Part 15

_Abdomen._—The first abdominal tergite contains 2 rows of about 4 bristles each, while the other tergites to the seventh contain a single row of from 12 to 16 bristles. The stigmata are large. There is a single antipygidial bristle on each side. The sternites from third to seventh have a single row of 4 bristles each.

_Legs._—The hind coxa has on its inner side a patch of from 6 to 12 spines, while the hind femur has a row of 10 or 12 bristles on its inner surface. The spines on the posterior border of the hind tibia, with the exception of the apical, are in pairs, while in the apical group are about 3 stout bristles. The apical spine of the second joint of the hind leg reaches to nearly the middle of the fifth joint. On the fifth joint of all the legs there are 4 lateral spines and a subapical pair, and between the third and fourth lateral spines there is a hair.

_Modified segments._—(♀) The eighth tergite has no hairs back of the stigma. The apical margin is rounded at the apex and contains 8 or 10 bristles. The stylet is short and wide and contains at its tip a long and a short bristle.

(♂) The manubrium is short and narrow. The movable finger of the clasper is short, thick, swollen at its middle, bluntly rounded at its extremity, and contains on its upper border numerous hairs and a few on its lower border.

Rothschild[209] has pointed out certain differences between the _Ctenocephalus canis_ and _Ctenocephalus felis_. The differences are that in the female of the felis the head is longer and more pointed. This difference is not so pronounced in the male. Also certain differences in the shape of the claspers and the number of bristles in the episternum and epimerum of the metathorax and the hind femur, those in the _C. canis_ being more numerous. Also that group of bristles on the posterior border of the hind tibia between the fifth pair and the apical bristles consists of two in the _Ctenocephalus canis_, while there is but a single bristle with a small hair in the _Ctenocephalus felis_.

REFERENCES.

Endnote 201:

1909, McCoy.—“Plague Bacilli in Ectoparasites of Squirrels.” Public Health Reports, Vol. XXIV, No. 16.

Endnote 202:

1908, Schumann.—“A Disease of Rats Caused by Mites.” Centralblatt f. Bact., Oct. 30th.

Endnote 203:

1909, McCoy and Mitzmain.—“An Experimental Investigation of the Biting of Man by Fleas Taken from Rats and Squirrels.” Public Health Reports, Vol. XXIV, No. 8.

Endnote 204:

1908, McCoy.—“A Report on Laboratory Work in Relation to the Examination of Rats for Plague at San Francisco, California.” Public Health Reports, Vol. XXIII, No. 30.

Endnote 205:

Wagner.—Aphanipterologische Studien aus dem zootomischen laboratorium der Universität zu St. Petersburg.

Endnote 206:

1908, Mitzmain.—“How a Hungry Flea Feeds.” Entomological News, December.

Endnote 207:

1908, Miller.—“Hepatazoon Perniciosum (N. G. N. SP.). A Hæmogregarine Pathogenic for White Rats; With a Description of the Sexual Cycle in the Intermediate Host; A Mite (Lælaps Echidninus).” Bull. No. 46, Hyg. Lab. U. S. Pub. Health and Mar. Hosp. Serv., Wash.

Endnote 208:

1908, Jordan and Rothschild.—“Revision of Non-Combed Eyed Siphonaptera.” Parasitology, Vol. I, No. 1.

Endnote 209:

1901, Rothschild.—“Notes on Pulex canis, Curtis, and Pulex felis, Bouché.” Entomologist’s Record, Vol. XIII, No. 4.

1905, Rothschild.—“Some Further Notes on Pulex canis, Curtis, and Pulex felis, Bouché.” Novitates Zoologicae, Vol. XII.

RODENTS IN RELATION TO THE TRANSMISSION OF BUBONIC PLAGUE.

By Surgeon RUPERT BLUE,

_United States Public Health and Marine-Hospital Service_.

Man has associated the rat with bubonic plague since the dawn of history. The monuments and coins of the earliest times yield abundant evidence of this association. Æsculapius, the god of the healing art, is represented by the Greeks with a rat at his feet. An early scriptural reference may be found in the first Book of Samuel in the fifth and sixth chapters. The historian records therein the occurrence of a fatal epidemic of “emerods” in the land of the Philistines coincident with an invasion of “mice.”

The inhabitants of southern China in recent times have learned to look upon the finding of sick and dead rats in their homes as a harbinger of evil, in fact, as a forerunner of that dread scourge—“wan-yick,” or plague. In the villages and cities of the Kwantung and Kwangsi provinces, as recorded by medical missionaries, epizootic plague almost invariably precedes an outbreak among human beings. So well is this fact known to the common people that many seek safety in flight, feeling assured that in a short time “yang-tzu” or “wan-yick” will claim a harvest of victims among those who remain.

