IMMUNOLOGY 857 



in the blood on the fourth day after infection and then drop precipitously 

 until on the tenth day of the infection they reach a low level (at location 

 1, in Figure 189), from which they do not thereafter deviate. Provided 

 such a large number of adult trypanosomes are injected intravenously 

 that they appear in the blood and can be studied immediately, the coeffi- 

 cient is low on the first day and rises precipitously, as may be seen in 

 control rat 980 in Figure 190. The inhibition of reproduction, as will 

 be shown later, is due to the development of an acquired immunity 

 involving an antibody which has been called ablastin (W. H. Taliaferro, 

 1924, 1932). The rate of reproduction of T. leivisi is similarly retarded 

 and inhibited when grown in an abnormal host, the guinea pig, as 

 ascertained by Coventry (1929) . Essentially the same results were found 

 for T. duttoni in the mouse, except that the rate of reproduction is never 

 as high and is not as completely inhibited, according to W. H. Taliaferro 

 and Pavlinova (1936) and W. H. Taliaferro (1938). Hence the 

 trypanosomes are never as numerous during the acute rise and may 

 increase slightly in numbers during the first part of the developed infec- 

 tion. T. ioivensh in the striped ground squirrel, as described by Rouda- 

 bush and Becker ( 1934) , closely parallels the development of T. duttoni. 

 Since T . nabiasi in its natural host, the rabbit, increases in numbers only 

 during the first few days of the infection and thereafter does not show 

 division forms, as reported by Kroo (1936), the rate of reproduction 

 of this trypanosome may also be inhibited. 



The question arises : Is there a natural immunity during the acute rise 

 of these infections? For it must be realized that in spite of the rise in 

 numbers a constant percentage of the parasites formed may be being 

 killed as was demonstrated in malaria. There are two ways of demon- 

 strating natural immunity. The first applies to the death of the organisms 

 and can be used only in such infections as malaria, in which it can be 

 demonstrated that all of the progeny formed do not survive. This is 

 impossible in the trypanosome infections, in which reproduction is not 

 synchronous and in which no method of ascertaining the total number 

 of progeny produced has so far been devised. The second method applies 

 not only to the death of the organisms, but also to the rate of reproduc- 

 tion, and involves various procedures such as comparisons of the same 

 species in various hosts and splenectomy combined with blockade. Posi- 

 tive experiments of this kind will indicate the existence of a natural im- 



