Volume 1 — GENERAL DISEASES. (continued 25)

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.

PYÆMIA AND SEPTICÆMIA.

BY B. A. WATSON, M.D.

HISTORY.—There is little to be learned from existing literature of the views which were maintained by the ancients, prior to the birth of Christ, in regard to the morbid conditions now designated pyæmia and septicæmia; although it is certain they were recognized by the "Father of Medicine," who reports a well-marked case of puerperal fever terminating fatally on the twentieth day of the disease, and also a case in which death was unquestionably caused by septic poisoning, as is clearly shown in the following:¹ "Criton, in Thasno, while still on foot and going about, was seized with a violent pain in the great toe; he took to his bed the same day, had rigors and nausea, recovered his heat slightly; at night was delirious. On the second, swelling of the whole foot, and about the ankle, erythema with distension and small bullæ (phlyctænæ); acute fever; he became furiously deranged; alvine discharges, bilious, unmixed, and rather frequent. He died on the second day from commencement." Additional confirmation of the fact that Hippocrates was familiar with the phenomena of these diseases may be found in his dissertation on empyema and fevers. Prof. C. Heuter says, under the head of septic fever,² "Hippocrates and Celsus observed the fever in cases of injuries which proved so dangerous that this danger could not have originated from the inflammation or from the wound alone." Jacotius, a commentator of Hippocrates, has even mentioned putrid fevers, the same as Adrianus Spigelius, who spoke of fevers which arise from putrefaction; but both authors, as well as their followers, did not discriminate between septicæmia arising from the putrescence of wounds and pyæmia. In the mean time both varieties were regarded as intermittent fever.

¹ Works of Hippocrates, trans. by Adams, vol. i. p. 377.

² Pitha und Billroth, Handbuch der Chirurgie, 1 Band, 2 Abth., 1 Heft, 1 Liefg., S. 6.

"Aretæus lived during the middle of the second century of the Christian era. In his remarks on pneumonia he observes that the subjects of this disease die mostly on the seventh day. 'In certain cases,' he says, 'much pus is formed in the lungs, or there is a metastasis from the side if a greater symptom of convalescence be at hand. But if, indeed, the matter be translated from the side to the intestine or bladder, the patients immediately recover from the peripneumony.' He speaks of a metastasis to the kidneys and bladder being peculiarly favorable in empyema. He ascribes suppuration of the liver to intemperance and protracted disease, especially dysentery and colliquative wasting. The symptoms described by him resemble those of chronic pyæmia."³

³ Braidwood on Pyæmia, p. 2.

Galen and some of the other ancient physicians recognized the existence of septic poisoning, as is shown by the opinions expressed on the subject of putrid fevers. According to Galen, putrid fevers may either arise from the conversion of ephemerals, or originally from putrefaction of the fluids within the vessels.

Aetius states that they arise from constriction of the skin or viscidity of the humors, whereby the perspiration is stopped, and the quantity of vital heat so altered as to give rise to putrefaction, first of the fluids, and afterward of the fat and solid parts. When these corrupted fluids are contained within the vessels they occasion synochous fevers, but when distributed over the body they give rise to intermittents. Synesius and Constantinus Africanus give a similar account. Alexander gives an interesting and ingenious disquisition on the origin and nature of putrid fevers, one of the most common causes of which he holds to be the conversion of ephemeral fevers, and the inseparable symptoms being want of concoction in the urine and quickness of the pulse with systoles. This is the account of them given by most of the other authorities, both Greek and Arabian, so that we need not enter into any circumstantial exposition of their views. We shall merely give the brief account of those furnished by Palladius. There are, he says, two kinds of synochous fevers, the one being occasioned by effervescence, and the other by putrefaction of the blood; of these the latter are the more protracted and dangerous. In them the pulse is contracted, the heat pungent, and the urine white and putrid.⁴

⁴ Paulus Ægineta, trans. by Adams, vol. i. p. 236 (Sydenham Soc., 1844).

A new era in the literature of this subject dawned during the sixteenth century. Ambrose Paré and Bartholomew Maggi each published a work in which they pointed out the old errors and announced new truths. Paré's Treatise on Gunshot Wounds was published in Paris in 1551, while Maggi's treatise appeared a year later at Bologna. Paré gained his first experience in the treatment of gunshot wounds in 1536, which is described as follows: "The storming of the small mountain-fortress Villane, near Susa, probably gave him for the first time full occupation, and he followed in all things the example of older colleagues. Like them, although hesitatingly, he poured into the gunshot wounds boiling oil of elder to destroy the poison, but the oil fell short, and then he was compelled to dress the other wounded men with an ointment of oil of roses and turpentine. Fearing that the latter would soon become victims of the wound-poison, he passed a sleepless night, got up early to see the ill consequences, but was greatly surprised to find those that he had half given up free from pain and without inflammation or swelling, while those who had been treated with boiling oil lay in a state of fever, with great pain and much swelling. He therefore determined, as he tells us, never again to burn the poor subjects of gunshot wounds so cruelly."⁵ It will be seen that Paré's treatise on gunshot wounds was published fifteen years after this impressive experience at the fortress of Villane. In this work he sought to correct the prevailing idea that gunshot wounds were poisonous, and was ably supported in his effort by Bartholomew Maggi; but it required all the respect which Paré enjoyed in riper years to gradually obtain consideration for the new view. The idea that gunshot wounds were poisonous is supposed to have originated in the fact that in every war there are cases of acute sepsis, developed after the infliction of these injuries, which agree in all their essential points with the results of the bites of poisonous snakes. We are even informed that during the late Franco-Prussian War there were cases which even excited suspicion among the laymen that the enemy had used poisoned missiles.

