Part 92

An importation of infected cattle into New Jersey was made in 1847, by Mr. Richardson, who on discovering the nature of the disease, made an end of that particular contagious centre, by slaughtering his whole herd at a cost of $10,000.

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.

Infection through food soiled by breath or nasal defluxion is a common cause. In our great swill stables during the prevalence of the plague, it was notorious that the disease advanced rapidly along the line of a feeding trough to the sixty or more animals using it, and that the rapidity of the advance was determined largely by the fact that the first animal was at the higher end of the trough. If at the lower end there was no upward current to carry infection to the others. Open pastures where the sick have fed and watering troughs or ponds are common sources of infection. The permanence of infection in and around large cities is largely due to the common pasturage by different herds in succession on the same unfenced lots waiting to be purchased for building. For this reason the plague always extended in summer when the cattle frequented these lots, and diminished in winter when they were strictly confined to stables and yards.

Mingling of different herds on great unfenced areas has been the main cause of the maintenance of the infection from time immemorial in the hills and forests of central Europe and on the boundless Steppes of Europe and Asia. This alone is chargeable with the permanence of the affection, in spite of all efforts for its extinction, in South Africa, Australia, Tasmania and New Zealand.

Contagion carried by attendants, cattle dealers and even dogs, is generally recognized, I have elsewhere quoted the case, in E. Lothian, Scotland, in which the son of the steward, who was cattleman on an infected farm, was the means of infecting first, his father’s cow, and later the whole of the stock on the place; also the case at Quincy, Mass., in which a farmer coming straight from the slaughter of sick cattle, infected his own herd; also the case of Mr. Jewell, of Long Island, who carried the infection from the herds visited, to his own family cow in a thoroughly secluded stable.

Infection through infected and emptied stables, was a common experience in dealing with the lung plague in America. Cows kept alone and only introduced after the predecessor had died habitually contracted the disease, though brought, through the most carefully guarded stockyards, from healthy districts. Stables have continued infecting for a year after having been vacated, (Friedberger and Fröhner).

Infection through manure spread on ground to which susceptible cattle had access was an occasional occurrence.

An active, unrestricted commerce is however the most prolific means of infection in cultivated countries. Slow as the disease progresses, and long as the animal diffuses infection, it soon attacks and kills or immunizes all the susceptible animals in the single herd, and if no other susceptible animal is bought or born into the herd, the germ in due time loses its pathogenic potency and infection is at an end. In this way many centres of infection started in herds on well fenced farms have worn themselves out. But the case was far otherwise in the city dairies and swill stables. The trade demanded that the stalls emptied by deaths should be filled up to consume the swill, or supply the milk route and thus fresh susceptible cattle were constantly exposed in the infected stable. The dairy cows were supplied by dealers who charged exorbitant prices for them and held a chattel mortgage for the amount. They had come through the infected dealer’s stable, and if they did not come up to the milk yield promised, they were either passed on to another dairy or returned to the dealer’s stable carrying back a new load of infection. The wagons used to carry the cows through the city were constantly infected and infecting. The swill stables became the final destination of the surviving cows that had gone dry and thus infection constantly gravitated into them.

In Europe where the great cattle and meat trade with England and the constant demand for cattle to consume the marc of the beet sugar and other factories, cause a continuous draught upon the infected districts the great western centres of enterprise and commerce have found it impossible to exterminate the plague.

In the country districts in England outbreaks were almost exclusively confined to the times when fresh cattle were purchased at one of the great fairs. Hence the late autumn, the period of laying in feeding cattle, witnessed the greatest extensions.

In Ireland, as shown by Ferguson, the whole cattle trade seemed to be arranged as if for the speedy and universal diffusion of infection. Calves, bought by jobbers from all sources, were bunched together with every opportunity for intercommunication and infection. As soon as they were a little further matured, they were assorted in lots and sent to a fair, where they were sold, and found their way to great common pastures, and this process was repeated again and again until they had reached full maturity. On the way to and from each market they were quartered over night in a public yard which had just been vacated by other animals, often diseased, traversed the same roads, and drank and fed from the same troughs which diseased ones had just used.

The introduction of apparently recovered cattle is generally credited with the infection of a fresh herd and Friedberger and Fröhner quote with approval Walley’s assertion that a recovered animal with a sequestrum in the lung can infect a herd into which it is taken. I have failed to produce even local exudate, subcutem or in the lung, from sequestra which were much more recent, but the animals operated on were rendered immune and inspired me to carry out a system of immunization by the use of the sterilized fresh exudate. The actual date of the expiration of virulence in the necrotic lung tissue has never been demonstrated and probably varies in different cases.

