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, 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.
1 Wochenschrift f. Thierheilkunde und Thiersucht, Nos. 24 and 25, 1879.
2 Rec. de Med. Vet., Mar. 15, 1879.
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, 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 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.
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 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 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.
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, 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 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, 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 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.
PROPHYLAXIS.—In prophylaxis the soil demands the first attention. If this is damp and calcareous or rich in organic matter, the remainder of the herd should be at once removed to a drier and more porous soil, where the germ is less likely to be preserved and increased. In an enzoötic in Livingston County, N.Y., in 1875, 40 bullocks out of 200 had perished in ten days, yet after removal to an adjacent dry pasture and the use of antiseptics with the food and water the attacks abruptly ceased and 48 out of 50 head already sick recovered. The drainage of anthrax soils leads to a steady reduction of the poison, favoring as it does the germination of the spores and the destruction or modification of the germ. When drainage is impossible, the mortality may be reduced by driving the stock to drier grounds during the hot, dry season, by stabling them morning and night when the dews are on the grass, also in wet times, when they are likely to pull up the plants by the roots, or, better still, by cutting the fodder and soiling the stock in stables or yards. Yet in all these cases the germs will at intervals find access to the animals in the green food or hay, so that badly infected soils must be secluded from live-stock, and either be abandoned or devoted to other cultures. A point of the very first importance is the safe disposal of the products and carcases of the sick. These should be thoroughly burned, or, failing this, deeply buried (4 feet) and the graves covered with coal tar and fenced in from all other stock for from five to ten years. Contaminated litter and fodder should share the same fate. Stables and yards where the sick have been, and all vehicles and implements used for them or their products, should be thoroughly disinfected. In the epizoötic in Livingston County, above referred to, these measures seem to have eradicated the disease in the course of six years, though the land was neither drained nor subjected to cultivation, and the dangerous meadows are now again pastured with impunity.
In the case of sick animals the greatest care is requisite to keep them from common drinking- or feeding-troughs; to exclude all other animals, even the smaller quadrupeds and birds, which may become the bearers of the poison; to avoid the chance of the drainage of infected excreta into other yards and pastures, and to carefully disinfect and guard the human attendants against contamination. The sale of animals out of an infected herd, and, above all, for the meat-market, and the use of the milk or other products of such animals, until attested sound, are highly reprehensible.
Finally, there are the different methods of protecting the system by inoculation with modified virus. The first of these is that of Burdon-Sanderson, Dugnid, and Greenfield, who in 1878 and 1879 inoculated six cattle with the blood of guinea-pigs dead of anthrax, all of which survived except an old, emaciated, worn-out, and pregnant cow, and all the survivors would only afterward contract anthrax in a mild form. The anthrax blood of the guinea-pig inoculated on the sheep proved fatal. The second mode is that of Pasteur, who cultivated the anthrax-germ artificially in flasks of meat-infusion, and after the nourishment in the latter had been used up left the bacilli to degenerate until their virulence had been so far decreased that the liquid could be safely inoculated on animals, so as to produce a mild anthrax infection and thereafter secure immunity from this poison. For all the larger domestic animals he found that the eighth day of the culture sufficed, provided there had been no formation of spores; and the method has now been applied on many scores of thousands of domestic animals. Klein, however, has found that cultures in pork-broth of the same age are invariably fatal to rodents, and that a guinea-pig which survived inoculation with culture a month old did not possess immunity against fresh virus. The third method, that of Toussaint, consists in heating the fresh virus, so as to lessen its activity, and then inoculating it on the animals to be protected. He found that a temperature of 55° C. (131° F.) maintained for one hour rendered the virus non-fatal, without impairing its prophylactic powers on animals inoculated. In spite of a partial failure at Alfort from insufficient heating of the virus, the method has now been firmly established as at once easy and effective.
