South Africa was infected in 1854 by the landing of a Dutch bull at Cape Town. As there were no railroads and all inland carriage was conducted by ox-wagons, it soon spread over the colonies and extended thence into the native states, and has continued to the present time.
Australia was infected in 1859 through an English cow landed at Melbourne. When the disease was identified, the whole herd was slaughtered and paid for, and the farm quarantined. But the quarantine was broken by a teamster turning his work oxen into the pastures under cover of night, and the infection escaped and has prevailed over Australia to the present day.
Later the disease extended in a similar manner, to Tasmania and New Zealand.
Causes. The one essential cause of lung plague is contagion from a preëxisting case. Before the days of bacteriology, this had been demonstrated as conclusively as any truth can be. All extensions into a new country or district could be traced to direct importation from a preëxisting area of infection. Until such importation such lands have been immune from time immemorial; at once after, the infection has spread from the imported animals as a centre; if the stock is divided up and scattered, several primary centres are formed from each of which the plague makes extension. Again, isolated islands (Channel Islands) and purely breeding districts (Scottish Highlands) into the herds of which no store cattle from outside are admitted, remain immune through centuries, no matter how prevalent lung plague may be in the countries immediately around. The immemorial immunity of the Western Continent, up to the date of the arrival of the now famous Dunn cow, the continued immunity of Canada and Mexico after the infection of the Eastern United States, and the immunity of the United States since the last infected cattle were destroyed in 1892, are equally conclusive in this respect.
Bacteriology. The history of lung plague forcibly illustrates how harmless microbes of large size, that may be easily discovered, and which existing in the environment, readily find their way into diseased and susceptible parts (in this case into the bronchia), may be held to be the pathogenic cause. Willems and Van Kempen, in 1852, found microbes in the exudate. Lustig in 1885 found four separate microbes in the lesions, 1st, a short, thick, liquefying bacillus to which he attributed the disease; and 2d, 3d, and 4th, three forms of micrococcus. Poels and Nolen, in 1886, demonstrated bacilli of variable size (0.9μ), solitary, in pairs and chains, cultivable in different media, and inoculable by injecting such cultures into the lungs, but the resulting lesions were not marked by the full lung plague exudate. Arloing, in 1887, separated from the exudate the bacillus liquefaciens bovis, a very short, slender bacillus, often in pairs with flagella, motile, staining easily in anilin but not in Gram’s solution, quickly liquefying gelatine as a culture medium and assuming a form that might be taken for micrococci, quickly obscuring peptonized bouillon, and growing on potato. The exudate placed in a thermostat at 95° F. encreases in potency. The bouillon cultures injected under the skin or into the lung, produced characteristic lesions of lung plague.
In the light of the later experiments of Nocard and Roux in 1897–8, it would appear that Arloing’s bouillon cultures were probably complex, containing not only the bacillus liquefaciens bovis, but also, the infinitesimal microbe which is the true cause of the lung plague. In seeding culture media with the exudate taken with all possible precaution against contamination, from the interlobular pulmonary connective tissue, they and others constantly failed to obtain results. Better success attended their efforts with Martin’s culture bouillon for producing diphtheritic toxin. Five pigs’ stomachs are minced, pounded to pulp, mixed as follows: stomach 200 grs., pure muriatic acid 10 grs., water 50° C., 1000 grs., left in a thermostat at 50° C. for 12 hours, (to 24), then heated to 100°C. to destroy the action of the pepsin, then lowered to 80° C., alkalized, filtered from flocculi that formed, heated to 120° C., and filtered. This is then mixed with peptonized meat juice prepared as follows: fresh beef or veal, minced and pulped, 500 grs., and water, 1 litre, are kept for 20 hours at 35° C., the liquid expressed, 5 grs. common salt added, mixed in equal proportions with the peptonized liquid from the pig’s stomach, heated to 70° C. to coagulate albuminoids, filtered, alkalized and sterilized. To this mixture is added ¹⁄₂₅th part of blood serum (sterile) from the rabbit or cow.
This bouillon was inoculated with the pulmonary interlobular exudate, enclosed in collodion capsules, having very thin walls, and inserted aseptically into the abdomen of the rabbit. In 15 days the rabbit was sacrificed, and the capsules enucleated from their envelopes of exudate and cells. The contents showed the slightest possible shade of opacity, but they contained neither cells nor any other definite organism. Under a magnifying power of 2000 diameters the liquid contents were found to be full of brilliantly refrangent points, actively mobile, but so minute that their form could not be made out even when staining was resorted to. The contents of these capsules when inoculated on cattle produced the unequivocal phenomena of lung plague infection in a period of from 8 to 15 days. Other collodion culture cases inoculated from this produced the same cultures in the peritoneum of the rabbit. Collodion cases charged with the uninoculated peptonized bouillon, and placed in the rabbit’s peritoneum remained absolutely clear, with no refrangency nor motility under high powers and with no infectivity when inoculated. The rabbits used for the infective cultures often became emaciated to the last degree and even died, but their tissues proved in no respect infecting to culture media nor when inoculated. The attempt to cultivate the germs in collodion cases in Guinea pigs completely failed.
This ingenious form of culture devised by Metchnikoff for experiments on the more delicate organisms, has been used by Nocard to accustom the tubercle bacillus of mammals to grow in the bird and opens up great possibilities for future investigators. The collodion, being impermeable to leucocytes and bacteria, allows these to grow almost together, only on the opposite sides of the collodion wall, restrains phagocytosis, and protects the microbe against the destruction which would otherwise overtake it.
Modes of transmission. The exhalations from the sick convey the infection to susceptible healthy cattle. Yet even this was denied by one veterinary teacher in Great Britain in the latter half of the 19th century. The transmission of the disease by mediate contagion was denied by those in authority in Great Britain up to the end of the century and this delusion contributed largely to the loss of many millions by the nation. Experiments made at Brown Institution were held to sustain this, but not an atom of evidence was furnished to show that the exposed animals were susceptible ones. Diseased lungs kept for a year at 21° F. proved infecting when inoculated (Laguerriere).
Contagion through the air in the same stable was admitted even by the English sceptics. It may be carried in this way for forty yards, or if dried on dust or light materials to a great distance.