⁵ German Clinical Lectures, 2d series (New Sydenham Soc., 1877), p. 65 et seq.

The nature of the error which Paré and Maggi endeavored to correct is shown by the declaration made by Johannes de Vigo at the commencement of the sixteenth century, who expressed in dogmatic form the views then firmly held by physicians. "A gunshot wound is a contused wound, he says, for the bullet is round; it is burnt, for the bullet is heated; it is poisoned, for the powder is poisonous. The poisoning is the essential condition; therefore the treatment must be directed above all to counteract this."

The next step was that a poisonous substance may develop itself or settle in the wound, and especially in gunshot wounds—a substance which has nothing to do with powder or lead. Paré himself adopted this view. When he took part in the siege of Rouen many wounds sloughed and had a cadaverous smell, and on opening the bodies of those who died numerous collections of pus were found in different parts full of greenish ill-smelling ichor. Besiegers and besieged believed themselves to be wounded with poisoned bullets. Paré looked for the cause in a deterioration of the air by the large quantity of decomposing substances, and he appears to have assumed, as is done at this day, a direct action of the so-called deteriorated air upon the wound itself.

The evil influence of air vitiated by the products of decomposition, not upon wounds only, but upon the organism generally, has never been lost sight of by physicians since that time. That rotten straw, decomposing bodies of men and animals, surfaces saturated with excrement, and overcrowding of badly-ventilated hospitals give rise to infectious fevers and unhealthy state of wounds is not a result of modern observation only. That it was a question of the processes of fermentation which became communicated to the body by means of the exciters of fermentation contained in the air was a view frequently adopted. "To quote one only out of many; John Pringle, in his Observations on the Diseases of the Army, published in 1775, devotes a chapter especially to 'Diseases resulting from Bad Air,' and his forty-eight experiments on septic and antiseptic substances contain numerous hints at attempts resembling those made at the present day to determine the antiseptic power of certain things. No advance was made, however, beyond vague surmises concerning the nature of the exciters of putrefaction, and they were for the most part looked for amongst the volatile, ill-smelling products of decomposition, and were believed to be extremely subtle gaseous matters."⁶

⁶ German Clinical Lectures, Second Series (New Sydenham Soc., 1877), p. 67 et seq.

Ambrose Paré (1582) first taught that secondary abscesses in surgical cases, "which he had observed in the spleen, lungs, liver, and other viscera, were due to a changed condition of the fluids produced by some unknown alteration in the atmosphere and determining a purulent diathesis."⁷ The following quotations force the conclusion that in the early history of medicine there was supposed to be some important relation between wounds of the head and multiple abscesses. "Nicholas Massa (1553) mentions a case of abscess of the left lung, following an injury of the head."⁸ "Valsalva (1707) was induced by his own observation to say that the viscera of the thorax were sometimes affected in wounds of the head." "Desault (1794) considered abscesses of the liver to be a very frequent sequence of head injuries."⁹ The fact that wounds of the head were frequently followed by abscesses of the lungs, liver, and other organs probably led to the opinion expressed by Desault, Barthez, Brodie, W. Phillips, Copeland, and others, that the disease had its origin in a nervous agency.¹⁰ "Bertrandi and Audouille (1819) sought for a mechanical explanation of the occurrence of hepatic abscesses after head injuries and in cases of apoplexy." Morgagni (1740) somewhat obscurely hinted at the doctrine of the reabsorption of pus—a doctrine which was afterward elaborated by Quesnay in 1819. Morgagni, after quoting a great number of instances of wounds of the head followed by visceral abscesses, opposes the idea of a mechanical transportation of pus thither, and states that abscesses are not confined to the liver and that they may follow wounds and ulcers of other parts besides the head. He ascribes their formation to particles of pus (not always deposited in the form of pus) resulting from the softening and suppuration of small tubercles, which, having been mixed with the blood and disseminated, are arrested in some of the narrow passages, perhaps of the lymphatic glands, and by obstructing and irritating these, as happens in the production of venereal buboes, and by retaining the humors therein, distend them and give origin to the generation of a much more copious pus than what is carried thither; and by this means, he says, we may also conceive how it is that much more pus is frequently formed in the viscera and cavities of the bodies than a small wound could have produced.¹¹

⁷ Braidwood on Pyæmia, p. 2 et seq.

⁸ Ibid., p. 2.

⁹ Ibid., p. 3.

¹⁰ Ibid., p. 10.

¹¹ Ibid., p. 3 et seq.

Cheston (1766) believed that the translation of matter from one point to another was a frequent occurrence after amputations of the larger limbs. John Hunter (1793), and after him Velpeau, demonstrated the existence of pus in the blood. Hunter believed that the pus was derived from the interior of the inflamed veins. He described three forms of inflammation of these vessels—viz. adhesive, suppurative, and ulcerative. Pyæmia he considered to be an aggravated form of phlebitis. Arnott (1829) concluded from his observations—1, That death does not result from the extension of the inflammation of the veins to the heart; 2, that the dangerous consequences of phlebitis have no direct relation to the extent of the vein which is inflamed; and, 3, that the presence of pus in the veins, though the principal, is not the sole, cause of the secondary affection. He accordingly opposes the idea of Abernethy, Carmichael, and others that the constitutional affection is owing to the extension of the inflammation to the heart. The publication of Arnott's and Dance's treatises led to the general opinion being held in England and in France that phlebitis and purulent infection were identical affections, or, at least, that the latter was invariably caused by the former.¹²

¹² Ibid., p. 14.

