Part 15

Bronchiectasis is reasonably common with pulmonary diseases of man, particularly of chronic character, but is certainly not frequent among animals. Under the first group (a) we can record one case, a Siberian tiger which died of enteritis and its complications to which were added a mild inactive bronchitis and a bronchiectasis of diffuse distribution. The lungs were irregular in shape, dull, gray-red in color and gave a variable boggy and vesicular sensation to the fingers. On opening the lung, dilatations of the bronchi were found, affecting chiefly the larger secondaries but apparently not the bronchioles. Parasites were not found nor were inflammatory reactions apparently adequate to explain the distentions, so that we looked upon this case as congenital. Cases coming under the headings b and c are not recorded. Inflammation almost certainly represents the most important single factor in the pathogenesis of this lesion and could be demonstrated in two cases, a Clouded Leopard (_Felis nebulosa_) and a Red River Hog (_Potamochærus porcus_). While I feel that parasites probably laid the foundation for the dilatations in these cases, none were found after, in one case at least, a very thorough search, although in the second animal a single cyst of _Cysticercus tenuicollis_ was found in the peritoneum. In both animals there was a low grade interstitial pneumonitis and peribronchitis with dilatations of the middle sized and end bronchi, these being supplied with thick walls but containing very scanty secretion.

We have on record chronic ulcerative pulmonary tuberculosis in six primates, two carnivores and nine ungulates. It is highly probable that among this number some cases of ulcerative bronchiectasis occurred but if so they were not conspicuous enough to mention in the diagnosis and in only two protocols do I find a discussion thereof, once in a monkey and once in a carnivore. All the cases of our records were diffuse ectasias, fusiform, or irregular and none of the distinct saccular variety.

From the foregoing facts it would seem that in human cases more weight should be laid to the effect of the dilating power of coughing and its preparatory exertions. While I am aware that the comparative incidence of human and lower animal bronchiectasis cannot be based upon the meager figures at our command, these dilatations certainly can be expected in a general autopsy service more in man than in lower animals. Chronic bronchitis is relatively rare, aside from the verminous varieties. I have seen little retained exudate in the bronchi, probably because quadrupeds seem with ease to raise and swallow the secretions. Nor do animals give vent to paroxysms of coughing such as the human being feels forced to do. Suggestive deductions from these points are that inflammation is the principal factor in acquired bronchiectasis and that the retention of secretion with violent inspiratory efforts are potent in man for the dilatation of the tubes.

THE LUNGS.

The essential respiratory organ of the animal body, the lung, is all through this kingdom a structure intended to expose the blood to free or combined atmosphere in order to permit gaseous interchange, therefore being arranged so that there is a close apposition of the two factors, separated only by such cells and membranes as may be necessary to protect the circulation; perhaps these anatomical elements possess at the same time some vital force to further the exchange of useful and useless matter. In the two classes under discussion there is no difference whatsoever in the primary factors of respiration albeit some variations exist in reference to oxygen and carbon dioxide interchange, moisture of the air, and the physics of inspiration and expiration. The chemical variables have in our limited knowledge of comparative physiology apparently little effect upon morbid anatomy but it is probable that some pathology may be in part explained on physical grounds.

The mammalian respiratory box is a relatively elastic affair, but collapsed at the end of expiration which is largely a passive or recoil process. The avian thorax is believed to be normally a tensely distended space from which air is expelled by pressure of the pectoral contraction upon the broad sternum driving the latter back upon the air sacs which in turn drives it from the lungs. Also by this means, air is distributed through the bones and air spaces, a measure necessary in flight, especially in a head wind when tracheal inspiration is said to be suspended at times. The communications of the lungs, air sacs and bones make it possible for birds to breathe internally when the trachea is closed and externally as well if a bone be opened. The balance of air pressure in the lungs and related spaces is dependent upon the patency of the ostia communicating between the bronchial ends and the air sacs, from which the bony cavities obtain their supply. Should all these be closed there is first a standstill of current and a limitation of the respiration of the lungs. Fortunately it is extremely rare that this occurs for it is obvious that it is incompatible with flight, and with life indeed. The principal effect upon the lungs of obstruction to the passages seems to be expressed in congestion but in how far this is due actually to the closure of foramina and how far to the cause of obstruction is sometimes difficult to evaluate. It should be remembered that the air sacs are usually looked upon as mucous surfaces continuous with the bronchial wall, there being a deep layer to each membrane possibly continuous with the serous membranes. In mould disease of the lungs there is very commonly a colony lying in the ostium supplying the anterior, lateral and posterolateral cavities.

