In this disease, also, like in typhoid, the difficulties in this attempt are multiplied by the fact that individuals, perfectly healthy or showing only indefinite symptoms, certainly not exhibiting the picture of a dysenteric, may carry in their intestines and, therefore, disseminate with their stools the dysentery bacillus, thus becoming sources of infection. In Germany the importance of this factor is fully recognized and the directions published for the performance of all these measures are as strict as are those for typhoid cases. Since we have learned that the bacillus is highly adapted to life in the human organism, the latter is its main source for its dissemination. If we destroy them, as they leave it, the principal source of infection is eliminated.

The means for recognition and detection of the bacillus have been highly elaborated and allow today to establish its presence with a high degree of certainty in a short time.

It is only natural that attempts have not lacked that intended to deal with the disease by means of specific remedies. Since the bacillus was known it seemed promising to influence the course of its ravages by antitoxic or bactericidal

sera.

All of these attemps have failed. Like the typhoid and cholera bacillus, the dysentery organism does not secrete a toxin, so that the production of an antitoxin was, a priori, excluded, like it is in typhoid and cholera. The hope to achieve success by a báctericidal serum could only be entertained under a wrong impression of the action of such a serum on an infected organism. If destruction of the bacillus through such a serum was the object to be obtained it was easy to do. Animals, even horses, are easily immunized against the dysentery bacillus and furnish a material of high bactericidal potency. The same experience was had before with other bactericidal sera, they prevented disease, if given before or at the time of infection, but in no case had such a serum influenced the course of a fully-established infection, in spite of the numerous favorable reports to the literature of cured cases of typhoid or cholera. On the contrary, in animal experimentation it can be shown that the administration of fresh sera acts deleteriously and kills the animal. The toxic effect of diseases. like typhoid or dysentery is not due to a toxin secreted but to the toxic effect of the proteids of the bacilli disintegrating in the tissues of the infected organism. These proteids may be called endotoxins and a certain amount of them means a fatal

quantity. Small doses are withstood by the normal reactive properties of our organism, fatal doses overpower it. If the chances would be there in the form of the necessary complement a large dose of typhoid-immune serum would kill the patient at a stage of the disease when we know his system is flooded with a number of bacteria, the suddenly-freed disintegration-products of which would form certainly more than the necessary fatal dose of endotoxin. Just the same conditions obtain for the dysenteric infection; such a serum may be used for prophylactic purposes or during the stage of incubation of the disease, where the number of bacilli present would not as yet aggregate if dissolved to the fatal dose; it can never do any good in an organism flooded with innumerable bacteria. That hopes for a success could be entertained was due, as said before, to a wrong conception of the action of bactericidal sera. The less said about the work done in this line, the better.

The remarks so far made deal with bacillary 'dysentery from the point of view that the disease is etiologically a unit. However, this belief that Shiga's discovery has aroused has been dispelled by the researches made during the last few years. Holding to the belief that a bacillus is the causative agent of the disease, we must admit today that it is etiologically different, although clinically identical forms of dysentery exist caused by different bacilli. Very soon after the comparative work on the various forms of organisms isolated in different parts of the world as Shiga's bacilli was begun, discrepancies between their biologic character were noticed, that at first were charged to the sources of error inherent to our methods of experiment. But after a short time it became clear that the differences found were real, and that in fact there existed a number, perhaps a great number, of altogether different dysentery bacilli, each of them able to produce the picture of what is called, clinically, dysentery. Five or six different forms are so far known, that by their biologic qualities can be differentiated, and that in their reactive effect on the infected individual differ entirely. It is very probable, even certain, that in our country alone we have not to deal with a single form of every where identical type, but with a greater number of species or varieties. Several of these have been closely studied and compared, so that, if found, they can be identified, but it is very unlikely that the supply is already exhausted and

that the coming years will not reveal a great variety of dysentery bacilli in different groups of cases. We have to figure with a great family of dysentery bacilli, that is at the bottom of the totality of the cases of dysentery occurring, although we know that certain members of it are found very widely disseminated. The future will spread more light on the importance and frequency of the single ones and, perhaps, thereby enable us to act upon them. At present the investigation of the etiology of dysentery is as yet in such an unsettled state that definite ideas can not be entertained.

