WILLIAM H. TALIAFERRO 685 



infection, which proceeds by crises and relapses, one of the two possible effects of 

 resistance is operative, i.e., the host's resistance is directed toward a destruction of the 

 parasites after they are formed but not toward an inhibition of the rate of reproduc- 

 tion per se. 



A long series of investigations are in accord in showing that the wholesale de- 

 struction of the trypanosomes at each crisis is due to the sudden acquisition by the 

 host of a trypanolytic property of its serum and that the trypanosomes reaccumulate 

 during the relapse, not because the trypanolysin disappears, but because the trypa- 

 nosomes become biologically altered so that they are no longer susceptible to the 

 trypanolysin. 



The first investigators to recognize the phenomenon of trypanolysis were probably 

 Schilling (1902), Lingard (1904), and Franke (1905). The last also noted that the 

 blood of the host could contain both trypanosomes and strong trypanocidal anti- 

 bodies, which led him to point out that such parasites had evidently become biologi- 

 cally changed from the original strain and resistant to the antibodies. Credit is due 

 Rodet and Vallet (1906) for the first systematic study of the lysins arising during the 

 course of uninfluenced infections and their relation to crises and relapses. Massaglia 

 (1907) showed that a definite correlation exists between the crisis and the lytic prop- 

 erty of the serum. Thus, when tested against the original strain of trypanosomes, 

 serum from a guinea pig before the crisis was only slightly lytic, whereas during and 

 after the crisis it was strongly lytic. Furthermore, serum collected during and after 

 the crisis had no deleterious effect on the trypanosomes reappearing after the crisis. 

 This is clear experimental proof that the trypanolysin which effected the crisis re- 

 mains in the blood (as shown by the activity of the serum against the original passage 

 strain) and that the trypanosomes accumulate during the relapse because they have 

 become biologically altered so that they are no longer susceptible to the lytic prop- 

 erty. The work of Massaglia was greatly extended by Levaditi and Muttermilch 

 (1909) who showed that trypanolysis like other immune lytic phenomena is a "com- 

 plement-amboceptor" reaction, and by Leger and Ringenbach (1911a and b) who 

 found the usual group specificity between a given trypanolytic immune serum and 

 different species of pathogenic trypanosomes. 



Simultaneously with the studies of these investigators, others, chiefly Ehrlich 

 and his co-workers, were demonstrating the biological difference between the original 

 strain of trypanosomes and the relapse strain in mice incompletely cured with drugs. 

 Previous to their experiments, Ehrlich and Shiga (1904), Halberstaedter (1905), and 

 Franke (1905) had shown that if a mouse is cured of an infection with a pathogenic 

 trypanosome, it is refractory for about twenty days to a second infection with the 

 same strain of parasites. Ehrlich (1909), Ehrlich, Roehl, and Gulbransen (1909), 

 Rosenthal (1913), and Ritz (1914) found that the original strain of trypanosomes 

 and the relapse strains were so different as to be differentiable by cross immunity 

 tests. Thus, a mouse, infected with the original (passage) strain of trypanosomes and 

 cured, is refractory to a second infection with the passage strain, but can be infected 

 with a relapse strain and vice versa. With the same methods, Ritz (1916) dift'eren- 

 tiated the original and relapse strains arising during the uninfluenced course of an 

 infection in the rabbit. 



