In a Preliminary Note [Comptes rendus, t. 165, 1917, p. 373] I described a filtering microbe found in the excreta of convalescents from bacillary dysentery. The use of a technique less perfect than the one I had used at first [Comptes rendus du la Société de Biologie, séance du 7 décembre 1918] combined with the systematic examination of the stools of thirty-four patients, all suffering from dysentery due to Shiga bacilli, and several of whom could be followed daily from the beginning of the illness until the end of convalescence, allowed me to study in a more complete manner the mode of action of the bacteriophage microbe and to specify its role in the evolution of the disease.
In cases of bacillary dysentery, even very serious ones, but in which the patient’s condition improves rapidly, the bacteriophage microbe manifests its presence in a very active manner from the outset, both on cultures of the bacillus isolated from the patient’s excrement and on laboratory Shiga strains, from the moment when the symptoms begin to improve. The bacteriophage power with respect to the dysentery bacillus abruptly ceases to be detectable at the beginning of convalescence. From this moment on, repeated examinations also show the absence of pathogenic bacilli.
In cases where the disease is prolonged, the bacteriophage microbe shows only a nonexistent or slightly marked action, as long as the patient’s condition remains stationary. If, in some cases, the bactericidal action is relatively high on strains which have undergone numerous passages on culture media, on the other hand, it is always inappreciable or very weak on cultures of the bacillus coming from the patient under observation. The improvement is manifested as soon as the bacteriophage action becomes energetic with respect to the latter.
In long-term and relapsing forms, the bacteriophage power of the filtering microbe may, at certain times, be very energetic with respect to cultured bacilli and variable from one day to the next, although always relatively weak, with respect to the patient’s bacillus. Recovery closely follows the moment when the action of the bacteriophage microbe manifests itself in an equally intense manner for both strains. This action persists, with fluctuations in activity, as long as the patient remains a carrier of germs. This latter fact would even be likely to facilitate the detection of germ carriers, the detection of the bacteriophage microbe being simpler and more reliable than the search for the pathogenic bacillus in the stools.
I was able to verify that the action of the bacteriophage microbe was preponderant, not only with regard to the disappearance of the dysentery bacillus from the intestine once the disease had declared itself, but also during its outbreak. During the recent epidemic, I had the opportunity to observe several extremely mild cases in which the symptoms were limited to a few sputum and two or three diarrheal stools: now, in all these cases, the bacteriophage microbe was, from the beginning, present and endowed with a high antagonistic power. Despite the benignity of the affection, it was indeed dysentery because, in three of these cases, I was able to isolate from the first diarrheal stool emitted a typical Shiga bacillus.
The bacteriophage microbe pre-exists in the intestine where it normally lives at the expense of B. coli. In normal stools, its antagonistic power towards the latter bacillus is always very weak; it can become considerable in various morbid states, in certain forms of enteritis and common diarrhea, for example. The presence of dysenteric bacilli in the intestine first determines a considerable exaltation of the virulence of the bacteriophage microbe towards B. coli, then, by a more or less rapid habituation, this virulence is exalted towards the dysenteric bacillus; it immediately or gradually reaches a considerable power leading to the rapid or gradual disappearance of the pathogenic bacillus. If the virulence of the bacteriophage microbe is immediately exalted [“very active”?], the dysenteric bacilli are destroyed from the start of their culture in the intestinal contents, the disease aborts before any symptoms or is limited to a few temporary disorders. If, for a cause which remains to be determined, the virulence of the bacteriophage microbe with respect to the pathogenic microbe does not manifest itself immediately or only manifests itself weakly, a fight is established between the two organisms, the dysentery bacilli multiply in the intestinal contents, infiltrate the mucous membrane, the disease breaks out and the patient’s condition then faithfully records the fluctuations in the fight. In summary, the pathogenesis and pathology of bacillary dysentery are dominated by two opposing factors: the dysentery bacillus, the pathogenic agent, and the filtering microbe bacteriophage, the agent of immunity. As a corollary, the experiment on the rabbit shows that cultures of the bacteriophage microbe have a preventive and curative power in the experimental disease; on the other hand, the bacteriophage microbe is invariably present in the intestine of the sick as soon as the symptoms improve; it therefore seems logical to propose, as a treatment for bacillary dysentery, the administration, as soon as the first symptoms appear, of active cultures of the bacteriophage microbe.
A Smaller Flea 