Responses to prolonged selection for resistance and susceptibility to acute cecal coccidiosis in the auburn strain single comb white leghorn.

Selection in the parental Auburn Strain Leghorn (A line) for resistance (R line, 13 filial generations) and susceptibility (S line, 7 filial generations) to acute cecal coccidiosis (ACC) caused by Eimeria tenella resulted in a sixfold difference in the ACC mortality rates of the two lines. Relaxation of selection for resistance in line RR, derived entirely from R line, resulted in gradual regression of the ACC mortality rate toward that of the parental A line nonselected control. Progress of selection in R line based on the same low dose of oocysts employed in S line neared a plateau of low mortality after six generations. Average ACC mortality in the first four generations of S line was 50% greater than that in A line. Before infection, chicks of S line were smaller than those of lines A, R, and RR. After infection, growth of S line survivors was inferior to that of survivors of the other lines. Uninfected controls of S line and A line grew at similar rates; those of R line grew at a significantly lower rate. In R line, large doses of oocysts caused high mortality. The largest dose caused mortality approaching 90% in both sexes; at lower doses, males died at higher rates than females. Among the survivors, growth rates of females were inferior to those of males; the difference increased with increasing dose. Large doses of oocysts resulted in spreading of the infection beyond the typical site. In R line, severe infection occurred in the necks of the cecal pouches and rectum with comparatively mild infection in the bulbar portion of the pouches. In contrast, the chief focus of infection remained in the bulbar pouches in S line. Selection for resistance seemingly disrupted the typical host tissue specificity of E. tenella. Thus, genes mediating the response of the host to ACC are possibly identical or complementary to genes controlling tissue specificity.