From the AAAP Avian Disease Manual
C. HISTOMONIASIS
(Blackhead; Enterohepatitis)
DEFINITION
Histomoniasis is a protozoal disease caused by
Histomonas meleagridis affecting turkeys, chickens,
peafowl, grouse, quail and possibly other gallinaceous birds characterized by necrotizing lesions involving
the ceca and liver.
OCCURRENCE
Histomoniasis occurs most frequently in exposed, unmedicated turkeys, especially turkeys under 3
months of age. It also occurs in chickens and in many captive game birds. Young birds are more
frequently and severely affected. The disease is infrequent in areas where there are no earthworms i.e.,
where there is dry, sandy soil and where there are no vectors for transmission of histomonads.
Histomoniasis occurs infrequently where proper measures are taken for its prevention.
HISTORICAL INFORMATION
1. Histomoniasis once limited the expansion of the turkey industry. Prior to development of safe
antihistomonal drugs, it could be controlled only by cumbersome and relatively ineffective measures
designed to prevent exposure of turkeys to the embryonated ova of cecal worms (
Heterakis
gallinarum
).
2. Significant growth of the turkey industry occurred after safe antihistomonal drugs were developed.
The disease is now uncommon and these drugs are no longer used routinely. It occurs sporadically
when turkeys are raised where chickens were previously located. The disease is still common in
chickens but its effect on production is mild and rarely recognized. Histomoniasis remains an
important cause of death among other galliformes including peafowl, pheasant and quail.
ETIOLOGY
1. The etiologic agent is the protozoan
Histomonas meleagridis, assisted by secondary bacteria. In the
experimental absence of bacteria, the histomonad appears not to be pathogenic.
H. meleagridis is a
flagellate in the lumen of the cecum but assumes an ameboid form in tissue.
2. A larger histomonad distinguished by its 4 flagella,
H. wenrichi, also occurs in the cecum but is not
pathogenic.
EPIDEMIOLOGY
Transmission of
H. meleagridis to susceptible birds is possible via three routes:
1. Ingestion of fresh feces. This route probably is relatively unimportant except for spread within a flock.
2. Ingestion of embryonated cecal worm ova containing the protozoan. Within these resistant ova the
histomonad can survive for years.
H. meleagridis is liberated in the intestine when ingested ova hatch,
then invades the cecal wall and initiates the disease.
3. Ingestion of earthworms containing cecal worm larvae within their tissues. Earthworms serve as
transport hosts for the cecal worm and the cecal worm acts as a transport host for the histomonad.
Infection results after the cecal worm larvae are liberated during digestion.(Blackhead; Enterohepatitis)
DEFINITION
Histomoniasis is a protozoal disease caused by
Histomonas meleagridis affecting turkeys, chickens,
peafowl, grouse, quail and possibly other gallinaceous birds characterized by necrotizing lesions involving
the ceca and liver.
OCCURRENCE
Histomoniasis occurs most frequently in exposed, unmedicated turkeys, especially turkeys under 3
months of age. It also occurs in chickens and in many captive game birds. Young birds are more
frequently and severely affected. The disease is infrequent in areas where there are no earthworms i.e.,
where there is dry, sandy soil and where there are no vectors for transmission of histomonads.
Histomoniasis occurs infrequently where proper measures are taken for its prevention.
HISTORICAL INFORMATION
1. Histomoniasis once limited the expansion of the turkey industry. Prior to development of safe
antihistomonal drugs, it could be controlled only by cumbersome and relatively ineffective measures
designed to prevent exposure of turkeys to the embryonated ova of cecal worms (
Heterakis
gallinarum
).
2. Significant growth of the turkey industry occurred after safe antihistomonal drugs were developed.
The disease is now uncommon and these drugs are no longer used routinely. It occurs sporadically
when turkeys are raised where chickens were previously located. The disease is still common in
chickens but its effect on production is mild and rarely recognized. Histomoniasis remains an
important cause of death among other galliformes including peafowl, pheasant and quail.
