Chapter C: F. Dawson, in investigating a wasting disease of well fed Brahma (1)

fowls in Maryland in which there was no appreciable symptom except the gradual and extreme loss of flesh and weight found in all cases a catarrhal duodenitis, with the presence in the contents of a bacterium in pure cultures, and apparently allied to bacillus coli communis.

_Bacteriology._ The bacterium is 1 to 1.3μ long, by .5μ wide, with rounded ends, often in pairs. It does not stain in acid nor alkaline methylene blue, carbol fuchsin, nor alcoholic dyes, but stains easily in aqueous solutions of the same stains and by Gram’s method. It is ærobic, facultative anærobic, grows at 50° to 120° F. in acid or alkaline beef bouillon, with fœtor; in glucose, saccharose, or lactose bouillon with the production of acid; in milk causing coagulation; on gelatine, agar and potato. Growth in Bouillon ceased at 131° F. and sterilization took place at 135° to 140° F. Vitality was not lost under freezing nor drying. It was killed by a 1 per cent. solution of carbolic acid in five minutes, or by formaldehyde gas, but not by lime water.

_Pathogenesis._ Inoculated subcutem, in a _Guinea pig_ caused death in 24 hours, with a necrotic œdematous condition of the adjacent tissues like malignant œdema, and containing the microbe. It was further found in the liver, spleen, abdominal exudate, heart, blood and lungs, but not in the kidneys.

It proved harmless to _rabbits_ when injected subcutem, but fatal in 24 hours when thrown into the peritoneum. The lesions were severe duodenitis and omental inflammation, and the bacterium was found in the liver and duodenal wall.

Pigeons, rats and mice proved refractory to the artificial cultures, also chickens. The latter were injected subcutem, intraabdominally and intravenously. Yet in view of the constancy of the lesion in hens with the microbe in pure cultures and the absence of all other morbid conditions, Dawson felt justified in attributing the disease to this microörganism. It is possible that his experimental hens had become immune from a previous attack, or failed in some condition of food or environment which is essential to pathogenesis, or finally there may possibly be some other infinitesimal microbe present which escaped observation, but which furnished the occasion for the coincident development of the colon bacterium.

_Treatment._ The indications are: the expulsion of the offending bacterium to be followed by nutritious, easily digested food, pure water and tonics. Dawson advises castor oil in dose of two teaspoonfuls, or calomel ¼ grain repeated till purgation occurs; and to be followed by powdered fennel, anise, coriander, cinchona of each 30 grains; powdered gentian and ginger of each ½ dram; powdered copperas 15 grains. The addition of bismuth, pepsin, or orexin may be suggested.

APOPLECTIFORM SEPTICÆMIA IN CHICKENS.

Streptococcic infection in hens. Most violent in pullets and hens;
less so in capons and cockerels. Found dead, or sick 24 hours,
ruffled, prostrate, neck limp, head drooped, indisposed or unable to
rise, liquid icteric fæces, blood-stained skin of neck and breast,
death without agony. Lesions: Soiled anal feathers, plump carcass,
skin pallor save neck and breast, extravasation of blood subcutem and
intramuscular, mucosæ anæmic, peritoneal engorgement and effusion,
enlarged, engorged liver, cell proliferation, degeneration,
coagulation necrosis, gall bladder full. Enlarged congested spleen,
degeneration. Congested swollen kidneys, epithelial degeneration,
casts, streptococcus. Congested, consolidated bronchioles, alveoli,
lungs, with microbe. Meningeal congestion, exudate. Bacteriology:
Streptococcus, pure cultures in lesions, size, chains, tetrads,
staining qualities, culture media, colonies, action on sugars, acid,
no gas, on milk no coagulation, on gelatine no liquefaction. History:
Stagnant water; no evident source of infection, buzzards, etc.
Pathogenesis: Inoculation, intravenous or intramuscular, feeding. On
duck, pigeon, rabbits, mice, dogs. Guinea pigs and sheep immune.
Immunization by injection of sterilized cultures.

Under this name Norgaard describes a hæmorrhagic streptococcic infection which prevailed in 1901 in a flock of 200 to 250 Plymouth Rocks in Loudon County, Va. Forty birds died within six weeks, and later the mortality reached 200, death often occurring suddenly while feeding, or the birds would drop from their roosts in the night and be found dead in the morning.

_Symptoms._ In the majority, the pullets which died suddenly, no symptoms whatever were observed, yet a certain number of the capons and cockerels were noticeably ill for 12 to 24 hours. In these the feathers were ruffled, the prostration extreme, the head drooped between the wings, the neck was weak and wobbling (limber neck), the wings and tail drooped, and the animal lay on its breast often unable to rise. Sometimes there was a passage per anum of liquid bile-stained mucus. Close examination of the neck and breast might detect hæmorrhagic discoloration of the skin, though the skin elsewhere was pale and smooth. Death takes place without a struggle.

_Lesions._ The anal feathers were usually stained, indicating diarrhœa; the picked carcass was plump and fat, with pale, healthy looking skin, except on the neck and breast, where it was discolored by extravasated blood; at such points the connective tissue and muscles were infiltrated with blood in areas of an inch in diameter, more or less, and with irregular outlines. The buccal mucosa was clear, pale and bloodless. The cavity of the body contained an abundance of sero-sanguinolent exudate, and the mesenteric veins were engorged. The _liver_ was greatly enlarged and congested, the greater part of its substance being apparently composed of the distended blood vessels. The hepatic cells were granular and fatty, and if death had been delayed over twenty-four hours their outline became indistinct and the nucleus stained only faintly. In the foci of disease were clumps of round cells and leucocytes in and between the acini, and in still more tardy cases points of coagulation necrosis. The streptococcus was abundant in the necrotic centres, among the clumps of leucocytes, in the parenchyma and capillaries. The _gall bladder_ was usually distended with bile. The _spleen_ had the large size and well developed Malpighian bodies that characterize the well-fed bird, but it showed still greater enlargement, combined with sanguineous congestion and circumscribed blood extravasations. With a hand lens were seen numerous round, semi-transparent points, the size of pin holes, which the microscope revealed to be centres of coagulation necrosis, surrounded by embryonic tissue. The centres consisted of a granular debris with abundance of the streptococcus. The _kidneys_ were congested and swollen, and in cases that had survived two or three days there was granular degeneration of the epithelium of the tubules, and the lumen of the tubes contained casts with leucocytes and streptococci. The organism was also present in the capillaries. The _lungs_ presented areas of congestion and consolidation, exudation into the walls of the bronchioles and the alveoli, and an abundance of streptococci in the lesions. In the cranium were a subdural exudate and meningeal congestion. For examination of the tissues they were hardened in specimens of alcohol of encreasing strengths, embedded in paraffin and stained with carbol fuchsin with a counterstain of methylene blue.

