Responses to Prolonged Selection for Resistance and Susceptibility to Acute Cecal Coccidiosis in the Auburn Strain Single Comb White Leghorn

Abstract

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.

Exoerythrocytic development of Plasmodium gallinaceum in the White Leghorn chicken

“…ii) We excluded the possibility that our chicks harbored residual coccidiostats, which are frequently included in chicken feed to prevent devastating outbreaks of the related apicomplexan parasite Eimeria tenella (Takaya et al, 1999;Pines et al, 2000), which could have affected the exoerythrocytic stages of P. gallinaceum. iii) One remaining possibility is that White Leghorns have gained resistance to tissue stages of P. gallinaceum, because modern commercial chicken breeds have been selected for increased resistance to disease, including E. tenella infection (Edgar et al, 1951;Champion, 1954;Rosenberg et al, 1954;Johnson and Edgar, 1982;Caron et al, 1997). 4) Finally, the quinine used in the 1940s may have been of lesser purity thus permitting the generation of secondary exoerythrocytic stages from a low level parasitemia.…”

Problématique du contrôle et de la prévention de la coccidiose du poulet

“…L'influence de la souche hôte sur l'expression de la maladie fut clairement démontrée. Après 12 générations de sélection par rapport à la sensibilité à Eimeria tenella, les mortalités pour le groupe témoin, le groupe résistant, le groupe peu résistant et le groupe plus sensible, étaient respectivement 41%, 21%, 29% et 35% (Johnson et Edgar, 1982). Pinard et al (1998) (Kim et al, 2009).…”

Ea-B and Ea-C Cellular Antigen Genes in Leghorn Lines Resistant and Susceptible to Acute Cecal Coccidiosis ,

“…The gene frequencies of certain generations beginning with 1957 are given in Table 1 (Table 1) with an increase in the inoculating dose of oocysts employed in the 1957 and 1958 generations of the R line (Johnson and Edgar, 1982). The 1956 generation, inoculated with the dose of 15,000 oocysts/individual employed from the beginning of selection, produced the 1957 generation having about equal frequencies of B 2 and B 5 .…”

“…Cellular antigen studies were begun on consanguineous Single Comb White Leghorn lines R and S after respective selection for resistance and susceptibility to acute cecal coccidiosis (Johnson and Edgar, 1982) was largely completed. The two lines were shown to possess A and E (abbreviations of Ea-A and Ea-E) alloantigen alleles linked in distinctly different AE haplotypes (Johnson and Edgar, 1984).…”