by comparisons made between sections of the city which, though lying side by side, exhibit in a marked degree the two extremes of wealth and poverty. Thus, the mortality among the representatives of the lower social strata, in proportion to population, was from three to six times as great as that among the more fortunate classes.

RELATIONS TO ZYMOTIC DISEASES.--In investigating, some years ago, the nature, causes, and prevention of puerperal fever,[55] I prepared, from the statistics of the Health Board of New York City, tables extending over a period of nine years to answer the inquiry as to whether there was any relation between the frequency of deaths from scarlatina, diphtheria, and erysipelas and those from metria. Previous to their publication I was anticipated in my deductions by a paper upon the same subject by Matthews Duncan.[56] Neither Duncan nor myself found any such relation existing between the statistical frequency of puerperal fever and the zymotic diseases mentioned. There was, however, nothing in our investigations to invalidate any direct testimony which tends to show that, in individual cases, a real connection between puerperal fever and the zymotic diseases may exist. Indeed, it seems to me to be fairly established that a poison may be conveyed from patients suffering from either of the foregoing morbid processes which may be absorbed by the puerperal woman, and may in her give rise to an infectious fever possessing an intense degree of virulence. My friend Prof. Barker has recently drawn attention to the important relations of intermittent fever to the puerperal state. I have not, however, thought it advisable to complicate {1021} the present discussion with any extended notice of his very valuable observations. So far as malarial fever occurs unequivocally as such in puerperal women, there is no more reason for establishing a special category for puerperal malaria than for puerperal typhoid or puerperal small-pox. In the class of cases characterized by sharp chills, intense fever, irregular remissions, and profuse perspiration, which pursue a pernicious course unaffected by antiperiodic remedies, the nature is extremely dubious. The same symptoms are likewise characteristic of certain forms of pyæmia, and I cannot learn that such cases are familiar in the practice of those of our physicians who practise outside of cities in districts where malarial affections are most prevalent.

[Footnote 55: _Trans. of the International Med. Congress_, Philadelphia, 1876.]

[Footnote 56: "On the Alleged Occasional Epidemic Prevalence of Puerperal Pyæmia, or Puerperal Fever and Erysipelas," _Edinburgh Med. Journal_, March, 1876, p. 774.]

PREVENTION.--Of the 3342 deaths from puerperal causes in New York City from 1868 to 1875, inclusive, 420 occurred in hospital, or one-eighth of the entire number. Of the 1947 cases of metria, about 300, or not quite one-sixth, were contributed by the hospitals. After such a showing the first impulse would be to cry out loudly for the suppression of the maternities. But a wiser policy suggests an inquiry as to whether the large mortality mentioned is an evil necessity. The following reports will show how much may be done in the present state of our scientific knowledge to so control the conditions which favor the generation of puerperal diseases in large hospitals as to make them safe asylums for the needy.

Goodell[57] has stated that at the Preston Retreat in 756 cases of labor there have been but 2 deaths from septic disease. Winckel[58] of the Lying-in Institution in Dresden reported, in 1873, 18 deaths from metria, or 1.8 per cent., but from the 10th of January to the 7th of July in 570 births there was but 1 case of septic disease; in the year 1872 the death-rate exceeded 5 per cent. The reduction in mortality was no fortuitous circumstance, but was due to rigid measures for the prevention of disease. Stadfeldt[59] reduced the mortality from puerperal fever in the Maternity Hospital of Copenhagen from 1 to 37, the proportion between the years 1865 and 1869, to 1 in 87 between the years 1870-74. Johnston[60] reports, in the Rotunda Hospital of Dublin, during the seven years of his mastership, 7860 births with 169 deaths, of which 85, or 1 in 91, were from metria. Braun von Fernwald[61] in sixteen years reports 61,949 confinements in the vast Maternity Hospital of Vienna, with 825 deaths from puerperal fever, or 1.3 per cent. In a visit made by me to the Vienna Maternity in 1883, I was informed that the recent mortality, including difficult operations, had been reduced to one-half of 1 per cent. Spiegelberg[62] lost, in 901 confinements at Breslau, only 5 cases of puerperal fever. Beurmann[63] reports that in the Hôpital Lariboisière, under the administration of M. Siredey, the death-rate in 1877 was 1 in 145, and in 1878, 1 in 199, confinements; in the Hôpital Cochin, under the charge of M. Polaillon, the total mortality from 1873 to 1877 was 1 to 108.7. In 1877 there was but 1 death from puerperal causes in 807 confinements. Upon Prof. Streng's division of the magnificent {1022} maternity in Prague, I was told that, in 1882-83, in over 1100 confinements there had been no death from septic causes.

[Footnote 57: _On the Means employed at the Preston Retreat for the Prevention and Treatment of Puerperal Diseases_, p. 13.]

[Footnote 58: _Berichte und Studien_, Leipsic, 1874, S. 183.]

[Footnote 59: _Les maternités, leur organsation et administration_, Copenhagen, 1876.]

[Footnote 60: _Clinical Reports_, from 1870 to 1876, inclusive.]

[Footnote 61: _Lehrbuch der gesammten Gynaekologie_, S. 885.]

[Footnote 62: _Ibid._, S. 748.]

[Footnote 63: _Recherches sur la mortalité des femmes en couches dans les hôpitaux_, Paris, 1879.]

When the maternity service was transferred in 1872 from Bellevue Hospital to Blackwell's Island, it became necessary to make some provision for so-called street-cases--_i.e._ women taken suddenly in labor without homes, and representing the extremes of penury and want. At first they were received, in part, by the various private institutions of charity in New York City, but these in 1877 decided to exclude them thenceforth, on the ground that their condition at the time of their reception was such as to endanger the lives of the inmates for whom the charities were specially provided. An old engine-house was then put in readiness by the city, and under the name of the Emergency Hospital was placed under the charge of Henry F. Walker[64] and myself. The number of confinements in the Emergency has averaged 220 annually. The death-rate from all causes has been 2 per cent., which, though large, is not an unfavorable showing when we remember that the patients all belong to the homeless class, that all were taken in labor before their entrance, and that many of them were in a deplorable condition at the time of their admission. The hospital, too, receives a considerable number of patients annually who are sent there only after protracted, and often severe, operative measures have been fruitlessly attempted outside its walls.[65] The building possesses, for maternity purposes, two fairly ventilated rooms. Excellent nurses are furnished by the New York Training School for Nurses. Mr. Osborn, a liberal private citizen, has had constructed in the rear, but detached from the main house, a small pavilion, modelled after that of Tarnier, for the reception of infectious cases. The Commissioners of Charities have promptly responded to every call made upon them to extend the facilities for the care of patients.

[Footnote 64: Dr. Walker has since resigned, and my present colleague is Prof. Wm. M. Polk.]

[Footnote 65: From Oct., 1883, to Aug., 1884, there have been confined 168 women in the hospital. Twenty were brought in from the street just after the birth of the child. Of these 188, not one suffered from any puerperal affection. There were 2 deaths--1 from intestinal ulcerations, possibly the result of the corrosive sublimate irrigations, and 1 from exhaustion. This latter patient had been thirty-six hours in labor before she was brought to the hospital, and died four hours after admission. Under the admirable management of Miss Hart, the matron, in addition to the slight mortality, there has likewise been almost complete absence of even trivial temperature elevations.]

Surely these results do not support the idea that it is better for a woman to be confined in a street-gutter than to enter the portals of a lying-in asylum. Goodell's experience shows that a hospital for respectable married women may be so conducted that its inmates may enjoy absolutely a greater degree of safety than do women in their homes surrounded by all the aids that wealth can command. Equally good results are not to be obtained in hospitals which are open to unfortunates of every class. But there is much misapprehension and confusion of ideas respecting the fate of these women when no charitable provision is made for them. In Copenhagen the Maternity Hospital is closed for from six to eight weeks in the summer-time. During this period unmarried parturient women receive pecuniary assistance from the hospital to enable them to obtain a place in which to be confined. Now, Stadfeldt reports a larger mortality among this class than among those delivered in the hospital. Yet they are confined at a favorable season of the year, without any communication with the furniture, the sage-femmes, or the {1023} physicians of the hospital. As they fortunately receive nothing but money, that can hardly be suspected of communicating contagion. What their fate would be in New York City perhaps may be judged from the following facts: Excluding cases confined in hospitals, nearly one-thirtieth of all the deaths and one-twenty-fourth of the cases of metria between 1867 and 1875 are reported by four practitioners. Ten practitioners out of twelve hundred signed the death-certificates of one-fifteenth of the women dying from puerperal causes, and one-tenth of the cases of metria. But it is not to be supposed that these deaths were all the result of malpractice and incompetence. The true history of most of them probably was that the doctor was engaged to attend the case of confinement for a small fee, with the understanding that he should make no calls subsequently, unless specially summoned by the friends of the patient. The latter, left to ignorant care or perhaps without any assistance whatever, and exposed to all the pernicious influences bred by poverty, when illness supervened probably did not call the physician to her aid until the time for help had passed, so that in the end his professional functions were confined to procuring the requisite permit for burial.

Humanity demands that charity should furnish places of refuge in which poor outcasts can receive assistance during the perils of child-bearing. If we must, then, have maternities, we should make them safe, and this can be in great measure accomplished by remembering the twofold source of danger arising from a poisoned atmosphere and direct inoculation. A hospital must be clean, spacious, and well-ventilated, or its atmosphere will become charged with the spores of septic fungi and produce nosocomial malaria. The most rigid sanitary precautions observed by the attendants will not prevent a badly-ventilated ward from becoming unwholesome, unless unoccupied wards are kept to which patients can be transferred upon the first admonition of danger. Goodell states that at the Preston Retreat the wards are used invariably in rotation. In connection with the Maternity at Copenhagen there are a number of small supplementary hospitals scattered through the city, which serve as safety-valves for the central institution. Artificial methods of ventilation render the task of keeping the wards wholesome comparatively easy. They do not need, however, to be complicated and expensive. The good repute of the Rotunda Hospital, it seems to me, is in large measure due to the natural ventilation afforded by open fireplaces.

In the Vienna Clinic, according to C. Braun, the mortality between 1834 and 1862 averaged 6 per cent., and in 1842 the enormous total of 521 deaths to 3067 confinements was reached. With the introduction in 1862 of what is known as Böhm's heating and ventilation system an immediate improvement was experienced. In the sixteen years from 1863 to 1878, inclusive, the total mortality has been 1.6 per cent., though in that time 5464 practitioners have received an obstetrical training in its wards. In commenting upon this change, Braun says: "I have now from practical experience arrived at the knowledge of the fact that the rapid and thorough prevention of putridity by adequate ventilation is to be regarded as a good preventive measure against puerperal fever; that it is not the number of patients in a lying-in hospital, nor yet the number of patients in a single room, but the deficient circulation of air--a fault {1024} which may inhere to separate compartments in the smallest maternities--which is the important feature in the spread of puerperal fever; that puerperal women are to be protected from childbed diseases not by isolated buildings and gardens, nor by walls, but by the permanent introduction of great quantities of pure, warm air." He then adds, what is in thorough accord with my own experience, "Before new institutions are built greater attention than heretofore should be paid to the ventilation of the old structures, and, where this is found defective, a system should be substituted corresponding to the scientific requirements."

In the year 1872 puerperal fever destroyed 28 women of 156 who were confined in the Bellevue Hospital. The service was then broken up, and a great outcry arose against "tainted hospitals." Wooden pavilions were accordingly erected on Blackwell's Island for the reception of lying-in women. These buildings were constructed upon what is known as the cottage plan. They were favorably situated in an airy location remote from the general hospital. They were, however, heated by large iron stoves, and no means of ventilating the wards was provided, except by lowering the windows. In less than three months from their occupancy an epidemic of puerperal fever made it necessary to remove the service for a time to the Charity Hospital. The same result followed every subsequent attempt to utilize them for maternity purposes, until, after three years' trial, it was found necessary to abandon them altogether.

In private practice it is likewise important that the lying-in room should be provided with plenty of light and air. The physician should insist upon the value of ventilation as a means of contributing to the speedy recovery of childbed women. By hermetically sealing the windows, through false fears of his patient's taking cold, he exposes her to the risk of becoming poisoned with her own exhalations.

But the early experiences of the Hôpital Cochin and the Hôpital Lariboisière, costly, palace-like structures, with every appliance of art, prove that fresh air alone does not protect patients from the consequences of inoculation.

The great improvement in the condition of maternity patients in recent years has been due to the application of Lister's principles to obstetric practice. Complete antisepsis in the surgical sense is, of course, impracticable. Adequate antisepsis has, however, been proved to result from the observance of a variety of precautions which have been the slow outcome of experience. These, in brief, in hospitals, consist in protecting the patient from every known form of contamination, and in the prompt removal and isolation of every puerperal woman who manifests febrile symptoms.

In citing the examples of the Hôpital Cochin and the Hôpital Lariboisière, I was led to the selection because these hospitals most strikingly illustrate the extent of the triumph of the new doctrines. Whereas at the Lariboisière the mortality in 1854, the year of its opening, exceeded 10 per cent., as a result of the prophylactic measures adopted by M. Siredey the mortality was 1 to 145 in 1877, and 1 to 199 in 1878. And at the Hôpital Cochin, in 1878, Lucas-Champonnière, with 770 confinements, was able to report but 2 deaths from puerperal causes.

{1025} As regards details, the bedsteads should be of iron and should be frequently scrubbed with a carbolic solution; after each confinement the palliasse upon which the woman lay should be washed in boiling water and the straw should be burned; in place of the usual rubber covering to the bed, Tarnier recommends tarred paper, which is antiseptic, and costs so little that it need be used in but a single case; all soiled linen should be instantly removed from the ward, either to be burned or disinfected by prolonged boiling; sponges should be banished, as, when they have once been soaked with blood, not even carbolic acid can make them safe; nurses employed in the puerperal wards ought not to have access to cases of labor, as D'Espine and Karewski[66] have shown that the lochia of even a healthy person on the third day will poison a rabbit; a patient attacked with fever should be immediately removed, and the nurse in attendance should go with her. At the Emergency Hospital, with the first appearance of catarrhal affection of the genital organs or of so-called milk fever, the wards are immediately emptied and fumigated with sulphurous acid. In spite of recent scepticism regarding the value of the fumes of sulphurous acid as a germicide and disinfectant, I do not hesitate to express, after long experience, my firm conviction as to their efficacy.

[Footnote 66: D'Espine, _"Contributions à l'étude de la septicémie puerpérale,"_ p. 18; Karewski, _loc. cit._]

Doléris[67] formulates the indications for effective prophylaxis as follows: 1, prevent the introduction of germs (antisepsis before confinement); 2, paralyze their action (antisepsis after confinement); 3, shut up the doors--veins, lymphatics, and Fallopian tubes (employment of means which promote uterine contraction).

[Footnote 67: _La fièvre puerpérale_, 1880, p. 303.]

The first duty of the physician is to refrain from attending a case of labor when fresh from the presence of contagious diseases or from contact with septic materials, whether derived from the dissecting-room or the clinic. Scepticism regarding these sources of danger is sure in the long run to be severely punished. In a doubtful case the least concession should consist in a full bath and a complete change of clothing. A special coat for confinement purposes, stained with blood and amniotic fluid, is liable to convey infection. In every case of labor, whether in hospital or private practice, the hands and forearms should be freely bathed in a carbolic solution before making a vaginal examination. A nail-brush should form a part of the ordinary obstetric equipment. Frequent examinations during labor should be avoided. All instruments employed during or subsequent to confinement should be carefully disinfected. In prolonged labors, after operation, in cases of dystocia, or where the membranes have ruptured prematurely and the foetus is dead, it is a useful precaution after delivery to wash both uterus and vagina with warm carbolized water or solution of corrosive sublimate (1:2000). In Vienna both Spaeth and Braun after difficult labors introduce a suppository of iodoform, 2 to 2-1/2 inches in length, into the uterine cavity. The formula recommended consists of--

Rx. Iodoformi, 20 grammes; Gummi Arabici, Glycerinæ, Amyli puri, _aa._ 2 grammes; Ft. Bacilli, No. iij.

{1026} In their introduction the half-hand (left) should be passed to the cervix; the iodoform bacillus should be seized by a pair of polypus forceps and pushed into the cervical canal. The hand in the vagina should then be used to shove the suppository upward past the internal os. No symptoms of poisoning from the iodoform have been observed. The disinfection is complete and prolonged. In hospitals the woman should be bathed before entering the lying-in ward, and the vagina should in all cases be disinfected with carbolic acid or corrosive sublimate both before and immediately after labor. The conduct of labor under carbolic acid spray is commended by Fancourt Barnes. Doléris advises the application of a compress soaked in carbolic fluid to the external genitals during the progress of labor. Tarnier advises dressing the vulva, so soon as the head begins to emerge, with a pledget soaked in carbolized oil (1:10). With the recession of the head during the interval between pains a portion of the oil is carried upward into the vagina.

In the puerperal period the warm carbolized douche stimulates uterine retraction and promotes the rapid healing of wounds in the vaginal canal; in hospital practice it possesses the additional advantage of preventing the accumulation of putrid albuminoid matters in the air. In private practice the patient should employ a new syringe; in hospitals every woman should be supplied with a glass tube to be attached to the irrigator. When not in use these tubes should be immersed in carbolic acid. The stream injected into the vagina should be continuous, like that furnished by the fountain syringe. With my hospital patients, in place of cloths to the vulva I have been in the habit of using oakum. By soaking the latter in a solution of carbolic acid the vulva is surrounded by an antiseptic atmosphere.[68]

[Footnote 68: I know that of late there has been a strong reaction against the use of vaginal injections in normal childbed, but personally I have experienced none of the disagreeable effects ascribed to them. Indeed, both my hospital and private patients alike speak of them as soothing and grateful. I therefore have had no ground to discontinue them. That they are indispensable I do not claim. They are no longer used in Vienna, in Prague, nor in the New York Maternity, and yet, none the less, their results have since been in the highest degree satisfactory. At these institutions, however, vaginal disinfection is vigorously resorted to during and immediately subsequent to labor, and during childbed some form of antiseptic pad over the vulva is employed.]

Pedantic as these directions may seem, they are justified by experience, and the carrying out of the details given easily becomes a matter of habit. That by such precautions puerperal fever is destined to be erased from the list of dangerous diseases attacking the woman in childbed is saying more than is warranted. Nevertheless, it is true that a physician ought never to lose the sense of personal responsibility for its occurrence. Indeed, puerperal fever ought to be regarded as a preventable disease, and an attack as the evidence that some source of danger has been overlooked, though, owing to the imperfection of our knowledge, it may easily happen that even with the keenest scrutiny the precise cause in an individual case may escape detection.[69]

[Footnote 69: Since the above was written Dr. Garrigues has furnished a most extraordinary example of the efficacy of the antiseptic treatment at the New York Maternity Hospital. From the years 1875 to 1882, inclusive, the number of confinements was 2827; the deaths 116, or a little over 4 per cent. The highest percentage was reached in 1877--viz. 6.67; the lowest in 1881, when it fell to 2.36. In 1883, of 345 women confined, 30 died. In September of that year there were 9 deaths, and of 5 puerperæ who were seriously ill, 1 died later. At this time he introduced a series of reforms of which the following, omitting details, gives the essentials: Wards fumigated with sulphurous acid fumes, and the floors and furniture washed with a solution of corrosive sublimate (1:1000). Every patient, on entering the lying-in ward after the bath, had her abdomen, buttocks, genitals, and thighs washed with sublimate solution (1:2000). During labor vagina irrigated with latter solution. In prolonged labors irrigation repeated every three hours. Great care of hands on part of doctor and nurses. Glycerine and corrosive sublimate (1:1000) used for lubricating fingers before making internal examinations. Antiseptic pad applied to the head during its egress, and to the vulva until the secondines had been expelled. Absorbent cotton covered with netting soaked in corrosive sublimate solution applied to external genitals during childbed period. This latter applied and removed with the same care as in dressing a wound after a capital operation. Irrigation, first of the vagina and afterward of the uterus, immediately after labor in cases where the hand or instruments had been passed into the uterine cavity.

When the details of this treatment were first published by Garrigues, many took a humorous view of it, but mark the result: In the following 162 confinements there were no deaths, and from October to July, inclusive, of the present year, of 409 patients confined, though many operations were performed, 5 died; but of these, 3 only were from septic causes, and they, Garrigues believes, were the result of the neglect of certain of the prescribed details.]

{1027} Before terminating this section upon the prophylaxis of puerperal fever, I take great satisfaction in furnishing from Tarnier's recent treatise the following description, by Pinard, of the ingenious pavilion designed by Tarnier to make it possible to secure for hospital patients, at the minimum expense, the benefits of isolation, and to provide for each room in the pavilion all the conditions favorable to rapid and complete disinfection.

The pavilions are two-storied and of a rectangular shape, twenty-four feet in width by forty-six feet in length. The front and rear face to the north and south, the ends to the east and west. Two main partitions divide the interior into three divisions. Each end division is subdivided by a central partition into two chambers, so that each story has five compartments--a central one for the attendants, and four at the four corners destined for the reception of patients. On the ground floor the central compartment consists of a vestibule facing to the north, and an office facing to the south. On the former are placed the staircase, the water-closet, and a reception-closet. In addition to the main entrance there are three interior doors--one leading to the water-closet, one to the closet, and one to the office. The latter, for the occupation of the person on duty, contains a heater, a portable bath, a table, chairs, and wardrobe. Two windows face the south. The office has two doors, one opening into the vestibule, and the other, in the opposite side, opens directly outward. The four corner rooms for patients have each a door and a window, the latter looking from the end of the partition and reaching to the floor, and the former opening out from the façade. These four rooms are therefore not only independent of one another, but have no communication with the vestibule or the central office. On the second floor the arrangement is similar, except that the rooms open upon a balcony, by means of which communication from the outside is rendered possible. Upon each façade a glazed screen furnishes shelter in rainy weather. The screen extends to the roof, but is not in direct contact with the walls, a space being left for a current of air. The eight rooms for patients, four on each story, are severally fourteen feet long, eleven and a half feet wide, and ten feet high. Below, the floors are of asphaltum; above, of flags or slates. The walls and ceilings are stuccoed and covered with oil paint. The corners are rounded to prevent the accumulation of dust. To facilitate {1028} washing, the floors slant toward a gutter communicating by means of a pipe with the sewer. In each room panes of glass enable patients and the office attendant to see one another, so that surveillance is secured without sacrificing the principle of isolation. The furniture of the rooms consists of an iron bedstead with metallic springs. The pillow, bolster, and palliasse are stuffed with straw. In addition, each room is provided with a night table, a round table, a chair, a stool, and a crib--all of iron. A bell-rope at the bedside, the wire of which passes to the office by the outside of the building, enables the patient to summon assistance. Each room likewise contains a washstand, with faucets for hot and cold water, the latter supplied from a cistern on the roof, the former from the office heater. The patients remain in the rooms where they are confined until they are discharged. When this takes place the chamber is aired, the furniture is removed and washed with care, the straw is burned, and the walls are washed with an abundant supply of water. If a patient is taken ill, she is carefully isolated, and has assigned to her her own especial attendant and physician, who do not come into contact with other puerperal patients.

That the plans of construction in the Tarnier pavilions would require some modification to adapt them to the rigor of our winters seems probable, but the principles which they illustrate are sufficiently vindicated by the results so far reported--viz. 6 deaths in 1062 confinements, whereas in the old Maternity the death-rate, formerly amounting to 5 per cent., still aggregates 2 to the 100.

TREATMENT.--When the septic germs characteristic of putrid infection have once entered the blood, they are beyond the reach of the physician. Except, however, in cases of acute septicæmia, where the quantity of poison introduced at the outset is excessive, the patient rallies from the immediate shock, and, provided no fresh pyrogenic material finds its way into the system, recovery is to be anticipated. The indications for treatment are, therefore, to neutralize the puerperal poison at the point of production, in order to prevent its causing further mischief, and to adopt measures calculated to enable the patient to tolerate its presence, when once absorbed, until it is either eliminated or loses its harmful properties.

Toward the fulfilment of the first indication it is to be recommended that in every case of fever of puerperal origin the vagina be cleansed with a 2 to 3 per cent. solution of carbolic acid or corrosive sublimate (1:3000) every four to six hours. The douche in itself is absolutely harmless. In most cases the infection starts from the wounds of the vagina and of the cervix. Then, too, the tendency of the secretions to stagnate in the vaginal cul-de-sac, bathing as they do the cervical portion, is a prolific source of septic trouble. In all but the mildest cases the vaginal orifice should be examined with reference to the existence of puerperal ulcers. All necrotic patches should be touched with hydrochloric acid, with a 10 per cent. solution of carbolic acid, with iodoform, or, what I personally prefer, a mixture composed of equal parts of the solution of the persulphate of iron and the compound tincture of iodine. The latter acts as a powerful antiseptic, while the former, by corrugating the tissues, closes the lymphatics and shuts up the portals through which the septic germs penetrate into the system.

{1029} Intra-uterine injections should be resorted to with extreme circumspection. They are not indicated by a simple rise of temperature. A very large proportion of the febrile attacks which occur in childbed run an absolutely favorable course. Unless the infection--and this is not the rule, but the exception--proceeds from the uterine cavity, they are unnecessary. In circumscribed inflammations, where the morbific poison loses its virulence at a short distance from the puerperal lesion, they are often injurious. It is difficult, if not impossible, to so conduct them as to avoid opening up afresh recent granulating wounds. Yet the practice of local disinfection is warmly advocated by Fritsch, Schüller, Langenbuch, and Schroeder as a prophylactic against puerperal affections. On the other hand, Braun von Fernwald, with his vast opportunities for judging obstetrical questions, writes with reference to this: "We must protest against injections made by physicians into the uterine cavity. Such meddlesomeness is more likely to do harm than good." This corresponds with my own experience. In theory, the proposition to treat the uterus as one would any other pus-secreting cavity seems rational, but I have found that every attempt to carry the theory to its logical conclusion in hospital practice has been followed by a rise in the puerperal death-rate. Runge reports an epidemic of puerperal fever in Gusserrow's clinic brought about by the employment of intra-uterine irrigations, during which the mortality rose to 3.8 per cent. With the abolition of the irrigations the mortality sank to .39 per cent. In 1880, Fischel[70] introduced the so-called permanent irrigations into the Prague maternity. Of 880 patients, 9 died of sepsis. The irrigations were then prohibited. The following year, of 933 patients, only 2 died from the same cause, and in 1882, of 521 patients, there were no deaths from sepsis. Fehling, who limited the use of intra-uterine injections to special momentary indications, reported, in 1880, 415 confinements without a single death.

[Footnote 70: "Zur Therapie der Puerperalen Sepsis," _Arch. f. Gynaek._, vol. xx. p. 41.]

Among the accidents which have been referred to the use of injections are convulsions, shock, and carbolic-acid or corrosive-sublimate poisoning; but the chief danger lies in the possibility of conveying the infectious materials from the vagina to the previously normal uterus. There seems to be no question as to the superior effectiveness of corrosive sublimate as a germicide. It not only acts more rapidly than carbolic acid, but its action is more permanent. In the usual proportion of 1:2000 it is apt, when repeated frequently as a vaginal douche, to corrugate the vagina and cervix. When used for intra-uterine irrigation great pains should be taken that no portion of the fluid remain behind in the uterine cavity. Since its introduction into the Emergency Hospital there has been one death from ulceration in the colon, which possibly was attributable to its use. It is to be hoped the claim that corrosive sublimate is an efficient antiseptic in the proportion of 1:10,000 may prove well founded.

In pressing the necessity of caution and discrimination, I have not, however, intended to discourage the employment of intra-uterine antisepsis in cases where it is strictly indicated. Thus, it would be folly, in a fever due to the decomposition of placental débris, of shreds of decidua, of strips of membrane, or of retained coagula, or in diphtheritis of the mucous membrane, to treat the general symptoms and neglect {1030} the local cause of difficulty. In a specific case it may prove difficult to decide as to the correct course to pursue. In general it may be stated that it is proper to wash out the entire length of the genital canal when fever follows prolonged operations conducted within the uterine cavity or the birth of a dead foetus, and in cases of fever associated with a fetid discharge which persists in spite of the vaginal douche, with the presence of recognizable portions of the ovum or its dependencies in the lochia, with the repeated discharge of decomposed coagula, or with a large, flabby uterus. It will, however, be seen that with proper disinfection during and immediately after labor, the occasions for late intra-uterine injections are extremely rare.

The operation of cleansing the uterus should be conducted with the most scrupulous care. The syringe employed should produce a continuous and not an interrupted stream, and all air should be expelled from the pipe. The tube to be passed through the cervix should be of glass, of the size of the little finger, and bent somewhat to conform to the pelvic curve. The vagina should first be subjected to a thorough disinfection, by way of precaution against conveying septic materials into the uterus. The introduction of the tube should be made with the guidance of two fingers passed through the external os. But slight force is requisite to reach the internal os. It is neither necessary nor desirable to push the tube to the fundus. The fluid injected should be tepid, and, if carbolic acid is used, of the strength of two or three drachms to the pint; if corrosive sublimate is employed, the strength should not exceed 1:3000. It should be introduced very slowly, and pains should be taken to ensure its unimpeded escape, which can usually be accomplished by pressing the anterior wall of the cervix forward by means of the glass tube. Langenbuch recommends securing permanent drainage by leaving a bit of rubber tubing in the cervical canal--a plan concerning the merits of which I am not able to speak from experience. The tube is said to be well tolerated, and to possess the advantage of enabling subsequent injections to be performed without disturbing the patient.

