224 



THE TELOSPORASIDA AND THE COCCIDIA PROPER 



infection and reach maturity at about 96 

 hours. They measure about 8 by 7/i and 

 differ from the second generation schi- 

 zonts in having a residuum. They produce 

 8 to 16 merozoites which measure about 

 7 by 1. 5ju 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 /i, and the 

 microgametocytes contain a rounded res- 

 iduum. 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. 



The duodenal mucosa occasionally seems 

 to have undergone coagulation necrosis, 

 and pieces of caseous material may be 

 scattered in the lumen of the entire intes- 

 tine along with a large amount of fluid 

 which may have a pinkish tinge. The re- 

 mainder 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 hemor- 

 rhage 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. 



Pathogenesis : This species is mod- 

 erately 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. Haw- 

 kins (1952) found that infection with 

 50,000 sporulated oocysts produced a high 

 mortality in young poults, in some in- 

 stances 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, respec- 

 tively. Food utilization is reduced in in- 

 fected 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 contain- 

 ing merozoites and small amounts of blood 

 and other cells. Five to 6 days after infec- 

 tion the duodenum is enlarged, its blood 

 vessels are engorged, and it contains a 

 reddish brown, necrotic core which ad- 

 heres firmly to the mucosa and extends a 

 little way into the upper small intestine. 



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 ab- 

 normalities 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 ap- 

 pear 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 in- 

 creased cellularity of the lamina propria. 



Immunity : According to Hawkins 

 (1952), the immunity produced by infections 

 with this species is not as solid as that 



