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Eimeria vermiformis: host strains and the developmental cycle.

M E Rose, B J Millard

    Experimental Parasitology
    |December 1, 1985
    PubMed
    Summary
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    This study compared Eimeria vermiformis development in resistant BALB/c and susceptible C57BL/6 mice. Susceptible mice showed prolonged parasite development and more extensive intestinal infection, indicating strain-specific host responses.

    Area of Science:

    • Parasitology
    • Immunology
    • Mammalian Genetics

    Background:

    • Eimeria vermiformis is an intestinal parasite affecting rodents.
    • Host susceptibility significantly influences parasitic infections.
    • Understanding host-parasite interactions is crucial for disease control.

    Purpose of the Study:

    • To compare the endogenous developmental cycle of Eimeria vermiformis in two mouse strains with contrasting susceptibility.
    • To quantitatively and qualitatively assess differences in parasite development and distribution.

    Main Methods:

    • Confirmatory studies of Eimeria vermiformis endogenous development.
    • Qualitative and quantitative comparison of parasite development in BALB/c (resistant) and C57BL/6 (susceptible) mice.
    • Monitoring parasite distribution, persistence, and developmental stages (schizogony, gametogony).

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  • Fecal oocyst production kinetics analysis.

    • Main Results:

    • No significant differences were observed in the first 5 days of development between resistant and susceptible mice.
    • Susceptible C57BL/6 mice exhibited increased parasite numbers, wider intestinal distribution, and prolonged tissue persistence.
    • Schizogony extended longer in C57BL/6 mice, potentially involving additional generations, alongside gametogony.
    • Oocyst production kinetics in feces correlated with intestinal epithelial events.

    Conclusions:

    • Host genetic background dictates the outcome of Eimeria vermiformis infection.
    • Susceptible hosts support more extensive and prolonged parasite development, suggesting a less effective immune response.
    • Further research into the immune mechanisms underlying differential susceptibility is warranted.