Doctor Mahē, sanitary officer for the port of Constantinople, in 1889, called attention to the fact that epidemics of plague were always announced by a great mortality among rats and mice. In 1894 Yersin reported the fatal epizootic among rats then prevailing in Canton and Hongkong coincident with the outbreak of plague among the Chinese. Recent researches have confirmed these observations and a great deal has been added to the literature of plague, especially in relation to its mode of transmission. Indeed, it should be said that wherever the disease has prevailed in recent years the relation of rats to its spread has been observed, and that since the discovery of the specific bacillus by Yersin and Kitasato, in 1894, bacteriological investigations have shown that there is no difference morphologically or culturally between the bacilli of human and rat plague. Moreover, the gross and microscopic lesions in the lymph nodes are practically the same, and the _B. pestis_ recovered in both fulfills the postulates of Koch.

Nothing was definitely known, however, of the mode of transmission of the disease from rat to rat or from rat to man until the completion of the experimental work of the Indian Plague Commission. Simond, Ogata, Thompson, and Koch each expressed the belief that the infection was transferred by the rat flea. Nuttall (1897) and Simond (1898) demonstrated the presence of _B. pestis_ in the bodies of bugs (_Cimex_) and fleas which had been taken from plague-sick rats, and the latter observer, in the same year, succeeded in transmitting the disease from rat to rat without contact.

The work of the Indian Plague Commission was undertaken (1905) with a view to establishing the exact relationship between epizootics among rats and epidemics among men, and included both field and laboratory observations. The experiments of Gauthier and Raybaud (1903) and of Simond were repeated on a larger scale and greatly improved in that all rats and fleas used were first identified as to species. The findings of the commission may be briefly summarized as follows: That fleas and bugs taken from plague-sick rats contain _B. pestis_, and that some of them remain alive in the bodies of the insects from five to sixteen days; that plague is conveyed by the bites of fleas which have previously fed on the blood of animals suffering with the disease; that rat fleas bite man; that under experimental conditions the infection is not transferred from rat to rat in the absence of fleas.

A careful study of the findings of the workers in India justifies the assumption that plague is a disease of the rodent primarily and accidentally, and secondarily a disease of man. An analysis of the epidemiological facts collected in San Francisco leads to the same conclusion. As a result our practice with regard to suppressive measures and quarantine procedure has undergone a radical change in the last decade. If the infection is flea-borne from rat to man in the majority of cases, then the extermination of the rat should be the first principle upon which to base a campaign. In the former contribution on the subject (1907) I stated that “if we destroy the host there is no longer danger of infecting the parasite.” This basic principle has been recognized and successfully applied in two campaigns against plague in San Francisco. First in the outbreak in Chinatown in 1903–4, and again in the larger epidemic of 1907.

The outbreak of 1907 began May 27, a little over a year after the great fire and earthquake, but no cases were discovered between that time and mid-August when the disease began to appear in various parts of the city. The source of infection was, in all probability, a recrudescence from a focus which was not destroyed in the campaign of 1903–4. There occurred 160 cases with 77 deaths, the last case appearing January 30, 1908. The following table shows the incidence of human plague:

─────────────────────┬───────┬─────── Year. │Cases. │Deaths. ─────────────────────┼───────┼─────── 1907. │ │ May │ 1│ 1 August │ 13│ 6 September │ 56│ 25 October │ 34│ 25 November │ 41│ 12 December │ 13│ 7 1908. │ │ January │ 2│ 1 ─────────────────────┼───────┼─────── Total │ 160│ 77 ─────────────────────┴───────┴───────

EPIDEMIOLOGICAL OBSERVATIONS IN SAN FRANCISCO.

Abundant epidemiological data associating the rat[AE] with plague have been collected in San Francisco. For the purpose of illustration a detailed reference to a few cases will be made. Two small boys (October, 1907) while playing in an unused cellar found the body of a dead rat. The corpse was buried with unusual funeral honors. In forty-eight hours both were ill with bubonic plague. A laborer finding a sick rat on the wharf picked it up with the naked hand and threw it into the bay. He was seized three days later with plague. Doctor C. and family lived in a second-story flat over a grocery store in the residence section. Being annoyed for some days by a foul odor the doctor caused the wainscoting around the plumbing to be removed. One or two rat cadavers were found in the hollow wall. In two or three days the two members of the family who used the room sickened, one dying on the fifth day of cervical bubonic plague. It is probable that infected rat fleas were set free by the removal of the wainscoting.

