During the recent outbreak of plague in Manila, several samples of bed-bugs from the beds of the plague patients and dog fleas from a plague-infected house were collected and examined, but with negative result.In spite of the fact that it adds nothing new to the question of whether or not plague can be transmitted by fleas, since the question has been conclusively answered by the work of the Indian Commission, nevertheless the following observations of a small outbreak of plague among animals, the spreading of which was due solely to fleas, are of interest.One wild rat was inoculated with strain Iloilo 3 ofBacillus pestis. The skin adjoining the root of the right ear was scarified, and a loopful of the culture was smeared on the scarified skin. The rat was found dead three days after the inoculation.The cage containing the dead rat was immersed in kreolin solution. At autopsy the cervical glands were found slightly swollen, somewhat reddened, but no hæmorrhagic œdema of the surrounding tissue was noticeable. There was slight necrosis at the place of inoculation, showing superficial, purulent discharge. Clear effusion in both pleural cavities and one hemorrhage in the pleura were found. The lungs were hyperæmic, but otherwise normal. The spleen was of somewhat darker color, but otherwise normal in size and appearance. The liver showed a slight degree of parenchymatous degeneration, the congestion making prominent the structure of the organ. The typical, although not constant, changes of the organ, which are characteristic of natural plague infection in rats, were absent. The kidneys were without macroscopic change. The lymph glands, with exception of the cervical nodes, were normal.Examination of the rat's fur revealed ectoparasites on the neck, under the chin, and back of the ears; these at the time of the examination apparently were dead. About 6 common rat fleas were found and identified asLœmopsylla cheopisRothsch. The parasites were immersed in sterile salt solution for three hours. When removed in a dry test tube, they began to move about sluggishly. The intestinal tract of these fleas contained blood.Five of the fleas were crushed by means of sterile forceps, and inserted in a pocket under the shaved skin of a guinea-pig. The animal died of plague within three days, showing considerable hemorrhagic œdema aroundthe place of inoculation, typical bilateral inguinal buboes, and characteristic changes in the spleen. Smears and cultures made from the bubo and spleen were positive forBacillus pestis.Another wild rat, which was in a separate cage in the same room where rat 1 had been kept, died twenty-four hours after rat 1. The two cages were at least 10 centimetres apart. Rat 2 harbored fleas of the same species as were found on rat 1.Numerous severe bites were detected back of the ears and on the neck of the dead animal. The post-mortem findings were identical with those described in rat 1; that is, cervical buboes, pleural effusion, and slightly enlarged spleen.It is well to remark that both rats had been kept in the same room for about six months. Fleas had never been noticed on our guinea-pigs. During the time the rats had been kept in the plague house no irregular results were noticed in plague-inoculated animals. At the time the first rat was inoculated no other plague-infected animals were in the plague house, and since that time another building has been used for plague-infected animals.Two days after the death of rat 2 three guinea-pigs, which were kept in separate cages in the same room, were found dead of plague (smears and cultures were both positive). Several fleas (Lœmopsylla cheopis) were found on the necks of these animals. They were collected and inoculated in the same way as the fleas from the first rat. The experimental animal, which was inoculated with the fleas, was killed and found to be infected with plague. The findings were local reaction, inguinal buboes, and typical spleen. Smears and cultures were positive forBacillus pestis.Although numerous healthy guinea-pigs were examined in the same plague house, no fleas could be found at that time, only the 2 rats and the first 3 guinea-pigs are positively known to have harbored fleas, the latter after the death of the rats and not before.The gross lesions in these naturally infected guinea-pigs were somewhat unlike those found in guinea-pigs infected either by vaccination or by intraperitoneal or subcutaneous inoculation. All except one showed primary buboes on the neck with more or less extensive hemorrhagic œdema extending in some cases over the thorax. There was little pleural effusion present; the spleen always showed typical changes of necrotic foci varying in size and number. In one instance similar foci were found also in the liver, large enough to be visible macroscopically. This was in a case where like changes were found in the lungs.Only one of the guinea-pigs showed an exception, in that the primary buboes were located in the inguinal region, with pelvic and axillary glands secondarily involved. These are the findings usually met within guinea-pigs artificially infected with plague by the vaccination method, if the lower part of the abdomen be chosen for inoculation. The reason for such a deviation from the findings in the rest of the guinea-pigs may lie in the fact that this animal was almost completely deprived of hair by a skin disease.It is of importance to mention the skin lesions which were found on the necks of the guinea-pigs, particularly under the chin. Besides small red spots which appeared to be fresh flea bites, small, elevated, and fairly deep infiltrations partly covered with moist scab were found in the skin under the chin. Other animals showed changesusually found in the scarified skin of guinea-pigs after artificial inoculation with plague material. The base of each cutaneous efflorescence was hemorrhagic and œdematous.A histological study of the tissues of these guinea-pigs known to be naturally infected by plague fleas showed the following changes:The Cervical Bubo.—The enlarged lymphatic gland was surrounded with a thickened capsule. Necrosis existed in the subcapsular part of the gland, where it formed an almost continuous circular zone, leaving the central part less changed. Smaller irregular necrotic foci were scattered throughout the section. Polymorphonuclears in various stages of disintegration were found throughout the section.The Lungs.—Very few blood extravasations were present in the alveoli; otherwise normal.The Spleen.—The capsule was thin. There were subcapsular hemorrhages. The Malpighian bodies were somewhat enlarged, but of normal structure. Throughout the parenchyma irregular multiple necrotic foci were found, leaving but little of spleen tissue intact. Numerous polymorphonuclears which were present showed varying degrees of karyorrhexis.The Kidneys.—The outline of the cells was indefinite; a few miliary hemorrhages existed in the cortical part of the organ.The Liver.—There was excessive congestion, fatty degeneration, and pigmentation of the cells. The capsule was slightly thickened.The Skin.—The epithelium was missing in one place in the section, and cellular infiltration extended from that place into the subepithelial layer of the surrounding skin.The same kind of infiltration reached deep into the skin, stripes of cellular infiltration penetrating into the tissue along the muscle fibres. There was no direct connection between the cellular infiltration and the follicles of the hair.It may be well to describe in detail the time of death from plague among these and the other animals in this outbreak, as well as the time when the plague house was disinfected.The first animal (rat 1) having been inoculated on August 27, in the afternoon, died of plague within three days (August 30). The second animal (rat 2) died twenty-four hours later. Guinea-pigs 3, 4, and 5 (see plan) were found dead on the morning of September 2; that is, two days after the death of rat 2 and three days after the death of rat 1.The same day that the three guinea-pigs were found dead of plague, rooms I, III, IV, and VI were thoroughly disinfected. The floor, the ceiling, and the walls were sprayed with kerosene and lysol solution. The remaining animals in room VI were destroyed, and the cages disinfected. No animals were kept in rooms I, III, and IV at that time.Three days after the death of animal 5, guinea-pigs 6 and 7 were found dead of plague, while the next day guinea-pigs 8 and 9 died. No death occurred on September 7, but the next two days each recorded two plague guinea-pigs (10, 11, 12, and 13). On September 11, the last guinea-pig died of plague in this outbreak. The whole building was then thoroughly disinfected. No plague-inoculated animals were kept in the rooms after the first sign of the epidemic. After September 11, no more cases of spontaneous plague infection were observed.
During the recent outbreak of plague in Manila, several samples of bed-bugs from the beds of the plague patients and dog fleas from a plague-infected house were collected and examined, but with negative result.
In spite of the fact that it adds nothing new to the question of whether or not plague can be transmitted by fleas, since the question has been conclusively answered by the work of the Indian Commission, nevertheless the following observations of a small outbreak of plague among animals, the spreading of which was due solely to fleas, are of interest.
One wild rat was inoculated with strain Iloilo 3 ofBacillus pestis. The skin adjoining the root of the right ear was scarified, and a loopful of the culture was smeared on the scarified skin. The rat was found dead three days after the inoculation.
