The same gentleman thus resumes the evidence for the belief that a disease in a puerperal woman, not having the characteristic symptoms of a zymotic disease, but resembling puerperal septicaemia, may really be of zymotic origin: 1. Even apart from the puerperal state, cases of zymotic disease occur in which the rash or other characteristic signs are not de veloped. 2. In undoubted cases both of puerperal scarlatina and puer peral erysipelas, symptoms of inflammation of the peritoneum and in the pelvis are common. 3. Undoubted scarlet fever is so modified in puer peral women, that while the mortality is very high, the sore throat is almost always slight. 4. Cases of puerperal pyrexia occur, often severe or fatal, in which sore throat is absent or very slight, and the rash so little defined that it is difficult to decide as to whether the disease should be reckoned as scarlatina or not. In these cases symptoms of inflamma tion of the peritoneum and in the pelvis are often marked. " There is strong evidence that a disease which cannot be distinguished from other forms of puerperal fever, may be originated by the conveyance of conta gion from certain zymotic diseases, especially erysipelas and scarlet fever. Accordingly the view is accepted by many, probably the majority of ac coucheurs in this country (England) that these diseases may give rise to puerperal fever." Gallabin, thus, must be ranked with those who claim that, although rare, a puerperal fever, sui yeneris, may exist.—Ed.] As we have seen, almost all authorities admit the necessity of a wound, and IIervieux and Depaul are about alone in the claim that there is some thing else than a septictemia of local origin in puerperal affections, thus championing the doctrine of essentiality.
We think that there is exaggeration in both these beliefs. Certainly, in the vast majority of cases, there is a wound, and by wound we under stand not only the uterine, but fissures, vulvar and vaginal erosions, tears of the cervix caused by the foetal head; and here it is that, ordinarily, in fection occurs. But this wound, these fissures, are not for us indispensa ble, and from this standpoint we agree with Hervieut and Depaul. Puerperal fever is the result of infection; it is contagious to the highest degree, but, according to our belief, no wound is necessary, and we claim that infection, aside from any local lesion, may take place through the respiratory tract, or the digestive, the patient thus infected being able to transmit the contagion to other puerpera. This contagion of puerperal fever is to-day no longer contested, and it has been proved by numerous researches both in France and abroad. It remains only to find the septic agent, the miasm, the poison, the infectious germ, the indispensable agent. What is it? Whence does it come? Such are the questions which it remains to study, and which have been answered by Pasteur, whose researches have been faithfully stated in Dol(ris's thesis.
According to Pasteur, this agent is a proto-organism, and this proto organism is not single, but multiple in variety, giving rise thus to those multiple affections which may be observed in puerperte.
Mayerhofer first determined, in 1865, that the lochia of infected women were in character putrid, and discovered motile vibrios, which, according to him, were the cause of the putridity. Recklinghausen, and Waldeyer, continuing his researches, proved the presence of these vibrios not only in the lochia, but on the surface of puerperal wounds, in the uterine lymphatics, in the exudations in the cellular tisane, in the serous cavities, and proved also that the fine grain-like masses described by V irchow and Hohl were purely microscopical organisms, multiform bacteria. Despine and Quinquaud, by injecting putrid lochia into animals, produced lesions similar to those of septicaemia.
Orth, in 1873, rejected cylindrical bacteria, which, he claimed, came from the interior, and stated that the puerperal lever germ was a micro coccus, sometimes in isolated globular points, sometimes joined infinitely together so as to form chaplets. Heiberg, 1873, Birsch-Hirschfeld, 1874, Spillmann (Nancy), 1876, Rohrer, 1876, believed both in the vibrios and the bacteria, and Hausmann, (Berlin) 1876, caused septic phenomena by injecting septic material into the vagina and uterus of rabbits, pregnant and not pregnant. In the latter instance, however, infection only oc curred in case there existed a lesion of the vagina.
In 1878, Hugh Miller, of Edinburgh, from a series of researches, claimed the presence of bacteria, micrococci and vibrios. Billroth, on the other hand, did not believe in the bacteria. " The etiological connec tion, he says,'between bacteria and septic disease, or putridity of the blood, has not been proved. In the living organism, certain forms of acute inflammation bring to the pus, from the surrounding tissues, materials which modify its chemical composition in such a manner that the microscopical spores may develop in an exuberant way. In addition to the wounds, there must exist certain determinate forms of inflamma tion of the connective tissue, erysipelas, abscess, pseudo-erysipelas, diph theria, or else traumatic inflammation must be transformed into these inflammatory affections, in order that the pus may, in turn, alter a little, and the microbe may develop in abundance. It has been indeed det3r mined that the pus corpuscles may change without the presence of any ' organism, and, on the other hand, these organisms may be carried in bandages, on instruments, the fingers of the accoucheur, and transplanted on the wound. The water with this wound is washed is of itself sufficient." It is to Pasteur, 1879 to 1880, that we owe the most valuable researches. Doleris has resumed the experiments of this distinguished teacher, and it is from his monograph that we borrow the following pages: " Puerperal infection is an infection which borrows nothing at all peculiar from the puerperal state, otherwise than that it is more or less linked with the weakened condition, the result of parturition, thus finding in diminished ability to resist the action of morbid agents a condition favorable for its development.