Andrew Watson Sellards AND
Max Theiler
From the Department of Tropical Medicine Harvard Medical School Boston, Massachusetts
I
1. Specimens of feces containing cysts of E. histolytica butno trophozoites were injected directly into the large bowelof kittens. Using material not more than six days old, 6 outof 8 animals were infected.
2. The circumstances of the experimentssuggest very stronglyindeed that excystation occurred in thelarge bowel.
3. Additional evidence was obtained that stasisis an importantfactor in producing an infection of the intestinewith E. histolytica.
II
4. Kittens were infected with E. histolytica and the large intestinewas then deprived of its normal supply of water by placing aligature around the gut.
5. The amoebae disappeared promptlyin three animals in whichthis procedure was carried out earlyin the course of the infection.The progress of the diseasewas not checked in one animal inwhich the operation was delayedfor several days after symptomsappeared.
III
6. According to our conception, the cysts of E. histolyticawhen ingested by mouth are carried rapidly by peristalsis throughthe small bowel and set up lesions at points of stasis in thelarge intestine. In 3 kittens amoebic infection of the colonreadily invaded the ileum when the ileo-colic sphincter wasrendered functionless. Under the conditions of these experiments,the sphincter was an important factor in the mechanical protectionof the ileum.
7. In 3 animals, ligation of the small boweland inoculationof active amoebae immediately above the ligaturefailed to producean infection. This failure to produce a primaryinfection ofthe small intestine suggests that the environmentalconditionsin the ileum are somewhat unfavorable for the developmentofamoebae. It does not necessarily indicate that the mucosaperse of the ileum is less susceptible than that of the colontothe action of E. histolytica.