The great value of these discoveries can hardly be overestimated, yet it is to be feared that the éclat of their reception has led to a far too general adoption of the methods. No one of the methods professes to destroy the life of the bacillus nor to impair its power of self-propagation. The bacillus, therefore, is likely to be planted in the localities where it is being employed, and, if the soil is favorable, to be perpetuated there. It follows also, from the susceptibility of the bacillus to change under varying conditions of life, that the modification impressed on it by the methods of Pasteur and Toussaint may be reversed under a reverse state of the environment, and that the harmless virus sown by our inoculators may in favorable soils produce the more deadly types. The methods secure the safety of the individual herd inoculated, at the expense of planting in the pasture a seed most perilous to all future uninoculated herds that may roam there. The only place for such protective inoculations is on pastures already charged with the anthrax bacillus, and from which that cannot be eradicated. On the dry, healthful soils where the bacillus cannot survive the inoculation is useless, while on the dense, damp, rich soils favorable to its preservation, but as yet uninfected or nearly so, this inoculation is but sowing deadly seed to secure a very temporary and questionable advantage.
TREATMENT.—Bloodletting and laxatives have been largely used in the treatment of anthrax, though both are mostly useless in acute cases, their possible good effects being anticipated by the early death. When of service at all, it is probably mainly in reducing that plethora which serves often to enhance the virulence and severity of the malady. Apart from these, the agents resorted to are more or less of an antiseptic nature, and probably exert their action mainly on the bacilli undergoing development near the surface of the skin or intestinal mucous membrane. In extensive outbreaks I have had the best results with the administration thrice daily of carbolic acid, nitro-muriatic acid, or bichromate of potassium, and hypodermically of iodide of potassium and sulphate of quinia. Alcoholic stimulants, chlorate of potassium, and muriate of iron are equally indicated, especially when the period of prostration has set in. If the local anthrax can be detected when there is as yet but a hard nodule, there should be no hesitation in cauterizing it to its depth and treating the resulting sore and surrounding parts with tincture of iodine or iodized phenol. After crucial incision the nodule may be treated with powerful caustics (potassa, nitric acid, chloride of zinc), to be followed by iodized phenol, with or without poultices or fomentations.
Anthrax in Man (Malignant Pustule or Vesicle, Anthrax Intestinalis, Mycosis Intestinalis).
Fournier in 1769 first traced the communicated anthrax of man to the consumption of the flesh of diseased animals and the handling of their wool. Until quite recently, however, the form which originated as a local external affection was the only type recognized, while internal anthrax was confounded with a multitude of other affections.
ETIOLOGY.—That anthrax in man is almost invariably derived from the lower animals by infection is now undoubted, while for the direct infection of man, as of animals, by the germs propagated in the soil, there is no absolute proof. The latter mode of propagation has only been recognized in the Herbivora, which are so much more exposed to contamination from the soil; yet, abstractly, there is no reason to suppose that man is less susceptible to the earth-grown bacillus than to that produced in the animal, if only he were as frequently exposed to its infection. The spontaneous development of anthrax apart from the pre-existent bacillus in animals or soil is a chimera. The principal modes of infection may be considered as direct and mediate. Among the direct are included infection from handling the sick animals, their carcases, their wool, hair, bristles, hides, fat, and guts; the inoculation of physicians, surgeons, and nurses from their patients; and the infection of men by the meat, milk, and cheese eaten. As attested modes of mediate infection may be cited the inoculation by insects (mosquitoes, bluebottles, and other bloodsuckers), and the introduction by water into which anthrax products have drained or been washed; there are also hypothetical cases in which anthrax-germs from the earth have entered the system in the air, drink, or food (raw vegetables). The direct inoculations are especially common in certain classes (shepherds, farmers, butchers, knackers, tanners, veterinarians, and workers in hides, hoofs, glue-factories, fat-rendering works, in hair, wool, bristles, and catgut, and in felting and paper-making). In such cases the disease usually begins as a local one, and occurs on uncovered portions of the body. Three such cases occurred in 1875 on one farm at Avon, N.Y., where the victims had assisted in burying forty dead cattle, and a number of other similar instances can be adduced in different parts of the same State, in one of which a physician was accidentally inoculated in dressing a farmer's hand. Physicians whose practice includes large tanneries become very familiar with the disease and recognize it very readily.
Infection through food is much less frequent in men than in animals, the process of cooking combining with the action of the gastric juice in destroying the poison. Yet it is by no means unknown. The records above given of infection in St. Domingo, Naples, and the Russian steppes can be easily supplemented. Dr. Keith of Aberdeen, Scotland, records the case of a family that suffered, two of them fatally, after partaking of broth and meat which had been boiled for hours, one member of the family (a vegetarian) having alone escaped. Infection through milk, butter, and cheese is less common, the gravity of the disease in animals leading to an early suppression of the mammary secretion. In all such cases the infection enters through sores in the mouth or from the bowels.
