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Read-Only Case Details Reviewed: Jan 2010

JPC SYSTEMIC PATHOLOGY
DIGESTIVE SYSTEM
October2021
D-P21

 

SLIDE A: Signalment (JPC #2550496):  Hare

 

HISTORY:  None

 

HISTOPATHOLOGIC DESCRIPTION:  Liver:  Expanding and effacing 70% of this section and compressing adjacent hepatocytes are multifocal to coalescing granulomas centered on eosinophilic cellular and karyorrhectic debris (lytic necrosis) admixed with numerous aphasmid nematode eggs.  These eggs are 40x60um, have a 10-15um thick, anisotropic, bioperculated shell with radial striations, and contain either an eosinophilic 15um diameter morula or small amounts of granular eosinophilic debris.   The central areas of necrosis are bounded by circumferential layers of numerous degenerate neutrophils and eosinophils, epithelioid macrophages and multinucleated giant cells (foreign body and Langhans types), numerous fibroblasts, numerous eosinophils, fewer lymphocytes and plasma cells, and fibrous connective tissue (fibrosis) with many entrapped bile ductules. The multinucleated giant cells measure up to 200um in diameter, contain up to 40 nuclei, and rarely contain a phagocytized nematode egg.  The adjacent hepatocytes are multifocally atrophied, occasionally swollen and microvacuolated (degenerate), or rarely shrunken and hypereosinophilic with pyknotic nuclei (necrotic).  Multifocally there are increased numbers of haphazardly arranged bile ducts (ductular reaction) as well as occasional ectatic bile ducts.  Multifocally there is minimal to mild hemorrhage, fibrin, and edema within the hepatic parenchyma. Portal areas are infiltrated by low numbers of eosinophils, lymphocytes and plasma cells.

 

MORPHOLOGIC DIAGNOSIS:  Liver:  Granulomas, eosinophilic, multifocal to coalescing, moderate to marked, with bi-operculate aphasmid eggs, etiology consistent with Capillaria hepatica, hare (Lepus sp.), lagomorph.

 

ETIOLOGIC DIAGNOSIS:  Hepatic capillariasis

 

CAUSE:  Capillaria hepatica (Calodium hepaticum); Capillaria spp. (birds)

 

SLIDE B: Signalment (JPC #3165178):  Adult male guinea fowl.

 

HISTORY:  This male guinea fowl was one of several group housed at a zoological institution that developed wasting and chronic diarrhea followed by multiple deaths.  On autopsy, this bird was in poor nutritional condition and the crop was markedly dilated, the crop wall measured 3-4mm thick, and the mucosa was tan, granular, and rugose.

 

HISTOPATHOLOGIC DESCRIPTION:  Esophagus:  Diffusely the mucosa is markedly thickened up to 1.5mm (mucosal hyperplasia), there are numerous variably sized mucosal papillary projections extending into the lumen that are variably cornified, and the mucosa is moderately undulant (rugose).  The mucosal glands are also either moderately hyperplastic or replaced by hyperplastic mucosal epithelium.  Multifocally throughout the mucosa there are numerous intact and degenerate cross and tangential sections of adult aphasmid nematodes and eggs.  The adult nematodes are 150um in diameter, have a 2-3um thick cuticle, polymyarian-coelomyarian musculature, hypodermal bacillary bands, stichosome, esophagus, gastrointestinal tract lined by uninucleate cuboidal cells, and reproductive tract often containing numerous eggs.  The eggs are 20x40um and have a 3-4um thick, eosinophilic, anisotropic, bioperculated shell containing eosinophilic flocculent material.  Within the lamina propria, the mucosa-associated lymphoid tissue is moderately expanded (reactive) and diffusely there are several scattered lymphocytes, plasma cells, and fewer heterophils admixed with increased clear space (edema).  Rarely, heterophils also transmigrate through the mucosa and either form intraepithelial aggregates, aggregate around degenerate nematode sections and eggs with fewer macrophages and lymphocytes, or are found within the lumen admixed with mixed intraluminal bacterial colonies and ingesta.

 

MORPHOLOGIC DIAGNOSIS:  Esophagus:  Esophagitis, proliferative, diffuse, marked, with numerous intraepithelial adult aphasmid nematodes and bi-operculate aphasmid eggs, etiology consistent with Capillaria spp., Guinea fowl, avian.

 

ETIOLOGIC DIAGNOSIS:  Esophageal capillariasis

 

CAUSE:  Capillaria spp. (C. contorta or C. annulata)

 

GENERAL DISCUSSION:

 

PATHOGENESIS:

 

LIFE CYCLE:

 

TYPICAL GROSS FINDINGS:

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

 

ADDITIONAL DIAGNOSTIC TESTS:

 

DIFFERENTIAL DIAGNOSIS:

Capillaria hepatica in hares:

 

COMPARATIVE PATHOLOGY:

 

REFERENCES:

  1. Barthold SW, Griffey SM, Percy DH. Pathology of Laboratory Rodents and Rabbits. 4th West Sussex, UK: John Wiley & Sons, Inc.; 2016:153, 301.
  2. Breshears MA and Confer AW. The Urinary Sytem. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017:680.
  3. Cullen JM, Stalker MJ. Liver and biliary system. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 2. 6th ed. St. Louis, MO: Elsevier Ltd; 2016:320.
  4. Delaney MA, Trueting PM, Rothenburger JL. In: Terio KA, McAloose D, St. Leger J ed. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier Inc. 2018:512-3.
  5. Fitz-Coy SH. Parasitic diseases. In: Boulianne M ed. Avian Disease Manual. 8th Jacksonville, FL: American Association of Avian Pathologists; 2019: 130-1.
  6. Gardiner CH, Poynton SL. Aphasmids. In: Gardiner CH, Poynton SL, eds. An Atlas of Metazoan Parasites in Animal Tissues. Washington, DC: Armed Forces Institute of Pathology; 1999:40-43.
  7. Lopez A and Martinson SA. Respiratory, Mediastinum, and Pleurae. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier; 2017:548.
  8. Lowenstine LJ, McManamon R, Terio KA. In: Terio KA, McAloose D, St. Leger J ed. Pathology of Wildlife and Zoo Animals. Cambridge, MA: Elsevier Inc. 2018:399.
  9. Rothenburger JL, Himsworth CG, La Perle KMD, et al. Pathology of wild Norway rats in Vancouver, Canada. J Vet Diagn Invest. 2019; 31(2):184-199.


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