Light and electron microscopic observations confirmed that Eimeria necatrix sporozoites first enter villous epithelial cells of the chicken small intestine and are transported to the crypts by mononuclear cells. Ultrastructurally, these cells resemble granulated intraepithelial lymphocytes (IEL) rather than macrophages, as suggested previously. The injection of chickens intraperitoneally (i.p.) with a variety of irritants, including proteose peptone, at the time of oocyst inoculation or up to 12 hr postinoculation (PI) resulted in a delay in the arrival of sporozoites at the crypt. Significantly fewer sporozoites had arrived at the crypt by 24 hr PI in i.p.-injected birds as compared to controls. This delay in the arrival of sporozoites at the crypts was reflected by a delay in the development of intestinal lesions and in peak oocyst production. However, there was no significant decrease in the total numbers of oocysts produced by these birds as compared to controls, indicating that no significant loss of sporozoites occurs during the possible rerouting of the parasites. The presence of infective stages in extraintestinal sites was detected by transferring various tissues to coccidia-free recipients. Infection was transferable by gut, liver, and spleen from irritant-injected and control birds at all time intervals studied (12, 24, 36, and 48 hr PI). Infection was also transferable with blood and kidney, but not consistently. A small number of oocysts was passed by the recipients of peritoneal wash from irritant-injected birds at 12 hr PI. In all transfers, the prepatent period was normal, suggesting that the migrant stages are sporozoites.

The development of second generation schizonts of Eimeria necatrix and E. tenella was studied with the electron microscope. Invasion of the crypt epithelial cells by merozoites of the first generation schizonts caused changes in the morphology of the infected cells and stimulated their migration into the lamina propria through breaks which appeared in the basement membrane of the crypts. Second generation schizonts developed in the lamina propria within these crypt cells whose epithelial origin was confirmed by their interconnection by desmosomes and tight junctions and by their possession of characteristic microvilli. A comparison is made between this invasion of the lamina propria by parasitized cells and invasion of connective tissue by malignant epithelial cells; the possible mechanisms involved are discussed.