_Bacteriology._ The streptococcus was found in pure cultures in all the diseased centres except in the intestinal contents. Smear preparations were made from the blood, the abdominal exudate, the intestinal contents, the bone marrow, the cerebral exudate and the sanguineous effusions into the muscles.

The coccus is .6 to .8μ in diameter, in short chains of 2 to 8 cells, or in some media much longer. Involution forms are common, and Norgaard claims to have seen indications of fission in two directions to form tetrads. The organism stains in the usual aniline dyes, as well as by Gram’s and Gram-Weigert’s method. It is nonmotile, ærobic, facultative anærobic, grows in solid and liquid media that is neutral, or slightly acid or alkaline (not if strongly acid), best at 98.6° F., and slower at the room temperature. In alkaline peptonized beef bouillon in 24 hours it forms threads and balls on the sides and bottom of the tube, leaving the liquid clear. On agar there are formed small shining, grayish colonies 1.5 mm. in diameter with brownish centre and bluish periphery. With all the sugars it produces acid, but no gas. It does not coagulate milk. On gelatine colonies are formed in four days, and there is no liquefaction.

_History of the Outbreak._ The outbreak commenced early in January, without any obvious occasion for the introduction of infection. There had been no chicken disease on the place for 25 years, and no chickens had been purchased except from a neighboring farm where the stock remained healthy. They had been fed on corn meal, wheat bran, wheat tailings and whole corn, together with scorched wheat from a burned barn. The poultry houses were clean and well aired, and after they had been closed there was no abatement of the disease. The water was from a stagnant pool receiving drainage from the stable, but this was no new condition and January is not the driest month with the foulest water. The suggestion may be hazarded that the infection may have been introduced by the usual infection bearer, the buzzard, or by some other wild bird, or mammal.

_Pathogenesis._ Among the _chickens_ the most rapid and fatal cases were in pullets, then among the laying hens, while the capons and cockerels were less severely affected, and some survived from three to seven days.

Those _inoculated intravenously_ as a rule sickened on the second or third day with a temperature of 110.7° F., and were found dead the following morning.

Some took injections of .25 to 1cc. in the _pectoral muscles_ with impunity.

Chickens that had fasted 24 hours, took each daily for 3 days, a few cubes of bread soaked in a fresh bouillon culture. Death followed in four out of six, in from four to thirteen days from the beginning of the experiment. The birds gradually became listless, refused to eat, and remained quiet in a corner of the cage, with closed eyes and head drooping until it rested on the ground. Diarrhœa was frequent but not invariably present.

Chickens fed on the chopped up viscera of rabbits that had died of the disease perished in 3 to 10 days.

A _white duck_ inoculated intravenously with .5cc. of peptonized beef bouillon culture, took ill on the 8th day, and died on the 12th. There was loss of coördination and use of the wings, temperature 109° F., and necropsy showed valvular endocarditis containing the streptococcus. A second duck sickened on the 11th day, but recovered after three days’ illness. Killed on 21st day, all cultures from heart, spleen and kidney remained sterile. Subcutaneous, intramuscular and feeding experiments failed to produce the disease in ducks.

A _pigeon_ injected with .5cc. bouillon culture intravenously died on the fourth day with the internal lesions of chickens, and blood extravasations on head and neck. Intra-muscular injections and feeding experiments were fruitless.

In _rabbits, intravenous_ injections of 1 to 1.5cc. led in 24 hours, to temperature of 105.3° F., without impairment of appetite, or other marked sign of illness, and as a rule the subject is found dead next morning. _Intra-abdominal_ and _intrapleural_ injections kill in two to four days, and _subcutaneous_ ones in three days. In addition to the lesions found in chickens, there is often bloody urine, a sanguineous lymph on and beneath the cerebral meninges and in the fourth ventricle, and deep congestion of the cancellated tissue of the vertebræ. Streptococci are abundant in the lesions.

In _mice intraabdominal_ injection of .01cc. killed in 48 hours, and _subcutaneous_ injections in 2 to 5 days. The lesions were like those seen in birds, and streptococci were abundant.

In _dogs_ after _intravenous_ injection there was hyperthermia (103.6° and 104.1° F.) and lameness of the right fore shoulder joint, followed in 5 to 8 days by recovery. Feeding on the viscera of the diseased chickens, was followed by anorexia, and vomiting only.

_Guinea pigs_ and _sheep_ proved refractory.

_Immunization._ The injection into the wing vein of .5 to 2.5cc. of bouillon culture, sterilized by heat proved protective to the chickens against inoculations of the virus while the check animals invariably died.

TUBERCULOSIS.

