BACTERIAL POISONS 39 



are not conceived as specific for individual bacteria but may be 

 formed from all bacterial proteins, both the pathogenic and the non- 

 pathogenic. The differences in pathogenicity between bacteria of 

 this class would then depend entirely upon their powers to invade 

 not at all upon their possession of individually peculiar cell poisons. 

 The differences in clinical course and toxemic manifestations would 

 1 be taken to depend entirely upon the accumulation and the distribu- 

 tion of the invading germs, and the consequently variable energy in 

 the production of the toxic split products from them. Considerable 

 experimental evidence has accumulated in favor of this point of 

 view. We will reserve a consideration of this for a later chapter. 



The entire question of "endotoxins," or rather the problem of 

 the mechanism by which such bacteria as typhoid bacilli, plague 

 bacilli (and other organisms which do not produce exotoxins) poison 

 the animal body, must be subjected to experimental revision. In 

 addition to the idea of toxic split products in the sense of Vaughan 

 and Friedberger, there are other alternatives. Jobling and Petersen 

 have shown that bacteria injected into the circulation may absorb 

 lipoidal substances which ordinarily act as anti-enzymes. In con- 

 sequence of this, serum protease may be liberated to act upon the 

 plasma itself, and produce toxic substances. 



Again, it is well known that the bacterial cells are relatively 

 poor in coagulable protein, and we have shown with one of our stu- 

 dents (Aronovitch) that primary and secondary proteoses may be 

 obtained in considerable quantities in bacterial extracts. It is not 

 impossible that these in themselves may have toxic functions when 

 liberated, without further splitting. This particular subject finds a 

 more extensive discussion in the chapter on bacterial anaphylaxis. 



In order to do injury to the infected individual the bacterial 

 poisons must be produced in such locations that they can easily enter 

 the physiological interior of the body. None of the poisons that 

 have been so far investigated can produce injury when introduced 

 into the alimentary canal. In this location they are, as a rule, de- 

 stroyed, or they pass through without doing harm. Neither diph- 

 theria toxin nor tetanus toxin will produce symptoms when intro- 

 duced intra-intestinally. 27 28 29 30 Even cholera poison does not pass 

 through the uninjured intestinal wall. Kruse 31 assumes, and Kolle 

 and Schiirmann 32 seem to agree with him, that the absorption of 

 cholera poison does not occur until the intestinal wall has been in- 



27 Meyer and Gottlieb. "Exp. Pharmakol.," Urban & Schwartzenberg, 

 Berlin, 1911. 



28 Ransom. Deutsche med. Woch., No. 8, 1898. 



29 Nencki. Centralbl. f. Bakt., Vol. 23, 1898. 



30 Carriere. Ann. de I'lnst. Past., Vol. 13, 1899. 



31 Kruse. "Allgemeine Mikrobiologie," Vogel, Leipzig, 1910, p. 934. 



32 Kolle and Schiirmann in "Kolle u. Wassermann Handbuch," 2d Ed.. 

 Vol. 4. 