The cage containing the dead rat was immersed in kreolin solution. At autopsy the cervical glands were found slightly swollen, somewhat reddened, but no hæmorrhagic œdema of the surrounding tissue was noticeable. There was slight necrosis at the place of inoculation, showing superficial, purulent discharge. Clear effusion in both pleural cavities and one hemorrhage in the pleura were found. The lungs were hyperæmic, but otherwise normal. The spleen was of somewhat darker color, but otherwise normal in size and appearance. The liver showed a slight degree of parenchymatous degeneration, the congestion making prominent the structure of the organ. The typical, although not constant, changes of the organ, which are characteristic of natural plague infection in rats, were absent. The kidneys were without macroscopic change. The lymph glands, with exception of the cervical nodes, were normal.
Examination of the rat's fur revealed ectoparasites on the neck, under the chin, and back of the ears; these at the time of the examination apparently were dead. About 6 common rat fleas were found and identified asLœmopsylla cheopisRothsch. The parasites were immersed in sterile salt solution for three hours. When removed in a dry test tube, they began to move about sluggishly. The intestinal tract of these fleas contained blood.
Five of the fleas were crushed by means of sterile forceps, and inserted in a pocket under the shaved skin of a guinea-pig. The animal died of plague within three days, showing considerable hemorrhagic œdema aroundthe place of inoculation, typical bilateral inguinal buboes, and characteristic changes in the spleen. Smears and cultures made from the bubo and spleen were positive forBacillus pestis.
Another wild rat, which was in a separate cage in the same room where rat 1 had been kept, died twenty-four hours after rat 1. The two cages were at least 10 centimetres apart. Rat 2 harbored fleas of the same species as were found on rat 1.
Numerous severe bites were detected back of the ears and on the neck of the dead animal. The post-mortem findings were identical with those described in rat 1; that is, cervical buboes, pleural effusion, and slightly enlarged spleen.
It is well to remark that both rats had been kept in the same room for about six months. Fleas had never been noticed on our guinea-pigs. During the time the rats had been kept in the plague house no irregular results were noticed in plague-inoculated animals. At the time the first rat was inoculated no other plague-infected animals were in the plague house, and since that time another building has been used for plague-infected animals.
Two days after the death of rat 2 three guinea-pigs, which were kept in separate cages in the same room, were found dead of plague (smears and cultures were both positive). Several fleas (Lœmopsylla cheopis) were found on the necks of these animals. They were collected and inoculated in the same way as the fleas from the first rat. The experimental animal, which was inoculated with the fleas, was killed and found to be infected with plague. The findings were local reaction, inguinal buboes, and typical spleen. Smears and cultures were positive forBacillus pestis.
Although numerous healthy guinea-pigs were examined in the same plague house, no fleas could be found at that time, only the 2 rats and the first 3 guinea-pigs are positively known to have harbored fleas, the latter after the death of the rats and not before.
The gross lesions in these naturally infected guinea-pigs were somewhat unlike those found in guinea-pigs infected either by vaccination or by intraperitoneal or subcutaneous inoculation. All except one showed primary buboes on the neck with more or less extensive hemorrhagic œdema extending in some cases over the thorax. There was little pleural effusion present; the spleen always showed typical changes of necrotic foci varying in size and number. In one instance similar foci were found also in the liver, large enough to be visible macroscopically. This was in a case where like changes were found in the lungs.
Only one of the guinea-pigs showed an exception, in that the primary buboes were located in the inguinal region, with pelvic and axillary glands secondarily involved. These are the findings usually met within guinea-pigs artificially infected with plague by the vaccination method, if the lower part of the abdomen be chosen for inoculation. The reason for such a deviation from the findings in the rest of the guinea-pigs may lie in the fact that this animal was almost completely deprived of hair by a skin disease.
It is of importance to mention the skin lesions which were found on the necks of the guinea-pigs, particularly under the chin. Besides small red spots which appeared to be fresh flea bites, small, elevated, and fairly deep infiltrations partly covered with moist scab were found in the skin under the chin. Other animals showed changesusually found in the scarified skin of guinea-pigs after artificial inoculation with plague material. The base of each cutaneous efflorescence was hemorrhagic and œdematous.
A histological study of the tissues of these guinea-pigs known to be naturally infected by plague fleas showed the following changes:
The Cervical Bubo.—The enlarged lymphatic gland was surrounded with a thickened capsule. Necrosis existed in the subcapsular part of the gland, where it formed an almost continuous circular zone, leaving the central part less changed. Smaller irregular necrotic foci were scattered throughout the section. Polymorphonuclears in various stages of disintegration were found throughout the section.
The Lungs.—Very few blood extravasations were present in the alveoli; otherwise normal.
The Spleen.—The capsule was thin. There were subcapsular hemorrhages. The Malpighian bodies were somewhat enlarged, but of normal structure. Throughout the parenchyma irregular multiple necrotic foci were found, leaving but little of spleen tissue intact. Numerous polymorphonuclears which were present showed varying degrees of karyorrhexis.
The Kidneys.—The outline of the cells was indefinite; a few miliary hemorrhages existed in the cortical part of the organ.
The Liver.—There was excessive congestion, fatty degeneration, and pigmentation of the cells. The capsule was slightly thickened.
The Skin.—The epithelium was missing in one place in the section, and cellular infiltration extended from that place into the subepithelial layer of the surrounding skin.The same kind of infiltration reached deep into the skin, stripes of cellular infiltration penetrating into the tissue along the muscle fibres. There was no direct connection between the cellular infiltration and the follicles of the hair.
It may be well to describe in detail the time of death from plague among these and the other animals in this outbreak, as well as the time when the plague house was disinfected.
The first animal (rat 1) having been inoculated on August 27, in the afternoon, died of plague within three days (August 30). The second animal (rat 2) died twenty-four hours later. Guinea-pigs 3, 4, and 5 (see plan) were found dead on the morning of September 2; that is, two days after the death of rat 2 and three days after the death of rat 1.
The same day that the three guinea-pigs were found dead of plague, rooms I, III, IV, and VI were thoroughly disinfected. The floor, the ceiling, and the walls were sprayed with kerosene and lysol solution. The remaining animals in room VI were destroyed, and the cages disinfected. No animals were kept in rooms I, III, and IV at that time.
Three days after the death of animal 5, guinea-pigs 6 and 7 were found dead of plague, while the next day guinea-pigs 8 and 9 died. No death occurred on September 7, but the next two days each recorded two plague guinea-pigs (10, 11, 12, and 13). On September 11, the last guinea-pig died of plague in this outbreak. The whole building was then thoroughly disinfected. No plague-inoculated animals were kept in the rooms after the first sign of the epidemic. After September 11, no more cases of spontaneous plague infection were observed.
