Histomoniasis in Poultry
(Blackhead, Infectious enterohepatitis)
Histomonas meleagridis, an anaerobic protozoan parasite of the order Trichomonadida, is the causative agent of histomoniasis (blackhead disease). It can exist in flagellated (8–15 mcm in diameter) and amoeboid (8–30 mcm in diameter) forms. H meleagridis is primarily transmitted in the egg of the cecal nematode, Heterakis gallinarum. Chickens and other gallinaceous birds act as a reservoir for H gallinarum. Nematode eggs infected with H meleagridis remain viable in the environment for years. Three species of earthworms can act as paratenic hosts for H gallinarum larvae containing H meleagridis. Chickens and turkeys that consume these earthworms can become infected with both H gallinarum and H meleagridis. In turkeys, transmission by direct cloacal contact with infected birds or via fresh droppings results in H meleagridis quickly spreading throughout the flock. Traditionally, histomoniasis has been thought of as affecting turkeys while doing little damage to chickens. However, outbreaks in chickens may cause morbidity and moderate mortality. Liver lesions tend to be absent or less severe in chickens but can involve secondary bacterial infections. In most cases, chickens recover from clinical signs but remain carriers, whereas turkeys succumb to the infection.
Signs of histomoniasis are apparent in turkeys 7–12 days after infection and include:
The origin of the name “blackhead” is obscure and misleading; birds do not display a cyanotic head. Young birds have a more acute disease course and die within a few days after signs appear. Older birds may be sick for some time and become emaciated before death.
The primary lesions of histomoniasis are in the ceca, where the parasite migrates into the submucosa and muscularis mucosae. This leads to inflammation and development of a yellowish green caseous exudate or, in later stages, a dry, cheesy core. Occasionally, these ulcers erode the cecal wall, leading to peritonitis and involvement of other organs. The clinical signs in the ceca are apparent 3–4 days after H meleagridis invasion. Histomonads can reach the liver either by the vascular system or via the peritoneal cavity. Liver lesions are highly variable in appearance; in turkeys, they appear 6–8 days after infection and may be up to 4 cm in diameter and involve the entire organ. In some cases, the liver will appear green or tan. Lesions are also seen in other organs, such as the kidneys, bursa of Fabricius, spleen, and pancreas.
PCR, examination of cecal contents under a microscope, and histopathologic examination can be used to diagnose histomoniasis.
The liver lesions must be differentiated from those of:
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.
Because healthy chickens and game birds often carry the cecal worm vector, any contact between turkeys and other galliformes should be avoided and care should be taken to reduce the worm population. Worm eggs, from contaminated soil, can be tracked inside by workers, causing infection. Arthropods such as flies may also serve as mechanical vectors. 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 turkey flock, infection spreads rapidly without a vector through direct contact. Dividing a facility into subunits using barriers can contain the outbreaks to specific units. Histomonads that are shed directly into the environment die quickly. Thus, in a turkey facility, where H gallinarum is unable to complete its life cycle, decontamination is not required.
Immunization has only been partially successful in controlling histomoniasis, and reports differ on its effectiveness. The immune response of turkeys to live, attenuated Histomonas requires 4 weeks to develop. Vaccination of 18-week-old pullets 5 weeks before experimental infection has been shown to prevent a drop in egg production. 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 do not offer protection.
No drugs are currently approved for use as treatments for histomoniasis. 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 H gallinarum worms that carry the infection.