History
One male and 1 female turkey, each 8 months old, from a flock of 13 birds were submitted for necropsy several days apart. The owner reported that the 2 turkeys were apparently normal and then died suddenly. He had lost 8 of 13 turkeys in a similar manner. The turkeys were housed with chickens. There were no signs of disease or any death losses among the chickens.
Gross Findings
The male turkey had a body score of 3/10. The liver size and shape were considered normal; however, it was mottled in color with five or six 2-mm-diameter pale white spots that extended into the parenchyma (Figure 1). The right cecal pouch was greatly enlarged and full of fibrous material with a thick cecal wall. The right cecal pouch was 15 cm in length and 3 cm in diameter. The cecal wall was 3 mm in thickness. The mucosal surface was red. The left cecal pouch was full of serosanguineous material and had a 5-mm-thick core of caseous material. There were no additional gross lesions.
Photograph of the liver of 1 of two 8-month-old turkeys, each of which was apparently normal and then died suddenly. Notice the white-mottled surface of the liver.
Citation: Journal of the American Veterinary Medical Association 249, 12; 10.2460/javma.249.12.1371
The female turkey had a body score of 4/10. A moderate amount (10 mL) of clear straw-colored fluid was free in the coelomic cavity. The liver was twice its expected size with rounded edges. The liver was dark red with 2- to 5-mm-diameter white flat circular lesions distributed evenly throughout the liver parenchyma. There were 15 to 20 lesions. The right and left ceca were each 11 cm in length and 2 cm in diameter. The cecal pouch wall was 1 mm in thickness. There were no additional gross lesions
Formulate differential diagnoses from the history, clinical findings, and Figure 1—then turn the page→
Histopathologic Findings
Samples of formalin-fixed liver and cecum from each bird were routinely processed and stained with H&E stain. Approximately 45% of the normal architecture of the livers was replaced by multifocal and focally extensive to coalescing foci of hepatocyte loss and replacement by eosinophilic debris (necrosis; Figure 2). There was a dense associated inflammatory infiltrate composed of macrophages, lymphocytes, plasma cells, and multinucleated giant cells in various numbers. Within the hepatocytes, macrophages, and multinucleated giant cells as well as free in the necrotic cellular debris, there were numerous spherical eosinophilic protozoal trophozoites, each approximately 10 to 20 μm in diameter (Figure 3). Occasionally, the intracytoplasmic trophozoites were surrounded by clear space. The normal architecture of the walls of the cecal pouches was expanded and replaced by numerous macrophages, lymphocytes, and plasma cells, with fewer multinucleated giant cells. The inflammatory infiltrate multifocally extended from the variably ulcerated and necrotic lamina propria through the submucosa, muscular tunics, and serosa into the associated mesenteric adipose tissue. Multifocally, there were large foci of necrosis with abundant eosinophilic cellular debris. In the lamina propria, submucosa, and muscular tunics, there were numerous protozoal trophozoites, approximately 10 to 20 μm in diameter. The lumens of the cecal pouches contained a coagulum composed of fibrin, degenerate inflammatory and epithelial cells, erythrocytes, bacteria of variable morphology, and degenerate protozoal organisms (cecal core).
Photomicrograph of a section of affected liver from one of the affected turkeys of Figure 1. Notice the focus of necrosis (N) and the mixed inflammatory infiltrate with multinuclear giant cells (arrow) containing protozoal trophozoites. H&E stain; bar = 40 μm.
Citation: Journal of the American Veterinary Medical Association 249, 12; 10.2460/javma.249.12.1371
Higher-magnification photomicrograph of the section of affected liver from one of the affected turkeys in Figure 2. Intracellular and extracellular protozoal trophozoites (arrows), typical of Histomonas meleagridis, are visible. H&E stain; bar = 10 μm.
Citation: Journal of the American Veterinary Medical Association 249, 12; 10.2460/javma.249.12.1371
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: severe multifocal coalescing granulomatous necrotizing hepatitis with intralesional protozoal organisms and severe multifocal coalescing transmural necrotizing typhlitis with intralesional protozoal organisms.
Case summary: hepatitis and typhlitis attributable to Histomonas meleagridis infection that caused sudden death in 2 turkeys housed with chickens.