ANIMAL HOUSE
ANIMAL HOUSE
It will be noticed that the epidemic lasted eleven days after the first animal died and fourteen days after animal 1 was inoculated. Altogether, 14 animals out of at least 200 animals exposed died of plague.No death occurred among rabbits, although these animals were distributed among the guinea-pigs. In fact, 2 rabbits were surrounded by plague guinea-pigs 8, 9, and 10, but did not contract plague.From the epidemiological standpoint it is interesting to know the dimensions and location of the cages in which the animals were kept.Aside from the 2 rats which were confined in ordinary traps that stood on a table 80 centimetres high, the rest of the animals were kept in regular metal animal cages. The dimensions of the cages are: Fifty centimetres long, 36 centimetres broad, and 30 centimetres high. The cage stands on four legs each 10 centimetres long; the centre of the bottom of the cage holds a drain opening 8 centimetres above the floor.The majority of the cages in room II were located on the floor; some on the second shelf of a wooden rack. This last-mentioned arrangement, judging from the construction of the wooden frame, allowed a continuous passageway for the fleas to the second shelf of the racks. On the other hand, the deaths among the guinea-pigs in room V were restricted to the cages standing on the floor, the majority of cages in that room being placed on tables 80 centimetres high.Only a theoretical explanation can be given of the short duration and sudden cessation of the outbreak. One can assume with great probability that the first partial disinfection drove the fleas away from the primary source of infection, and that they traveled as far as possible.They finally settled in those guinea-pig cages which had not been molested by the first disinfection. Having no new supply of plague blood (all of the plague-infected guinea-pigs having been removed, most of them before death), the fleas soon cleared themselves of plague bacilli. The peculiar feature of the outbreak, namely, the failure to find fleas on the animals in rooms II and V, finds its explanation in the observation of the Indian Commission who found that the fleas "died or disappeared very rapidly."The following conclusions can be drawn from these observations:The common rat flea (Lœmopsylla cheopis) prefers the rat to the guinea-pig.In the absence of rats it will attack guinea-pigs rather than rabbits.The fleas which have sucked blood from rats or guinea-pigs afflicted with plague septicæmia were found to harbor virulent plague bacilli inside of their bodies.The transmission of plague infection by direct or indirect contact being excluded in our case, the fact that fleas of the same species and harboring plague bacilli were found on the rat and on the guinea-pigs, the presence of flea bites on the rats and on the guinea-pigs with positive findings of skin lesions on that part of the body where the fleas and flea bites were located, together with the anatomical picture of the findings in the guinea-pigs, lead to but one explanation; namely, that the plague infection was transmitted by fleas.III.Observations on Animals Suspected of PlagueOut of the several tens of thousands of rodents examined during the antirat campaign, we have found onlytwo plague rats which showed the typical picture of natural plague infection in rat; that is, cervical buboes with surrounding œdema, subcutaneous injection, pleural effusion, enlarged spleen, and such changes of the liver as are characteristic of natural plague infection in rats. Microscopically, large numbers of plague bacilli were found in these cases, and pure cultures ofBacillus pestiswere recovered from the spleen. Histological examination of internal organs, particularly that of the liver, confirmed the bacteriological findings. The remainder of the plague rats exhibited only two of the signs of plague infection, namely, bubo and œdema of the surrounding tissue, and eventually hemorrhages.Besides plague infection, a great number of rats showed purulent conditions from causes other than plague. Abscesses of the lungs were frequently met with, and cervical or axillary buboes are not uncommon in Manila rats. Various pyogenic bacteria were found in the pus of such abscesses. Of the less common wasBacillus pyocyaneusand the pneumobacillus of Friedländer. Chronic plague was excluded in these cases since the animal inoculation failed to produce plague infection.More than half of the rats examined harbored parasites in their organs.Echinococcus taeniæformiswas found in the liver of practically every gray rat, while a smallAscarisandTænia diminutawere not uncommon in the intestines. Two rats were found to have sarcosporidiosis, 2.6 per cent. showed rat leprosy, and 7.4 per cent. trypanosomiasis. One tumor of the mammary gland and one tumor in the axillary region were encountered, while one tumor of the large curvature of the stomach proved to be a chronic inflammatory tumor due to parasites. One peritoneal tumor in a rat (Mus decumanus) gave the impressionof a malignant tumor on account of the miliary dissemination of the peritoneum. It was found to consist of muscle and spindle-cell sarcomatous tissue. Ectoparasites were very seldom noticed, on account of the method of collecting the rats. When present, they were mites and fleas.In the naturally infected plague rats the rigidity of the fresh cadaver was pronounced. The primary bubo was in every case cervical. Cervical glands were enlarged and hemorrhagic with slight œdema of the surrounding tissue. The subcutaneous injection extended over the neck and chest. The inguinal glands were small and pigmented. The lungs were collapsed, and showed hemorrhagic foci. The spleen was slightly enlarged, firm, and dark red. The liver was rather large, firm, pale red, with shade of yellow, which was caused by minute yellowish foci thickly scattered throughout the tissue and visible through the capsule. The kidneys were hyperæmic. The intestines were without change. The serous membranes were pale with no hemorrhages.Histological examination of the tissue of naturally infected plague rats showed the following changes:Liver.—The structure of the organ was well marked; the veins dilated, trabeculæ slightly compressed, nuclei well stained, and few of the liver cells showed vacuoles. Small foci, most numerous under Glisson's capsule, were scattered throughout the organ; they varied in size, but were not larger than a miliary tubercle. The small necrotic foci were found to consist of few necrotic liver cells. The centre of the larger foci was formed by degenerated and necrotic liver tissue, surrounded by round-cell infiltration. Polymorphonuclears were also found in the zone of cellular infiltration. There was a slight degree ofhemorrhage in each focus. Epithelioid cells and large vesicular cells with several nuclei were to be found. The foci, mentioned above, were sharply demarcated from the surrounding liver tissue, which appeared to be intact.Spleen.—The structure was well preserved, the capsule thin. The Malpighian bodies were normal as to the elements of which they consist. Cells with pycnotic nuclei were scattered throughout the organ, and vesicular cells with small, deeply stained, excentrically located nuclei were present. Polymorphonuclears were found in the tissue in considerable numbers. No localized necrotic foci could be found in sections through the spleen.Cervical Glands.—The blood-vessels were considerably distended. A few hemorrhages and polymorphonuclears were present. Œdema of the capsules and surrounding tissue existed. Part of the gland was necrotic.Lungs.—The blood-vessels were distended. The alveoli contained homogeneous masses and blood. There were numerous subpleural hemorrhages. The bronchi were collapsed, and contained mucus.Kidneys.—The cortical part showed subdued structure; the epithelial cells had an indefinite outline and occasionally showed vacuolization. The medullar part was better preserved. There were miliary subcapsular hemorrhages. A few small foci were scattered throughout both medullar and cortical parts. They consisted of round-cell infiltration.Natural Plague Infection in a CatThe experiments of the German Plague Commission proved that cats showed considerable resistance to plague infection as cutaneous and subcutaneous inoculations failed to infect them. According to the Austrian Commission,cats develop submaxillary buboes if fed on plague material. They are said by Albrecht and Gohn[13]sometimes to recover. Out of four cats fed on plague material two died of plague, one showing submaxillary, the other mesenterial buboes. Virulent plague bacilli were found in the discharge from the nose and also in the fæces of cats which apparently did not become infected after having been fed on plague material.[13]Über die Beulenpest in Bombay im Jahre 1897 (1897), II B, II C.One case of spontaneous plague infection of a cat was recorded by Thompson[14]in Sydney.[14]Report of an outbreak in Sydney, 1900. Referred to in Kolle and Wassermann (1903),2, 510.W. Hunter,[15]in Hongkong made observations on cats suffering from plague infection. The author also undertook a few experiments, and arrived at the following conclusions:Cats suffer from plague.The disease may be acute or chronic.The type of the disease is septicæmic.The animals may occasionally play a part in the dissemination of plague.In plague-infected areas cats probably become infected through rats, which they devour as food.In plague-infected districts possible plague infection in cats is of great importance from a domestic point of view.[15]Lancet (1905),I, 1064.On November 27, 1912, a sick cat was brought to the laboratory for examination. It was reported that the animal was found in a warehouse in which dead rats hadbeen found some time previously. The rats were not examined. In the morning of the 30th, the cat was found dead in the cage where it had been kept under observation. The following are the post-mortem findings:The animal was a fairly well-nourished female.[16]The subcutaneous tissue, pericardium, mediastinum, and mesenterium contained considerable amounts of fat.