Footnote AE:

_M. norvegicus_ and _M. rattus_.

Dead rats were frequently found in or near houses where plague had occurred. Immediately upon the discovery of a case of plague trained men were sent into the neighborhood and a thorough search made for rats. This work consisted in the removal of defective wooden floors and walls of insanitary buildings and other harboring places. Extensive rat catacombs were frequently found in these operations. In the yard of a house in which 4 cases had occurred 20 cadavers were found under the board covering. In the walls of a Chinese restaurant 87 dead rats were uncovered.

Very little can be said of the relation of mice (_M. musculus_) to the epidemic. While many thousands were trapped, only a few hundred were examined microscopically and in these no infection was found. They are nonmigratory in habit and for this reason are not considered of much importance from an epizoological standpoint.

Transmission from man to man was observed in but a small percentage of cases, 3 per cent to be exact. In these the probability of transference by fleas (_P. irritans_) or by bugs (_Cimex_) must be admitted. When more than one case occurred in a house a common source of infection was indicated, such cases occurring simultaneously or within from forty-eight to seventy-two hours after the first. Deratization was the measure mainly relied upon. After an infected house was rat proofed, and the harboring places in the block destroyed, no further cases occurred.

The course of epizootic plague was not interrupted at any time by climatic conditions, there being as many cases in proportion to the rat population in the winter of 1908 as there were at the height of the epidemic. The last case of human plague occurred January 30, 1908, but the infection remained active among rats for eight months longer, or until October 21, 1908. (See following table.)

─────────┬─────────┬─────────┬─────┬────────────┬────────┬───────────── Month. │ Number │ Number │ Per │ Average │Rainfall│Character of │examined.│infected.│cent.│temperature.│ in │ days. │ │ │ │ │inches. │ ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── 1907. │ │ │ │ °F. │ │{Clear, 13. September│ 1,002│ 27│ 2.69│ 60.6│ 0.11│{Part cloudy, │ │ │ │ │ │15. │ │ │ │ │ │{Cloudy, 2. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 10. October │ 2,679│ 23│ .86│ 60.6│ 1.36│{Part cloudy, │ │ │ │ │ │10. │ │ │ │ │ │{Cloudy, 11. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 14. November │ 3,954│ 36│ .88│ 57.8│ .04│{Part cloudy, │ │ │ │ │ │13. │ │ │ │ │ │{Cloudy, 3. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 6. December │ 4,308│ 48│ 1.11│ 52.4│ 3.66│{Part cloudy, │ │ │ │ │ │11. │ │ │ │ │ │{Cloudy, 14. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── 1908. │ │ │ │ │ │{Clear, 5. January │ 6,622│ 70│ 1.05│ 50.8│ 4.88│{Part cloudy, │ │ │ │ │ │11. │ │ │ │ │ │{Cloudy, 15. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 11. February │ 11,700│ 45│ .38│ 51.0│ 5.39│{Part cloudy, │ │ │ │ │ │12. │ │ │ │ │ │{Cloudy, 6. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 20. March │ 19,263│ 52│ .26│ 54.8│ .90│{Part cloudy, │ │ │ │ │ │10. │ │ │ │ │ │{Cloudy, 1. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 17. April │ 15,524│ 34│ .21│ 56.3│ .22│{Part cloudy, │ │ │ │ │ │10. │ │ │ │ │ │{Cloudy, 3. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 17. May │ 11,311│ 20│ .13│ 55.4│ .76│{Part cloudy, │ │ │ │ │ │12. │ │ │ │ │ │{Cloudy, 2. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 16. June │ 13,624│ 4│ 0.02│ 55.3│ 0.01│{Part cloudy, │ │ │ │ │ │9. │ │ │ │ │ │{Cloudy, 5. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 11. July │ 11,204│ 2│ .017│ 57.4│ .02│{Part cloudy, │ │ │ │ │ │17. │ │ │ │ │ │{Cloudy, 3. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 11. August │ 10,988│ 0│ .0│ 57.3│ .01│{Part cloudy, │ │ │ │ │ │10. │ │ │ │ │ │{Cloudy, 10. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 16. September│ 15,902│ 0│ .0│ 59.3│ .29│{Part cloudy, │ │ │ │ │ │9. │ │ │ │ │ │{Cloudy, 5. ─────────┼─────────┼─────────┼─────┼────────────┼────────┼───────────── │ │ │ │ │ │{Clear, 16. October │ 10,178│ 2│ .019│ 58.8│ .061│{Part cloudy, │ │ │ │ │ │7. │ │ │ │ │ │{Cloudy, 8. ─────────┴─────────┴─────────┴─────┴────────────┴────────┴─────────────

The rats examined for September, 1907, were very largely collected from the badly infected districts; the remaining months give a truer picture of the extent of the epizootic in the entire rat population.