In many cases the results of intra-uterine treatment are very striking. Often the temperature falls notably within an hour or two of the operation. This result is, however, rarely permanent. Usually the fever recurs, and the operation has to be repeated. The patient should be carefully watched, and with the first sign of returning danger the injection should be repeated. Two or three injections may thus be called for in twenty-four hours, and they may require to be continued for a week. Still, by the means indicated a certain pretty large proportion of women seemingly destined to destruction in the end make favorable recoveries.[71]

[Footnote 71: The admirable monograph of Dr. T. G. Thomas, entitled _The Prevention and Treatment of Puerperal Fever_, has already done much good in calling the attention of the profession at large to the practice of local disinfection. His experience, however, based upon a very large consulting practice, has perhaps been of a kind to furnish him with an undue proportion of puerperal cases calling for intra-uterine treatment. With increasing care in the management of labor and of the birth of the child there seems reason to hope that the necessity for the treatment he so eloquently advocates may, in the near future, disappear entirely.]

Ehrendorfer[72] relates a case of septic endometritis and erysipelas {1031} starting from the genital organs, in Spaeth's Clinic, where, after seven days of ineffective uterine irrigations, two bacilli, containing together ten grains of iodoform, were introduced into the uterus. The washings with carbolic acid were then stopped. On the next day the discharge was diminished and the odor was less marked. On the fourth day two new iodoform bacilli were introduced. The patient, in spite of the fact that the erysipelas spread over nearly the entire body, eventually recovered.

[Footnote 72: "Ueber die Verwendung der Jodoform staebchen bei der intrauterinen nach behandlung im Wochenbette," _Arch. f. Gynaek._, vol. xxii. S. 88.]

Of the symptoms, the first in order which calls for treatment is usually the peritoneal pain. It is, as we have seen, commonly of a lancinating character, and is associated with hurried breathing and extreme frequency of the pulse. So soon as the pain is once fairly under control the violence of the onset begins to abate. It should be met, therefore, by the hypodermic injection of from one-sixth to one-third grain of morphia in solution. The anodyne action should be maintained by doses administered by the mouth in quantities and at intervals suited to the severity of the case. The most important object to be secured is freedom from spontaneous pain. It is, moreover, good practice to push the opiate until pain elicited by pressure is likewise controlled, provided it can be accomplished without producing narcosis. In susceptible patients and in localized inflammations the quantity required may not be very great, while in acute general peritonitis the tolerance of the drug exhibited by puerperal women is sometimes extraordinary. Thus, a patient of Alonzo Clark took the equivalent of 934 grains of opium in four days; a patient of Fordyce Barker 13,969 drops of Magendie's solution in eleven days; and one of my own, at the Maternity, the equivalent of over 1700 grains of opium in seven days.[73] In this latter instance the patient was to all appearance moribund when the treatment was begun. Thus, the features were pinched, the face was drawn, the pupils were dilated, the finger-tips were blue and cold, the respirations were rapid, and the pulse was scarcely perceptible. In this condition the large doses of opium did not produce narcosis, but were followed by restoration of the circulation, by normal breathing, and by the disappearance of the symptoms of shock. Any attempt to relax the treatment was at once succeeded by a recurrence of the alarming symptoms. At the expiration of the disease the opium was discontinued abruptly without detriment to the patient.

[Footnote 73: The details of this case have been reported in the _Am. Jour. of Obst._, Oct., 1880, p. 864, by Dr. F. M. Welles, who conducted the administration of the opium.]

In contrast to cases of acute peritonitis an extreme susceptibility to opium is often observed in the pyæmic variety. Here opiates seem to me rarely to do good. They do not hinder the migrations of the round bacteria, there is rarely pain to relieve, and I have sometimes thought that their administration was simply the addition of a second poison to the one which already was overwhelming the nervous system.

In pelvic peritonitis, in the course of forty-eight hours plastic exudation is thrown out and the pain to a great extent subsides. From this time very moderate doses of opium, as a rule, are needed to make the patient comfortable.

In France leeches applied to the abdomen are much used as a means of relieving peritoneal sensitiveness. That they do this is beyond question. {1032} Their disuse in this country is due probably more to popular prejudice than to their inefficacy.

In the beginning of an attack a turpentine stupe to the abdomen is a source of comfort to many women, while the sharp counter-irritation exercises possibly a favorable influence upon the course of the disease. At a later period I commonly employ flannels wrung out in water and covered with oil-silk to prevent speedy evaporation. It is an old experience that in the beginning of a puerperal fever the provocation of loose stools by purgatives is frequently followed by a fall in the temperature and a great improvement in the patient's condition. The result, however, is far from uniform, as in other cases these artificial diarrhoeas have a tendency to aggravate the peritoneal symptoms. Owing to this uncertainty in their action, purgative remedies should be administered with caution, not from any theory as to their eliminative powers, but because of the ascertained existence of fecal accumulation. In pelvic inflammations castor oil in two- or three-tablespoonful doses, or five to ten grains of calomel rubbed up with twenty grains of bicarbonate of sodium, as recommended by Barker, may be given when thus indicated. After the bowels have once been freed, however, the purgative should not be repeated. In cases of intense local inflammation and in general peritonitis enemata should alone be employed for the removal of constipation.

Every increase of body-heat is associated with rapid tissue-waste, with enfeebled heart-action and with exhaustion of the nerve-centres. Since the modern recognition of the deleterious effects of high temperatures per se, antipyretic remedies in place of the old-time cardiac sedatives have come to play the leading rôle in the treatment of fevers.

Of internal antipyretic agents quinia enjoys a deservedly high repute. In the remitting forms of fever it may be administered in five-grain doses at intervals of four to six hours. Given thus in medium doses, it moderates the fever, diminishes the sweating, and in most patients lessens gastric and intestinal disturbances. In continued fevers it should, on the contrary, be given in a single dose large enough to procure a distinct remission. By making a break in the febrile symptoms, if only of a few hours' duration, a retardation of the destructive processes is accomplished. At the first administration twenty to thirty grains may be given. In favorable cases the temperature falls in the course of a few hours below 101°. When the high temperature is only temporarily held in check, at the end of twenty-four hours, if all symptoms of cinchonism have disappeared, the same dose should be repeated. If the doses mentioned, given in the manner prescribed, produce no perceptible effect upon the fever, their continuance may be regarded as unnecessary.

C. Braun and Richter speak favorably of the action of salicylate of sodium.[74] It possesses antipyretic properties, though in a less degree than quinia. It is, however, rapidly absorbed, circulates through all the parenchymatous organs, and finally is discharged unchanged in the urine. It is said by Binz, in small doses, to hinder the action of the disease-producing ferments, while it leaves untouched the normal ferments of the organism. It is of special service where quinia is not well tolerated, or when given fifteen to twenty grains at a time every four to six hours as {1033} an adjuvant to large single doses of quinia. The remedy should be continued until all traces of febrile disturbance have disappeared.

[Footnote 74: Richter, "Ueber intrauterine Injectionen," etc., _Zeitschr. für Geburtsk. und Gynaek._, Bd. ii. Heft 1, p. 146.]

A more powerful remedy than salicylic acid, where quinia has failed, is the Warburg's tincture. Some patients find, however, that it is somewhat difficult to retain upon the stomach.

Not many years ago, owing to the encomiums of Fordyce Barker,[75] the tincture of veratrum viride was in great favor in puerperal fever as a means of reducing the excited pulse of inflammation. The plan recommended was to administer five drops hourly, in conjunction usually with morphia, until the pulse was brought down to 70 or 80 beats to the minute. If the pulse had once been reduced, then three, two, or one drop hourly would be found sufficient to control it. Vomiting and collapse from its use were no cause for alarm, as they were temporary symptoms, and were followed by a fall of the pulse to 30 or 40 a minute, which was rather of favorable prognostic significance. In the rapid pulse of exhaustion, however, veratrum should not be given. Since the introduction of the thermometer into practice the reduction of the pulse by veratrum has been found to be associated with a fall in the temperature of the body. Of late, however, veratrum has gone rather out of vogue, not because it is not a very effective agent, but because its administration is an art to be acquired, and cannot safely be entrusted to an unskilled assistant. Then, too, in the last ten years there has grown up a better acquaintance with less dangerous remedies.

[Footnote 75: _The Puerperal Diseases_, p. 347.]

Braun recommends in severe cases, where quinia alone is without effect, to give in addition from twelve to twenty-four grains of digitalis in infusion per diem until its specific action is produced. Unlike veratrum, digitalis effects a permanent slowing of the heart. By prolonging the cardiac diastole and contracting the arterioles it allows the left ventricle to fill, restores the arterial tension, diminishes correspondingly the intravenous pressure, and promotes absorption. Its tendency to produce gastric disturbances and the distrust felt as to its safety have prevented its becoming popular in practice.

Alcohol as an adjuvant to treatment is indicated in all cases, whether quinia or salicylic acid or veratrum be simultaneously employed. It stimulates and sustains the heart, it retards tissue-waste, and is in itself an antipyretic of no mean value. Usually I give it in conjunction with quinia, one or two teaspoonfuls hourly of either whiskey, rum, or brandy, in accordance with the recommendation of Breisky.[76] But many years before I had learned from my friend Prof. Barker that the specific influence of veratrum was in many cases not obtained until the use of alcohol was combined with it.

[Footnote 76: _Ueber Alcohol und Chinin-behandlung_, Bern, 1875.]

The antipyretic action of drugs is probably due for the most part to some direct influence they exert upon the oxygenation of the tissues. Of course the less the fire the less the heat. It is well, however, to support their internal administration by the external employment of cold. Cold owes its effect in fevers partly to the abstraction of heat from the body-surface, and in a still more important degree to the impression which it produces upon the nervous system. In healthy persons the action of cold is to increase the consumption of oxygen and the production of carbonic {1034} acid. The additional heat thus generated renders it possible to sustain the vicissitudes of climate. In fevers the primary effect of cold is similar in character. Its main therapeutical action is derived from its secondary influence upon the nerve-centre which regulates the body-heat. If the cold employed be sufficiently intense or sufficiently prolonged, there follows, not always immediately, but in the course of an hour or two, a marked lowering of the temperature, which can only be accounted for by assuming an indirect influence exerted through the sympathetic nerve and the medulla oblongata. This peculiarity renders the external application of cold a most valuable addition to the therapeutical resources available in fevers.

In cases of moderate severity frequently sponging the patient with cold water will be found to be a grateful practice. An ice-cap to the head, where the blood lies near the surface, will often affect the entire temperature of the body. From immemorial times it has been employed to control delirium and promote sleep. An ice-bag placed over the inguinal region is locally beneficial to deep-seated pelvic inflammations, and, according to Braun, is capable of effecting a rapid fall of temperature. Ice-cold drinks should be freely allowed.

Schroeder recommends a permanent stream of cold water in the uterine cavity by means of a large irrigator and a drainage-tube; others advise cold rectal injections maintained for long periods by the aid of a tube with a double current.

In fevers of great violence the systematic application of cold by means of baths or the wet pack is capable in some cases of rendering important service. The temperature of the bath should range from 70° to 80°. Its duration should not exceed ten minutes. The patient should, when removed to the bed, be wrapped in a sheet without drying, and should be comfortably covered. In employing the wet pack two beds should be placed side by side. The body and thighs of the patient should be wrapped in a sheet wrung out in cold water, and be allowed to remain in the pack from ten to twenty minutes. As the sheet becomes heated the patient should be placed in a fresh one upon the second bed, and the transfers should be continued until the desired fall of temperature is effected. Braun claims that four packs are equivalent in action to one full bath.

Both these methods are, however, open to the objection that they cannot be carried out without considerable disturbance of the patient--a point of no small importance in cases of peritonitis. G. B. Kibbie has invented a fever-cot which obviates the ordinary difficulties of this mode of treatment. The cot is covered with "a strong, elastic cotton netting, manufactured for the purpose, through which water readily passes to the bottom below, which is of rubber cloth so adjusted as to convey it to a vessel at the foot." T. G. Thomas,[77] who has employed this apparatus extensively to reduce high temperatures after ovariotomies, explains as follows the modus operandi: "Upon this cot a folded blanket is laid, so as to protect the patient's body from cutting by the cords of the netting, and at one end is placed a pillow covered with india-rubber cloth, and a folded sheet is laid across the middle of the cot about two-thirds of its extent. Upon this the patient is now laid; her {1035} clothing is lifted up to the armpits, and the body enveloped by the folded sheet, which extends from the axillæ to a little below the trochanters. The legs are covered by flannel drawers and the feet by warm woollen stockings, and against the soles of the latter bottles of warm water are placed. Two blankets are then placed over her, and the application of water is made. Turning the blankets down below the pelvis, the physician now takes a large pitcher of water, at from 75° to 80°, and pours it gently over the sheet. This it saturates, and then, percolating the network, it is caught by the india-rubber apron beneath, and, running down the gutter formed by this, is received in a tub placed at its extremity for that purpose. Water at higher or lower degrees of heat than this may be used. As a rule, it is better to begin with a high temperature, 85°, or even 90°, and gradually diminish it. The patient now lies in a thoroughly soaked sheet, with warm bottles to her feet, and is covered up carefully with dry blankets. Neither the portion of the thorax above the shoulders nor the inferior extremities are wet at all. The water is applied only to the trunk. The first effect of the affusion is often to elevate the temperature--a fact noticed by Currie himself--but the next affusion, practised at the end of an hour, pretty surely brings it down. It is better to pour water at a moderate degree of coldness over the surface for ten or fifteen minutes than to pour a colder fluid for a shorter time. The water slowly poured robs the body of heat more surely than when used in the other way. The water collected in the tub at the foot of the bed, having passed over the body, is usually 8° or 10° warmer than it was when poured from the pitcher. On one occasion Dr. Van Vorst, my assistant, tells me that it had gained 12°. At the end of every hour the result of the affusion is tested by the thermometer, and if the temperature has not fallen another affusion is practised, and this is kept up until the temperature comes down to 100°, or even less. It must be appreciated that the patient lies constantly in a cold wet sheet, but this never becomes a fomentation, for the reason that as soon as it abstracts from the body sufficient heat to do so it is again wet with cold water and goes on still with its work of heat-abstraction. I have kept patients upon this cot enveloped in the wet sheet for two and three weeks, without discomfort to them and with the most marked control over the degree of animal heat. Ordinarily, after the temperature has come down to 99° or 100°, four or five hours will pass before affusion again becomes necessary."

[Footnote 77: "The Most Effectual Method of Controlling the High Temperature occurring after Ovariotomy," _N.Y. Med. Jour._, August, 1878.]

Since reading this account, I have made a good many trials of the method upon puerperal women, and have not found that it agrees with all in an equal degree. In some instances the affusions have been followed, in spite of hot bottles to the feet and the administration of stimulants, by such a degree of depression and impairment of cardiac force, as shown by the persistent coldness of the extremities, that it has been necessary to discontinue them. On the other hand, I can look back upon cases, apparently so desperate that the condition of the patients was looked upon as hopeless, where they proved the means of saving life as by a miracle. Of course, the difference depends upon whether the high temperature is the sole cause of the alarming symptoms, or whether the latter are in part due to blood-dissolution and secondary changes in the parenchymatous organs.

{1036} The use of the coil in fever, whether of rubber or of metal tubing, I can highly recommend. Either the night-dress or a towel should be placed between the coil and the skin. A current of cold water passing through the tube rapidly abstracts the surface heat, and is usually grateful to the patient. The lowering of the temperature by this means is much slower than by cold affusions. Disturbance of the patient is, however, avoided, and the method, so far as I have tried it, has been free from the objections incident to the direct application of water to the skin.

It is hardly necessary to state that in puerperal, as in other fevers, the patient's strength requires to be sustained and the waste of tissue to be repaired, as far as possible, by the regulated administration of liquid food, as milk and beef-tea, in such quantities as can be borne by the stomach, and at one to two hours' intervals.

In the treatment of encysted peritoneal effusions, and in inflammatory exudations into the pelvic and adjacent cellular tissue, after the acute symptoms have subsided the attention should be directed to the afternoon fever and to promoting the assimilation of food. So soon as the sweating and fever are checked the absorption of the plastic materials begins. The most important agents for accomplishing this object are quinia, in moderate doses, combined with some form of alcohol and with tepid sponging. Deep-seated pain in the iliac region is best relieved by a large blister upon the side over the point where the tenderness is felt. Prolonged rest in bed should be enjoined. Even after convalescence is well advanced, so long as the exudation remains unabsorbed the resumption of household duties is pretty certain to be followed by a relapse or by the development of a chronic condition of a most intractable description. The sooner the patient's stomach can be got to digest and absorb beefsteak and iron the more speedy will be her recovery.

In pelvic exudations the hot vaginal douche, warm baths, and the application of flannels wrung out in water to the abdomen aid in diminishing the local pain, and, perhaps, in causing a disappearance of the tumor. The action of mercurials or of iodide of potassium in melting away plastic inflammatory materials is sometimes very striking, but more frequently they either do no good or else do harm by disturbing the digestion.

If fever, chills, and sweating announce the presence of pus, the most careful exploration should be made to determine, if possible, the seat of suppuration. It is of great advantage to treat pelvic abscesses as abscesses are treated elsewhere in the body. If the redness of the skin above Poupart's ligament indicates a tendency to point in that direction, an aspirator-needle should be introduced to make sure of the diagnosis. If the sac is near the surface, a free incision should be made and the pus should be allowed to escape. In many cases I make these incisions three to four inches in length. The redness of the external skin makes it certain that the abscess has become adherent to the abdominal wall, and that the incision consequently will not communicate with the peritoneum. After the abscess has been opened it should be cleansed twice daily, and the cavity should be filled with oakum. If, after a time, the granulations become flabby, Peruvian balsam or iodoform should be introduced into the sac at each change of the dressing. I can recommend this plan as essentially a mild procedure. With a large opening for the discharge of {1037} pus the fever and sweating disappear, the appetite returns, and the abscess fills rapidly by granulation. With a small incision hectic is apt to persist, and the abscess to end in the formation of interminable fistulæ.

If softening and bagginess or distinct fluctuation indicate that the pus can be reached through the vaginal cul-de-sac, the aspirator-needle should be inserted deeply at the suspected point, and if a large amount of pus is detected, an incision should be made with a long-handled bistoury, using the needle as a director, and making the opening large enough to permit the introduction of a drainage-tube. I prefer for this purpose a self-retaining Nélaton catheter, which is easily passed by means of a uterine sound inserted into the eye at the extremity. Through the tube--without disturbing the patient--the pus-cavity can be washed as frequently as required, and with drainage and cleanliness cases of the longest standing may be expected to recover.

P. F. Mundé[78] has reported a number of cases of chronic character where the aspiration of pus has been followed by rapid absorption of the intra-pelvic exudation. The presence of pus was suspected because of a boggy, doughy feeling in the exudation tumor.

[Footnote 78: "Diagnosis and Treatment of Obscure Pelvic Abscess," etc., _Arch. of Med._, December, 1880.]

{1038}

BERIBERI.

BY DUANE B. SIMMONS, M.D.

DEFINITION.--Beriberi is a disease of inanition, most common in tropical countries, though found in high latitudes (41° N.), especially in low-lying seaboard towns, during the summer months, and is both endemic and epidemic. It is usually chronic in form, but is subject to exacerbations of varying degrees, and has for its characteristic symptoms anæsthesia of the skin, hyperæsthesia and paralysis of the muscles, anasarca, palpitation, cardiac and arterial murmurs (in the wet form), præcordial oppression, and abdominal pulsation.

HISTORY AND GEOGRAPHICAL DISTRIBUTION.--It was for a long time confounded with a great variety of other diseases. The Anglo-Indian physicians of Ceylon and the Malabar coast were no doubt the first to recognize the specific nature of the disease, though it is claimed that Chinese medical works of the thirteenth century contain a fairly accurate description of it.

The literature of beriberi, at the first glance, appears to be very meagre, as some of the most popular medical works make no mention of the disease at all, while others only give it a passing notice. Its bibliography, however, is very considerable, as may be seen in the exhaustive list in Billings' _Index Catalogue_, but for want of space we refer only to the most recent contributions to the subject. These are--an article by A. LeRoy de Mericourt;[1] an essay by Tarissan, entitled _Beriberi in Brazil_; an article by Anderson,[2] and an essay by myself.[3]

[Footnote 1: _Dictionnaire Encyclopédique des Sciences Médicales_, Paris, 1876.]

[Footnote 2: _Guy's Hospital Reports_.]

[Footnote 3: _Chinese Maritime Customs Medical Report_ (1880).]

For a long time beriberi was supposed to have a peculiar territorial limitation. It is now known to be more or less prevalent on all the islands and shores of Eastern Asia and Africa from Japan to the Cape of Good Hope, and in Brazil.

ETIOLOGY.--I know of no disease in regard to which a greater diversity of opinion exists as to its cause. Indeed, as one has observed, "autant d'auteurs, autant d'opinions diverses." Ten years' study and observation of the malady under a great variety of circumstances and conditions have led me to the definite conclusion that its exciting cause is a specific poison or germ, having many striking resemblances in its mode of production to paludal or marsh miasm, though entirely distinct and separate from it. A great variety of predisposing causes, however, exert a powerful influence in rendering individuals or classes susceptible to the {1039} disease, such as age, sex,[4] occupation, race, mode of life, diet, and climate.

[Footnote 4: Women suffer from the disease much less frequently than men.]

CLINICAL HISTORY AND SYMPTOMS.--There are three forms of the disease: 1st. Beriberi hydrops (wet beriberi), in which there is a hydræmic condition of the blood, distension of the general areolar tissue, with serum, and effusion into the serous cavities. 2d. Beriberi atrophia (dry or atrophic beriberi), in which there is a notable deficiency of fluids in the vessels and areolar tissue, and atrophy of the muscles. 3d. Mixed beriberi, in which the above forms lose the sharp lines of distinction and merge into each other. Cases complicated with dysentery, diarrhoea, and especially with continued fevers of the typhoid type, are not uncommon.[5] These last, besides being of grave prognosis, are frequently very embarrassing and difficult of diagnosis.

[Footnote 5: Some authors have designated fatty or convulsive forms of the disease, which I think unnecessary.]

In general terms, wet beriberi may be divided into two stages--the prodromic stage and the stage of attack; and into several types--the acute or pernicious, and the chronic. From the very insidious nature of the approach of the disease, sometimes extending over a period of several weeks, it is often very difficult, or even impossible, to determine the exact time of its invasion. It is generally admitted that a residence of some weeks in an infected locality is necessary before any decided symptoms make their appearance. As in many other diseases of slow development, the symptoms of the prodromic stage are certain not easily defined feelings of indisposition, such as an occasional sense of chilliness, inaptitude for mental exertion, and especially a tired feeling in the lower extremities. A period of uncertain length now intervenes, during which the characteristic symptoms appear and constitute the stage of attack. The first of these symptoms is, generally, anæsthesia of the skin over the anterior tibial muscles, in the tips of the fingers, and around the mouth, in the order given. Paralysis in varying degrees next declares itself in certain groups of muscles, usually those immediately underlying the regions of anæsthesia. One of the consequences of this is a drooping of the toes, causing the patient while walking to lift the feet high so as to clear the ground, thus occasioning the peculiar gait noticed by many observers as characteristic of the disease. A sense of constriction in the muscles of the calves is experienced at the same time, arising from a veritable contraction, which causes their apparent enlargement and hardening, with tension of the tendo achillis. A feeling of tightness in the chest usually accompanies this condition, due, no doubt, to partial paralysis of the muscles of respiration. If firm pressure be now made upon the muscles in various parts of the body, a greater or less degree of tenderness will be found to exist in many of them, and especially those occupying the posterior part of the leg, back of the forearm, inside of the arm, and upper part of the chest. Tenderness of the periosteum of the long bones and a peculiar roughness of their surfaces often exist also. Palpitation of the heart, especially on making any considerable exertion, is a frequent and often troublesome symptom, even at this stage of the disease.

Up to this point the above symptoms are common to both the wet and {1040} dry forms of the malady, and to them the characteristic features either of beriberi hydrops or atrophia are now added. The first manifestation of anasarca, the pathognomonic symptom of wet beriberi, is in an oedematous condition of the areolar tissue of the anterior part of the legs. This, in reality, is more or less general even at an early stage of the disease, as is evident from the plump appearance of the patient and a certain sallow-white color of the skin, especially of that of the face. In uncomplicated cases the temperature is normal, or it may be at times a little below the normal point. There is also little or no increase in the frequency of the pulse. Its quality, however, is changed, and somewhat characteristic for both forms of the disease. Thus in the wet form it is full, large, and easily compressible, indicating a great diminution of arterial tone, while in the dry form there is nearly an opposite condition. If the heart be now examined, a decided systolic murmur will be heard, most distinctly over the pulmonary valves; and in most cases of wet beriberi it exists in all the large arterial trunks. The heart furnishes the usual signs of dilatation and want of tone. In the dry form the cardiac murmurs are either slight or wanting altogether, and the area of cardiac dulness is variable, and frequently diminishes as the disease advances.

In both wet and dry beriberi the appetite is little impaired in the earlier stages, but if in the former the stomach is over-distended, there is increased præcordial oppression, and sometimes sudden death. The bowels in the wet form are sluggish, and urine scanty; in the other there is but little deviation from the normal in these respects.

The cases of the subacute type are by far the most numerous. From this it is evident that the acute or pernicious type of the malady is, in most cases, only an exaggeration of the subacute, as observed in some other diseases, notably rheumatism and those of marsh malarial origin. The term pernicious is, strictly speaking, applicable to the wet form of the disease only, as the dry form is rarely, if ever, rapidly fatal. A marked case of wet beriberi is always to be regarded as dangerous, from the suddenness with which pernicious symptoms often declare themselves. In these the anasarca (which, as has been stated, constitutes the leading clinical difference between the two forms of the malady) plays an important rôle. It often happens that in the course of a few hours the local oedema in the extremities and the slight puffiness of the face become general and extreme, and the neck is enormously swollen by the distension of the veins, both deep and superficial. The pleural and pericardial sacs are more or less distended with serum, thus mechanically embarrassing the action of the organs they contain. The action of the heart now becomes laborious, the lungs oedematous and filled with coarse râles, and a terrible sense of suffocation comes over the patient, causing him to seek relief by constant change of position. The stomach is irritable, a greenish-yellow fluid is vomited, and death closes the scene. The acute stage of dry beriberi, on the contrary, is characterized by a rapid diminution of the fluids of the body and muscular atrophy.

The annual appearance in the same individual of either wet or dry beriberi, and its long continuance, constitute the chronic type of the disease.

MORBID ANATOMY.--The morbid anatomical changes in beriberi vary considerably with its form. Few, if any, observers claim seriously to {1041} have found in either the wet or dry form of the disease evidences of acute inflammatory action in any of the tissues or organs. The blood undoubtedly undergoes important morbid changes, whereby its nutritive and oxygenating power is impaired, indicating that this is a disease of inanition. This shows itself most markedly in necrobiotic and degenerative changes, especially in the muscular tissues, which are the seat of the leading morbid phenomena in all stages of both forms of this disease. The respiratory, digestive, and glandular systems rarely undergo morbid changes other than those of a secondary or passive kind, such as engorgement with serum and venous blood.

The condition of the organs contained in the cranial and spinal cavities is variable and inconstant. According to some observers, the substance of the brain and spinal cord is hardened. The greater number by far, however, have found it more or less softened.[6] The heart in wet beriberi is habitually large and flabby, its muscular tissue softened and of a pale-yellow and macerated appearance. Its cavities are engorged with dark blood, sometimes fluid, but more often clotted. These clots are often voluminous in the right heart, semi-fibrinous, and extend into the pulmonary artery and great venous trunks, which are enormously enlarged. The cardiac muscular tissue I always found to have undergone metamorphic changes, varying from granular clouding to advanced fatty degeneration.[7] The tissue of the paralyzed voluntary muscles undergoes degenerative changes in both forms of the disease. In the extreme atrophy of dry beriberi I have not unfrequently found many of the sarcolemma sheaths completely emptied of their contents. The power of regeneration in these cases is often wonderfully displayed by an almost complete restoration of the lost elements, and, in a corresponding degree, of the function of the part.

[Footnote 6: The former condition was undoubtedly observed in autopsies made of the dry or atrophic form of the disease, though this fact is not mentioned. The latter, or softened, condition of the cerebro-spinal contents belongs to the wet form of the disease (my own cases being of this kind). I regard this softening as not ante-mortem, but as consecutive to serous imbibition (as observed by Eismann and Sanders in chlorosis), and as taking place during the last moments of life or after death, when the vital forces no longer oppose themselves to the mechanical disintegrating power of the fluid with which the nervous as well as all the other tissues of the body are engorged.]

[Footnote 7: I believe this to be the condition of the heart-muscle in all cases of death from the wet form of beriberi. In this opinion I am supported by Oudenhoven and many of the Dutch observers.]

It would appear that in wet beriberi the heart is first weakened by paresis of the cardiac ganglia, with consequent incomplete emptying of its cavities. This, in connection with rapid degenerative changes in its muscular tissue, causes the walls to yield to the blood-pressure, producing dilatation and tricuspid insufficiency, with regurgitation and consequent capillary stasis and dropsy. Vaso-motor nerve-paralysis, acting at the same time on the pulmonary artery and arterioles, and on other large arterial trunks, probably gives rise to the murmurs heard in them. In the dry form of the disease the vaso-motor nerve-paralysis is less pronounced, and the degenerative changes in the muscular tissue of the heart slower, while the marked decrease in the fluids of the system and the great failure of nutrition tend toward atrophic changes. From this it follows that we usually have, instead of a large dilated heart, a small weak one, with a narrow tricuspid orifice instead of a dilated one; little or no {1042} intercostal pulsation, and hence less cardiac dulness; no venous distension or capillary stasis, and hence no dropsy.

PROGNOSIS.--In temperate climates the prognosis of uncomplicated beriberi is favorable in a majority of cases. In seasons of its epidemic prevalence, however, all cases of the wet form of the disease must be carefully watched, as it not unfrequently happens that grave symptoms suddenly appear at a time when no danger has been anticipated. An unfavorable prognosis may be ventured when, in a case of wet beriberi, relief is not obtained by free purging or when vomiting sets in. In dry beriberi the termination in death is exceedingly rare as a direct result of the action of the poison producing the disease, so that when death does occur it is chiefly from exhaustion. The time of recovery depends on the amount of muscular degeneration, and also upon the season of the year when the attack occurred, as all cases of both forms of beriberi usually get well without treatment during the winter months.

