28 PROTOZOOLOGY 



"epithelial cells" (Fig. 1, h), a state comparable to the formation of 

 the ciliated epithelium from a layer of fibroblasts lining a cyst 

 formed around a piece of ovary inplanted into the adductor muscle 

 of Pecten as observed by Drew (1911). 



Practically all Microsporidia are cytozoic, and the infected cells 

 become hypertrophied enormously, producing in one genus the so- 

 called Glugea cysts (Fig. 257). In many cases, the hypertrophy of the 

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

 cytoplasm (Fig. 255). 



Information concerning toxic substances produced by parasitic 

 Protozoa is meager. Sarcosporidia appear to produce a certain toxic 

 substance which, when injected into the blood vessel, is highly toxic 

 to experimental animals. This was named sarcocystine (Laveran and 

 Mesnil) or sarcosporidio toxin (Teichmann and Braun). 



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 lewisi, a considerable number of 

 the parasites are destroyed during the developmental phase of the 

 infection and that after a variable length of time, resistance to the 

 parasites often develops in the host, as the parasites disappear from 

 the peripheral blood and symptoms subside, though the host still 

 harbors the organisms. In malarious countries, the adults and chil- 



