Eimeria Gallopavonis

Host: Turkey.

Hawkins (1952) transmitted this species experimentally to the Hungarian partridge but not to the pheasant or bobwhite quail. Gill (1954) claimed to have transmitted it from the turkey to the chicken.

Location: Ileum, rectum and, to a lesser extent, ceca.

Geographic Distribution: North America, India.

Prevalence: Uncommon.

Morphology: This species was described by Hawkins (1952, 1952a), who remarked that its oocysts cannot be differentiated with any certainty from those of E. meleagridis. The oocysts are ellipsoidal, smooth, 22 to 33 by 15 to 19 u with a mean of 27 by 17 u, without a micropyle. An oocyst polar granule is present. There is no oocyst residuum. The sporocysts are ovoid, with a Stieda body. A sporocyst residuum is present. The sporulation time is 1 day.

Life Cycle: Hawkins (1952) described the life cycle of this species. The endogenous stages are found in the epithelial cells at the tips of the villi, where they lie mostly above the host cell nuclei. The first generation schizonts occur in the ileum and rectum. They produce approximately 8 merozoites and a residual mass 3 days after infection. There are apparently two sizes of second generation schizonts. The smaller ones occur in the rectum, ileum and rarely in the ceca. They produce 10 to 12 merozoites and a residual mass 4 to 5 days after infection. The larger second generation schizonts occur only in the rectum. They are 20 u in diameter and produce a large, undetermined number of merozoites 4 days after infection.

There are a few third generation schizonts and merozoites in the rectum. They produce about 10 to 12 merozoites. These and most of the second generation merozoites develop into sexual stages. These are found primarily in the rectum and only occasionally in the ileum and ceca. The macrogametes and microgametocytes are similar to those of other turkey protozoa. Some oocysts are passed in the feces on the sixth day after infection, but most appear on the seventh day.

Pathogenesis: Little is known of the pathogenicity of this species. Hawkins (1952) noted marked edema, sloughing and lymphocytic infiltration in the intestines, but did not have sufficient material to make a thoro study.

Immunity: According to Hawkins (1952), infection with E. gallopavonis produces a more solid immunity than that elicited by E. meleagridis, E. meleagrimitis or E. dispersa.