Chapter LVII: Part II: , Showing Predominance of Malarial Element . . . . 617 (56)

Conveyance of glanders from man to man has taken place through using or handling the same dishes, towels, or handkerchiefs, through dressing the wounds, or, as in the case of the veterinarian Gerard, through making an autopsy of a victim of the disease.

Fortunately, the susceptibility of man is slight, but few out of the multitudes handling glandered horses becoming infected. It is essentially an industrial disease, 114 cases being distributed as follows among the different occupations: hostlers, 42; farmers and horse-owners, 19; horse-butchers, 13; coachmen and drivers, 11; veterinary surgeons and students, 10; soldiers, 5; surgeons, 4; gardeners, 3; horse-dealers, 2; policemen, shepherds, blacksmiths, employés at veterinary school, and washerwomen, 1 of each.

A condition of ill-health doubtless predisposes to this as to other invasions of infectious disease, yet men in apparently the most vigorous health have succumbed to the poison.

SYMPTOMS.--The incubation of acute glanders in inoculated cases usually varies from one to four days. In cases in which the mode of entrance is not so manifest it may apparently extend over one, two, or even three weeks. If the disease has occurred by external inoculation, the seat of the wound shows the first symptoms, consisting of tense swelling, pain, and a dark or yellowish erysipelatoid redness, while the edges of the wound are puffy and everted, the matter escaping is sanious, and the surrounding lymphatics are swollen and red and the lymphatic glands enlarged and tender. After a few days constitutional disorder sets in--languor, extreme weakness and prostration, aching in the limbs (muscles and joints) and in the head, rigors alternating with fever or a continued fever after the first violent chill, and in some cases nausea, vomiting, and even diarrhoea. In cases not resulting from external inoculation the febrile symptoms are the earliest to be noticed, and the muscular and articular pains may be at first mistaken for acute rheumatism. In other cases, in which the gastric and intestinal disorders are the most prominent and the prostration and weariness extreme, the symptoms at first strongly {921} suggest typhoid fever. Soon, however, with a sense of formication a local yellowish or livid erysipelatoid inflammation appears, by preference on the softer parts of the face, the nose, eyelids, cheeks, or on one of the principal joints, the shoulder, elbow, or knee. In the midst of the phlegmonous swelling, or even antecedent to it, there appear small firm red spots or nodules, sometimes as small as those of variola, at others like a pea or as large as a walnut or larger. These gradually blanch in the centre, soften, and change into pustules or abscesses, and, bursting, discharge a slimy, thick, sanguineous pus, often emitting a mawkish or fetid odor. The sores thus formed are ulcerous and unhealthy, with puffy, ragged, everted borders and a grayish or yellowish red base, which often extends deeply between the muscles and exposes tendons and bones. When several deposits of this kind are closely aggregated, they tend to combine in one slough, which may involve a great extent of tissue. In all cases there are the swollen, reddened, tender condition of the connecting lymphatics and the tumefaction of the lymphatic glands. At times the deposits and abscesses are deeply seated in the interstices of the muscles, and at other times the joints are enlarged by exudation.

In nearly one-half of the cases glanders supervenes on the cutaneous symptoms. At first a viscid, whitish nasal catarrh appears from one or both nostrils, mixed with striæ of blood; then upon the pituitary membrane appear ulcers like those already described in the horse; the same form on the buccal, pharyngeal, and laryngeal mucous membranes, and by physical examination they may even be found to have invaded the lungs. The margins of the nostrils become adherent through the drying of the tenacious mucus; the meati are blocked or narrowed by the swelling of the mucosa, the detachment of sloughs, and the accumulation of the discharges; the breathing becomes snuffling and difficult; the voice altered or lost; the cough weak, with a mucous and bloody expectoration, and the breath offensively fetid. The submaxillary lymphatic glands are inflamed and enlarged, and may even go on to suppuration and ulceration. The conjunctiva is usually involved, and at times the specific formation and ulceration extend to the stomach and intestines, and nausea, vomiting, indigestion, irregularity of the bowels, and fetid diarrhoea ensue. There is complete anorexia, but thirst is ardent, especially with diarrhoea. With the advance of the disease dyspnoea supervenes, and nervous disorder is shown by the extreme weakness, anxiety, sleeplessness, troubled dreams, nocturnal delirium, dilated pupils, and even coma. The temperature, though at first unaltered, may later rise to 104° F., and the pulse to 110 to 120 beats per minute. The diagnosis is confirmed by detection of the bacillus in the discharges, and, above all, in the liquids of freshly-opened pustules (Wassilieff).

The duration of acute glanders in man may be no more than three days, though usually it is protracted to fourteen or twenty-one, and exceptionally to twenty-nine days. The almost constant termination of this form of the disease is in death.

Chronic glanders occasionally appears in man, and is in most respects the counterpart of that of the horse. The morbid process shows itself in the integumental or other tissues of the body, and only attacks the nose and air-passages later, when the constitutional symptoms become more intense. The general malaise, languor, prostration, aching of {922} limbs and joints, and inappetence are usually present, complicated by a local swelling in the seat of inoculation (face, hands, etc.), with small nodules progressing to pustules, congestion of the lymphatics, and swelling of the lymphatic glands. These lesions may subside even before suppuration, and the disease is manifested for a week or two only by a general feeling of weariness and ill-health; but sooner or later the local symptoms reappear in the same or another seat, and the neoplasms, though indolent for an indefinite length of time, finally degenerate, soften, burst, and form ulcers. These ulcers have the general characters already described--a livid grayish or yellowish hue, with red, puffy, irregular edges, and a viscid greenish, yellowish, dirty white, or bloody discharge. They tend to increase, or they may appear to heal by the peculiar firm cicatricial formation, but on the swollen margins new deposits, abscesses, and ulcers tend continually to form. Sometimes these are of considerable size and seated deeply among the muscles, but when opened they show the same unhealthy serous or bloody pus, and manifest a tendency to extension rather than to healing. When the disease extends to the respiratory organs, often two or three months after the onset, there is cough and sore throat, blocking of the nose by the tenacious discharges and swollen mucosa, and in the pharynx, fauces, and nose the characteristic ulcer may be detected. The attendant constitutional symptoms are also much more marked--indigestion, nausea, vomiting, diarrhoea, rigors, profuse perspiration, high temperature, excited breathing and pulse, a yellowish or earthy hue of the skin, rapid emaciation, and great prostration. Though great emaciation, debility, and hectic ensue on the indolent chronic processes, yet the disease usually assumes all the characters of the acute type before terminating fatally.

