Eimeria spp. are a group of highly successful intracellular protozoan parasites that develop within enterocytes. Eimeria maxima from the chicken is characterized by high immunogenicity (a small priming infection gives complete immunity to subsequent homologous challenge) and naturally occurring antigenically variant populations that do not completely cross-protect. In this study we examined the expression of antigenic diversity in E. maxima, as manifested by cross-strain protection in a series of inbred chicken lines. The IAH line of Light Sussex chickens and all lines of inbred White Leghorns were susceptible to primary infections with either of two strains (H and W) of E. maxima and were protected completely against challenge with the homologous strain of parasite. The extent of cross-protection against the heterologous parasite strain varied from 0 to almost 100% depending on host genetics. Interestingly, in one inbred line of chickens (line 15I) the cross-protective phenotype was directional and intensely influenced by the infection history of the host. The basis for the observed variation in cross-protection is not known, but our results suggest that the major histocompatibility complex is not a major genetic component of the phenotype. These results are discussed in relation to the number of protective antigens presented by complex pathogens and the development of immunoprotective responses in hosts of different genetic backgrounds.

The effect of treatment with monoclonal antibodies (Mabs) which deplete CD4+ or CD8+ T lymphocytes, on infections with Eimeria spp. was examined in NIH mice. Treatment with anti-CD4 Mab increased susceptibility to primary infections with E. vermiformis or E. pragensis and reduced the subsequent resistance of the mice to homologous challenge. Similar treatment of immune mice did not affect their resistance to re-infection but this was reduced in mice depleted of CD8+ T lymphocytes. In mice immunized with E. vermiformis the effect of CD8(+)-depletion was very slight, apparent only as the presence of small numbers of oocysts in the faeces of some mice; in mice immunized with E. pragensis there was a small, though significant, increase in oocyst production, compared with controls and anti-CD4-treated groups. These results confirm the importance of mechanisms involving the function of CD4+ T lymphocytes in the control of primary infections with Eimeria spp. and indicate that CD8+ cells play some part in the expression of resistance to reinfection. They also show that a major part of this resistance was not affected by either of the treatments given.

The reproduction of Eimeria vermiformis in different strains of phenotypically normal mice and in mice with various immunological characteristics or defects was compared. In some strains of phenotypically normal mice there were marked differences in oocyst production, both in terms of numbers and in the duration of patency, allowing the strains to be classified as resistant or susceptible to infection with E. vermiformis. These differences were apparent only in primary infections; both types of strain were equally resistant to reinfection. Amongst the strains of mice with immunological deficiencies, reproduction of the parasite was greatest in the athymic (nu/nu) mutants and these mice were completely susceptible to reinfection. Strains of mice with lowered or defective antibody production, or with defective neutrophils and low NK cell activity (bg/bg) were more susceptible than the relevant controls to primary infection but all developed substantial immunity to reinfection. Asplenic (Dh/+) mutants were remarkably resistant to infection.

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