Overview of Histomoniasis in Poultry

The causative agent of histomoniasis is the anaerobic, single cell protozoan parasite Histomonas meleagridis that can exist in flagellated (8–15 μm in diameter) and amoeboid (8–30 μm in diameter) forms. Histomonas is most often transmitted in embryonated eggs of the cecal nematode Heterakis gallinarum. A large percentage of chickens and other gallinaceous birds harbor this worm, which serves as a reservoir. Three species of earthworms can act as vectors for 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 the ceca. 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. In turkeys, transmission is by direct cloacal contact with infected birds or via fresh droppings, resulting in histomoniasis quickly spreading throughout the flock. Infection has not been shown to spread in this manner in chickens.

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 but lack uniformity. Experimental infections with Histomonas of 16-wk-old layers have demonstrated reduced egg production during infection. Tissue responses to infection may resolve in 4 wk, but birds may be carriers for another 6 wk.

Signs of histomoniasis are apparent in turkeys 7–12 days after infection and include listlessness, reduced appetite, drooping wings, unkempt feathers, and yellow droppings in the later stages of the disease. The origin of the name “blackhead” is obscure and misleading, with only a few birds displaying a cyanotic head. 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.

Because healthy chickens and gamebirds often carry the cecal worm vector, any contact between turkeys and other galliforms 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 Heterakis 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 wk to develop. Vaccination of 18-wk-old pullets 5 wk 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. Nitarsone is available for prophylaxis by feed medication. Nitarsone is mixed with the feed at 0.01875% and fed continually. A 5-day withdrawal period is required for animals slaughtered for human consumption. Under most conditions, nitarsone 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.