In cases that recover the fever diminishes, exacerbations cease, ulcers granulate and cicatrize, vesicles dry up, the nodules and enlarged glands diminish, the erysipelatoid swellings of skin and nose subside, and a very tardy and imperfect convalescence is established.

The duration of chronic glanders, nasal or cutaneous (farcy), is exceedingly indefinite, varying from three months to ten or eleven years. One of the most protracted cases is that recorded by Bollinger of a veterinarian who, after an eleven years' illness, recovered with cicatricial contraction of the nose and larynx and a decided cachectic appearance.

MORBID ANATOMY.--Besides the lesions above mentioned as occurring in the skin and mucous membranes of the nose, mouth, and pharynx, the frontal sinuses, the larynx, and less frequently the lungs, are the seats of the specific glanderous processes. In the lungs there are then the nodules, hard, caseous, or purulent according to their age, and varying in size from a millet-seed and pea upward to the involving of the greater part of a lobe. Beneath the pleuræ may be seen ecchymoses, hard, fibrous nodules, and yellow elevations, which on being incised furnish grumous pus. The spleen is usually enlarged, gorged with blood, gray or black, and is the seat of suppuration. The liver is enlarged, softened, and may be the seat of glanderous processes, with ulcers in the bile-duct or gall-bladder. The joints, like other serous cavities, become the seat of specific suppuration. The bones are often implicated in adjacent deposits, especially in the face, cranium, and hands, so that the compact tissue may become reduced to the merest shell, while the medulla and periosteum {923} abound in the specific products. The cerebral meninges and brain-tissue are frequently the seat of specific growths and minute abscesses. It is noticeable that the enlargement of the lymphatic glands is usually less than it is in the horse, though they are never entirely free from lesions. Indeed, the tendency in man to the formation of considerable glanderous neoplasms is much less than in the solipede.

The microscopy of the lesions is essentially the same as in the horse. O. Wyss describes the cutaneous nodules as formed by a great proliferation of round cells (like pus-cells) in the upper layer of the corium just beneath the papillary layer. In a more advanced stage the corium and papillæ are filled with pus-cells, and, becoming disorganized, give rise to the formation of pustules and small abscesses. Lagrange describes in a chronic ulcer of the palm, a layer about 2 mm. in thickness of embryonic cells closely packed with an amorphous intercellular substance. The nuclei appeared larger than in ordinary ulcers or tubercles. Extending into this layer were capillary vessels packed with red globules and with blind extremities, or in some instances minute ruptures and hemorrhages. Beneath this superficial cellular layer was a stratum of striated muscle, especially noticeable for the excess of condensed connective tissue making up the intermuscular septa, and the great multiplication of nuclei with large, clearly-defined nucleoli, not only inside the sarcolemma, but also between the fibrillæ and separating them widely. At some points the muscular tissue had undergone a vitreous degeneration, while at others were many fusiform cells. At one point, where the ulcer extended to the phalanx, the compact layer of the bone was attenuated to the thinnest shell and perforated, so that the medulla was continuous with the ulcer. The medulla contained a great number of white globules, medulla-cells, and minute embryonic nuclei. The vessels were remarkable by the extensive fibroid thickening of their coats. On section of the ulcer many orifices stood widely open because of the rigidity of their walls. The internal coat was plicated, as if too large for the lumen. The external fibrous layers were at points abundantly interspersed with, and even replaced by, groups of embryonic cells, the active proliferation of which meant the destruction of the perivascular fibrous layer. These embryonic cells even invaded the lumen of the vessel and partly blocked it, so that the remnant of the tube remained as the centre of a disintegrating mass, or later a caseous or purulent focus.

DIAGNOSIS.--Acute glanders, when well developed, is unmistakable. The presence on or near the skin of the characteristic nodules, pustules, phlyctenæ, and ulcers, the oedema or erysipelatoid condition of the adjacent skin, the redness of the lymphatics, the presence of the neoplasms and ulcers in the nose, and the sticky, fetid, variously colored nasal discharge, with the acute fever, prostration, and pains in the limbs and joints, make a tout ensemble that is pathognomonic. In the initial stage only it may be confounded with rheumatism, but the arthritic pains are not usually attended by the same amount of redness and swelling of the joints, the prostration is far more profound, and there are in most cases an irritable, unhealthy-looking wound and a history of exposure to infection from glandered horses.

In chronic glanders, and especially in the external form (farcy), the diagnosis is often more difficult. From pyæmia and septicæmia it is {924} usually to be distinguished by the comparative absence or the slightness of the chills, by the less healthy character of the pus, and by the implication of the nasal mucosa, the larynx, and lungs. When the nose, larynx, or lungs are but slightly affected, there may be a strong resemblance to syphilis or miliary tuberculosis, but a close attention to the character of the lesions, the absence of any concomitant history or symptoms of syphilis, and deductions drawn from the occupation of the patient and the presumptive exposure, will greatly assist in reaching a diagnosis.

The detection of the bacillus is not conclusive, as in tuberculosis and some forms of septicæmia there are similar organisms, agreeing with the microbe of glanders even in the matter of size. In cases of doubt a little delay will usually allow the development of new and more characteristic symptoms.