Synonyms. Definition: infectious disease caused by bacillus, attended
by productive inflammation, tubercles, necrotic degeneration,
caseation, fibroid change, calcification or ulceration. Animals
susceptible: python, salamander, carp, fish, birds, rodents, sheep,
goats, solipeds, cattle, dogs, cats, apes, swine, wild ruminants,
kangaroo, carnivora, cage birds, civilized (housed) man. Geographical
distribution: with dense population, Central Europe, Britain, Eastern
States; little in absence of cattle products—Scottish Western Isles,
Iceland, Newfoundland, Greenland Highlands, Arctic North America,
Northern Norway, Sweden, Lapland: open air life protects. Virulence:
ancient records, modern, early antituberculous legislation, decimation
of herds, researches of Vilemin, Gerlach, Chauveau, Semmer, Parrot,
Tappeiner, etc. Bacillus tuberculosis: evolutionary changes, relation
to actinomyces, 1.5 to 3.5μ by 0.2μ shorter and thicker in ox,
solitary, exceptionally short chains, on blood serum may be
filamentous, staining slow, carbolated fuchsin, technique, sections;
biology, adaptation to environment, to genera, variation in same
genus, experiments showing real identity of variant forms; vitality:
in water human bacillus 50 to 70 days, bovine bacillus indefinitely,
avian 117 days, dried sputa 9 months, cow’s lung 102 days, putrid
material 43 days to years, survives gastric juice, sunlight kills in
some hours, if in thin layer, day light 7 to 18 days, dry heat (212°
F.) for an hour left living bacilli, moist heat 140° F. for 1 hour
kills, low temperatures (−25° F.) fail, after 15 days in salt failed
in rabbit, after 30 in Guinea pig. Chemical disinfectants. Accessory
causes: racial vulnerability, close buildings, dark, foul, damp
stables, poor scanty food, heavy milking, conformation, early
breeding, inbreeding, age, predisposing diseases, traffic in animals,
dairy extension, admission of tuberculous animals from other states,
assorting tuberculous for sale in a given State, sale of sound from
tuberculous herd, lack of indemnity for animals killed, private
testing of herds and sale of tuberculous, accustoming to tuberculin
test, antipyretics during tuberculin test, false certificates of
tuberculin tests, feeding hogs on tuberculous offal, feeding calves
and hogs on tuberculous milk, feeding hogs after tuberculous cattle,
feeding from a common trough, dry, dusty stables, extension through
vermin, flies and other insects carry virus. The tubercle: miliary,
pinhead, conglomerate, proliferation of cells—tissue and leucocytes,
in nests in stroma, giant cells in center, then epithelioid, then
lymphoid, caseation, calcification, fibrosis, pearl disease.
Localization: _Cattle_: pulmonary: miliary tuberculosis, aggregation
into larger tubercles, caseated centres, fibroid, cretified,
abscesses, vomicæ, complex infections, infiltrations, difference from
broncho-pneumonia, lesions of different ages; pleural lesions;
congestion, exudation, fringes, nodules, grapes, adhesions,
caseations: bronchial and mediastinal glands, congestion, swelling,
softening, induration, caseation, cretefaction: cardiac lesions:
lesions of mouth and throat, pharyngeal glands: gastro-intestinal,
peritoneal, mesenteric glandular; œsophagastoma; liver tubercle;
splenic; pancreatic; genito-urinary; mammary; cerebral; spinal;
orbital; skeletal; cutaneous; muscular; glandular; table of
distribution. _Swine_: lesions: pharyngeal, intestinal, mesenteric,
muscular, hepatic, splenic, glandular, pulmonary, skeletal, caseation,
liquefaction. _Horse_: lesions: thoracic, abdominal, glandular, of
serosæ, vertebræ, etc. _Sheep_ and goat: lesions: thoracic, abdominal,
glandular, hepatic, pharyngeal, facial, etc., verminous affections.
_Dog and Cat_: lesions: respiratory, abdominal, pharyngeal, tonsillar,
hepatic, pancreatic, splenic, skeletal, arthritic, cutaneous. _Apes
and Menagerie Animals_: lesions. _Chickens_: lesions: intestines,
liver, spleen, peritoneum: lungs and kidneys often escape. _Pheasant_:
lesions: as in hens, centre zone has epithelioid cells, fibroid,
cretefaction, amyloid degeneration. _Parrot_: lesions: eye, beak,
tongue, palate, larynx, bones, joints, lungs, liver, intestines,
muscles, skin. Primary and secondary infection, extension by
lymphatics, blood channels, tonsils, inhalation, deglutition.

_Synonyms._ Consumption; Tabes; Scrofula; Pining; Grapes; Great White Plague, etc.

_Definition._ An infectious disease common to man and a large number of animals, caused by the bacillus tuberculosis, and characterized by a productive inflammation giving rise to small, rounded bodies (tubercles), or diffuse infiltration, with a tendency to necrotic degeneration, and caseation, or to fibroid degeneration (sclerosis), calcification or ulceration.

_Animals susceptible._ Tuberculosis comes near to being a panzoötic, since although reptiles, fishes, birds and some mammals do not readily contract it under normal conditions, yet under abnormal and debilitating conditions nearly all will succumb to it.

_Reptiles._ Sutton found tuberculosis in a python which was kept so warm in the London Zoological Gardens that a thermometer between its folds registered 85° F. Kráhl, Battaillon and Ferre cultivated the bacillus in frogs, Kráhl in snakes. Blauvelt found tuberculosis in a salamander. Lechner found it in amphibia.

_Fishes._ Broussais records the prevalence of tuberculosis in carp in a pond which received the sputa of a consumptive man. Under the skin were found rounded tumors, containing abundance of bacilli, that infected rabbits and Guinea pigs on which they were inoculated.

_Birds._ In birds of the farmyard—hens, pheasants, turkeys, ducks and pigeons—it is very frequent and often occurs as an epizoötic. While the tuberculosis of barnyard fowl is a manifest variety and not readily interchangeable with the varieties affecting the mammal, yet, with a special predisposition, it can be transferred and can then be conveyed from animal to animal in the new genus in which it has been implanted. That of cage birds is interchangeable with that of man.

_Rodents._ Guinea pigs have a strong susceptibility to tuberculosis, whether from human or bovine source, and rabbits for that of birds, and by continuous transmission through the body of the rodent, all alike seem to tend toward acquiring common characters. The Guinea-pig, therefore, has been especially availed of for the experimental transmission of tuberculosis, and, as the disease in them becomes acute and rapid in its progress, these subjects permit the multiplying of experiments in a short period. _Rabbits_ are less vulnerable to the bovine or human form.

_Sheep and goats_, kept under usual conditions, show a remarkable immunity from tuberculosis, yet if directly inoculated an inherent susceptibility is easily shown. Habitual immunity may be in some degree due to their open air life, to the heavy winter fleece protecting them against chills, to the comparative absence of the heavy and continuous milk yield demanded of cows, to the more restricted development of the lymph plexuses in the lungs and elsewhere, and to the limited opportunity offered by the small tonsils for infection entrance.

