464 FAMILY: TEYPAXOSOMID^ 



panosomes appear in the peripheral blood from four to six days after 

 intraperitoneal inoculation of infected blood from another rat, and the 

 resulting infection may be divided into two phases. In the first, a great 

 variety of forms occurs in the blood, most of which are in process of 

 division (Fig. 197). This is the multiplication phase, but it gradually 

 subsides, giving place to a phase in which the trypanosomes are much more 

 uniform in character, and are the forms generally recognized as T. lewisi. 

 The first phase is of short duration, and multiplying forms are rarely 

 seen in the peripheral blood after the eighth or ninth day, when the only 

 forms to be found are those of the second phase, which lasts from one to 

 four months. When inoculation has been made intraperitoneally — and 

 this is the readiest method of bringing about infection — it is stated by 

 Laveran and Mesnil (1912) that multiplication first commences in the 

 peritoneal cavity, and that these stages are much more numerous in the 

 peritoneal exudate than in the blood. Before their appearance in the 

 peripheral blood after intraperitoneal inoculation, it appears, from still 

 unpublished observations by A. C. Stevenson, that active multiplication 

 has been taking place in the small vessels of the internal organs, especially 

 the kidneys. He was unable to demonstrate the active multiplication in 

 the peritoneal cavity, though in the later stages of an infection trypano- 

 somes occurred in the exudate. AYithin two days of peritoneal inocula- 

 tion, multiplying forms can be demonstrated in sections of the organs. 

 In the ordinary course of events, T. lewisi does not seriously injure the 

 rat, which recovers from its infection and nearly always has an immunity 

 to reinfection. Miss M. Robertson, however, informs the writer that if 

 only a slight infection occurs after a first inoculation, the rats may be re- 

 infected. In some cases, rats are reported to have died as a result of 

 heavy infections. 



Roudsky (1910-1911), by rapid passage from rat to rat of the whole 

 blood of an animal when the trypanosomes were at the multiplication 

 phase, was able to raise the virulence of T. lewisi till it became definitely 

 pathogenic to rats, and not only infected mice, which are seldom susceptible 

 to the ordinary strains, but sometimes killed them. Further, the infection 

 in mice was transmissible from mouse to mouse. This strain of heightened 

 virulence was also inoculable to rabbits, guinea-pigs, and other rodents, 

 which are rarely susceptible or entirely resistant to T. lewisi. It was 

 suggested by Reichenow (1917) that the numerous trypanosomes of mice 

 and other rodents, which morphologically resemble T. lewisi, and even 

 a trypanosome which he found in African apes, might actually be 

 T. lewisi. Yamasaki (1924) attempted without success to infect mice 

 and monkeys by means of fleas which had become infective after feeding 

 on rats. 