Cruveilhier (1829), admitting the doctrine of the formation of secondary abscesses being due to capillary phlebitis, further laid down an axiom, since proved untenable, that the foreign body introduced into the veins, whose elimination by the emunctories is impossible, will produce visceral abscesses similar to those which occur after wounds and operations, and that these abscesses are the result of capillary phlebitis of those viscera.¹³

¹³ Braidwood on Pyæmia, p. 14 et seq.

During the early part of the present century it was generally admitted by the best authorities that the symptoms and lesions in pyæmia were entirely due to the presence of pus in the blood, but whether absorbed from the wound or developed by an inflammation of the veins was at that time a disputed question.

Haller made the first experiments on animals with putrefying substances in the latter part of the eighteenth century, and was convinced that nothing destroys the animal fluids more powerfully than putrefaction. Gaspard (1822) published a complete work based upon his experimental research in regard to the action of putrefying substances on living organisms. He, having produced septic infection in animals by injecting into their blood pus or other putrefying substances, thus prepared the way for other experimenters, by whom he was quickly followed. Ernst R. Virchow repeated the experiments of Gaspard, and discriminated with greater precision between the surgical diseases—septicæmia with its sharply-defined group of symptoms, the opposite of pyæmia. Furthermore, "he showed that the changes in the veins which had been regarded as due to phlebitis were caused by the coagulation of the blood and by subsequent degenerative changes in the thrombi thus formed; that the infarctions and abscesses seen in the viscera were due to emboli which had become detached from softened thrombi; that, as the white blood-globules and pus-globules were identical in appearance, they could not be distinguished; and that it was improbable that pus-globules made their way into the blood."¹⁴

¹⁴ The International Encyclopædia of Surgery, ed. by Ashhurst, vol. i. p. 204.

Panum (1855) conducted a series of important experiments, and endeavored to separate the infectious substance and determine its real nature. He concludes that the real poison is not identical with any of the chemical combinations or any of the single substances which have until now been isolated by chemical analysis from the products of nitrogenous decomposition, but adds that it is probably a concealed ferment belonging to the so-called extractive matters—carbonate of ammonium, leucin, tyrosin, fatty acids, acetic acid, etc. Furthermore, that the putrid poison is stable, fixed, and non-volatile; that it is neither decomposed by boiling nor by evaporation to dryness; that it is insoluble in absolute alcohol, but soluble in water; that the albuminous substances found in putrefying liquids become venomous only because they are impregnated with the septic poison; and that washing these substances in a large quantity of water renders them innocuous; and that the energy of these putrid poisons can only be compared to the venom of serpents, curare, and other vegetable alkaloids.

The prize offered by the Faculty of Medicine at Munich for the best essay on the action of putrefying substances in the animal organism was awarded to Hemmer in 1866. His essay was distinguished for its accurate delineation of the pertaining literature and for the number of experiments reported, while his conclusions bear a striking resemblance to those of Panum.

Bergmann in 1868 sought to determine the poisonous element contained in decomposing animal substances, and for this purpose chemically treated putrid fluids, hoping to find the agent that would excite all symptoms of septic poisoning. He obtained a body of this nature from decomposing yeast, which he called sepsin, although we have no proof that either he or any one else has ever found the same in pus or any decomposing animal matters; and even if it had been found in these, it would then become necessary to demonstrate the fact that no other substance contained in the putrefying liquids could produce septic poisoning. Many other experiments, similar to those which have just been mentioned, were made in the mean while by Magendie, Stich, Billroth and Hufschmidt, O. Weber, Duprey, Learet, Urfrey, Saltzman, Fischer, Frese, Muller, and others. Bergmann had extracted the sepsin from yeast, but Schmidt and Petersen (1869) were able to obtain it from putrefied blood. In 1869, Zuelzer and Sonnenschein claimed, on the contrary, to have separated a new, unnamed septic alkaloid, which was not the sepsin, and the action of which resembled that of atropine and hyoscyamine. Nevertheless, the separation of the sepsin or of the alkaloid of Zuelzer seemed to demand a talent in the manipulator which is not possessed by everybody, and rare are the chemists who possess it—so rare that these substances are not yet either officinally recognized or classified. The attention of the medical profession had now become thoroughly fixed on the chemical character and the physiological action of these newly-discovered substances. It is therefore only natural that we should find during the next few months that the medical societies were much occupied with discussions on these subjects, although no important progress seems to have been made.

Political events now gave a new direction to thought, and the Franco-Prussian War filled the hospitals of both nations with wounded in which there was opened a grand field for the practical study of purulent infection in all its various forms. Humanity now demanded the best efforts of the medical profession. Neither the mechanical nor chemical theories had ever yielded practically any beneficial results; consequently, something better was demanded in this emergency. It was during this important epoch that the germ theory began to assume form and to attract some general attention in the medical profession, although Schroeder and Dusch had shown in 1854 that the filtration of the air through cotton was sufficient to prevent the putrefaction of albuminous substances which had been previously boiled. Pasteur also demonstrated the existence of germs in the air in 1863, and likewise showed their agency in the process of fermentation.

