Blackhead (histomoniasis) in small turkey flocks
Marina Brash, Lloyd Weber
Blackhead disease, also known as histomoniasis and enterohepatitis, is a disease that is diagnosed frequently at the AHL in late summer and fall in small turkey flocks, and because there are no approved preventive or treatment medications, mortalities can persist resulting in very high losses.
Blackhead is caused by a protozoan parasite, Histomonas meleagridis, which is carried by the common poultry cecal worm Heterakis gallinarum, found in the ceca of chickens and turkeys. Histomonas is fragile and cannot live outside the bird host for long but can survive for long periods of time in the environment when in the cecal worm or its eggs. Earthworms can also carry infected cecal worm eggs and are important in transmitting blackhead. Flies, beetles, including darkling beetles, grasshoppers, sowbugs, and crickets can also serve as mechanical vectors. Cecal worms and eggs can also be transferred via contaminated manure on equipment and shoes.
Typically, outbreaks in turkeys begin with the ingestion of infected earthworms or cecal worms or eggs from contaminated soil or concrete-floored pens where flocks of chickens or turkeys have been raised. Wild grouse and quail may also carry the infection to turkey yards. In turkeys, bird-to-bird transmission, through direct cloacal contact or with infected droppings, can contribute to maintenance of the outbreak. Chickens, pheasant, partridge, and peafowl are also susceptible.
Once the H. meleagridis organisms are ingested, they travel to the cecum, penetrate the mucosa, multiply, resulting in necrosis, inflammation, and thickening of the cecal wall, enter the bloodstream and travel to the liver inciting necrosis and inflammation. In the intestine, interaction with coccidia and bacteria including Clostridium perfringens and E. coli increases the severity of disease with more tissue damage. Turkeys can show clinical signs of illness 7-12 d post-ingestion including anorexia, drowsiness, ruffled feathers, drooping of the wings, placement of the head down and close to the body or tucked under the wing, and the excretion of yellow feces described as sulfur-yellow droppings (Fig. 1). The head may or may not be cyanotic. Death follows shortly thereafter.
At postmortem, lesions are characteristic with enlargement of the cecal pouches and marked thickening of cecal walls with thick caseous cores (Fig. 2). Extension of inflammation through the cecal serosa will result in localized peritonitis. The liver is enlarged, with multiple circular depressed areas of necrosis circumscribed by raised yellow rings described as targetoid lesions (Fig. 1). Lesions can also be found in other organs, including kidneys, bursa of Fabricius, spleen, lungs, pancreas, and proventriculus. Histopathology can confirm the diagnosis as the histomonad organisms will be present in cecal and liver tissues.
There are no approved preventive or treatment medications, therefore prevention of this disease is the key and the approach is multipronged.
(For more detail on recommendations, please see our LabNote 54.)
1. Do not raise turkeys where chickens have been housed.
2. Concrete-floored pens are preferred to dirt floors.
3. Prevent fecal contamination of bedding and housing.
4. The cecal worm burden can be evaluated by inspection of cecal contents during PMs. Ascarid and cecal worm eggs can be differentiated by size on fecal flotations.
5. Moving sick turkeys will only contaminate the new site.
6. Contaminated litter must be removed. Washing and disinfecting concrete or wood floors works well.
If possible, move up the processing date for the remaining healthy birds. If the turkeys are dehydrated and/or in poor body condition at processing, and/or have grossly affected internal organs, they will be be condemned. AHL
Figure 1. Sulfur-yellow droppings on the underside of the tail feathers. Typical targetoid lesions in liver.
Figure 2. Enlarged cecal pouches containing typical caseous cecal cores.