JPC SYSTEMIC PATHOLOGY
DIGESTIVE SYSTEM
October 2018
D-P26

Signalment (JPC #2439475):  Two adult (6- and 10-year-old) male marmosets

HISTORY:  Both marmosets presented with weight loss and progressive weakness and were euthanized.

HISTOPATHOLOGICAL DESCRIPTION: Exocrine pancreas and duodenum:  Diffusely, effacing and replacing interlobular septa, peripancreatic fat, and perilobular acini and ducts are coalescing areas of lytic necrosis characterized by loss of cellular architecture and replacement by abundant eosinophilic cellular and karyorrhectic debris admixed with fibrin, edema, minimal hemorrhage, and moderate numbers of viable and degenerate neutrophils.  Areas of necrosis are bordered by moderate numbers of lymphocytes, eosinophils and macrophages, occasionally laden with cytoplasmic golden granular pigment (hemosiderin), fewer neutrophils, rare plasma cells, and variable amounts of fibrous connective tissue (fibrosis) that separates, surrounds and often replaces pancreatic acini.  Remaining pancreatic acini are either degenerate, characterized by pale vacuolated cytoplasm that lacks zymogen granules, or atrophied.  Multifocally, there are increased numbers of small pancreatic ducts (tubular complexes)with hyperplastic epithelium and that are often surrounded by fibrous connective tissue.  Ductular lumina are often ectatic and contain scant necrotic debris, few previously described inflammatory cells, and multiple cross and tangential sections of a 200um diameter adult spirurid nematode with a 5um thick smooth cuticle, lateral cords, polymyarian-coelomyarian musculature, a pseudocoelom that contains granular eosinophilic material (spirurid), a tri-radiate esophagus, an intestinal tract lined by uninucleate cells with an indistinct brush border, and reproductive structures.  Previously described inflammatory cells and necrotic debris multifocally extend into and replace the outer longitudinal and, to a lesser extent, the inner circular layer of the duodenal tunica muscularis and serosa.   Adjacent myocytes are vacuolated with swollen cytoplasm (degeneration).  The submucosa and remaining serosa of the duodenum are expanded by increased clear space and ectatic lymphatics (edema).

Lymph node, mesenteric:  Diffusely, subcapsular and medullary sinuses are expanded by macrophages with foamy cytoplasm which occasionally contains intracytoplasmic golden pigment (hemosiderin), along with few eosinophils and edema.

MORPHOLOGIC DIAGNOSIS:

  1. Exocrine pancreas:  Pancreatitis, necrotizing, lymphocytic and eosinophilic, chronic, diffuse, moderate, with fibrosis, acinar degeneration, atrophy and loss, tubular complexes, duct hyperplasia, necrotizing peripancreatic steatitis, and multiple intraductal adult spirurid nematodes, etiology consistent with Trichospirura leptostoma, marmoset, nonhuman primate.
  2. Duodenum, tunica muscularis and serosa: Necrosis, focally extensive, with mild eosinophilic and lymphoplasmacytic inflammation and edema.
  3. Lymph node, mesenteric: Sinus histiocytosis, diffuse, mild with eosinophils and edema. 

ETIOLOGIC DIAGNOSIS:  Pancreatic trichospiruriasis

CAUSE:  Trichospirura leptostoma

GENERAL DISCUSSION:

LIFE CYCLE:

TYPICAL CLINICAL FINDINGS:

TYPICAL GROSS FINDINGS:

TYPICAL LIGHT MICROSCOPIC FINDINGS:

ADDITIONAL DIAGNOSIS:  

DIFFERENTIAL DIAGNOSIS:

COMPARATIVE PATHOLOGY:

REFERENCES:

  1. Cosgrove GE, Humason G, Lushbaugh CC. Trichospirura leptostoma, a nematode of the pancreatic ducts of marmosets (Saguinus ). J Amer Vet Med Assoc. 1970;157:696-698.
  2. Gardiner CH, Poynton SL. An Atlas of Metazoan Parasites in Animal Tissues. Washington, DC: Armed Forces Institute of Pathology; 2006:34.
  3. Jones TC, Hunt RD, King NW. Veterinary Pathology, 6th ed., Baltimore, MD: Williams and Wilkins; 1997:625,1107.
  4. Toft JD. The pathoparasitology of the alimentary tract and pancreas of nonhuman primates: A review. Vet Pathol. 1982;19:44-92.
  5. Strait K, Else JG, Eberhard ML. Parasitic diseases of nonhuman primates. In: Abee CR, Mansfield K, Tardif S, Morris T, eds. Nonhuman Primates in Biomedical Research: Diseases. Vol. 2. 2nd ed. San Diego, CA: Elsevier; 2012:237-238.


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