Those cases in which the bacillus enters the system with the inspired air are probably the least numerous. Yet the germ may reach the lungs in fine dust, and then find in the delicate respiratory mucous membrane the most accessible of all channels into the system.
The proportion of men affected is much greater than that of women and children, doubtless by reason of their greater exposure to infection, and, as in the lower animals, the summer months are most productive of anthrax. The susceptibility of the human race appears to be less than that of the Herbivora, and doubtless varies, as in these animals, with the nature of the food. It is at least temporarily exhausted by a first attack, though in exceptional cases and under a strong dose of the poison a man may be affected a second time.
SYMPTOMS.—Symptoms usually set in within twenty-four hours after inoculation of the poison, though it is alleged that the incubation may be extended to twelve or fourteen days. Itching draws attention to a small red spot like a mosquito bite, but with a black central point. This speedily increases to a small rounded swelling (papule), and in fifteen hours is surmounted by a minute vesicle with dark-red or bluish contents. From the size of a millet-seed this increases to that of a pea, and in thirty hours bursts spontaneously or under friction and forms a dark-red, indurated, comparatively painless nodule (parent nucleus, Virchow). The adjacent skin shows a swollen areola livid and red, on which there appear vesicles similar to the first, which pass through the same stages, burst, and leave a livid, hard, or doughy gangrenous surface. By this time the surrounding skin is red, shining, and puffy, and the disease continues to spread by the same method of extension. The diseased part now becomes the centre of an oedematous swelling which may invade the entire arm, face, or neck, and is attended with more or less constitutional symptoms. The affected part may be cold or hot, and it may show the red lines of lymphangitis and the swelling of the adjacent lymphatic glands.
The pyrexia, at first slight, often reaches a high grade, attended with occasional chilliness, pains in the back and loins, great prostration, languor, dulness, and even delirium, with cold sweats, anxiety, dyspnoea, and at times muscular spasms. As in beasts, there are the dusky skin and mucous membranes, petechiæ, and cyanosis, and in bad cases there may be sudden collapse and death. The symptoms vary much, however, according to the extent of the local lesion, to the amount of poisonous chemical products thrown into the blood, to the degree of the invasion of the blood by the bacillus, and to the complication (not infrequent) of the affection with septicæmia. In the very mildest cases the affection never proceeds beyond a local slough, the size of a quarter or half dollar, the germs do not enter the blood in sufficient numbers to survive, the constitutional symptoms are few or absent, and the sore heals by granulation.
The disease usually lasts from six to ten days, and for the first forty-eight hours the symptoms are generally purely local.
Malignant anthrax oedema (oedeme maligne) was first observed by Bourgeois as occurring in the eyelid, and has since been recognized in other parts of the body (arm, forearm, head). It differs mainly from malignant pustule in the absence of the preliminary vesicle, of the hard nodule (parent nucleus), and of the early circumscribed gangrene. It has this further peculiarity, that the local disease often appears as a sequel rather than a precursor of the constitutional disturbance. It corresponds in the main to the diffuse erysipelatoid anthrax of the lower animals, and has been attributed to the anthrax poison introduced by inhalation. It has been observed to follow eating of anthrax flesh (Leube, Müller). Inasmuch as the active disease is often delayed a week or ten days after exposure to infection, it may reasonably be supposed that the bacillus has been imprisoned on the mucous membrane, or, entering the blood in small quantity only, has been held in check by the antagonism of the blood-globules until some elements, escaping into the connective tissue, have started the local disease. The symptoms are usually first languor, sleeplessness, restlessness, with some sense of chill, debility, and headache, and finally, after a few days, the formation of the specific oedema at one point or more. This has a pale, semi-translucent, slightly yellowish or greenish aspect, pits on pressure nearly equally at all points, and tends to a rapid extension, with concomitant aggravation of the constitutional symptoms, and in many cases nausea and vomiting. Gangrene sets in—not progressively, as in malignant pustule, but simultaneously over a more extensive surface—and is followed by great prostration, stupor, dyspnoea, cyanosis, collapse, and death.