The _horse, ass and mule_ rarely contract tuberculosis casually, the more spacious stall, outdoor life, hard muscular condition, the very small tonsils, the exclusive nasal respiration, the paucity of connective tissue lymph plexuses, and the abundance of red globules, probably favor immunity. Yet on inoculation by Chauveau, Nocard and others, the horse readily succumbed to infection, generalization taking place more certainly than in the ox.

_Cattle._ The bovine races are remarkably subject to tuberculosis. This is probably due in part to the great amount of connective tissue lymph plexus in the lungs and elsewhere, the habit of using the mouth in hurried breathing, the deep, sudden inspiration through the mouth and over the tonsils that follows a cough, the habitual restricted size of the cow stables, the absence of individual separated stalls, the habit of feeding from the same trough with the cattle adjacent, the great drain of yearly breeding and heavy milking, the retention in the herd of old, failing cows for their milk product and high priced offspring, and the bovine habit of licking each other with the infected tongue. In many European cities and even in country districts the disease is very prevalent. In Copenhagen a few years ago 17.7 per cent. of all oxen and cows killed in the abattoirs were tuberculous; in Berlin 15 per cent.; in Holland 20 per cent.; in Pomerania and Bomberg 50 per cent.; in Hildesheim, Hanover, 50 per cent.; in Berlin dairies 75 per cent. (Ostertag): in Leipsic and Edinburgh 20 per cent. The great variation in the data for the different cities is suggestive of different inspection standards. American figures as given by the Bureau of Animal Industry are for Baltimore (mostly cows recently from the country) 2.5 to 3.5 per cent.; and for the packing centers (among 2,273,547 mostly fat steers, and therefore selected) 0.02 per cent. It is here largely a matter of locality and infection, I have seen large herds with 100 per cent. tuberculous, and extensive districts, in the north and especially in the south entirely free from the disease.

_Dogs and cats_ in their natural condition rarely show the disease, but contract it readily on inoculation. Cadiot found 40 cases in 9,000 _post mortems_ of dogs. The young are apparently more susceptible than the old, and primary lesions in the abdomen are common and suggest infection through the food. The majority belonged to consumptive persons, and gnawed the bones that had been first picked by the owner, and ate from his plate what he left. Jacobi records the case of a dog, with general tuberculosis, which habitually licked up the expectorations of his phthisical master.

_Apes and Monkeys_, in confinement, almost all die of tuberculosis.

_Swine_ contract tuberculosis readily, the large tonsils, the habit of breathing through the mouth, and the abundance of connective tissue and lymph plexuses in the lungs and elsewhere contributing to this. Yet in them the affection is mainly a dietetic disease. Swine kept in the country and fed on vegetable food are rarely affected. In Saxony, where 17 per cent. of the cattle are tuberculous only a shade over one per cent. of swine were so, and in Baden only 0.02 per cent. In hogs raised on our western farms and corn-fed the proportion is much less. Yet in those fed on uncooked skim milk, kitchen scraps and the refuse of slaughterhouses in a raw state, tuberculosis becomes very common. In one case, in a large public institution, where the dairy herd was universally affected, and where, on their slaughter, their raw offal had been thrown to the hogs, I found that the latter were almost all tuberculous. Similarly, in feeding experiments, from the time of Gerlach, pigs and especially young pigs, have shown themselves to be very susceptible.

Among the less domesticated animals that contract tuberculosis may be named _deer_, _elk_, _gazelle_, _antelope_, _camel_, _dromedary_, _giraffe_, _kangaroo_, _lion_, _tiger_, _jackal_, _jaguar_, _bear_, _arctic fox_, _rat_, _mouse_ and the _common cage birds_, etc. Fröhner found 36 per cent. of parrots affected in Berlin.

_Man_ has long been recognized as standing in the front rank of susceptibility to tuberculosis. Yet even in his case the prevalence of the affection bears an intimate relation to his indoor life. In large cities _post mortems_ often show that one-third have suffered, and that one-seventh and upward of the whole population die of tuberculosis. Natives of tropical islands and countries, living in the open air and apart from close association with civilized man, often escape entirely. In South Africa the herdsmen living in close buildings suffer encreasingly, while their cattle, kept constantly in the open pasture, escape.

_Geographical Distribution._ The prevalence of tuberculosis shows a direct relation to the opportunity for infection rather than to climate, latitude or altitude. It is the prevailing disease of civilized communities with dense populations, and especially in large cities where the general vitality is lowered and the crowded buildings give every opportunity for infection. It is preëminently the disease of Central Europe, of Great Britain and of our Eastern States, where there is the greatest activity in business, manufacture and commerce. Yet in the Scottish Hebrides, Iceland, Newfoundland, the Greenland Highlands, Arctic North America, the northern parts of Norway and Sweden, Lapland and Finland it is hardly known. The absence of commerce and cattle and the sparse population have much to do with this. The coasts of Greenland with their Danish stations have two-thirds of the population tuberculous (Cook); the Indians of Barrow’s Straits, when infected in 1899 by the frozen-in whalers, suffered from it as from a plague; in Christiana, Stockholm and St. Petersburg it is as prevalent as in the large cities of Central Europe. Elevated and dry climates have often been found to be free from the affection, yet it prevails inside the double windows of houses in the higher Alps, and has, within a generation established a notorious prevalence in Minnesota, Dakota and westward, as it has in Australia, mainly owing to the advent of consumptives who sought for health in the dry atmosphere. The hills and dry tablelands in North and South America, Africa and Asia which have acquired a reputation for salubrity, owe this largely to the sparse population and the absence of facilities for infection. In South Africa, in spite of the dry and genial climate, the disease is constantly encreasing in the human (housed) population. The sea-coasts, which are the seats of large cities and the centres of population and trade, are also the most extensively affected with tuberculosis—in the West Indian Islands, Panama, Nicaragua, Mexico, Yucatan, Columbia, Equador, Peru, Chili, Ceylon, Guinea coast—while the sparsely peopled highlands of the same countries are practically free.