The final resort, however, is to inoculation. Auto-inoculation, as practised by Poland, is rarely satisfactory, as the system has acquired a partial tolerance of the disease and local lesions are not so certainly developed as in the healthy subject (St. Cyr). Inoculation on a healthy goat, sheep, or rabbit can always be availed of, and if practised on more than one subject can be relied upon, as the virus loses nothing of its power in passing through the human system, but usually determines an acute form of the disease in the animal inoculated.

PROGNOSIS.--Acute glanders is almost constantly fatal to man. Of chronic cases, and especially the external form (farcy), from one-third to one-half of the subjects recover. When both internal and external (farcy--glanders), the issue is usually fatal. Kütner claims that cases caused by external inoculation are more favorable than those caused by the inhaled poison. This accords with the general principle, that a poison viable in the comparatively vitiated air of the lungs or on the surface of the intestinal canal is better fitted by its habit of life for survival in the blood and plasma, and is consequently more redoubtable. The greater the duration of the disease in any particular case, the more favorable is the prognosis.

TREATMENT.--In the treatment of glanders in man the same principles must guide as in animals. In external, inoculated cases the wounded tissues should be early destroyed by potent caustics--fuming nitric acid, corrosive sublimate, iodized phenol, chlorine, sulphate of copper, carbolic acid, or the hot iron. The erysipelatoid swellings may be treated by leeching, followed by solutions of carbolic acid, iodine, or chlorine-water, by ice, and internally by laxatives and iodide of potassium. The first two antiseptics may be freely used by hypodermic injection. Abscesses and tumors should be laid open and cauterized as above, and then treated by weaker solutions of the same agents. Nasal ulcers may be treated by insufflation of iodoform and injections of creasote, carbolic acid, nitrate of silver, or permanganate of potash solutions. Of the greatest importance is a general tonic and stimulating regimen. A nutritious diet (including beef-tea), abundance of pure air, alcoholic stimulants, quinia, tincture of the chloride of iron, and, above all, arseniate of strychnia, have been used with advantage. Various anti-ferments, such as the bisulphites in full doses, carbolic acid, and iodide of potassium, have apparently proved beneficial, and deserve a further trial. As in the horse, a great {925} variety of other agents, mostly of a tonic nature, have been employed, but with very variable results.

PREVENTION.--The first step toward the prevention of glanders in man is the systematic restriction and extinction of the affection in animals. This has been already sufficiently referred to above. Further measures of prophylaxis embrace the following: the avoidance of contact with glandered and suspected horses by all persons having any wounds, abrasions, or ulcers on their skins; the cauterization with nitrate of silver of all such sores on persons necessarily brought in contact with glandered or suspected animals or their products; the general diffusion of information as to the danger from glandered animals; washing of hands and face in a solution of carbolic acid or chloride of lime after handling infected or suspected animals or their carcases or products; the thorough disinfection or destruction (preferably by fire) of harness, clothing, racks, mangers, wagon-poles, buckets, troughs, brushes, combs, litter, and fodder that have been exposed to infection; and, finally, the exclusion from the markets of all meat derived from suspected or infected animals. It is generally held that the flesh of the horse alone demands inspection, but with the known susceptibility of sheep, goats, and rabbits it can easily be conceived how the infection may reach man through his food, though horse-flesh is never consumed. That glanders has never been recognized as arising from the consumption of diseased sheep or rabbits does not prove that it has never reached man by this channel, any more than the absence of all recognition of the infection of man from the horse would prove the non-occurrence of such infection until the beginning of the present century. The knowledge that the animals used for food in this country are liable to contract and convey this disease is an additional reason for the systematic and universal suppression of the disease among the equine population.

{926}

ANTHRAX (MALIGNANT PUSTULE).

BY JAMES LAW, F.R.C.V.S.

SYNONYMS.--_Latin_, Ignis Sacer, Anthrax Epizoöticus, Pustula Maligna, Pustula Pestifera, Erysipelas Carbunculosum, Carbunculo Contagioso, Glossanthrax, Angina Carbunculosa, Anthrax Hæmorrhoidalis, Mycosis Intestinalis, Apoplexia Splenitis, etc. _English_, Black Erysipelas, Malignant Vesicle, Anthrax Fever, Splenic Apoplexy, Splenic Fever, Inflammatory Fever, Carbuncular Fever, Black Quarter, Blood-Striking, Bloody Murrain, Blain, etc. _French_, Pustule maligne, Charbon, Fièvre putride, Typhohémie, Pélohémie, Mal de Rate, Splenite Gangréneusé, etc. _German_, Karbunkelkrankheit, Contagiose Karbunkel, Milzbrand, Milzseuche, Milzbrandfieber, Brandbeulenseuche, Rothlauf, etc. _Russian_, Jaswa (boil-plague). _Italian_, Antrace. _Spanish_, Carbunculo, Lobado. _Swedish_, Boskapssjukan. _Mexican_, Calentura del piojo.

DEFINITION.--Anthrax is an acute, infectious, bacteridian disease, occurring mostly in the Herbivora and Omnivora, but communicable to other mammals (including man), to birds, and even fishes. Its local manifestations are exceedingly varied in kind, but the malady is characterized by the presence in the tissues or blood, or both, of specific spherical and linear bacteria (micrococcus and bacillus anthracis), leading to arrest of hæmatosis, to disintegration of the blood-globules, to sanguineous engorgement of the spleen, to capillary embolism, and to a spreading gangrenous inflammation.