The lungs in birds are not free as in mammals, being fitted into the troughs made by the anterior ridges of the ribs, to the serous covering of which they are lightly attached by delicate fibres running between the two. This more or less definite fixation, together with the pressure of the air in the sacs give the free play of the lungs a limited excursion. They are naturally very elastic by reason of a good supply of elastic fibers and large air spaces, a condition aided by their attachments to the supports of the diaphragm and to the insertions of the air sac walls. Notwithstanding this elasticity and the great capacity of the organ for blood, it seems as if congestion of the lungs is a very serious matter, since from the foregoing review of anatomy, accommodation of excess blood and any consolidation must be difficult. As a matter of fact the mere excess of blood known as active congestion seems able to kill small varieties.

CONGESTION OF LUNGS.

Birds of flight seem to have little resistance to this condition and often it is the only diagnosis one can make at autopsy. The causes of this condition include exposure, dust, gorging (?), indigestion, enteritis and infection in birds while in mammals acute gastrointestinal disease stands out as the most prominent accompaniment. To what extent dust and exposure operate I do not see, although they are frequently mentioned as causes. The overfilling of the crop, esophagus and proventricle, the turgescence incident to gastric indigestion or the pressure of foreign bodies in large amount are supposed to operate by exerting pressure on the anterolateral air sacs with closure of their ostia and also by right lateral torsion of the heart with twisting of the very delicate pulmonary veins.

I have sought to show that protozoa or embryo nematodes in the blood might embarrass the lungs to a state of congestion, a thought suggested by some findings in the London Gardens, but only about ten per cent. of our cases of hemic parasitism are accompanied by it.

The incidence of congestion of the lungs not due to stasis as from cardiac diseases, is 2.4 per cent. in mammalian autopsies, in only 7 per cent. of which figure did it represent the principal morbid anatomy, whereas in birds it occurred to the extent of 7.6 per cent. of postmortems, in 17 per cent. of which it was the sole or principal cause of death. This seems to bear out the feature of delicacy of the pulmonary vascular mechanism in these latter animals. This condition seems to be indicated by simple dyspnœa in birds, relief for which has occasionally been afforded by removal from the exhibition cages and protection separately in a warm dry room; this is partly hypothetical of course and congestion is to be looked upon as serious, particularly in passerine birds.

PNEUMONIA.

Pneumonia as a clinical disease is a relatively uncommon, although quite serious sporadic condition in animals. However accompanying the specific, more or less epizoötic diseases such as influenza, distemper and the choleras it may be a frequent and quite pronounced complicating feature of the case. Pneumonia _per se_ has exacted a reasonable toll in this Garden but unfortunately recognition being impracticable, diagnosis and treatment have not progressed. Nor has it been practicable to group our cases pathologically because of the lack of history and the difficulty of making bacteriological observations at many autopsies. Fortunately we have had practically no epizoötic pneumonias, an experience shared with other gardens judging by their published reports. Etiologically, and of course this applies to non-verminous, non-mycotic and non-tuberculous cases, the pneumococcus has stood out prominently as a cause with a few additional cases due to the streptococcus and the Bact. aerogenes mucosum group; London reports four cases in monkeys due to the Friedlander bacillus. Some time ago Doctor Weidman subjected our pneumonias to an analysis and was able to show that there is no parallelism between the seasonal incidence of pneumonia in man and animals, rather indeed that the Garden is more apt to have a greater number of cases in the summer, a sort of “closed season” for man. This I am inclined to interpret as connected with the larger number of visitors during that season. Doctor Weidman was further able to show that the only real examples of lobar fibrinous pneumonia strictly comparable to the human infection occurred in the Primates. I have uncovered one in a lemur and one in a carnivore. The pneumococcus has been far and away the greatest producer of our pneumonias, in two typed cases being of the IV variety. There will be given below a summary of the pathological types of pneumonia encountered, to be followed by some notes upon the principal gross and minute anatomy in special orders. Table 9 will show the numerical distribution of types among the orders. All the principal mammalian orders are represented while the birds seem relatively less susceptible to the disease and, except the Passeres, show a trifling incidence.

