Goodpasture: Histopathology of the Intestine 



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villi in the first case may possibly be due to direct action of 

 absorbed toxic material, but it is not constant and, in the 

 absence of degenerative changes in the overlying epithelium, it 

 seems more probable that some local condition within the villi 

 is responsible for it. It is not a progressive degenerative 

 change, and the necrotic cells are rapidly phagocytized. Mac- 

 Callum(5) speaks of a widespread necrosis of the intestinal 

 epithelium in cholera. This I have not seen. 



In the presence of subepithelial oedema disconnecting the epi- 

 thelial sheet from its basement membrane it can be readily 

 understood how the least mechanical disturbance or post-mortem 

 maceration would be sufficient to strip off this layer, especially 

 from the more-exposed folds and villous projections. Even after 

 the tissue is fixed the utmost care is necessary in embedding to 

 prevent its removal. Preparations from the intestine of an 

 executed criminal used for comparative study, fixed within one 

 hour after death, show many denuded villi, evidently the result 

 of mechanical dislodgment. 



However, the abundant surface growth of intestinal bacteria 

 with penetration of some of these organisms beneath the epi- 

 thelial coat and into the tissue of villi in the lower portions of 

 the ileum, as demonstrated in the first case, cannot be attributed 

 altogether to post-mortem activity, and the desquamation of 

 epithelium here is out of proportion to that in the duodenum 

 and the jejunum; yet in this case there is no necrosis of epithe- 

 lium nor indication of inflammatory reaction. Patients dying of 

 cholera may lie in a moribund state with barely perceptible 

 pulse for some time before death. The child (case 1) under 

 consideration was in this dying state for at least two hours. 

 Under such conditions active growth of intestinal bacteria, espe- 

 cially in the lower ileum, and the presence of digestive enzymes 

 in the intestinal fluid would seem sufficient to macerate the 

 projecting epithelial layer so that it may soften and fall away, 

 thus admitting bacteria whose penetration and growth can no 

 longer elicit an inflammatory response. In fact, this was shown 

 in case 2, but it is not a part of the disease ; it is the beginning 

 of disintegration. 



That ulceration of intestinal mucosa can occur in the course 

 of the disease is evident from the presence of desquamated 

 epithelium in the stools during life and the occurrence of diph- 

 theritic enteritis or even necrosis of the intestinal wall post 

 mortem. This must be regarded, however, as a complication 

 and not a part of the pathology of typical cholera. 



