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Histomoniasis is caused by a protozoan that infects the ceca, and later the liver, of turkeys, chickens, and occasionally other galliform birds. In turkeys, most infections are fatal; in other birds, mortality is less common.
Etiology
The protozoan parasite Histomonas meleagridis is transmitted most often in embryonated eggs of the cecal nematode Heterakis gallinarum, and sometimes directly by contact with infected birds. Outbreaks spread quickly through flocks by direct contact. A large percentage of chickens harbor this worm, and histomonads have been located in adult worms of both sexes. Three species of earthworms can harbor H gallinarum larvae containing H meleagridis, which are infective to both chickens and turkeys. H meleagridis survives for long periods within Heterakis eggs, which are resistant and may remain viable in the soil for years. Histomonads are released from Heterakis larvae in the ceca a few days after entry of the nematode and replicate rapidly in cecal tissues. The parasites migrate into the submucosa and muscularis mucosae and cause extensive and severe necrosis. Histomonads reach the liver either by the vascular system or via the peritoneal cavity, and rounded necrotic lesions quickly appear on the liver surface. Histomonads interact with other gut organisms, such as bacteria and coccidia, and depend on these for full virulence.
Traditionally, histomoniasis has been thought of as affecting turkeys, while doing little damage to chickens. However, outbreaks in chickens may cause high morbidity, moderate mortality, and extensive culling. Liver lesions tend to be less severe in chickens, but often involve secondary bacterial infections. Morbidity can be especially high in young layer or breeder pullets. Layer flocks recover and produce eggs normally, but lack uniformity. Tissue responses to infection may resolve in 4 wk, but birds may be carriers for another 6 wk. Wild or feral chickens, pheasants, chukars, and bobwhite quail are common sources of infection for turkey flocks.
Clinical Findings
Signs are apparent in turkeys 7–12 days after infection and include listlessness, drooping wings, unkempt feathers, and yellow droppings. The origin of the name “blackhead” is obscure and misleading. Young birds have a more acute disease and die within a few days after signs appear. Older birds may be sick for some time and become emaciated before death.
Lesions
The primary lesions are in the ceca, which exhibit marked inflammatory changes and ulcerations, causing a thickening of the cecal wall. Occasionally these ulcers erode the cecal wall, leading to peritonitis and involvement of other organs. The ceca contain a yellowish green, caseous exudate or, in later stages, a dry, cheesy core. Liver lesions are highly variable in appearance; in turkeys, they may be up to 4 cm in diameter and involve the entire organ. The liver and cecal lesions together are pathognomonic. However, the liver lesions must be differentiated from those of tuberculosis, leukosis, avian trichomoniasis, and mycosis. Lesions are also seen in other organs, such as the kidneys, bursa of Fabricius, spleen, and pancreas. Studies by PCR show that Histomonas nucleic acids can be found in the blood and in the tissues of most organs, whether lesions are present or not. Histopathologic examination is helpful for differentiation of diseases.
Histomonads are intercellular, although they may be so closely packed as to appear intracellular. The nuclei are much smaller than those of the host cells, and the cytoplasm less vacuolated. Scrapings from the liver lesions or ceca may be placed in isotonic saline solution for direct microscopic examination; Histomonas spp must be differentiated from other cecal flagellates. Molecular diagnosis is possible with published PCR primers.
Prevention and Treatment
Because healthy chickens and gamebirds often carry the cecal worm vector, any contact between turkeys and other birds should be avoided. Wild birds may contaminate soil around turkey farms, so that worm eggs can be tracked inside by workers, causing infection. Because H gallinarum ova can survive in soil for many months or years, turkeys should not be put on ground contaminated by chickens. Once established in a flock, infection spreads rapidly without a vector.
Immunization does not control histomoniasis. The immune response to infection develops slowly and gives only modest protection. Most workers have concluded that immunization of birds against this disease using live cultures is not practical. Killed organisms stimulate some immunity when given SC or IP but 2–3 inoculations are necessary over several weeks. Further study is needed to define a workable immunization plan.
There are currently no drugs approved for use as treatments for histomoniasis. A single drug (nitarsone) is available for prophylaxis by feed medication. Nitarsone is mixed with the feed at 0.01875% and fed continuously. Under most conditions this product is effective, although some outbreaks in turkeys on medication have been reported. Historically, nitroimidazoles such as ronidazole, ipronidazole, and dimetridazole were used for prevention and treatment and were highly effective. Some of these products can be used by veterinary prescription in non-food-producing birds. Frequent worming of chickens with benzimidazole anthelmintics helps reduce exposure to heterakid worms that carry the infection.
Last full review/revision March 2012 by Larry R. McDougald, PhD
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