Some Factors in the Defense Mechanism against Reinfection with Trypanosoma lewisi

Abstract

Early in experimental studies on Trypanosoma lewisi it was discovered that rats having spontane ously recovered from an infection are refractory to reinfection (Kanthack, Durham and Blanford1). The immunity thus acquired lasts, with an occasional exception, for life of rat. The numerous immunological studies with T. lewisi have been chiefly centered on determining factors involved in recovery of rats from an initial infection (Taliaferro,2 Regendanz and Kikuth,3 and others). Our knowledge of defense mechanism against reinfection is at present meager and largely based on in vitro studies. Only a few observations have been made directly on parasite during course of reinfection. Laveran and Mesnil4 noted that when recovered or hyperimmunized rats are inoculated intraperitoneally with living T. lewisi parasites seldom appear in circulating blood. They be lieved that phagocytosis was chief mechanism involved in both active and passive immunity. Agglutination of parasites was observed by Laveran and Mesnil, but they did not consider it an important event in defense mechanism since parasites were apparently uninjured by reaction. Recent workers have generally failed to observe typical phagocytosis of trypanosomes. Taliaferro5 has noted trypanosomes attached to leucocytes under conditions similar to experiments of Laveran and Mesnil and when inactivated immuna rat serum was mixed with washed T. lewisi and washed guinea pig leucocytes. It would appear that, at present time, phagocytosis is not con sidered to be important or usual manner of destruction and disposal of T. lewisi in either initial infection or in reinfection. Taliaferro5 injected intravenously large quantities of washed adult trypanosomes into recovered rats? but otherwise normal?and also into recovered rats splenectomized during course of their initial infection. In first experiments, 27 rats were inoculated from 6 to 325 days after end of initial infection. There was no apparent correlation between length of time from recovery to second inoculation and duration of reinfec tion. No reproduction by parasites was noted in 8 rats whose reinfections lasted from 2 to 3 days. Dividing forms occurred in 6 rats whose reinfections lasted 2 to 13 days and, for others, trypano somes remained in blood too short a time to determine reproductive activity. In many of rats recovery was apparently rapid, since the parasites were swept from blood in 5 to 15 minutes. To what extent reproduction developed and whether a numerical increase of trypanosomes occurred is not stated. In splenectomized series, 10 rats were reinfected from 31 to 353 days after end of initial infection. The reinfec tions lasted from 1 to 40 days and in 2 rats slight variation of trypanosomes but no division was noted. It was concluded that, in most cases, trypanocidal antibody is so strong in recovered rats that it is largely effective before ablastin (repro duction-inhibiting antibody) has time to play any particular r?le. The nature of trypanocidal antibody has not been determined, but according to Taliaferro,6 it is a lytic antibody which may act as an opsonin in vivo. In vivo studies, thus far, have failed to indicate specific character of this antibody. From a review of literature it would appear that in most attempts to establish reinfection experimental animal was injected intraperitoneally with a dilute suspension of infective blood. Since trypanosomes injected into peritoneal cavity must traverse one or more lymph nodes before they can enter blood stream, possibility was early considered that in spontaneous recovery lymph nodes might become sensitized and thus produc? an effective barrier against parasites entering circulation. In present study, experiments designed to gain information on this question clearly demon strated that trypanosomes pass without hindrance