TREATMENT.--The well-established fact of the influence of certain localities in the production of beriberi makes the removal of the patient from them a hygienic measure of great importance, and this is frequently the only treatment necessary if it can be done early. The effect of the change is often almost magical, especially if it be made to an elevated locality and among the mountains.

Diet is an important element in the treatment of beriberi. At the head of the list of foods to be avoided is rice. Coarsely prepared grains, such as wheat, barley, certain kinds of beans,[8] apparently because of more or less laxative properties, are preferable as articles of food.

[Footnote 8: A small red bean called adzuke, possessing both laxative and diuretic properties, is a favorite remedy with the Japanese for beriberi. It is used alone or mixed with rice, and is not unfrequently the only means resorted to for the successful cure of mild cases.]

No drug has been discovered possessing specific properties in this disease. In the wet form, medication consists in the administration of drugs calculated to draw off the excess of serum in the areolar tissues and in the serous sacs. First in point of efficacy for this purpose are the hydragogue cathartics. In my own practice the sulphate of magnesia, in large and repeated doses, has given the best results; elaterium, a powder of jalap, squill, and digitalis, and, in fact, any medicine which will give frequent and copious stools, are sure to afford marked relief to the more urgent symptoms, and in many cases will alone effect a cure. Care must be taken, however, not to exhaust the patient, though I have never seen the judicious use of this method of treatment do harm.

Copious bleeding is recommended by Anderson, especially in the stage of greatest danger, but I have never been able to convince myself of its safety.

The almost specific virtue claimed by the old Indian physicians for treeak farook is no doubt due to its cathartic properties.

Diuretics are indicated for the same reason as cathartics, and any of the more active are productive of good results. They are too slow in their action, however, to be relied on otherwise than as adjuvants to cathartics. I have found juniper gin to answer an excellent purpose, both as a stimulant and diuretic, where there was danger of exhaustion from the free use of cathartics.

The medical treatment of dry beriberi differs materially from that of {1043} the wet disease. Cathartics and diuretics are alike useless, and the former injurious. The ordinary means, such as electricity, strychnia, frictions, etc., employed in cases of muscular atrophy and paralysis from other causes, are indicated when the active stage has passed, but they are useless, and even injurious, before this time. The muscular hyperæsthesia common to both forms of the disease may be generally greatly relieved by anodyne liniments containing aconite. The internal use of the latter is highly recommended by some. Hypodermic injections of morphia afford relief to the painful sense of constriction in the calves of the legs so often complained of.

{1045}

INDEX TO VOLUME I.

A.

Abdomen, state of, in cholera, 741 in general peritonitis of puerperal fever, 1010 in relapsing fever, 390 in septicæmia, 977 in septicæmia lymphatica, 1011 in septicæmia venosa, 1012

Abdominal cavity, lesions of, in general peritonitis of puerperal fever, 989 glands, lesions of, in typhoid fever, 264 organs, alterations of, in scarlet fever, 531

Abortion from septicæmia, 972

Abortive form of the plague, 777 of relapsing fever, 395 of typhoid fever, 298 of typhus fever, 354

Abortive treatment of erysipelas, value, 638

Abscess in symptomatic parotitis, date of pointing, 627 metastatic, of lungs, complicating relapsing fever, 404

Abscesses complicating cholera, 735 variola, 445 following the plague, 781 frequency of, in pyæmia, 976 in erysipelas, treatment, 638 in para- and perimetritis, 1008 in puerperal fever, 989 metastatic, of pyæmia, modes of production, 963 of pyæmia, treatment, 981 pelvic, of puerperal fever, treatment, 1036 pulmonary, in puerperal fever, 989

Acids, mineral, use of, in cholera, 768

Aconite, use of, in rubeola, 580 in scarlet fever, 543 in yellow fever, 651

Acute diseases, relation of, to rubeola, 561 form of glanders in man, 920 in horse, 914

Adenitis complicating scarlet fever, 511 vaccination, 468

Adenopathy complicating erysipelas, 634

Adhesions from infiltration, 55

Adulteration of food, 197

Adynamic form of typhus fever, 354

Age, influence of, on causation of anthrax in man, 940 of cerebro-spinal meningitis, 802 of diphtheria, 680 of erysipelas, 630 of influenza, 860 of idiopathic parotitis, 620 of the plague, 775 of pertussis, 839 of relapsing fever, 371 of rötheln, 583 of rubeola, 561 of typhoid fever, 242 of typhus fever, 342 proper for vaccination, 477

Aged, typhoid fever in the, 301

Agminated glands, lesions of, in cholera, 745

Air, amount supplied in ventilation, 179 carbonic acid as a cause of impurity, 177 -currents, direction of, test, 178 distribution of, in ventilation, 180 estimation of carbonic acid, 178 fresh, value of, in convalescence, 206 humidity of, as a cause of disease, 133 impure, as a cause of disease, 177 influence of, on causation of glanders, 912 impurities of, due to offensive effluvia, 181 sources of impurity, 177 standards of impurity, 178 transmission of the plague by, 776 velocity of, in ventilation, 180 vitiated, as a cause of pyæmia, 959 supply, method of calculating amount of, in ventilation, 179

Albuminoid infiltration, 72

Albuminuria complicating diphtheria, 674 relapsing fever, 407 scarlet fever, 525 typhus fever, 355 following rubeola, 574 in typhoid fever, treatment, 334

Alcohol, use of, in algid form of pernicious malarial fever, 608 in anthrax, 938, 944 in cerebro-spinal meningitis, 831 in cholera, 767 in influenza, 876 in puerperal fever, 1033 in pyæmia, 982 in scarlet fever, 544 in typhoid fever, 324 in typhus fever, 366

Algid form of pernicious malarial fever, 606 causes of death, 607 frequency, 607 mortality-rate, 607 symptoms, 606 treatment, 607

Alum, use of, in pertussis, 845

Ammonium bromide, use of, in pertussis, 846 carbonate, use of, in scarlet fever, 544 chloride, use of, in diphtheria, 704, 705

Amyloid bodies, 86 degeneration, 84

Anæsthesia of skin in beriberi, 1039 significance of, in general diagnosis, 165

Anæsthetic form of leprosy, 790

Analysis of urine, importance of, in general diagnosis, 165

Anasarca, 69 complicating scarlet fever, 529 date of appearance in scarlet fever, 529 in beriberi, 1040

Anginose form of anthrax, 941 of scarlet fever, 510

Animals, cerebro-spinal meningitis in, 804 diphtheria in, 683 transmission of diphtheria from, 683

Animal vaccine, advantages, 475

Anodyne liniments, use of, in beriberi, 1043

Anorexia in relapsing fever, 389 in typhoid fever, 285 in typhus fever, 350 significance of, in general diagnosis, 162

ANTHRAX, OR MALIGNANT PUSTULE, 926 Synonyms, 926 Definition, 926 History, 926 Geographical distribution, 926 Etiology--specific origin, 928 Modes of transmission, 928 Transmission from eating flesh of anthrax animals, 928 by milk, 929 by insects, 929 by alkaline soils, 929 Season, relation of, to causation, 931 Plethora, relation of, to causation, 931 Sex, relation of, to causation, 931 Age, relation of, to causation, 931 Bacillus, 931 relation to causation, 931 physical characters, 932 effect of heat and cold on activity, 933 effect of oxygen on activity, 933 mode of entering body, 933 effect on blood-vessels, 934 Forms, 934 Symptoms--Incubation period, 934 duration of, 934 Apoplectiform form, 934 Anthrax fever, 934 Localized external anthrax, 935 Character and seat of lesions, 935 Morbid anatomy--changes in blood, 935 Spleen, 935 Lymphatic glands, 935 Connective tissue and muscles, 935 Gastro-intestinal tract, 936 Vagina and uterus, 936 Liver and kidneys, 936 Diagnosis--from other bacteridian diseases, 936 Swine plague, 936 Prognosis, 936 Mortality, 936 Treatment, 937 Preventive, 936 Drainage of anthrax soil, 937 Disinfection of stables, etc., 937 Disposal of carcases of sick animals, 937 Isolation, 937 By inoculation, 937 Methods of, 937 Pasteur's method, 937 Dangers in, 938 General, alcohol, 938 Use of carbolic acid, 938 nitro-muriatic acid, 938 potassium iodide, hypodermically, 938 quinia sulphate, hypodermically, 938 Local, 938 Cauterization, 938 Incision of nodule, 938

_Anthrax or Malignant Pustule in Man_, 939 Synonyms, 939 History, 939 Etiology, 939 Origin from lower animals, 939 Modes of infection, 939 direct, 939 by handling sick animals, 939 by insect-bites, etc., 939 by food, 939 by blood, 939 by air, 939 Occupation, relation of, to causation, 939 Age and sex, relation of, to causation, 940 Relative susceptibility of man and animals, 940 Forms, 940 Symptoms--of incubation period, 940 Local lesions, 940 Temperature, 940 Relation of, to local lesions, 940 Malignant anthrax, 940 Symptoms, 940 local, 940, 941 general, 941 Anthrax intestinalis, 941 Symptoms, 941 general, 941 eruptions, 941 gastro-intestinal tract, 941 nervous system, 941 Duration, 941 Anthrax angina, 941 Symptoms, 941 general, 941 local, 941 Duration, 941 Morbid anatomy, 941 Changes in blood, 942 Spleen, 942 Lymphatic glands, 942 Liver and kidneys, 942 Skin and mucous membranes, 942 Appearance of pustule, 942 Position of bacillus, 942 Diagnosis--signs, pathognomonic of, 942 From bites of insects, 942 Boils and carbuncles, 942 Plague-boil, 942 Glanderous nodule, 942 Importance of detection of bacillus, 942 Of malignant anthrax oedema, 942 Internal anthrax, 943 Prognosis, 943 Mortality, 943 Treatment--Preventive, 943 Disinfection, 943 Local, 943 Cauterization of preliminary papule in external form, 943 Method of cauterization, 943 Excision of parent nucleus, 943 Caustics used in, 943 Hypodermic injections into swelling, 943 Constitutional, 944 Carbolic acid, use of, 944 Alcohol, use of, 944 Diet, 944 Of anthrax oedema, 944

Antipyretics, use of, in relapsing fever, 428 in cerebro-spinal meningitis, 833

Antisepsis in septicæmia, 983 value of, in prevention of puerperal fever, 1024

Antiseptic treatment of scarlet fever, 545

Antiseptics, use of, in cholera, 770 in glanders in man, 924 in pyæmia, 980

Aphasia in cerebro-spinal meningitis, 810

Apoplectic form of anthrax in animals, 934

Appetite in cerebro-spinal meningitis, 814 as a guide to necessary amount of food, 195 loss of, significance, in general diagnosis, 162

Arcus senilis, significance, in general diagnosis, 151

Argyria, 93

Arsenic, use of, in relapsing fever, 427

Arsenical poison as cause of obscure diseases, 193

Arterial emboli, 63 murmur in beriberi, 1040 thrombosis following typhoid fever, 293

Arteritis from thrombosis, 61 in pyæmia, 967

Articular enlargement, significance of, in general diagnosis, 160

Artificial alimentation in diphtheria, 713

Asthenic form of simple continued fever, 233 of inflammation, 46

Ataxic form of typhus fever, 354

Ataxo-adynamic form of typhus fever, 354

Atmosphere, impure, influence of, on causation of puerperal fever, 1013, 1014 necessity of, for prevention of pyæmia and septicæmia, 980

Atmospheric variations as a cause of diphtheria, 682

Atrophy following diphtheritic paralysis, 676

Atropia, use of, in relapsing fever, 429

Auditory nerve, lesion of, in cerebro-spinal meningitis, 824

B.

Bacillus of anthrax, characters of, 931, 932 mode of entering body, 933 of glanders, 914 of pearly distemper, innocuousness of, from cooking, 105 species of, 142 tuberculosis, 99 _et seq._ description, 100 duration of effects, 104 cultivation, 100 local and general effects of invasion, 103 methods of detection, 102 milk as a means of dissemination, 105 mode of entrance into intestinal canal, 104 into respiratory organs, 104 typhosus, 258

Bacteria in healthy bodies, 144 influence of, on causation of pyæmia, 958 liability to error, from minuteness, 143 of cholera, 748 of leprosy, 791 of puerperal fever, 995

Bacterium termo as a cause of putrefaction, 142

Barometric variations, influence of, on course and causation of disease, 134

Bartholini's glands, suppuration of, complicating typhoid fever, 296

Baths, cold, use of, in puerperal fever, 1034 in relapsing fever, 428 warm, use of, in hydrophobia, 907 in variola, 453

Bed-linen, as a means of disseminating typhoid fever, 253

Bed-sores, complicating relapsing fever, 400 typhoid fever, 297 typhus fever, 355 in typhoid fever, treatment of, 335

Belladonna as a prophylactic in scarlet fever, 536 use of, in cerebro-spinal meningitis, 833 in pertussis, 846

Benignant tumors, 114

Benzoic acid as a prophylactic in scarlet fever, 537

BERIBERI, 1038 Definition, 1038 Geographical distribution, 1038 History, 1038 Etiology--Specific poison, 1038 resemblance of, to marsh-miasm, 1038 Predisposing causes, 1039 Varieties, 1039 Symptoms--Anæsthesia of skin, 1039 Muscular paralysis, 1039 Peculiarity of gait, 1039 Cramps, 1039 Muscular tenderness, 1039 Periosteal tenderness, 1039 Palpitation of heart, 1039 Symptoms, special--Of wet form, 1040 Anasarca, 1040 Quality of pulse, 1040 Cardiac murmur, 1040 Arterial murmur, 1040 Of dry form, 1040 Quality of pulse, 1040 Condition of heart, 1040 Morbid anatomy, 1040 Alterations in blood, 1041 Heart, 1041 Muscles, 1041 Prognosis, 1042 Treatment--By change of residence, 1042 By diet, 1042 Of wet form by hydragogue cathartics, 1042 Sulphate of magnesium, 1042 Elaterium, 1042 Treeak farook, 1042 Diuretics, 1042 Juniper gin, 1042 Of the dry form by electricity, 1043 Strychnia, 1043 Frictions, 1043 Use of anodyne liniments, 1043 Use of hypodermics of morphia, 1043

Bites of rabid dogs, treatment, 905

Bladder, diphtheria of, general sepsis from, 674 lesions of, in rabies, 903 in relapsing fever, 414 symptoms of diphtheria of, 674

Blindness in cerebro-spinal meningitis, 811

Blisters, use of, in cerebro-spinal meningitis, 830

Blood, alterations of, in anthrax, 935-942 in beriberi, 1041 in cerebro-spinal meningitis, 824 in cholera, 747 in pyæmia, 968 in relapsing fever, 411 in scarlet fever, 530 in septicæmia, 971 in typhoid fever, 268 in typhus fever, 356 altered, as a cause of symptomatic parotitis, 626 condition of, in pyæmia, 963 contamination of, sources, in pyæmia, 958 degeneration of, complicating diphtheria, 675

Blood-vessels, calcification of, 88, 90 changes in inflammation, 43 lesions of, in typhoid fever, 267 new formation of, 55

Body, portion of, most suitable for vaccinating, 477

Bones, chronic diseases of, following rubeola, 574 cranial, lesions of, in symptomatic parotitis, 626 in glanders, 922 in pyæmia, 967

Bone-marrow, lesions of, in relapsing fever, 417

Boric acid, use of, in diphtheria, 709

Bovine vaccine, 473

Bowels, state of, in relapsing fever, 390 in remittent fever, 602 condition of, in typhus fever, 350

Brain, lesions of, in cerebro-spinal meningitis, 823 in cholera, 746 in glanders, 923 in relapsing fever, 413 in typhoid fever, 266 in typhus fever, 358 and membranes, lesions of, in cerebro-spinal meningitis, 822 in pyæmia, 966 and spinal cord, lesions of, in rabies and hydrophobia, 903 softening of, following cerebro-spinal meningitis, 820

Breath, odor of, in typhus fever, 353

Bright's disease, aggravation of, by influenza, 870

Bromine, use of, in diphtheria, 708

Bromide of potassium, use of, in relapsing fever, 430

Bronchi, lesions of, in rabies and hydrophobia, 902 symptoms of formation of diphtheritic membrane, 671

Bronchial glands, lesions of, in influenza, 872

Bronchitis, complicating influenza, 868 rubeola, 571 typhoid fever, 294 typhus fever, 355 frequency of, in typhoid fever, 277 in rubeola, treatment, 581 in septicæmia, 977 in typhus fever, 353, 354

Broncho-pneumonia, complicating diphtheria, 672

Bryce's test of vaccinal infection, 461

Buboes, characters of, in grave form of the plague, 778 date of appearance of, in grave form of the plague, 778 of the plague, treatment, 784 pathology of, in the plague, 781 seat of, in grave form of the plague, 778

C.

Cadaveric rigidity after cholera, 741

Cæcum and colon, lesions of, in typhoid fever, 263

Calcification, 87 causes, 87 of blood-vessels, 88, 90 of thrombi, 60, 89

Calabar bean, use of, in cerebro-spinal meningitis, 834

Calm stage of yellow fever, 645

Calomel as a specific in typhoid fever, 336 use of, in cholera, 766 in hemorrhagic form of pernicious malarial fever, 613

Camphor, use of, in cholera, 768

Cancer, 117, 123 hereditary nature, 129 relation of, to epithelial tumors, 118

Capillary bronchitis, complicating influenza, 868

Capillaries, intestinal, lesions of, in cholera, 745

Carbolic acid, use of, in anthrax, 938 in diphtheria, 707 in glanders, 924 in scarlet fever, 545

Carbonic acid, as a cause of impure air, 177 amount of, in pure and impure air, 178

Carbuncles, character of, in grave form of the plague, 778 seat of, in grave form of plague, 778

Cardiac degeneration, complicating diphtheria, 675 following typhoid fever, 293 complicating typhus fever, 355 dilatation, complicating scarlet fever, 523 inflammation, complicating scarlet fever, 522 murmur in beriberi, 1040 sounds in typhoid fever, 276 thrombi in diphtheria, 687

Caseation, 79

Cataract, hereditary, nature, 129

Catarrh, absence of, in rubeola, 568 of influenza, treatment, 874

Catarrhal affections as predisposing causes of pertussis, 839 inflammation, 52 pneumonia, complicating influenza, 869 pock in vaccinia, 463 symptoms in influenza, 866 in prodromal stage of rubeola, 564

Causes of otitis in scarlet fever, 520

Caustics, use of, in hydrophobia, 905

Cauterization, use of, in external anthrax, 938, 943

Cathartics, use of, in wet beriberi, 1042 in scarlet fever, 554

Cellular tissue, lesions of, in pyæmia, 966

Cellulitis, pelvic, in puerperal fever, 988

Cerebral softening from embolism, 65 symptoms in yellow fever, 644

Cerebro-spinal meningitis, 795

Certificates of death, duty of a physician in regard to, 210

Cesspools beneath dwellings, dangers of, 192 contamination of water by, 192 evils of, 126

Change of residence as cause of typhoid fever, 244

Cheesy degeneration, 79 metamorphosis, 79

Chicken-pox, 481

Child-bed fever, relation to erysipelas, 630

Childhood, influence of, on occurrence of pertussis, 839

Children, causes of frequency of diphtheria in, 682 typhoid fever in, 301

Chills in pyæmia, 973

Chinolin, use of, in diphtheria, 703

Chloral hydrate, use of, in cerebro-spinal meningitis, 834 in hydrophobia, 907 in pertussis, 846 in relapsing fever, 430

Chloride test for detecting pollution of water-supply, 192

Chloroform, use of, in cholera, 768 in hydrophobia, 907 in relapsing fever, 431

CHOLERA, 715 Definition, 715 Synonyms, 715 History, 715 _et seq._ Etiology--predisposing causes, 720 Influence of high temperature in origin and spread, 720 Season, influence of, on causation, 720 Over-crowding and filth as causes, 720 Intemperance as a cause, 721 Contagiousness, 721 Modes of transmission, 721 Channels of entrance into system, 721 Propagation of, by fomites, 721 by drinking-water, 723 Cases illustrating spread of, by drinking-water, 724 Influence of height of subsoil-water on prevalence, 722 Humidity of soil as a cause, 722 Special fomites of, 723 Cases illustrating spread of, by fomites, 727 Cases illustrating contagiousness, 728 Objections to contagious nature, 729 Individual immunity, 730 Different grades of, from intensity of poison, 731 Specific origin, 747 Nature of poison, 748 Influence of bacteria in production, 748 Koch's investigations in regard to bacilli, 745, 749 Symptoms, 731 Mild forms, 732 "Cholerine" stage, 732 Number of stools in mild forms, 732 Character of stools in mild forms, 732 Grave forms, 733 Physiognomy in grave forms, 733 Stools in grave forms, 733 Typhoid state, 734 Stage of collapse, 734 Reaction, 734 Convalescence, 735 Temperature, 736 Difference between axillary, vaginal, and rectal temperature, 736 Special symptoms--Low temperature of mouth, 736 Condition of skin, 736 Color of skin, 737 Condition of heart and pulse, 737 Veins, 737 Vomiting, 738 Character of vomit, 738 Diarrhoea, 738 Results of diarrhoea, 738 Characters of stools, 739 Condition of urine, 739 Cramps, 740 Causes of cramps, 740 State of abdomen, 741 of nervous system, 741 Complications and sequelæ, 735 Complicated by diphtheritic exudations, 735 Inflammation of parotid and submaxillary glands, 735 Abscesses and ulcers, 735 Cutaneous eruptions, 735 Morbid anatomy--general appearance after death, 741 Cadaveric rigidity, 741 Muscular contractions after death, 741 Appearance, post-mortem, of abdominal cavity, 743 Changes in stomach, 743 Intestinal canal, 743 Intestinal mucous membrane, 743 Nature of exfoliation from intestinal canal, 744 Changes in isolated and agminated glands, 745 Capillaries and veins of intestinal canal, 745 Liver, 745 Gall-bladder, 746 Spleen, 746 Heart, 746 Pericardium, 747 Lungs, 746 Brain and spinal marrow, 746 Kidneys, 746 Blood, 747 Diagnosis--from cholera morbus, 750 from irritant poisoning, 752 Order of symptoms as a ground for, 753 Prognosis, 753 Symptoms indicating favorable and unfavorable, 754 Mortality--in different epidemics, 754 Influence of age, 754 Sex, 754 Social condition, 754 Treatment, 759 Preventive, 755 Disinfection, 758 Modes of applying disinfectants, 758 Importance of maintaining high degree of health during epidemics, 758 Quarantine and sanitary cordons for prevention, 755 _et seq._ Mode of carrying out quarantine, 757 Cases illustrating value of quarantine, 757 Use of drinking-water during epidemics, 759 General management, 760 Importance of early recognition, 732 Necessity of rest, 760 of prompt, 760 Diarrhoea, 760 Vomiting, 761 Hiccough, 762 Injection of sodium chloride into veins, 762 Stage of collapse, 763 Diet of stage of reaction, 763 For restoration of circulation in stage of collapse, 763 Stage of reaction, 763 Undue reaction, 764 Urinary suppression in stage of reaction, 764 Convalescence, 764 Use of venesection in, 764 Emetics, 765 Calomel, 766 Alcohol, 767 Opiates, 767 Mineral acids, 768 Camphor, 768 Chloroform, 768 Intravenous injections, 768 Hot applications, 769 Cold affusions, 769 Of cramps, 769 Necessity of cold water to allay thirst, 770 Use of antiseptic remedies, 770

Cholerine, 732

Chorea, following typhoid fever, 293

Chronic diseases, relation of, to rubeola, 561 forms of erysipelas, 634 of glanders, 915, 923

Cicatrix, condition during incubation of hydrophobia, 895 in hydrophobia, excision, 906-908 in vaccinia, description, 460

Classification of puerperal inflammations, 986

Cleanliness, importance of, in prevention of pyæmia, 980 in variola, 454

Climate, as a cause of disease, 185 definition of term, 185 influence of, on causation of influenza, 860 on causation of rabies and hydrophobia, 887 of rubeola, 560

Clinical history of influenza, 864

Clothing as a cause of disease, 198

Cloudy swelling, 72

Coagulation of exudations, 43

Cohnheim's theory of production of morbid growths, 106

Colchicum, use of, in dengue, 885

Cold as a cause of disease, 133 and damp, influence of, on causation of glanders, 912 bath, use of, in diphtheria, 702 in puerperal fever, 1034 in typhoid fever, 327 Contra-indications to use of, in diphtheria, 703 Use of, in algid form of pernicious malarial fever, 608 in cerebro-spinal meningitis, 830 in cholera, 769 in diphtheria, 702 in puerperal fever, 1033 in the hyperpyrexia of scarlet fever, 541 in scarlet fever, 542 in yellow fever, 651 water, intra-uterine injections of, in puerperal fever, 1034 mode of applying, in scarlet fever, 542

Cold stage of intermittent fever, 592 of intermittent fever, theory of cause, 593 treatment, 594 of yellow fever, treatment, 653

Cold water, use of, in typhus fever, 364

Collapse in cerebro-spinal meningitis, treatment, 831 in cholera, 734 treatment, 763 of lungs, complicating influenza, 869

Collections of water, influence on health of a community, 187

Colloid degeneration, 83 metamorphosis, 83

Color of skin, significance of, in general diagnosis, 159

Coma, in cerebro-spinal meningitis, 812 significance of, in general diagnosis, 166

Comatose form of pernicious malarial fever, 608 Diagnosis, 609 Symptoms, 609 Treatment, 609

Coma-vigil in typhus fever, 349

Compresses, hot water, use of, in variola, 453

Complications of cholera, 735 of erysipelas, 633 of idiopathic parotitis, 623 of influenza, 868 of pertussis, 843 of plague, 780 of relapsing fever, 396-410 of rötheln, 587 of rubeola, 570 causes, 570 of scarlet fever, 510 of typhoid fever, 292 treatment, 335 of vaccination, 468 of vaccinia, 464 of varicella, 483 of variola, 445

Confluent small-pox, 440

Conjunctiva, condition of, in human glanders, 921 symptoms of diphtheria of, 670

Conjunctival diphtheria, local treatment, 712

Conjunctivitis, diphtheritic, symptoms, 670

Consanguineous marriages, effects, 131

Constipation in cerebro-spinal meningitis, 814 in grave form of the plague, 779 in rubeola, treatment, 581 in typhoid fever, treatment, 333 in typhus fever, treatment, 367 significance of, in general diagnosis, 163

Constitutional infection, absence of, in vaccinia, 460 of syphilis, hereditary nature, 127 taints, conveyance of, by vaccination, 471 treatment of anthrax, 944 of pyæmia, 982

Contagion as a cause of disease, 135, 200 definition of, 200 of dengue, 884 of erysipelas, manner of propagation, 630 nature, 630 of influenza, 862 of relapsing fever, transmission, 373 of rabies and hydrophobia, 891 dissemination, 891 of rötheln, nature, 583 of rubeola, modes of dissemination, 558 mode of entering the body, 558 nature, 557 in typhus fever, nature, 343 modes of transmission, 344

Contagium of variola, duration of activity, 435 mode of entering body, 435 nature, 435 period of greatest activity, 435

Contagious diseases, characteristics, 137

Contagious nature of cholera, objections to, 729

Contagiousness of anthrax, 928 of cerebro-spinal meningitis, 803 of cholera, 721 of dengue, 884 of diphtheria, 678 of erysipelas, 630 of glanders, 911 of influenza, 862, 863 of leprosy, 788 of the plague, 776 of puerperal fever, 1017 of pyæmia, 960 of rabies and hydrophobia, 891 of scarlet fever, 494 of typhoid fever, 248 of typhus fever, 343 period of greatest, 345 of varicella, 481 of variola, 435

Convalescence, choice of diet, 206 in cerebro-spinal meningitis, 819 management, 835 in cholera, 735 management, 764 in chronic glanders in man, 922 in dengue, 882 in grave form of the plague, 779 in erysipelas, management, 639 in influenza, treatment, 875 in relapsing fever, 393 in scarlet fever, management, 544 in typhoid fever, management, 335 in typhus fever, management, 368

Convulsions during hot stage of intermittent fever, treatment, 597 in cerebro-spinal meningitis, 810 in relapsing fever, 384 complicating rubeola, 572 in prodromal stage of rubeola, 565 in rubeola, treatment, 581 in yellow fever, treatment, 653

Cooking, necessity of a physician's knowledge of, 196

Corpuscles, pus-, 43

Corrosive sublimate, use of, as antiseptic in puerperal fever, 1025, 1029

Coryza, chronic, following rubeola, 574 complicating scarlet fever, 520 of scarlet fever, treatment, 546

Cough, in rubeola, treatment, 581 significance of, in general diagnosis, 158

Counterirritants, use of, in pertussis, 848

Course of vaccinia, 458 irregularities, 460

Cow-pox, 456 spontaneous, 456

Cramps in beriberi, 1039 in cholera, 740 treatment, 769 causes, 740

Cretinism and goitre, hereditary nature, 128

Croup, respiration, 157

Croupous inflammation distinguished from croup, 49 of fauces, complicating scarlet fever, 516 membrane, 685 characters, 685 mode of formation, 685 metamorphosis, 80

Crust in vaccinia, composition, 464

Crusts, objections to use of, in vaccination, 476

Cubebs, use of, in diphtheria, 709

Cultivation of bacillus tuberculosis, 100

Curare, use of, in treatment of hydrophobia, 907

Cutaneous deposits in glanders, microscopic characters, 917 diphtheria, treatment, 713 lesions of glanders in man, 922 symptoms of glanders in man, 921

Cysts, definition, 115, 121

D.