HISTORY AND GEOGRAPHICAL DISTRIBUTION.--While ancient history is not clear as to the specific diseases of animals, yet there is the strongest presumption that nearly all great plagues that attacked indiscriminately animals and man were of this nature. Thus, the plague of murrain, with boils and blains breaking out on man and beast, in the days of Moses, was probably of this kind (Gen. ix. 3.); also that which at the siege of Troy extended from animals to man, and many later epizoötics in all parts of the world. No infectious disease of man and animals, with the single exception of tuberculosis, has been more widely diffused, and none can be considered as more cosmopolitan. Heusinger, in his classic work on _Milzbrandkrankheit_, traces the ravages of the disease from the highest to the lowest latitudes in the northern and southern hemispheres and in the Old World and the New. He adduces outbreaks in Siberia, Astrakan, Lapland, and Finland, in Russia, Prussia, Poland, Silesia, Bavaria, Holland, Belgium, France, Spain, Portugal, Italy, Switzerland, Austria, Hungary, Greece, Turkey, Egypt, East and West Indies, {927} North and South America, etc. We can now add all the great English, French, and other European colonies not included in the above (South Africa, Australia, New Zealand, Algeria, etc.), together with China and Japan. We find, moreover, that the disease is always most prevalent where agriculture is in its most primitive condition, so that there can be little doubt of the prevalence of the affection in the less-civilized countries as well. But while the disease is prevalent in all parts of the world, its ravages are largely subordinate to the nature of the soil. Wherever this is close, impervious, marshy, or charged with an excess of organic matters, the gaseous emanations of which drive out most of the oxygen, the anthrax-germs, once introduced, tend to be preserved indefinitely. Thus, in drying up basins with no natural drainage, on lake and river margins, on deltas, in forests, in mucky, mossy, or peaty soils, and on those that are habitually over-manured, the germs of anthrax are especially liable to be perpetuated. It has long been noticed that herbivorous animals are the most susceptible to anthrax, while the purely carnivorous, and to a less extent the omnivorous, have relatively a far higher resisting power. That the immunity is largely due to the food is manifest from the experiments of Feser on rats. Those fed on vegetable aliment contracted anthrax readily from inoculation, while those kept on an exclusive diet of flesh successfully resisted. The same rats that escaped while on a flesh diet were afterward placed on a vegetable diet, and then perished after inoculation.[1] Davaine found the same to be true of foxes kept on meat and vegetables respectively, and inoculated with the virulent blood of the allied disease, septicæmia. He found, moreover, that guinea-pigs were much more susceptible to anthrax than rabbits. One-thousandth of a drop of virulent anthrax blood invariably killed the guinea-pig, while it left the rabbit unharmed.[2] Klein has never found a rabbit insusceptible. It has recently been claimed that pigs are insusceptible, but I have known of many instances in which the offal of anthrax cattle, when devoured by pigs, has determined fatal anthrax in the latter. Chickens too prove much less susceptible to anthrax than the Herbivora. Inoculations made by Cohn and others proved invariably unsuccessful, while Pasteur has showed that they can be infected easily after the body has been cooled by partial immersion in cold water.[3] Pasteur attributes this immunity to their normally high temperature, yet rabbits, sheep, pigs, wolves, and foxes, though maintaining a correspondingly high temperature, are still subject to anthrax. Even the herbivorous mammal suffering from acute anthrax fever has its temperature raised to that of the chicken, yet the disease progresses none the less surely to a fatal result. Again, anthrax liquids inoculated under the skin of a fox proved harmless, while if thrown into the warmer peritoneal cavity they proved fatal. It may well be suspected that the relative insusceptibility of chickens is in part due to the large amount of animal food consumed by them, and that the chilling process increases the receptivity by deranging sanguinification and nutrition.

[Footnote 1: _Wochenschrift f. Thierheilkunde und Thiersucht_, Nos. 24 and 25, 1879.]

[Footnote 2: _Rec. de Med. Vet._, Mar. 15, 1879.]

[Footnote 3: _Ibid._, Mar. 15, 1880.]

The insusceptibility to anthrax is often characteristic of certain individuals or families or of the animals living in a particular district. Thus, Chauveau found that some French sheep, and nearly all Algerian ones, {928} resisted inoculation with a moderate amount of anthrax virus, while the introduction of a maximum amount proved fatal to these as to others. In the same way, it is often noticed that animals living in an anthrax region escape the evil effects of the poison, while strange animals brought in either fall ready victims or for a time do badly until they have become habituated to the locality. In view of the subsequent protective effect on the system of a first and non-fatal attack of anthrax, it is probable that all these examples of immunity in the Herbivora depend on a previous mild attack of the same disease or on the extinction of the more susceptible races. Even in the case of the animals that do badly on first coming into an anthrax district, and recover better health with immunity later, we may well infer that a mild form of the anthrax infection has been passed through.

ETIOLOGY.--The one essential cause of anthrax is the introduction into the system of a specific bacteridian germ (bacillus anthracis or its spores). This is not, as a rule, carried far on the atmosphere, but demands for its propagation contagion, immediate or mediate. Unless, therefore, it meets in the soil the conditions necessary to the preservation and propagation of the germ, it is transmitted with some uncertainty from animal to animal, and thus the disease does not spread widely and rapidly, like an ordinary plague, but tends to become localized in particular districts as an enzoötic.

But its dangers are none the less real nor its existence less to be dreaded. In predisposed localities, where the disease-germ has gained a footing, the animal mortality may exceed that caused by the great plagues, while the risk to human beings is incomparably greater than from any other acute infectious disease of the lower animals. Thus, in San Domingo, in 1770, 15,000 people perished in six weeks from eating the carcases of anthrax animals, and the mortality was only arrested when the meat was legally interdicted. In the worst anthrax years on some of the Siberian steppes as many as one-fourth of the whole human population suffer from the malady. The prevalence and death-rate, however, vary greatly in different localities and seasons. Sometimes only one or two solitary cases of the affection are observed; at other times the disease becomes moderately prevalent, but a lack of virulence in the poison or a previously acquired insusceptibility of the individual protects the great majority of the animals exposed, while at others, still, the poison attacks nearly all exposed to its contagion.

The animal products that mainly convey the disease are the blood, the liquid exudations, portions of the diseased carcase, and the bowel dejections. The virus is most potent when derived from an animal still living or only recently dead, yet under certain conditions (with spore-formation) it may long retain its virulence under the most extreme changes of climate, temperature, dryness, and humidity. Russian hides tanned in England or America frequently convey anthrax, which is known especially as a tanner's malady, and wool and hair sent from Buenos Ayres have repeatedly produced malignant pustule (woolsorter's disease) in Britain and the United States. The preserved scabs of malignant pustule have been often successfully inoculated on the lower animals, so that, like other forms of poison, this seems to be preserved indefinitely by desiccation.

