228 



THE TELOSPORASIDA AND THE CCXCIDIA PROPER 



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. 



Since E. adenoeides is found in the same 

 locations as E. meleagridia and E. gal- 

 lopavonis, and since its oocysts are ap- 

 parently similar to theirs, this lack of 

 reciprocal immunity is an important dif- 

 ferentiating criterion. The only other dif- 

 ferences are its greater pathogenicity ancj 

 its location in the crypts and deep glands 

 rather than only in the tips of the villi. 



On the 6th to 8th days in birds infected 

 with 10,000 oocysts, the terminal intestine 

 contains white, creamy mucus, and pete- 

 chiae are present in the mucosa. By the 

 9th day the intestinal contents appear nor- 

 mal, altho they still contain large numbers 

 of oocysts (Clarkson, 1958). 



Infiltration with eosinophiles commen- 

 ces as early as 2 hours after infection, 

 and enormous numbers of eosinophiles 

 may be found in the terminal small intes- 

 tine, ceca and rectum from the 3rd to the 

 10th days. 



Beginning 4 days after infection, ed- 

 ematous 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 epithel- 

 ial denudation increase progressively until 

 the 6th day. In birds which recover from 

 the disease or which have received rela- 

 tively few oocysts, resolution is very 

 rapid. Vascularity is greatly reduced, 

 the deep glands are almost free of para- 

 sites 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. Clark- 

 son (1959a), too, found no cross immunity 

 between E. meleagridis and E. adenoeides . 



EIMERIA INNOCUA 

 MOORE AND BROWN, 1952 



Host : Turkey. 



Moore and Brown (1952) were unable 

 to infect the chicken, guinea fowl, ring- 

 necked pheasant and bobwhite quail with 

 E. innocua. 



Location: Thruout the small intestine. 



Geographic Distribution : 

 America (New York). 



North 



Prevalence : Apparently uncommon. 



Morphology : The oocysts of this 

 species were described by Moore and 

 Brown (1952). They are subspherical, 

 smooth, 19 to 26 by 17 to 25 ji with a mean 

 of 22 by 21 ^t, and without a micropyle or 

 oocyst polar granule. No other morpho- 

 logical information was given. The sporu- 

 lation time is 2 days. 



Life Cycle : Unknown. The endogen- 

 ous stages occur in the epithelial cells of 

 the villi. The tips of the villi are most 

 heavily parasitized, while the crypts and 

 deep glands are never affected. According 

 to Moore and Brown (1952), oocysts first 

 appear in the feces 5 days after infection, 

 and the patent period is up to 9 days. 



Pathogenesis : This species is non- 

 pathogenic according to Moore and Brown 

 (1952). They observed no macroscopic 

 lesions, even in heavy infections; poults 

 less than 5 weeks old showed no signs of 

 illness and had no diarrhea. 



Immunity : Moore and Brown (1952) 

 immunized turkey poults by infecting them 