What is true of man is equally so of cattle. In the Gulf states of this country, herds living in the open air are practically free from tuberculosis, while in New Orleans and other large cities, the cows shut up in the confined stables and yards, are as tuberculous as those of the great cities of the north. So in many districts in the northern states we find no bovine tuberculosis, while in others, differing in no essential particular as regards geological formation, altitude, exposure, and industrial use of the animal, a large proportion are affected.

_Virulence._ Tuberculosis has long been recognized as virulent. “It is indicated in the Mishna and other Jewish works as rendering the meat unfit for consumption, but to come to more modern times, we find that throughout the seventeenth and eighteenth centuries the flesh of tuberculous animals was excluded from human food, alike by the civil and ecclesiastical laws of Europe. Tuberculosis in cattle was erroneously identified with syphilis of man, which made a frightful extension in the end of the fifteenth century, spreading from the army of Charles VIII which had been engaged in the siege of Naples. This conviction lasted until it was disproved about 1782. Though mistaken in the identity of the two diseases, the fact that for centuries the common people and physicians both associated tuberculosis with a malady so notoriously contagious as syphilis, speaks strongly for the forcible evidence of contagion manifested at that time. Morgagni, who must have begun practice about 1700 A. D., testifies to the strong conviction of the contagious element in tuberculosis. Indeed it became a common practice to isolate the consumptive person from the public, and after his death to burn his clothes and sometimes even the house, or at least to subject them to a careful disinfection. It is recorded that in 1750, in Nancy, the magistrates ordered the burning, in the public square, of the personal property of a woman who had died of phthisis, from sleeping in the bed of another consumptive person.

“At Naples, a royal edict of September 20, 1782, prescribed the sequestration of the phthisical, the disinfection of the rooms, chattels, movables, books, etc., with vinegar, eau-de-vie, lemon juice, sea-water, fumigations, etc., under a penalty of three years at the galleys, or in the case of nobles, of three years imprisonment and a fine of 300 ducats. A physician who failed to report a case of consumption was fined 300 ducats for the first offense, and banishment for ten years in case of a second. Any one assisting in such evasion of the law was sent to prison for six months.

“Chateaubriand found that, in 1803, he could not sell his carriages in Rome, because Mme. Beaumont, who had died of consumption, had ridden in them three or four times. George Sand, who was with the phthisical Chopin in Minorca in 1839, was refused a lease of the house for the second month, and the price of repainting and purifying was demanded. Later, in Barcelona, they were assessed for the bed on which Chopin had slept, as the police regulations prescribed it should be burned.

“This was not a mere survival of vulgar prejudice. Jacobi tells us of a dog which died of consumption from eating the sputa of his phthisical master. Laennec, the discoverer of auscultation, and the great authority on pulmonary consumption, records that he himself contracted a tuberculous nodule, through a wound with a saw, while making a necropsy in a case of phthisis. Laennec died of tuberculosis later, although he seemed to have checked this lesion by caustics. Andral joins Laennec in enjoining the greatest caution and cleanliness in taking care of, or associating with persons having advanced tuberculosis.

“Cullen, who started with a strong prejudice against the doctrine of contagion, leaves us the following instance of its occurrence: ‘A young man predisposed to phthisis married a Dutch girl of a sanguine temperament and good constitution. Some days after the marriage the woman lost her fresh color and was attacked by a bad cough; a month later she commenced spitting blood. The physician advised her not to sleep in the same bed with her husband, but she refused to follow his advice, and six months later she died of phthisis. The servant who took care of her and the domestic, who avoided, as far as possible, staying in the sick chamber, both died of consumption.’

“Wickmann, court physician in Hanover, in 1780, pronounces emphatically for contagion. In Zurich, at that time, one death in every six was from phthisis. The contagion of phthisis was slow in its operation, and was, therefore, less evident than that of plague, smallpox, scarlatina and other affections attended by a skin eruption, but it was no less real and deadly. It was also less frequently indirect, or carried from victim to victim by intermediate agents. He cited instances of the transmission of consumption from husband to wife and vice versa, and claimed that the marriage of a phthisical person should be legally prevented. As a means of preventing the disease, he proposed a strict surveillance of establishments for the sale of old clothes, and the avoidance of leaving infants with consumptives.

“Valsalvi and Sarconi refused to make necropsies of persons who had died of phthisis.

“Dr. Ruhling, of Gottingen, writing in 1774, of the disease in animals, says: ‘The malady is transmitted to sound animals by direct contact of animals standing side by side in the stall, and licking each other, and breathing the expired air direct from the diseased lungs; the frequenting of the same pastures will also serve to propagate it.’ In Krunitz’s encyclopedia, published in Berlin, in 1787, is the following: ‘The heifers show an ardent desire for the male, and remarkably enough, do not become pregnant, but part with the fruit of conception. When opened these animals show the first stomach, kidneys and surface of the lungs, covered with pustules like dried mulberries or in suppuration. The affection is contagious, and communicates itself from one animal to another by contact.’

“Fromage, in the Dictionaire de Rozier, Article Phthisis, says: ‘Men of art are very much in accord that this malady is not contagious, but some stock owners think differently.’

“Huzard, who saw much of tuberculosis in the Parisian dairies in the concluding decade of the last century, said that most of the veterinarians looked upon the disease as contagious, and that some of the physicians believed the same of the phthisis of man.

“Dewar, speaking of his experience in Scotland in 1839, and succeeding years, in a particular herd, says: ‘The proprietor agreed to remove partition walls, and to make openings opposite one another in the outside walls, so that there might be a current of fresh air passing through. These alterations combined with cod liver oil, tonics and stimulants, may have prolonged life but yet no cure was effected, and that herd died out. I resorted to every precaution when new cattle were purchased to prevent infection; as I had an idea, even at that time, that the disease might be communicated from one to another when in immediate contact. The precautions adopted when fresh cattle were purchased had the desired effect, for in a few years afterward, they were as good a lot of cattle as any in the district. That herd left an impression on my mind that never can be effaced, and made me always dread the evil consequences of tuberculosis. Having practiced in the same locality, which is an extensive breeding and rearing district, I have seen several herds decimated. Though I have sometimes foretold the owner what he might expect, yet he did not believe me until so many were infected that the byres were infested with the fearful malady, and your remarks in regard to nose contamination are so true that I do not think it possible any can escape that are so exposed. I have also seen, as Grad has, the same stall infecting beast after beast until a thorough cleaning and disinfecting, with plenty of fresh air had removed all infection.’