The simple contact of the virus with the slightest abrasion will suffice {929} to convey the disease. It has often been communicated where no lesion of the epidermis could be found, yet the presumption is that even in such cases the cuticle had been in some way wounded. Eating the flesh of animals killed while suffering from anthrax has often conveyed the disease. In an outbreak in Swineshead, Lincolnshire, England, in 1863, I found a dog and a number of swine suffering from eating the bodies of dead bullocks. In 1864 an East Lothian (Scotland) farmer fed his pigs with the offal of a slaughtered anthrax bullock, and lost nearly the whole herd. The carcase of the bullock had been sent to market. About 1860 cattle, and even horses, died yearly on a swampy meadow at Brighton, Mass. On one occasion the owner, John Zoller, fed the offal of a dead bullock to his pigs, which were speedily attacked with anthrax, and as speedily killed to save their bacon (Dr. Thayer). Even when cooked the flesh is not always safe. Of this we have the undoubted case in San Domingo above noticed, the alleged death of 60,000 people in the vicinity of Naples from the same cause in 1617 (Kircher), and the thousands that die on the Russian steppes every anthrax year from eating the sick horses (Rawitch). But in all these, and in the ever-recurring cases in which families suffer from eating anthrax meat, there is the possibility, if not the probability, of the contamination of the meat subsequently to cooking by the knives, forks, tables, and dishes used. The San Domingo slaves had few appliances for cleanliness, much less disinfection, and the Tartars eat their meat from the same board on which it has been chopped up raw.

In accurate experiments it has been found that the bacilli are destroyed by a temperature of 145° F. maintained for five minutes, but the spores are capable of surviving the boiling temperature for five or even ten minutes. The varying power of resistance may be compared to that of the green stalk of the pea and the dry flinty seed. The first is destroyed by a very moderate heat, while the second will sprout after having had boiling water poured over it. The resisting bacillus-spores are never found in the living animal, but may be developed in the blood and tissues after death, and may account for the occasional extraordinary viability of the poison when exposed to a boiling temperature.

Milk, though often used with impunity, conveyed the disease when inoculated by Bollinger, and the same was true of the vaginal mucus. Innocent in the early stages of the disease while the germs are still localized, they become virulent after the bacilli swarm into the blood.

Healthy men and animals often carry the poison, though themselves insusceptible. The question of its conveyance by insects has been much debated, but the constant occurrence of malignant pustule on the uncovered parts of the body goes far to settle the question. Bourgeois long ago noticed that it was most frequent on the face, hands, neck, and arms, and rare on the trunk. In sixty cases recorded by A. W. Bell of Brooklyn, all occurred on the face except two on the hands, one on the wrist, and one on the forearm. The bite of a fly or mosquito had in many of these cases proved the starting-point of the malady. Bollinger has shown the presence of the bacillus in the stomach of such flies as fed on flesh and blood (horse-flies, bluebottles, etc.), and, together with Raimbert and Davaine, has produced anthrax by inoculations with the stomachs, legs, and proboscides of these insects.

{930} Surgical instruments occasionally convey anthrax. At Cockburnspath, East Lothian, Scotland, a yearling heifer contracted anthrax, and the whole herd was bled, commencing with the sick one. Next morning seven were found dead, the disease in each case extending around the fleam-wound. At Brunt, in the same county, a shepherd skinned an anthrax bullock, and after washing and taking a turn among his sheep, on the same day castrated several litters of pigs, all of which perished. In St. Lawrence Co., N.Y., in 1870, a surgeon inoculated himself while opening a vesicle on the hand of a farmer.

Harness, stables, stable utensils, vehicles, fodder, and litter are frequent bearers of contagion. At Geneseo, N.Y., in 1877, three horses and a cat died in midwinter after licking the blood from a stone-boat which had conveyed the skin of an anthrax bullock to market. Green fodder or hay harvested from ground formerly occupied by anthrax victims or from their graves often convey the poison, but probably only by the adherent earth and dust containing the anthrax-germ.

That the anthrax bacillus and its spores may be long preserved in earth is abundantly proved. At Avon, N.Y., nine months after any cases of the disease, the liquid leaking out on the river-bank near to the grave of a victim of the year before was licked by six cattle, and in two days they all perished. On the same pasture victims were seized yearly for seven years, but with a rigid seclusion of these, their products, and their graves the malady has finally disappeared. The persistent deadly effect of some soils on animal life, apart from the presence of the carcases, seems to show that in certain soils we find the normal home of the anthrax bacillus, while the migration into the animal economy is but an accident of its existence. The soils that are especially subject to anthrax are the dense clays, the limestones, and the rich alluvials. Among the essential conditions are the exclusion of oxygen, excepting a limited amount bearing some relation to what is found in the animal fluids, and the abundance of some alkaline agent (lime, potash, soda, ammonia), so that the earth is either neutral or only very slightly alkaline or acid. An acid vegetable infusion is inimical to the germ, which soon disappears from such a medium. The requisite paucity of air is found in all the dense, less pervious soils (clays, etc.), in soils habitually waterlogged (swamps, deltas, river-bottoms, low meadows, natural basins, drying lakes and ponds), and in soils rich in decomposing organic matter (peat, alluvial, over-manured). The antacid is often found present as lime or potash, or is constantly being produced in the form of ammonia, etc. by organic decomposition. Such places are known to farmers as "dead lots," because no stock will live on them. The bacillus in the buried carcase does not produce spores (Bollinger), though it may in the soil at any temperature between 59° and 110° F. In the graves, therefore, at a lower temperature, the poison can only be preserved by a continuous generation of the bacillus.

