THE TELOSPORASIDA AND THE COCCIDIA PROPER 



229 



with 4 to 7 doses of oocysts over a period 

 of 22 to 29 days. The immunized birds 

 were not immune to E. dispersa, the 

 species which E. innocua most closely 

 resembles, and turkeys immunized against 

 E. dispersa were susceptible to infection 

 with E. innocua. 



EIMERIA SUBROTUNDA 



MOORE, BROWN AND CARTER, 1954 



Host : Turkey. 



Moore, Brown and Carter (1954) were 

 unable to infect the chicken, guinea fowl, 

 ringnecked pheasant or bobwhite quail with 

 this species. 



Location: Duodenum, jejunum and 

 upper ileum as far as 2 inches anterior to 



the yolk stalk rudiment. 



Geographic Distribution : 

 America. 



North 



Prevalence : Apparently uncommon. 



Morphology : This species closely 

 resembles E. innocua, according to 

 Moore, Brown and Carter (1954). The 

 oocysts are subspherical, smooth, 16 to 

 26 by 14 to 24 jj. with a mean of 22 by 20 ji , 

 without a micropyle or polar granule. No 

 other morphological information was given. 

 The sporulation time is 48 hours. 



Life Cycle : Unknown. According to 

 Moore, Brown and Carter (1954), the en- 

 dogenous stages occur in the epithelial 

 cells of the tips of the villi, extend along 

 the sides of the villi to some extent, but 

 never invade the crypts and deep glands. 

 Oocysts first appear in the feces 96 hours 

 after infection, and the patent period is 12 

 to 13 days. 



Pathogenesis : This species is appar- 

 ently non- pathogenic. Moore, Brown and 

 Carter (1954) observed no signs of infec- 

 tion, diarrhea or gross lesions in poults 

 less than 5 weeks old which had been in- 

 fected with massive doses of sporulated 

 oocysts. 



Immunity : Moore, Brown and Carter 

 (1954) immunized turkey poults by feeding 

 them 10,000 to 15,000 sporulated oocysts 

 every 4 days until they ceased to shed 

 oocysts; this occurred in less than a month. 

 Poults which had been immunized against 

 E. subrotunda were not immune to E. 

 innocua and E. dispersa, and poults which 

 had been immunized against the latter two 

 species were not immune to E. subrotunda. 

 This was the primary basis for separating 

 E. subrotunda from E. innocua. 



COCCIDIOSIS IN TURKEYS 



Epidemiology : Coccidiosis in turkeys 

 has been discussed by Morehouse (1949), 

 Hawkins (1952), Moore (1954) and Becker 

 (1959) among others. The U. S. Dept. of 

 Agriculture (1954) estimated that it caused 

 an annual loss of $466,000 from 1942 to 

 1951, and it is becoming of increasing im- 

 portance to the turkey grower. 



Of the 7 species of Eimeria, 1 of 

 Isospora and 1 of Cryptosporidium reported 

 from turkeys, by far the most important 

 are E. meleagriniitis and E. adenoeides. 

 The former affects the jejunum and the 

 latter the lower ileum, ceca and rectum. 



Coccidiosis is primarily a disease of 

 young birds. Older birds are carriers. 

 Poults become infected by ingesting 

 oocysts along with their feed or water. 

 The severity of the disease depends on the 

 number of oocysts they receive. If they 

 ingest relatively few, they may develop 

 immunity without ever showing signs of 

 illness, while if they ingest large numbers, 

 they may become seriously ill or die. 

 Crowding and lack of sanitation greatly 

 increase the disease hazard. 



Diagnosis : Coccidiosis of turkeys 

 can be diagnosed in the same way as coc- 

 cidiosis of chickens by finding endogenous 

 stages of the coccidia in scrapings of the 

 affected parts of the intestinal tract of 

 birds which show signs of the disease. 

 The mere presence of coccidia in the ab- 

 sence of disease cannot be relied on. Since 

 several species of turkey coccidia 



