418 The Philippine Journal of Science 1923 



tions. There are karyolysis and faintly staining cytoplasm, 

 although the outlines of cells are in position. In places where 

 the process of disintegration is more advanced, there are com- 

 plete disappearance of nuclei and dissolution and softening of 

 epithelium with dislodgment of fragments, leaving the tips of 

 villi denuded; but there is no inflammatory reaction in these 

 places. Overlying such areas is an abundant growth of bacilli, 

 giving the impression that they are partially responsible for 

 this rapid disintegration ; rarely, however, are they found within 

 subepithelial spaces, and then only where epithelium has disap- 

 peared at some point. 



In contrast to this evident post-mortem disintegration there 

 are minute areas of ulceration, obviously ante mortem, for there 

 is necrosis of epithelium, fibrin thrombi in capillaries and veins, 

 as well as polymorphonuclear and epithelioid cell infiltration. 

 In the superficial necrosis there is a sharply limited zone of 

 bacilli having the morphology of Bacillus coli, and these bacilli 

 are evidently responsible for the lesion. In the preparations 

 no vibrios are demonstrable on the surface, in the lesions, or 

 within glandular crypts. Had this intestine been examined an 

 hour or so later there would undoubtedly have been extensive 

 desquamation and the areas of ulceration could easily have been 

 overlooked. Agglutinable vibrios were demonstrated in cultures 

 post mortem. 



It seems almost too obvious for further consideration that, 

 if ulceration occur in cholera before the agonal period, an 

 inflammatory reaction will appear which can be easily identified. 

 Yet a third case in this series, autopsied one hour and fifteen 

 minutes after death, showed even more strikingly evidences of 

 ante-mortem necrosis of epithelium and ulceration due certainly 

 in part to the local action of vibrios. 



This case also was an adult Japanese. The patient, a male, 

 aged 28 years, was admitted to the hospital three hours after 

 the onset of illness. He was in complete collapse, pulse hardly 

 perceptible, extremities cold, with clammy perspiration and 

 cramps. Bowels had moved twice; stools watery in character. 

 The diagnosis, clinically and bacteriologically, was cholera. He 

 died on the sixth day of illness, showing toward the end indica- 

 tions of uraemia. On opening the peritoneal cavity one hour and 

 fifteen minutes after death the upper portion of the small 

 intestine was found to be tremendously distended with gas and 