Deaf-mutism following cerebro-spinal meningitis, 819

Deafness in cerebro-spinal meningitis, 811

Death, causes of, in cerebro-spinal meningitis, 818 in glanders, 915

Debility in cerebro-spinal meningitis, 813 in influenza, treatment, 876 influence of, in causation of glanders, 912 in relapsing fever, 386

Decline, stage of, in pertussis, 841

Decubitus, significance of, in general diagnosis, 150

Definition of anthrax, 926 of beriberi, 1038 of cerebro-spinal meningitis, 795 of cholera, 715 of contagion, 200 of cysts, 115, 121 of dengue, 880 of diphtheria, 656 of erysipelas, 629 of glanders, 909 of idiopathic parotitis, 620 of influenza, 851 of leprosy, 785 of pernicious malarial fever, 605 of pertussis, 836 of the plague, 771 of puerperal fever, 984 of pyæmia, 953 of rabies and hydrophobia, 886 of relapsing fever, 369 of remittent fever, 598 of rötheln, 582 of rubeola, 557 of septicæmia, 953 of simple continued fever, 231 of symptomatic parotitis, 625 of term "climate," 185 of typhoid fever, 237 of typho-malarial fever, 614 of vaccinia, 455 of varicella, 481 of variola, 434 of yellow fever, 640

Degeneration, 72 amyloid, 84 cheesy, 79 colloid, 83 fibrinous, 80 fatty, 74 granular, 72 hyaline, 80 lardaceous, 84 mucous, 82 of tubercle, 96 parenchymatous, 73 waxy, 84

Deglutition, difficult, in idiopathic parotitis, treatment, 624

Delirium in cerebro-spinal meningitis, 812 in erysipelas, treatment, 637 in idiopathic parotitis, treatment, 624 in pyæmia, 971 in relapsing fever, 384 in typhoid fever, 278 treatment, 334 in typhus fever, 348 treatment, 366 in yellow fever, treatment, 653 significance of, in general diagnosis, 166

Demonstration of bacillus of glanders, 914

DENGUE, 879 Synonyms, 879 History, 879 Definition, 880 Etiology, 883 Specific origin, 884 Contagiousness, 884 Symptoms--prodromal stage, 880 Mode of onset, 880 Temperature, 881 Pulse, 881 Delirium, 881 Facies, 881 State of gastro-intestinal tract, 881 State of tongue, 881 Stomach and bowels, 881 State of urine, 881 Eruptions, 881 Hemorrhages, 882 Prostration, 882 Convalescence, 882 Duration of, 882 Morbid anatomy, 882 Specific nature of, 882 Relation to acute articular rheumatism, 883 Changes in abdominal organs, 883 Diagnosis, 884 From acute articular rheumatism, 884 From yellow fever, 884 Prognosis, 885 Treatment, 885 Use of colchicum, 885 quinia, 885 opium, 885

Depletion, local, use of, in cerebro-spinal meningitis, 830

Depressing emotions, as a cause of typhoid fever, 245

Dermatitis, complicating vaccination, 468 vaccination, treatment, 469

Desquamation, date of, in mild scarlet fever, 506 in erysipelas, 633 in relapsing fever, 377

Desiccation in varicella, 482 in variola, 440

Diagnosis, general, 148 divisions of, 148 main direction of inquiries, 148 proper method of procedure, 150 significance of alteration of voice in, 158 of anthrax in animals, 936 in man, 942 of cerebro-spinal meningitis, 826 of cholera, 750 of comatose form of pernicious malarial fever, 609 of dengue, 884 of diphtheria, 689 of erysipelas, 635 of idiopathic parotitis, 624 of glanders in horse, 918 of glanders in man, 923 of influenza, 872 of intermittent fever, 594 of leprosy, 792 of the plague, 782 of pyæmia from septicæmia, 978, 979 of remittent fever, 600 of rabies and hydrophobia, 900 of relapsing fever, 418-422 of rötheln, 587 of rubeola, 575 of scarlet fever, 532 of simple continued fever, 234 of symptomatic parotitis, 627 of typhoid fever, 311-314 of typho-malarial fever, 616 of typhus fever, 358, 359 of vaccinia, 464 of varicella, 483 of variola, 447 of varioloid, 444 of yellow fever, 648

Diaphoretics, use of, in yellow fever, 649

Diarrhoea in cerebro-spinal meningitis, 814 in cholera, 738 results, 738 treatment, 760 in mild scarlet fever, 503 in pyæmia, 975 in relapsing fever, 405 in rubeola, treatment, 581 in septicæmia, 977 treatment, 983 in typhoid fever, 287 treatment, 331

Diarrhoeal diseases from impure water, 182

Diathesis, 127 hereditary, transmission, 130

Diet in anthrax, 944 in beriberi, 1042 in cerebro-spinal meningitis, 834 in cholera, 763 in convalescence, 206 in erysipelas, 639 in glanders, 924 in influenza, 874 in relapsing fever, 430 in pertussis, 848 in puerperal fever, 1036 in pyæmia, 982 in rubeola, 579 in typhoid fever, 323 in typho-malarial fever, 619 in typhus fever, 362 in yellow fever, 654 of convalescence, 206

Digestion, condition of, in cerebro-spinal meningitis, 814

Digestive tract, condition of, in glanders, 921 in idiopathic parotitis, 623

Digitalis, use of, in puerperal fever, 1033 in relapsing fever, 428 in scarlet fever, 543 in typhoid fever, 330 in yellow fever, 651

DIPHTHERIA, 656 Synonyms, 656 Definition, 656 History, 656 _et seq._ Panum's view regarding relation of bacteria to, 667 Etiology--Age, influence of, on causation, 680 Sex, influence of, on causation, 680 Causes of frequency of, in childhood, 680 Pharyngeal, buccal, and nasal catarrh a cause of, in children, 680 Physiological causes of, greater frequency in childhood, 681 Family predisposition, 681 Thermometric and barometric changes a cause, 682 Season as a cause, 682 Filth as a cause, 682 Polluted air as a cause, 682 water as a cause, 683 milk as a cause, 683 Contagiousness, 678 Modes of transmission of poison, 678 In the lower animals, 683 Transmission of, from lower animals to man, 683 Artificial production of membrane, 684 Invasion, 676 duration of incubation period, 679 Symptoms--Prodromal stage, 667 duration, 667 localized redness of mucous membranes, 667 Different manifestations of diphtheritic process, 668 Severe form, 668 appearance of membrane in severe form, 668 Gangrenous condition of membrane, 669 Swellings of glands at angle of jaw as sign of invasion of nasal cavities, 669, 670 Mode of invasion of nasal cavities, 669 Mode of spread to nasal cavities, 669 Nasal form, 669 Conjunctival form, 670 Aural form, 670 Laryngeal form, 671 Formation of membrane in larynx, 671 Tracheal and bronchial forms, 671 primary form, 672 Oral form, 672, 673 Intestinal form, 673 Of wounds, 673 Eruption of, 674 Vulvar and vaginal forms, 674 In puerperal women, 674 Vesical form, 674 Placental, 674 Liability of open wounds, 672, 679 Tendency to second attacks from chronic nasal and pharyngeal catarrh following, 670 Complications and sequelæ, 672 complicated by fibrinous pneumonia, 672 by broncho-pneumonia, 672 by erysipelas, 673 by urticaria and purpura, 674 by kidney affections, 674 by albuminuria, 674 by granular degeneration of blood, 675 by cardiac degeneration, 675 by symptoms of cardiac degeneration, 675 by embolism, 675 by acute endocarditis, 675 by leucocythæmia and Hodgkin's disease, 675 by nervous diseases, 675 by paralysis, 676 seat of, 676 date of appearance, 676 fatty degeneration and atrophy following, 676 sensory, 676 Secondary form, 671 Morbid anatomy--characters of the membrane, 685 Mode of formation of membrane, 685 Varieties of membrane in, 686 Rindfleisch's definition of diphtheritic inflammation, 686 Changes in the heart, 686 fatty and granular degeneration, 686 endocarditis, 687 cardiac thrombi, 687 Changes in lungs, 687 Spleen, 687 Liver, 687 Kidneys, 687 Muscles, 687 Lymphatic glands, 687 Mucous membranes, 688 Influence of different mucous membranes upon characters of false membrane, 688 epithelia upon growth and spread of false membrane, 688 Changes in intestines, 689 nervous system, 689 Diagnosis--significance of localized pharyngeal injection, 689 From muguet or thrush, 690 Follicular stomatitis, 690 Significance of glandular swelling, 690 lymphadenitis in nasal form, 690 Of laryngeal form, 691 Significance of absence of fever, 691 Of paralysis, 691 Prognosis--symptoms indicating favorable, 692 unfavorable, 692 Significance of glandular swelling, 692 In nasal, 692 Of fetid and putrid discharges, 693 Of epistaxis, 693 In laryngeal, 692 In tracheal, 692 Of tracheotomy, 692 significance of state of pulse after, 692 of dry respiration after, 692 of temperature-range after, 692 of character of membrane, 692 Influence of temperature, 693 state of pulse, 693 complications, 693 bronchitis and pneumonia, 693 endocarditis, 693 albuminuria, 693 affections of sensorium, 693 purpura, 693 icteric discoloration of skin, 693 Of relapses, 694 Treatment--hyperpyrexia, 694 Reflex symptoms, 694 Vomiting, 694 Futility of expectant, 694 Use of stimulants, 694 Amount of stimulants necessary, 695 Importance of general treatment, 695 Futility of venesection, 695 Prophylactic, 696 Danger of self-infection, 696 Prevention of self-infection, 696 Isolation, 696 Closure of schools and public places during epidemics, 697 Disinfection, 698 Special, 701 Local, 701, 709 by steam, 701 Use of water, 702 Ice and cold, 702 Cold baths, 702 Mode of applying cold, 702 Contra-indications to use of cold, 703 Solvents of pseudo-membrane, 703 Use of lime-water, 703 Slaking lime, 703 Lactic acid, 703 Pepsin, neurin, and chinolin, 703 Papayotin, 703 Pilocarpine, 704 objections to, 704 Turpentine inhalations, 704 Ammonium chloride, 704 Mercury, 705 Tincture of chloride of iron, 706 Carbolic acid, 707 Salicylic acid, 707 Quinia, 708 Bromine, 708 Boric acid, 709 Sodium salicylate, 709 Ozone, 709 Sulphur and cubebs, 709 Chlorate of potassium, 699 Dose of chlorate of potassium, 700 Danger in large doses of chlorate of potassium, 701 Mechanical removal of membrane, 709 Cauterization of membrane, 709 Glandular swellings, 710 Abscess of glands, 710 Of nasal form, 710 danger of permitting sleep in, 712 local applications, 710 Of conjunctival form, 712 Of laryngeal form, 712 use of emetics, 712 Of paralysis, 713 by strychnia, 713 by electricity, 713 artificial alimentation, 713 Of cutaneous form, 713

Diphtheria, complicating rubeola, 573 scarlet fever, 514 of genitalia in puerperal fever, 1002

Diphtheritic endometritis, 987 exudations, complicating rubeola, 735 membrane, cauterization, 709 mechanical removal, 709 conjunctivitis, 670 treatment, 712 inflammation, causes, 51 distinguished from diphtheria, 50 paralysis, treatment, 713 pock in vaccinia, 463

Disease, 35 Causes, 125, 175 arsenical poisoning, 193 climate, 185 cold, 133 contagion, 135, 200 epidemic influences, 135 errors of diet, 135 exciting, 125 exercise, abnormal, 134, 198 deficient, 135 functional, 134 habitation, 186 heat, 133 hereditary, 132 humidity of atmosphere, 133 improper clothing, 198 impure air, 177 ice, 185 water, 182 ingestive, 135 intemperance, 197 mental, 204 minute organisms, 141 predisposing, 125 pre-natal, 126, 175 poisons and misuse of medicines, 135 soil, condition of, 187 Definition of, 135 Elevation of site, influence of, 134 Means of discovery, 175 Abdominal, hot climate as a cause, 133 Respiratory, cold as a cause, 133 Prevention, 175 Respiration in, 156 Theory of--bioplastic, 140 chemical, 138, 140 fermentation, 138 germ, 138 points of objection, 142 undecided state, 147 Zymotic, table of, 136

Disinfectants, varieties, 202

Disinfection in anthrax, 937, 943 in cholera, 758 in diphtheria, 698 of glanders, 925 in the plague, 784 in puerperal fever, 1025, 1028 in pyæmia and septicæmia, 980 in scarlet fever, 201, 538 in typhus fever, 362 methods, 201 practical difficulties, 201 principles, 201

Dissecting poison, relation of, to causation of puerperal fever, 1018 wounds, relation of, to causation of septicæmia, 962

Dissemination of influenza, 863 in typhoid fever, 249 of puerperal fever by physicians, 1018

Diuretics, use of, in scarlet fever, 555 in wet beriberi, 1042

DRAINAGE AND SEWERAGE, 213 Back, ventilation of traps, 221 Disposal of liquid wastes by irrigation, 225 Frequency of leakage in waste-pipes, 222 Necessity of, in prevention of typhoid fever, 321 Of houses, 188 Necessity of abundant water-supply in, 220 Of soil, 226 Perfect, fundamental requirements, 213 Removal of human excrement, 215 of liquid household wastes, 220 Varieties of grease-traps, 221 Ventilation of waste-pipes, 223

Drainage-pipes, effects of large traps, 220 of too large bore, 220 of vertical position, 220

Drinking-water as a medium of disseminating typhoid fever, 248 propagation of cholera by, 723

Dropsies, 67-71

Drugs, use of, in the plague, 784

Dry form of beriberi, symptoms, 1040 treatment, 1043

Duration of cerebro-spinal meningitis, 818 of dengue, 882 of anthrax, 940, 941 of acute form of glanders in horses, 915 of chronic form of glanders in horses, 915 of acute form of glanders in man, 921 of chronic form of glanders in man, 922 of influenza, 865 of malignant scarlet fever, 508 of mild scarlet fever, 506 of prodromal stage of rubeola, 565 of remittent fever, 602 of rabies and hydrophobia, 900 of septicæmia lymphatica, 1012

Dysentery complicating relapsing fever, 406 typhus fever, 355

Dysphagia, significance of, in general diagnosis, 162

Dyspnoea, causes, 157

E.

Ear, affections of, in rubeola, treatment, 581 diseases of, complicating rubeola, 570 displacement of lobe in idiopathic parotitis, 624 internal, lesions of, in cerebro-spinal meningitis, 824 lesions of, in pyæmia, 967 in symptomatic parotitis, 626 middle, suppuration of, in cerebro-spinal meningitis, 811 symptoms of diphtheria, 670

Ears, significance of appearance of, in general diagnosis, 151

Early stages of yellow fever, treatment, 649

Earth-closets, 218

Effluvia, offensive, symptoms due to, 181

Effusions, 67 causes, 68-71 distinguished from exudations, 67

Elaterium, use of, in wet beriberi, 1042 in dry beriberi, 1043

Electricity, use of, in diphtheritic paralysis, 713

Elevated temperature as a cause of typhoid fever, 246

Emaciation, causes, 160 significance of, in diagnosis, 159

Emboli, action of, in production of metastatic abscesses in pyæmia, 967

Embolism, 62 complicating diphtheria, 675 from septic thrombus, 66 hemorrhagic results, 64, 65 in typhoid fever, treatment, 335 mechanical effects, 63 necrosis from, 64, 65 results, 64 softening, cerebral, from, 65 symptoms, 66

Embolus, 62 arterial, 63 venous, 63 terminations, 65

Emetics, use of, in cerebro-spinal meningitis, 830 in cholera, 765 during cold stage of intermittent fever, 595 in influenza, 876 in laryngeal diphtheria, 712 in pertussis, 845

Emphysema, aggravation of, by influenza, 870 significance of, in general diagnosis, 159

Endocarditis, acute, complicating diphtheria, 675 in diphtheria, 687 in puerperal fever, 990

Endo- and pericardium, lesions of, in septicæmia, 972

Endocolpitis in puerperal fever, 986, 1005

Endometritis in puerperal fever, 986

Enthetic febrile diseases, hereditary nature, 130

Epidemic causation of disease, 135

Epidemics of rubeola, frequency, 560 frequency in the new-born, 563

Epiglottis, symptoms of diphtheria, 671

Epistaxis in relapsing fever, 393 complicating rubeola, 570 in remittent fever, 602 in rubeola, treatment, 580 in typhoid fever, 273 treatment, 335

Epithelia, influence of different, in spread of diphtheritic membrane, 688

Ergot, use of, in cerebro-spinal meningitis, 833

Ergotine, use of, in pyæmia, 982

Eruption, absence of, in rubeola, 568 causes of absence of, in mild scarlet fever, 505 in cerebro-spinal meningitis, 816, 817 in dengue, 881 in diphtheria, 674 in influenza, 866 in malignant scarlet fever, 507 in mild scarlet fever, 504 in pyæmia, 974 in relapsing fever, 376 in rötheln, 585, 586 in rubeola, 566 peculiarities in character, 569 in seat, 509 relapses, 570 retrocession of, in rubeola, treatment, 580 in tubercular form of leprosy, 789 in typhoid fever, 273 in typhus fever, 351 in varicella, 487 in variola, 437 characters, 438 position, 438 in varioloid, 444

Eruptive stage of rubeola, duration of, 567 symptoms of, 565 of variola, treatment, 452

ERYSIPELAS, 629 Definition, 629 Synonyms, 629 Classification, 629 History, 629 Etiology, 629 Unity of the origin, 629 Age and sex as a cause, 630 Season as a cause, 630 Contagiousness, 630 Nature of contagion, 630 Manner of propagation, 630 Relation to childbed fever, 630 Symptoms--initial, 631 Characters of cutaneous lesions, 631 Course of cutaneous lesions, 631 Severe varieties of cutaneous lesions, 632 Migration of cutaneous lesions, 632 Swelling of integument, 632 Starting-point of cutaneous lesions, 632 Physiognomy, 632 Condition of tongue, 633 of fauces and buccal membrane, 633 General symptoms of grave form, 633 pulse, 633 temperature, 633 Occurrence of gangrene, 633 Resolution, 633 Desquamation, 633 Complications and sequelæ, 633 Complicated by lymphangitis and adenopathy, 634 By pneumonia, 634 By pleuritis, 634 By inflammation of joints, 634 By inflammations of serous membranes, 634 By pyæmia and septicæmia, 634 By eye diseases, 634 Followed by seborrhoea of scalp, 633 By loss of hair, 633 Modification of previous skin disorders, 634 Chronic forms, 634 Variety and nature of chronic forms, 634 Morbid anatomy, 635 Changes in skin, 635 Viscera, 635 Mucous surfaces, 635 Diagnosis, 635 From dermatitis, 636 From eczema, 636 From erythema, 636 From pemphigus, 636 From scarlet fever, 636 From urticaria, 636 Prognosis--symptoms indicating unfavorable, 636 Treatment--preventive, 636 Hygienic, 637 General, 637 Hyperpyrexia, 637 Delirium, 637 Local, 637 Value of abortive, 638 Surgical, 638 Mouth complications, 638 Nasal complications, 638 Abscesses, 638 Value of expectant, 639 Convalescence, 639 Diet, 639 Use of quinia, 637 tincture of the chloride of iron, 637

Erysipelas, complicating diphtheria, 673 typhus fever, 355 vaccination, 469 variola, 445 relation of, to puerperal fever, 1002

Etiology, general, 125 of anthrax in animals, 928 in man, 939 of beriberi, 1038 of cerebro-spinal meningitis, 801 of cholera, 720 of dengue, 883 of diphtheria, 680 of erysipelas, 629 of glanders in horse, 911 in man, 919 of idiopathic parotitis, 620 of influenza, 859 of leprosy, 787 of pertussis, 838 of the plague, 774 of puerperal fever, 1013 of pyæmia, 955 of rabies and hydrophobia, 887 of relapsing fever, 370 of remittent fever, 598 of rötheln, 583 of rubeola, 557 of scarlet fever, 487 of septicæmia, 960 of septo-pyæmia, 963 of simple continued fever, 232 of symptomatic parotitis, 625 of typhoid fever, 242 of typhus fever, 341 of varicella, 481 of variola, 435 of yellow fever, 640

Eucalyptus, use of, in typhoid fever, 331

Excision of cicatrix for prevention of hydrophobia, 908 of primary nucleus in anthrax, 943

Exciting cause, mechanical nature of, in symptomatic parotitis, 626 of the plague, 775 of typhoid fever, 248 of typhus fever, 343

Excrement, human, disposal of, by privy-vaults, 219 dry conservancy, 218 _et seq._ removal of, by water-carriage, 215

Exercise, abnormal, as a cause of disease, 134 amount necessary for health, 198 as a part of a systematic education, 199 deficiency of, a cause of disease, 135 Du Bois Reymond's definition, 198 importance of, in preservation of health, 198 relation of, to mental work, 199

Expectant treatment of erysipelas, value, 639

Expectoration, significance of, in diagnosis, 158

External anthrax, localized, 935

Exudation, distinction from transudation, 42 in inflammation, 42 in peri- and parametritis of puerperal fever, 1007 in pelvic peritonitis, 989

Eye, affections of, following cerebro-spinal meningitis, 819 in rubeola, treatment, 581 condition of, in cerebro-spinal meningitis, 810 diseases of, complicating erysipelas, 634 rubeola, 571 variola, 445 lesions of, in cerebro-spinal meningitis, 824 in pyæmia, 967

Eyes, appearance of, significance in general diagnosis, 151

F.

Face, appearance of, in typhus fever, 348

Family predisposition to diphtheria, 681

Faradization, use of, in rabies and hydrophobia, 907

Farcy, 909

Fatigue as a cause of typhus fever, 342

Fat, sources of, in the body, 74

Fatty degeneration, 74 causes, 78 following diphtheritic paralysis, 676 infiltration, 76 metamorphosis, 74, 79

Fauces, condition of, in cerebro-spinal meningitis, 814 in erysipelas, 633 in malignant scarlet fever, 508 in typhoid fever, 286 inflammation of, complicating rubeola, 571 significance of appearance of, in general diagnosis, 152

Faucial and nasal mucous membrane, condition of, in mild scarlet fever, 504

Febrifuge, use of, in relapsing fever, 428

Febrile stage of grave form of the plague, 778

Fermentation theory of disease, 138

Fever, agents producing heat in, 40, 41 definition, 38 inflammatory, 37 distinguished from idiopathic, 37 influence of vaso-motor system on production of heat in, 39 intermittent, 592 malarial, 589 pernicious malarial, 605 puerperal, 984 relapsing, 369 remittent, 598 sanitary effects, 41 scarlet, 486 secondary, in variola, 439 simple continued, 231 symptoms, 38 temperature, 38-40 traumatic, 37 typho-malarial, 614 typhoid, 237 typhus, 338 yellow, 640

Fibrinous degeneration, 80 inflammation, 49

Filtering power of soil, 187

Filth as a cause of cholera, 721 diphtheria, 682 the plague, 774 relapsing fever, 370

Foetus, effects of maternal impression upon, 131

Fomites, propagation of cholera by, 721 special, of cholera, 723

Food, adulterations, 197 appetite as a guide to necessary amount, 195 as a cause of disease, 195 infants, 196 patient's sensations as a guide to choice of, in disease, 205 popular errors in regard to, 195 to overeating, 195 preparation of, necessity of a physician's knowledge of, 196 proper, necessity of, in prevention of pyæmia and septicæmia, 980 transmission of anthrax by, 929

Formad on peculiarities of scrofulous habit, 101

Forms of anthrax in animals and man, 934, 940 of leprosy, 789 of the plague, 777 of rabies, 895 of relapsing fever, 395 of vaccine, 476

Fourth ventricle, lesions of, in cerebro-spinal meningitis, 824

Frænum linguæ, ulceration of, in pertussis, 841

Frequency of puerperal fever, 984 of typho-malarial fever, 616

Frictions, use of, in dry beriberi, 1043

Frontal pains in influenza, 867

Fruit, propagation of malaria by, 591

Fulminant form of the plague, 779

Furious form of rabies, 896

Furuncles, complicating variola, 445

G.

Gait, peculiarity of, in beriberi, 1039

Gall-bladder, lesions of, in cholera, 746 in typhoid fever, 266

Gangrene, 56 complicating vaccination, 468 following typhoid fever, 293 typhus fever, 355 in erysipelas, 633 in symptomatic parotitis, treatment of, 628 of neck, complicating scarlet fever, 512 pulmonary, complicating relapsing fever, 404

Gangrenous affections following rubeola, 574

Gastro-intestinal canal, condition of, in dengue, 881 condition of, in yellow fever, 644 lesions of, in anthrax, 936 in influenza, 872 in rabies and hydrophobia, 902 in relapsing fever, 413 symptoms in influenza, 866 in mild scarlet fever, 505 in malignant scarlet fever, 507 of septicæmia lymphatica, 1011

Gelsemium, use of, in yellow fever, 651

GENERAL ETIOLOGY, 125

General dropsies, 71 treatment of erysipelas, 639 of glanders in horse and man, 919, 920

Genitalia, gangrene of, complicating variola, 446

Geographical distribution of anthrax, 926 of beriberi, 1038 of glanders, 909 of rabies and hydrophobia, 886 of relapsing fever, 369 of typhoid fever, 241

Germ, specific, of glanders, nature of, 914 of rabies and hydrophobia, 892 point of election of, 892

Germ-theory of disease, 138 of scarlet fever, 488

Giddiness, significance of, in general diagnosis, 166

GLANDERS (FARCY), 909 Synonyms, 909 Definition, 909 History, 909 Geographical distribution, 909 Etiology--Contagiousness, 911 Specific nature, 911 Predisposing causes, 912 Ill-health, relation of, to causation, 912 Cold and damp stables, relation of, to causation, 912 Debility from chronic diseases, relation of, to causation, 912 Infection, channels of, 913 Particular nature of the germ, 914 Virulence of the germ, 914 Modes of culture of germ, 914 Demonstration of bacillus of, 914 Symptoms--in horses, 914 Acute form, 914 Incubation period, 914 Mode of onset, 914 Local lesions, 915 Appearance of nostrils, 915 of lymphatics, 915 Enlargement of joints, 915 Appearance of ulcers, 915 Mode of death in, 915 Chronic form, 915 Premonitory symptoms, 915 Condition of general health, 915 Local lesions, 915 Lymphatics, 915 Bronchial and pulmonary form, 916 Acute cutaneous form (farcy), 916 Local lesions, 916 Chronic cutaneous form (chronic farcy), 916 Local lesions, 916 Duration, 915 Morbid anatomy, 916 Nasal lesions, characters of, 917 Pulmonary lesions, characters of, 917 Cutaneous lesions, characters of, 917 Diffuse glanderous swellings, 917 of nose, 918 of lungs, 918 of muscles, 918 Diagnosis, 918 Value of inoculation in, 918 Prognosis, 918 Unfavorable nature of, 918 Treatment--in animals, 918 Not commendable, 918 Local, 918 General, 919 Diet in, 919 Preventive, 919 Extermination of disease in animals, 919

_Glanders in Man_, 919 History of, 919 Etiology, 919 Modes of infection, 919 immediate, 919 mediate, 920 Influence of occupation, 920 Influence of ill-health, 920 Symptoms--incubation period, 920 Appearance of wound, 920 General, 920 Mode of onset, 920 Character and seat of local lesions, 921 Appearance of sores, 921 Condition of nasal mucous membrane, 921 of submaxillary glands, 921 of conjunctiva, 921 Digestive tract, 921 Nervous system, 921 Temperature in, 921 Pulse in, 921 Chronic form, 921 General, 921 Local, 921 Cutaneous lesion, 922 Respiratory lesions, 922 Lymphatic glands, 922 Digestive tract, 922 Convalescence, 922 Duration of acute forms, 921 of chronic forms, 922 Morbid anatomy--changes in mucous membranes, 922 Lungs and pleuræ, 922 Gastro-intestinal tract, 922 Spleen and liver, 922 Joints, 922 Bones, 922 Brain and membranes, 923 Microscopy of lesions, 923 Diagnosis, 923 Pathognomonic signs in, 923 From rheumatic fever, 923 Chronic form, from pyæmia and septicæmia, 923 From syphilis, 924 From miliary tuberculosis, 924 Presence of bacillus not conclusive, 924 Value of inoculation in, 924 Prognosis--unfavorable nature of, 924 Treatment--External cases, 924 Erysipelatoid swellings, 924 Abscesses and tumors, 924 Nasal ulcers, 924 Importance of general treatment, 924 Use of antiseptics, 924 Diet, 924 Preventive, 925 Extinction of affection in animals, 925 Necessity of disinfection, 925

Glanderous swelling, diffuse, 917

Glands at angle of jaw, swelling of, symptomatic of nasal invasion, in diphtheria, 669, 670

Glandular abscesses in diphtheria, treatment, 710 degenerations, 72 swellings in diphtheria, treatment, 709

Glycosuria, complicating relapsing fever, 410

Gout, hereditary nature, 127

Granuloma, 120, 124

Grave forms of cholera, physiognomy, 734 stools, 733 symptoms, 732 of the plague, 777 of relapsing fever, 395

Grease-traps, varieties, 221

GROWTHS, MORBID, 105

Gums, significance of state of, in general diagnosis, 151

H.