Lister began the antiseptic treatment of compound fractures in 1865, although he did not publish his report until 1867. The cotton-wadding treatment of wounds, which is based on the fact that the air passed through cotton is freed by it from all germs, was first employed by Alphonse Guérin, who refers to it in the following language: "In the latter part of 1870 I had the idea that the cause of purulent infection existed in the germs or ferments which Pasteur had discovered in the air. It was at the end of the war; all the cases of amputation had succumbed to the purulent infection, and not a single large wound escaped the scourge. The studies which I had made from the month of September to the end of December in 1870 had confirmed me in the opinion that purulent infection is neither due to phlebitis nor to the absorption of pus. I believed more firmly than ever that the miasms emanating from the pus of the wounds were the real cause of this frightful malady to which I had been compelled to see the wounded succumb, whether they were treated with charpie or cerate, whether with the lotions of alcohol or of carbolic acid applied several times a day, and which was soaked up by the linen which remained in contact with the wounds. But this miasmatic theory remained, nevertheless, useless, since from 1847, when I professed it, the cases of amputation in my service succumbed to purulent infection in about the same proportion as those who were cared for by my partisan colleagues did from the absorption of pus or the inflammation of the veins. In my despair, seeking constantly a means to prevent this terrible complication of wounds, I had thought of the miasm of which I had admitted the existence, because I was not otherwise able to explain the production of the purulent infection, and which was not only known to me by its deleterious influence, but which appeared to consist of living corpuscles of the nature of those that Pasteur had seen in the air; and then the history of the miasmatic poison possessed for me a new clearness. So, said I then, the miasms are the ferments. I am able to protect the wounded against their fatal influence by filtering the air, as Pasteur had done, while maintaining, in opposition to Pouchet of Rouen, that there is no spontaneous generation. I thought then of the cotton-wadding treatment, and had the satisfaction of seeing my anticipation realized. It was from this time that dates in reality the theory of germs or of ferments as a cause of purulent infection."¹⁵

¹⁵ Nouveau Dictionnaire de Médicine et de Chirurgie pratiques, t. xxx. p. 265.

A series of important experiments were made in 1872 by Coze and Feltz, which consisted in injecting into the jugular vein and the subcutaneous cellular tissue putrid liquids; and they record, among other interesting results observed by them, that the blood of the animal thus destroyed always contained infusoria. These experiments have been repeated and their results confirmed by several observers, and in particular by Davine in 1872.

Another series of experiments were made by Behier and Lionville, which absolutely confirmed those of Coze and Feltz; they likewise found in the blood rounded and rod-shaped corpuscles possessed of movements more or less energetic. Vulpian also confirmed the results obtained by Davine and Behier. He says: "It will not do to deny to the immovable or movable vibriones and corpuscles found by Coze, Behier, and Davine a very important rôle, because they are not the essential contagion of the poisonous blood; it is at least necessary that they should be there in order to produce the alterations which have occurred in this fluid." Chauveau has experimented extensively, and likewise admits the action of the septic vibriones of Pasteur.

Pasteur has made known the result of his investigation in communications to the Academy of Medicine in 1877, 1878, and 1879. There exist, according to him, two principal vibriones—the pyogenic, or the producer of pus, and the septic, the producer of the properly so-called septicæmia. But the latter is not a unique disease, and, as we have seen from the outset, there are confounded under this name different states, light or grave, corresponding with as many forms of vibriones.

The questions of greatest practical importance in regard to this whole group of diseases seem to us to be, as expressed by Dr. Budd, where and how the specific poisons which cause them breed and multiply; and all who have closely followed the scientific investigations bearing on these points which Prof. Tyndall has conducted during the past few years, and who have repeated even a portion of his experiments, cannot fail to be powerfully impressed with the value of the views which he embodied in his work entitled Floating Matter of the Air.

NOMENCLATURE.—The want of a systematic classification of the various morbid conditions arising from septic infection has long embarrassed alike authors and students, and even at the present time the vague manner in which the terms pyæmia and septicæmia are used leads to much confusion. The Pathological Society of London appointed, in 1869, a committee to investigate the nature and causes of those infectious diseases known as pyæmia, septicæmia, and purulent infection. This committee, having spent ten years in the study of these affections in connection with nearly all the large hospitals of London, report the following: "Summary.—It would seem, from a careful study of all the cases here collected, that it is probable that the diseases commonly known clinically as pyæmia and septicæmia may be grouped as follows: 1. Septic intoxication.—The effects of poisoning by the chemical products of putrefaction. A non-infective disease. 2. Septic infection.—A general infective process arising from the introduction of some peculiar constituent of putrid matter into the blood-stream. It is supposed by some to be due to the multiplication of living organisms in the blood, and by others to the effect of a non-organized ferment. It terminates fatally without secondary inflammations. 3. Pyæmia (for want of a better name).—An infective process probably, similar in nature to septic infection, but differing from it by giving rise to local inflammation and suppurations, often complicated by thrombosis and embolism, probably due to the blood condition. 4. Thrombosis with softening and decomposition of the thrombus and embolism, causing local abscesses in the viscera wherever the septic emboli lodge, but without the development of any general infective process. 5. Various combinations of one or more of the foregoing conditions in the same subject. 6. Infective periostitis or acute necrosis. 7. Infective endocarditis or ulcerative endocarditis. 8. Infective myositis. 9. A group of obscure cases in which it is impossible to form any idea as to the exact nature, often called spontaneous septicæmia or pyæmia."¹⁶

¹⁶ Trans. Pathological Soc. of London, vol. xxx. p. 38.

