Hawkins (1952) was unable to transmit this species to the bobwhite quail or Hungarian partridge. Gill (1954) claimed to have transmitted it to the chicken.
Location: The asexual stages occur mainly in the upper jejunum, but a few are present in the duodenum and ileum as far as the yolk stalk. The first generation schizonts lie below the host cell nuclei of the epithelial cells of the glands. The second generation schizonts develop in colonies in the epithelial cells of the deep glands but also spread up the sides of the villi. They usually lie just beneath the brush border of the cell but are sometimes found below the host cell nucleus. The third generation schizonts are found in the epithelial cells of the villi but never in the glands. Most of them lie above the host cell nucleus, but some are below it.
The sexual stages are found mainly in the epithelial cells at the tips of the villi but also spread down the sides. The great majority lie above the host cell nucleus (Clarkson, 1959).
Geographic Distribution: Presumably worldwide.
Prevalence: Quite common. Four out of 22 outbreaks studied by Clarkson and Gentles (1958) in Great Britain were due to this species, and 3 to a mixture of it and E. adenoeides.
Morphology: The morphology of this species has been studied especially by Tyzzer (1929), Hawkins (1952) and Clarkson (1959). The oocysts are subspherical, smooth, 16 to 27 by 13 to 22 u with a mean of 19 by 16 u; 150 oocysts measured by Clarkson (1959) were 20.1 ± 1.95 by 17.3 ± 1.7 u. A micropyle is absent. One to 3 oocyst polar granules are present. An oocyst residuum is absent. The sporocysts are ovoid, with a Stieda body. A sporocyst residuum is present. The sporozoites have a colorless globule at the large end. The sporulation time is 2 days according to Hawkins (1952), 1 day at 26° C according to Clarkson (1959).
Life Cycle: Tyzzer (1929), Hawkins (1952) and Clarkson (1959) studied the life cycle of this species, the last using a strain derived from a single oocyst. The account below is that of Clarkson, which is the most complete. The sporozoites invade the tips of the villi and migrate down the villi in the lamina propria until they reach the glands. Young first generation schizonts can be found in the gland epithelial cells as early as 12 hours after infection, and many are mature by 48 hours. They usually measure 17 by 13 u and enlarge the host cell, pushing its nucleus into the gland lumen. They contain 80 to 100 merozoites which measure about 4.5 by 1.5 u and have the nucleus at the larger end.
The first generation schizonts rupture and release the merozoites, which invade the adjacent epithelial cells, forming colonies of second generation schizonts. Most of these are mature by 66 hours after infection. They measure 8 by 7 u and contain 8 to 16 merozoites which measure about 7 by 1.5 u and have the nucleus near the center.
Third generation schizonts may be recognized as early as 72 hours after infection and reach maturity at about 96 hours. They measure about 8 by 7 u and differ from the second generation schizonts in having a residuum. They produce 8 to 16 merozoites which measure about 7 by 1.5 u and have the nucleus much nearer the large end than do the second generation schizonts.
Macrogametes and microgametocytes first appear 114 hours after infection. They measure about 15 by 11 u, and the microgametocytes contain a rounded residuum. The microgametes have 2 long flagella.
According to Hawkins (1952), the prepatent period is 6 days. Clarkson (1959) found that it ranged from 114 to 118 hours with an average of 116 hours.
Pathogenesis: This species is moderately to markedly pathogenic, causing catarrhal enteritis. The death rate is high in young poults up to 6 weeks of age, but older birds are more resistant. Hawkins (1952) found that infection with 50,000 sporulated oocysts produced a high mortality in young poults, in some instances killing 100% of 2- to 3-week-old poults. Clarkson and Gentles (1958) and Clarkson (1959) observed mortalities of 62%, 36% and 0%, respectively, in poults 1.5, 3 and 4 weeks old fed 100,000 oocysts; of 40% and 100%, respectively, in 4-week-old poults fed 300,000 and 400,000 oocysts; and of 0% in 5- and 10-week-old poults fed 200,000 and 2 million oocysts, respectively. Food utilization is reduced in infected birds, and those which recover do not gain weight well for some time.
Lesions first appear at the end of the 4th day after infection (Hawkins, 1952; Clarkson and Gentles, 1958; Clarkson, 1959). The jejunum is slightly thickened, dilated, and contains an excessive amount of clear, colorless fluid or mucus containing merozoites and small amounts of blood and other cells. Five to 6 days after infection the duodenum is enlarged, its blood vessels are engorged, and it contains a reddish brown, necrotic core which adheres firmly to the mucosa and extends a little way into the upper small intestine. The duodenal mucosa occasionally seems to have undergone coagulation necrosis, and pieces of caseous material may be scattered in the lumen of the entire intestine along with a large amount of fluid which may have a pinkish tinge. The remainder of the intestine is congested, and petechial hemorrhages may be present in the mucosa of most of the small intestine.
Regeneration of the mucosa begins on the 6th or 7th day. A few petechiae are present in the duodenum and jejunum, and there are a few minute streaks of hemorrhage and spotty congestion in the ileum. The posterior part of the jejunum and ileum may contain greenish, mucoid casts 5 to 10 cm long and 3 to 6 mm in diameter, and necrotic material may be found in the ileum or feces.
Feed consumption begins to drop 2 to 3 days after infection, and 4 days after infection the birds huddle together with closed eyes, drooping wings and ruffled feathers. Their droppings at this time are scanty and slightly fluid. At the peak of the disease, 5 to 6 days after infection, some of the feces form cylinders 1 to 2 cm long and 3 to 6 mm in diameter. The droppings are not bloody, altho a few flecks of blood may occasionally be seen. Death usually occurs 5 to 7 days after infection.
The first reaction of the host is local infiltration of the whole intestine with eosinophiles (Clarkson, 1959). This begins within 2 hours after infection, reaches a maximum in 1 to 2 days, and persists at least 10 days. There are no striking abnormalities at 4 days, but at 5 days many of the infected villi appear to have lost their tips, all the duodenal blood vessels are congested, and many of the epithelial cells around the villi stain poorly and appear necrotic. These changes are present also in birds which die on the 6th or 7th days, but resolution is rapid in recovered birds, and Clarkson (1959) saw very little abnormality by the 8th day except for increased cellularity of the lamina propria.
Immunity: According to Hawkins (1952), the immunity produced by infections with this species is not as solid as that produced by E. meleagridis, E. dispersa and E. gallopavonis, but it is still considerable.