32 PROTOZOOLOGY 



Practically all Microsporidia are cytozoic, and the infected cells 

 become hypertrophied enormously, producing in one genus the so- 

 called Glugea cysts (Figs. 287, 290). In many cases, the hypertrophy 

 of the nucleus of the infected cell is far more conspicuous than that 

 of the cytoplasm (Figs. 287, 291) (Kudo, 1924). 



When the gonads are parasitized heavify, the germ cells of the 

 host animal often do not develop, thus resulting in parasitic castra- 

 tion. For example, the ciliate, Orchitophrya steUarum, a parasite in 

 the male reproductive organ of Asterias rubens, was found by Vevers 

 (1951) to break down completely all germinal tissues of the testes in 

 the majority of the host starfish. In other cases, the protozoan does 

 not invade the gonads, but there is no development of the germ cells. 

 The microsporidian, Nose ma apis, attacks solely the gut epithelium 

 of the honey bee, but the ovary of an infected queen bee degenerates 

 to varying degrees (Hassanein, 1951). Still in other instances, the 

 Protozoa invade developing ova of the host, but do not hinder their 

 development, though the parasites multiply, as in Nosema bombycis 

 in the silkworm (Stempell, 1909) and Babesia bigemina in the cattle 

 tick (Dennis, 1932). 



For the great majority of parasitic Protozoa, there exists a de- 

 finite host-parasite relationship and animals other than the specific 

 hosts possess a natural immunity against an infection by a particular 

 parasitic protozoan. Immunity involved in diseases caused by Pro- 

 tozoa has been most intensively studied on haemozoic forms, es- 

 pecially Plasmodium and Trypanosoma, since they are the causative 

 organisms of important diseases. Development of these organisms 

 in hosts depends on various factors such as the species and strains 

 of the parasites, the species and strains of vectors, and immunity of 

 the host. Boyd and co-workers showed that reinoculation of persons 

 who have recovered from an infection with Plasmodium vivax or P. 

 falciparum with the same strain of the parasites, will not result in a 

 second clinical attack, because of the development of homologous 

 immunity, but with a different strain of the same species or different 

 species, a definite clinical attack occurs, thus there being no hetero- 

 logous tolerance. The homologous immunity was found to continue 

 for at least three years and in one case for about seven years in P. 

 vivax, and for at least four months in P. falciparum after apparent 

 eradication of the infection. In the case of leishmaniasis, recovery 

 from a natural or induced infection apparently develops a lasting 

 immunity against reinfection with the same species of Leishmania. 



It has been shown that in infections with avian, monkey and hu- 

 man Plasmodium or Trypanosoma hwisi 1 a considerable number of 