It will be observed that the earlier writers on medicine, although aware of the existence of septic diseases, wholly failed to discriminate between pyæmia and septicæmia until 1848, and even since that date these terms have been only partially adopted by authors, by whom frequently the meaning of the same word has been so modified as to refer to essentially different conditions. Custom having fully sanctioned the use of these terms, it is now thought that a separate consideration of their nomenclature may be advantageous, and consequently we shall pursue this course.

NOMENCLATURE OF PYÆMIA.—In Dunglison's Medical Dictionary the definition given to pyæmia is, "Pyohæmia," and the latter word is defined as follows: "Pyohæmia, Pyæmia, Pyohémie (F.), from pyo, and [Greek: haema], 'blood;' alteration of the blood by pus, giving occasion to the diathesis seu infectio purulentia."

The committee appointed by the Pathological Society of London in 1869 report on this subject as follows: "The most common definition of pyæmia is, no doubt, that adopted by the College of Physicians in the nomenclature of diseases. It is as follows: 'A febrile affection resulting in the formation of abscesses in the viscera and other parts.'"

Birch-Hirschfeld includes under the name pyæmia "all cases in which any general infective process is set up as a secondary consequence of a wound."¹⁷ Virchow has proposed the name ichorrhæmia. O. Weber uses the name embolhæmia for the condition in which emboli are found in the blood. Hueter in pure cases of purulent infection without metastasis calls the disease pyohæmia simplex; in cases with metastasis, pyohæmia multiplex; and when complicated with septicæmia he designates it as septo-pyohæmia. The term hospitalism has been applied to this disease by Erichsen and Sir James Y. Simpson, and the former remarks that "the term pyæmia is used in a very wide and elastic manner, and by many is made to include various forms of blood-poisoning."¹⁸ Billroth says: "Pyæmia is a disease which we believe to arise from the taking up of pus, or of the constituent parts of pus, into the blood." Koch employs the term pyæmia merely to denote a general affection accompanied by metastatic inflammation and suppuration.

¹⁷ Trans. Pathological Soc. of London, vol. xxx. p. 22.

¹⁸ On Hospitalism, p. 73.

The French definition and nomenclature of pyæmia, according to Guérin, is as follows: "Purulent infection, or pyohæmia, purulent fever, surgical typhus." The purulent infection is a poisoning of the blood, which terminates by the formation of multiple abscesses, which have been improperly known under the name of metastatic abscesses.

From 1820 to 1870 surgeons admitted that these abscesses were the result of a phlebitis having its origin in a wound exposed to the air. Therefore, this disease was variously designated under the name of phlebitis, pyohæmia, or purulent infection. Tessier called it purulent diathesis; "in 1847, I compared it to the typhus, and, as the poison is absorbed from the surface of the wound in the purulent infection, I gave it the name of surgical typhus or purulent fever."¹⁹

¹⁹ Nouveau Dict. de Méd. et de Chir. pratiques, t. xxx. p. 222.

Having given enough on this subject to answer our purpose, we will consider the nomenclature of another septic complication.

NOMENCLATURE OF SEPTICÆMIA. The term septicæmia was first employed by Piorry, and was applied for a considerable time to all those diseases in which the blood was submitted to a septic influence. Therefore, the term was made applicable to the morbid conditions existing in anthrax, glanders, typhus and typhoid fevers, variola, and also all forms of purulent and putrid infections. Guérin now adds: "Fortunately, for several years the most competent authors seem to have wished to reserve the name of septicæmia for what surgeons call putrid infection, and for the morbid state that the experimenters produce by the injection of putrid material into healthy animal tissues; it is consequently the experimental septicæmia which we aim at first and foremost."²⁰

²⁰ Nouveau Dict. de Méd. et de Chir. pratiques, t. xxx.

Dunglison defines septicæmia with a single word, septæmia. The same authority gives the following derivation and definition to septæmia: "From [Greek: sêptos], 'rotten,' and [Greek: haema], 'blood.' A morbid condition of the blood produced by septic or putrid matters."

Sanderson says: "What I mean by septicæmia is a constitutional disorder of limited duration, produced by the entrance into the blood-stream of a certain quantity of septic material. It must, therefore, be regarded less as a disease than as a complication, differing from pyæmia not only in the fact that it has no necessary connection with any local process, either primary or secondary, but also in the important particular that it has no development."²¹

²¹ British Medical Journal, Dec. 22, 1877.

Both Davine and Koch designate as septicæmic all cases of general infection from wounds in which no metastatic changes occur. "Birch-Hirschfeld limits the term septicæmia much in the same way as Sanderson. He describes as septicæmia those cases in which the disease results merely from the absorption of the products of putrefaction, and regards it merely as a process of poisoning, such as might arise from the injection of any other noxious chemical substance into the blood. Pyæmia, on the other hand, he considers a truly infective process, probably due to the entrance of specific organisms into the body. He would therefore include many of the cases described by Koch as septicæmia under pyæmia."²²

²² Trans. Pathological Soc. of London, vol. xxx. p. 9.

Billroth defines septicæmia as an "acute general affection which arises from the taking up of various kinds of putrid substances into the blood, and it is believed that these putrid substances so change the quality of the blood that it can no longer fulfil its physiological functions."²³

²³ Lectures on Surgical Pathology and Therapeutics (trans. from 8th ed.), vol. ii. p. 41.

