520 Messrs. W. E. Bullock and W. Cramer, On a New 



There can be little doubt that the presence of certain simple chemical 

 constituents of the soil which have the property of producing the kata- 

 phylactic phenomenon is responsible for the occurrence of gas gangrene and 

 of tetanus. This statement does not imply that every case of gas gangrene 

 and of tetanus can be accounted for in this way. Experimentally, mice 

 infected with detoxicated B. Welchii and exposed to cold have occasionally 

 developed gas gangrene. As a rule, gas gangrene does not develop in mice 

 exposed to cold either before or after the injection of a suspension of B. 

 Welchii. But out of 16 mice, two animals, in which the exposure to cold 

 had been exceptionally severe so that the animals were already ill when they 

 received the injection of B. Welchii, did develop gas gangrene. The experi- 

 ments with cold are complicated by the fact that mice frequently develop an 

 enteritis as the result of a severe exposure to cold. The general depression 

 of the vitality of an animal which has received such a severe exposure to 

 cold may be reasonably assumed to involve also the processes of lysis and 

 phagocytosis which constitute the defensive mechanism of the infected 

 animal against the infected bacteria, and thus account for the development 

 of gas gangrene in the two positive experiments. In the human subject, 

 where such a depression may be the result not only of exposure to cold but 

 also to shock, it will probably be responsible also for the development of gas 

 gangrene in some cases. But it cannot be looked upon as the only or even 

 most frequent exciting cause, since gas gangrene develops in men who, apart 

 from the wound, are in good health, are not in a state of shock, and have not 

 been exposed to cold. 



There is another way in which tetanus and gas gangrene can be produced 

 experimentally in animals infected with the detoxicated bacteria without 

 making use of the phenomenon of defence rupture. Tulloch* has shown that 

 tetanus spores will produce tetanus in guinea-pigs if they are injected together 

 with a non-lethal dose of the toxin of B. Welchii. We have found that gas 

 gangrene can be produced in mice if the detoxicated B. Welchii are injected 

 together with diphtheria toxin, which happens to be non-lethal for mice but 

 has a transient local action. The explanation of this fact is probably to be 

 found in the aggressin-like nature of the toxins. We have pointed out in 

 the introduction that the toxin of B. Welchii acts at first by paralysing the 

 defensive mechanism of lysis and phagocytosis by which the animal defends 

 itself against infection with the detoxicated B. Welchii, and diphtheria toxin 

 has probably a similar effect in mice. It seems possible, therefore, that the 

 presence of a n-on-specific and non-lethal toxin with an aggressin-like action 

 may have to be considered as a factor in the causation of gas gangrene or of 

 * Tulloch, ' British Medical Journal,' June 1, 1918. 



