JPC SYSTEMIC PATHOLOGY

DIGESTIVE SYSTEM

October 2024

D-P05

 

Signalment (JPC #3166610): Young male turkey (Meleagris gallopavo).

 

HISTORY: Found dead.

HISTOPATHOLOGIC DESCRIPTION: Liver: Approximately 70% of the section is effaced by a single, large focus of lytic necrosis characterized by abundant eosinophilic cellular and karyorrhectic debris, hemorrhage, fibrin, and edema admixed with numerous macrophages that are often hemosiderin-laden, lymphocytes, scattered foreign body type multinucleated giant cells, and heterophils. Multifocally within these areas of necrosis there are numerous extracellular and intrahistiocytic, 10-20 µm diameter, irregularly round, lightly eosinophilic, protozoal trophozoites (histomonads) that occasionally contain single, central, 3-5 µm diameter basophilic nuclei. Trophozoites are often surrounded by a 3-5 µm clear zone. Bile ducts are multifocally ectatic and contain luminal debris and low numbers of heterophils and macrophages, and often exhibit piling up of epithelial cells (bile duct hyperplasia). Hyperplastic bile duct epithelia occasionally contain previously described trophozoites. Adjacent less affected hepatic parenchyma is characterized by swollen vacuolated hepatocytes (degeneration) with cytoplasm occasionally expanded by one to multiple discrete vacuoles (lipid-type vacuolation), and there are increased numbers of small bile duct profiles (ductular reaction) and increased numbers of macrophages. There are low numbers of periportal lymphocytes, plasma cells, and macrophages. 

 

Cecum: Affecting 95% of the section, there is diffuse, transmural, lytic necrosis and granulomatous inflammation characterized by loss of normal, well-defined intestinal layers and replacement by large numbers of macrophages, lymphocytes, fewer plasma cells, and heterophils, admixed with eosinophilic and karyorrhectic debris, fibrin, edema, and mild hemorrhage. Transmurally there are numerous previously described protozoal trophozoites, often found within vacuoles or within macrophages. The overlying mucosa is nearly diffusely effaced to the level of the muscularis mucosa. In the one small focus of remaining mucosa, crypts are either hyperplastic characterized by cells piling up to 2-3 layers deep with increased mitoses, or are dilated and filled with necrotic cellular debris, fibrin, degenerate protozoal trophozoites, macrophages, and heterophils (crypt abscess). The inflammatory infiltrate surrounds and separates often necrotic or degenerate myofibers of the tunica muscularis. 

 

MORPHOLOGIC DIAGNOSES: 

1. Liver: Hepatitis, necrotizing and granulomatous, random, multifocal to coalescing, marked, with numerous intrahistiocytic and extracellular protozoal trophozoites, turkey, avian.

2. Cecum: Typhlitis, necrotizing and granulomatous, diffuse, transmural, severe, with numerous intrahistiocytic and extracellular protozoal trophozoites.

ETIOLOGIC DIAGNOSIS: Hepatic histomoniasis

 

CAUSE: Histomonas meleagridis

 

CONDITION: Histomoniasis 

 

SYNONYMS: Blackhead, infectious enterohepatitis, typhlohepatitis

GENERAL DISCUSSION:

• Well-known, economically important anaerobic protozoan that causes severe necrotizing typhlitis, local peritonitis, and necrotizing hepatitis in a wide range of birds including turkeys, chickens, peafowl, grouse, quail, other gallinaceous birds, ostrich, rhea, and ducks 
• Exists in flagellated (luminal) or amoeboid (in tissue) forms 
• The cecal worm, Heterakis gallinarium, is the intermediate host; earthworms can be paratenic hosts for H. gallinarum larvae

• Adult worms are 1.5-3 inches long 
• Heterakis gallinarum is not considered a major threat, but is a major carrier/vector for Histomonas meleagridis
• Lifecycle of H. gallinarum is similar to other ascarids (direct, eggs passed in feces become infective within 2-3 weeks, eggs viable in environment for years and are resistant to disinfecting agents)

• This disease once limited expansion of the turkey industry, but is now uncommon, occurring typically when turkeys are raised where chickens were previously located; 

• Disease can be mitigated by keeping turkeys on separate farms from chickens and not using ranges until they are at minimum 4 years chicken-free. 

• Turkey poults are most susceptible (as well as pheasants and peafowl); in chickens, disease is common but mild and rarely recognized therefore they may serve as carriers
• Common in chickens but its effect on production is mild and rarely recognized except for commercial pullet flocks where outbreaks are reoccurringHHet
• CContclGood sanitation is the best control method; raising on sandy, dry, loose soil is best; no current approved preventative and treatment measures in food animals

LIFE CYCLE: 

PATHOGENESIS:

• Disease occurs when birds have access to the outdoors and are exposed to the intermediate host or its ova in the environment
• Disease appears to require secondary infection (cohabitating cecal bacteria such as E. coli, Clostridium perfringens, Bascillus subtilis in turkeys, and protozoa in chickens such as Eimeria tenella); experimentally, H. meleagridis was not pathogenic in the absence of bacteria

TYPICAL CLINICAL FINDINGS:

• Morbidity and mortality is high in young turkeys (up to 100%), older birds tend to be more resistant
• In turkeys, incubation period between exposure and disease is 7-12 days
• Initial signs include listlessness, depression, moderate anorexia, drooping wings, and yellow feces (“sulfur colored”); chicken feces may contain some blood; head parts may be cyanotic (“blackhead”) but often are not; biliverdiurea 
• Later signs include depression, standing with its wings, eyes closed, head drawn close to the body, emaciation and ultimately death 

