Eimeria Acervulina

Host: Chicken.

Location: Anterior small intestine.

Geographic Distribution: Worldwide.

Prevalence: Common.

Morphology: The oocysts are ovoid, smooth, 12 to 23 by 9 to 17 u with a mean of 16 by 13 u. A micropyle is absent. An oocyst polar granule is present. An oocyst residuum is absent. The sporocysts are ovoid, with a Stieda body but without a sporocyst residuum. The sporulation time is 1 day. Edgar (1955) found that the minimum sporulation time for this species at 28° C was 17 hours.

Life Cycle: The life cycle of this species was described by Tyzzer (1929). The schizonts are found in the epithelial cells of the villi of the anterior small intestine, where they lie above the host cell nuclei. The gland cells may also be invaded. Sometimes more than one parasite is found in a cell. The schizonts produce 16 to 32 merozoites which measure about 6 by 0.8 u. There are at least 2 and possibly more asexual generations. Asexual reproduction lasts longer than in E. tenella.

The sexual stages occur above the host cell nuclei in the epithelial cells of the villi and to a lesser extent in the gland cells in the anterior small intestine. They first appear 4 days after infection. The microgametocytes are relatively small, measuring 11 by 9 u.

The prepatent period is 4 days, and oocysts continue to be produced for relatively longer than with some other chicken coccidia.

Brackett and Bliznick (1950) found that the maximum number of oocysts produced per oocyst fed in their studies was 72,000. This occurred in a group of 3-week-old birds fed 2000 oocysts each. In another experiment in which similar birds were fed the same number of oocysts, only 35,000 oocysts were produced per oocyst fed. Oocyst production was lower with both larger and smaller inocula. Following inoculation with 200, 10,000 and 20,000 oocysts, respectively, 9000, 35,000 and 7,600 oocysts were produced per oocyst fed.

Pathogenesis: E. acervulina is generally considered only slightly pathogenic, but very large inocula may cause severe signs and even death. Generally, however, this species causes only a temporary setback. Dickinson (1941) found that administration of as many as 25 million oocysts to pullets produced only a temporary drop in weight and temporary cessation of egg production. Between 4 and 9 days after infection, the birds were droopy, ate relatively little and passed slimy, mucoid feces. Peterson (1949) reported losses from E. acervulina infection in the Pacific Northwest in older birds 3 to 4 weeks after they had been brought in off the range and placed in houses. The birds lost weight, egg production ceased, the combs shriveled and keratin pigment disappeared. There were few if any deaths. After about 6 weeks the birds recovered and egg production returned to normal.

Brackett and Bliznick (1950) found that inoculation with 500,000 oocysts reduced weight gains of 2-week-old chicks. Moynihan (1950) obtained similar results. Becker (1959) found that 300,000 oocysts produced only loss of appetite for 2 or 3 days and watery feces on the third day after infection in White Leghorn chicks. Morehouse and McGuire (1958) found that infection of chicks with 100,000 oocysts retarded weight gains somewhat but did not affect the final weight. Larger inocula produced increasingly severe effects. Single and multiple doses of 5 million or more oocysts caused 6 to 75% mortality.

The lesions produced by E. acervulina are not as marked as with E. necatrix. The intestine may be thickened and a catarrhal exudate may be present, but hemorrhage is rare. The maturing oocysts lie massed in limited areas, and form whitish or grey spots or streaks running transversely in the intestinal mucosa. In heavy infections the entire mucosa may be involved and may appear greyish, mottled and somewhat thickened. Morehouse and McGuire (1958) described a severe inflammatory reaction in chicks infected with 1 to 20 million oocysts. The intestine was edematous and thickened, with extensive vasodilation and marked reddening of the mucosa, and there was also degeneration or necrosis and sloughing of the intestinal epithelium.