THEORIES AS TO THE CAUSE OF SEASONAL PREVALENCE.

The marked seasonal prevalence of plague in man in San Francisco may be given as additional proof of the association of the rat with its spread. In the cold, rainy season, from December to April, the epidemic ceases while the epizootic is apparently not influenced. The anomaly is accounted for when we remember that the rat and its parasites are very susceptible to cold and rain. It is then that the animal seeks a warm, comfortable place from which it does not venture until driven thence by dire necessity. In other words, the association of the rat with man is not so intimate in winter, while the reverse is true of the relation of rat with rat. The rains, while interrupting the overground migrations and domiciliary visits of rats, drive them to overcrowded burrows and harboring places. Another factor should be mentioned in this connection. Human fleas (_P. irritans_), and probably rat fleas also, are markedly reduced in numbers at that season of the year. We must conclude, therefore, that the seasonal prevalence of plague in man is due to the effect of climatic conditions upon the habits of rats and the life history of the insect carriers of the bacilli.

An examination of the foregoing should convince everyone that all former theories as to the prolonged viability of _B. pestis_ in contaminated soil or in polluted streams, and of the periodical spread of the infection therefrom, are no longer tenable. It may also be stated that insanitary conditions, except in so far as they furnish food and shelter to rats and other vermin, play no important rôle in the continuance of plague. This general revision has also eliminated overcrowding as an important factor. In the absence pneumonic cases, and of suctorial insects, this _bête noire_ of the sanitarian may be disregarded.

THE OCCURRENCE OF PLAGUE IN THE MARMOT OF ASIA AND THE GROUND SQUIRREL OF CALIFORNIA.

Rudenko (1900) first pointed out the possibility of contagion by the “Tarbagan,” a species of the _arctomyinæ_ found in Siberia. He observed a connection in 1894 between this rodent and an outbreak of plague in a Cossack family of Soktuewsk. According to Beliatsky and Zabolotny, each having been an observer in the same field, the natives of Siberia and Mongolia often acquire plague in this manner. Le Dantec and other writers have called attention to the probable susceptibility of the marmot (_Arctomys bobac_), a hibernating rodent of India and China. The marmot of Thibet, in the opinion of this writer, is the natural animal host and purveyor of the virus. The literature of the subject presents no bacteriological evidence, however, of such a relationship, and plague in the _arctomyinæ_ of Asia is merely an hypothesis. There is positive evidence though of the susceptibility of the tree squirrel (_Sciurinæ_) to plague infection. Dr. Alice Corthorn (1898) reported the finding of a plague-infected squirrel in one of the outbreaks in the Bombay Presidency.

PLAGUE INFECTION IN GROUND SQUIRRELS.[AF]

Footnote AF:

Genus Citellus, Oken; subgenus Otospermophilus. “California Mammals,” Frank Stephens.

The demonstration of natural plague in the California ground squirrel (_Otospermophilus beecheyi_) is perhaps the most important observation of the antiplague work of the service in 1908. The existence of a plague epizootic in Contra Costa County was suspected as early as the summer of 1903, and efforts were made at that time to collect sick and dead rodents for bacteriological examination. In August (1903) two fatal cases of human infection occurred in widely separated sections of the county. The investigation which followed failed to connect either with a previous case of human plague, but showed an association with ground squirrels. These deaths occurred during a fatal epizootic among ground squirrels and suggested a connection which unfortunately was not confirmed.

None of the circumstances were forgotten, however, and in the second campaign, begun in September, 1907, in San Francisco, inspectors were detailed to examine all persons dying in the area under suspicion. No plague was reported that autumn and winter. Fatal cases occurred and were reported by the inspectors in July, 1908, as follows: A boy (J. F.) died July 15, near Concord, and a young woman (M. P.) died July 28, on a ranch 10 miles from Martinez. The two were not associated. An investigation was ordered at once and a force of trappers was hurried to the scene with instructions to collect squirrels from the ranches in the vicinity. The first plague-infected squirrel was found August 5 on the ranch where the boy had died July 15. Of 425 squirrels collected from August 1 to October 12, 4 showed the gross and microscopic lesions of natural plague.