Anthrax intestinalis may be looked upon as the counterpart of the internal anthrax or anthrax fever of animals, described above. As in animals, the constitutional symptoms may result early in a fatal issue, with scarcely any local lesion save in the blood and spleen (Carganico, Leube, Müller, Winkler, Lorinser). As in animals too, the sanguineous engorgement of the spleen and the intestinal anthrax are often complicated by external anthrax oedema or malignant pustule (Heussinger, Virchow, Buhl, Waldeyer, etc.). In this form pyrexia and other constitutional disturbances are first seen. There is a general feeling of languor and depression, with some chilliness, fever, pains in the limbs, back, and head, vertigo, and ringing in the ears. Even at this early stage there is noticed a dusky hue of the skin and visible mucous membranes, which goes on increasing to a brown or yellow tinge, to petechiæ, or, with the supervention of dyspnoea, to cyanosis. Digestive derangement is early shown in abdominal pain, nausea, vomiting, tenderness, some swelling, and finally diarrhoea, often bloody and sometimes profuse and exhausting. In acute cases the symptoms become rapidly worse, and then follow discharge from the mouth and nose of uncoagulable blood, dyspnoea, cyanosis, small pulse, dilated pupils, great anxiety or drowsiness, and stupor, or there may be tonic spasms of the trunk or extremities. Death usually results from asphyxia or collapse, as in animals. These cases are almost invariably fatal within a period of thirty-six hours, though some linger six or seven days.
Allied to the intestinal anthrax is anthrax angina, a not unknown occurrence in man. This begins as a bad sore throat, with an especially dark-red hue of the pharyngeal mucous membrane. As it advances the shade becomes increasingly darker, the power of deglutition is lost, serous phlyctenæ with gangrene and deep ulceration set in, but without any tendency to the formation of false membrane as in diphtheria. There are early superadded the constitutional symptoms above described, and the patient dies in a state of collapse or asphyxia.
MORBID ANATOMY.—The lesions closely agree with those already described for animals in general. The blood presents the same dark-red or black, tarry, incoagulable, or only slightly coagulable condition in the worst cases, yet this is less constant in man, as the bacteria are less constant or numerous in the blood, in keeping with the more prolonged localization of the external anthrax in man, and the more pronounced antagonism between the blood and the bacillus which results from feeding exclusively or largely on flesh. The red globules do not tend to adhere together, and the white globules are in excess and very granular. The spleen is less extensively enlarged than in animals, but is highly charged with blood, bacilli, and micrococci. The lymphatic glands too are enlarged, hyperæmic, cloudy, hemorrhagic at points, of a dark grayish, deep red, or blackish color, and highly charged with the bacillus. The surface of the skin and mucous membranes (mouth) presents hemorrhagic spots and patches, with serous vesicles and eschars. The malignant pustule when cut into presents a central slough and a surrounding hard indurated mass, both of a dark blood-red, with similar prolongations downward into the adipose tissue, and around all the characteristic oedematous infiltration, often streaked with blood. The bacillus is found in tufts or dense groups at intervals in the rete mucosum, the dermis, and the subcutaneous connective tissue. The serous membranes present the same general lesions as in animals. The walls of the stomach and bowels are the seat of cloudy red infiltration, with at intervals small hemorrhagic foci, and on the mucous surface distinct sloughs. Jelly-like exudations are also found in these membranes in the mesentery and in the retro-peritoneal tissue. The liver and kidneys are usually congested or are infiltrated with an oedematous exudate, and in these, as in all the local anthrax lesions, the characteristic bacilli are found.
DIAGNOSIS.—Malignant pustule is distinguished by its commencing from a minute red point with dark centre, and by its progressive extension from this point by a dark-red, puffy, and vesicular areola, with steadily advancing induration and gangrene. The bites of insects have a yellowish central point with red areola. A boil lacks the dark centre and the rapidly rising elevated red areola. Carbuncles and plague-boils tend to appear on clothed parts of the body, respectively on the back of the neck and shoulders and on the trunk and extremities. In carbuncle several boils rise and burst simultaneously, though they may finally slough into one sore, while in anthrax the extension is from one point. The plague-boil is usually multiple and much more painful than anthrax. The glanderous nodule is usually multiple, situated at intervals on the course of a lymphatic, the intervening portion of which is inflamed, hard, and cord-like. It is also usually associated with the specific glairy discharge from the nose, the nasal ulcers and nodules, and the enlarged painless, nodular, and indolent submaxillary lymphatic glands. As a last resort the detection of the bacillus in the indurated nucleus and the inoculability of the disease on the lower animals (rabbit, guinea-pig), may be appealed to.