“Spinola, writing in 1858, of bovine tuberculosis, gives contagion as a possible cause, and Lafosse, in 1867, says: ‘Physicians begin in imitation of Morgagni to believe in the contagion of phthisis. The facts published by Villemin appear to support this opinion, which has been held by our colleague, Dupont, of Bordeaux, for several years.’

“Cruzel in his work of date, 1868, is much more positive; he says: ‘This fœtid expired air, inhaled immediately by another cow upon a sound lung, gives the latter tuberculous infection. It is a matter of every day experience to the veterinarian. Two oxen or cows are kept in the same stable, take their food from a common rack or manger, lie in the same stall, and respire nose to nose. The one is, to all appearances, perfectly sound, the other is in as good a condition, and is vigorous, but it coughs from time to time, and its breath is foul. Soon we notice that the animal that does not cough, eats with less appetite, he loses flesh and soon he is unequivocally affected with the same malady as the first.’ The foregoing quotations show clearly that in spite of the misleading teachings of Broussais and others, the doctrine of contagion in tuberculosis could not be overcome, and that up to the time of the remarkable experiments of Villemin, in 1865, it maintained its hold upon the minds of extensive and careful observers. In animals, especially, the evidence was so frequent and clear, animal following animal in the same stall, and eating from the same infected manger, only to be infected in turn, and two animals stalled together, and licking the same manger with their prehensile tongues, transmitting the infection with certainty the one to the other, were facts that could not possibly be ignored. Other cattle in the same building might escape for a length of time, but the eating in common from the same fatal manger, by a tuberculous and a healthy animal, quickly sealed the fate of the latter.

“Physicians, too, who were compelled to investigate the causes of the extraordinary fatality from tuberculosis in the armies and navies, could not shut their eyes to the fact notwithstanding that they came to the task strongly prejudiced through education against the acceptance of contagion. Thus, Dr. Bryson, in his report to the Epidemiological Society, in 1860, on consumption in the several ships of the English navy on the Mediterranean station, says distinctly that the disease appeared to be propagated by contagion. Dr. Parkes, quoting this in his Practical Hygiene, says: ‘It may be inferred that pus cells were largely thrown off during coughing, and floating through the air, were received into the lungs of other persons. The production of phthisis in animals confirms this view. The case of monkeys in the zoological gardens, narrated by Dr. Arnot, is a striking instance. Cows in close stables frequently die of phthisis. But not only phthisis may reasonably be considered to have one of its modes of origin in the breathing of an atmosphere contaminated by respiration, but other lung diseases, bronchitis and pneumonia, appear also to be more common under such circumstances.’

Villemin in 1865, published his investigations in which he had produced tuberculosis in a great number of animals, by inserting particles of fresh tubercle or injecting the tuberculous sputa of man into the subcutaneous connective tissues, the peritoneum and the trachea. There resulted in nearly every case a chronic disease, the marked phenomena of which were caseated centers devolving from firm inflammatory nodules in the seat of inoculation, in the adjacent lymphatic glands, in the lungs, serous membrane, liver, spleen and kidneys. The centers of such nodules were at first transparent and grayish, but soon the center underwent necrobiosis, forming a soft cheesy mass the size of a pin’s head, and gradually enlarging to that of a pea, a bean, a hazel nut or larger. After a period of about 14 days the lymphatic gland nearest the seat of injection could be felt as a firm pea-like nodule, and in two weeks more a second gland on the line of the lymph circulation, had become enlarged and nodular, while the first, now the size of a large bean, had probably undergone distinct softening. This became adherent to the skin, burst and discharged continuously or at intervals with little or no tendency to heal. If killed at this date, the animal showed only the open sore and a chain of nodular pea-like caseated lymphatic glands leading up from it. The lungs might be apparently sound, but the spleen and liver usually showed miliary elevations on the surface, with clear grayish centers, as viewed under a magnifying glass, opaque patches were found on the omentum, and the lymphatic glands of the mesentery, of the portal fissures of the liver and of the Hilus of the spleen were distinctly enlarged and resistant. If not killed, the subject usually died 100 to 120 days after inoculation, and then the lungs were found studded with tubercles miliary or larger and more or less caseated; the bronchial mediastinal, subdorsal, pectoral, prepectoral, phrenic, mesenteric, hepatic, and splenic lymphatic glands were more or less enlarged and caseated, while the liver and spleen were enlarged and studded with multiple tubercles. Guinea pigs give the most extensive and intensive lesions, rabbits much less so, but in both emaciation and wasting are very marked. In short the lesions are essentially and unmistakably those of generalized tuberculosis.

“At first, however, incredulity prevailed and experiments on a large scale were inaugurated all over Europe and America to put the question to crucial test. Martin, Conheim, Burdon-Sanderson, Simon, Wilson, Fox, Lebert and Wyss, Fraënkel, Waldenbourg, and others inoculated with all sorts of non-tuberculous organic materials (bronchial mucus, foul pus, cancer juice, diseased liver, simple cotton setons, etc.) and from these in Guinea pigs there resulted local caseated foci, and implication of the adjacent lymphatic glands. It was found that the liquids from low types of pneumonia produced these apparently tubercular deposits, while that from acute sthenic pneumonia did not; that the cotton thread seton failed to produce the disease if it were first steeped in carbolic acid, and that the lesion caused by breaking a bone without injury to the skin failed to produce the characteristic lesions even in the very susceptible Guinea pig. It became evident, therefore, that the morbid results in these cases, were due to accidental inoculations with the poison of the tubercle, which is widely distributed, or with some pyæmic or other germs.

“Gradually the truth triumphed, and those who had at first been loudest in their opposition were led by their own experiments to become the firmest supporters of the new truth.

“As early as 1874, Gerlach had experimented largely in feeding the milk of tuberculous cows, and had infected calves, pigs, sheep and rabbits in this way. Chauveau in (1874), Klebs (1873), Semmer (1880) and Parrot (1870) fed calves, cats, Guinea pigs, pigs, sheep and a variety of other species of animals with tuberculous flesh or lungs, or saliva, producing tuberculosis in a large proportion of cases. In this manner they escaped the charge of the operation of a wound and of ærial bacteria, and yet succeeded in producing infection. The lesions in this case began in the intestinal mucous membranes and mesenteric glands.

