Adult male Chukar partridge, Alectoris chukarFarm raised chukar, found dead.
Hepatic necrosis, multifocal, severe.
Typhlitis, necrotizing, multifocal, severe.
Nematodiasis, small intestine and cecae, severe.
Liver: Multifocal, variably sized, random areas of coagulative and lytic necrosis replace hepatocytes throughout all lobules. Large numbers of macrophages, degenerative and intact heterophils intermixed with foreign body-type multinucleated giant cells are adjacent to areas of necrosis. Fewer lymphocytes and plasma cells surround these areas. Large numbers of macrophages and multinucleated giant cells contain myriads of intracytoplasmic, approximately 15 um diameter, round, lightly eosinophilic protozoal trophozoites.
Cecum: Similar trophozoites fill macrophages and multinucleated giant cells surrounded by degenerative heterophils, karyorrhectic debris and proteinaceous material cover the ulcerated lamina propria.
Hepatocellular necrosis, lymphocytic-histiocytic hepatitis, with intracellular and intralesional trophozoites consistent with Histomonas meleagridis
Typhlitis, necrotizing, multifocal, severe, and histiocytic, with intrahistiocytic and intralesional trophozoites consistent with Histomonas meleagridis
Histomoniasis is caused by a flagellated protozoan parasite, Histomonas meleagridis, that colonizes earthworms and the cecal nematode, Heterakis gallinarum (1, 2). Histomoniasis primarily affects gallinaceous birds (chickens, grouse, partridge, peafowl, pheasants, quail, turkeys); lesions are primarily found within the liver and cecum (5, 6). Turkeys, either wild or domestic, almost always develop severe disease following infection. Chukar partridge, peafowl and ruffed grouse also are prone to severe disease (4). Ring-necked pheasants, chickens and junglefowl rarely become sick; these species serve as carriers of the parasite. Bobwhites, guinea fowl and Hungarian partridge exhibit high morbidity, but intermediate mortality.
Liver: Hepatitis, necrotizing, multifocal to coalescing, severe, with numerous protozoal trophozoites.
Brain: No significant lesions.
This historically important disease has caused more losses to the turkey industry than any other disease, and occurs especially in poults, as well as chickens and captive game birds. Although the disease is less severe in chickens, economic losses are often greater than in turkeys due to the frequency of occurrence and greater number of birds affected(7). Histomonas was originally classified as an amoeba, but was reclassified as a flagellated protozoan by Tyzzer in 1920 based on the presence of a flagellum when in the cecal lumen and absence of a cyst form(6). Although histomoniasis is colloquially called blackhead for the development of cyanosis of the head, this inconsistent sign is not pathognomonic. The conversion of hemoglobin to methemoglobin in acute disease may also contribute to cyanosis(7).
Transmission is by ingestion of 1) infected feces; 2) embryonated Heterakis eggs containing histomonads; or 3) an earthworm containing infected Heterakis larvae. Histomonads are released into the intestinal lumen when the Heterakis eggs hatch and then invade the cecal wall. Two to three days after cecal infection, the protozoa reach the liver via hepatic-portal circulation, and can also be found in the bursa of Fabricus, kidney, pancreas, and spleen(7). In addition to vector-borne transmission, histomoniasis can spread directly through cloacal drinking, which is the retrograde peristalsis of urine and fecal contaminants from the vent into the bursa and ceca; this is important in rapid spread of the disease through turkey flocks(6).
In addition to the gross lesions seen in this case, the ceca are often bilaterally enlarged and hyperemic with thickened walls, and may contain a central caseous, laminated core, necessitating differentiation from Eimeria tenella and Salmonella spp. The liver may have depressed targetoid lesions which often coalesce. Histomonas may be difficult to identify histologically in chronic lesions, and the presence of rounded empty spaces within a marked inflammatory response should raise the specter of histomoniasis, especially within the liver or ceca(2).
Histomonas achieves its full virulent potential when Escherichia coli, Clostridium perfringens, or Bacillus subtilis is present in the cecum, and is avirulent in gnotobiotic poults. Conversely, Histomonas mitigates Eimeria infections in the cecum by creating an inhospitable environment for coccidia to flourish. In chickens with histomoniasis, coinfection with Eimeria tenella significantly increases the development of hepatic necrosis(7).
1. Callait-Cardinal M, Chauve C, Reynaud M, Alogninouwa T, Zenner L. Infectivity of Histomonas meleagridis in ducks. Avian Pathology. 35:109-116, 2006.
2. Charlton BR. Avian Disease Manual. 4th ed., Atlanta, GA:American Association of Avian Pathologists; 2006:152-3.
3. Grabensteiner E, Hess M. PCR for the identification and differentiation of Histomonas meleagridis, Tetratrichomonas gallinarum and Blastocystis spp. Vet Parasitol. 20:223-230, 2006.
4. Janildo L, Reis R, Beckstead C, Brown A, Gerhold R. Histomonas meleagridis and Capillarid Infection in a Captive Chukar (Alectoris chukar). Avian Diseases. 53:637-639, 2009.
5. McDougald L, Fuller L. Blackhead disease in turkeys: direct transmission of Histomonas meleagridis from bird to bird in a laboratory model. Avian Disease.49:328-331. 2005.
6. McDougald L. Blackhead disease (histomoniasis) in poultry: a critical review. Avian Disease. 49: 462-476. 2005.
7. McDougald LR. Histomoniasis (Blackhead) and Other Protozoan Diseases of the Intestinal Tract. In: Saif YM ed., Diseases of Poultry. 12th ed., Ames, IA:Blackwell; 2008:1095-1100.