The difficulties have become more serious through the bewitching complexity that a closer study of the agglutination reaction, alleged to be one of the most reliable footholds of the investigations, has revealed. If we follow Park's publications the possibilities of errors and misinterpretations are so immense that it will take a long time before a satisfactory basis is created for the building up of a systematic procedure. This obtains, too, for the investigations designed to carry the conception of bacillary dysentery to so far illy-understood classes of diseases-the summer diarrheas of infants. I need not remind you of the work of Duval and Bassett, that is well known to you and that seemed to lift a load from the heart of every pediatrist baffled by the capricious and intangible peculiarities of these disturbances. Dysentery bacilli were found in almost all of them, slight agglutinations were considered as sufficient proof for their etiologic meaning.

I do not want to say that nothing of this work will withstand the critic of future investigations, but that in its entirety it will not persist. The mere presence of dysentery bacilli means very little, some even think that they are frequent or normal inhabitants of the infantile intestinal tract. Their etiologic relation to summer diarrhea has not been proven, but in a few cases, although that may be due simply to the insufficiency of our methods. The very careful research instituted with all means of our present knowledge is unable to establish the correctness of the bacillary origin of summer diarrhea in the sense of the authors mentioned, is shown by a late publication in the Journal of Infectious Diseases of February, 1905. Clinical identical cases of ileocolitis were exhaustively investigated without there being any evidence found, that in each of them at least dysentery bacilli were only present, much less that they had any relation to the pathologic process.

As you see, the depth of our knowledge on the relations of Shiga's bacillus to so called dysentery is as yet not very great. The importance of the disease in influencing the public welfare will continue to be a stimulus for further research and elucidation. So far, we may assume that the only benefit derived from the bacteriologic study of dysentery is the recognition of its bacillary origin and of its dissemination. This at least, has given a definite means to work against it-by preventing it.

PRIC

Vesicovaginal Fistulæ.

BY ROLAND HILL, M.D,

ST. LOUIS, MO.

RIOR to the year 1845, vesicovaginal fistulæ, either large or small, were considered to be practically incurable. In this year, J. Marion Sims made the first successful operation in a case of this kind that has been reported. He pared the edges of the fistula, sutured the freshened surfaces together, and was pleased to find his patient cured.

Some years later, another advance was made in the treatment of these lesions, when Thomas A. Emmet showed the necessity of bringing these tissues together without tension, and devised the plan of making parallel incisions through the vaginal mucous membrane so as to entirely relieve tension on the sutures.

In 1894, Machenrodt, of Berlin, conceived a plan of operation applicable to even large fistulæ, that were hitherto considered incurable. His idea was to separate the bladder from the vagina, and suture each separately. This principle is the one that practically underlies the successful treatment of those extensive cases in which the vesicovaginal septum is completely torn across.

Thus, Kelly' states that in operating on cancer of the uterus the bladder is sometimes injured, and a vesicovaginal fistula results. He advises in these cases the opening of the abdominal cavity widely, from side to side, so as to free its (the bladder's) connections from the vaginal vault, and render it moveable.

Read before the St. Charles Medical Society, November 18, 1904.

McGannon, of Nashville,' reports having operated on six cases of extensive fistula, in which the bladder around the lesions was thoroughly freed from its surroundings, and sutured separately, with perfect results.

Paul F. Munde,3 and other observers have reported the suturing of the uterus in position to partly fill the gap in some of these extensive cases, with good results. However, by the use of Machenrodt's principle, it is doubtful if this will often be necessary.

My object in reporting this case today is to call attention to a new method of treatment, applicable to small fistula that has proved a success in my hands, and also in the work of some of my friends.

Mrs. T., white, aged 23 years, was referred to me by Dr. James Stewart, of Holstein, Mo., October 23, 1903. Her previous history is uninteresting, as she had always been in good health.

On January 26, 1903, she was confined; labor started at 12 p.m., and at 10 a.m. the baby was delivered after very severe use of the forceps, the child being stillborn. Immediately after labor, urine began to escape entirely through the vagina, and ran away just as it was secreted, rendering the patient from that time on perfectly miserable.

An examination showed a small vesicovaginal fistula.

On May 13, 1904, an operation was performed for the closure of the fistula, but it failed to heal, and the wound reopened on the third day. A second operation was performed on May 21st, but it was also unsuccessful, as the fistula again became patulent on the fourth day after the operation. A third operation was performed early in June, but failed to produce the desired result, as the fistula began to leak again on the fifth day.

I do not know what technic was employed in these operations.

When she came to me her condition was deplorable, as the urine was all coming through the vagina, rendering the patient most wretched. An examination showed a vesicovaginal fistula that must have entered near the center of the trigone of the bladder. The patient was sent to the Baptist Sanitarium, and on October 23, 1903, operation was performed.

The patient was put under general anesthesia, chloroform being used. The parts were retracted, and the fistula brought