The receptivity of different breeds has been discussed and the Holsteins and Shorthorns have been thought to show the greatest susceptibility. These are among the cattle that are most prized, bought and sold, and exposed to infection. The Shorthorn especially has a great development of the circulatory system, including the connective tissue with its great lymph sacs and channels, and the microbe we are dealing with shows a marked preference for the lymph system, in which it finds its appropriate field of development. Susceptibility is greatly encreased by a warm climate or hot season, under which large herds may die without a single exception, the disease running a fatal course in two or three days. In cooler climates 20 per cent. will often escape at first (French Commission Experiments, 1849).

Lesions. If death has taken place early, the lesions are usually essentially pulmonary, though they may implicate the pleuræ and mediastinum. In many cases the lung alone is involved, yet even then the predilection of the microbe for the lymph network of the interlobular tissue is strongly manifested in the serous infiltration of that, rather than of the lung structure proper. This determines the much talked of marbled lung, the pulmonary lobules standing out at first as a more or less deep red brown or black, while the marbling is caused by the yellowish or grayish infiltrated tissue surrounding each pulmonary lobulette which appear set in, as in mosaic on the surface of a section. Sometimes a blood extravasation discolors the interlobular exudate as well, yet it retains its soft liquid appearance which sufficiently distinguishes it from the firmer lung tissue. These yellowish interlobular markings vary much in thickness, but in acute cases this may be up to half an inch or even more. In the lesions of longer standing the interlobular exudate has usually coagulated, or even undergone fibroid organization, so that it compresses and condenses the lobules which it surrounds.

The pulmonary lobules may show the earliest changes of the alveolar and lobular capillaries, with formation of an exudate, and an active proliferation of small round cells in and around the alveoli. Later the exudate coagulates, forming the familiar red hepatization, and this in its turn may pass into the gray, or it may liquefy and undergo absorption and resolution. Other changes are not uncommon. The excess of interlobular exudate will compress the pulmonary lobules so as to reduce their size and expel the blood from their structure, giving them a pale color, or this compression becomes still greater, completely arresting the circulation and inducing lobular gangrene. Thrombi in the afferent and efferent vessels contribute to the necrotic change, and sequestra of varying size, from that of a nut to that of an infant’s head or larger, are formed. The earliest stage of this necrosis is usually infarction of the lung, a definite area of which becomes saturated with dark blood cells so that in contrast with the rest of even the hepatized lung, it is almost as characteristic as the marbling. The further progress of this necrosis is varied. Most commonly the exudate surrounding the necrotic mass becomes organized into white fibrous tissue and forms an investing sac in the interior of which is the dead lung tissue, showing for a time distinctly, the bronchia, blood vessels, lobulettes, and interlobular tissue. This gradually becomes detached and floating in a liquid debris, slowly undergoes solution, and is absorbed, the sac meanwhile closing in on the cavity. A large sequestrum may be a year or sixteen months in undergoing complete solution. In other cases the pulmonary lobulettes undergo an individual softening while the interlobular tissue becomes organized and when cut across, the lung presents a distinct honeycombed appearance. In still other cases a considerable area of both lobulettes and interlobular tissue is necrosed and liquefied, while the exudate, around the bronchial tubes, that supplied it, becomes organized, and on the necropsy the latter are found to constitute a thick branching mass of a very characteristic appearance.

The newly affected lobulettes have a watery or gelatinoid or dropsical appearance and if freely incised give out a large amount of serum and flatten down in doing so. When hepatized the cut surface is granular, and microscopic examination shows the terminal bronchia and alveoli filled with a fibrinous exudate containing great quantities of red blood globules and leucocytes. The distension of the lung is enormous, so that when the entire organ is infiltrated it may weigh from 50 to 100 pounds.

In recent cases the lung may be extensively affected without affecting the pleuræ; in other cases both are early involved. In advanced cases the pleuræ are always implicated. First there is the subpleural infiltration over the affected part of the lung; later the pleural surface has reddened arborescent patches, with a slight solid exudate, and a yellowish (sometimes blood-stained) serum collects in the bottom of the cavity; later still the affected portion of the lung is covered more or less thickly with false membranes, while others cover the organ or the parietal pleura below this level, and hang in shreds or bind the lung to the ribs. In old standing and recovered cases these may be largely represented by dense, white fibrous investments covering the lung or the rib, or establishing permanent adhesions. The amount of pleural effusion may be about two gallons in bad cases, and like the invasion is either unilateral or bilateral. The pericardium is usually more or less involved in pleuritic cases.

The larger bronchia sometimes contain false membranes.

The bronchial, prepectoral and mediastinal lymph glands are often enlarged, congested and infiltrated with an abundant exudate.