ETIOLOGY
1. The etiologic agent is the protozoan
Histomonas meleagridis, assisted by secondary bacteria. In the
experimental absence of bacteria, the histomonad appears not to be pathogenic.
H. meleagridis is a
flagellate in the lumen of the cecum but assumes an ameboid form in tissue.
2. A larger histomonad distinguished by its 4 flagella,
H. wenrichi, also occurs in the cecum but is not
pathogenic.
EPIDEMIOLOGY
Transmission of
H. meleagridis to susceptible birds is possible via three routes:
1. Ingestion of fresh feces. This route probably is relatively unimportant except for spread within a flock.
2. Ingestion of embryonated cecal worm ova containing the protozoan. Within these resistant ova the
histomonad can survive for years.
H. meleagridis is liberated in the intestine when ingested ova hatch,
then invades the cecal wall and initiates the disease.
3. Ingestion of earthworms containing cecal worm larvae within their tissues. Earthworms serve as
transport hosts for the cecal worm and the cecal worm acts as a transport host for the histomonad.
DIAGNOSIS
1. Diagnosis can be made on the basis of clinical signs and characteristic lesion. Typical well-developed
lesions are pathognomonic [
Fig. 1; Histomoniasis; NCSU].
2. In turkeys histomoniasis appears 7-12 days after exposure. Initially there is listlessness, moderate
anorexia, drooping wings and yellow ("sulfur colored") feces. Head parts may be cyanotic
("blackhead") although they often are not. In chickens with histomoniasis there may be some blood in
the feces.
3. Later the affected turkey is depressed and stands with its wings drooping, eyes closed, head drawn
close to the body. Emaciation is common in chronic cases, usually in older birds. In young turkeys
morbidity and mortality are high, up to 100%. Older birds tend to be more resistant.
4. Gross lesions. Bilateral enlargement of the ceca with thickening of the cecal walls [
Fig. 2;
Histomoniasis; UC Davis
]. The mucosa usually is ulcerated. The ceca often contain caseous cores
which are yellow, gray or green and may be laminated. In chronic cases the cores may have been
expelled. Peritonitis occurs when the cecal wall becomes perforated.
5. Liver contains irregularly-round, depressed, target-like lesions that vary in color [
Fig. 3;
Histomoniasis; UC Davis
]. They often are yellow to gray but may be green or red. They vary greatly
in diameter but often are 1-2 cm and may coalesce to produce larger lesions.
6. Lesions may not be entirely typical in birds under treatment, less susceptible avian species or young
turkeys in the early stages of the disease. In most infected flocks typical lesions usually can be found
if an adequate number of birds are examined. In quail, cecal lesions may not occur even though
mortality is high.
7. Microscopically, histomonads can be found in the inflamed cecal walls and necrotic foci which
develop in the liver. In birds killed for necropsy the agent sometimes can be identified in smears from
the ceca or in scrapings from the margin of hepatic lesions.
CONTROL
1. Histomoniasis usually can be prevented by adding antihistomonal drugs to the ration in proper dosage.
No current preventive medication is approved in the U.S. Histostat (nitarsone) is still used in poultry
outside the U.S. In quail, a cholinesterase inhibiting carbamate (Sevin) increases susceptibility to
histomoniasis.
2. Control by the use of antihistomonal drugs may fail unless reasonably good sanitation is practiced.
3. Other measures that assist in control follow:
A. Do not keep chickens and turkeys (or other susceptible birds) on the same farm.
B. Do not use chicken ranges for turkeys or other susceptible birds unless those ranges have been
free of chickens for at least 4 years.
C.
H. meleagridis is quickly destroyed by disinfectants and drying unless protected within
earthworms or within the cecal worm ova. Avoid exposure to vectors. If possible, raise
susceptible birds on sandy, dry, loose soil. Prevent access to earthworms after rains. In range
birds, rotate ranges periodically if possible. Some operators with small lots replace the top
few inches of soil every few years using power equipment or plow the lots to reduce the
number of cecal worm ova and other pathogens.
