THE TELOSPORASIDA AND THE COCCIDIA PROPER 



215 



an alcoholic horse kidney extract produced 

 fewer oocysts than untreated, infected 

 controls. Burns and Challey (1959) found 

 that when chicks which had been previously 

 infected thru a fistula into a cecal pouch 

 which had been isolated from the intestine 

 were challenged with E. tenella orally, 

 they were somewhat more resistant than 

 the controls, indicating that there is some 

 generalized host response. 



Less research has been done on the 

 development of immunity in other species 

 of coccidia. Tyzzer, Theiler and Jones 

 (1932) found that chickens which had re- 

 covered from E. necatrix infections were 

 immune, as did Grumbles and Delaplane 

 (1947). Dickinson (1941) and Brackett 

 and Bliznick (1950) showed that immunity 

 developed following infection with E. 

 acervulina. The latter found the same 

 thing with E. maxima. Similar results 

 have been obtained for the other species 

 (Brackett and Bliznick, 1950). 



Diagnosis : Avian coccidiosis can be 

 diagnosed by finding lesions containing 

 coccidia at necropsy. Diarrhea with or 

 without blood in the droppings, inappetence 

 and emaciation are suggestive, but scrap- 

 ings of the affected intestinal mucosa must 

 be examined microscopically to determine 

 whether coccidia are present. It is not 

 enough to look for oocysts, but schizonts, 

 merozoites and young gametes should be 

 recognized also. 



Coccidiasis is much more common 

 than coccidiosis; hence the mere presence 

 of oocysts in the feces cannot be relied 

 upon for diagnosis. Conversely, the ab- 

 sence of oocysts does not necessarily mean 

 that coccidiosis is not present, since the 

 disease may be in too early a stage to 

 produce oocysts. 



Since some species of coccidia are 

 highly pathogenic for the chicken while 

 others are practically non-pathogenic, 

 the species present must be identified to 

 establish a diagnosis. This can often be 

 done in a rough way from the type and lo- 

 cation of the lesions. 



Treatment : Many hundreds of papers 

 have been written on the treatment of coc- 



cidiosis in chickens, and there is no space 

 here for more than a relatively brief dis- 

 cussion. By far the greatest part of the 

 research has been done on E. tenella. 



The first compound found effective 

 against coccidia was sulfur, which Herrick 

 and Holmes (1936) introduced. When 2 to 

 5% sulfur is mixed with the feed, coccid- 

 iosis is largely prevented in young chicks. 

 The use of sulfur had a certain vogue, but 

 it was soon found unsatisfactory because 

 it causes a condition known as sulfur rick- 

 ets. Even tho the chicks are on an ordin- 

 arily adequate diet, the sulfur interferes 

 with calcium utilization and causes rickets. 



The use of borax in E. tenella coccid- 

 iosis was introduced by Hardcastle and 

 Foster (1944). Several others have done 

 research on it (Wehr, Farr and Gardiner, 

 1949), and the consensus is that 0. 3 to 

 0. 5% borax in the feed prevents death from 

 coccidiosis if administered beginning 1 or 

 2 days after experimental infection and 

 continued for 3 days or longer. However, 

 it does not prevent cecal hemorrhage or 

 weight losses. It is also toxic, causing 

 loss of weight even when fed alone. 



P. P. Levine (1939) was the first to 

 use sulfonamides against coccidiosis. His 

 discovery that sulfanilamide was active 

 opened up the field. Many different-- 

 probably several hundred--sulfonamides 

 were tested, and a number of them were 

 found of practical value. Sulfaguanidine 

 was introduced after sulfanilamide. It 

 was followed by sulfamerazine and sulfa- 

 methazine (called sulfamezathine in Eng- 

 land), and still later by sulfaquinoxaline 

 and N'*-acetyl-N'-(4-nitrophenyl) sulfanil- 

 amide. All of these compounds are effec- 

 tive against E. tenella, the last 2 are 

 quite effective against E. necatrix, and 

 sulfaquinoxaline and sulfaguanidine are 

 quite effective against E. acervulina. 

 Sodium sulfadimidine is active against 

 E. mitis, but does not completely elim- 

 inate it (Joyner, 1958). 



Sulfaguanidine is fed at the rate of 

 0. 5% in the mash, sulfamethazine and sul- 

 famerazine at 0. 1 to 0.25%, and sulfaquin- 

 oxaline at 0.025%. Sodium sulfamethazine 

 and sodium sulfadimidine are given in the 



