866 IMMUNOLOGY 



inhibited, these infections may be considered with the constantly repro- 

 ducing experimental infections discussed in this section. 



Little is known about natural immunity because, as pointed out in 

 the consideration of the T. lewisi group of trypanosomes, the rate of 

 reproduction of the trypanosomes cannot be measured directly and few 

 attempts have been made to raise the rate of reproduction ( see T . duttoni 

 in the mouse) or to increase the percentage of surviving trypanosomes. 

 Nieschulz and Bos (1931), however, reported a slightly shorter incuba- 

 tion period in dogs infected with T. evansi as the result of splenectomy. 



Acquired immunity, which develops later and which is superim- 

 posed on any natural immunity which may be present, is entirely para- 

 siticidal, with no evidence of an inhibition of reproduction. When the 

 infection shows a typical acute rise in numbers, the first manifesta- 

 tion of acquired immunity is a crisis (see guinea pig, in Figure 193). 

 Thereafter, one or several relapses and crises follow. When a pro- 

 longed chronic low-grade infection ensues, with no typical acute rise 

 as in Figure 192, it is probable that parasiticidal effects of acquired 

 immunity, similar to those produced at the two typical crises later, hold 

 the numbers down. Since all the animals die, the acquired immunity 

 is obviously ineffective. In other words, once the parasites are intro- 

 duced into the host, they reproduce during the entire infection, and 

 although at intervals most of those that have accumulated in the blood 

 are destroyed, the few that escape destruction repopulate the blood 

 again and again until the host dies. 



An extensive series of in vivo and in vitro investigations (see Laveran 

 and Mesnil, 1912; W. H. Taliaferro, 1929, for reviews of the pioneer 

 work) indicate (1) that the periodic destructions of the trypanosomes 

 are due to typical trypanolysins which can be demonstrated in vivo and 

 in vitro and which are acquired by the host as a result of specific infec- 

 tion or specific immunization; (2) that the trypanosomes reaccumulate 

 during the relapses not because the trypanolysins disappear, but be- 

 cause the parasites have become resistant to them; and (3) that the 

 relapse trypanosomes differ antigenically and that the majority of them 

 are subsequently killed by a new trypanolysin. In all of this work, the 

 strains of trypanosome used and their continuous maintenance are of 

 paramount importance. The experimental infection is started with what 

 is known as the passage strain and is usually maintained in mice by 



