Moore and Brown (1951) were unable to transmit this species to the chicken, guinea fowl, ringnecked pheasant or bobwhite quail. Clarkson (19 59a) was unable to transmit it to the chicken.
Location: The first generation schizonts (Clarkson, 1958) occur in the neck of the ceca and in the terminal inch or so of the ileum, where 80% of them lie below the host cell nuclei of the epithelial cells. The second generation schizonts occur thruout the ceca, and some are found in the rectum and posterior ileum. They lie above the host cell nuclei of the epithelial cells, just beneath the brush border. The sexual stages occur thruout the ceca, rectum and posterior third of the small intestine. A few are found even more anteriorly, but none more than halfway to the yolk sac stalk. They invade the epithelial cells of the crypts and deep glands, a location which distinguishes them from E. meleagridis and E. gallopavonis, and also apparently the epithelial cells of the villi. Clarkson (1958) illustrated them as lying above the host cell nuclei.
Geographic Distribution: North America, Great Britain.
Prevalence: Quite common. Fifteen out of 22 outbreaks studied by Clarkson and Gentles (1958) in Great Britain were caused by this species and 3 by a mixture of it and E. meleagrimitis.
Morphology: The oocysts have been described by Moore and Brown (1951) and Clarkson (1958). They are similar to those of E. meleagridis and E. gallopavonis. They are ellipsoidal, sometimes ovoid, smooth, 19 to 31 by 13 to 21 u with a mean of 26 by 17 u. A micropyle is sometimes present. One to 3 oocyst polar granules are present. An oocyst residuum is absent. The sporocysts are elongate ovoid, apparently with a Stieda body. A sporocyst residuum is present. The sporozoites contain a clear globule at the large end. The sporulation time is 1 day. Edgar (1955) found sporulated oocysts as early as 18 hours at 29° C.
Life Cycle: Clarkson (1958) studied the life cycle of this species, using a strain derived from a single oocyst. First generation schizonts can be found in the epithelial cells as early as 6 hours after infection. They become mature 60 hours after infection; by 66 hours most of them have released their merozoites, altho a few remain up to 84 hours. The mature first generation schizonts measure 30 by 18 u and contain about 700 merozoites measuring 4.5 to 7 by 1.5 u, with a central nucleus.
The second generation schizonts become mature 96 to 108 hours after infection. They measure 10 by 10 u and contain 12 to 24 merozoites measuring about 10 by 3 u, with the nucleus a little nearer the rounded than the pointed end.
Sexual stages can be found as early as 114 hours and recognized as early as 120 hours after infection. The mature macrogametes measure about 20 by 18 u and contain many large, plastic granules which stain black with Heidenhain's hematoxylin. The mature microgametocytes are about the same size as the macrogametes.
The prepatent period was given by Moore and Brown (1951) as 112 hours. Edgar (1955) found oocysts in the feces as early as 104 hours, and Clarkson (1958) found that the prepatent period varied from 114 to 132 hours in 30 birds.
The patent period is 7 to 8 days according to Moore and Brown (1951). Clarkson (1958) found that very few oocysts were passed more than 14 days after infection, and none after the 20th day.
Pathogenesis: This species is highly pathogenic. Moore and Brown (1951) were able to kill 100% of experimental poults up to 5 weeks of age with large doses of sporulated oocysts. Older poults developed a severe enteritis with few or no deaths. Clarkson (1958) and Clarkson and Gentles (1958) observed mortalities of 0%, 0%, 45% and 100%, respectively, in 3-week-old poults fed 10,000, 25,000, 100,000 and 200,000 oocysts; of 33% in 6-week-old poults fed 1 million oocysts; and of 0% in 11-week-old poults fed 3 million oocysts. Birds which did not die had decreased food consumption and weight gains.
Poults develop signs of anorexia, droopiness and ruffled feathers during the 4th day after experimental infection. If death occurs, it is usually on the 5th or 6th days but may be a little later (Moore and Brown, 1951).
The gross lesions have been studied by Moore and Brown (1951), Clarkson (1958) and Clarkson and Gentles (1958). The intestines appear quite normal until the 4th day. The walls of the lower third of the small intestine, ceca and rectum become swollen and edematous, petechial hemorrhages which are visible from the mucosal but not from the serosal surface appear, and the lower intestine becomes filled with mucus.
During the 5th day, most of the terminal intestine is congested and contains large numbers of merozoites and long streaks of blood. By the end of the day, the intestine contains caseous material composed of cellular debris, gametes, and a few immature oocysts. A little later the caseous exudate is composed largely of oocysts. The feces in severe cases are relatively fluid and may be blood-tinged and contain mucous casts 1 to 2 inches long. Caseous plugs are sometimes present in the ceca.
On the 6th to 8th days in birds infected with 10,000 oocysts, the terminal intestine contains white, creamy mucus, and petechiae are present in the mucosa. By the 9th day the intestinal contents appear normal, altho they still contain large numbers of oocysts (Clarkson, 1958).
Infiltration with eosinophiles commences as early as 2 hours after infection, and enormous numbers of eosinophiles may be found in the terminal small intestine, ceca and rectum from the 3rd to the 10th days.
Beginning 4 days after infection, edematous changes are seen in the intestine, and infected epithelial cells begin to break off, leaving the villi denuded. The blood vessels become engorged, and cellular infiltration of the submucosa and epithelial denudation increase progressively until the 6th day. In birds which recover from the disease or which have received relatively few oocysts, resolution is very rapid. Vascularity is greatly reduced, the deep glands are almost free of parasites by the 7th day, and the intestine is almost normal by the 9th or 10th day (Clarkson, 1958). Clarkson (1958)found no changes in the blood picture of infected poults.
Immunity: Moore and Brown (1951) produced solid immunity to E. adenoeides by infecting turkey poults with 25 doses of sporulated oocysts over a period of 2 months. These birds were not immune to E. meleagridis. Conversely, poults which had been immunized against E. meleagridis were not immune to E. adenoeides. Clarkson (1959a), too, found no cross immunity between E. meleagridis and E. adenoeides. Since E. adenoeides is found in the same locations as E. meleagridis and E. gallopavonis, and since its oocysts are apparently similar to theirs, this lack of reciprocal immunity is an important differentiating criterion. The only other differences are its greater pathogenicity and its location in the crypts and deep glands rather than only in the tips of the villi.