Heuter defines septicæmia as a fever caused by the entrance into the circulation of the products of putrefaction from local centres of decomposition. He draws no clear distinction between an infective and a non-infective form, but the affection he describes as pyæmia simplex or pyæmia without metastasis seems to include many cases which Davine, Koch, and others would include under septicæmia.²⁴

²⁴ Trans. Path. Soc. of London, vol. xxx. p. 9, 1879.

Having before us the views of some of the prominent authors who have written upon the nomenclature of pyæmia and septicæmia, we observe that the use of these terms is based either on known or imaginary morbid conditions of the body, more especially of the blood. It therefore seems that the first step toward determining the proper limit within which these terms can be employed consists in learning their accurate meaning, which is fortunately clearly shown by their derivation. The next step consists in the application of these terms to the morbid conditions which are described more or less completely by these words. It may be here added that there will be frequently required for a full and definite expression certain modifying words, and consequently we may properly employ such phrases as puerperal septicæmia, spontaneous pyæmia, etc.

Having carefully examined the terms employed by various authors in connection with the morbid changes which are known to occur in certain cases of septic contamination, we give our preference to the following nomenclature: Septicæmia, septo-pyæmia, pyæmia simplex, and pyæmia multiplex.

The term septo-pyæmia is applied to a morbid condition possessing certain peculiarities of both septicæmia and pyæmia, and it is supposed to arise from the absorption of both poisons; the term pyæmia simplex is applied to a pyæmic condition in which there is no metastasis; while the name pyæmia multiplex is given to that form of disease which is characterized by the existence of metastatic abscesses. It may be well to add here that this nomenclature is not intended to cover all cases of septic poisoning, but to be applied to those cases only in which the morbid changes give to the terms a certain degree of appropriateness.

Septic poisoning may be justly regarded as a single chain composed of many links. Take, for example, a case of amputation of the thigh, followed within a few hours by traumatic fever, later by septicæmia; afterward there may be developed secondary fever; formation of ichorous pus, with absorption and its concomitants; pyæmia, accompanied by embolism, thrombosis, abscess in the lungs, liver, etc. To these may also occasionally be added phlebitis and inflammation of the joints, terminating speedily in suppuration. This chain may in this case be further lengthened or varied with traumatic erysipelas or with hospital gangrene. In fact, the variations in these cases are very numerous, and all these conditions, together with many others, are due to septic blood-poisoning.

ETIOLOGY OF PYÆMIA.—Four theories have been advanced at different times to explain the etiology of pyæmia, and they have been designated as follows: the mechanical, the nervous, the chemical, and the germ theories respectively; and their action is based on the following hypotheses: 1, that pus enters the blood, circulates in it, and acts as a poison; 2, that an irritation is excited in certain visceral organs in sympathy with inflammation of the fibrous membranes of the cranium or the bones of the upper or lower extremity, and there is thus produced a metastasis to these organs of an ichorous miasm or of a fluid which is more or less acrid; 3, that a chemical poison is generated from the pus in the wound, and when it is absorbed produces pyæmic manifestations; 4, that the putrefaction of pus in wounds is caused by a microscopic organism which enters the circulation and produces pyæmia.

The first hypothesis was somewhat modified, as we have already mentioned, by John Hunter and others, who advanced the idea that pyæmia consisted essentially of a phlebitis, and that the pus found in the circulation had its origin within the veins. However, it has since been shown conclusively that pyæmia cannot be produced by the injection of healthy pus into the cellular tissue or veins. This fact having been generally admitted by the profession, it is thought unnecessary to adduce here either the experiments or the arguments which have been accepted as conclusive on this important point. It is not even necessary to bring forward the disputed question of the possibility of the entrance of pus into the blood, since laudable pus does not produce pyæmia. In fact, we have reached a point in the progress of medicine when the discussion of either the first or second hypothesis ceases to be interesting to medical men. Consequently, our chief interest in the study of the etiology of pyæmia centres in the third and fourth hypotheses; and we believe that it may be safely asserted that the origin of this disease has been fully demonstrated by an almost unlimited number of experiments.

The injection of pus into living animals produces local, remote, and constitutional symptoms. The character of these symptoms depends principally on the kind of pus, laudable or ichorous, the quantity injected, and the site of the injection. It will be readily perceived that in cases where the pus is thrown directly into a vein the local symptoms would be unimportant, while the danger of remote trouble—metastatic abscesses in the lungs, liver, etc.—would be very great; but should the injection be made into the connective tissue, then the relations would be reversed. Constitutional symptoms may exist in both cases, but will differ in character and degree.

In regard to the character of the pus, and its agency in the production of this disease, Billroth says: "The old view, that pyæmia is only induced when decomposed pus (ichor) is reabsorbed, is entirely erroneous. There are cases where decomposed, putrid pus enters the blood, and which present a combination of the symptoms of septicæmia and pyæmia (septo-pyæmia of Hueter)."²⁵ Dupuytren failed to produce metastasis by injections of pus into the veins of dogs; these results were confirmed by Boyer, who only obtained metastasis when he used ichorous pus in his experiments. The same results are recorded in the works of Günther and Sedillot, based on numerous experiments. Beck made fourteen experiments very carefully, but did not succeed in producing metastasis in a single case. The same results are recorded by a commission of the Physiological Society of Edinburgh. O. Weber has recently shown by extended experiments that carefully filtered pus will not produce metastatic abscesses in the lungs. Therefore, it may be considered as proved that fluid pus injected into the veins of an animal produces no metastatic points of inflammation.

²⁵ Surgical Pathology, p. 344.