Pasteur, who successfully inoculated the casts of earth-worms taken from anthrax graves, attributes to these an important rôle in bringing the germs to the surface. A more important agent, however, is probably the rise and fall of water in the soil. By this means the bacilli and spores are washed up toward the surface, and when the superficial layers dry out they are easily carried by the winds. Hence it is that anthrax is usually prevalent in late summer and when the soil is dried and heated to its {931} greatest depth. Thus it is, too, that wet seasons followed by specially dry and hot ones are, above all, productive of anthrax in herds. Wet seasons fulfil the further purpose of carrying off the germs into rivers and depositing them on the banks or on inundated meadows, where after the subsidence of the flood the disease appears, for the first time perhaps.

There is, however, good reason to believe that the effect of a warm season is not confined to its influence on the soil and its germs. The high temperature deranges the vital functions of the animal economy, and, inducing a febrile disturbance, lessens the power of resistance to the anthrax virus, just as the cooling of the warm-blooded bird lays it open to infection. On this account, and because of the frequently recurring electric storms, the hot dry season is especially the season of anthrax. The hottest, driest autumns of Siberia always coincide with the anthrax years, and in the last fifteen years in the United States I have noticed the wide extension of anthrax whenever the season has been unusually hot and dry. In Corsica the herdsmen confidently pasture their stock in the close still valleys throughout spring and early summer, but whenever the surface soil is dried out they make all haste to remove it to the hills, well knowing that delay means devastation and ruin.

Plethora is undoubtedly an important predisposing cause of anthrax, and so is the alternation of cold nights with hot days. The febrile condition induced in the animal economy is perhaps the main factor at work in each case. Finally, youth is on the whole more liable than age, but whether because of the greater receptivity of the growing system and its tissues, or because it has not yet acquired some immunity by exposure to the milder effects of the poison, is not certainly determined. Sex is without influence.

It is not a little remarkable that the bacillus germ has not yet been found in the placental liquids nor foetal blood of sheep, goats, or rabbits, though swarming in that of the mother. Bollinger attributes this to the action of the placenta as a "physiological filter"--a conclusion seemingly at variance with the passage of the bacillus through all the other animal membranes, including those lining the mammary glands and the vagina. Two other possible explanations remain: first, that the secretions of the uterine glands are inimical to the bacillus; and, second, that the foetus, being in some sense a carnivorous animal, possesses the immunity characteristic of Carnivora. Bacilli have recently been found in the foetal guinea-pig.

The bacillus anthracis was first observed by Pollender and Branel in 1849 (Birch-Hirschfeld), but it was only publicly claimed as the cause of the disease in 1855 by Davaine. Branel discarded Davaine's theory, because blood in which he had failed to find bacillus produced anthrax with bacillus in the blood of two foals inoculated. Later observations by Bollinger and others have shown that cultures of bacillus can always be made from such infecting blood, and that in most cases the presence in the infecting blood of spherical bacteria can be demonstrated by the microscope. That the bacillus is the true pathogenic element is proved by the following facts: 1st. That the bacillus is the only ectogenous, particulate, organized structure constantly found in the anthrax blood and fluids; in cases in which it is apparently absent cultures show its actual presence. 2d. After cultivation in pork or beef infusion to the {932} hundredth generation the virulence is unimpaired, though it must be assumed that all non-organized poisons derived from the infected animal body must have been diluted or decomposed to extinction. 3d. That filtration of the anthrax liquids through a plaster or other efficient filter renders the filtrate innocuous, while the solids retained in the filter remain infecting (Chauveau, Bert, Toussaint). 4th. That the clear filtrate injected to excess killed by virtue of its contained chemical products in twelve hours, while the solids filtered out and containing the bacillus or its spores only killed after thirty hours.[4] 5th. Anthrax blood from the living animal or one just dead, and destitute of spores, when subjected to compressed oxygen (50 atmospheres), is non-infecting (Bert). 6th. The same anthrax liquid, destitute of spores, after boiling is completely innocuous. 7th. The same liquid, if kept in a closed tube apart from oxygen for eight days, shows the bacilli broken down by granular degeneration, and proves absolutely harmless when inoculated in small quantity. 8th. The same sporeless anthrax fluid when treated with absolute alcohol loses its virulence. 9th. The anthrax liquid which has been cultivated with free access of air in a temperature varying from 25° C. (77° F.) (Klein, Löffler) to 41° C. (105.5° F.) forms spores, and then remains infecting, though it may have been subjected to compressed oxygen, boiling for several minutes, absolute alcohol, dilution with water, putrefaction, or the exclusion of oxygen.

[Footnote 4: Bert, _Compt. Rend. de la Société Biol._, p. 355, 1879.]

The bacillus anthracis, as found in the blood and animal fluids, is in the form of fine rods, straight (rarely bent or angular), motionless, and 0.007 to 0.012 Mm. in length. Smaller forms are seen to be minute ovoid or oblong bodies, and the smallest absolutely spherical (micrococcus); but in all cases, as seen under the highest powers of the microscope, they have clear-cut, even margins, linear or curved, which easily distinguish them from the irregular normal granules of the blood and tissues. Under the highest powers of the microscope the bacillus is seen to be made up of a series of oblong (Koch) or cubical (Klein) cells enclosed in one common sheath. This is rendered more manifest if they are first swollen by the addition of water. The motionless form of the anthrax bacillus is of especial value in distinguishing it from the motile bacteria of putrefaction (saprophytes).

Within the living animal body the development never goes aside from these forms. The growth appears limited to micrococcus and bacillus rods, while spores or bacillus threads are never found. This finds its counterpart in the micrococcus poisoning caused by the inoculation with the spores of common moulds (Grawitz); and in septicæmia also micrococcus and bacillus forms only are found, the filamentous never.