Habits, depressing, as a cause of cerebro-spinal meningitis, 802

Hæmatemesis, significance of, in general diagnosis, 163 in relapsing fever, 390

Hæmatoidin, 91

Hæmatoma, 115, 122

Hæmaturia in relapsing fever, 390

Hæmoglobin, 90

Hæmophilia, hereditary nature, 129

Hæmoptysis, significance of, in general diagnosis, 163

Hæmostatics, use of, in yellow fever, 652

Hair, appearance of, in typhoid fever, 275 loss of, following erysipelas, 633

Headache in cerebro-spinal meningitis, 808 in idiopathic parotitis, 624 in influenza, 867 treatment, 874 in relapsing fever, 383 in typhoid fever, 277 treatment, 334 in typhus fever, 348 treatment, 366

Health, importance of exercise in preservation, 198

Health-resorts, disease from, 185

Hearing, impairment of, following cerebro-spinal meningitis, 819 disorders of, in relapsing fever, 400 modifications of, in typhoid fever, 279 significance of, in general diagnosis, 166

Heart, alterations of, in beriberi, 1041 condition of, in beriberi, 1040 in cholera, 737 in pyæmia, 976 in typhus fever, 351 disease, complicating influenza, 870 lesions of, in cholera, 746 in diphtheria, 686 in relapsing fever, 411 in septicæmia, 972 in typhoid fever, 267 in typhus fever, 357 and blood-vessels, lesions of, in rabies and hydrophobia, 902 palpitation of, in beriberi, 1039

Heart-clot, complicating relapsing fever, 402 rubeola, 672 scarlet fever, 523

Heat as a cause of disease, 133 use of, in cholera, 769

Hemorrhages in dengue, 882 in hemorrhagic form of pernicious malarial fever, treatment, 612 in remittent fever, treatment, 605 in yellow fever, 646 treatment, 651 intestinal, in typhoid fever, 287, 288 treatment, 332

Hemorrhagic form of pernicious malarial fever, 609 causes, 610 seat of hemorrhages, 610 symptoms, 611 treatment, 612 of scarlet fever, 509 of variola, treatment, 454 infarction, 64 rubeola, 569 small-pox, 442 variola, morbid anatomy of pock in, 447

Hepatic abscess following typhoid fever, 295

Heredity as a cause of disease, 175 influence of, on marriage, 176 relation of, to life insurance, 175 as a cause of leprosy, 787

Hereditary diathesis, transmutation, 130 nature of syphilis, 127 of non-malignant morbid growths, 129 of nervous diseases, 129 of organic disease, 129 of rickets, 128 predisposition to disease, 126

Herpes labialis, complicating influenza, 874

Hiccough in cholera, 762 in relapsing fever, 405 significance of, in general diagnosis, 158

Histoid tumors, 116

History of anthrax in animals and man, 926, 939 of beriberi, 1038 of cerebro-spinal meningitis, 796 of cholera, 715 of dengue, 879 of diphtheria, 656 of erysipelas, 629 of glanders in horses, 909 in man, 919 of influenza, 852 _et seq._ of pertussis, 836 of rabies and hydrophobia, 886 of relapsing fever, 369 of rötheln, 582 of rubeola, 557 of pyæmia and septicæmia, 945-952 of scarlet fever, 486 of simple continued fever, 231 of typhoid fever, 238 of typhus fever, 338 of vaccination, 465 of vaccinia, 456 of varicella, 481 of variola, 434

Hodgkin's disease, complicating diphtheria, 675

Horse-pock vaccine, 473

Hospitals for infectious diseases, necessity, 203

Hospital, maternity, advantages, 1021

Hot stage of intermittent fever, treatment, 595

House-drainage, 188 disconnection of, from sewer, 190 testing, 190

House-plumbing, 190

Houses, sanitary inspection, 187, 193

House-sewerage, 188 dangers to health from, 189, 191 examination of a system, 188 main points in a good system, 191 peppermint-test for defects, 190

Human excrement, removal of, by drainage, 215

Humanized and animal vaccine, relative merits, 473 vaccine, points of superiority, 473

Humidity of air as a cause of disease, 133

Hunger, influence of, on causation of rabies and hydrophobia, 888

Hyaline degeneration, 80

Hydro-bilirubin, 91

Hydrocephalus, following cerebro-spinal meningitis, 819

Hydrochloric acid, local use of, in puerperal fever, 1028

Hydrophobia, 886

Hygiene, 173 importance of perfect, in cholera epidemics, 758 in pertussis, 848 public, relation of physicians to, 207

Hygienic treatment of erysipelas, 637 of hydrophobia, 906 of scarlet fever, 539 of typhoid fever, 322 of yellow fever, 654

Hygroma, 116, 122

Hyperpyrexia in diphtheria, treatment, 694 in erysipelas, treatment, 637 in puerperal fever, treatment, 1032 in relapsing fever, treatment, 426 in rubeola, treatment, 579 in scarlet fever, treatment, 541 in typhoid fever, treatment, 327 in typhus fever, treatment, 364 in yellow fever, treatment, 651

Hypodermatic injection of anthrax swellings, 938, 943

I.

Ice, impure, as a cause of disease, 185 use of, in diphtheria, 702 in scarlet fever, 542

Idiopathic parotitis, 620

Idiosyncrasy as a cause of typhoid fever, 245 influence of, in causation of variola, 436

Ill-health, influence of, in causation of glanders, 912, 920

Impure air as a cause of disease, 177 evil effects of, 181 water, as a cause of disease, 182

Impurities of water, from living organisms, 184 nature, 184

Incubation of relapsing fever, 376 of scarlet fever, 492 of typhus fever, 346 of varicella, 481 of variola, 436 period of anthrax in animals, 934 in man, 940 of diphtheria, duration of, 679 of glanders in horse, 914 in man, 920 of influenza, 863 of intermittent fever, 592 of the plague, 777 of rabies and hydrophobia, 894 of rötheln, 585 of typhoid fever, 259 of yellow fever, 643 stage of idiopathic parotitis, duration, 621 of idiopathic parotitis, 621 of puerperal fever, 1004 of pyæmia, 973 of rubeola, 563

Indications for treatment of puerperal fever, 1028 of septicæmia, 982 of yellow fever, 649

Infants' food, 196

Infarction, hemorrhagic, 164

Infection, 200 channels of, in glanders, 913 modes of, in human anthrax, 939

Infiltration, albuminoid, 72 amyloid, 84 fatty, 76

INFLAMMATION, 37 Characteristics, 37 Heat, 37 Redness, 37 causes, 37 Pain, 41 causes, 41 Swelling, 41 causes, 41 Exudation, 42 Reuss on distinction of exudation from transudation, 42 Migration of white corpuscles, 42 Coagulation of exudation, 43 Changes in the blood-vessels, 43 Disturbance of functions, 44 Varieties of--hemorrhagic, 48 Diphtheritic, 50 Productive, 51 Catarrhal, 52 Phlegmonous, 52 Acute, 53 Chronic, 53 Interstitial, 53 Parenchymatous, 53 Termination, 54, 55, 56 Resolution, 54 New formations, 54 Cicatrization, 55 Abscesses, 56 Destruction of tissue, 56 Causes, toxic, 43 traumatic, 44 parasitic, 45 infectious, 45 constitutional, 46 trophic, 46 Course, 46 Sthenic and asthenic, 46 Serous, 47 Typhoidal, 47 symptoms, 47 Purulent, 48 Suppurative, relation of microbia, 48 Fibrinous, 49 of fauces, catarrhal and diphtheritic, complicating typhoid fever, 295 of neck, complicating parotitis, 511 simple, complicating vaccination, 468

Inflammations, serous, complicating typhus fever, 355

Inflammatory fevers, 37 form of typhus fever, 354 rubeola, 568

INFLUENZA--Definition, 851 Synonyms, 851 History, 852 _et seq._ Etiology, 859 Predisposing causes, 859 Age, relation of, to causation, 860 Social condition, relation of, to causation, 860 Sex, relation of, to causation, 860 Occupation, relation of, to causation, 860 Race, relation of, to causation, 860 Over-crowding and filth, relation of, to causation, 860 Season, relation of, to causation, 860 Climate, relation of, to causation, 860 Air, condition of, to causation, 860 Winds, relation of, to spread, 860 Mode of onset of epidemics, 860, 861 Duration of epidemics, 861 Exciting causes, 862 Specific poison, 863 Contagiousness, 862 Dissemination, 863 Relation of, to other epidemic diseases, 863 Incubation period, 863 Clinical history, 864 Variations in intensity of symptoms, 864 Symptoms of mild cases, 864 of severe cases, 864 Symptomatology, 865 Analysis of symptoms, 865 Fever, 865 Temperature, 865 Pulse, 866 Urine, 866 Skin, 866 Eruptions, 866 Gastro-intestinal system, 866 Nausea and vomiting, 866 Physiognomy, 866 Catarrhal symptoms, 866 Condition of mucous membrane, 866 Hoarseness, 867 Cough and dyspnoea, 867 Nervous system, 867 Headache, 867 Frontal pain, 867 Pains in limbs, 868 Pleurodynia, 868 Delirium, 868 Dizziness, 868 Sleeplessness, 868 Hebetude and torpor, 868 Muscular twitchings, 868 Mental condition, 868 Duration, 865 Complications and sequelæ, 868 Inflammations of lungs, 868 Bronchitis and capillary bronchitis, 868, 869 Catarrhal pneumonia, 869 Lobar pneumonia, 869 Localized pulmonary collapse, 869 Gangrene of lungs, 870 Pleurisy, 870 Pericarditis, 870 Laryngitis and chronic bronchitis, 870 Inflammation of middle ear, 870 Parotitis, 870 Herpes labialis, 870 Phthisis, 870 Emphysema, aggravation, 870 Old neuralgias, aggravation, 870 Heart disease, aggravation, 870 Bright's disease, aggravation, 870 Pregnancy, 870 Intermittent fever, 870 Morbid anatomy, 871 Essential lesions, 871 Appearance of respiratory tract, 871 Changes in gastro-intestinal tract, 872 Bronchial glands, 872 Lung tissue, 872 Pathology--Not a simple acute inflammation, 871 Specific character, 871 Diagnosis--From non-specific catarrhal affections, 872 From typhoid fever, 872 Prognosis--Influence of age, 872 pre-existing organic disease, 872 of character of epidemic, 872 Mortality, 872, 873 Variability in different epidemics, 873 Rate of, 873 Cause of death, 873 Treatment--preventive, 873 Mild forms, 874 Catarrh, 874 Headache, 874 Cough, 875 Use of quinine, 874 Opium, 874 Fat inunctions, 874 Diet, 874 Severe forms, 875 Indications for treatment, 875 High temperature, 875 Cough, 876 Sub-sternal and chest pains, 876 Use of diaphoretics, 875 Bloodletting, 875 Emetics, 876 Purgatives, 876 Quinine, 876 Mineral acids, 876 Expectorants, 877 Opium, 876 Alcohol, 877 Chloral, 877 Diarrhoea, 877 Debility, 877 Lung complications, 877 Diet in, 875 Convalescence, 878 Danger of depressing measures, 878

Inhalations, use of, in pertussis, 844

Initial stage of pertussis, 840 symptoms of yellow fever, 644

Injections, intravenous, use of, in cholera, 768 in hydrophobia, 908 in puerperal fever, 1029 vaginal, use of, in prevention of puerperal fever, 1026

Inoculation as a means of diagnosis in glanders, 918 in hydrophobia, 902 as a prophylactic in anthrax, 937 in rabies and hydrophobia, 905 in scarlet fever, 536 of leprosy, 788 of rubeola, 559 of small-pox, 465

Insects, propagation of anthrax by, 929

Insomnia in typhoid fever, treatment, 334 in typho-malarial fever, treatment, 619 in typhus fever, treatment, 366

Inspection of houses, sanitary, 187

Insusceptibility to rabies and hydrophobia, 894

Intellect, impairment of, following cerebro-spinal meningitis, 819 following typhoid fever, 292

Intellectual condition in typhus fever, 348

Intemperance as a cause of cholera, 721 of disease, 197 of relapsing fever, 370 of typhoid fever, 245 of typhus fever, 342

Intermission in intermittent fever, 594 in relapsing fever, 381

INTERMITTENT FEVER, 592 Incubation period, 592 Symptoms--prodromal stage, 592 Paroxysm, 592 Cold stage, 592 theory of cause of cold stage, 593 Hot stage, 593 duration of hot stage, 593 relation of type to duration of hot stage, 593 Sweating stage, 593 Nausea and vomiting during paroxysm, 593 Intermission, 594 Duration of intermission, 594 Relative frequency of different types, 594 Convertibility of different types, 594 Morbid anatomy, 594 Treatment--cold stage, 594 Use of quinia, 595 Opium, 595 Emetics, 595 Hot stage, 595 Use of opium, 595 Quinia, 596 Purgatives, 596 Of convulsions, 597 Sweating stage, 597 Use of quinia, 597 Causes of failure of quinia, 597 Adjuvants to quinia in preventing return of paroxysms, 598 Use of nitric acid to prevent return of paroxysms, 598

Internal anthrax in animals, 934

Interstitial inflammation, 53

Intestinal anthrax in man, 941 canal, lesions of, in cholera, 743 catarrh, chronic, following rubeola, 574 complicating rubeola, 572 tract, lesion of, in typhus fever, 357

Intestines, lesions of, in diphtheria, 689 symptoms of diphtheria of, 673

Intravenous injection of warm water in hydrophobia, 908

Inunction in scarlet fever, 541

Inunctions, use of, in rubeola, 580

Invasion of cerebro-spinal meningitis, 806 of diphtheria, 676 of variola, 438 stage of grave form of the plague, 777 of idiopathic parotitis, duration, 621 treatment, 624 of variola, treatment, 452 of varioloid, 443

Iodine as a specific in typhoid fever, 336, 337

Iodoform, intra-uterine use of, in puerperal fever, 1025

Iron, persulphate, local use of, in puerperal fever, 1028 tincture of the chloride, use of, in diphtheria, 706 in erysipelas, 637 in yellow fever, 652

Irregular forms of scarlet fever, 508

Irrigation, disposal of liquid wastes by, 225

Irritability of nervous system in hydrophobia, 899

Irritants, influence of, in production of morbid growths, 108

Isolated glands, lesions of, in cholera, 745

Isolation in anthrax, 937 in diphtheria, 696 in the plague, 783 in rubeola, 578 in scarlet fever, 536 necessity of, in typhus fever, 361 principles of, in disease, 203

J.

Jaborandi, use of, in scarlet fever, 552 in yellow fever, 650

Jaundice in relapsing fever, 391 in septicæmia venosa, 1012 complicating typhoid fever, 295 typhus fever, 356 in remittent fever, 601 in yellow fever, 646

Joints, chronic diseases of, following rubeola, 574 condition of, in glanders in man, 920 inflammation of, complicating erysipelas, 634 lesions of, in pyæmia, 967 purulent inflammation of, in puerperal fever, 990 suppuration of, in pyæmia, 976 swelling of, in cerebro-spinal meningitis, 814 in relapsing fever, 400

Jugular veins, pulsation of, significance in general diagnosis, 156

Juniper gin, use of, in wet beriberi, 1042

K.

Kibbie's fever-cot, use of, in puerperal fever, 1034, 1035

Kidney affections, complicating diphtheria, 676 complications in hemorrhagic form of pernicious malarial fever, treatment, 612

Kidneys, lesions of, in anthrax in animals, 937 in man, 942 in cholera, 746 in diphtheria, 687 in pyæmia, 969 in rabies and hydrophobia, 903 in relapsing fever, 414 in scarlet fever, 526 in septicæmia, 972 in typhoid fever, 268 in typhus fever, 357

Koch's investigation of bacillus tuberculosis, 99 of cholera bacilli, 745-749 of bacteria of puerperal fever, 997

L.

Lactic acid, use of, in diphtheria, 703

Lardaceous degeneration, 84

Laryngeal diphtheria, local treatment, 712 prognosis, 692

Laryngitis, complicating rubeola, 571 typhoid fever, 294

Larynx, inflammation of, complicating variola, 446 lesions of, in hydrophobia, 902 in relapsing fever, 413 in typhoid fever, 266 symptoms of diphtheria, 671

Latent form of typhoid fever, 300

Leeches, use of, in puerperal fever, 1031

LEPROSY, 785 Definition, 785 Synonyms, 785 History, 785 Etiology, 787 Heredity as a cause, 787, 788 Contagiousness, 788 Transmission, by inoculation, 788, 789 Sex as a cause, 789 Forms, 789 Symptoms--prodromal stage, 789 Duration of prodromal stage, 789 Tubercular form, 789 Local, 789 Eruptions, 789 Earlier eruptions, 790 Characteristic eruptions, 790 General, 790 Duration, 790 Anæsthetic form, 790 Local, 790 General, 791 Duration, 791 Morbid anatomy, 791 Changes in nerves, 791 Skin, 791 Bacteria, 792 Seat of bacteria, 792 Diagnosis, 792 Prognosis, 793 Treatment, 793 Futility of specific, in, 793 Indications, 793 Prophylaxis, 794 Segregation of afflicted, 794 Quarantine in, 794 Local, 794

Lesions characteristic of anthrax, 935

Lethargic form of rabies in dogs, 897

Leucocytes, death of, as a cause of thrombosis, 57 migration, 42

Leucocythæmia, complicating diphtheria, 675

Lime-water, use of, in diphtheria, 703

Limbs, significance of appearance in general diagnosis, 160

Listerine as a prophylactic in scarlet fever, 537

Liver, abscess of, following typhoid fever, 295 enlargement of, in pyæmia, 976 lesions of, in cholera, 745 in diphtheria, 687 in glanders, 918, 922 in pyæmia, 969 in remittent fever, 602 in relapsing fever, 414 in scarlet fever, 531 in typhoid fever, 265 in typhus fever, 357 in yellow fever, 649

Local dropsies, 71 lesions of glanders, 915, 921 symptoms of glanders in animals, 914 of glanders in man, 921 treatment of anthrax in animals, 938 of anthrax in man, 943 of diphtheria, 701, 709 of erysipelas, 637 of glanders in horse, 918 in man, 924 of pyæmia, 981 of septicæmia, 983

Lochial discharge, influence of, on causation of puerperal fever, 1015

Lung diseases, complicating influenza, 868 complicating influenza, treatment, 877

Lungs, gangrene of, in influenza, 870 hypostatic congestion of, in typhus fever, 353 lesions of, in cholera, 746 in diphtheria, 687 in glanders, 917, 922 in influenza, 872 in pyæmia, 968 in relapsing fever, 413 in septicæmia, 972 in typhoid fever, 266

Lymph, dried, use of, in vaccination, 477 of vaccinia, microscopical characters, 463 vaccine, proper time for collecting, 479

Lymphangitis, complicating erysipelas, 634 vaccination, 468

Lymphatic glands, condition of, in anthrax, 940 in glanders in horses, 915 in man, 921 in malignant scarlet fever, 508 in rötheln, 586 lesions of, in human anthrax, 942 in anthrax of lower animals, 935 in diphtheria, 687 in relapsing fever, 417 pigmentation of, 92

Lymphatics, as channel of entrance of poison of septicæmia, 963 lesions of, in symptomatic parotitis, 626

Lymphatic swellings, seat of, in grave form of the plague, 778 system, lesions of, in the plague, 781

Lymphoma, 120, 124

M.

Magnesium sulphate, use of, in wet beriberi, 1042

Malaria, 89 action of poison on system, 591 entrance into system, modes of, 591 communicability by drinking-water, 590 by fruit, 591 by milk, 590 conditions necessary to mature the poison, 589 duration of incubation of poison, 591 from impure water, 182 influence of moisture in production, 187 means of access of the poison, 590 nature of the poison, 589 non-interchangeableness of the poison, 591 ponderability of the poison, 590 production, 187 specific nature of poison, 591

MALARIAL FEVER, PERNICIOUS, 605 Definition, 605 Varieties, 606 Algid or congestive form, 606 Causes, 606 Frequency, 607 Cases illustrating clinical history, 606 Causes of death, 607 Mortality-rate, 607 Treatment, 607 General indications for treatment, 608 Use of ice and cold in treatment, 608 Opium, 608 Alcohol, 608 Comatose form, 608 Symptoms, 608 Previous condition of persons attacked, 609 Diagnosis from congestive form, 609 Treatment, 609 Hemorrhagic form of, 609 Causes, 610 Seat of hemorrhages, 610 Cases illustrating clinical history, 611 Treatment, 612 Indications for treatment, 612 Use of quinia, 612 Hemorrhages, 612 Renal complications, 613 Depurative, 613 Use of calomel and purgatives, 613

Malarial fevers, 589 definition, 589 nature of remittent fever, 598

Malignant anthrax oedema, 940 pustule, 926 tumors, 114

Mania following cerebro-spinal meningitis, 819

Maternity hospitals, advantages of, 1021

Marriages, influence of, hereditary, 176 of diseased persons, 176 transmission of hereditary proclivities by, 131

Marriages, consanguineous, 131

Marson's theory of multiple vaccination, 467

Masked forms of yellow fever, symptoms, 654

Maturation in variola, 439

Measles, 557 relations of, to idiopathic parotitis, 620

Mechanism of transudation, 68

Medical diagnosis, general, 148

Melanæmia, 92

Melanin, 92

Membrane, appearance of, in severe form of diphtheria, 668 diphtheritic, artificial production, 684 characters, 685 mode of formation, 685 varieties, 686 gangrenous condition of, in diphtheria, 669

MENINGITIS, EPIDEMIC CEREBRO-SPINAL, 795 Definition, 795 Synonyms, 795 History, 796 Etiology, 801 Seasons as a cause, 802 Meteorological agencies, 802 Localities, 802 Age, influence, 802 Sex, influence, 802 Depressing and debilitating habits, 803 Contagiousness, 803 Morbific principle, 803 Pandemic nature, 804 In the lower animals, 804 Types, 804 Forms, 805, 806 Symptoms--summary of, 806 Modes of onset, 806, 807 Individual, 808 Pain in the head, 808 spine, 808 Hyperæsthesia and anæsthesia of skin, 808 Spinal rigidity or opisthotonos, 809 duration of, 809 Convulsions, 809 Paralysis, 810 Aphasia, 810 Condition of eyes, 810 pupils, in, 810 strabismus, 810 blindness, 811 Deafness, 811 Suppurative inflammation of middle ear, 811 Physiognomy, 812 Delirium, 812 Coma, 812 Vertigo, 812 Debility, 813 Condition of tongue, 813 Nausea and vomiting, 813 Characters of matter vomited, 813 Appetite and digestion, 814 Thirst, 814 Constipation and diarrhoea, 814 Condition of fauces, 814 Urine, 814 Swelling of joints and limbs, 814 Respiration, 814 Pulse, 815 Temperature, 815 fluctuations of, 816 Eruptions, 816 irregularity of, 816, 817 petechiæ and ecchymoses, 816, 817 bullæ and pemphigus, 817 Cause of death, 818 Duration, 818 Convalescence, 819 characters, 819 cause of tardy, 819 Relapses, 820 frequency, 820 Sequelæ, 819 Followed by eye affections, 819 Impairment of hearing, 819 Deaf-mutism, 819 Impaired intellect and mania, 819 Hydrocephalus, 819 Paresis and paralysis, 819 Softening of brain, 820 Difficulty of speech, 820 Severe neuralgic pains, 820 Mortality of, 820, 828 variability of death-rate, 820, 828 influence of age upon, 828 Morbid anatomy, 820 General appearance of body after death, 820 Changes in the muscles, 821 in brain and membranes, 821 Changes due to congestion of brain and membranes, 821 to inflammation of meninges, 822 to softening of the brain, 823 Changes in pia mater, 821 in brain-tissue, 823 in spinal cord and membranes, 823 position of, 823 in internal and auditory apparatus, 824 Softening of fourth ventricle and auditory nerve, 824 Changes in eye and optic nerve, 824 in the viscera, 824 Absence of enlargement of spleen, 824 Changes in blood, 824 Amount of fibrine in blood before death, 825 after death, 825 Changes in blood-corpuscles, 825 Summary of pathology, 826 Diagnosis of, 826 From sporadic meningitis, 827 Functional and hysterical nervous affections, 827 Typhoid fever, 827 Typhus fever, 827 Prognosis of, 828 Symptoms indicating unfavorable, 829 favorable, 829 Imprudence of absolute, in, 829 Treatment, 829 Emetics, 830 Purgatives, 830 Futility of venesection, 830 Local depletion, 830 Cold applications, 830 Blisters, 830 Mode of using blisters, 831 Of coldness of skin, 831 Of collapse, 831 Use of alcohol, 831 Opium, 832 Value of opium, 833 Use of quinia, 833 Antipyretics, 833 Mercury, 833 Calabar bean, 834 Belladonna, 833 Ergot, 833 Potassium bromide, 834 Hydrate of chloral, 834 Potassium iodide, 834 Management of convalescence, 835 Diet in, 834

Meningitis, granular, following rubeola, 574

Menstrual disorders, complicating relapsing fever, 410 typhoid fever, 296

Menstruation, complicating typhus fever, 356 significance of abnormal, in general diagnosis, 165

Mental condition in hydrophobia, 899 in influenza, 868 in septicæmia lymphatica of puerperal fever, 1012 in typhoid fever, 277 disorders following the plague, 781 impressions, influence of, in causation of yellow fever, 643 overwork as a cause of typhus fever, 342 strain, symptoms due to, 205 work, relation of, to exercise, 199

Mercury, use of, in cerebro-spinal meningitis, 833 in diphtheria, 705

Metamorphosis, cheesy, 79 colloid, 83 croupous, 80 fatty, 74, 79 mucous, 82

Metastasis in idiopathic parotitis, 623, 624 treatment, 625 in pyæmia, pathology, 964 of tumors, 110

Methods of disinfection, 201 of vaccinating, 478

Metritis in puerperal fever, lesions, 987

Meteorism in typhoid fever, 286

Micro-organisms of puerperal fever, 1015 in pyæmia, blood-changes effected, 970

Microbes, as poison producers and carriers, 141 difficulty of separation of, from surrounding material, 146 liability to error from minuteness, 143

Microbia in inflammation, 45, 48

Micrococci, 141 in healthy bodies, 144

Microscopic organisms, classification, 141

Microscopy of glanderous lesions in man, 923

Migration of leucocytes, 42

Mild forms of cholera, 731 character of stools, 732 number of stools, 732 of influenza, treatment, 874 form of typhus fever, 354 of yellow fever, symptoms, 644

Milk, adulteration, 197 as a cause of disease, 197 as a medium of dissemination of anthrax, 929 of malaria, 590 of rabies and hydrophobia, 891 of scarlet fever, 491 of typhoid fever, 252 as a vehicle of bacillus tuberculosis, 105 polluted, as a cause of diphtheria, 683

Mind, state of, in relapsing fever, 384

Miscarriage, complicating typhus fever, 356

Modern conveniences questionable benefits, 215

Moral sense, perversion of, following typhoid fever, 292

Morbid anatomy, of anthrax in animals, 935 in man, 941 of beriberi, 1040 of cerebro-spinal meningitis, 820 of cholera, 741 of dengue, 882 of diphtheria, 685 of erysipelas, 635 of glanders in horses, 916 in man, 922 of idiopathic parotitis, 621 of influenza, 871 of intermittent fever, 594 of leprosy, 791 of pertussis, 843 of the plague, 781 of puerperal fever, 985 of pyæmia, 966 of pyæmia simplex, 970 of rabies and hydrophobia, 902 of relapsing fever, 413-417 of remittent fever, 602 of rubeola, 575 of scarlet fever, 530 of septicæmia, 971 of septo-pyæmia, 972 of simple continued fever, 235 of symptomatic parotitis, 626 of typhoid fever, 260 of typhus fever, 356 of vaccinal pock, 463 of varicella, 483 of variola, 446 of yellow fever, 649 growths, 105 classifications, 114, 122 Cohnheim's theory of origin, 106 influence of an irritant in production, 108 method of origin, 106 non-malignant, hereditary nature, 129 processes, 35

Morbific principle of cerebro-spinal meningitis, 803

Morphia, hypodermic use of, in beriberi, 1043 use of, in rabies and hydrophobia, 907

Mortality of anthrax in animals, 936 in man, 943 of cerebro-spinal meningitis, 820, 828 in cholera, 754 of glanders in man, 924 of influenza, 872 of pertussis, 841 of the plague, 780 of puerperal fever, 1020 of rabies and hydrophobia, 894 in relapsing fever, 422 of remittent fever, 599 of rubeola, 577 of scarlet fever, 534 of typhoid fever, 316-320 of typho-malarial fever, 616 of typhus fever, 360, 361 of yellow fever, 647, 648

Mouth, condition of, in idiopathic parotitis, 622 of mucous membrane of, in erysipelas, 633 complications in erysipelas, treatment, 638 symptoms of diphtheria, 672, 673

Mucous degeneration, 82 membranes of palate and fauces, appearance of, in prodromal stage of rubeola, 564 condition of, in confluent small-pox, 441 in rötheln, 586 eruptions of varicella on, 483 influence of different, upon the character of diphtheritic membrane, 688 lesions of, in diphtheria, 688 in glanders in man, 922 in rabies and hydrophobia, 902 in erysipelas, 635 localized redness of, symptomatic of prodromal stage of diphtheria, 667 variolous pustules upon, 439 metamorphosis, 82 softening, 82

Multiple tumors, 110

Mumps, 620

Murmurs, arterial, in beriberi, 1040 cardiac, in beriberi, 1040

Muscles, alteration of, in beriberi, 1041 lesions of, in cerebro-spinal meningitis, 821 in diphtheria, 687 in pyæmia, 966 in typhoid fever, 267 of neck, suppuration of, in symptomatic parotitis, 626 voluntary, lesions of, in relapsing fever, 410

Muscular pains in yellow fever, 644 paralysis in beriberi, 1039 rigidity after cholera, 741 spasm, in typhoid fever, 279 tenderness in beriberi, 1039 tremor in typhoid fever, 279 in typhus fever, 349

N.

