BACTERIAL METABOLISM WITHIN THE BODY 699 



mentation of its activity beyond normal. Indol and other substances are 

 formed in increased amounts and, for a time at least, appear to be ab- 

 sorbed from the intestinal contents [which are not desiccated at these 

 levels] into the blood stream. Very shortly thereafter the normal capacity 

 of the liver to oxidize the indol to indoxyl, and to pair the latter with 

 sulphuric acid [or, more accurately, with the monopotassium salt of sul- 

 phuric acid] is exceeded, and there is an overflow of indol into the general 

 circulation. 



Normally, the indol and phenols, and other products arising from the 

 bacterial decomposition of aromatic amino acids, are oxidized in the liver, 

 as indicated in a preceding article, before they enter the general circu- 

 lation. They are excreted from the circulation chiefly as aromatic sul- 

 phates, but whenever the available sulphate is decreased in amount, the 

 body produces glycuronic acid, and pairs these aromatic nuclei with that 

 substance prior to elimination through the kidneys into the urine. By 

 this process the body is rid of these somewhat toxic putrefactive sub- 

 stances, their toxicity being reduced materially by the dual process of 

 oxidization and pairing with sulphuric or glycuronic acid. 



The phenomena of intoxication ordinarily ascribed to indol, and 

 probably participated in by other aromatic residues of amino acids, are 

 frequently associated with one or more of three factors; first, the con- 

 tinued production of unusual amounts of indol formed in the alimentary 

 canal as the result of an unsuitable amount of protein in the diet, or 

 persistent intestinal stasis, or both. This may lead to the absorption of 

 amounts of the aromatic nucleus beyond the normal capacity of the liver, 

 and the excess of indol then may appear as such in the general circulation. 

 Secondly, defective oxidative power of the liver, leading again to the sys- 

 temic flooding with indol; or, finally, an impaired power of combining 

 the oxidized indol with sulphuric or glycuronic acid. 



Any of these processes, imperfectly carried out, may result in the 

 slow, cumulative effects which eventually are recognized clinically by 

 lassitude, malaise, headache, and dizziness, and other symptoms spoken 

 of as "auto-intoxication." 



It is quite as possible for an individual to suffer from an excessive 

 production of lactic acid of intestinal origin as it is to be injured by an 

 overproduction of indol or other bacterial derivatives of the aromatic 

 amino acids. Such conditions have been described by Escherich, Finkel- 

 stein and Salge. The few cases on record occurred in young children, 

 once in almost epidemic proportions, in a hospital in Gratz. 



The causative factor appears to be an upward extension of the normal 

 zone of growth of Bacillus acidophilus, or a closely related organism, into 

 the small intestine. The most prominent symptom is a profuse, watery 

 diarrhea. The dejections are yellowish and have a very sour smell. The 

 acidity in the few cases studied was found to be four to eight or even 



