Abstract
Parasites of the genus Eimeria are characteristically host specific. Peritoneal macrophages obtained from nonspecific hosts (guinea fowl and turkeys) were found to greatly reduce the viability of sporozoites of E. tenella from the chicken in vitro (Long and Millard, 1979, Parasitology 78: 239-247). We have demonstrated here that the in vivo inhibition of macrophage activity enabled infection with Eimeria to occur in a nonspecific host. It has been shown that crystalline silica particles are selectively toxic to macrophages in vivo and in vitro without altering the viability of lymphocytes (Lotzova and Cudkowicz, 1974, J. Immunol. 13: 343-345; Kessel et al., 1963, Brit. J. Exptl. Pathol. 44: 351364; Vigliani and Pernis, 1963, Adv. Tuberc. Res. 12: 230-282). After phagocytosis, silica has a cytotoxic effect on the macrophage probably by interacting with the macrophage lysosomal membrane releasing hydrolytic enzymes into the cytoplasm (Allison et al., 1966, J. Exp. Med. 124: 141-154). For the present study, silica particles were used to investigate the possible role of macrophages in the host specificity of Eimeria. Two-week-old male, White Leghorn chickens were inoculated per os with a mixture of 500,000 sporulated oocysts of turkey coccidia (a mixture of E. dispersa, E. meleagrimitis and E. adenoeides). Silica particles of an average size of 5 /im were obtained from Dr. K. Roback, Steinkoklenbergbauverein, Germany. Doses of 3 mg/0.5 ml buffered saline were injected i.v. twice daily into the wing vein. Chickens were given the silica injections by group on days 1 through 4 PI. All the feces discharged were collected and examined for oocysts daily, starting on the 5th day PI, and terminating on the 15th day PI. The combined results of two identical experiments are given in Table I. Oocysts were produced in all groups that were treated with silica; the predominant oocysts produced were identified morphologically as E. dispersa. In one of the two experiments, untreated, infected chickens discharged oocysts on only one day (5th day). Silica-treated chickens produced 17 to 126 times more oocysts over periods ranging from 5 to 15 days after oocyst inoculation. The greatest number of oocysts was discharged in all groups between 5 and 9 days PI. This corresponded with the minimum prepatent periods of Eimeria dispersa species used in this study. More oocysts were produced in those birds given the silica injections 3 to 4 days PI than those birds given the injections on days 0 through 3 PI. The treatment given 3 to 4 days PI coincided with the termination of schizogony and the start of gametogony. Thus, macrophages may play some role, either directly or indirectly, in the host specificity of coccidia by affecting the asexual cycle and perhaps the sexual cycle as well. The treatment inhibited host specific mechanism(s) of those chickens given silica on days 0 to 2 PI, but the effect was greater when silica was given 3 to 4 days PI. Thus, the mechanisms involved in the innate resistance of nonspecific hosts to Eimeria may be effective against early gametocytes. After 2 to 4 days in the chickens' circulation, most of the silica may have been sequestered in lymphoid tissue (Pearsal and Weiser, 1968, J. Reticuloendothel. Soc. 5: 107-120). The increase in the number of oocysts produced on days 13 to 15 PI may reflect the delayed effects of the silica treatment. However, more evidence is needed to adequately explain this finding. The oocysts collected from these birds completed their life cycle when inoculated into turkeys, confirming that the oocysts produced by chickens given the silica treatment were indeed turkey coccidia. Doran (1978, J. Parasitol. 64: 882-885) was able to produce a light
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