Nævi, vaccination as a means of destroying, 468

Nails, appearance of, in typhoid fever, 275

Nasal cavities, condition of, in malignant scarlet fever, 508, 520 mode of invasion of, in diphtheria, 669 complications in erysipelas, treatment, 638 diphtheria, local treatment, 710 prognosis, 692 form of diphtheria, symptoms, 669 lesions in glanders, 917 mucous membrane, condition of, in influenza, 866

Nationality in relation to relapsing fever, 371

Nature of puerperal fever, views concerning, 990-1004 of vaccinia, 455

Nausea, during intermittent fever paroxysm, 593 in cerebro-spinal meningitis, 813 in influenza, 866 in relapsing fever, 390 in rubeola, treatment, 581 in typhoid fever, 285 in typhus fever, 350 in yellow fever, treatment, 652 significance of, in general treatment, 162

Negroes, insusceptibility of, to yellow fever, 644

Neck, significance of appearance of, in diagnosis, 152

Necrosis from embolism, 64, 65

Neoplasms, 105

Nephritis, complicating scarlet fever, 525 in scarlet fever, treatment, 550-555

Nerves, lesions of, in leprosy, 791 in symptomatic parotitis, 626

Nervous diseases, complicating diphtheria, 675, 676 hereditary nature of, 129 influence of, upon susceptibility to rubeola, 561 symptoms in relapsing fever, 383-385 complicating scarlet fever, 510 of dengue, 882 of influenza, 867 of malignant scarlet fever, 507

Nervous system, chronic diseases of, following rubeola, 574 condition of, in cholera, 741 in remittent fever, 602 lesion of, in diphtheria, 689 in septicæmia, 972

Neuralgia, following cerebro-spinal meningitis, 820 in yellow fever, 644

Neuralgias, old, aggravation of, in influenza, 870

Neurine, use of, in diphtheria, 703

Nitric acid, use of, to prevent the return of intermittent fever paroxysm, 598

Nitro-muriatic acid, use of, in anthrax, 938

Nodule, nasal, in glanders, 917

Nomenclature of pyæmia, 953 of septicæmia, 953

Nose, inflammation of, complicating variola, 445

Nostrils, condition of, in glanders in man, 921

Nourishment, necessity of, in typhus fever, 363

Nuisance, legal views as to what constitutes, 182

O.

Obesity, tendency to, following typhoid fever, 298

Obstetrical scarlatina, 498

Occupation, influence of, in causation of anthrax, 939 of glanders, 920 of influenza, 860 of typhoid fever, 244 of typhus fever, 343 relation of, to relapsing fever, 372

Odor of body, significance of, in general diagnosis, 159 of relapsing fever, 378

Oedema, 69 complicating relapsing fever, 400 scarlet fever, 529 typhoid fever, 297 from nervous influence, 71 of glottis, complicating scarlet fever, 512, 529 of lungs, Welch on cause of, 72 significance of, in general diagnosis, 159

Oesophagus, lesions of, in typhoid fever, 265

Offensive effluvia, symptoms due to, 181

Oil, inunctions of, in the plague, 784

Open wounds, liability of, to diphtheria, 679

Opisthotonos in cerebro-spinal meningitis, 809

Opium, use of, during cold stage of intermittent fever, 595 during hot stage of intermittent fever, 595 in algid form of pernicious malarial fever, 608 in cerebro-spinal meningitis, 832 in cholera, 767 in dengue, 885 in influenza, 874, 877 in puerperal fever, 1031 in relapsing fever, 429 in remittent fever, 604 in typhus fever, 366

Ophthalmia, chronic, following rubeola, 574

Optic nerve, lesions of, in cerebro-spinal meningitis, 824

Organic disease, hereditary nature of, 129

Organisms, microscopic, classification, 141 minute, convertibility, 145

Organoid tumors, 116

Origin of vaccinia, 457

Origins, specific, of the plague, 776

Ossification, 87

Otitis, chronic, following rubeola, 574 complicating scarlet fever, 520 in scarlet fever, results, 521 treatment, 547

Ovaries, lesions of, in septicæmia, 972 in pelvic peritonitis in puerperal fever, 989

Overcrowding as a cause of cholera, 721 of typhus fever, 341

Overwork as a cause of disease, 204 of the plague, 775

Ozone, use of, in diphtheria, 709

P.

Pain, in idiopathic parotitis, 623 in inflammation, 41 significance of, in general diagnosis, 165

Pains, muscular and joint, in relapsing fever, 385 of general peritonitis in puerperal fever, 1010 peritoneal, in para- and perimetritis of puerperal fever, 1007 rheumatic, in relapsing fever, 399

Palpitation of heart in beriberi, 1039

Pancreas, lesions of, in relapsing fever, 417

Pandemic nature of cerebro-spinal meningitis, 804

Panum's view of bacteria of diphtheria, 667

Papayotin, use of, in diphtheria, 703

Papule in variola, morbid anatomy, 446

Paralysis, complicating diphtheria, 676 variola, 445 diphtheritic, date of appearance, 676 seat, 676 treatment, 713 following cerebro-spinal meningitis, 819 typhoid fever, 293 in cerebro-spinal meningitis, 810 local, in relapsing fever, 398 motor, in relapsing fever, 385 muscular, in beriberi, 1039 sensory, in diphtheria, 676

Paralytic form of rabies in dogs, 896 stage of hydrophobia in man, 900

Parenchymatous inflammation, 53

Para- and perimetritis in puerperal fever, symptoms, 1005

Parametritis in puerperal fever, lesions, 987

Paresis following cerebro-spinal meningitis, 819

Parotid glands, lesions of, in idiopathic parotitis, 621 gland, lesions of, in symptomatic parotitis, 626 in pyæmia, 967 swelling, character of, in symptomatic parotitis, 627 complicating typhoid fever, 296

PAROTITIS, IDIOPATHIC, 620 Definition, 620 Nature, 620 Etiology--predisposing causes, 620 Age, influence, 620 Sex, influence, 620 Season, influence, 620 Relation to measles, diphtheria, and scarlet fever, 620 Peculiarities in mode of occurrence, 621 Anatomical appearance, 621 Changes in parotid gland, 621 Symptoms, 621 Duration of incubation stage, 621 Of invasion stage, 621 Actual attack, 621 Local, 621 Physiognomy, 622 Mouth and tongue, 622 Digestive tract, 622 Temperature and pulse, 623 Respiration, 623 Pain, 623 General, 623 Complications, 623 Metastasis, 623 Frequency, 623 Date of appearance, 623 Orchitis, 623 Symptoms, 624 Diagnosis, 624 Significance of outward displacement of lobe of ear, 624 Prognosis, 624 Result of metastatic orchitis, 624 Treatment, 624 Delirium and headache, 624 Difficult deglutition, 624 Sleeplessness, 625 Local, 625 Suppuration of gland, 625 Incomplete resolution, 625 Metastasis, 625 in females, 625 with depression, 625

PAROTITIS, SYMPTOMATIC or METASTATIC, 625 Definition, 625 Etiology, 625 Mechanical nature of exciting cause, 626 Altered blood as a cause, 626 Morbid anatomy, 626 Changes in parotid gland, 626 Suppuration of muscles of neck, 626 Changes in periosteum and cranial bones, 626 lymphatics, veins, and nerves, 626 in middle ear, 626 Thrombi of jugular veins, 626 Symptoms, 626 Characters of swelling, 627 Date of pointing of abscess, 627 Physiognomy, 627 Prognosis, 627 Of bilateral form, 627 Diagnosis--from idiopathic parotitis, 627 Treatment of, 627 Local, 628 Of incomplete resolution, 628 Of gangrene, 628

Parotitis, complicating cholera, 735 influenza, 870 relapsing fever, 404 typhus fever, 356 treatment, 367

Paroxysm of intermittent fever, 592 primary, of relapsing fever, 375, 378 of remittent fever, 599

Paroxysms of hydrophobia in man, 899 of pertussis, characters, 837 duration, 840 frequency, 840 of rabies in dogs, 896

Pasteur's experiments as to infectiveness of rabies, 892, 893 method of inoculation in anthrax, 937 for prevention of rabies and hydrophobia, 905

Pathognomonic lesions of rabies in dogs, 903

Pathology of glanders in man, 916, 918 of influenza, 871 of pyæmia, 963

Pearly distemper, relation of, to tuberculosis, 99

Pelvic abscesses in puerperal fever, treatment, 1036 cellulitis in puerperal fever, lesions, 988 exudations, treatment of, in puerperal fever, 1036 peritonitis, in puerperal fever, lesions, 988

Peppermint-test for defects in plumbing, 190

Pepsin, use of, in diphtheria, 703

Perforation, intestinal, in typhoid fever, 289, 290 in typhoid fever, treatment, 333

Pericarditis in relapsing fever, 402 complicating influenza, 870

Pericardium, lesions of, in cholera, 747 in pyæmia, 968

Peri-glandular lesions in the plague, 782

Periostitis, complicating typhoid fever, 297

Peritoneal effusions, encysted, in puerperal fever, treatment, 1036

Peritoneum, lesions of, in relapsing fever, 417

Peritonitis, complicating relapsing fever, 406 typhoid fever, 295 general, in puerperal fever lesions, 989 in puerperal fever, symptoms, 1010 pelvic and diffused, of puerperal fever, 988

Pernicious malarial fever, 605

Perspiration in pyæmia, 974 in yellow fever, 645

PERTUSSIS, 836 History, 836 Definition, 836 Etiology, 838 Specific poison, 838 seat, 838 period of greatest virulence, 838 inoculation of animals with, 839 Childhood, influence of, in occurrence, 839 Age at which most prevalent, 839 Sex, influence of, in causation, 839 Catarrhal affections as predisposing causes, 839 Symptoms, 840, 841 Initial stage, 840 Second stage, 840 Stage of decline, 841 Paroxysm, characters of, 837 duration, 840 frequency, 840 Frænum linguæ, ulceration, 841 Urine, condition, 841 Mortality, 841 Morbid anatomy, 843 Complications, 843 Prophylaxis, 843 Treatment, 844 Inhalations, 844 Emetics, 845 Potassium carbonate, 845 Alum, 845 Belladonna, 846 Ammonium bromide, 846 Chloral hydrate, 846 Quinia, 847 Pilocarpine muriate, 847 Sodium benzoate, 847 Caustic irritation, 848 Diet, 848 Hygiene, 848

Pertussis, following the plague, 781

Petechiæ, characters of, in grave form of the plague, 779

Petrifaction, 87

Peyer's patches, lesions of, in typhoid fever, 261

Pharyngeal spasm in rabies and hydrophobia, 899

Pharyngitis in scarlet fever, treatment, 545 and tonsillitis, complicating relapsing fever, 405

Pharynx, lesions of, in rabies and hydrophobia, 902 in relapsing fever, 413 in typhoid fever, 265

Phlebitis and phlebo-thrombosis, lesions of, in puerperal fever, 989

Phlegmonous inflammation, 52

Phthisis, complicating influenza, 870 following typhus fever, 355 from damp soil, 187 pulmonary, hereditary nature of, 128

Physicians as carriers of contagion in puerperal fever, 1017 mortality in, 207 relation of, to public hygiene, 207

Physiognomy of cerebro-spinal meningitis, 812 of dengue, 881 of erysipelas, 632 of hydrophobia, 899 of idiopathic parotitis, 622 of influenza, 866 of symptomatic parotitis, 627 of relapsing fever, 376 of typhoid fever, 272 of yellow fever, 644 significance of, in general diagnosis, 150, 151

Pigmentation, 90

Pilocarpine, use of, in diphtheria, 704 in rabies and hydrophobia, 907 muriate, use of, in pertussis, 847

Pitting, frequency of, in varicella, 482 prevention of, in variola, 452

Placenta, symptoms of diphtheria, 674

PLAGUE, THE, 771 Definition, 771 Synonyms, 771 Classification, 771 History, 772 Etiology--Predisposing causes of, 774 Poverty and filth, 774 Bodily and mental overwork, 775 Sex and age, influence, 775 Season, 775 Exciting causes, 775 Dissemination by bodies dead from, 775 Specific origin, 776 Contagiousness, 776 Nature of the poison, 776 Air as a medium of transmission, 776 Period of incubation, 777 Forms of, 777 Grave or ordinary form, 777 Fulminant form, 779 Abortive form, 780 Symptoms, 777 Grave form, different modes of onset, 779 Invasion stage, 777 Second stage, or stage of fever, 778 Stage of fully-developed local manifestations, 778 Seat of enlarged lymphatics, 778 of buboes, 778 Characters of bubonic swellings, 778 Date of appearance of buboes, 778 Seat and character of carbuncles, 778 of petechiæ, 779 Character of vomited matter, 779 Constipation, 779 Condition of urine, 779 Stage of convalescence, 779 Fulminant form, 779 duration, 779 Abortive form, 780 General duration of, 780 Complications and sequelæ, 780 Followed by catarrhal pneumonia, 781 Pertussis, 781 Mental troubles, 781 Ulcers and abscesses, 781 Morbid anatomy, 781 Changes in lymphatic system, 781 Appearance of buboes, 781 Peri-glandular tissue, 782 Abdominal viscera, 781 Diagnosis, 782 Prognosis, 780 Mortality, 780 Treatment, 782 Preventive, 782 Isolation, 783 Quarantine, 783 Disinfection, 784 Clinical, 784 Inunction of oil, 784 Buboes, 784 Drugs used, 784

Pleura, lesions of, in pyæmia, 968 in relapsing fever, 413 in septicæmia, 972

Pleurisy, complicating typhoid fever, 294 typhus fever, 355 in septicæmia lymphatica of puerperal fever, 1012

Pleuritis, complicating erysipelas, 634 influenza, 870 relapsing fever, 404 scarlet fever, 523 in scarlet fever, treatment, 556

Plumbing, examination of defects, 190 of houses, 188

Pneumonia, catarrhal, complicating influenza, 869 following the plague, 781 complicating erysipelas, 634 relapsing fever, 404 rubeola, 571 typhoid fever, 294 typhus fever, 355 fibrinous, complicating diphtheria, 672 in rubeola, treatment, 581 in typhoid fever, treatment, 335 lobar, complicating influenza, 869

Pneumonias, nature of, complicating influenza, 870

Pock of vaccinia, date of appearance, 459 depression, 459 desquamation, 460 development, 459 incrustation, 460 in variola, characters of mature, 439

Poison, diphtheritic, fixity, 678 transmission, 678 influence of intensity of, on severity of cholera, 730, 731 of anthrax, modes of transmission, 929 of cholera, nature, 749 of malaria, nature, 589, 591 of the plague, nature, 776 of yellow fever, birthplace, 641 characteristics, 641 influence of heat and cold on development, 641 transportability, 641 specific, of beriberi, 1038 of pertussis, 838

Polluted soil as a means of disseminating typhoid fever, 253

Potassium bromide, use of, in cerebro-spinal meningitis, 834 carbonate, use of, in pertussis, 845 chlorate, danger of large doses, 701 use of, in diphtheria, 699, 700 iodide, use of, in cerebro-spinal meningitis, 834

Poverty as a cause of typhus fever, 342

Predisposing causes of beriberi, 1042 of cholera, 720 of glanders in horse, 912 of idiopathic parotitis, 620 of the plague, 774 of typhoid fever, 242 of typhus fever, 341

Predisposition to disease, hereditary nature, 126

Predispositions, inherited, evidence, 132

Pregnancy, complicating influenza, 871 typhoid fever, 296

Preliminary papule of anthrax, treatment, 943

Premonitory symptoms of rabies and hydrophobia, 895 of scarlet fever, 502

Prevention of anthrax by inoculation, 937

Preventive treatment of anthrax in animals, 936 in man, 943 of cholera, 755 of erysipelas, 636 of glanders in horses, 919 in man, 925 of influenza, 873 of the plague, 782 of puerperal fever, 1021 of pyæmia and septicæmia, 979, 980, 983 of rabies and hydrophobia, 903 of scarlet fever, 536 of typhoid fever, 321 of typhus fever, 361

Previous attacks of variola, protection from, 436

Primary vaccine, 473

Privy vaults, contamination of water-supply by, 192 dangers from, 192

PROCESSES, GENERAL MORBID, 35

Prodromal stage of diphtheria, 667 of intermittent fever, 592 of leprosy, 789 of remittent fever, 599 of rötheln, 585 of rubeola, 564 of varicella, 482

Prognosis, general, 167 of anthrax in animals, 936 in man, 943 of beriberi, 1042 of cerebro-spinal meningitis, 828 of cholera, 753 of dengue, 885 of diphtheria, 692-694 of erysipelas, 636 of idiopathic parotitis, 624 of influenza, 872 of intermittent fever, 594 of glanders in horse, 918 in man, 924 of leprosy, 793 of the plague, 782 of relapsing fever, 422-425 of remittent fever, 602 of rötheln, 588 of scarlet fever, 533 of simple continued fever, 235 of symptomatic parotitis, 627 of typho-malarial fever, 616 of typhoid fever, 314-316 of typhus fever, 359, 360 of vaccinia, 464 of varicella, 484 of variola, 450 of varioloid, 444 in yellow fever, 646, 647 effect of constitution, 168 of nature of malady, 169 of present state of patient, 169 influence of nursing, 169 modifying effects of medicinal agents, 169

Prophylactic treatment of diphtheria, 696

Prophylaxis, individual, in contagious diseases, 206 of leprosy, 794 of pertussis, 843 of puerperal fever, 1021

Prostration in dengue, 882 in typhus fever, 348 treatment, 365

Protective power of vaccination, 466 duration of, 468 against pertussis, 468

Pseudo-membrane, solvents of, 703

Psoas abscess in puerperal fever, 1010

Psychical treatment of hydrophobia, 906

Public sewers, 224

PUERPERAL FEVER, 984 Definition, 984 Frequency, 984 Etiology, 1013 Atmosphere, impure, influence on causation, 1013, 1014 Malaria, nosocomial, influence on causation, 1013 Micro-organisms, influence on causation, 1013-1015 Lochial discharge, influence on causation, 1015 Atmosphere, peculiar states of, on causation, 1016 Direct inoculation, 1016 Contagiousness of, 1017 Contagion, physicians as carriers of, 1017 Dissecting poison, 1018 Self-inoculation, 1019 Morbid anatomy, 985 Spiegelberg's classification of puerperal inflammations, 986 Endocolpitis and endometritis, 986 Diphtheritic ulceration, 986 Metritis and parametritis, 987 Diphtheritic endometritis, 987 Pelvic cellulitis, 988 Cellulitis from specific infection, 988 Peritonitis, pelvic and diffused, 988 exudation in, 989 general, 989 appearance of abdominal cavity, 989 ovaries, 989 Phlebitis and phlebo-thrombosis, 989 Thrombi in uterine and pelvic veins, 989 Abscesses, 989 pulmonary, 989 Veins, inflammation, 989 Thrombi, growth, 990 Septicæmia, 990 Abscesses, metastatic, 990 Endocarditis, ulcerative, 990 Pleuritis, 990 Joints, purulent inflammation, 990 Earlier views concerning nature, 990 Modern view concerning nature, 992 Septic origin, 993-1003 Bacteria, relation to causation, 994 Koch's investigations of, 997 physical characters, 999 modes of entering the circulation, 1000 action of, upon the blood, 1000 Diphtheria of genitalia, characters, 1002 Relation of, to erysipelas, 1002 Inflammatory affections of non-specific origin, 1003 Symptoms, general, 1004 Incubation period, 1004 Chill, significance of, 1005 Of endometritis and endocolpitis, 1005 temperature, 1005 Parametritis and perimetritis, 1005 Incubation, 1006 Temperature, 1006 Pulse, 1006 Relapse, 1006 Headache, 1007 Pains, 1007 Vomiting, 1007 Duration, 1007 Exudation, 1007 Uterus fixity of, 1007 Tumors in iliac fossa, 1008 Abscesses, 1008 location, 1008 pointing of, 1008 Local peritonitis, 1009 Of psoas abscess, 1010 Of peritonitis, general, 1010 Pains, 1010 Abdomen, state, 1010 Respiration, 1010 Vomiting, 1010 Vomit, characters, 1010 Fever, 1010 Skin, 1010 Pulse, 1010 Pyæmic form, 1011 Of septicæmia lymphatica, 1011 Mode of onset, 1011 Temperature in, 1011 Abdomen, state, 1011 Skin, state, 1011 Vomiting, 1011 Tongue, condition, 1011 Pulse, condition, 1011 Respiration, 1012 Pleurisy in, 1012 Endocarditis, 1012 Mental condition, 1012 Joint affections in, 1012 Duration, 1012 Of septicæmia venosa, 1012 Chills in, 1012 Fever in, 1012 Temperature in, 1012 Pulse in, 1012 Abdomen, state of, 1012 Uterus in, 1012 Of pure septicæmia, 1013 Mortality, 1020 Relation of, to zymotic diseases, 1020 Prophylaxis, 1021 Maternity hospitals, advantages, 1021 Necessity of light and air, 1024 Antisepsis, value, 1024 methods, 1025 Sulphurous acid, use, 1025 Corrosive sublimate, use, 1025 Iodoform, use of, intra-uterine, 1025 Vaginal injections, carbolized, use, 1025 Tarnier's maternity pavilions for prevention, 1027 Treatment--indications, 1028 Disinfection, 1028 Local, 1028 Use of hydrochloric acid, 1028 Persulphate of iron, 1028 Intra-uterine injections, use, 1029 dangers of, 1029 methods, 1029 Corrosive sublimate, use, 1025, 1029 Pain, peritoneal, 1031 Use of opium, 1031 in pyæmic variety, 1031 Leeches, 1031 Turpentine stupes, 1032 Hyperpyrexia, 1032 Use of purgatives, 1032 Quinia, 1032 Sodium salicylate, 1032 Veratrum viride, 1033 Digitalis, 1033 Alcohol, 1033 Cold in, 1033 Cold, method of applying, 1034 Cold water, intra-uterine injections, 1034 Baths, cold, use, 1034 Kibbie's fever-cot, use, 1034, 1035 Coil, 1036 Diet, 1036 Encysted peritoneal effusions, 1036 Quinia, use, 1036 Pelvic exudations, 1036 Pelvic abscesses, 1036

Puerperal septicæmia, relations of, to obstetrical scarlatina, 499 women, general sepsis from diphtheria in, 674 symptoms of diphtheria in, 674

Pulmonary abscess in puerperal fever, 989 collapse, complicating influenza, 869 complications of typhus fever, treatment, 367 oedema, complicating rubeola, 572

Pulsation of jugular veins, significance of, in general diagnosis, 156

Pulse and temperature, relation of, in yellow fever, 644 average frequency in health and disease, 154 characters of, in erysipelas, 633 in idiopathic parotitis, 623 in general peritonitis of puerperal fever, 1010 in septicæmia, 977

Pulse, characters of, in septicæmia lymphatica of puerperal fever, 1011 venosa of puerperal fever, 1012 condition of, in acute glanders in man, 921 in beriberi, 1040 in cerebro-spinal meningitis, 815 in cholera, 737 in dengue, 881 in influenza, 866 in pyæmia, 975 in relapsing fever, 382 in typhus fever, 351 significance of, in general diagnosis, 152 in malignant scarlet fever, 507 in typhoid fever, 275 kinds of, 154 methods of examining, 153 relation to respiration, 154 temperature, relation of, in relapsing fever, 382

Pupil, significance of state of, in general diagnosis, 151

Pupils, condition of, in cerebro-spinal meningitis, 810

Pure septicæmia of puerperal fever, 1013

Purgatives, use of, during hot stage of intermittent fever, 596 in cerebro-spinal meningitis, 830 in hemorrhagic form of pernicious malarial fever, 613 in puerperal fever, 1032 in remittent fever, 604

Purity of water, standards of, 184

Purpura, complicating diphtheria, 674

Pus, 48 influence of, in production of pyæmia, 955 in stools, significance in diagnosis, 164

Pustule, malignant, 926

Putrefaction of cadaver, rapidity of, in puerperal fever, 971

Putrified flesh as a means of disseminating typhoid fever, 257

PYÆMIA AND SEPTICÆMIA, 945-955 History, 945-952 Nomenclature, 952 Pyæmia, 953 Definition, 953 Septicæmia, 953 Definition, 954 Etiology of pyæmia, 955 Theories concerning, 955 Pus, influence of, in production, 955 Character of production, 956 Thrombosis, relation of, to causation, 957, 958 Contamination of blood, influence of, in causation, 958 sources, 958 Germs, disease-, influence of, in causation, 958 Wounds, characters of, influence on causation, 958 Etiology of spontaneous pyæmia, 959 Wounds of alimentary canal and genito-urinary apparatus as cause, 959 Air, vitiated, influence of, on causation, 959 Spontaneous origin, 959 Contagiousness, 960 Chemical origin, 960 Living organisms, influence of, on causation, 958-960 Etiology of septicæmia, 960 Septic intoxication, relation of, to, 961 Traumatic fever, relation of, to, 962 Dissecting wounds, relation of, to causation, 962 Putrid substances, maximum toxic action of, on the body, 962 Lymphatics as channel of entrance of poison, 963 Etiology of septo-pyæmia, 963 Pathology, 963 Condition of blood, 963 in pyæmia simplex, 963 multiplex, 963 Metastasis, conditions, 964 Pus, mode of entering the circulation, 964 Metastatic abscesses, production, 964 from primary infection, 964 from secondary infection, 964 Emboli, action of, in production of metastatic abscesses, 964 Thrombi, action of, in production of metastatic abscesses, 965 Seat of pathological changes, 965 Fat emboli, influence of, in production, 966 Morbid anatomy, 966 Of pyæmia, 966 Appearance of body, 966 Rigor mortis, 966 Lesions of cellular tissue, 966 Muscles, 966 Brain and membrane, 966 Retina and choroid, 967 Cornea, 967 Ear, 967 Bones, 967 Joints, 967 Parotid gland, 967 Arteries and veins, 967 Blood, 968 Pericardium, 968 Pleuræ, 968 Lungs, 968 Liver, 969 Spleen, 969 Kidneys, 969 Micro-organism in blood, changes effected by, 970 Pyæmia simplex, 970 Absence of abscesses in, 970 Septicæmia, 971 Putrefaction of bodies, rapidity of, 971 Blood, lesions of, 971 Sepsin, nature, 971 Lesions, nervous system, 972 Endo- and pericardium, 972 Lungs, 972 Pleuræ, 972 Kidneys, 972 Spleen, 972 Uterus, 972 Ovaries, 972 Bladder, 972 Of septo-pyæmia, 972 Symptoms, 972 Of pyæmia, 972 Prodromal stage, 973 Chills, date of appearance, 973 frequency, 973 Temperature, 974 Perspiration, 974 Eruptions, 974 Pulse, 975 Tongue, condition of, 975 Vomiting, 975 Singultus, 975 Diarrhoea, 975 Stools, character of, 976 Heart, condition of, 976 Lungs, condition of, 976 Liver and spleen, enlargement, 976 Urine, 976 Joints, suppuration, 976 Abscesses, frequency, 976 Delirium, 976 Breath, odor of, 976 Wound, changes, 976 Of septicæmia, 976 General, 976 Wound, condition of, 977 Temperature, 977 Abdomen, state of, 977 Pulse, 977 Diarrhoea, 977 Vomiting, 977 Tongue, 977 Singultus, 977 Bronchitis in, 977 Of gangrene foudroyante, 977 Skin, condition, 977 Diagnosis, 978 Of pyæmia from septicæmia, table showing, 978, 979 Treatment, 979 In fully-developed cases unsuccessful, 980 Preventive, 979, 980 Cleanliness, necessity of, in prevention, 980 Atmosphere, pure, necessity of, in prevention, 980 Food and drink, proper, necessity of, in prevention, 980 Cheerful and pleasant surroundings, in prevention, 980 Antiseptics, use of, 980 Local, 981 Of wound, 981 Metastatic abscesses, 981 Constitutional, 982 Sulphites of magnesium, sodium, potassium, and lime, use of, 982 Use of alcohol, 982 Quinia, 982 Ergotine, 982 Diet, 982 Stimulants, 982 Of septicæmia, 982 Indications for, 982 Local, 983 Preventive, 983 Of wound, 983 Diarrhoea, 983 Antisepsis, 983 Sulphites and hyposulphites, use of, 983 Quinia, use of, 983 Of puerperal septicæmia, 983 complicating erysipelas, 634 typhoid fever, 295 typhus fever, 356

Pyæmic form of general peritonitis of puerperal fever, 1010

Q.

Quarantine in cholera, 204, 755 in leprosy, 794 in the plague, 783

Quinia, use of, in cerebro-spinal meningitis, 833 in dengue, 885 in diphtheria, 708, 712 in erysipelas, 637 in influenza, 874-876 during cold stage of intermittent fever, 595 hot stage of intermittent fever, 596 sweating stage of intermittent fever, 597 to prevent the return of intermittent fever, paroxysm, 598 in hemorrhagic form of pernicious malarial fever, 612 in pertussis, 847 in puerperal fever, 1032, 1036 in pyæmia, 982 in relapsing fever, 426 in remittent fever, 603 in rubeola, 580 in scarlet fever, 543 in septicæmia, 983 in typhoid fever, 330 in typho-malarial fever, 618 in typhus fever, 365 in yellow fever, 651 and opium, use of, in yellow fever, 651

R.