Malignant anthrax oedema is less easily recognized, but may be inferred from the sudden swelling with a dusky yellow or greenish hue and a tendency to vesiculation and gangrene, the whole preceded and attended by the constitutional symptoms of anthrax, and, above all, from the presence of the bacillus in the exudate.
In both of these forms much may be deduced from the known liability of the district to anthrax, from the occupation of the subject as being exposed to infection (worker in hair, wool, bristles, hides, catgut, etc.), or from his having eaten meat which was open to suspicion.
Internal anthrax is less certainly diagnosed because of the absence of local symptoms until the constitutional disorder is well advanced. Yet the reasonable suspicion of infection and the sudden and violent eruption of the disease (headache, nausea, vomiting, bloody diarrhoea, extreme anxiety, debility, dyspnoea, cyanosis, convulsions, collapse, with petechiæ, and local discharges of diffluent blood) serve to identify it. The bacillus is not always to be detected in the blood under the microscope, but its presence can usually be demonstrated by inoculation.
PROGNOSIS.—The prognosis of malignant pustule energetically treated in its early stages is good. The disease is as yet a local one, and the germs can be extinguished by local treatment. In anthrax districts, where the disease is feared and early recognized, the mortality may be from 5 per cent. (Nicolai) to 9 per cent. (Lengyel, Koranyi). Even this mortality is mainly due to delay in treatment. In districts, on the other hand, where the malady is infrequent, and where efficient measures are applied too late, the mortality is often 30, 40, or even 50 per cent. After internal infection, and where local symptoms only appear after general infection, the case is very hopeless.
PROPHYLAXIS AND TREATMENT.—The prophylaxis of anthrax in man is to a large extent identical with that for animals. All considerations as regards soil, culture, drainage, sick and dead stock, cremation, burial, disinfection, etc. have a most important if only a secondary bearing on the protection of man. Still more important is the free use of carbolic acid, chloride of lime, or tincture of iodine for the hands of those dressing unhealthy sores in animals or handling suspicious cases of sickness or cadavers, and of those working in hides, wool, hair, horns, hoofs, guts, etc. Similarly, all products of animals with anthrax should be withheld from general use.
In external anthrax of man, before the system has been contaminated, the thorough destruction by caustic of the diseased part with its contained poison is most effectual. Where there is as yet but the preliminary papule it may be incised and thoroughly destroyed by a stick of chloride of zinc, caustic potassa, or nitrate of silver, or, if more convenient, by fuming nitric acid, muriatic or sulphuric acid, or, perhaps preferably to all others, iodized phenol. Should the parent nucleus have already formed, it should be excised with the knife or deeply incised in a crucial direction, and then thoroughly cauterized with one of the more potent escharotics (caustic potassa, strong nitric acid) or with the iodized phenol. The latter agent may be further applied on the sound skin adjacent, especially if there is the slightest swelling or redness. Should the peripheral oedema persist or reappear after the cauterization, the latter should be repeated until this tendency is overcome. Hypodermic injections of a solution of iodine and iodide of potassium may be made into the entire swelling. After the caustic has done its work the eschar may be softened and its separation favored by a warm poultice containing a small amount of carbolic acid or iodized phenol. This treatment is often highly beneficial, even after constitutional symptoms have set in, by arresting the propagation of the bacillus and checking its introduction and that of its chemical products into the circulation.
Constitutional treatment is not to be forgotten. Carbolic acid may be profitably given to the extent of fifteen drops daily, iodide of potassium ten to twenty grains thrice a day, and sulphate of quinia ten grains at the same intervals. The strength should be sustained by iron (tincture of the chloride) and wine or other alcoholic beverage, both being, like the agents already named, calculated to retard if not to limit the propagation of the bacillus. The diet throughout should be nutritious and easily digested.
When a person is known to have eaten anthrax meat an emetic will be indicated, followed by a smart oleaginous purgative combined with five drops of carbolic acid, and subsequently by the constitutional treatment above recommended. In case of extensive anthrax oedema, incisions may be made into the part as far as the yellow exudate extends, and a poultice containing carbolic acid may be applied. Or, preferably, the swelling may be freely injected with a weak solution of iodized phenol (1:100 water), and then painted with the same agent or with tincture of iodine.