Comments
There has been a large increase in the establishment of organic and organic free-range small chicken and turkey flocks in Virginia. These enterprises raise both meat and eggs for sale in the organic food marketplace. The birds are exposed to diseases and parasites that can be difficult to treat with methods perceived as natural. Consultation with a veterinarian is recommended to aid in the prevention and treatment of infectious disease and parasitic infestations commonly found in poultry.
Histomoniasis (blackhead disease) in turkeys is a protozoal infection of the cecal pouches and liver caused by H meleagridis.1 Turkeys of any age are susceptible. In addition to turkeys and chickens, chukar partridges, peacocks, pheasant, and ruffed grouse can be severely affected. Guinea fowl, bob-white quail, and ostriches can develop a milder form of the disease, and ducks can be nonclinical carriers.2 Histomonas meleagridis infects the embryonated eggs of the cecal nematode Heterakis gallinarum. The cecal nematode H gallinarum normally infects chickens and does not cause major illness. Infections with the protozoal organism H meleagridis can cause death among chickens but the mortality rate is low (approx 20%). However, infections with H meleagridis in turkeys are usually fatal with a mortality rate as high as 100%.
Infection of a bird with H meleagridis can occur in 3 ways. The bird can ingest heterakid eggs infected with H meleagridis. When the cecal nematode eggs hatch in the cecal pouch, the H meleagridis organisms migrate through the cecal pouch wall into the bloodstream or coelomic cavity to the liver, where the protozoal organisms divide and multiply causing severe liver damage. Heterakid eggs can survive for years in the soil. A second mode of infection is via earthworms. Earthworms ingest H gallinarum eggs and serve as transport hosts for the protozoa. Histomonas meleagridis infects the turkeys when they consume the earthworms. A third mode of infection in turkeys is by a process called cloacal drinking or cloacal drop. In this process, infected material is transferred from the surface of the cloaca to the ceca by reverse peristalsis.2 Close contact among birds is required for this means of infection, and chickens do not commonly transmit the disease to each other in this manner. Infection by ingestion of fresh feces containing H meleagridis is possible, but less likely, because free protozoa are not very viable in the environment without the protection of the cecal worm egg. This type of direct transmission requires the birds to be in close contact.
Currently, there is no FDA-approved drug available for treatment of histomoniasis in turkeys, making the prevention and control of histomoniasis difficult. The most important methods for limiting the disease are good biosecurity practices and cecal nematode control. Biosecurity measures include prevention of H meleagridis entering the property on contaminated vehicles, shoes, clothing, and animals. The poultry houses should only be entered by personnel wearing coveralls and gloves that are clean and specific for that house, and disinfected boots. Foot baths should be used to disinfect boots when entering and leaving the poultry house. The poultry houses should be constructed with nonporous materials that can be cleaned easily. Birds from flocks from other locations should not be added to existing flocks. Although not commonly practiced in backyard flocks, the all-in all-out method of raising birds can be used.
Worm control can be accomplished through monitoring the birds' parasite load by performing fecal egg counts and, except on organic farms, treating birds that have heavy parasite loads with benzimidazole anthelmintics. Because most organic farms cannot use anthelmintics, management of the flock then becomes important. Raising turkeys and chickens together should be avoided because chickens are more resistant to histomoniasis than are turkeys. Also, in chickens, concurrent infection with the cecal coccidium Eimeria tenella increases the severity of H meleagridis-associated liver lesions. It is important to control exposure to coccidia to prevent histomoniasis in chickens.3 Turkeys should not be in houses or on ground that has previously been used to raise chickens.4 The cecal worm eggs from chickens are viable for long periods in the soil and will contain the H meleagridis protozoa, which will infect the turkeys. By practicing good biosecurity, animal husbandry, and flock health monitoring, histomoniasis among turkeys can be prevented.
References
1. McDougald LR. Histomoniasis (blackhead) and other protozoan diseases of the intestinal tract. In: Saif YM, ed. Diseases of poultry. 12th ed. Ames, Iowa: Blackwell Publishing, 2008; 1095–1100.
2. McDougald JR. Blackhead disease (histomoniasis) in poultry: a critical review. Avian Dis 2005; 49: 462–476.
3. McDougald LR, Hu J. Blackhead disease (Histomonas meleagridis) aggravated in broiler chickens by concurrent infection with cecal coccidiosis (Eimeria tenella). Avian Dis 2001; 45: 307–312.
4. The Merck Manual website. Overview of histomoniasis in poultry. Available at www.merckmanuals.com/vet/poultry/histomoniasis/overview. Accessed Jul 22, 2014.