RABIES AND HYDROPHOBIA, 886 Synonyms, 886 Definition, 886 History, 886 Geographical distribution, 886 Etiology, 887 Climate, relation of, to causation, 887 Season, relation of, to causation, 887 Summer heats, relation of, to causation, 887 Hunger and thirst, relation of, to causation, 888 Improper food, relation of, to causation 888 Sex, relation of, to causation, 888 Liability of special breeds, 889 From skunk-bite, 889 Spontaneous origin, 890 Contagion, 891 Modes of dissemination, 891 Milk, propagation by, 891 Saliva, propagation by, 891 Specific germ, 892 Pasteur's experiments as to infectiousness, 892 Point of election of germ, 892 Antagonism between blood and germ, 892, 893 Localization of the virus in the wound, 893 Relation of successful inoculation to bites, 893 Insusceptibility to, 894 Incubation, 894 Duration of, in lower animals, 894 in man, 894 Condition of cicatrix during, 895 Symptoms, 895 In dogs, 895 Importance of recognizing premonitory, 895 Of prodromal stage, 895 Of furious form, 896 During paroxysms, 896 Between paroxysms, 896 Of paralytic form, 896, 897 Of lethargic form, 897 Popular fallacies regarding, 897 In horse and other animals, 897 In man, 898 Symptoms, 898 Prodromal stage, 898 Appearance of wound, 898, 899 Of paroxysms, 899 Duration, 899 Reflex irritability during, 899 Facies during, 899 Mental condition, 900 Delirium during, 900 Relative severity in men and women, 900 Paralytic stage, 900 duration, 900 Without paroxysms, 900 Diagnosis, 900 Pathognomonic features in, 900 From tetanus, 900 From diphtheria, 900 From pharyngeal anthrax, 900 From acute mania, 900 From epilepsy, 901 From hysteria, 901 From pseudo-hydrophobia, 901 Inoculation in doubtful cases, 902 Morbid anatomy, 902 Post-mortem appearance of body, 902 Changes in mucous membranes, 902 Bronchi and pharynx, 902 Lungs, 902 Heart and blood-vessels, 902 Gastro-intestinal tract, 902 Liver and spleen, 902 Kidneys, 902 Bladder, 902 Brain and spinal cord, 902 Pathognomonic changes in dogs, 903 Treatment, 903 Preventive, 903 Registration of dogs, 904 Modes of preventing diffusion, 904 Inoculation, 904 Pasteur's method, 905 Of bites, 905 Use of caustics, 905 Excision of cicatrix, 906, 908 Futility of eliminating measures, 906 Hygienic, 906 Psychical, importance of, 906 Therapeutic, 907 Use of chloroform, 907 Chloral, 907 Pilocarpine, 907 Curare, 907 Morphia, 907 Atropia and daturia, 907 Vaccine virus, 907 Warm baths, 907 Faradization, 907 Inhalation of oxygen, 907 Importance of rest and quiet, 907 Intravenous injections, 908 Venesection, 908

Race, influence of, in causation of variola, 436 protection as a preventive of small-pox, 130 relation of, as causation of rubeola, 561

Rachialgia in cerebro-spinal meningitis, 808

Rash of variola, date of appearance of, 437 significance of, 437 variolous, 437

Raspberry excrescence in vaccinia, 461

Reaction in cholera, 734 treatment, 763

Reflex irritability in hydrophobia, 899 symptoms in diphtheria, treatment, 694

Registration of dogs for prevention of rabies, 904

Relapse, in relapsing fever, 381

Relapses, cause of, in typhoid fever, 309 duration of, in typhoid fever, 304 frequency of, in typhoid fever, 302 in cerebro-spinal meningitis, 820 of diphtheria, prognosis of, 694 in rubeola, 563

RELAPSING FEVER, 369 Definition, 369 Synonyms, 369 History and geographical distribution, 369 Etiology, 370 Destitution and filth as causes, 370 Intemperance as a cause, 370 Starvation and over-crowding as a cause, 371 Age, relation of, to causation, 371 Sex, relation of, to causation, 371 Nationality, relation of, to causation, 371 Season, relation of, to causation, 371 Occupation, relation of, to causation, 372 Specific origin, 370, 372 Contagious nature, 372 Transmission of contagion, 373 Area of contagious atmosphere, 373 Spirillum, 373 Mode of detecting, 373 Inoculation, 374 Incubation period, 376 General clinical description, 374 Invasion, 376 Special symptoms, 376 Odor, 378 Physiognomy, 376 Bronzing of face, 376 Eruptions, 377 Hepatic eruptions, 377 Sudamina, 377 Desquamation, 377 Primary paroxysms, duration, 378 Temperature, 378 at crisis, 378 peculiarities, 382 Relapse, 381 Duration, 381 Absence, 380 Frequency, 382 Later relapses, 381 Cases illustrating frequency of relapses, 394 Average duration of paroxysms, 381 Intermission, duration, 381 Pulse, 382 Relation of pulse to temperature, 382 Character of pulse during paroxysm, 383 Pulse at crisis, 382 During intermission, 383 Character of heart-sounds, 383 Convulsions, 384 Mental condition, 384 Headache, 383 Wakefulness, 384 Vertigo, 384 Delirium, 384 General tremor, 384 Muscular rigidity, 384 Muscular and joint pains, 385 Cause of muscular and joint pains, 385 Seat of muscular and joint pains, 385 Motor paralysis, 385 Debility, 386 Perversion of special senses, 386 Respiration, 386 Relation of respiration, temperature, and pulse, 386 Bronchitis and pneumonia, 387 Condition of urine, 387 Urine of paroxysm, 388 of intermission, 388 Thirst, 389 Anorexia, 389 Condition of tongue, 389 Nausea and vomiting, 390 Hæmatemesis, 390 Condition of bowels, 390 of abdomen, 390 Spleen, enlargement, 391 Liver, enlargement, 391 Jaundice, significance of, 391 Epistaxis, 393 Hemorrhages, 393 Convalescence, 393 Varieties, 395 Grave form, 395 Multiple or protracted form, 395 Abortive form, 395 Case illustrating subintrant form, 396 Complications, 396 Peculiarities of temperature, 397 Mental hebetude, 398 Local palsies, 398 Severe rheumatic pains, 399 Disorders of vision, 399 Ophthalmia, 399 Disorders of hearing, 400 Otorrhoea, 400 Swellings and effusions of joints, 400 Bed-sores, 400 Gangrene, 400 Abscesses, 400 Anæmia, 400 Oedema, 400 Sudden collapse and syncope, 401 Hemorrhages from mucous surfaces, 401 Pericarditis, 402 Heart-clot, 402 Thrombosis and embolism, 402 Laryngitis, 403 Bronchitis, 403 Splenic enlargement, 403 Rupture of spleen, 403 Parotitis, 404 Pleurisy, 404 Pneumonia, 404 Pulmonary gangrene, 404 Metastatic abscesses of lungs, 404 Pharyngitis and tonsillitis, 405 Hiccough, 405 Diarrhoea, 405 Dysentery, 406 stools, 406 Suppuration of mesenteric glands, 406 General and local peritonitis, 406 Emaciation, 407 Renal disorders, 408 Albuminuria, 407 Suppression of urine, 407 Incontinence of urine, 407 Hæmaturia, 409 Glycosuria, 410 Metastatic inflammation of kidneys, 410 Disorders of menstruation, 410 Pregnancy, 410 Sequelæ, 398 Local palsies, 398 Acute miliary tuberculosis, 404 Dyspepsia, 406 Anæmia, 400 Morbid anatomy, 410 Post-mortem appearance of body, 410 Changes in voluntary muscles, 410 Blood, 411 Granule-cells of blood, 412 Changes in pericardium, 411 Heat, 411 Gastro-intestinal canal, 412 Solitary and agminated glands, 413 Mesenteric glands, 413 Larynx and pharynx, 413 Pleura, 413 Lungs, 413 Brain and membranes, 413 Liver, 414 Bile-ducts and gall-bladder, 415 Spleen and capsule, 416 Pancreas, 417 Peritoneum, 417 Kidneys, 414 Bladder, 414 Lymphatic glands, 417 Marrow of bones, 417 Diagnosis, 418 Presence of spirillum as a means, 418 From typhus fever, 418 From typhoid fever, 419 Grave form of, from typhoid fever, 420 From bilious remittent fever, 420 Yellow fever, 420 Small-pox, 421 Acute gastro-hepatic catarrh, 421 Simple febricula, 421 Rheumatic fever, 421 Acute yellow atrophy of liver, 422 Parotitis, 422 Cerebral diseases, 422 Prognosis, 422 Symptoms indicating unfavorable, 424 Influence of variations of temperature, 424 Cerebral symptoms, 424 Character of eruption, 425 Hiccough upon, 425 Epistaxis, 425 Cough upon, 425 Heart complications on, 425 Hepatic enlargement upon, 425 Splenic enlargement upon, 425 Jaundice upon, 425 Albuminuria, 425 Mortality--bilious typhoid form, 422 Influence of type of disease, 423 Stage of disease, 423 Season, 423 Habits and previous health, 424 Sex, 424 Age, 424 Race, 424 Cause of death in, 426 Treatment--indications for treatment in regular cases, 426 Hyperpyrexia, 426 Cause of failure of antipyretics, 429 Insomnia, 429 Headache, 429 Nausea and vomiting, 430 Constipation, 430 Jaundice, 431 Muscular tremor, 432 soreness and pains, 432 At critical fall of temperature, 432 Renal complications, 432 Epistaxis, 432 Collapse, 433 Necessity of absolute rest in, 432 Résumé of treatment, 432 Diet, 430 Special remedies, 431 Use of antiperiodics, 428 Arsenic, 427 Atropia, 429 Bromide and chloral, 430 Blisters, 431 Chloroform, 431 Cold baths, 428 Digitalis and other antipyretics, 428 Hyposulphite of sodium, 428 Opium, 429 Quinia, 426 Salicylic acid and salicylates, 428 Simple febrifuges, 428 Stimulants, 430 Venesection, 431

REMITTENT FEVER, 598 Definition, 598 Malarial nature, 598 Etiology, 598, 599 Relation of, to intermittent fever, 599 Symptoms, 599 Prodromal stage, 599 Paroxysm, 599 Temperature, 599 Epistaxis, 602 State of tongue, 600 Stomach, 602 Bowels, 602 Urine, 602 Jaundice, 600 cause, 600 Nervous symptoms, 602 Physiognomy, 600 Pulse in, 602 Duration of, 602 Diagnosis, 600 From intermittent fever, 600 From typhoid fever, 600 From yellow fever, 600 Prognosis, 602 Mortality, 599 Morbid anatomy, 602 Changes in skin, 603 Liver, 602 Spleen, 602 Treatment, 603 Main indications, 603 Use of quinia, 603 Amount of quinia, 603 Causes of failure of quinia, 604 Adjuvants to quinia, 604 Use of depuratives, 604 Purgatives, 604 Opium, 604 Of hemorrhage, 605 Of tympanites, 605 Of vomiting, 605

Renal disease, complicating relapsing fever, 408 scarlet fever, 525

Residence, change of, in treatment of beriberi, 1042

Resolution, incomplete, in idiopathic parotitis, treatment, 625 of symptomatic parotitis, treatment, 628 of erysipelas, 633 of inflammation, 54

Respiration in cerebro-spinal meningitis, 814 characters of, in idiopathic parotitis, 623 in general peritonitis of puerperal fever, 1010 in mild scarlet fever, 504 in relapsing fever, 386 in septicæmia lymphatica, 1012 in typhoid fever, 276 in typhus fever, 352 in croup, 157 in disease, 156 kinds of, 156 significance of, in general diagnosis, 156

Respiratory diseases, relation of, to rubeola, 561 organs, lesions of, in typhus fever, 356 spread of diphtheria into, 671 tract, alterations of, in scarlet fever, 531

Rest, necessity of, in cholera, 760 in rabies and hydrophobia, 907 in relapsing fever, 432 in yellow fever, 654

Retention-cysts, 116, 122

Retro-vaccine, 473

Re-vaccination, time of, 467

Rheumatic and cardiac inflammation in scarlet fever, treatment, 556

Rheumatism, complicating scarlet fever, 521

Rickets, hereditary nature, 128

Rigidity, muscular, in relapsing fever, 384

Rindfleisch's definition of diphtheritic inflammation, 686

RÖTHELN, 582 Definition, 582 Synonyms, 582 History, 582 Etiology, 583 Age as a cause, 583 Sex as a cause, 583 Specific origin, 583 Nature of contagion, 583 Modes of transmission, 583 Period of greatest contagiousness, 583 Distinct nature, 584 Frequency of second attacks, 584 Relapses, 584 Symptoms, 585 Incubation period, 583, 585 Duration of incubation period, 583 Prodromal stage, 585 Eruption, 585 Duration of eruption, 585 Characters of eruption, 586 Types of eruption, 586 Condition of mucous membranes, 586 Swelling of lymphatic glands, 586 Temperature, 587 Complications and sequelæ, 587 Diagnosis, 587 From measles, 587 From scarlet fever, 587 From symptomatic skin eruptions, 588 Prognosis of, 588 Treatment of, 588

RUBEOLA, 557 Definition, 557 Synonyms, 557 History, 557 Etiology, 557 Nature of contagion, 558 Relation of straw fungus, 558 Mode of entrance into body, 558 Modes of dissemination of contagion, 559 Inoculation, 559 Stage when most easily propagated, 560 Race, influence of, 561 Age, influence of, 561 Sex, influence of, 562 Climate as a cause, 560 Pregnancy and parturition as a cause, 561 Scrofula as a cause, 561 Diseases of respiratory organs as a cause, 561 Relation of, to acute diseases, 561 to chronic diseases, 561 to whooping cough, 561 Influence of nervous diseases upon susceptibility, 561 Frequency of epidemics, 560 in new-born, 562 second attacks, 563 Relapses in, 563 Symptoms, 563 Incubation stage, 563 Duration of incubation stage, 560 Prodromal stage, 564 Temperature, 564 Catarrhal symptoms, 564 Punctated appearance of palatal and faucial mucous membrane, 564 Convulsions, 565 Duration of, 565 Eruptive stage, 565 Temperature of, 566 Character and seat of eruption, 566 General symptoms, 567 Symptoms at decline, 567 Temperature at decline, 567 Duration of eruptive stage, 567 Varieties of, 568 Inflammatory or synochal, 568 Hemorrhagic (rubeola nigra), 569 Without eruption, 568 catarrh, 568 Deviations from ordinary course, 569 Peculiarities in seat of eruption, 569 in character of eruption, 569 Relapses of eruption, 570 Complications, 570 Causes, 570 Complicated with epistaxis, 570 Skin disorders, 570 Pemphigoid eruptions, 571 Ear diseases, 570 Eye diseases, 571 Faucial inflammation, 571 Laryngitis, 571 Bronchitis and capillary bronchitis, 571 Pneumonia, 571 Pulmonary oedema, 572 Acute miliary tuberculosis, 572 Heart-clot, 572 Intestinal catarrh, 572 Convulsions, 572 Diphtheria, 573 Sequelæ, 573 Followed by general miliary tuberculosis, 574 Chronic pulmonary tuberculosis, 573 Coryza, 574 Ophthalmia, 574 Otitis, 574 Intestinal catarrh, 574 Cutaneous diseases, 574 Bone and joint disease, 574 Nervous affections, 574 Granular meningitis, 574 Albuminuria, 574 Gangrenous affections, 574 Morbid anatomy, 575 Changes in skin, 575 Diagnosis, 575 Value of punctated appearance of palatal and faucial mucous membranes, 575 Salient points in diagnosis, 575 From rötheln, 576 Scarlet fever, 576 Variola, 576 Roseola and erythema, 577 Typhus, 577 Roseola syphilitica, 577 Prognosis, 577 Factors to be considered in making, 577 Influence of hygienic surroundings, 577 previous health, 578 complications, 578 Mortality, 578 Influence of stage of disease, 578 of age, 578 Treatment, 578 Preventive, 578 Isolation, 578 Hygienic, 579 Diet, 579 Uncomplicated cases, 579 Results, 579 Hyperpyrexia, 580 Retrocession of eruption, 580 Epistaxis, 580 Diarrhoea, 581 Nausea and vomiting, 581 Constipation, 581 Cough, 581 Eye complications, 581 Aural complications, 581 Bronchitis and pneumonia, 581 Convulsions, 581 Use of aconite, 580 Inunctions, 580 Quinia, 580 Stimulants, 580

S.

Salicylic acid, use of, in diphtheria, 707 in relapsing fever, 428

Saliva, propagation of rabies and hydrophobia by, 891

Salivary glands, lesions of, in typhoid fever, 268

Sanitary inspection of houses, 187

Sarcoma, 118

SCARLET FEVER, 486 History, 486 Etiology--Specific origin, 487 Germ theory, 488 Microbes, 488 Modes of cultivation of microbes, 488 Modes of entering the system, 490 Modes of communication, 490 Dissemination of, by milk, 491 Fixity of the poison, 491 Solid nature of the poison, 492 Duration of incubation, 492, 493 Contagiousness, 494 Area of contagiousness, 494 Age, influence of, in causation, 500 Variations in type, 494 Surgical, 495 distinguished from septicæmic efflorescence, 497 effect of poison upon inflammation of wounds, 498 Obstetrical, 498 liability of parturient women to, 498 relation of, to puerperal septicæmia, 499 Immunity of infants, 500 Clinical facts regarding, 501 Relapses in, 501 Frequency of second attacks, 501 Sympathetic sore throat in, 502 albuminuria in, 502 Symptoms, 502 Ordinary form, 502 Premonitory, 502 Nervous system, 503 Vomiting in, significance, 503 Diarrhoea, 503 Condition of tongue, 504 of faucial and nasal membranes, 504 Respiratory, 504 Efflorescence, 504 Seat of greatest intensity of eruption, 504 Cause of absence of eruption, 505 Date of desquamation, 506 Temperature, 505 Digestive system, 505 Urine, characters, 505 Duration, 506 Malignant or grave form, 507 Digestive system, 507 Pulse, 507 Eruption, 507 Temperature, 507 Nervous symptoms, 507 Condition of fauces, 508 Of throat, 508 Nasal cavities, 508 Lymphatic glands, 508 Duration, 508 Irregular form, 508 Causes, 508 Absence of eruption, 508 Hemorrhagic form, 509 Anginose form, 510 Complications and sequelæ, 510 Complicated by severe nervous symptoms 510 Throat symptoms, 511 Adenitis, 511 Inflammation of neck, 511 Gangrene of neck, 512 Oedema of glottis, 512 Diphtheria, 514 course of diphtheria, complicating, 516 Croupous inflammation of fauces, 516 Coryza, 520 Otitis, 520 course of otitis, complicating, 520 results of otitis, complicating, 521 By rheumatism, 521 By cardiac inflammations, 522 By dilatation of heart, 523 By heart-clot, 523 By pleuritis, 523 By nephritis, 525 By glomerulo-nephritis, 527 By albuminuria, 525 By anasarca and oedema, 529 Order and date of appearance of anasarca, 529 By head symptoms due to uræmia, 530 Morbid anatomy, 530 Changes in the blood, 530 Respiratory tract, 531 Abdominal organs, 531 Post-mortem appearance of eruption, 532 Changes in the kidneys, 526 hyaline degeneration of kidneys, 527 intestinal nephritis, 528 parenchymatous nephritis, 526 Changes in the liver, 531 Diagnosis, 532 From measles, 532 From erythema, 533 From rötheln, 533 From diphtheria, 533 Prognosis, 533 Influence of complications upon, 533, 535 type upon, 534 age upon, 534 Of grave cases, 535 Mortality, 534 Treatment, 536 Preventive, 536 Isolation in, 537 Inoculation as a prophylactic, 536 Belladonna as a prophylactic, 536 Sodium sulpho-carbolate as a prophylactic, 537 Listerine as a prophylactic, 537 Boric acid as a prophylactic, 537 Disinfection in, 201, 538 Hygienic, 539 Therapeutic, 539 Mild cases, 540 Inunction in, 541 Hyperpyrexia, 541 by cold, 541 Mode of applying cold, 542 Antiseptic, 545 Complications and sequelæ, 545 Pharyngitis, 545 local, 546 Coryza, 546 local, 547 Otitis, 547 local, 549 paracentesis of tympanum, 548 Nephritis and albuminuria, 550 modes of producing diaphoresis, 551 local, 555 Convulsions, 556 Rheumatic and cardiac inflammation, 556 Pleuritis, 556 Convalescence, 544 Use of aconite and veratrum viride, 543 Alcohol, 544 Ammonium carbonate, 544 Carbolic acid, 545 Cathartics, 554 Diuretics, 555 Digitalis, 543, 555 Ice, 542 Jaborandi and pilocarpine, 552 Sodium salicylate, 543 Quinia, 543

Scarlet fever, relation of, to idiopathic parotitis, 620

Scarlatina, disinfection in, 201, 538

Schools, closure of, for prevention of disease, 203

Scrofula, relation of, to causation of rubeola, 561 relation to tuberculosis, 96, 101

Scrofulosis, hereditary disposition to, 127

Scrofulous habit, peculiarities of tissue, 101

Scurvy, complicating typhus fever, 355

Season, influence of, on causation of anthrax, 931, 940 of cerebro-spinal meningitis, 802 of diphtheria, 682 of typhoid fever, 245 of erysipelas, 630 of idiopathic parotitis, 620 of influenza, 860 of the plague, 775 of rabies and hydrophobia, 887 of relapsing fever, 371 of typhus fever, 343 of variola, 435 on cholera, 720 proper, for vaccination, 477

Seborrhoea, following erysipelas, 633

Second attack of rubeola, frequency of, 563 stage of pertussis, 840

Secondary form of diphtheria, 671

Segregation of lepers, 794

Self-infection, danger of, in treating diphtheria, 696 prevention of, in treating diphtheria, 696

Sensibility, altered, significance of, in general diagnosis, 161 modifications of, in typhoid fever, 279

Sepsin, 971

Septicæmia, 945 complicating erysipelas, 634 distinguished from pyæmia, 978, 979 lymphatica of puerperal fever, 1011 venosa, 1012

Sequelæ of cerebro-spinal meningitis, 819 of cholera, 735 of erysipelas, 633 of grave form of the plague, 780, 781 of influenza, 868 of relapsing fever, 396 of rötheln, 587 of rubeola, 573 treatment, 580 of scarlet fever, 510 of vaccinia, 464 of variola, 445

Serous inflammation, 47 inflammations complicating erysipelas, 634

Severe form of diphtheria, symptoms, 668 of influenza, treatment, 875 of typhus fever, 354

Sewerage, 213

Sewer- and soil-pipes, importance of position, 188

Sewer-gas, 189 diseases produced by, 190 symptoms due to, 189

Sewers, characters of efficient, 224 public, 224 ventilation of, 224

Sewer-traps, test as to their efficiency, 190 varieties, 191

Sex, influence of, on causation of cerebro-spinal meningitis, 802 of diphtheria, 680 of erysipelas, 630 of idiopathic parotitis, 620 of influenza, 860 of leprosy, 789 of pertussis, 839 of the plague, 775 of rabies and hydrophobia, 880 of relapsing fever, 371 of rötheln, 583 of variola, 436 typhoid fever, 243 relation of, to causation of rubeola, 563

Silver nitrate, use of, in typhoid fever, 332

Simon's triangles, 437

SIMPLE CONTINUED FEVER, 231 Definition, 231 Synonyms, 231 History, 231 Etiology, 232 Symptoms, 233 Asthenic form, 233 Morbid anatomy, 235 Diagnosis, 234 From typhoid fever, 234 From typhus fever, 234 From relapsing fever, 235 From tubercular meningitis, 235 Prognosis, 235 Treatment, 236

Simple form of yellow fever, treatment, 649

Singultus in pyæmia, 975 in septicæmia, 977 significance of, in general diagnosis, 158

Skin, alterations in sensibility of, in cerebro-spinal meningitis, 808 anæsthesia of, in beriberi, 1039 appearance of, in typhoid fever, 273 character of lesions in erysipelas, 631 chronic diseases of, following rubeola, 574 color of, in cholera, 737 condition of, in cholera, 736 in influenza, 866 in septicæmia, 977 coolness of, in cerebro-spinal meningitis, treatment, 831 diseases of, complicating vaccination, 471 effects on course of erysipelas, 634 following vaccination, 471 disorders of, complicating rubeola, 570 eruptions of, complicating cholera, 735 in pyæmia, 974 erysipelas of, migration, 632 hyperæsthesia of, in typhus fever, 352 lesions of, in erysipelas, 635 course of, 631 in leprosy, 791 in remittent fever, 603 in rubeola, 575 morbid anatomy of lesions of, in variola, 446 odor of, in typhoid fever, 273 in typhus fever, 352 significance of color of, in general diagnosis, 159 swelling of, in erysipelas, 632

Skunk-bites as cause of rabies and hydrophobia, 889

Slaking lime, use of, in diphtheria, 703

Sleep, danger of prolonged, in nasal diphtheria, 712

Sleeplessness in idiopathic parotitis, treatment, 625

Small-pox, 434 black, 442 freedom of liability to, from race-protection, 130

Sodium benzoate, use of, in pertussis, 847 chloride, venous injection of, in cholera, 762, 768 hyposulphite, use of, in relapsing fever, 428 salicylate, use of, in diphtheria, 707 in puerperal fever, 1032 in scarlet fever, 543 in typhoid fever, 330 sulpho-carbolate as a prophylactic in scarlet fever, 537

Softening, cerebral, from embolism, 65 mucous, 82

Soil, character of, as cause of disease, 187 composition of, 187 diminished dryness of, a cause of phthisis, 187 drainage of, for prevention of anthrax, 937 of disease, 226 examination, 188 filtering power, 187 humidity of, as a cause of cholera, 722

Soils, alkaline, relation of, to causation of anthrax, 930

Soil-pipes, importance of position of, 188 tests as to their efficiency, 190 ventilation of, 189

Solitary glands, lesions of, in typhoid fever, 261

Spasm of pharyngeal and respiratory muscles in hydrophobia, 899

Special senses, perversion of, in relapsing fever, 386 in typhus fever, 349

Specific origin of anthrax, 720, 726 of cholera, 727 of glanders, 911 of rötheln, 583 of yellow fever, 640

Speech, impairment of, following cerebro-spinal meningitis, 820

Spinal cord, lesions of, in cerebro-spinal meningitis, 823 marrow, lesions of, in cholera, 746 rigidity in cerebro-spinal meningitis, 809

Spirillum, 142 of relapsing fever, 373

Spleen, condition of, in relapsing fever, 391 enlargement of, in pyæmia, 976 lesions of, in anthrax in animals, 935 in man, 942 in cholera, 746 in diphtheria, 687 in glanders, 922 in hydrophobia, 903 in pyæmia, 969 in relapsing fever, 416 in remittent fever, 602 in septicæmia, 972 in typhoid fever, 264 in typhus fever, 357 rupture of, in relapsing fever, 403

Spontaneous cow-pox, 456 origin of pyæmia, 959 of typhoid fever, 254

Stages of yellow fever, 645

Standards of purity of water, 184

Starvation and over-crowding as causes of relapsing fever, 370

Steam, use of, in diphtheria, 701

Sthenic inflammation, 46

Stimulants, use of, in diphtheria, 695 in relapsing fever, 431 in rubeola, 580 in variola, 453

Stomach, lesions of, in cholera, 743 state of, in remittent fever, 602

Stools, as a medium of disseminating typhoid fever, 249 character of, in cholera, 739 in pyæmia, 976 in typhoid fever, 287 in typho-malarial fever, necessity of disinfecting, 619 necessity of disinfection in prevention of typhoid fever, 321 significance of, in general diagnosis, 163

Strabismus in cerebro-spinal meningitis, 810

Straw-fungus, relation of, to rubeola, 558

Strychnia, use of, in diphtheritic paralysis, 713 in dry beriberi, 1043

Stupor in typhoid fever, treatment, 334 in typhus fever, treatment, 366

Subsoil-water, level of, 188

Sudamina in typhoid fever, 274 in typhus fever, 352

Sulphites and hyposulphites, use of, in pyæmia, 982 in septicæmia, 983

Sulphur, use of, in diphtheria, 709

Summer heats, relation of, to causation of rabies and hydrophobia, 887

Suppuration in idiopathic parotitis, treatment, 625 influence of minute organisms in production of, 144

Suppurative stage of variola, 439

Surgical scarlatina, 495 treatment of erysipelas, 638

Swelling of parotid glands in cerebro-spinal meningitis, 814

Swellings, significance of, in diagnosis, 159

Sweating stage of intermittent fever, 593 of intermittent fever, treatment, 597

Symptomatic parotitis, 625

Symptomatology, general, 148

Symptoms at decline of eruptive stage of rubeola, 567 constitutional, of vaccinia, 459 due to sewer-gas, 189 general, of idiopathic parotitis, 623 of anæsthetic form of leprosy, 791 of tubercular form of leprosy, 790 of confluent small-pox, 441 local, of anthrax, 935, 940 of idiopathic parotitis, 621 anæsthetic form of leprosy, 790 of glanders, 914, 915, 921 of tubercular form of leprosy, 789 nervous, in mild scarlet fever, 503 in typhus fever, 348 special, in typhus fever, 347 of anthrax in animals, 934 in man, 940 angina, 941 intestinalis, 941 of malignant anthrax, 940 of beriberi, 1039 of cerebro-spinal meningitis, 806 of cholera, 731 of comatose form of pernicious malarial fever, 608 of dengue, 884 of diphtheria, 667 of endometritis and endocolpitis of puerperal fever, 1005 of erysipelas, 631 of glanders in horses, 914 in man, 920 of hydrophobia, in man, 898 of influenza, 865 of idiopathic parotitis, 621 of intermittent fever, 592 of gangrene foudroyante, 977 of general peritonitis of puerperal fever, 1010 of leprosy, 789 of malignant scarlet fever, 507 of para- and perimetritis in puerperal fever, 1005 of pertussis, 840 of the plague, 777 of puerperal fever, 1004 of pyæmia, 972 of rabies and hydrophobia in dogs, 895 of relapsing fever, 374 of remittent fever, 599 of rötheln, 585 of rubeola, 563 of scarlet fever, 502 of septicæmia, 976 lymphatica of puerperal fever, 1011 venosa of puerperal fever, 1012 of simple continued fever, 233 of symptomatic parotitis, 626 of typho-malarial fever, 615 of typhoid fever, 268 of typhus fever, 346 of vaccinia, 458 of varicella, 481 of variola, 436 of varioloid, 443 of yellow fever, 644

Synonyms of anthrax, 926 of cerebro-spinal meningitis, 795 of cholera, 715 of dengue, 879 of diphtheria, 656 of erysipelas, 629 of glanders, 909 of influenza, 851 of leprosy, 785 of the plague, 771 of rabies and hydrophobia, 886 of relapsing fever, 369 of rötheln, 582 of rubeola, 557 of simple continued fever, 231 of typhoid fever, 237 of typhus fever, 338 of vaccinia, 455 of vaccination, 465 of varicella, 481 of variola, 434 of yellow fever, 640

Syphilis, complicating vaccination, 469 modes of preventing, 470 treatment of, 471 constitutional, hereditary nature of, 127

T.