[16]The cat was the mother of 4 kittens which were about 3 weeks old at the time the cat was delivered for examination. They were kept under observation for several weeks, but showed no signs of plague infection.The subcutaneous tissue of the neck showed œdema and small hemorrhages. The submaxillary tissues were swollen on both sides. When the fasciæ and superficial muscles of the neck were removed, enlarged glands were found on both sides. These were closely attached to the submaxillary salivary glands. The surrounding tissue was œdematous, but no hemorrhages were noticed in the vicinity of the enlarged glands. Upon section the glands were found to be necrotic, and upon pressure a thin purulent liquid escaped. There were no hemorrhages within the glands. Several enlarged lymph-nodes, smaller in size, could be followed down the neck on the left side. The lymph-nodes in the axillæ as well as in the groins and peribronchial nodes were normal. The mesenteric glands were slightly enlarged and reddened.The lungs were slightly collapsed. A clear, sanguineous, slightly coagulated effusion was observed in both pleural cavities. The tissue of the lungs showed considerable œdema and hypostasis. The bronchi and pharynx showed no changes, the mucous membrane being pale and thin.The heart was normal.The spleen was enlarged, of light red color, with follicles slightly prominent.The stomach contents was blackish in color; there were no hemorrhages or ulcers in the mucosa.The liver was somewhat enlarged. The organ showed prominent structure, the centres of the acini being red, the periphery lighter in color.The kidneys were slightly enlarged and pale. The capsule peeled off easily, the venæ stellatæ were prominent, the surface smooth; there were no hemorrhages. The cortex was increased in breadth and was of the same color as the surface; the pyramids were darker in color. The organ was of fragile consistence.Suprarenals were normal, as were also intestine and bladder.The histological findings were as follows:Bubo.—The capsule of the gland was œdematous. The whole gland as seen in cross section had undergone necrosis, except a few foci which still showed cellular structure.Lungs.—The alveoli were filled with homogeneous masses, containing but few degenerated epithelial cells and leucocytes. The blood-vessels were dilated, particularly in the subpleural part of the organ. In some places capillary mycotic emboli with subsequent hemorrhage were encountered. The large blood-vessels and bronchi were normal.Salivary Glands.—Those glands attached to the primary bubo showed the normal structure of a combined mucous and serous gland.Liver.—There was considerable congestion. The centres of the acini showed parenchymatous and fatty degeneration. The cells on the periphery of the aciniexhibited typical fatty infiltration. The large blood-vessels and small ducts were without change.Kidney.—The cells of the kidney showed various degrees of degeneration, ranging from parenchymatous to fatty infiltration. There were a few capillary hemorrhages and hyaline casts present.Suprarenals.—These showed slight degeneration.Spleen.—This organ showed congestion, a few hemorrhages, and bacterial emboli; otherwise normal.The bacteriological examination of the material from this cat gave the following results:Smears:From the buboes showed degenerated leucocytes, many lymphocytes, and numerous bacteria, some of which resembledBacillus pestisin their polar staining.From the spleen showed numerous plague-like, polar-stained bacilli. Round involution forms were present.Cultures:From the buboes were badly contaminated withBacillus coliandBacillus pyocyaneuscolonies.From the spleen: A few scattered colonies ofBacillus pyocyaneusdeveloped on the surface of the agar. Between the large colonies a scanty growth of dewy appearance was noticed. Smears made from this growth revealed plague-like bacilli of the cultural type, showing a few club-shaped involution forms. Subcultures were made in order to secure pure culture. They showed a pure growth ofBacillus pestisas indicated by the morphology of bacilli and shape of the colonies. Agglutination with plague-immune serum was positive.Inoculation experiments (vaccination method):One guinea-pig was inoculated with the material from the left bubo, another one with material from the right bubo. They died of plague on the third and fifth days, respectively.One guinea-pig was inoculated with the material from the spleen. It died of plague on the third day.One guinea-pig was inoculated with material from the nostrils obtained by swab. The animal survived, showing no indication of plague.One guinea-pig was inoculated with material from the rectum obtained by swab. It died of plague on the fifth day.Although plague infection among cats is apparently a rare occurrence, the fact that cats may contract the disease in spite of the high degree of resistance to plague infection has to be considered from the hygienic standpoint.To appreciate the important rôle which cats may play in the spreading of the disease one need only consider the close contact of these animals with rats on one side and human beings on the other. It is also a well-established fact that not only plague-infected cats, but also those which have devoured plague-infected material and remained apparently normal, may excrete plague bacilli which have retained their full virulence.
It will be noticed that the epidemic lasted eleven days after the first animal died and fourteen days after animal 1 was inoculated. Altogether, 14 animals out of at least 200 animals exposed died of plague.
No death occurred among rabbits, although these animals were distributed among the guinea-pigs. In fact, 2 rabbits were surrounded by plague guinea-pigs 8, 9, and 10, but did not contract plague.
From the epidemiological standpoint it is interesting to know the dimensions and location of the cages in which the animals were kept.
Aside from the 2 rats which were confined in ordinary traps that stood on a table 80 centimetres high, the rest of the animals were kept in regular metal animal cages. The dimensions of the cages are: Fifty centimetres long, 36 centimetres broad, and 30 centimetres high. The cage stands on four legs each 10 centimetres long; the centre of the bottom of the cage holds a drain opening 8 centimetres above the floor.
The majority of the cages in room II were located on the floor; some on the second shelf of a wooden rack. This last-mentioned arrangement, judging from the construction of the wooden frame, allowed a continuous passageway for the fleas to the second shelf of the racks. On the other hand, the deaths among the guinea-pigs in room V were restricted to the cages standing on the floor, the majority of cages in that room being placed on tables 80 centimetres high.
Only a theoretical explanation can be given of the short duration and sudden cessation of the outbreak. One can assume with great probability that the first partial disinfection drove the fleas away from the primary source of infection, and that they traveled as far as possible.They finally settled in those guinea-pig cages which had not been molested by the first disinfection. Having no new supply of plague blood (all of the plague-infected guinea-pigs having been removed, most of them before death), the fleas soon cleared themselves of plague bacilli. The peculiar feature of the outbreak, namely, the failure to find fleas on the animals in rooms II and V, finds its explanation in the observation of the Indian Commission who found that the fleas "died or disappeared very rapidly."
The following conclusions can be drawn from these observations:
III.Observations on Animals Suspected of Plague
Out of the several tens of thousands of rodents examined during the antirat campaign, we have found onlytwo plague rats which showed the typical picture of natural plague infection in rat; that is, cervical buboes with surrounding œdema, subcutaneous injection, pleural effusion, enlarged spleen, and such changes of the liver as are characteristic of natural plague infection in rats. Microscopically, large numbers of plague bacilli were found in these cases, and pure cultures ofBacillus pestiswere recovered from the spleen. Histological examination of internal organs, particularly that of the liver, confirmed the bacteriological findings. The remainder of the plague rats exhibited only two of the signs of plague infection, namely, bubo and œdema of the surrounding tissue, and eventually hemorrhages.
Besides plague infection, a great number of rats showed purulent conditions from causes other than plague. Abscesses of the lungs were frequently met with, and cervical or axillary buboes are not uncommon in Manila rats. Various pyogenic bacteria were found in the pus of such abscesses. Of the less common wasBacillus pyocyaneusand the pneumobacillus of Friedländer. Chronic plague was excluded in these cases since the animal inoculation failed to produce plague infection.
More than half of the rats examined harbored parasites in their organs.Echinococcus taeniæformiswas found in the liver of practically every gray rat, while a smallAscarisandTænia diminutawere not uncommon in the intestines. Two rats were found to have sarcosporidiosis, 2.6 per cent. showed rat leprosy, and 7.4 per cent. trypanosomiasis. One tumor of the mammary gland and one tumor in the axillary region were encountered, while one tumor of the large curvature of the stomach proved to be a chronic inflammatory tumor due to parasites. One peritoneal tumor in a rat (Mus decumanus) gave the impressionof a malignant tumor on account of the miliary dissemination of the peritoneum. It was found to consist of muscle and spindle-cell sarcomatous tissue. Ectoparasites were very seldom noticed, on account of the method of collecting the rats. When present, they were mites and fleas.
In the naturally infected plague rats the rigidity of the fresh cadaver was pronounced. The primary bubo was in every case cervical. Cervical glands were enlarged and hemorrhagic with slight œdema of the surrounding tissue. The subcutaneous injection extended over the neck and chest. The inguinal glands were small and pigmented. The lungs were collapsed, and showed hemorrhagic foci. The spleen was slightly enlarged, firm, and dark red. The liver was rather large, firm, pale red, with shade of yellow, which was caused by minute yellowish foci thickly scattered throughout the tissue and visible through the capsule. The kidneys were hyperæmic. The intestines were without change. The serous membranes were pale with no hemorrhages.
Histological examination of the tissue of naturally infected plague rats showed the following changes:
Liver.—The structure of the organ was well marked; the veins dilated, trabeculæ slightly compressed, nuclei well stained, and few of the liver cells showed vacuoles. Small foci, most numerous under Glisson's capsule, were scattered throughout the organ; they varied in size, but were not larger than a miliary tubercle. The small necrotic foci were found to consist of few necrotic liver cells. The centre of the larger foci was formed by degenerated and necrotic liver tissue, surrounded by round-cell infiltration. Polymorphonuclears were also found in the zone of cellular infiltration. There was a slight degree ofhemorrhage in each focus. Epithelioid cells and large vesicular cells with several nuclei were to be found. The foci, mentioned above, were sharply demarcated from the surrounding liver tissue, which appeared to be intact.
Spleen.—The structure was well preserved, the capsule thin. The Malpighian bodies were normal as to the elements of which they consist. Cells with pycnotic nuclei were scattered throughout the organ, and vesicular cells with small, deeply stained, excentrically located nuclei were present. Polymorphonuclears were found in the tissue in considerable numbers. No localized necrotic foci could be found in sections through the spleen.
