persons suffering from chronic intestinal putrefaction have shown no diminution in the putrefactive products excreted in the urine where the patients have added a soured milk to their usual diet. It is, of course, clear that in cases of this sort the failure of the putrefactive process to decline may be attributable to the introduction of more than the habitual amount of protein material. The observation is, however, of interest in that it emphasizes the fact that the ingestion of lactic acid, even if probably associated with lactic acid fermentation within the intestine, may not suffice to exert any beneficial influence in reducing putrefaction.
I do not wish to be understood as maintaining that the presence of lactic acid in soured milk is of no value in checking intestinal putrefaction. I wish merely to point out that the administration of lactic acid per se can not be regarded as a significant anti-putrefactive procedure. It seems to me probable, on the other hand, that the presence of lactic acid in the large intestine would at least in a degree tend to restrict putrefactive decomposition. But I must own that positive evidence on this point seems to be at the present time entirely wanting. In my judgment only very carefully planned studies would suffice to enable us to form a final opinion on the value of lactic acid as an antiputrefactive agent. We are not justified in developing an enthusiastic attitude toward lactic acid as an agent in the inhibition of intestinal putrefaction on the basis of our present knowledge.
Let us now consider the effects derivable from the bacteria used in lactic fermentation. As an example of a strong lactic acid producer we may take B. bulgaricus, used in the production of lacto-bacilline. This organism is a powerful lactic acid ferment, forming large amounts of lactic acid from milk sugar while forming very little alcohol. The organism grows well in milk and on some media containing an abundance of soluble carbohydrates, as, for instance, in malt extracts. We may take the behavior of B. bulgaricus in the digestive tract as being typical of efficient lactic acid bacilli in general. There are two questions which we must put to ourselves regarding the therapeutic effects of such bacteria. First, to what extent do the lactic acid bacilli replace obligate normal types of bacteria or the undesirable saprophytic forms present in disease? Secondly, to what extent is it desirable that there should be a replacement of the intestinal flora by lactic acid bacilli?
It is one of the fundamental assumptions of the sour milk treatment of intestinal diseases that the lactic acid producing microorganisms establish themselves throughout the digestive tract and through their more or less aggressive growth directly or indirectly inhibit the development of putrefactive or other undesirable forms of bacteria. In some of the statements put before the public in regard to the action
