Chapter LVIII: Part II: , Showing Predominance of Malarial Element . . . . 617 (57)

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 {937} 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, {938} 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.

{939} 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 {940} 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 {941} 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 {942} 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.

{943} 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 {944} 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.

{945}

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.

[Footnote 1: _Works of Hippocrates_, trans. by Adams, vol. i. p. 377.]

[Footnote 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, {946} especially dysentery and colliquative wasting. The symptoms described by him resemble those of chronic pyæmia."[3]

[Footnote 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]

[Footnote 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 {947} 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.

[Footnote 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]

[Footnote 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 {948} 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]

[Footnote 7: Braidwood on _Pyæmia_, p. 2 _et seq._]

[Footnote 8: _Ibid._, p. 2.]

[Footnote 9: _Ibid._, p. 3.]

[Footnote 10: _Ibid._, p. 10.]

[Footnote 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]

[Footnote 12: _Ibid._, p. 14.]

{949} 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]

[Footnote 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]

[Footnote 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 {950} 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 {951} 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]

[Footnote 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 {952} 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]

[Footnote 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 {953} 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.

[Footnote 17: _Trans. Pathological Soc. of London_, vol. xxx. p. 22.]

[Footnote 18: _On Hospitalism_, p. 73.]