Some Factors in the Defense Mechanism against Reinfection with Trypanosoma lewisi

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Abstract
Rats which have spontaneously recovered from a trypanosome infection are highly resistant to reinfection. In an effort to determine the defence mechanism involved, Wistar white rats were infected 2, and even 3 times, with a strain of T. lewisi, the course of infection then being followed by examination of fresh blood taken from the tail or toes, of stained blood smears, of peritoneal fluid, of portions of lymph nodes, liver, spleen, and bone marrow teased apart in saline, and of stained sections. Injn. was intraperitoneal, or, in a few cases, directly into the heart. Massive doses were used, estimated by hemocytometer counts. The tryp-anosomes used in each case were from heparinized blood of a heavily infected donor rat and were concentrated and largely freed from blood cells by a series of centrifugations and dilutions with "normal" saline. The course of reinfection and recovery was observed to be as follows. Tryp-anosomes readily pass from the peritoneal cavity, through the lymph system, into the blood. There some single individuals (which evidence suggests to be dividing cells only) are immobilized, presumably by a trypanocidal antibody, and are then ingested whole by macrophages. After a certain time agglutination of other individuals occurs, or they become entangled within clumps of blood platelets, presumably either by the action of a higher titer of the same antibody or by a distinct "agglutinin." Evidence suggests that the agglutinated clumps are phagocytized in the liver and spleen. All trypanosomes are removed from the blood in from a few minutes to 5 days. The trypanosomes may commence to divide, this apparently not being inhibited by an antibody like the "ablastin" developed during an initial infection. No trypanocidal antibody is present in the peritoneal cavity. One, seemingly exceptional, case is reported of agglutination of donor [red] blood cells in a lymph node.

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