Cervical Glands.—The blood-vessels were considerably distended. A few hemorrhages and polymorphonuclears were present. Œdema of the capsules and surrounding tissue existed. Part of the gland was necrotic.
Lungs.—The blood-vessels were distended. The alveoli contained homogeneous masses and blood. There were numerous subpleural hemorrhages. The bronchi were collapsed, and contained mucus.
Kidneys.—The cortical part showed subdued structure; the epithelial cells had an indefinite outline and occasionally showed vacuolization. The medullar part was better preserved. There were miliary subcapsular hemorrhages. A few small foci were scattered throughout both medullar and cortical parts. They consisted of round-cell infiltration.
Natural Plague Infection in a Cat
The experiments of the German Plague Commission proved that cats showed considerable resistance to plague infection as cutaneous and subcutaneous inoculations failed to infect them. According to the Austrian Commission,cats develop submaxillary buboes if fed on plague material. They are said by Albrecht and Gohn[13]sometimes to recover. Out of four cats fed on plague material two died of plague, one showing submaxillary, the other mesenterial buboes. Virulent plague bacilli were found in the discharge from the nose and also in the fæces of cats which apparently did not become infected after having been fed on plague material.
[13]Über die Beulenpest in Bombay im Jahre 1897 (1897), II B, II C.
One case of spontaneous plague infection of a cat was recorded by Thompson[14]in Sydney.
[14]Report of an outbreak in Sydney, 1900. Referred to in Kolle and Wassermann (1903),2, 510.
W. Hunter,[15]in Hongkong made observations on cats suffering from plague infection. The author also undertook a few experiments, and arrived at the following conclusions:
[15]Lancet (1905),I, 1064.
On November 27, 1912, a sick cat was brought to the laboratory for examination. It was reported that the animal was found in a warehouse in which dead rats hadbeen found some time previously. The rats were not examined. In the morning of the 30th, the cat was found dead in the cage where it had been kept under observation. The following are the post-mortem findings:
The animal was a fairly well-nourished female.[16]The subcutaneous tissue, pericardium, mediastinum, and mesenterium contained considerable amounts of fat.
[16]The cat was the mother of 4 kittens which were about 3 weeks old at the time the cat was delivered for examination. They were kept under observation for several weeks, but showed no signs of plague infection.
The subcutaneous tissue of the neck showed œdema and small hemorrhages. The submaxillary tissues were swollen on both sides. When the fasciæ and superficial muscles of the neck were removed, enlarged glands were found on both sides. These were closely attached to the submaxillary salivary glands. The surrounding tissue was œdematous, but no hemorrhages were noticed in the vicinity of the enlarged glands. Upon section the glands were found to be necrotic, and upon pressure a thin purulent liquid escaped. There were no hemorrhages within the glands. Several enlarged lymph-nodes, smaller in size, could be followed down the neck on the left side. The lymph-nodes in the axillæ as well as in the groins and peribronchial nodes were normal. The mesenteric glands were slightly enlarged and reddened.
The lungs were slightly collapsed. A clear, sanguineous, slightly coagulated effusion was observed in both pleural cavities. The tissue of the lungs showed considerable œdema and hypostasis. The bronchi and pharynx showed no changes, the mucous membrane being pale and thin.
The heart was normal.
The spleen was enlarged, of light red color, with follicles slightly prominent.
The stomach contents was blackish in color; there were no hemorrhages or ulcers in the mucosa.
The liver was somewhat enlarged. The organ showed prominent structure, the centres of the acini being red, the periphery lighter in color.
The kidneys were slightly enlarged and pale. The capsule peeled off easily, the venæ stellatæ were prominent, the surface smooth; there were no hemorrhages. The cortex was increased in breadth and was of the same color as the surface; the pyramids were darker in color. The organ was of fragile consistence.
Suprarenals were normal, as were also intestine and bladder.
The histological findings were as follows:
Bubo.—The capsule of the gland was œdematous. The whole gland as seen in cross section had undergone necrosis, except a few foci which still showed cellular structure.
Lungs.—The alveoli were filled with homogeneous masses, containing but few degenerated epithelial cells and leucocytes. The blood-vessels were dilated, particularly in the subpleural part of the organ. In some places capillary mycotic emboli with subsequent hemorrhage were encountered. The large blood-vessels and bronchi were normal.
Salivary Glands.—Those glands attached to the primary bubo showed the normal structure of a combined mucous and serous gland.
Liver.—There was considerable congestion. The centres of the acini showed parenchymatous and fatty degeneration. The cells on the periphery of the aciniexhibited typical fatty infiltration. The large blood-vessels and small ducts were without change.
Kidney.—The cells of the kidney showed various degrees of degeneration, ranging from parenchymatous to fatty infiltration. There were a few capillary hemorrhages and hyaline casts present.
Suprarenals.—These showed slight degeneration.
Spleen.—This organ showed congestion, a few hemorrhages, and bacterial emboli; otherwise normal.
The bacteriological examination of the material from this cat gave the following results:
Although plague infection among cats is apparently a rare occurrence, the fact that cats may contract the disease in spite of the high degree of resistance to plague infection has to be considered from the hygienic standpoint.
To appreciate the important rôle which cats may play in the spreading of the disease one need only consider the close contact of these animals with rats on one side and human beings on the other. It is also a well-established fact that not only plague-infected cats, but also those which have devoured plague-infected material and remained apparently normal, may excrete plague bacilli which have retained their full virulence.
Notes on Plague in Hong Kong by Dr. Roberg.—During the Hong Kong epidemic of plague which preceded and was coincident with thatof Manila, I visited that city twice (December, 1913, and July, 1914), but I did not closely investigate the methods adopted and carried out by the authorities there, for the reason that the Manila plan was so much more productive of results, as shown by the apparent inability of the Hong Kong officials to gain control of the disease. However, I received from Dr. David Roberg, of the Oregon State Board of Health, a copy of a report made by him to the Secretary of his State Board of Health, following an investigation of the Hong Kong epidemic and the methods there followed. I have Dr. Roberg's permission to use his report and it is herewith presented. It is dated Manila, April 16, 1914, and is as follows:
I have the following notes to present on the epidemic of bubonic plague in Hongkong.On April 5th when I arrived in Hongkong the epidemic was rapidly approaching its height. With its onset in January there were 47 cases, in February 42, and in March 223. During the week previous to April 5th, there were 91 cases; during the six days I was in Hongkong they averaged 15 a day.Judging from previous epidemics the present one will be exceptionally severe. The season for the occurrence of human plague is from the months of February to July.The onset is gradual; in May it reaches its maximum and then declines. In the epidemic of 1912, for the city of Victoria the monthly rate showed the following, January 9, February 22, March 61, April 265, May 513, June 346, July 105, August 11, and September 1. Comparing these rates with those of the present year it will be seen that the number for March far exceeds that of two years previous.Illustrating the season for human plague, with its onset, maximum and decline, are the monthly rates for the city of Kowloon during 1912, when the following cases occurred: February 2, March 12, April 52, May 246, June 152, July 39, August 8, and September 3.The season for human cases is determined by the condition of the rats. At the close of the season in July the rats die off from plague in great numbers as it is then the hottest time of the year. During the months from September to February the rats increase in number and in susceptibility to the extent of being sufficient to again infect human beings. Moreover every other year shows a marked severity in the epidemics of human bubonic plague. This is explained by the fact that it requires two years' time for the rat population to become of sufficient greatness and susceptibility to cause a severe human outbreak. This is shown by the yearly number of cases since the year 1911. During the years 1911, 1912 and 1913 respectively, there were 253, 1847, and 408 cases. During the present year the monthly rate is exceeding that of the heavy year of 1912.The severe epidemic in 1912 was a result of the influx of 50,000 Chinese refugees into Hongkong during the revolution in 1911. The number of rats in the nativedistrict depends upon the available food supply, and as a result of this human overcrowding the amount of waste food so increased in the houses, yards and streets, that the over accumulation of garbage could not be kept pace with. This influx also brought in great numbers of susceptible rats.The number of rats killed off during the epidemic in 1912 were so great that in 1913 they had not recovered sufficiently to cause a severe outbreak during that year, and as a result of the lightness of epidemic in 1913, they are so increased in number and susceptibility now that they are causing a very severe epidemic in human beings.Of rats in Hongkong they have theMus decumanusor drain rat and theMus rattusor house rat. It is noteworthy that the drain rat is found plague-infected throughout the year, while the house rat is found infected only during the period in which the human epidemics occur, namely from February to July. The number of infected rats a year run