Complete 18S ribosomal RNA gene sequences were determined for 8 Eimeria species of chickens and for Eimeria bovis of cattle. Sequences were aligned with each other and with sequences from 2 Sarcocystis spp., Toxoplasma gondii, Neospora caninum, and 4 Cryptosporidium spp. Aligned sequences were analyzed by maximum parsimony to infer evolutionary relationships among the avian Eimeria species. Eimecia bovis was found to be the sister taxon to the 8 Eimeria species infecting chickens. Within the avian Eimeria species, E. necatrix and E. tenella were sister taxa: this clade attached basally to the other chicken coccidia. The remaining Eimeria spp. formed 3 clades that correlated with similarities based on oocyst size and shape. Eimeria mitis and Eimeria mivati (small, near spherical oocysts) formed the next most basal clade followed by a clade comprising Eimeria praecox. Eimeria maxima, and Eimeria brumetti (large, oval oocysts), which was the sister group to Eimeria acervulina (small, oval oocysts). The 4 clades of avian Eimeria species were strongly supported in a bootstrap analysis. Basal rooting of E. necatrix and E. tenella between E. bovis and the remaining Eimeria species and the apparent absence of coccidia that infect the ceca of jungle fowl all suggest that E. necatrix and E. tenella may have arisen from a host switch, perhaps from the North American turkey, Meleagris gallopavo.

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Abstract. Twenty-four 5-month-old battery-hatched Japanese quail were inoculated orally with 10 5

Susceptibility to disease and the subclass-specific antibody response to Eimeria tenella, E. acervulina, and E. maxima were compared in two inbred strains of chickens, FP (B15B21) and SC (B2B2). FP strain was more susceptible to coccidiosis than SC chickens based on oocyst production, lesion score, and clinical signs. FP chickens infected with E. tenella had more severe cecal lesions and a significantly lower hematocrit level than SC chickens. FP chickens infected with E. acervulina excreted five times as many oocysts at 6 days postinfection as SC and showed a 71% reduction in plasma carotenoid level compared with controls (56% reduction in SC chickens). Body-weight change did not correlate with other signs of disease. Both SC and FP chickens produced high levels of serum IgM and IgG and biliary IgA. Although SC chickens had a slightly higher antibody response than FP chickens at 7 days postinoculation, both strains maintained high levels of IgM, IgG, and IgA for a prolonged period post primary inoculation. Although SC and FP chickens show different disease susceptibility to coccidiosis, they demonstrate similar antibody response.

Fourteen 2-3-wk-old turkeys were inoculated orally with 10(5) or 10(4) infective oocysts of the ME 49 strain of Toxoplasma gondii. Of the 8 turkeys given 10(5) oocysts in experiment 1, 3 died or were killed 12 or 14 days after inoculation (DAI) because of respiratory distress associated with a concomitant Aspergillus-like fungus infection. The remaining 5 turkeys remained normal and were killed 62 DAI. Toxoplasma gondii was isolated in mice from the heart of all 5, from the breast muscles of 2, leg muscles of 3, and from the brains and livers of none of the turkeys. All 6 turkeys fed 10(4) oocysts in experiment 2 remained clinically normal until necropsy on 41 DAI; T. gondii was isolated from pooled tissues from each turkey. All 14 turkeys developed high antibody titers to T. gondii in the modified agglutination test (MAT) using formalinized tachyzoites. The enzyme-linked immunosorbent assay (ELISA) was as sensitive as MAT for detecting T. gondii antibodies in turkey sera. The latex agglutination and indirect hemagglutination tests were less sensitive than the MAT and ELISA. No dye-test-measurable antibodies were found in sera of any turkey.

Chickens infected with any one of the six major species of chicken coccidia had lower levels of blood carotenoids (plasma pigmentation) than did uninoculated control birds. The species were Eimeria acervuUna, E. mivati, E. maxima, E. necatrix, E. brunetti, or E. tenella. Carotenoids decreased as early as 4 days postinoculation (PI) (E. acervuUna), but returned to a normal level by 14 days PI (E. mivati, E. acervuUna, and E. tenella). The maximum decrease occurred at 7 or 8 days PI in all species and was 49.8% with E. tenella and 62.4%-74.0% with the five intestinal species. Additional studies with E. tenella, E. acervuUna, and E. brunetti indicated that the magnitude of the decrease was related to the number of oocysts given within any one species. Increasing oocyst number also resulted in a more rapid reduction of longer duration in carotenoid levels.

Infections with single species of Eimeria acervulina, E. mivati, E. maxima, E. tenella, E. necatrix, and E. brunetti, and the six species mixed, were utilized in three separate battery experiments to evaluate the anticoccidial efficacy of various levels of salinomycin (AHR-3096), a fermentation product of a strain of Streptomyces albus. At the 60 to 100 p.p.m. treatment levels, this compound showed significant anticoccidial activity for all parameters studied (mortality, weight gain, feed conversion, dropping scores, and lesion scores). The mortality due to coccidiosis was reduced to 0.1% in the medicated infected birds. Some activity, as measured by weight gain, was seen in the lower levels of salinomycin medication (12.5 to 50 p.p.m.), but other parameters, including mortality and lesion scores, indicated less activity than that seen with the higher treatment levels. At 100 p.p.m., there was no apparent effect on the compound on bird performance in uninfected control birds. Salinomycin at the 100 p.p.m. treatment level was statistically as effective as 121 p.p.m. monensin (reference anticoccidial) in controlling coccidiosis.

The relative importance of MHC genes and background genes in the genetic control of disease susceptibility and the development of protective immunity to E. tenella infection was investigated in eight different strains of 15I5-B congenic and four inbred chicken strains. RPRL 15I5-B congenic chickens that share a common genetic background but express different B haplotypes demonstrated wide variations in disease susceptibility and the development of acquired resistance to E. tenella infection. Infection of chickens sharing a common B haplotype but expressing different genetic backgrounds showed quite contrasting levels of susceptibility to secondary E. tenella infection. In all chicken strains examined, infected chickens developed high levels of serum and biliary anti-coccidial antibodies regardless of their B haplotypes. Furthermore, no correlation between antibody levels and the phenotypically expressed levels of disease resistance was demonstrated. These findings lend support to the view that interaction of MHC genes and non-MHC genes influences the outcome of host response to E. tenella infection.