It should not be supposed, however, that because injection of fresh (non-ichorous) pus failed to produce metastatic abscesses, it was therefore without results, as the earlier experimenters thought. Billroth and O. Weber have shown by their recent experiments that these injections are uniformly followed by fever, and, if subcutaneous, by abscess; and further, that injections of fresh pus produce even a higher temperature than do those of ichorous pus; but the pus taken from cold abscesses has apparently very slight effect. The fresh non-ichorous dried pus was found to possess in a similar degree the power to excite inflammation and suppuration; even the removal of the albumen did not change its character or power. It will be observed that these injections caused not only local inflammations, but severe constitutional symptoms, as high temperature, etc. Experiments have thus far completely failed to show the agent that excites the inflammation, although it is generally admitted that it at least exists in the molecular bodies.

Virchow and Panum have shown conclusively by their experiments on living animals that the introduction of foreign bodies into the veins—as powdered coal, wax balls, and quicksilver—fail in all cases to produce metastatic abscesses in the visceral organs or symptoms of pyæmia. These foreign bodies were frequently found blocking up the terminal branches of the pulmonary artery, in some cases encapsulated, frequently resembling miliary tubercles, and occasionally surrounded by evidences of slight local inflammation, but in every instance without suppuration. The same experimenters, however, observed that the introduction of ichorous pus and decomposing animal tissue into the veins was attended with the formation of metastatic abscesses and other symptoms of pyæmia. They therefore conclude that the introduction of putrid animal substances into the veins, and the further transport of the same to the branches of the pulmonary artery, produce metastatic abscesses, and that the origin of these deposits is independent of the mere stopping up of the branches of this artery.

The occlusion of the blood-vessels in this diseased condition is a subject which has given rise to much discussion. Some of the earlier writers supposed this phenomenon constituted the disease pyæmia, while others believed it to be the essential cause. Roser says: "But the thrombus is, as can be easily proved, not the cause, but only a symptom, of pyæmia. If a surgical patient—e.g. one suffering with an injury of the head—is attacked by inflammation, and occlusion of a large vein, as of the common iliac vein, for instance, then there are three different theories for the inflammation of the occluded vessel—viz. Hunter's, Rokitansky's, and Virchow's. According to the old Hunterian phlebitic theory, the coagulation of the blood should be the result of the inflammation of the vein. On account of the circumstances under which the coagulation of the blood in the vein has occurred, one might suppose that the cause must be the oozing of coagulable exudation from the inflamed wall of the vein, but pathological dissections, especially Rokitansky's, would not accord with it. Large veins were found plugged up without the existence of corresponding indications of inflammation, and perfectly clear indications were often present that occlusion had preceded the inflammation. Consequently, the occlusion of the vein was the primary condition, and this must be explained in some other way than by its inflammation. Rokitansky in his theory recognized an independent disease of the blood. Yet it does not appear, on examination of the morbid conditions, that this theory can account for them. If it is recognized as correct that a primary disease of the blood is to be admitted, yet the coagulation of the blood in a large vein has not been traced back to it. It remained wholly unexplained why a single vein, especially one so large and strong as the common iliac, should become the seat of the local coagulation. The necessity of finding a local basis for the local coagulation could not be denied. For that reason it was greeted as a highly desirable advance when Virchow pointed out that the occlusion of such large veins could be dependent on the coagulation of the blood in the concave spaces behind the valves of the veins, or through the coagulation in the small branches—e.g. the hypogastric veins, which is gradually carried forward until it reaches the common iliac, and by continual increase this vein may also be filled up. At the same time, it was demonstrated that not infrequently, much oftener than was formerly supposed, the coagulated masses of blood are broken up and carried farther on in the circulation, in this manner producing occlusion of the pulmonary artery or its branches."²⁶

²⁶ Archiv der Heilkunde, Erst. Jahrg., Erst. Heft, S. 4.

The examination of this subject finally brings Roser to this conclusion: "Contamination of the blood is essentially the primary cause of pyæmia; thrombosis is only a result of this morbid contamination, and cannot, therefore, be regarded as the cause of pyæmia, but only as an apparent part, as one of the symptoms of the same."²⁷ The opinion here expressed by Roser I believe to be the one generally entertained by the profession at this time.

²⁷ Ibid., S. 43.

In cases of pyæmia there are recognized two principal sources of contamination of the blood—viz. the wound itself, and the vitiated condition of the atmosphere surrounding the patient—contamination, in the first place, directly from the wound through the blood-vessels; and in the second, by the passage of disease-germs or of the poisonous elements into the blood along the respiratory tract. E. Wagner says: "The latest examinations in regard to the vegetable parasites have made it very probable not only that these are the active agents, but also—what has been clinically quite generally accepted—that septicæmia and pyæmia owe their origin to different plants (the first to rod bacteria, the latter to globular bacteria); and, finally, that both may combine."²⁸ These germs may be generated in the wound or be received into it from the surrounding atmosphere. The character of the wound and the conditions surrounding the patient thus become important subjects for the consideration of the surgeon.

²⁸ Manual of General Pathology, p. 593.