parallel to the number of monthly cases.The bulk of human infection is due to the spread of house rats. Man also becomes infected by the drain rat when the drains are flooded by rain storms and the rats are driven into the houses.What has made plague permanent in Hongkong is the overcrowding of the native districts. Besides there is a floating population entering and leaving the native quarters, numbering about 4000 a day. The native houses have been built with double floors and walls which harbor the rats. Where the construction is of wood it is possible to remove the rat spaces. It has been found since the introduction of plague into Hongkong in 1894, that those districts containing the greatest number of softbrick houses with hollow walls, have shown the greatest incidence of plague. This can not be remedied as it would involve the destruction of buildings on too large a scale.The Work of the Sanitary BoardThe area under the control of the Board comprises the Island of Hongkong containing 32 square miles, with a sea frontage of 13 miles in length. Included also is the old city of Kowloon which is situated one mile and a third across the harbor and contains two and three-fourths square miles. The city of Victoria on the northern shore of the Island of Hongkong has a sea frontage of 5 miles, contains about ten thousand domestic buildings, of which about one thousand are non-Chinese.The population of Hongkong is difficult to estimate, as the floating population is so great. In the 1912 census there were 446,614 Chinese and 21,163 non-Chinese.The city of Victoria is divided into 10 Urban Health Districts and old Kowloon into 2. There is an inspector in charge of each. These districts are built over an area averaging from 31 to 140 acres. The houses in these districts average one thousand and the population from 8000 to 33,000. There are four inspectors in charge of the scavenging work, one for the disinfection stations in Victoria and old Kowloon, one for the cemeteries and two for general duty.The measures employed by the Sanitary Board are summarized as follows:The exclusion of rats from all dwellings by means of concreted ground surfaces, the protection of all drainopenings and ventilating openings by iron gratings, and the prohibition of ceilings and of hollow walls in new buildings and in those existing buildings from which they have been removed by order.The collection and bacteriological examination of all dead rats. Facilities for the collection of rats in the quarters are provided in the shape of small covered bins attached to lamp posts, telephone posts, electric light poles, etc. These bins contain a carbolic acid disinfectant, and the inhabitants are invited to at once put into them all rats found or killed by them. There are 650 of these bins distributed throughout the city and its suburbs, and each of them is visited twice daily by rat collectors who take all rats found by them to the City Bacteriologist. Each rat is at once labelled with the number of the bin from which it is taken, and if subsequently found to be plague infected, a special survey is immediately made of the block of houses in that vicinity. All rat-holes and rat runs are filled up with broken glass and cement, defective gratings and drains dealt with, and rat poison distributed free to the occupants. If several plague-infected rats are found in one locality, a special house-to-house survey and cleansing of that district is made.The destruction of rats by poison, traps and birdlime boards; special efforts in this direction being made just before the onset of the regular plague season which is in the months of from March to July.The encouraging of the community to keep cats.The systematic cleaning and washing out of all native dwellings at least once in three months with a flea killing mixture made by emulsifying kerosene in water.An efficient daily scavenging of all streets and lanesand the daily removal of refuse from the houses, coupled with the provision of covered metal dust-bins, to reduce as far as possible the amount of food available for rats.The disinfection of plague-infected premises by stripping them and washing them out thoroughly with a kerosene emulsion. The bedding, clothing, carpets, rugs, etc., are conveyed in a huge covered basket to the disinfecting plant and sterilized with superheated steam. No objection is made to the treatment of plague cases in native hospitals, and no restrictions are imposed in regard to the burial of those dead with plague except the provision of a substantial coffin.Every effort is made by means of lectures, addresses and explanations to induce the native population to participate in the above preventive measures.
I have the following notes to present on the epidemic of bubonic plague in Hongkong.
On April 5th when I arrived in Hongkong the epidemic was rapidly approaching its height. With its onset in January there were 47 cases, in February 42, and in March 223. During the week previous to April 5th, there were 91 cases; during the six days I was in Hongkong they averaged 15 a day.
Judging from previous epidemics the present one will be exceptionally severe. The season for the occurrence of human plague is from the months of February to July.The onset is gradual; in May it reaches its maximum and then declines. In the epidemic of 1912, for the city of Victoria the monthly rate showed the following, January 9, February 22, March 61, April 265, May 513, June 346, July 105, August 11, and September 1. Comparing these rates with those of the present year it will be seen that the number for March far exceeds that of two years previous.
Illustrating the season for human plague, with its onset, maximum and decline, are the monthly rates for the city of Kowloon during 1912, when the following cases occurred: February 2, March 12, April 52, May 246, June 152, July 39, August 8, and September 3.
The season for human cases is determined by the condition of the rats. At the close of the season in July the rats die off from plague in great numbers as it is then the hottest time of the year. During the months from September to February the rats increase in number and in susceptibility to the extent of being sufficient to again infect human beings. Moreover every other year shows a marked severity in the epidemics of human bubonic plague. This is explained by the fact that it requires two years' time for the rat population to become of sufficient greatness and susceptibility to cause a severe human outbreak. This is shown by the yearly number of cases since the year 1911. During the years 1911, 1912 and 1913 respectively, there were 253, 1847, and 408 cases. During the present year the monthly rate is exceeding that of the heavy year of 1912.
The severe epidemic in 1912 was a result of the influx of 50,000 Chinese refugees into Hongkong during the revolution in 1911. The number of rats in the nativedistrict depends upon the available food supply, and as a result of this human overcrowding the amount of waste food so increased in the houses, yards and streets, that the over accumulation of garbage could not be kept pace with. This influx also brought in great numbers of susceptible rats.
The number of rats killed off during the epidemic in 1912 were so great that in 1913 they had not recovered sufficiently to cause a severe outbreak during that year, and as a result of the lightness of epidemic in 1913, they are so increased in number and susceptibility now that they are causing a very severe epidemic in human beings.
Of rats in Hongkong they have theMus decumanusor drain rat and theMus rattusor house rat. It is noteworthy that the drain rat is found plague-infected throughout the year, while the house rat is found infected only during the period in which the human epidemics occur, namely from February to July. The number of infected rats a year run parallel to the number of monthly cases.
The bulk of human infection is due to the spread of house rats. Man also becomes infected by the drain rat when the drains are flooded by rain storms and the rats are driven into the houses.
What has made plague permanent in Hongkong is the overcrowding of the native districts. Besides there is a floating population entering and leaving the native quarters, numbering about 4000 a day. The native houses have been built with double floors and walls which harbor the rats. Where the construction is of wood it is possible to remove the rat spaces. It has been found since the introduction of plague into Hongkong in 1894, that those districts containing the greatest number of softbrick houses with hollow walls, have shown the greatest incidence of plague. This can not be remedied as it would involve the destruction of buildings on too large a scale.
The Work of the Sanitary Board
The area under the control of the Board comprises the Island of Hongkong containing 32 square miles, with a sea frontage of 13 miles in length. Included also is the old city of Kowloon which is situated one mile and a third across the harbor and contains two and three-fourths square miles. The city of Victoria on the northern shore of the Island of Hongkong has a sea frontage of 5 miles, contains about ten thousand domestic buildings, of which about one thousand are non-Chinese.
The population of Hongkong is difficult to estimate, as the floating population is so great. In the 1912 census there were 446,614 Chinese and 21,163 non-Chinese.
The city of Victoria is divided into 10 Urban Health Districts and old Kowloon into 2. There is an inspector in charge of each. These districts are built over an area averaging from 31 to 140 acres. The houses in these districts average one thousand and the population from 8000 to 33,000. There are four inspectors in charge of the scavenging work, one for the disinfection stations in Victoria and old Kowloon, one for the cemeteries and two for general duty.
The measures employed by the Sanitary Board are summarized as follows:
Upon my last visit to Hong Kong, in July last, plague was abating.The South China Morning Postof July 15, 1914, contained the following statement:
Plague is gradually disappearing from Hongkong. Last week's return shows that there were 26 cases, of which 19 were fatal. All were Chinese. The total number of cases for the current year to date is 2093, with 1939 deaths resulting.