“Another essay in the same direction was made by Tappeiner (1878), who infected rabbits, Guinea pigs and dogs, by enclosing them in boxes and compelling them to breathe tuberculous liquids intimately mixed with the air atomization. In these cases lesions began in the lungs and bronchial and mediastinal glands.[1]”

Footnote 1:

(From Report to the N. Y. Legislature, 1895. James Law.)

_Bacteriology._ The _bacillus tuberculosis_, the essential cause of tubercle, was demonstrated by Koch in 1882. It was at first supposed to be peculiar in its indisposition and tardiness to take a stain, and in its retention of the stain once imparted, even when it is treated with acids. Later observations have shown that these characteristics are common to certain other bacilli, notably to those of leprosy, smegma, and to specimens found in timothy hay and other grasses, cow dung, milk and butter. These furnish sources of fallacy in the milk and butter especially, but when the specimens examined are taken from the interior of a tubercle, lymph gland or serous cavity the danger of error may be practically ignored. What is quite as important is the fact that the tubercle bacillus is subject to evolutionary changes in adapting itself to a habitat in different genera of animals, and to a lesser extent in different parts of the same animal, by which its pathogenesis is modified, but these variations do not materially affect the staining qualities. Still more striking variations have been found in old cultures, ovoid forms (Metchinkoff), club-shaped microbes and filaments (Metchinkoff, Klein, etc.), branching filaments (Fischl, Coppen Jones), divergent club-shaped groups, like actinomyces (Babes and Levaditi). The last named, seen in inoculated rabbits, have been held to establish a relationship between the microbes of tuberculosis and actinomycosis, as the club-shaped cells do not take the usual Ziehl-Neelsen stain for tubercle bacilli, but the Birsch-Hirshfeld’s actinomyces stain. Apart from the rabbit such variations are not likely to prove sources of fallacy in identification of the microbe.

_Morphology._ As met with in the tubercle of man or ox the bacillus is a minute rod with rounded ends, 1.5 to 3.5μ long, by 0.2μ in thickness. In the ox it is shorter and thicker on an average than in man. They are usually solitary, but two and exceptionally even three or four elements may be united. In stained specimens unstained portions are frequently seen (spores?). When cultivated on blood serum there is a tendency to form elongated rope-like colonies having a waving outline. Other evolution forms have been already noted.

_Staining._ The resistance to staining is overcome by a heated alkaline watery solution of methylene blue (Koch), or better by a carbolated solution of fuchsin (Ziehl-Neelsen). To a 5 per cent. watery solution of carbolic acid add one tenth of its volume of saturated alcoholic solution of fuchsin. The suspected sputum or scraping from a section of a lesion is spread in a thin layer on a cover glass by drawing over it the straight edge of a second cover glass, dried in the air, and passed three times through an alcohol flame with the smeared side up. It may then be floated on the surface of the staining fluid with the specimen side down, then gently heated for three or four minutes almost to ebulition, drying being prevented by the addition of more of the carbol-fuchsin solution as required. It is then washed in water to remove excess of the staining fluid and treated with a bleaching acid solution (sulphuric acid 5 per cent. or nitric acid 15 per cent.) When decolorized it is well rinsed in two or more portions of a 60 or 70 per cent. alcohol and then in water. Next stain with a 1 or 2 per cent. aqueous solution of methylene blue for one minute and wash off the excess with water. The tubercle bacilli will appear of a deep red and other bacteria blue.

_Gabbett’s_ counter-staining and decolorizing solution is especially useful in economizing time. After staining, as above directed, in the carbol-fuchsin solution for one minute, wash in water, then cover with a solution of 2 grams methylene blue (powder) in 100cc. of 10 per cent. sulphuric acid, until the film has a faintly bluish tint: then wash thoroughly in water and examine. Tubercle bacilli come out red, others blue.

In _examination of tissues_ the microscopic sections are steeped for twenty-four hours in the carbol-fuchsin solution (or 1 hour at a temperature of 45° to 50° C.), then decolorized in a 5 per cent. sulphuric acid for a few seconds, then in a 70 per cent. alcohol: they are then counter-stained in an aqueous solution of methylene blue, washed in water dehydrated with absolute alcohol, cleared up in xyol or oil of cedar, and mounted in Canada balsam.

_Biology._ The _bacillus tuberculosis_ is notorious for its variant forms, assumed in adapting itself to given environments, and which it retains with considerable tenacity for a time, even when placed in a new and different medium. It is largely held to be an obligatory parasite, and incapable of survival as a saprophyte, yet Straus, Nocard and others, have shown that the form obtained from the tuberculosis of birds can easily be made to live in suitable dead mixtures of organic matter. It is also notorious that the bacillus taken direct from the tubercle of the mammal, and which, as a rule, fails to grow at once in glycerined bouillon, yet, after a first successful culture in the new medium, often adapts itself completely, and thereafter it can in many cases be transferred from bouillon to bouillon, with as great certainty as it could formerly be inoculated from ox to ox. The difference is one of habit and adaptability, rather than any primary and permanent distinction of species. There is every reason to believe that the microbe has lived, and under given conditions can still be made to live as a saprophyte, with a greatly reduced adaptability to parasitic life in the animal, just as we see to-day that it is only with great difficulty transferred from certain genera of animals to certain other genera (from bird to ox and vice versa). Trudeau tells us of a culture of a bacillus tuberculosis from man, inoculated on the rabbit and then cultivated _in vitro_ in successive generations for six years, that was in this way robbed of its pathogenesis for Guinea pigs, which, after inoculation, lived for many months, some two and a half years, and some even recovered. The average duration of life in the Guinea pig, after tuberculosis inoculation from man, rabbit, Guinea pig or recent culture is but seventeen days. The bacillus of human sputum often produces only localized tuberculosis in the ox. Even in the same species and individual the pathogenesis often varies materially. Nothing is more familiar than the slow progress of tuberculosis in the bones and lymph glands of man, on the one hand, and its frequently rapid progress in the lungs, liver and brain, on the other. As inoculated on the lower animals bacilli from the lungs of man are usually more virulent than those from the lymph glands (Creighton, Arloing, F. Craven Moore, Courmont and Denis). Among seven specimens of human sputum, the bacilli in six cases showed a fair average vitality, whereas those of the seventh failed to grow on blood serum of the dog (Theobald Smith). In both man and cow a large proportion of cases of tuberculosis remain localized, the disease lasting for years with little or no appreciable advancement, and not a few subjects appear to make a permanent recovery.

