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 

 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. 



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 intraintestinally. 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 

 injured by the actual growth of the living bacteria. Kruse calls 

 attention to experiments by Burgers in which enormous quantities of 

 cholera poison, i. e., 200 cultures of dead or living cholera bacilli, 

 could be administered to healthy guinea pigs and rabbits by mouth 

 without harm in spite of the fact that these animals are definitely 

 susceptible to the poisons and although the poisons are not injured 

 by the intestinal ferments. It is likely therefore that the absorption 

 of poison begins only after the bacteria have extensively invaded the 

 intestinal mucosa and, by injuring tissue, have opened paths for ab- 

 sorption. In thei case of diphtheria probably a similar condition 

 exists in that the localized injury to the mucous membrane at the 

 point of lodgment of the primary infection prepares a portal of 

 entry. The poison of the Bacillus botulinus alone seems to form an 

 exception to this rule, 33 since this substance, though apparently a 

 true bacterial toxin, is absorbed directly from the intestinal canal. 

 With most bacteria this problem does not arise, since the poisons are 



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'Inst. Past., Vol. 13, 1899. 



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

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

 Vol. 4. 



33 Madsen in "Kraus u. Levaditi, etc.," Vol. 1. 



