BACTERIAL METABOLISM WITHIN THE BODY 7u 



usually may be predicted. Secondly, apparent exceptions to the practical 

 working out of these principles may be caused by the abrupt development 

 of latent, unrecognized organisms whose activities are favored by the 

 regimen which controls those of the primary infective agent. 



Such instances are not indicative of a failure of the principle; in 

 fact, they are supplementary evidence of the correctness of the principle. 

 They do suggest the necessity of a complete survey of the residual intestinal 

 flora as a basis for the formulation of a correct dietotherapy. The 

 gradual, or rapid, reestablishment of a normal lactic acid flora, antago- 

 nistic to the development of the dysentery bacilli was readily determined 

 by direct examination of the fecal flora, by cultural methods, and by 

 chemical determinations of lactic acid. The shifting of the metabolism 

 of intestinal organisms of the colon type was rendered probable. The 

 shifting of the metabolism of the dysentery bacilli from toxicogenic to 

 acidogenic was surmised. It could not be definitely proven. 



The clinical results were, generally speaking, favorable. In no in- 

 stance was any harm to the patient discernible. If it were possible to 

 determine the initial damage to the patient by the dysenteric infection 

 before specific food therapy was started, much more accurate statements 

 could be made with reference to the probable beneficial effects of dietary 

 treatment as a means of preventing subsequent poisoning. It may be 

 stated without reservation that whatever was accomplished by direct 

 dietary interference with the antagonistic activities of the dysentery 

 bacilli was entirely in the interest of the host. 



It is unfortunate that accurate chemical studies of the metabolism of 

 at least a few of the cases so treated could not have been made. It 

 was apparent that the dysenteric intoxication produced a deep-seated and 

 unfavorable effect upon the metabolic processes of these patients. 



The only available evidence is qualitative, not quantitative. The re- 

 duction of signs and symptoms of toxemia, the general suggestion of an 

 amelioration of the severity of the infection, improvement of intestinal 

 conditions with respect to digestion, and a tendency toward a relatively 

 early recovery from loss of weight suggested that those same dietary 

 factors which would theoretically restrict the pernicious activities of the 

 invading microbe were favorable to the return of the host to a normal 

 state. 



Although metabolic studies upon dysentery cases fed with the lactose- 

 protein diet are not available, the effects of the Shaffer-Coleman high 

 calorie diet in typhoid fever offer a somewhat parallel condition. It 

 has long been known that there is a "toxic destruction of body protein" 

 in infectious febrile diseases, as typhoid, which is probably due in part 

 to 'simple pyrexia, and in part attributable to the toxins originating with 

 the organisms causing the morbid condition. The loss of tissue nitrogen 

 and of body weight may be very considerable in typhoid fever, particu- 