It has been observed, and is now generally admitted, that wounds complicated with a fracture of the long bones of the extremities, opening large medullary cavities and accompanied by extensive laceration of the soft parts, always increase the danger of blood-poisoning. This fact may be more thoroughly understood by a brief consideration of the condition of the parts. Frequently in open fractures large quantities of pus constantly remain in contact with the surface of the wound, while detached fragments of bone, which become speedily necrosed, move about with every motion of the injured limb, lacerating more or less the surrounding tissues, and thus exciting inflammation and suppuration. The periosteum becomes inflamed; a widespread suppurative periostitis is the result; necrosis of the bone from insufficient nutrition follows, while mechanical pressure on the pus aids in its absorption. The medulla frequently takes on suppurative inflammation, and here the surgeon fails to receive prompt warning of danger; slowly the suppuration progresses, without pain or other symptoms unless the disease has extended to the other tissues; the medullary cavity at the fractured end of the bone may be completely or partially occluded by a new osseous formation; and in such cases the absorption of pus by the comparatively large venous vessels of this cavity is greatly facilitated.

The soft parts may also be the seat of dangerous trouble. The same force that produced the wound and fracture may have also contused the soft parts, destroying in a greater or less degree their nutrition, thus giving rise to gangrenous sloughs, or in other cases to the formation of abscesses, etc. I will also call attention to the fact that the laudable pus in these cases is most favorably situated for a rapid change into that commonly called ichorous. The heat of the parts and the contact of the pus with the atmosphere will not fail to effect its rapid decomposition.

ETIOLOGY OF SPONTANEOUS PYÆMIA.—It is unquestionable that cases of true pyæmia have been observed in which the etiology was not traceable to a wound; and it is equally certain that this failure to discover such a source of contamination in the majority of cases is no proof that it did not exist. When it is remembered that a large portion of the alimentary canal, the respiratory and the genito-urinary tracts, are so situated that the existence of a contaminating wound might be absolutely undiscoverable, we are compelled to admit the possibility of a local centre of contamination in all these cases. But the question may be asked here with propriety, "Is fatal pyæmia, independent of a wound, ever produced by breathing vitiated air?" The answers to this question must generally be a negative, although it is certainly true that poisoning of the blood does take place to a certain degree, as is abundantly shown by the different symptoms arising in patients thus exposed who are not suffering with wounds. It is said that dogs exposed in this way are found to rapidly emaciate and suffer from severe and constant diarrhoea. The various symptoms arising in patients confined in overcrowded and pus-infected wards, among which may be mentioned loss of appetite, with diarrhoea and emaciation, are too well known to require an enumeration here. Therefore it appears highly probable that living in and breathing a vitiated atmosphere may act as a strongly predisposing cause, only requiring a slight scratch or abrasion of the skin, in which the infection may be said to act as an exciting cause of pyæmia.

In reference to such complications the following questions are asked by Roser: "Is it a specific deleterious material, a miasmatic or contagious disease-poison, or, as it is generally expressed, a zymotic agent? Must we regard each particular typhus-like fever, with its remarkable changes of blood, with its various localizations in all the organs and membranes, with its chills, furred tongue, petechiæ, delirium, etc., as we regard typhus, scarlatina, variola, etc.? or, as Virchow teaches us, is this pyæmia, so greatly feared by all surgeons, only an ontological idea? Is the word pyæmia only a general name for three different conditions—viz. leucocythæmia, thrombosis, and embolism, or ichorrhæmia and septicæmia? or are there, as many have supposed, two ways in which pyæmia may originate? Is there one primary miasmatic pyæmia analogous to the other epidemic, so-called zymotic diseases? and again, a secondary pyæmia arising from suppurative inflammation, wherein the poison is formed in the patient's own body, which is infected by a single organ?"²⁹

²⁹ Loc. cit., S. 39.

That this disease is caused by a specific deleterious material in the large majority of cases is no longer a question for discussion. The only question to consider is, whether it always arises from the same cause. Is it possible for pyæmia to originate spontaneously? Are there any cases of sporadic origin, or are they always due to endemic or contagious influences? No definite answer can be given to these questions, although, undeniably, the weight of the argument is strongly opposed to a sporadic origin. The term miasmatic, as used by Roser, probably refers to the vitiated condition of the atmosphere, as seen in the overcrowded surgical and obstetrical wards of hospitals. In no other sense can the word be appropriately used in connection with the subject of pyæmia. It is true, pyæmic diseases are found to prevail at certain seasons and in certain localities much more extensively than under other circumstances. The same, however, is true of cholera, typhus fever, scarlatina, variola, and other contagious diseases. That pyæmia is contagious has been frequently demonstrated. I therefore conclude that the prevalence and spread of this disease must be explained by the same rules as are applied to the existence and propagation of these allied affections.

This inquiry into the etiology of pyæmia brings before us again the four hypotheses which have been given in explanation of the same number of theories. The first and second have been already abandoned by the medical profession, after it was satisfactorily demonstrated that they were based on false theories, and consequently there remain for our consideration only the third and fourth.

The third hypothesis assumes that a chemical poison is developed in the wound-secretions, which when absorbed produces pyæmia. An examination of the subject does not justify us in asserting that this proposition has been proved, although it is certain that the results of experimental inquiry demand for it a more extended investigation. In all the analyses which have thus far been made the investigators have entirely failed to give us an adequate knowledge of this poison, and not a word has ever been said in regard to the agency by which it is produced, although it is universally admitted to have been only obtained from decomposing animal substances. It is therefore pertinent to the continuation of this inquiry to ask, By what agency is the putrefaction of animal substances produced? It has now been fully shown that there can be but one answer given to this question—viz. the putrefaction of albuminoid substances can only be effected by living organisms. We therefore conclude that the fourth hypothesis brings us at least one step nearer the correct explanation of the etiology of pyæmia than the third, since we justly assume that if there is a chemical poison in decomposing albuminoid substances, it is produced through the agency of living organisms.