When grown in organic infusions out of the animal body the anthrax-germ develops from micrococcus or bacillus into a long, branching, filamentous product, which in the presence of oxygen develops into spores. Apart from oxygen or when the proper nourishment of the bacillus is exhausted the protoplasmic elements within the filamentous sheath undergo granular degeneration, and finally the empty envelope disintegrates and disappears. The spores appear at intervals in the protoplasm of the filament as clear, brightly refrangent bodies, at first spheroidal, afterward larger and oblong. Unlike the micrococcus and bacillus, {933} they do not stain. Under favorable circumstances the primary cell is capable of forming one, or if extra long, two spores (Koch, Klein). Cossar-Ewart claims to have seen the formation of motile flagellate organisms aggregating themselves into zooglæa masses, but as these were not found in the carefully-conducted cultures of Koch and Klein, they are supposed to have been aërial microphytes accidentally introduced.

The great tenacity of life in the spores in heat and cold, dryness and wet, excluded from air and under several atmospheres of oxygen, in the midst of putrefaction and in pure watery fluids, well accounts for the persistence of infection in buildings and localities where the poison has gained a foothold. In order to their destruction in a natural manner it seems necessary that they should germinate and develop into the anthrax micrococcus, bacillus, or mycelium. This germination may take place in the presence of moisture, oxygen, and suitable nourishment, whether in the soil, the animal body, or elsewhere, and then the exhaustion of the aliment, the exclusion of the oxygen by putrefaction, the submergence in a medium unfavorable to development, or exposure to a very high temperature, may suddenly destroy the poison.

There is reason to believe that a too free exposure to oxygen proves destructive to the virulence, if not to the life, of the poison, and thus in all porous, well-drained soils the anthrax poison, even when introduced from without and concentrated by the death and burial of many victims, soon disappears. This feature, which is common to many zymotic diseases the germs of which live and multiply outside the animal body (typhoid, yellow fever, tuberculosis, swine plague, chicken cholera, diphtheria, etc.), offers countenance to the claims of Buchner that he had by prolonged culture, in the presence of air, metamorphosed the bacillus anthracis into a harmless mycrophyte, and that, conversely, by continuous cultivation under the surface of a suitable beef infusion he had changed the harmless bacillus subtilis of hay into the deadly bacillus anthracis. Koch, Klein, and others have discredited Buchner's results, on the ground that he had not, in their opinion, taken due precautions against impure cultures, and that his alleged transitions took place too abruptly; yet further observation must determine whether he has been condemned too hastily. The diminished virulence of Pasteur's attenuated virus, which is unaffected by the next subsequent culture or by the formation of spores, shows plainly enough that the bacillus anthracis is capable of physiological changes under the influence of varying conditions of growth, and that such changes are not at once undone by a return of the former conditions.

How anthrax-germs enter the body is partly known and partly conjectured. Direct inoculation on a sore by contact, by insects, by harness, by accidents, etc. is an undoubted method. The sound cuticle is probably an efficient barrier, since bacteria habitually inhabit, without hurt, the surface and gland-ducts of the skin; yet the entrance of these saprophytes through the shell and membranes of the egg leaves a doubt as to the efficiency of the cuticular obstacle. The mucous membranes are manifestly frequently penetrated by the parasite. Hence the local affections in the mouth and throat (glossanthrax, anthrax angina) and in the lungs (pulmonary anthrax). Cohn claims that the gastric juice of Carnivora especially is destructive to the anthrax poison, yet the constant recurrence of intestinal anthrax (mycosis) seems to imply that the germs often escape destruction {934} in the stomach. Pasteur supposes that anthrax-infected food is only injurious when there are inoculable sores in the mouth or pharynx, but it seems as if in that case the disease would be first shown at these points and in the nearest lymphatic glands rather than in the bowels, the rule for the inoculated anthrax being to develop first in the tissues and thence to reach the blood-vessels through the lymphatics.

The anthrax poison expends its fatal energy especially on the blood and blood-vessels. The bacilli in the blood use up the available oxygen, so that the circulating liquid becomes venous, dark, and unfitted for the maintenance of the normal functions of life. What is even worse, the ability of the blood to absorb oxygen is greatly impaired. In men and dogs suffering from anthrax the consumption of oxygen was found to be reduced in one instance even by two-thirds, probably in part by reason of the action of the chemical products of the bacillus. A third condition constantly found is embolism of the capillaries by the bacillus and the occurrence of local gangrene.

SYMPTOMS.--Anthrax shows itself in three principal forms: 1st, the apoplectiform; 2d, anthrax fever without local external lesions; and 3d, external localized anthrax. The two last forms correspond in the main to the acute and subacute forms.

The period of incubation varies according to the dose of the poison and the receptivity of the animal. In some cases infection is at once followed by illness. In these it is probably the chemical products that produce the first effect, while the disease caused by the propagation of the bacillus appears later should the animal survive. Such incubation is shortest for the smaller animals (mice, rabbits, guinea-pigs, cats), in which illness usually sets in in from twenty-four to forty-eight hours. In sheep and goats incubation may be extended to three or four days, while in horses and cattle it may last a day longer.

The apoplectiform type attacks animals which a few minutes before seemed in fine health, appetite, and spirits, striking them down as if by lightning, and the victims struggle convulsively for some minutes, expel blood perhaps by the nose or anus, and expire. In the less suddenly fatal cases there may be muscular trembling, unsteady gait, excited breathing, accelerated pulse, tumultuous heart's action, bleeding from some natural orifice, and death in from one to several hours. Occurring as these cases often do in summer, the sudden death is probably hastened by insolation.

In anthrax fever or acute internal anthrax there is loss of appetite, and, in ruminants, of rumination, suppression of milk, dulness, languor, staring coat, or even a rigor, and thirst. Then follows the hot stage, in which the temperature may rise to 106° or 107° F.; there are acceleration of pulse and breathing, petechiæ or a brown or yellowish tinge of the mucous membranes and white parts of the skin, tenderness of the spine, often jerking or clonic spasms of the muscles of the extremities, and much prostration and weakness, the patient hanging back on the halter, leaning against a wall, or swaying when made to move. The feces are usually more or less mingled with blood-clots, or may be at once liquid and bloody. Bloody urine and the discharge of blood from other natural channels are frequent. Some cases are manifestly delirious, and in others the skin crackles on being handled. Remissions are not uncommon, {935} during which the animal remains dull and prostrate. As the disease advances and the blood is robbed of its oxygen, the temperature descends below the natural standard, great weakness and stupor set in, the pupils are widely dilated, and death from asphyxia occurs in one or two days from the onset.

