420 The Philippine Journal of Science m» 



DISCUSSION 



Until the relation of vibrios to the inflammatory process in 

 the third case was observed, it seemed to me very doubtful that 

 vibrios of cholera were ever directly responsible for intestinal 

 ulceration. Evidently they are capable of invading tissue 

 locally and inciting an acute inflammatory process with poly- 

 morphonuclear leucocytic exudate. This fact is of importance 

 for understanding the pathology of the intestine in cholera and 

 is suggestive with respect to the pathogenesis of the disease. 

 Since cholera vibrios are capable of tissue invasion and the 

 production of ulceration and inflammatory exudate, it seems 

 obvious that, if desquamation of epithelium occurred to any 

 extent ante mortem, the pathology of the intestine would be 

 very different from what it is found to be, unless desquamation 

 is always followed by immediate death before inflammatory 

 reaction can occur. We would expect to find an acute ulcerative 

 enteritis the typical lesion, but this is the exception, and prac- 

 tically always late in the disease after reaction has begun. The 

 finding of desquamated epithelium in cholera stools means ulcera- 

 tion of the mucosa if the patient survives. 



The evidence at hand indicates that it is the growth of vibrios 

 within the lumen of the small intestine that is directly or 

 indirectly responsible for the production of intoxication, and if 

 toxic substances are formed in the intestine they are at first 

 absorbed through a mucous membrane which is anatomically 

 intact except for oedema. 



Whether the constant subepithelial oedema is caused by direct 

 action of injurious intestinal material or is a result of splanch- 

 nic congestion associated with general intoxication is an open 

 question. Experimental evidence shows the possibility that the 

 latter may be the correct explanation. 



Toxic protein products, such as those derived from closed 

 duodenal loops in experimental intestinal obstruction in dogs, 

 when injected intravenously into dogs cause a profound splanch- 

 nic congestion, especially of the upper portions of the small 

 intestine, associated with a rapid excretion of intestinal fluid. 

 Histologically, the congested intestinal mucosa shows a similar 

 accumulation of fluid beneath the epithelial layer which becomes 

 elevated, especially over the villi, to a degree equal to that found 

 in the intestine of cholera, and this change is also most marked 

 in the duodenum and the jejunum. The presence of fluid here 

 represents apparently a phase in the great excretory activity of 

 the intestine. The necrosis of a few cells at the tips of the 