Plague is gradually disappearing from Hongkong. Last week's return shows that there were 26 cases, of which 19 were fatal. All were Chinese. The total number of cases for the current year to date is 2093, with 1939 deaths resulting.
I regret that circumstances do not permit me to relate in detail the work done and the observations made during the closing six months of the Manila epidemic.
Up to the day of my departure from the Philippines, in July, 1914, I remained in charge of plague suppression, but the added duties of administration at San Lazaro Hospital and the coincident occurrence of a cholera epidemic prevented me from keeping a detailed record in such form as to permit reproduction here. It will therefore suffice to say that the first six months of 1914 witnessed the passing of the most threatening situation that has confronted the city of Manila in years. The record of plague rats found does not convey an accurate idea of the prevalence of rat plague by any means, for the simple reason that, when found, the rat cadavers were in such condition as to forbid bacteriologic examination; and inasmuch as the bacteriologic test of plague had been used exclusively in determining rat plague up to this time, it seemed desirable to adhere to the original method.
In February we found in one of the districts, in which we undertook systematic work in consequence of a few cases of human plague, a very large number of dead rats, in and adjacent to houses which furnished human plague cases. In one building alone more than 150 rat cadavers werefound during our cleaning and rat-proofing operations. It is this district concerning which the letter to the public (already quoted) was written.
The methods followed in treating this new and dangerous focus of infection did not differ from those practised during the previous year, except in the matter of intensity. Forces of the cleaning and rat-catching gangs were increased and the utmost thoroughness of treatment was insisted upon. The results fully justified our policy and demonstrated again how feasible it is to fight plague successfully if adequate authority be given.
During the last year of the epidemic in Manila it became the rule for us to expect our plague workers to locate and find the identical rat cadaver from which the infected fleas bore the disease to the human victim, provided the spot upon the floor where the patient's sleeping mat had been placed was known. In the better class of houses the rat (sometimes more than one) was found dead beneath the floor, behind some post casing, or in other space caused by double construction. Time and again I have directed the removal of some panel of woodwork, some post casing, or a board of the floorwith the full expectation (seldom unrealized) of finding a dead rat or a rat nest. These experiences were positively uncanny at times. In the houses of the poorer class, usually of bamboo and thatch construction, the finding of the rat was less easy and more uncertain, although the nest was repeatedly found, and as related elsewhere the dead rat itself might be found in a hollow bamboo timber, or in the thatch construction of the wall. In a house on Calle Echague, from which a Filipino and his wife were removed, dead, within a few hours of each other, several dead rats were found in the floor (the only piece of double construction in the whole house) within four feet from the spot where the sleeping mats were placed. A rat hole led to the nest and through this hole the fleas from the dead rats found their way to the human victims sleeping on the floor above the encased nest.
These instances could be multiplied many times, but there is no longer any special reason to do so, as the rat and the rat-flea are so completely incriminated as to render these repetitions quite unnecessary, however interesting they may be to the plague worker. The danger of pursuing these investigations,to the persons so engaged, must not be lost sight of, and exposure of such nests and rat cadavers should invariably be preceded by thorough spraying of the place, and particularly of the spot where tearing out of double construction is to be done. I know of no more dangerous employment than this, both for laborer and bystander.
Itwas not my original intention to include the subjects of diagnosis and treatment in this presentation, except in so far as I have already referred to them in the relation of my Manila experiences in the preceding pages. I have decided, however, to add a chapter upon Diagnosis and Treatment, for the sake of completeness. No attempt will be made to present these subjects in the orthodox way.
Rather, my remarks will be confined to such matter as I believe to be thoroughly practical and relevant.
In my opinion, the day has arrived when we may properly exclude from such handbooks as this one (intended for practical guidance), all such methods of diagnosis and treatment as have failed to meet the test of actual experience through a reasonable length of time. Twice in recent years,[17]I have described the diagnosis and treatment ofplague, attempting in each case to present a reasonably full account of the methods employed and advocated by authorities, for theoretic reasons and from the recorded personal experiences of medical men throughout the world. There comes a time, however, when wheat and chaff must be separated and when methods which have failed, in application, to justify preformed expectations must be relegated to the department of historical medicine.
[17]Tropical Medicine (1907) and Hare's Modern Treatment (1911), vol. 1.
Judging from recent medical text books it is evident that medical writers are generally accepting this view as the proper one. At any rate, my experiences and those of my medical friends during the Manila epidemic of 1912–1914, have led me to discard as impracticable, unproven, disproven or unpromising, certain plans of treatment formerly deemed worthy of trial. I do not refer to these methods individually but will content myself, instead, with reciting briefly the methods which I believe, from personal experience and the collected experience of others, to be worthy of continuance and of further trial.
Diagnosis.—The rapid diagnosis of plague is always of the utmost importance, both from the view-point of prognosis and treatment, in the individualcase, and from the community view-point of the recognition of the presence of a dangerous communicable disease, with the resultant obligation falling upon the health authorities.
The Biologic Diagnosis.—Let us understand, first and finally, that but one diagnosis is absolutely and irrefutably dependable, viz.: the biologic diagnosis. Herein I would include not only the recovery of the pest bacillus from the patient, but the recovery and identification of the organism from inoculated animals, infected from blood, tissues, secretions or cultivated plague bacilli derived from the human patient or cadaver.
This entire process involves a lapse of time of several days, and, while it is indispensable in the earliest cases of an epidemic, and highly desirable for the proper study of all cases of plague, it is impracticable and unnecessary, in communities where plague is known to exist, to carry out more than the first steps of the biologic diagnosis, viz.: the recovery ofB. pestis(morphologic identification) from the patient.
Necessity for Trained Bacteriologist.—It is evident that the services of a trained bacteriologist are indispensable in the accurate diagnosisof plague, unless (as rarely is the case) the observer himself is both clinician and bacteriologist. Even in this case it is far better for two persons, clinician and bacteriologist, to work together. I will not discuss the technic of the procedures of biologic diagnosis, which is described by Dr. Schöbl in the preceding pages. Except under circumstances of necessity, the clinician should always turn this work over to the bacteriologist.
Serum reactions, when present, occur too late to be of service in practical diagnosis.
The necessary procedures of the biologic diagnosis include blood-culture, smear examination (microscopic) of aspirated material from the œdematous tissues surrounding gland masses and from glands themselves; examination of sputum smears and of thick-blood smears.
All should be practised but, according to our Manila experiences, smear examinations of aspirated material and blood cultures are the most reliable methods, in the hands of a competent bacteriologist. Attention is invited to the reports of Dr. Otto Schöbl, already quoted.
Bacteriologic Procedure.—Dr. Schöbl was able to secure positive blood cultures, within 24hours, from all of a long series of cases of plague, both bubonic and septicæmic. As much blood as it was possible to secure was aspirated from superficial veins and introduced into the culture media at the bedside, ten c.c. being secured whenever it was possible.
The smear preparations for staining and culture inoculations upon slants were also made at the bedside from aspirated matter obtained from œdematous periglandular tissues or from gland puncture, an aspirating syringe being used. The drop or two of fluid which can be expelled from the hollow needle is usually sufficient for smears and tube inoculations.
Non-biologic Diagnosis.—I do not contend that other diagnostic means than biologic ones should not be used in plague.
On the contrary, it will inevitably happen at times that resort must be had to methods of diagnosis which are purely clinical. When this is the case, treatment, along lines to be detailed presently, should be instituted upon the establishment of a presumptive diagnosis. This presumptive diagnosis may be reached after due consideration of physical signs and symptoms. A carefully takenhistory of the onset and course of the disease will be valuable but unfortunately such histories can rarely be secured. It is far safer to mistakenly pronounce a case "plague" and to institute appropriate treatment, than it is to hesitate in the absence of a perfect clinical picture and to permit the golden moment for treatment to pass.
It must be remembered that septicæmic, bubonic and pneumonic plague are all manifestations of systemic infection withB. pestis; that they are all expressions of the same disease; that they call for the same treatment and that when the distinctive signs of bubo or pneumonia appear the disease is dangerously advanced.