TABLE 9. _Showing the Number of Cases of the Various Forms of Pneumonia Found in Each of the Orders._ ════════════╤═════════╤═════════╤═══════╤══════╤══════════╤═══════╤═══════════ │Fibrinous│Catarrhal│ Acute │Septic│Hypostatic│Chronic│Pleurogenic │ Lobar │ │Inter- │ │ │Inter- │ │ │ │stitial│ │ │stitial│ ────────────┼─────────┼─────────┼───────┼──────┼──────────┼───────┼─────────── Primates │ 4│ 22│ 2│ 1│ 1│ 2│ 2 Lemures │ 1│ 3│ │ │ │ │ Carnivora │ 1│ 34│ │ 4│ │ 1│ Insectivora │ │ │ │ │ │ │ Chiroptera │ │ │ │ │ │ │ Rodentia │ │ 6│ │ 3│ │ │ Ungulata │ │ 14│ │ 5│ 1│ 1│ Proboscidea │ │ 1│ │ │ │ │ Hyracoidea │ │ │ │ │ │ │ Edentata │ │ 1│ │ │ │ │ Marsupialia │ │ 13│ 1│ │ 1│ │ Monotremata │ │ │ │ │ │ │ │ │ │ │ │ │ │ Passeres │ 1│ 59│ 2│ 2│ │ │ Picariæ │ │ │ │ │ │ │ 1 Striges │ │ 3│ │ │ │ │ 1 Psittaci │ 1│ 15│ │ │ │ 1│ Accipitres │ │ 1│ │ │ │ │ Columbæ │ │ 2│ │ │ │ │ Galli │ │ 2│ │ │ │ │ Hemopodii │ │ │ │ │ │ │ Fulicariæ │ │ 1│ │ │ │ │ Alectorides │ │ │ │ │ │ │ Limicolæ │ │ │ │ │ │ │ Gaviæ │ │ │ │ │ │ │ Impennes │ │ │ │ │ │ │ Steganopodes│ │ │ │ │ │ │ Herodiones │ 1│ │ │ │ │ │ Odontoglossæ│ │ │ │ │ │ │ Palamedes │ │ │ │ │ │ │ Anseres │ 1│ │ │ │ │ │ Struthiones │ │ │ │ │ │ │ ────────────┴─────────┴─────────┴───────┴──────┴──────────┴───────┴───────────

Primates present a definite group of variations from the other orders, notably in having four clear cases of lobar fibrinous pneumonia, and in certain histological findings. In reference to the lobar cases, a review of their history does not indicate that any might have been surely diagnosed by their symptoms, and only possibly by signs in one case during the stage of red hepatization; unfortunately no temperature records are at hand. In one case it was possible to see a group of alveoli with the fibrin collected in a strand which, according to classical description, passes through the septum to the adjoining alveolus.

There were two cases, a Chimpanzee (_Pan niger_) and a Galago (_Galago maholi_) with a microscopical picture suggestive of those we met in the influenza epidemic, and indeed the lung of the former resembles grossly the lung of influenza pneumonia. The spotty areas of watery purple color correspond under magnification to celluloedematous semisolid sections showing a sanguineous exudate, few polynuclear cells and many swollen epithelia. The microscopic picture of the bronchocatarrhal pneumonias shows conspicuously thickened septa decidedly wider than one is accustomed to see in human cases and apparently due more to round cell infiltration than to congestion or polynuclear increase.

Bronchopneumonia or capillary bronchitis with zones of cellular edema in the vicinity is a rather usual picture in the deaths from degenerative bone disease. It cannot be said that there is anything very peculiar about it, although a frequent note met in the autopsies describes spotty areas of hemorrhage and nearby atelectasis.

The case of lobar pneumonia found in a ring tailed lemur (_Lemur catta_) showed very delicate fibrinous reticulum and relatively few cells in the exudate, a picture apparently due in part to beginning resolution since the whole upper left lobe was in a stage of gray hepatization.

The peculiarity of the Carnivora seems to lie in the reaction of the epithelia, these cells being quite large, swollen and occasionally much vacuolated. Such a picture was most pronounced in the terminal bronchitic pneumonias in cases which might be called distemper. Many instances of pseudolobar catarrhal or bronchopneumonia are recorded but we also observed the fibrinous lobar form at the stage of red hepatization in a Texas skunk (_Mephitis mesomelas_). Concerning the orders Rodentia and Edentata no especial notes seem necessary for their inflammatory reactions are essentially like the others in that epithelial cells are much swollen and prominent.

Pneumonias of Ungulata are well known to pathology and offer in causation and microscopy little that is peculiar. It might be emphasized however that the gross appearance of the bronchocatarrhal variety closely simulates that of lobar pneumonia, therefore to be called a pseudolobar form, in that extension to various parts of a lobe seems to occur. Moreover in the bronchitic varieties associated with enteritis, with or without infectious foci in the pharynx or larynx, there may be two or even three stages of the pneumonitic process in one lung or lobe. It seems that this pseudolobar appearance occurs definitely more often in ungulates than in the other orders.