On every hand this evolutionary tendency of the bacillus tuberculosis places itself in evidence, demanding a recognition of the fact, that more or less transient or lasting variations in accordance with previous or existing environment, control to a large extent the transmissibility of the disease among different genera and even among individuals of the same genera and species, and also the fatal progress, or the mild and evanescent issue of the infection.

Even the most widely divergent of these evolutionary forms can often be made to approach each other and apparently merge into one type. Profiting by the example of Metchnikoff, Nocard enclosed in collodion capsules the bacilli of the human sputum and inserted the capsules into the peritoneal cavity of chickens which had proved refractory to their direct inoculation. This excluded the direct action of the leucocytes from the encapsuled bacilli, but allowed the endosmosis of the serum of the fowl for their nourishment. After a sojourn of four months or more they were transferred to other capsules and again enclosed in the peritoneum and after a second and third transference of this kind it was found that the bacillus had become actively pathogenic for the chicken, having acquired the infecting potencies of the bacillus of avian tuberculosis.

In keeping with the above is the fact that both rabbit and horse are easily infected by the bacillus obtained from birds, and that after a certain number of transmissions through the rabbit the issue of the bacilli of bird and mammal appear to become identical. No less instructive are the cases of the infection of carp by human sputa and the conveyance of tuberculosis to rabbits and Guinea pigs by inoculation with the nodules of the infected carp.

The _vitality_ of bacillus tuberculosis is strong but variable. In sterilized water at 46° to 64° F. the human bacillus survived for fifty to seventy days (Chantemesse and Vidal), the bovine indefinitely (Galtier) and the avian bacillus at a higher temperature one hundred and seventeen days (Straus and DeBarry). In dried expectoration the bacillus of man still infects after nine or ten months (Koch, Schill, Fischer, De Thoma). In infected cow’s lung, dried and pulverized, it infected Guinea pigs at 102 days (Cadeac and Malet). In putrid matter it infected after 43 days (Schill, Fischer), 167 days (Cadeac and Malet), several years in a grave (Schottelius).

It is not destroyed by gastric juice (Fischer, Falk). The bacillus from tubercle of birds has a much greater vitality than that of mammals. Marfucci successfully seeded new media from a culture of two years old, and cultures in artificial media can be started more successfully.

Full _sunlight_ renders sputum on a solid nonabsorbent surface noninfecting in several hours, varying according to the thickness of the layer (Koch, Straus). When sputum is mixed in soil it may survive until the 137th day (Feltz). On woolen cloth it may live five hours (Migneco).

_Diffuse daylight_, with shading from the sun, killed in seven days (Koch), to eighteen days (Lucibelli).

_X-Rays_ do not arrest the growth of cultures (Blaikie, Pott, Ausset).

A _dry temperature_ of 212° F. for an hour left some of the bacilli still infecting to Guinea pigs (Lartigan).

A _moist heat_ of 140° F. for one hour sterilizes (De Man, Th. Smith, etc.). The scum formed on the milk may still prove infecting (Th. Smith). Half an hour of a moist temperature of 212° F. is sterilizing. Yet in the case of steaks, roasts and boiled meats the size of the piece often prevents the reaching of this temperature throughout, and it becomes unsafe to use any meat in which the redness of the juice shows, that the albumen has not all been fully coagulated (162° F.).

A _freezing temperature_, −16° to −26° F., does not devitalize the bacilli, even when alternated with thawing at intervals for several weeks (Galtier, Cadeac and Malet).

_Heavy salting_ of meats has been thought to kill the bacillus in a month. After 15 days in salt the microbe failed to kill rabbits, but still killed the Guinea pig, whereas after 30 days it killed neither (Galtier). The fact that salted meats are always unequally impregnated in different parts, renders this extremely unreliable and more of a snare than a guide.

The action of chemical disinfectants varies not only with the agent but also with the medium in which the bacillus is found. In simple liquid media (bouillon) the following results were obtained:

_Parts per 1000._ _Killed in._ Carbolic Acid 50:1000 30″ (Yersin) „ „ 10:1000 1′ „ Alcohol (absolute) 1000:1000 5′ „ Ether 1000:1000 10′ „ Iodoform ether 10:1000 5′ „ Mercuric chloride 1:1000 10′ „ Salicylic acid 2.5:1000 6 hrs. „ Anilin water Saturated ———————— ——————— ———————— Thymol 3:1000 3 hrs. (Yersin) Formalin vapor 60:1000 40 hrs. (Murray) Sulphurous Acid (Sulphur 1 oz. to cubic metre) ————————— 14 hrs. (Vallin).

The following agents proved ineffective: Saturated aqueous solution of creosote, or of B-naphthol, of naphthalin, of potassium iodide, of potassium bromide:—bromine water, iodine water (1:500), iodoform solution or vapor, vapor of oil of turpentine.

ACCESSORY CAUSES OF TUBERCULOSIS IN ANIMALS.

While recognizing that in the absence of the tubercle bacillus there can be no tuberculosis yet we must not ignore the fact that many conditions of the animal system and its environment contribute largely to the propagation of the disease on the one hand, or to hinder its progress on the other. None of these conditions can call the germ into being _de novo_, but in its presence, they greatly favor its diffusion or even its malignancy. Like any other seed, this bacillus requires a suitable soil and favorable climate, to bring out its most destructive development. In striking the balance, we have to guard against the error of so many, who would attribute to the germ alone the deadly results and who assume that these should be the same under all conditions, and the opposite error no less prevalent, that ascribes the evil to the conditions, and holds that without these the germ would be harmless.