Sporozoites of Eimeria tenella were treated with different anticoccidial drugs in vitro and their subsequent viability was tested by inoculating them into chicken embryos. Monensin, salinomycin, lasalocid, and arprinocid, at concentrations between 0.01 and 1.0 micrograms/ml, greatly reduced sporozoite viability as judged by mortality, hemorrhage and specific lesions in the embryo chorioallantois. Monensin was also effective in reducing the viability of sporozoites of E. mivati and E. tenella as judged by oocyst production occurring in embryos; activity of monensin was greater against E. tenella than against E. mivati. Monensin (0.1 mg) inoculated into embryos inhibited development of E. tenella. Oocysts which were produced in the presence of the drug sporulated normally and sporozoites obtained from them were fully infective. By initiating treatment of chickens with monensin at different times in relation to infection, it was shown that the drug exerts its anticoccidial effect on the primary invasive stage and on the gametogonous stage of E. tenella and E. necatrix. The effect of gametogony was tested by initiating infections with second generation merozoites of E. tenella. Significant reduction in oocyst production occurred in three of four strains of E. tenella tested. Medication with monensin initiated before merozoite inoculation was effective in inhibiting oocyst production, but medication starting 5 hr after merozoite inoculation was not. This differed from the effects of arprinocid and sulfaquinoxaline which were expressed both before and 5 hr after merozoite inoculation. The results show that the ionophorous anticoccidial drugs exert their anticoccidial action primarily against the invasive stages of Eimeria.
Four species of Eimeria from fowls were able to develop in chicken embryos following the inoculation of sporozoites. Three species (E. brunetti, E. mivati and E. tenella) were able to complete the whole of their endogenous cycle in embryos. E. necatrix developed to late schizogony, E. acervulina and E. maxima did not develop.The life-cycles appeared to be delayed, and in the case of E. tenella embryo mortality was associated with heavy parasitism of the chorioallantoic membranes. Oocysts recovered from urate deposits in the allantoic cavity sporulated normally and induced infections in chickens.Attempts to infect turkey and quail embryos with E. tenella or chicken and turkey embryos with E. stiedae were unsuccessful.The implications of the findings are discussed.I wish to thank Dr C. Horton-Smith for his encouragement and guidance with this work; Dr M. E. Rose for help in the preparation of the manuscript and Mr B. J. Millard for careful technical assistance.
Sporulated oocysts or oocyst hulls of Eimeria acervulina given via the crop, and oocyst juice or sporozoites inoculated directly into the in testinal lumen, were tested for their effects on the hypersensitivity of the intestines of immunized and susceptible birds. Only viable sporozoites consistently caused an increase in the permeability of the immunized intestine to macromolecules, shown by the leakage of intravenously injected dye. Repulsion of epithelium and disruption of the villi were seen more often in immunized than in susceptible chickens but there was no correlation with treatment or with dye leakage.The hypersensitive response of immune intestines challenged with a heterologous organism was approximately half as intense as the response to homologous challenge.The significance of these findings in relation to immunity to coccidiosis is discussed.
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