Marsupialia offer two rather easily grouped classes of bronchopneumonia— one associated with enteritis and one secondary to “Kangaroo disease” of the jaw; they differ in microscopy correspondingly. The simple bronchitic and peribronchitic infiltrate and superficial exudate occurring with enteritis or with a general infection is relatively diffuse, giving in some instances the impression of an interstitial process and showing notably swollen septa; there may be fibrin but this is exceptional and scanty. When mycosis of the jaw has been the origin or occasion of the infection the picture is that of frank aspiration pneumonia, therefore more like a septic infarct. However the amount of fibrin is sometimes very great and whole alveoli will be filled with it, perhaps accompanied by red cells, polynuclears and epithelia. Epithelial cells however play a small part in the minute anatomy. Hemorrhage and edema are prominent but true abscess formation and gangrene are not. Possibly the animals die too soon for the latter to develop.

Pneumonia in Aves aside from that due to moulds is apparently much less common than among the Mammalia, one order only, the Passeres, showing an incidence comparable to the important orders of the latter class. The other orders, and this applies particularly to those of which we have an adequate number, are quite insusceptible to simple pneumonia, none of them showing over two per cent. There are listed for Aves three instances of lobar fibrinous pneumonia. These cases can be described together since in all the findings were about the same. A whole lung or goodly portion thereof was uniformly involved in a red or gray consolidation of rather fine granular character which on section study seemed to be made up of the same lesion all over, with fibrin a prominent part of the exudate. The coagula were largely within the secondary alveoli but the primaries also contained it. The microscopic section may not have represented the process at all places, and since the arrangement of fibrin is similar in definitely catarrhal lesions, these may of course have been instances of pseudolobar pneumonia.

Our data are too few to draw any conclusions as to the behavior of the various orders but one note may be permitted. The passerine birds have a great tendency to dense cellular infiltrates while parrots show more coagulative or fluid exudates.

PRODUCTION OF INSULAR PNEUMONIA IN BIRDS.

Insular consolidations in which catarrhal and infiltrative processes are prominent, the bronchopneumonias, seem to arise in two ways. One course of events apparently follows infection _via_ the bronchial mucosa, the other _via_ the blood stream and a study of the resulting lesions may help toward an understanding of the development of pneumonia in man.

When infection unquestionably has been superficial, that is _via_ the bronchus, the first thing to happen is a swelling of the septal prolongations dividing the primary alveoli and an extension of their ends farther into the secondary alveoli with the result that the inlet to the primary air sacs is narrowed and the space in the secondaries is reduced. Upon the surfaces there then develops the usual catarrhal exudate while in the deeper parts marked congestion makes its appearance. Fibrin may develop and be mixed with the cells both in the larger and smaller alveoli but it is more evident in the former. (Figs. 8, 9, 10.)

The other process by which insular pneumonia develops seems to begin in the septa of the smaller alveoli and in the perivascular areas. This has been looked upon as hematogenic or pleurogenic. The first change occurs in the surroundings of the primary alveoli where there appears a richness of nuclei, of round, moderately well stained character, among which one may see a few granular and red blood cells. Soon the epithelia of adjacent alveoli increase in number and a fibrinocellular exudate appears, at first probably in the smaller sacs. However when the lesion is intensive the course of events must be rapid for the identity of a group of primary alveoli is soon lost and the exudate may extend to the larger air space. (Fig. 11) In severe or late cases a decision as to the course of origin is often impossible. The most instructive point of this part of the study is the closing of primary alveoli by the swelling of their septal ends and the early occlusion of the secondary alveolus by a catarrhofibrinous or even pus-like material. It is quite possible that a similar course of events transpires in the pathogenesis of human pneumonia, the superficial avian form being comparable to the aspiration form, the interstitial form comparable to the septicemic variety.

ABSCESS AND GANGRENE OF LUNG.

Abscess and gangrene of the lung are degenerative processes dependent upon embolism, or inspiration of infective matter and it is usually assumed that gangrene succeeds upon abscess when the blood or air supply of a part of the pulmonary tissue has been obstructed mechanically or by inflammation. A review of our material adds little to the etiology or pathogenesis of these two lesions, well recognized as they are by veterinarians. As opposed to human beings, lower animals probably suffer more from them, for an explanation of which one can probably look to the B. necrosis or necrophorus, an organism quite common in feed, and acknowledged to be of great importance as a secondary invader during specific infectious diseases. It has been found in embolic abscesses and in the organs in calf diphtheria and similar other conditions. It has been cultivated here twice, once from a lung abscess, once from Kangaroo disease. It doubtless occurs in human necrotizing processes but is seldom emphasized or even heard about; possibly none is due to it or its congeners.

TABLE 10.

_Table giving Analysis of 20 Mammalian and 3 Avian Cases of Abscess and Gangrene of the Lung_