692 INFECTION BY THE BLOOD PROTOZOA 



variation for total length for each of these rats showed that the trypanosomes in 

 experimental rat 977 lived in the blood for eleven days (infection died out at this 

 time) without showing any reproduction whatever, whereas in control rat 980 re- 

 production began on the second day and followed the course of a normal infection. 

 In this experiment it is to be noted that not only did the immune serum, i.e., the 

 serum taken from the seed rat on the tenth day, prevent adult trypanosomes from 

 reproducing in a fresh rat, but normal rat serum failed to prevent adult trypano- 

 somes from reproducing in a fresh rat. This is a clear-cut case of the passive transfer 

 of this type of immunity from an infected to an uninfected rat. 



The changes in titre of this immune property of serum through the course of an 

 ordinary infection have been studied in detail by Coventry (1925). She was unable 

 to demonstrate its presence in serum prior to the fifth day of the infection although it 

 is probably present as the rate of reproduction has already begun to decline, but 

 between the fifth and sixth days she found a sudden and very great increase with 

 a subsequent gradual increase until the thirty-fifth day and then a gradual de- 

 crease. 



As this immune property of serum which inhibits reproduction without affecting 

 the viability of the parasites emphasizes a new effect of resistance, the author has 

 attempted to compare it with the well-estabhshed immune bodies (1925 and un- 

 published work). Like most antibodies, it is non-ether soluble and is precipitated in 

 the globulin fraction of the immune serum. Strange to say, it comes down with both 

 the euglobulin and pseudoglobulin. It differs from others, however, in its lack of in 

 vitro affinity for its supposed antigen. Thus, when serum containing it is left for 

 twelve hours in contact with large numbers of dividing T. lewisi and the parasites 

 are subsecjuently removed, the serum does not lose any of its titre. 



Regendanz and Kikuth (1927) have verified the author's conclusions in regard to 

 the formation of the reproduction-inhibiting reaction product in infections with T. 

 lewisi, and similarly found that it exerted no trypanolytic or trypanocidal activity. 

 They have added the important finding that it is not formed in splenectomized rats. 



As far as the author is aware, there has been no experimental work nor any ex- 

 planation advanced to account for the second manifestation of resistance, i.e., the 

 first number crisis which occurs between the eighth and twelfth day of the infection. 

 Regendanz and Kikuth (1927) have not encountered this number crisis, but we have 

 invariably found it in the hundreds of infections studied in this laboratory. 



Some work on the immunological basis for the immunity of recovered rats to a 

 second infection, however, probably explains the third manifestation of resistance, 

 i.e., the crisis which terminates the infection. Laveran and Mesnil (1901) came to the 

 conclusion that the immunity and the final crisis are due to the phagocytosis of li\'ing 

 trypanosomes. MacNeal (1904), on the other hand, holds that the crisis and subse- 

 quent immunity are due to a trypanolysin, just as has been described for the patho- 

 genic forms. Manteufel (1909) also essentially agrees with this view. The author's 

 (1924) investigations and unpublished work of Coventry substantiate the formation of 

 a lysin which terminates the infection, but indicate that the lysin in conjunction with 

 the reproduction-inhibiting property is the basis for immunity to second infection. 

 For example, a rat recovered from an infection of T. lewisi receives a few parasites 

 from an infected flea. These find their way eventually into the blood stream, but on 