Tâches bleuâtres in typhoid fever, 275 in typhus fever, 352

Tarnier's maternity pavilions for prevention of puerperal fever, 1028

Taste, modifications of, in typhoid fever, 280 significance of modification, in general diagnosis, 162

Technics of vaccination, 472

Teeth, significance of condition, in diagnosis, 152

Temperature in anthrax in man, 940 at decline of eruptive stage of rubeola, 567 elevated, influence of, in origin and spread of cholera, 720 in cerebro-spinal meningitis, 815 in cholera, 736 in dengue, 881 in eruptive stage of rubeola, 565 in erysipelas, 633 in fevers, 38-40 in general peritonitis of puerperal fever, 1010 in idiopathic parotitis, 623 in influenza, 864 in malignant scarlet fever, 507 in mild scarlet fever, 505 in para- and perimetritis in puerperal fever, 1006 in prodromal stage of rubeola, 564 in pyæmia, 974 in relapsing fever, 378, 382 in remittent fever, 599 in rötheln, 587 in septicæmia, 977 venosa of puerperal fever, 1012 in typhoid fever, 280 in typhus fever, 349 significance of, in general diagnosis, 158 respiration and pulse, relations of, in relapsing fever, 386

Tenderness, muscular, in beriberi, 1039

Teratoid tumors, 124

Test, peppermint, for defects in plumbing, 198

Tests as to efficiency of soil-pipes, 190

The plague, 771

Thermometer, use of, in typhoid fever, 284

Thirst in cerebro-spinal meningitis, 814 in rabies and hydrophobia, 899 in relapsing fever, 389 in typhoid fever, 285 in typhus fever, 350 treatment, 367 significance of, in general diagnosis, 162 treatment of, in cholera, 770

Throat symptoms, complicating scarlet fever, 511

Thoracic duct, obstruction of, as cause of dropsy, 69

Thrombi, action of, in production of metastatic abscesses in pyæmia, 965 calcification of, 60, 89 in uterine pelvic veins, 989 growth of, in puerperal fever, 989

Thrombosis, 56 relation of, to causation of pyæmia, 957 and embolism, 56 causes, 57 symptoms, 66 in relapsing fever, 402 in typhoid fever, treatment, 335

THROMBUS, 56 Calcification, 60, 88 Characteristics, 59 Changes, 60 Composition, 56 Distinguished from thrombosis, 56 From compression, 58 From death of leucocytes, 57 From dilatation, 58 From marasmus, 59 From traumatism, 58 Mechanical effects, 62 Organization, 60 Softening, 61 Varieties, 57, 58

Tongue, condition of, in cerebro-spinal meningitis, 813 in dengue, 881 in erysipelas, 633 in idiopathic parotitis, 622 in mild scarlet fever, 504 in typhus fever, 350 in yellow fever, 644 state of, in pyæmia, 975 in relapsing fever, 389 in remittent fever, 600 in septicæmia, 977 in typhoid fever, 285 signification of state of, in diagnosis, 152

Tracheal diphtheria, prognosis of, 692

Trachea, formation of diphtheritic membrane in, 671

Tracheotomy in diphtheria, prognosis of, 692

Transmission of cholera, 721, 723 of variola, 435

Transudation, 68 causes, 69 mechanism, 68

Traps, ventilation, 221

Traumatic fever, relation of, to septicæmia, 961 fevers, 37

Treatment of anthrax in animals, 938 in man, 943 preventive, of anthrax, 936, 943 of beriberi, 1042 of cerebro-spinal meningitis, 829 of cholera, 759 of dengue, 885 of diphtheria, 694 general, importance of, in diphtheria, 695 of erysipelas, 636 of idiopathic parotitis, 624 local, of idiopathic parotitis, 625 of intermittent fever, 594 of leprosy, 793 local, of leprosy, 794 of comatose form of pernicious malarial fever, 609 of glanders in horse, 918 in man, 924 preventive, in horse, 919 in man, 925 of influenza, 873 of pertussis, 844 of the plague, 782 of puerperal fever, 1028 of septicæmia, 983 of pyæmia, 979 of rabies and hydrophobia, 903 preventive, 903 of relapsing fever, 426-433 of remittent fever, 603 of rötheln, 587 of rubeola, 578 hygienic, of rubeola, 579 preventive, of rubeola, 578 of scarlet fever, 536 of septicæmia, 982 of simple continued fever, 236 of symptomatic parotitis, 627 local, of symptomatic parotitis, 628 of typhoid fever, 320 of typho-malarial fever, 618 of typhus fever, 361 of variola, 451 hygienic, of variola, 451 of variola, preventive, 451 of varioloid, 451 of yellow fever, 649

Treeak farook, use of, in wet beriberi, 1042

TUBERCLE, 94 Calcification, 96 Cheesy degeneration, 96 Fibrous transformation, 96 Histology, 95 Horn-like change, 96 Infectious origin, 97 Inoculability, 97 Miliary and gray, cause of infectious qualities, 99 Origin of, from absorption of cheesy products, 97

Tubercular form of leprosy, 789

TUBERCULOSIS, 94 Bacilli of, 99, 100 _et seq._ Dissemination, 103 Hereditary nature, 101 Primary seat, 104 Relation of, to pearly distemper, 99 to scrofula, 101

Tuberculosis, acute miliary, complicating rubeola, 572 chronic pulmonary, following rubeola, 573 general miliary, following relapsing fever, 404 following rubeola, 574 relation of, to pearly distemper, 99 to scrofula, 96, 101

TUMORS, 105 Method of origin, 106 Cohnheim's theory of origin, 106 Influence of irritants in producing, 108 Growth, 109 concentric, 109 continuous, 109 eccentric, 109 influence of seat, 109 rapidity, 109 Primary, 110, 111 Secondary, 110, 112 Metastasis, 110 Multiple, 110 Recurrence, 110 Transplantation, 110 Embolic nature, 112 Changes occurring, 113 inflammatory, 113 Analogy of structure in primary and secondary, 113 Benignant, 114 Cachexia, 114 Malignant, 114 Resemblance of, to normal tissue of body, 115 Histoid, 116 Organoid, 116 Relation of, to each other, 117 Connective tissue, 118, 122 Cystic, 115, 116, 121 Influence of age upon development, 119 Classification, 114, 121 Infective group, 120, 124 Epithelial group, 123 Congenital, 124

Turpentine inhalations in diphtheria, 704 stupes, use of, in puerperal fever, 1032 use of, in typhoid fever, 326

Tympanites in remittent fever, treatment, 605 in typhoid fever, 286 treatment of, 332 in typho-malarial fever, treatment, 619 in typhus fever, 350

Tympanum, paracentesis of, in scarlet fever, 548

Types of cerebro-spinal meningitis, 804 of intermittent fever, 594 of scarlet fever, 494 of varioloid, 444

TYPHOID FEVER, 237 Synonyms, 237 Definitions, 237 History, 238 Geographical distribution, 241 Etiology, 242 Predisposing causes, 242 Age, influence of, 242 Sex, influence of, 243 Occupation, influence of, 244 Change of residence, influence of, 244 Idiosyncrasy, influence of, 245 Depressing emotions, influence of, 245 Intemperance, influence of, 245 Previous ill-health, influence of, 245 Season, influence of, 245 Elevated temperature, influence of, 246 Rise and fall of subsoil-water, influence of, 247 Exciting causes, 248 Contagiousness, 248 Dissemination, 249 Cases illustrating modes of dissemination, 250 Dissemination of, by drinking-water, 248 By stools, 249 By milk, 252 By atmosphere, 252 By bed-linen, etc., 253 By polluted soil, 253 By putrefied flesh, 257 Spontaneous origin, 254 Duration of virulence of germs, 256 Bacillus typhosus, 258 Incubation period, 259 Morbid anatomy, 260 Lesions peculiar to, 261 Changes in Peyer's patches, 261 Solitary glands, 261 Softening of Peyer's patches and solitary glands, 263 Cicatrization of Peyer's patches and solitary glands, 263 Changes in cæcum and colon, 263 Spleen, 264 Abdominal glands, 264 Lesions not peculiar to, 265 Changes in liver and gall-bladder, 265 Pharynx and oesophagus, 265 Larynx and lungs, 266 Brain and membranes, 266 Muscles, 267 Heart and blood-vessels, 267 Blood, 268 Salivary glands, 268 Kidneys, 268 Symptoms, 268 Clinical description, 268 Physiognomy, 272 Epistaxis, 273 Condition of skin, 273 Odor, 273 Eruption, 273 Sudamina, 274 Tâches bleuâtres, 275 Condition of hair and nails, 275 Pulse, 275 Heart-sounds, 276 Respiration, 276 Frequency of bronchitis, 277 Mental condition, 277 Headache, 277 Delirium, 278 Muscular spasm, 279 tremor, 279 Modifications of sensibility, 279 Hearing, 280 Vision, 280 Taste, 280 Temperature, 280 State of tongue, 285 Fauces, 286 Nausea and vomiting, 285 Anorexia, 285 Thirst, 285 Gurgling, 286 Meteorism or tympanites, 286 Diarrhoea, 287 Character of stools, 287 Intestinal hemorrhage, 287 frequency, 288 causes, 288 importance, 288 Intestinal perforation, 289 frequency, 290 causes, 290 date of appearance, 290 importance, 289 Condition of urine, 291 amount of solids, 291 presence of albumen, 292 Complications and sequelæ, 292 Complicated by pyæmia, 294 Laryngitis, 294 Bronchitis and pneumonia, 294 Pleurisy, 294 Jaundice, 295 Peritonitis, 295 Catarrhal and diphtheritic inflammation of fauces, 295 Parotid swelling, 296 Menstrual disorders, 296 Pregnancy, 296 Suppuration of Bartholini's glands, 296 Periostitis, 297 Oedema, 297 Bed-sores, 297 Followed by impaired intellect, 292 Perversion of the moral sense, 292 Paralysis and chorea, 293 Cardiac degeneration, 293 Arterial thrombosis, 293 Venous thrombosis, 294 Gangrene of vulva and vagina, 293 Hepatic abscess, 295 Tendency to stoutness, 298 Varieties of, 298 Abortive form, 298 Latent form, 300 In children, 301 In aged persons, 302 Relapses in, 302 frequency, 302 course, 303 cases illustrating, 304 causes, 308 Duration, 310 Diagnosis, 311 From typhus, 311 From influenza, 312 From relapsing fever, 312 From epidemic cerebro-spinal meningitis, 313 From simple continued fever, 313 From remittent fever, 312 From the eruptive fevers, 313 From acute tuberculosis, 313 From trichinosis, 314 From the specific inflammations, 314 From acute tubercular meningitis, 314 Prognosis, 314 Symptoms indicating unfavorable, 314 favorable, 316 Influence of hyperpyrexia upon, 314 Nervous symptoms, 315 Heart symptoms, 316 Condition of pulse, 316 Abdominal symptoms upon, 316 Mortality, 316 Tables showing, 317, 318 Influence of season, 318 Sex, 319 Age, 319 Treatment, 319 Habits, 320 Social condition, 320 Recent residence, 320 Corpulence, 320 Organic disease, 320 Childhood, 320 Treatment, 320 Preventive, 321 Necessity of proper drainage in prevention, 321 Disinfection of stools, 321 Hygienic, 322 Importance of ventilation, 323 administering water, 325 Diet, 323 Mild cases, 326 Hyperpyrexia, 327 by cold baths, 327-329 Typho-malarial form, 331 Vomiting, 331 Diarrhoea, 331 Tympanites, 332 Intestinal hemorrhage, 332 perforation, 333 Constipation, 333 Headache, 334 Insomnia, 334 Stupor, 334 Delirium, 334 Albuminuria, 334 Complications, 335 Epistaxis, 335 Pneumonia, 335 Hypostatic congestion of lungs, 335 Thrombosis and embolism, 335 Bed-sores, 335 Convalescence, 335 Use of alcohol, 324 Digitalis, 330 Eucalyptus, 331 Quinia, 330 Silver nitrate, 332 Sodium salicylate, 330 Turpentine, 326 Specific, 336 By calomel, 336 By iodine, 336, 337 Use of thermometer, 284

Typhoidal inflammation, 47

Typhoid state of cholera, 734 following variola, 445

TYPHO-MALARIAL FEVERS, 614 Definition, 614 Frequency, 616 Symptoms, 615 Diagnosis, 616 Prognosis, 616 Mortality, 616 relative mortality of white and black races, 616 Treatment, 618 Of typhoidal element, 618 Of malarial element, 618 Use of quinia, 618 Depurative treatment, 618 Necessity of disinfection of stools, 619 Of tympanites, 619 Of insomnia, 619 Diet, 619

Typho-malarial form of typhoid fever, treatment, 331

TYPHUS FEVER, 338 Synonyms, 338 History, 338 Etiology--Predisposing causes, 341 Over-crowding as a cause, 341 Age, influence of, 342 Debility and fatigue, influence of, 342 Mental and physical overwork, 342 Intemperance, 342 Poverty, 342 Barometric and thermometric variations, 343 Season, 343 Occupation, 343 Individual susceptibility to, 343 Exciting causes, 343 Contagiousness, 343 Nature of contagion, 343 Modes of transmission of contagion, 344 Communication of, by fomites, 345 Period of contagiousness, 345 Spontaneous origin, 345 Period of incubation, 346 Symptoms--Clinical description, 346 Special symptoms, 347 Prostration, 348 Nervous symptoms, 348 Appearance of face, 348 Intellectual condition, 348 Headache, 348 Delirium, 348 Wakefulness, 349 Coma vigil, 349 Perversion of special senses, 349 Muscular tremor, 349 Temperature, 349 Condition of tongue, 350 Anorexia, 350 Thirst, 350 Nausea and vomiting, 350 Condition of bowels, 350 Tympanites, 350 Gurgling, 350 Eruption, 351 Duration of eruption, 351 Tâches bleuâtres, 352 Sudamina, 352 Hyperæsthesia of skin, 352 Odor, 352 Condition of pulse, 351 of heart, 351 Respiration, 352 Pneumonia, 353, 355 Bronchitis, 353, 355 Odor of breath, 353 Hypostatic congestion of lungs, 353 Changes in urine, 353 Varieties of, 353 Mild form, 354 Severe form, 354 Ataxic form, 354 Adynamic form, 354 Ataxo-adynamic form, 354 Inflammatory form, 354 Walking form, 354 Abortive form, 354 Complications and sequelæ, 354 Complicated by erysipelas, 355 Cardiac degeneration, 355 Bronchitis and pneumonia, 353, 355 Pleurisy, 355 Albuminuria, 355 Bed-sores, 355 Scurvy, 355 Dysentery, 355 Jaundice, 356 Parotitis, 356 Serous inflammations, 356 Pyæmia, 356 Disorders of menstruation, 356 Miscarriage, 356 Followed by pulmonary gangrene and phthisis, 355 Morbid anatomy, 356 Alteration of blood, 356 Changes in respiratory organs, 356 Heart and membranes, 357 Liver and kidneys, 357 Spleen, 357 Intestinal tract, 357 Brain and membranes, 358 Diagnosis, 358 From typhoid fever, 358 From meningitis, 358 From measles, 358 From typhoid pneumonia, 359 From delirium tremens, 359 From purpura, 359 Prognosis of, 359 Symptoms indicating favorable, 360 unfavorable, 360 Influence of age, 359 Sex, 359 Former habits, 359 Convalescence from previous illness, 359 Obesity, 359 Mental and physical overwork, 360 Social condition, 360 Race, 360 Mortality, 360 Difference of, in hospital and private cases, 361 Treatment, 361 Preventive, 361 Necessity of isolation, 361 Disinfection, 362 Diet, 362 Quantity of nourishment necessary, 363 Futility of abortive treatment, 363 General treatment, 364 Mild cases, 364 Hyperpyrexia, 364 By cold water, 364 By cold baths, 364 Mode of using cold bath, 364 Prostration, 365 Headache, 366 Delirium, 366 Insomnia, 366 Stupor, 366 Urinary complications, 366 Thirst, 367 Vomiting, 367 Constipation, 367 Parotitis, 367 Pulmonary complications, 367 Use of alcohol in, 366 Opium in, 366 Quinia in, 365 Of convalescence, 368 Necessity of continuing stimulants during convalescence, 368

Tyrosis, 79

U.

Ulceration, complicating vaccination, 468

Ulcers, complicating cholera, 735 following the plague, 781

Umbilication in vaccinia, mechanism of, 464 in varicella, 482 in variola, 438 cause of, 447

Uræmia in scarlet fever, 530

Urinary complications in typhus fever, treatment, 366

Urine, analysis of, importance in general diagnosis, 165 condition of, in cerebro-spinal meningitis, 814 in cholera, 739 in dengue, 881 in influenza, 866 in mild scarlet fever, 506 in grave form of the plague, 779 in pertussis, 841 in pyæmia, 976 in relapsing fever, 387 in remittent fever, 602 in typhoid fever, 291, 292 in yellow fever, 644 suppression of, complicating relapsing fever, 407 in cholera, treatment, 764 in yellow fever, treatment, 653

Urination, difficult, significance of, in diagnosis, 164

Urobilin, 91

Urticaria, complicating diphtheria, 674

Uterus, fixity of, in para- and perimetritis of puerperal fever, 1007 lesions of, in septicæmia, 972

V.

VACCINIA, 455 Definition, 455 Synonyms, 455 History, 458 Etiology, 458 Nature, 455 Variolous origin, 457 Meteorological conditions as a cause, 458 Symptoms, 458 General course, 458 Constitutional, 459 Development of pock, 459 Date of appearance of pock, 459 incrustation of pock, 460 falling off of crust, 460 Description of cicatrix, 460 Irregularities in course, 460 Raspberry excrescence of pock, 461 Lack of elevation in pock, 461 Absence of a constitutional infection, 460 Bryce's test for determining constitutional infection, 461 Diphtheritic pock, 463 Catarrhal pock, 463 Morbid anatomy, 462 Pock, 463 Microspheres and vaccinals of lymph, 463 Microscopical characters of the lymph, 463 Mechanism of umbilication, 464 Composition of crust, 464 Complications and sequelæ, 464

VACCINATION, 465 Synonyms, 465 History of, 465 Protective power of, 461 theories regarding, 461 duration of, 468 against pertussis, 468 Marson's theory of multiple insertions, 467 Time of revaccination, 467 As a means of destroying nævi, 468 Complications, 468 Simple inflammatory, 468 Complicated by dermatitis, 468 Treatment of dermatitis, 469 Complicated by lymphangitis and adenitis, 468 By ulceration and gangrene, 468 Erysipelas, 469 treatment, 469 Complicated by syphilis, 469 treatment, 471 Modes of preventing transmission of syphilis, 470 Complicated by skin diseases, 471 by eczema, 472 Impetigo contagiosa, its relations to, 472 Followed by cutaneous affections, 471 by eczema, 472 Conveyance of constitutional taints in, 471 Technics of, 472 Varieties of virus, 472 Primary vaccine, 473 Horse-pox vaccine, 473 Retro-vaccine, 473 Bovine vaccine, 473 Variola vaccine, 473 So-called points of superiority of humanized vaccine, 473 Relative merits of animal and humanized vaccine, 473 Advantages of animal over humanized virus, 475 Forms of vaccine, 476 Objections to use of crust, 476 Use of dried lymph, 477 liquid or tube lymph, 476 Proper season, 477 Age, 477 Part of body most suitable for, 477 Modes of operating, 478 applying the virus, 478 Storage and preservation of virus, 479 Proper time of collecting lymph for storage, 479 Proper manner of transporting, 480

Vaccination, neglect of, as a cause of variola, 436

Vaccine virus, varieties of, 472 use of, in treatment of rabies and hydrophobia, 907

Vagina, symptoms of diphtheria of, 674

Vaginal injections, use of, for prevention of puerperal fever, 1025

Variations, barometric, influence of, upon course of diseases, 134

VARICELLA, 481 Definition, 481 Synonyms, 481 History, 481 Etiology, 481 Contagiousness, 481 Symptoms, 481 Period of incubation, 482 General, 482 Prodromal stage, 482 Eruption, 482 Umbilication of eruption, 482 Date of appearance of desiccation, 482 Frequency of scarring, 482 Appearance of vesicles on mucous membrane, 483 Morbid anatomy, 483 Complications, 483 Diagnosis, 483 From variola and varioloid, 484 From vaccinia, 484 From impetigo, 483 contagiosum, 483 From eczema pustulosum, 483 Prognosis, 484 Treatment, 485

_Varicella Prurigo_, nature, 484

Varieties of beriberi, 1039 of grease-traps, 221 of pernicious malarial fever, 606 of rubeola, 568 of sewer-traps, 191 of typhoid fever, 298

VARIOLA, 434 Definition, 434 Synonyms, 434 History, 434 Etiology, 435 Contagiousness, 435 Nature of contagium, 435 Mode of entrance of contagium, 435 Duration of activity of contagium, 435 Period of greatest activity of contagium, 435 Modes of transmission, 435 Race, influence of, 436 Season, influence of, 436 Sex, influence of, 436 Neglect of vaccination as a cause, 436 Individual idiosyncrasy, 436 Protection from, by previous attacks, 436 Effect of pre-existing skin disorders, 436 Symptoms, 436 Stage of incubation, 436 Invasion, 436 Variolous rash, 437 date of appearance, 437 significance, 437 Simon's triangle, 437 Stage of invasion, 438 Eruptive stage, 438 Characters of eruption, 438 Position of eruption, 438 Stage of vesication, 438 Umbilication, 438 Maturation, 439 Characters of mature pock, 439 Condition of patient in suppuration stage, 439 Pustules on mucous surfaces, 439 Stage of desiccation, 439 General, during desiccation, 440 Secondary fever, 439 Date of appearance of secondary fever, 439 Confluent variety, 440 Seat of lesion, 441 Condition of mucous surfaces in confluent, 441 General condition in confluent, 441 Hemorrhagic variety, 442 First form, 442 Second form, 443 Lesions of, 443 Variolic purpura, 442 Complications and sequelæ, 445 Complicated by eye diseases, 445 Erysipelas, 445 Nasal inflammation, 445 Furuncles and abscesses, 445 Muscular paralysis and hemiplegic attacks, 445 Laryngitis, 446 Gangrene of genitalia, 446 Followed by a typhoid state, 445 Pathology and morbid anatomy, 446 Cutaneous lesions, 446 Formation of papule, 446 Vesicle, 446 Cause of umbilication, 447 Repair of pock, 447 Hemorrhagic variety, 447 Changes of viscera, 447 Diagnosis, 447 From measles, 448 From scarlatina, 449 From pustular skin diseases, 449 From dermatitis medicamentosa, 449 From syphiloderm, 449 From acneform disease, 449 From typhoid fever, 450 From typhus fever, 450 Prognosis, 450 Symptoms indicating unfavorable, 450 Influence of sudden defervescence of eruption, 450 Pregnancy and childbed, 450 Fatality of, in the unvaccinated, 450 Influence of vaccination after development, 451 Treatment, 451 Preventive, 451 Hygienic, 451 Necessity of cleanliness, 454 Invasion stage, 452 Eruption, 452 Exclusion of sunlight for prevention of pitting, 452 Use of warm baths, 453 Hot water compresses, 453 Stimulants, 454 Hemorrhagic form, 454 Disposition of clothes and body after death, 454

Variola of vaccine, 473

Variolic purpura, 442

VARIOLOID, 443 Symptoms, 443 Invasion stage, 443 Eruption, 444 Types of, 444 Identity with variola, 444 Treatment, 451

Veins, condition of, in cholera, 737 intestinal, lesions of, in cholera, 745 jugular, thrombi of, in symptomatic parotitis, 626 lesions of, in pyæmia, 967 in symptomatic parotitis, 626

Venesection in cholera, 764 in rabies and hydrophobia, 908 in relapsing fever, 431 futility of, in cerebro-spinal meningitis, 830

VENTILATION, 177 _et seq._ Defects, 179 Distribution of air, 180 Estimation of carbonic acid in air, 178 Insufficient, evil effects, 181 Importance of, in treatment of typhoid fever, 323 Methods of calculating amount of air-supply, 179 Modes of investigating merits of a plan, 179 Of waste-pipes in drainage, 223 Of soil-pipes, 189 Proper size of flues and registers, 179 Relation of, to heating apparatus, 180 Varieties of ventilators, 180 Velocity of air, 180

Ventilators, varieties, 180

Venous emboli, 63 thrombosis, following typhoid fever, 294

Veratrum viride, use of, in puerperal fever, 1033 in scarlet fever, 543 in yellow fever, 651

Vertigo in cerebro-spinal meningitis, 812 in relapsing fever, 384 significance of, in general diagnosis, 158

Vesication in variola, 438

Vesicle in variola, morbid anatomy of, 446

Views, earlier, concerning nature of puerperal fever, 990 modern, concerning nature of puerperal fever, 992

Virus of anthrax, period of greatest virulence, 928 of rabies, localization of, in wound, 893 of vaccination, varieties of, 472 vaccine, manner of transporting, 480 storage, 479

Viscera, lesions of abdominal, in the plague, 781 in cerebro-spinal meningitis, 824 in erysipelas, 635 in variola, 447

Vision, modifications of, in relapsing fever, 399 in typhoid fever, 280

Vital statistics, registration, 208

Voice, alteration of, in diagnosis, 158

Vomit, character of, in cerebro-spinal meningitis, 813 in cholera, 738 in grave form of the plague, 779

Vomiting during intermittent fever paroxysm, 593 in cerebro-spinal meningitis, 813 in cholera, 738 treatment, 761 in diphtheria, treatment, 694 in general peritonitis of puerperal fever, 1010 in mild scarlet fever, 503 in para- and perimetritis of puerperal fever, 1007 in pyæmia, 975 in remittent fever, treatment, 605 in rubeola, treatment, 581 in septicæmia, 977 in typhoid fever, 285 treatment, 331 in typhus fever, 350 treatment, 367 in yellow fever, 644 treatment, 652 significance of, in general diagnosis, 162

Vulva, symptoms of diphtheria, 674

W.

Wakefulness in relapsing fever, 384 in typhus fever, 349

Walk, significance of, in diagnosis, 161

Walking form of typhus fever, 354 of yellow fever, symptoms, 654

Washstands, stationary, dangers from, 216

Waste-pipes, effects of large bore in, 220 leakage in, 222 tests for, 222 ventilation, 223

Water, collections of, effect upon public health, 187 fear of, in rabies and hydrophobia, 899 height of subsoil, influence of, on prevalence of cholera, 722 importance of, in treatment of typhoid fever, 325 impure, microscopic characters of, 184 diarrhoeal affections from, 182 disease from, 182 chemical examination of, 183, 184 value of chemical examination of, 183, 184 impurity of, from metallic salts, 182 from organisms, 184 nature of impurities, 182 polluted, as a cause of diphtheria, 683 stagnant, production of malaria by, 187 standards of purity, 184 subsoil, level of, 188 supply, contamination of, from privy-vaults, 192 cess-pools, 192 chloride test for detecting impurities in, 192 tables of analyses, 184 use of, in diphtheria, 702

Water-closets, defects of, 217 location, 218 varieties, 191 ventilation, 192, 217

Waxy degeneration, 84

Welch on cause of oedema of lungs, 72

Wet form of beriberi, symptoms, 1040 treatment, 1042

Whooping cough, 836 relation of, to rubeola, 561

Winds, influence of, on spread of influenza, 860

Wound, appearance of, in rabies and hydrophobia, 895, 899 changes in, in pyæmia, 976 condition of, in septicæmia, 977 influence of characters of, in causation of pyæmia, 958 treatment of, in pyæmia, 981 in septicæmia, 983

Wounds, diphtheria of, 673

Y.

YELLOW FEVER, 640 Synonyms, 640 Definition, 640 Etiology, 640 Specific origin, 640 Poison of, inconvertibility, 840 Birthplace, 641 Characteristics, 641 Ponderability, 641 Vitality, 641 Influence of heat and cold on development, 641 Impossibility of transportation of, by air, 641 Transportability of, by fomites, etc., 641 Nature of fomites, 641, 642 Fixity of, 643 Slowness of extension, 643 Medium of admission to system, 642 Localization of epidemics by atmospheric impregnation, 642 Anxiety, grief, and fatigue as causes, 643 Insusceptibility, in negroes, 644 from idiosyncrasy, 643 Protective power of previous attacks, 643 Duration of incubation period, 643 Symptoms, 644 Mild cases, 644 Initial, 644 Physiognomy, 644 Neuralgia and muscular pains, 644 Cerebral, 644 Condition of tongue, 644 Gastro-intestinal canal, 644 Vomiting, 644 Character of matters vomited, 644 Condition of urine, 644 Pulse, 644 Relation of pulse to temperature, 645 Perspiration, 645 Stages, 645 Masked forms, 653 Walking forms, 654 Paroxysmal stage, 645 Calm stage, 645 Hemorrhages and jaundice, 646 Prognosis, 646 Symptoms indicating unfavorable, 646 Influence of crowding the sick, 646 Pregnancy and parturition, 647 Condition of patient at time of attack, 647 Temperature, 647 In hospital cases, 647 Mortality, 647 Variableness, 647 Difference in hospital and private cases, 648 Diagnosis, 648 Significance of physiognomy, 648 State of pulse, 648 Albuminous urine, 648 Hemorrhagic tendency, 648 Yellow discoloration of skin, 648 Morbid anatomy, 649 Changes in liver, 649 Treatment, 649 Futility of abortive, 649 Importance of early, 649 Indications for, 649 Simple form, 649 Early stages, 649 Diaphoresis, 650 Jaborandi, 650 Neuralgias and muscular pains, 651 Hyperpyrexia, 651 by cold, 651 Hemorrhages, 651 by tincture of iron, 652 Nausea and vomiting, 652 Urinary suppression, 652 Failure of reaction from cold stage, 653 Convulsions and delirium, 653 Use of digitalis, 651 Aconite, 651 Veratrum viride, 651 Gelsemium, 651 Hæmostatics, 652 Quinia, 650, 651 Quinia and opium in combination, 651 Hygienic, 654 Necessity of absolute rest, 654 Diet, 654 Children, 655 Typhoid cases, 655 Time of return to solid food, 655

Z.

Zymosis, meaning of term, 137

Zymotic diseases, relation of, to puerperal fever, 1020 table, 136

END OF VOL. I.