It should also be realized that every case is, almost from its onset, a septicæmic case, either mildly or overwhelmingly so. Accordingly the treatment should invariably be the treatment of septicæmic plague.
The attitude of the diagnostician should be one of suspicion and he should have the courage to carry out antiplague treatment, practically upon suspicion. In this way only can the mortality of plague be greatly reduced. It is true of plague, just as it is true of cholera, that many of the fatalcases develop and become hopeless before the disease is suspected or diagnosticated. It is also true that many fatal cases of plague, in times of epidemic, completely escape recognition during life, the diagnosis being made in the autopsy room.
Therefore, I lay great stress upon the necessity for an attitude of suspicion on the part of practitioners, wherever even a single case of plague (human or rodent) is known to have occurred.
When it becomes necessary to establish a presumptive diagnosis,i.e., without resort to the microscope, the following symptoms and physical signs will be found to be most significant.
Symptomatology.—Acuteness of onset; rapidity of fever development; rapidity of the development of mental dulness or cloudiness, impairment of speech, delirium, stupor or restlessness; early and extreme prostration (perhaps more pronounced than in any other acute disease); extreme tenderness over involved gland masses, in the bubonic type of plague; cough, with considerable frothy sputum, soon becoming blood-discolored, in the pneumonic type of plague; and early cardiac asthenia in all clinical types of plague, septicæmic, pneumonic and bubonic.
The following diseases may be confounded with plague, if symptoms alone are considered: typhus (exanthematicus), influenza pneumonia, broncho-pneumonia, severe malaria, septicæmia, acute toxic typhoid, venereal bubo, mumps and tonsillitis.
I call attention again to the fact that mild cases of plague, septicæmic and bubonic, occur at times, clinical pictures in such cases being incomplete.
The statement that the prognosis in all cases of septicæmic plague is hopeless is not confirmed by my experience.
It should also be remembered that primary pneumonic plague and secondary pneumonia developing in the course of systemic plague are quite different in their significance and mortality, primary pneumonic plague being well nigh invariably fatal.
Pathologic Considerations.—Only the student of plague pathology, who has seen a large number of complete autopsies, can understand how universal is the involvement of organs, glands and tissues in systemic plague and how widespread is the distribution ofB. pestisthroughout the body, and he will best understand how treatment, to bein the least effective, must be given in the very earliest hours of the disease.
Plague is an exquisitely septicæmic disease and this fact must never be lost sight of by the therapeutist, who must realize that from the earliest moment of infection all plague is septicæmic plague.
Treatment, Conditions and Prognosis.—Passing to the subject of treatment let us, first of all, admit that even under the most favorable and approved conditions of treatment the mortality is extremely high. On account of the delay which usually occurs in the recognition of plague,—a delay which in the natural order of things is and must be the rule rather than the exception, because of the rapidity of onset of the disease and the fact that it occurs much more frequently in the lower social classes than elsewhere,—no brilliant results are to be expected from any plan of treatment.
The matter of plague treatment is far from being in the same satisfactory state as the matter of preventive control. I do feel, however, that biologic treatment from the earliest possible moment, with serum, is of the greatest promise, however discouraging the general prognosis may be in plague.
Serum Treatment.—Recent writers agree that there is no treatment with curative value except that with antipest serum. To this belief I subscribe assent, as I find it entirely in accord with my experience and that of my colleagues in Manila during 1912–1914.
Holding this view, I can see no reason for repeating here the details of purely symptomatic treatment. Symptomatic treatment has for its object the securing of comfort and of relief from suffering for the patient and is highly proper in its place, remembering always that it is not curative and that if employed alone it is worse than inadequate.
Symptomatic Treatment.—Opiates (morphine by needle) for pain, delirium and excitement; application of ice bags and cold or tepid sponge bathing for high temperature; stimulants for heart weakness, are all indicated and are required in nearly every case of plague.
As a rule surgery is not called for nor appropriate, except in cases which develop secondary surgical conditions, which conditions we need not consider at this time.
Statistical Studies in Mortality.—The statisticalstudy of plague mortality from the point of view of treatment is misleading and unsatisfactory for reasons already given in our discussion of treatment, viz.: failure to secure early recognition and early serum treatment, and the greater incidence of plague in the lower social classes.
Few statistical compilations divide the cases studied into moribund and non-moribund, and indeed such division, being a matter of judgment, largely involves the personal equation of the observer.
The ease with which statistics may be moulded to support theories, or to break them down, all with perfect honesty of purpose, is proverbial.
To me, the spectacle of a single case of plague, apparently ill unto death, recovering under the administration of antiplague serum, is more impressive than the contemplation of statistics; and I have seen more than one such case respond to serum treatment and recover.
So far as it goes, however, the study of statistics supports the view that treatment with antiplague serum is effective.
I have not at hand the records of the last20 or more cases, but of the first 68 cases of plague in the recent Manila epidemic, 32 were either found dead or died upon the same day that they were found.
If we exclude these cases from consideration there remain 36 cases. All of these patients received serum treatment and ten of them recovered.
It is at once apparent that this percentage of recoveries (27 per cent. plus) is far more favorable than the actual percentage of recovery in the series in which cases found dead and moribund are considered, the recovery percentage here being a little more than 14 per cent. It is also quite fair, it seems to me, to make this separation of cases, or even a more liberal one, if we are to consider the effects of serum treatment statistically.
Dosage and Technique of Serum Administration.—The amount of antiplague serum to be given will vary somewhat with the age and weight of the patient and with the apparent severity of the case.
In general terms it may be said that adults should be given from 300 c.c. to 500 c.c. of serum by injection, 100 c.c. being given every four hours.The injection may be either intramuscular or intravenous.
In view of the improvements in technic of intravenous administrations and its comparative simplicity, and especially in view of the uncertainties and delays of absorption from the tissues, the intravenous route should be given the preference. The serum may be delivered intravenously from a large glass syringe, the introduction being very slowly made, or through a gravity apparatus, as in the administration of salvarsan. The serum should not be diluted.
The use of antiplague serum for protective (immunizing) purposes is also recommended—especially when exposure to infection has occurred—in the same way in which diphtheria antitoxin is used. Its protective properties are conceded to be somewhat superior to those of plague vaccines as the protection conferred is immediate, whereas plague vaccines do not protect until sometime after their administration. The dose is from 30 c.c. to 50 c.c.
Prophylactic Serum and Anaphylaxis.—On one occasion in Manila in 1913, when some 30 persons were given prophylactic doses of serum, intramuscularly, following a particularly dangerousexposure to fleas from rats dead from plague, there occurred a number of cases of "serum sickness" (anaphylaxis). These persons suffered from severe urticarial, arthralgic and nervous symptoms, lasting for several days and a few were obliged to enter a hospital. In one case the symptoms did not entirely abate for a week. It has been stated that newly-prepared serum is particularly apt to produce serum sickness when used for immunizing purposes. This form of protection is brief (1 to 2 weeks) and is best suited for use where there has been special exposure.
Plague Vaccines.—Haffkine originally proposed prophylactic immunization, using killed broth cultures ofB. pestis(carbolized to ½ per cent.), giving two injections at intervals of 10 days. Statistically it seems to be shown that this prophylactic immunization with dead bacteria reduces the incidence and mortality one-fourth or one-half (approximately). Experimentally, also, it appears that antibodies (agglutinins) are produced by the vaccine (and modifications thereof). Instead of broth cultures, normal salt solution suspensions of killed pest bacilli are usually used in vaccines at present.
Castellani[18]has prepared a combined cholera and plague vaccine for use in countries where both diseases coincidentally prevail. It is a mixed vaccine, so prepared that 1 c.c. of the emulsion contains 1000 millions of plague bacilli and 2000 millions of cholera vibrios. The cultures are grown on agar, killed by phenol and suspended in normal salt solution.
[18]A. Castellani: Journal of Ceylon Branch of British Medical Association, June, 1914.
He finds (1) that inoculation of the vaccine in the lower animals induces a production of protective substances for the plague bacillus and the cholera vibrio; (2) that the inoculation of human beings is harmless (producing less reaction than the Haffkine inoculation); (3) that a small amount of agglutinins, both for plague and cholera, appear in the blood of most inoculated persons (similar to amounts produced by Haffkine's vaccine), a rough index only of the amount of immunity produced.
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