Feeding Hogs on Fresh Offal from Abattoirs. It has been a common practice, especially in country districts, to turn the raw offal of slaughterhouses to pigs, and as the tubercle is usually concentrated in internal organs, the hogs become infected in large numbers. In public institutions which slaughtered their own meat I have found the hogs all but universally tuberculous. The danger is only slightly lessened when the hogs are fed raw butcher and kitchen scraps in swill. It suggests the compulsory boiling of all swill or garbage containing raw meat.
Feeding Calves and Hogs on infected Milk. Though it has been repeatedly shown that the majority of moderately tuberculous cows do not yield infected milk, yet in every tuberculous herd, at irregular intervals, one or more are attacked with tuberculosis of the mammæ, and the drinkers of the milk take in the tubercle bacilli. This will happen in the most strictly supervised tuberculous herds, while in those that are less carefully managed, the milk that is considered unfit for human consumption is fed to pigs or calves. In one dairy, I found that the calves, all fed in this way afterward reacted under the tuberculin test, while the following year the crop of calves, though fed on the milk of the same diseased cows, with this difference that the milk had been first heated to 180° F., without exception grew up healthy, and not one reacted under the tuberculin test.
Feeding hogs after Tuberculous Cattle. Where cattle and hogs are kept on the same place, it is a common practice to let the swine clean up all food left by the satiated cattle. If there are tuberculous cattle, affected either in the air passages or alimentary tract, the pigs become infected by taking in the expectoration by which the food is soiled, or by rooting around where the cow manure has fallen.
Feeding from a Common Trough. In an infected herd, a common cause of extension is found in the use by the whole herd of a common feeding trough, in which the food soiled by virulent discharges, is taken by healthy animals. The habit of tying a cow in different stalls in succession as she happens to strike one, in place of keeping each cow by its own stall is a fruitful source of infection. Even when each cow is kept by its own stall, she often becomes infected by reaching into the feeding trough in front of the next cow on the left or right and taking in soiled and infected fodder. In swill stables the evil reaches its maximum, as the feeding trough for 50 or 60 animals is slightly inclined so that the liquid food runs from the supply end to the other, and infecting expectorations are carried in front of all in turn.
Dry, Dusty Stables. Tubercle bacilli are not carried out on the expired air, unless there is forced expulsion as in coughing, snorting or sniffing. In such cases the solid particles are thrown off in masses or fine spray and lodged on surrounding objects. These, together with infecting discharges from bowels, urinary or generative organs, open sores, etc., dry up, and rise on the dust, and, as sterilization occurs slowly indoors, they cause more or less infection of the animal inmates. Cornet, Tappenier and others have thoroughly established this as a common form of transmission, and shown the great importance of cleanliness, disinfection and the removal of infecting materials without raising dust. In an establishment in Paris, a consumptive had served for 3 years. In the following 10 years, 15 of the 20 employés died of phthisis.
Extension through Vermin. As rats and mice (and other rodents) are susceptible to tuberculosis by ingestion (Galtier) it follows that they may become the media for extension of the infection through fodder in which their droppings are scattered, or from their feeding in the same troughs as the cattle or swine. For swine in particular the danger is greater because of their carnivorous habits; the rat acquires tuberculosis through eating the offal of the abattoir, or the scraps of the butcher’s stall, or kitchen, and the sick rat is thereafter easily caught and devoured by the pig to its own undoing. To block this channel of infection the destruction of vermin about slaughter houses, stables and pig pens is a most important consideration.
Flies and Other Insects as Carriers of Tuberculosis. These congregating on tubercular sores, around the nares or lips, on the skin contaminated by the virulent bowel discharges, on dishes holding infecting milk, on objects soiled by infecting discharges, on diseased carcasses at abattoirs, rendering works and elsewhere, (Spillman, Hoffmann, Lartigan, etc.,) and on graves where the earth worms have brought the bacillus to the surface, (Lortet, etc.) become more or less active agents in disseminating the virus. In this way food and water are contaminated, and exceptionally, infection may even be implanted on sores. As the excreta of the flies contain the virulent bacilli, the latter are deposited on windows, walls, furniture, etc., and may be later disseminated in the dust of the apartment.
Dewevre found tubercle bacilli in the bedbugs infesting a bed in which successive cases of consumption had developed, showing that other parasitic or rapacious insects besides flies must be looked on as possible propagators of the bacilli. There is reason to suspect, lice, fleas, ticks and acari especially. The same is true of leeches and other rapacious invertebrates.
LESIONS. THE TUBERCLE.
The characteristic lesion in tuberculosis is the tubercle, taking its name from the small rounded nodule which, at first virtually invisible, encreases often to the size of a millet seed, or a pinhead or even larger, and which by confluence with others, forms conglomerate masses of all sizes to which the term tubercle is still applied. Where the bacillus tuberculosis is implanted, the fixed tissue cells are stimulated to an undue proliferation, and a diapedesis of leucocytes takes place from the neighboring capillary blood vessels, the whole eventuating in the formation of a rounded cluster or nest of epithelioid and giant and later small rounded lymphoid cells in a fine fibrous stroma. Baumgarten and his followers claim that the larger epithelioid and giant cells result from the karyokinesis and proliferation of the fixed tissue cells, epithelial and endothelial cells, and that the lymphoid cells which later (often after the eighth day in experimental cases) invade the lesions, are alone the product of the migrating leucocytes. Metchnikoff, Yersin and others contend, on the other hand, that epithelioid and giant cells are directly derived from the leucocytes and endothelial cells and like these are possessed of actively phagocytic qualities. As the final outcome before caseous degeneration, is the great predominance of the small lymphoid cell, it may well be questioned whether this is not the result of active encrease in both kinds of cells, as appears to happen in many other inflammations. For our present purpose it is well to note the early characters: Centrally often a large (giant) cell with a number of peripheral nuclei and at times, branching processes; around this as a second zone epithelioid cells of large size, with round or oval nuclei, and sometimes giant cells; outside this a third zone of small rounded lymphoid cells with large nuclei. There is a delicate fibrous network between the cells, but no indication of capillary blood vessels, the absence of which may partly explain the constant tendency to degeneration, necrosis, and caseation. The tissue around the miliary tubercle is red and congested.