Location: First generation schizonts occur thruout the small intestine. Second generation schizonts, gametes and gametocytes occur in the posterior small intestine, rectum, ceca and cloaca.
Geographic Distribution: North America.
Morphology: P. P. Levine (1942) described this species, and Becker, Zimmermann and Pattillo (1955) made a biometric study of its oocysts. The oocysts are ovoid, smooth, 14 to 34 by 12 to 26 u with a mean of 23 by 20 u. A micropyle is absent. An oocyst polar granule is present. An oocyst residuum is absent. The sporocysts are elongate ovoid, about 13 by 7.5 u, with a Stieda body. A sporocyst residuum is present. The sporulation time is 1 to 2 days. Edgar (1955) found infective oocysts as early as 18 hours at 24° C.
Life Cycle: The life cycle of this species was described by Boles and Becker (1954). The sporozoites are liberated in the intestine and invade the epithelial cells of the villi. They round up to become first generation schizonts, which lie below the host cell nuclei on the sides of the villi of the upper, middle and lower small intestines. They are present 51 to 76 hours after infection, measure 30 by 20 u, and contain approximately 200 first generation merozoites when mature. These invade other cells in the posterior small intestine, rectum, tubular part of the ceca and cloaca. They are found primarily at the tips of the villi, and usually lie below the host cell nuclei. They turn into second generation schizonts, which are present 4 days after infection. These average 30 by 16 u and contain 50 to 60 merozoites. Small schizonts about 10 by 9 u were also seen on the 4th day, but their significance was not determined.
The second generation merozoites invade fresh cells in the lower small intestine, ceca, rectum and cloaca and turn into sexual stages. These first appear on the 5th day and lie at the tips and sides of the villi, either above the host cell nuclei or on the basement membrane. The microgametocytes have a multicentric appearance, and are larger than the macrogametes, which measure about 25 by 22 u. The macrogametes contain eosinophilic plastic granules which later coalesce and form the oocyst wall. The prepatent period is 5 days.
Brackett and Bliznick (1952) found that E. brunetti could produce a maximum of 400,000 oocysts per oocyst fed. This figure was obtained in 2- to 3-week-old chickens fed 50 oocysts each. With larger inocula, relatively fewer oocysts were obtained. With inocula of 250, 1250, 6250, 20,000 and 40,000 oocysts, respectively, 150,000, 26,000, 7000, 800 and 400 oocysts were produced per oocyst fed.
Pathogenesis: E. brunetti is markedly pathogenic, but its effects depend upon the degree of infection. In light infections, no gross lesions may be seen. In heavier infections, Levine (1942) found that the gut wall becomes thickened and a pink or blood-tinged catarrhal exudate appears 4 or 5 days after experimental infection; the droppings are quite fluid and contain blood-tinged mucus and many mucus casts. The birds become somewhat depressed. These signs continue for 5 days and then subside if the birds recover.
In early or light infections, hemorrhagic, ladder-like streaks are present on the mucosa of the lower intestine and rectum. In heavy infections, a characteristic necrotic enteritis appears. It may involve the entire intestinal tract, but is more often found in the lower small intestine, large intestine and tubular part of the ceca. A patchy or continuous, dry, caseous necrotic membrane may line the intestine, and the intestine may be filled with sloughed, necrotic material. Circumscribed white patches may be visible thru the serosa, and there may even be intestinal perforation with resultant peritonitis.
Boles and Becker (1954) did not observe the extensive coagulation necrosis described by Levine (1942) in their experimentally infected chicks, but the other lesions were similar to those of his moderately infected birds. The birds became listless 82 hours after infection, and petechial hemorrhages were found, mostly in the lower small intestine but also in the middle and upper small intestine. These became more severe the next day but had disappeared from the upper and middle intestine. The lower small intestine and large intestine were hyperemic and hemorrhagic, there was epithelial sloughing, and the intestinal contents were watery and blood-tinged. The tubular part of the ceca was involved, and the dilated portion was plugged with dehydrated material. The epithelial denudation was most probably caused by the asexual stages, and was most prominent on the 4th day. Signs of illness continued until the 6th day.
Field outbreaks of the disease were studied by Levine (1943). The disease occurs most commonly in chicks 4 to 9 weeks old. The mortality is high, and typical necrotic lesions are present. We have seen the same condition in field outbreaks in Illinois.