In localized external anthrax the local swellings may be first seen. There are usually some tenderness of the skin, erection of the hair, and the formation of a little nodule, like a hazel-nut or walnut, adherent to the deeper parts of the skin, firm and comparatively painless even when cut. Sometimes the swelling is diffuse, with a dropsical or erysipelatoid aspect, and crackles like parchment when handled. Whether the affection attacks the tongue, the throat, or some part of the head, body, or limbs, the tendency is to gangrene of the part, and, if the subject survives long enough, to an extensive sloughing and unhealthy sore. The sloughs and sores have either a black sanguineous appearance or they are lardaceous and intermixed with streaks of dark red. If fever is not present at the outset, it sets in early, and passes through the same stages as in the acute internal anthrax, the animals being suddenly plunged in prostration and stupor, with dusky yellow or blood-stained mucous membranes, dyspnoea, dilated pupils, convulsions, and death. On the mucous membranes (gloss-anthrax, anthrax angina) the engorgement is usually complicated with bullæ with red or yellow contents, and which on bursting leave unsightly gangrenous ulcers. In all such cases the morbid liquids of the swellings teem with bacilli.

MORBID ANATOMY.--The most characteristic changes are usually met with in the blood. This is black, thick, tarry, uncoagulable or coagulates only in loose diffluent clots, which are redissolved before squeezing out the serum; the fibrin is diminished (often by two-thirds), the red globules are not adherent in rouleaux, and are crenated and broken down and the hæmatin diffused through the liquid, so that it stains the hands or paper deeply; the white globules are increased, probably by reason of the early irritation of the lymphatic glands and spleen by the poison; and it reddens slowly and but slightly on exposure to the air, and speedily passes into decomposition. The blood can scarcely be made to flow in a full stream, but often trickles down the hair and skin by reason of its thick, consistent character. The microphytes above described are usually found in the blood, and always in the affected tissues if examined just after death.

Next to the blood, the spleen presents the most constant lesions, being enlarged (by one-third, one-half, or to double, triple or quadruple its normal size) and gorged with blood (sometimes even to rupture). The lymphatic glands, and especially those adjoining the local anthrax swellings of the tissues, are always enlarged, marked with petechiæ, friable, easily reduced to a pulp, and swarming with bacilli and micrococci. Next to the glands of the affected parts the central ones, the axillary, prepectoral, thoracic, sublumbar, and abdominal, are the most constantly affected. The lymph is reddish and opaque.

Decomposition sets in early, and the resulting gases cause a puffy, emphysematous condition of the connective tissue. The fat and other white tissues are dusky brown or yellow, and petechiated; the muscles are soft, flabby, and dark red or brown, with occasional blood {936} extravasations; the blood-vessels, especially the veins, and the right heart are gorged with black, uncoagulable blood, and have their inner coats blood-stained. The serous membranes present numerous petechiæ, and contain more or less of a reddish serum. The intestines, and sometimes the stomach, are dark red throughout, marked by petechiæ, and are often the seat of thickening from sanguineous or transparent colloid infiltration. The lesions are especially extensive on the small intestines and rectum. The vagina and womb are also the frequent seats of sanguineous infiltration. The liver and kidneys are enlarged, congested, softened, and friable, and the ganglia of the sympathetic are enlarged, congested, and softened. The swellings are of two kinds, sanguineous and colloid. The former, when cut into, present one or more loose clots of black blood or a grumous mass of blood-elements, separating the tissues and often mixed with fetid gases. The colloid exudations are glairy, semi-solid, jelly-like masses, infiltrating the tissues. The tissues affected and the skin covering them are the seat of bacterial embolism and gangrene, and there is no tendency to suppuration. These products swarm with the specific microphytæ.

DIAGNOSIS.--The differential diagnosis of anthrax from other affections due to the propagation of microzymes in the system is not always easy--so much so that a variety of bacteridian and allied diseases (septicæmia in its various forms, erysipelas, swine plague, chicken cholera, poisoning by the micrococci of fungi, black quarter from bacteria, milk sickness, and Texas fever) have been erroneously confounded with this affection. These all show the same dusky or cyanosed mucous membranes, disintegrating blood-globules, loose blood-clots, petechiæ, blood-extravasations, sudden and great prostration, and enlargement and congestion of the lymphatic glands or spleen. In some of these the duration of incubation (in swine plague six to fourteen days and in Texas fever one month) serves to distinguish, while in the majority the microzyme is globular (Texas fever, micrococcus of fungi-poisoning, chicken cholera); in swine plague the cocci are arranged in pairs; in black quarter the microbe is a refrangent ovoid, single or in chains of two or three and a motile linear body with a refrangent nucleus in one end; and in milk sickness the germ is a spirillum. The germs are far more likely to be detected in the local lesions and lymphatic glands than in the blood. The specific nature of the symptoms and lesions can usually be relied on, but in cases of doubt the inoculation of a small animal (rabbit, guinea-pig, sheep) will be a material guide.

PROGNOSIS.--True anthrax leads to a very high mortality. The apoplectiform cases are fatal almost without exception; the acute cases of anthrax fever in many outbreaks perish to the extent of 75 or 80 per cent., and the more tardy ones to the number of 50 per cent. In a general outbreak the earlier cases are usually the most fatal, while later, when the less susceptible animals are attacked, the mortality is often decreased. Again, the mortality is often at once arrested by the emigration of the herd to a more healthy soil, a large proportion of those already attacked recovering.