TYPICAL GROSS FINDINGS:

• Well-developed gross lesions are pathognomonic: necrotizing typhlitis and characteristic target-like hepatic lesions

• Ceca: Bilateral distension/enlargement of ceca with thickening of the walls, typically ulcerated mucosa, and often contain caseous cecal cores (yellow, gray, or green, may be laminated) that may have been expelled in chronic cases
• Liver: Irregularly round, depressed, target-like (bulls-eye) areas of necrosis surrounded by a raised ring of hemorrhage; often yellow to gray but may be green to red, are often 1-2cm in diameter but may coalesce 

• Other lesions: Kidney and spleen may have small white nodules on surface, peritonitis if the cecal wall becomes perforated

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Histomonads: Extracellular and intrahistiocytic, round, 10-20µm, PAS-positive trophozoites with central dark nuclei; may be difficult to distinguish from macrophages on H&E

• Found in inflamed cecal walls or liver necrotic foci; can be seen on cecal smears or liver scrape at margins of foci

• Cecum: Bilateral, mucosal to transmural, fibrinonecrotic typhlitis with fibrinonecrotic to hemorrhagic cecal cores

• Extensive expansion of the lamina propria, with large numbers of lymphocytes, macrophages, giant cells, and histomonads in necrotic foci, often in groups of 1,4, or 8
• Fibrinoheterophilic and lymphocytic inflammation of the serosa; granulomatous inflammation in more chronic lesions

• Liver: Portal to multifocal-to-coalescing heterophilic recessed granulomas (up to 2 cm) and hepatocellular necrosis, histomonads in necrotic foci

• In advanced lesions, the trophozoites are scant as they degenerate and appear faintly eosinophilic, granular bodies 

• Kidney, spleen, bursa of Fabricius, air sacs, lungs, pancreas, proventriculus: May also have foci of necrosis with associated histomonads, granulomatous inflammation, few multinucleated giant cells

ADDITIONAL DIAGNOSTICS TESTS:

• PCR
• Histochemical stains: PAS-positive
• Cytology: Histomonads may be identified on smears of cecal contents or scrapings of cecal or liver lesions

DIFFERENTIAL DIAGNOSIS: 

Necrotic cecal cores:

• Eimeria tenella
• Salmonella sp. (Pullorum disease, Paratyphoid)

Other histomonads of the cecum:

 

COMPARATIVE PATHOLOGY:

• Chickens and ring-necked pheasants may carry the disease and show minimal/no clinical signs; in gallinaceous birds the disease is known as blackhead and has low prevelance in wild populations
• Turkeys, pheasants (other than ring-necked), and peafowl are highly susceptible; ostrich, rhea, guinea fowl, chukar, grouse, quail tend to not develop cecal lesions despite high mortality; and partridges can be infected
• In quail, cecal lesions may not occur but mortality remains high 
• Young ostriches can have cloacal prolapse due to histomoniasis 

 

REFERENCES:

1. Abdul-Aziz T, Fletcher OJ. Chapter 2: Lymphoid System. In: Abdul-Aziz T, Fletcher OJ, Barns HJ, eds. Avian Histopathology. 4th ed. Madison, WI: Omnipress; 2016: 46-47.
2. Abdul-Aziz T, Fletcher OJ. Chapter 8: Hepatobiliary System. In: Abdul-Aziz T, Fletcher OJ, Barns HJ, eds. Avian Histopathology. 4th ed. Madison, WI: Omnipress; 2016: 407-408.
3. Crespo R, Franca MS, Fenton H, Shivaprasad HL. Galliformes and columbiformes. In: Terio KA, McAloose D, St. Leger J. Pathology of Wildlife and Zoo Animals. London, England: Elsevier; 2018:759-761.
4. Fitz-Coy SH. Parasitic diseases. In: Boulianne M., ed. Avian Disease Manual. 8^th ed. Jacksonville, FL: American Association of Avian Pathologists; 2019: 130, 139-140, 145.
5. Fletcher OJ, Abdul-Aziz T. Chapter 7: Alimentary System. In: Abdul-Aziz T, Fletcher OJ, Barns HJ, eds. Avian Histopathology. 4th ed. Madison, WI: Omnipress; 2016: 276, 338-339.
6. Myers EA, Sander JE. Appendix. In: Boulianne M, ed. Avian Disease Manual. 8th ed. Jacksonville, FL: American Association of Avian Pathologists, Inc; 2019:191, 198-1988.
7. Smith DA. Palaeognathae: apterygiformes, casuariiformes, rheiformes, struthioniformes; tinamiformes. In: Terio KA, McAloose D, St. Leger J. Pathology of Wildlife and Zoo Animals. London, England: Elsevier; 2018:645.
8. Schmidt R, Reavill DR, Phalen DN. Pathology of Pet and Aviary Birds. 2nd ed. Ames, IA: John Wiley & Sons, Inc.; 2015: 83-84, 86, 110-111. 
9. Wallner-Pendleton E. Diseases of the Game Birds. In: Boulianne M, ed. Avian Disease Manual. 8th ed. Jacksonville, FL: American Association of Avian Pathologists, Inc; 2019:187.

Click the slide to view.

---