No abstract

Madin-Darby Bovine Kidney cells were treated with sodium flouride, iodoacetate, and 2-deosyglucose, reagents that block glycolysis, and thus reduce phagocytosis. Sporozoites readily entered cells whose ATP stores were largely depleted. They also entered cells treated with colchicine, colcemid, and vinblastine. These latter agents did not inhibit sporozite motility after 6 hr incubation. Cytochalasin B prevented penetration of cells by inhibiting the motility of sporozoites. This effect was reversible. Warm sporozoites entered cold cells 4 times more radily than cold sporozoites into warm cells. The above findings suggest that phagocytosis is not the mechanism for entry of E. magna sporozoites into cultured cells, but that sporozoite motility is of primary importance.

Ultrastructure of the penetration of Eimeria magna sporozoites into embryonic bovine trachea cells demonstrated that the host cell membrane was not broken during entry of the parasite. This membrane did, however, undergo alterations characterized by blebbing of vesicles, thickening, and eventual disorganization once penetration was completed. Concurrent with the entrance of the parasite into the cell, and the subsequent membrane alterations, was the appearance of empty membrane saccules, probably rhoptries, in the apical region of the sporozoite. It was proposed that rhoptry secretions aided penetration by changing cell surface characteristics which produced an eventual breakdown of the invaginated protion of the host cell membrane.

Alloantigen genes B and C of respective loci Ea-B, the major histocompatibility complex (MHC) of chickens, and Ea-C were detected in Leghorn lines R and S selected from common ancestry for resistance and susceptibility to acute cecal coccidiosis, Eimeria tenella (ACC). The lines share genes B2 and C1; R line has B5, Br, and C4, and S line has B1, B3, B4, B6, C2, and C3. Haplotype Br is an apparent recombinant of B2 and B5, possibly F2G2-5. Expression of the F2G2- region of B2 and Br is strong in graft-vs.-host reactions but weak on erythrocytes; in contrast, that of F5G5- of B5 is reduced in graft-vs.-host reactions but strong on erythrocytes. Extinction of B4 in R line and B5 in S line occurred in the last stages of selection, and the frequency of B5 in R line increased as a result of intensification of selection pressure for resistance to coccidiosis. The respective C genes of highest frequency in lines R and S are C1 and C3. The latter is a probable recombinant of C1 and C2. Evidence of roles of the B and C systems in resistance and previous similar evidence for the AE system indicates that genes other than the chicken MHC have measurable effects on infectious diseases.

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.