130 INFECTION 



duced by bacterial action upon various albumens, these toxic, alkaloid- 

 like substances being known as ptomains. It was soon found, however, 

 that the ptomains produced by pathogenic bacteria were insufficient of 

 themselves to cause the symptoms and lesions characteristic of the re- 

 spective microorganisms; that they were in general less toxic than the 

 cultures themselves; that the majority of ptomains are not very poison- 

 ous; and that they are not specific, since equally potent ptomains are 

 produced by non-pathogenic bacteria. This lack of specificity is in 

 sharp contrast to the toxins. No matter upon what medium a true 

 toxin producer is grown, the toxin is qualitatively the same, whereas the 

 nature and toxicity of ptomains depend upon the microorganism, the 

 culture-medium used, the duration of growth, and the quantity of oxygen 

 furnished. The same microorganism, when grown on different media 

 or under different conditions, may produce totally different ptomains. 



Ptomains may, however, produce disease, and even death, when they 

 are ingested with food that has undergone bacterial decomposition. In 

 most instances of meat-poisoning, however, which are frequently as- 

 cribed to the presence of ptomains, a specific microorganism, the 

 Bacillus botulinus, or a member of the Bacillus enteritidis group of 

 Gartner, is usually responsible. The commonest sources of ptomain 

 poisoning are improperly preserved meats, fish, sausages, cheese, ice- 

 cream, and milk. This subject received full consideration in Vaughan 

 and Novy's " Cellular Toxins." 



Besides occurring in food-poisoning, ptomains may be formed as the 

 result of putrefactive processes going on in abscesses, gangrenous areas, 

 and within the gastro-intestinal canal, and enough of these may be 

 absorbed to produce symptoms of intoxication. Under these condi- 

 tions it is possible for bacteria to produce ptomains that may be absorbed 

 and produce symptoms of intoxication without the bacteria themselves 

 actually gaining entrance to the tissues, and therefore not constituting, 

 according to our definition, a true infection. Pernicious anemia, 

 chlorosis, and allied conditions have been ascribed to the absorption of 

 such ptomains from the intestinal canal. Obviously it is difficult or im- 

 possible to always differentiate between bacterial toxins and bacterial 

 ptomains, or the products of protein decomposition dependent upon 

 bacterial activity, and we can but admit the possibility of the produc- 

 tion and absorption of both bacterial toxins and ptomains under certain 

 pathologic conditions. Most ptomains probably are produced as the re- 

 sult of decomposition of the dead protein medium upon which the bacteria 

 grow, and to a lesser extent by the destruction of the bacterial cells them- 



