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 importance 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. meleagrimitis 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 coccidiosis 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 absence of disease cannot be relied on. Since several species of turkey coccidia (E. innocua, E. subrotunda and E. meleagridis in particular) are non-pathogenic or nearly so, they must be differentiated from the pathogenic E. meleagrimitis and E. adenoeides. The sporulated oocysts of both the latter have polar bodies, which differentiates them from all but E. meleagridis and E. gallopavonis. The oocysts of E. meleagrimitis are ellipsoidal, but apparently only pathogenesis and absence of cross-immunity differentiates E. adenoeides from the other two. This last is hardly a practical diagnostic test, since it requires a colony of turkeys immunized against the various species.

Treatment

The sulfonamides are effective against a number of the turkey coccidia. Morehouse (1949a) found that only one of 6 sulfonamides was ineffective against E. meleagridis. Peterson (1949a) found that several sulfonamides were effective against E. meleagrimitis. Moore (1949) found that 0.031% sulfaquinoxaline, 1% sulfaguanidine or 0.5% sulfamerazine in the feed was effective against turkey coccidiosis. Wilson (1951) reported that 0.06% sodium sulfaquinoxaline in the drinking water stopped losses from E. meleagridis and E. meleagrimitis in a natural outbreak. (Their cultures of E. meleagridis may have contained E. adenoeides, a species which had not yet been named at the time.) Boyer and Brown (1953) found that 0.0175% acetylsulfaquinoxaline in the feed or 1-1000 to 1-2000 sulfamethazine in the water was effective against E. adenoeides, E. gallopavonis, E. meleagridis, E. innocua, E. subrotunda, E. dispersa and£. meleagrimilis. Horton-Smith and Long (1959) found that 0.0125% sulfaquinoxaline in the feed was effective against E. meleagrimitis.

Other coccidiostats used in treating chickens have not been found so useful in turkeys. Morehouse (1949) found that sodium 4-chlorophenyl arsonate was the most effective of 10 organic arsenic compounds to be tested against E. meleagridis, but that its effective dose was too close to the toxic one. Another organic arsenic compound, 3-nitro-4-hydroxyphenyl arsonic acid was of less value.

Boyer and Brown (1953) found that nitrophenide, 2-amino-5-nitrothiazole, sulfisoxazole, nitrofurazone and furoxone were not effective coccidiostatic agents in the turkey. Cuckler et al. (1955) reported that nicarbazin was effective against E. gallopavonis and E. meleagrimitis, but Horton-Smith and Long (1959) found that it was ineffective against E. meleagrimitis and in addition found that nitrofurazone and glycarbylamide were also ineffective against this species.

Prevention and Control

The same measures should be used for the prevention and control of coccidiosis in turkeys as in chickens.