A POISONOUS CONSTITUENT IN CHOLERA STOOLS 



By Ernest W. Goodpasture 



Of the Department of Pathology and Bacteriology, College of Medicine and 



Surgery, University of the Philippines 



The histopathology of the intestine in cholera indicates that 

 if poisonous materials are produced in the intestine, directly or 

 indirectly as a result of the growth of vibrios, they are formed 

 within the lumen of the bowel and n<tf on an inflamed and 

 denuded mucosa, for cholera vibrios are not primarily invaders 

 of tissue. This is in contrast to the lesions found in infections 

 with such toxin poducers as Bacillus diphtherias and B. dysen- 

 teric which regularly produce local necrosis, and which elaborate 

 their poisonous products on and within inflammatory exudate. 

 It is in contrast also to the effect of infection with B. typhosus. 

 which brings about not only a local necrosis but also a bac- 

 teriaemia. 



The vibrios of cholera do not produce an exotoxin and they 

 do not cause septicaemia, two sources of profound intoxication 

 which may be eliminated; and search for the poisonous agent 

 of the disease has led most investigators to the conclusion that 

 it is the endotoxin which has been demonstrated to exist in the 

 substance of these organisms. Pfeiffer was unable to demon- 

 strate a soluble toxin in young broth cultures, but showed that 

 young killed cultures were very toxic. Wasserman confirmed 

 this finding and showed that the toxin exists as a constituent 

 of the bacterial cell, becoming soluble only by disintegration 

 of the cellular body. Strong (l) also demonstrated an intracel- 

 lular toxin, and found that much of it was destroyed by heat at 

 60° C. and that it appeared to be completely destroyed by boiling. 

 He suggests that the stage of most violent symptoms in human 

 cholera may coincide with a period during which rapid dying 

 off of spirilla and, possibly, the setting free of the largest amount 

 of toxic substance occur. 



The sudden and often violent onset of the disease with early 

 collapse, fall in blood pressure, low body temperature, and loss 

 of fluid through the intestine are sufficiently unique to suggest 

 the possibility of a fundamental element in the pathogenesis of 