D. Reduce access of birds to their own droppings or to feed and water contaminated with
droppings. Place feeders and waterers on large wire platforms or keep them outside of the lot
but accessible through a wire fence.1. Diagnosis can be made on the basis of clinical signs and characteristic lesion. Typical well-developed
lesions are pathognomonic [
Fig. 1; Histomoniasis; NCSU].
2. In turkeys histomoniasis appears 7-12 days after exposure. Initially there is listlessness, moderate
anorexia, drooping wings and yellow ("sulfur colored") feces. Head parts may be cyanotic
("blackhead") although they often are not. In chickens with histomoniasis there may be some blood in
the feces.
3. Later the affected turkey is depressed and stands with its wings drooping, eyes closed, head drawn
close to the body. Emaciation is common in chronic cases, usually in older birds. In young turkeys
morbidity and mortality are high, up to 100%. Older birds tend to be more resistant.
4. Gross lesions. Bilateral enlargement of the ceca with thickening of the cecal walls [
Fig. 2;
Histomoniasis; UC Davis
]. The mucosa usually is ulcerated. The ceca often contain caseous cores
which are yellow, gray or green and may be laminated. In chronic cases the cores may have been
expelled. Peritonitis occurs when the cecal wall becomes perforated.
5. Liver contains irregularly-round, depressed, target-like lesions that vary in color [
Fig. 3;
Histomoniasis; UC Davis
]. They often are yellow to gray but may be green or red. They vary greatly
in diameter but often are 1-2 cm and may coalesce to produce larger lesions.
6. Lesions may not be entirely typical in birds under treatment, less susceptible avian species or young
turkeys in the early stages of the disease. In most infected flocks typical lesions usually can be found
if an adequate number of birds are examined. In quail, cecal lesions may not occur even though
mortality is high.
7. Microscopically, histomonads can be found in the inflamed cecal walls and necrotic foci which
develop in the liver. In birds killed for necropsy the agent sometimes can be identified in smears from
the ceca or in scrapings from the margin of hepatic lesions.
CONTROL
1. Histomoniasis usually can be prevented by adding antihistomonal drugs to the ration in proper dosage.
No current preventive medication is approved in the U.S. Histostat (nitarsone) is still used in poultry
outside the U.S. In quail, a cholinesterase inhibiting carbamate (Sevin) increases susceptibility to
histomoniasis.
2. Control by the use of antihistomonal drugs may fail unless reasonably good sanitation is practiced.
3. Other measures that assist in control follow:
A. Do not keep chickens and turkeys (or other susceptible birds) on the same farm.
B. Do not use chicken ranges for turkeys or other susceptible birds unless those ranges have been
free of chickens for at least 4 years.
C.
H. meleagridis is quickly destroyed by disinfectants and drying unless protected within
earthworms or within the cecal worm ova. Avoid exposure to vectors. If possible, raise
susceptible birds on sandy, dry, loose soil. Prevent access to earthworms after rains. In range
birds, rotate ranges periodically if possible. Some operators with small lots replace the top
few inches of soil every few years using power equipment or plow the lots to reduce the
number of cecal worm ova and other pathogens.
D. Reduce access of birds to their own droppings or to feed and water contaminated with
droppings. Place feeders and waterers on large wire platforms or keep them outside of the lot
TREATMENT
There is currently no approved medication for treatment of histomoniasis in food animals. Small
groups of birds not being raised for consumption can be effectively treated individually with metronidazole
at a dose of 30 mg/kg orally SID for 5 days. Antihelmentic treatment may help suppress the population of
cecal worms.There is currently no approved medication for treatment of histomoniasis in food animals. Small
groups of birds not being raised for consumption can be effectively treated individually with metronidazole
at a dose of 30 mg/kg orally SID for 5 days. Antihelmentic treatment may help suppress the population of
But sounds like you have some strong possibilities of what it is and they are better than the unsolvable possibilities. Hope you are able to get it sorted without too much trouble. 
