Tularemia was confirmed as the cause of death in a necropsied beaver from the site. Trappers noted “white liver lesions” in several muskrats from the same area. Tyzzer’s disease had been identified in muskrats from the same county five years prior to this event (see Case of the Month February 2020). Liver from a muskrat was submitted for histologic examination and testing for Tyzzer’s disease and tularemia.  

Histopathological Findings: Clusters of nematode eggs are scattered randomly throughout the liver. Eggs measure up to 28 x 52 µm, have an approximately 3 µm, light brown to eosinophilic, birefringent, bi-operculated shell with radial striations, and contain eosinophilic flocculent material. The egg clusters are often surrounded by low numbers of macrophages and occasionally by multinucleated giant cells. (Fig. 1A, B).

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Morphologic Diagnosis: Hepatitis, granulomatous, multifocal, moderate, chronic with intralesional Calodium hepaticum eggs.

Etiologic Diagnosis: Hepatic capillariasis

Etiology: Calodium hepaticum (syn. Capillaria hepatica), a nematode of the family Capillaridae (order Trichocephalida).

Distribution: Worldwide; C. hepaticum has been found in more than 60 countries in North, Central and South America, Europe, Asia, Africa, and Oceania. It was first reported in muskrats in North America in 1931.

Seasonality: All seasons.

Host range: Found in Muroidean rodent species with the Norway rat (Rattus norvegicus) being the main host species globally.

Transmission: The life cycle is direct. A host ingests embryonated eggs from the environment which hatch as larvae in the cecum and migrate to the liver via the portal vein where they develop to adults. Adult female nematodes lay eggs in the liver which develop only to the eight-cell stage and then, upon the death of the host, are released into the environment. Embryonated eggs, which can survive up to 25 months, are then ingested by a mammalian host.

Pathology: On gross examination, “curled whitish tracts” occur under the hepatic capsule and white foci may be observed on the hepatic surface and on cut section. The nematode causes a mild to severe granulomatous hepatitis with intralesional adult worms or eggs. Adult worms might not be observed as they have a short life span (18–60 days). Fibrosis may also be observed.

Diagnosis: Diagnosis can be made via touch impressions or histologic examination of the liver. Fecal examination is not diagnostic because eggs are not shed from the infected host. Differential diagnoses for pinpoint white foci in the liver of muskrats include tularemia, Tyzzer’s disease, or other causes of septicemia. PCR was performed in this case to rule out tularemia and Tyzzer’s disease and neither Francisella tularensis nor Clostridium piliforme were detected.

Public health concerns: Calodium hepaticum is a zoonotic parasite with more than 70 human cases documented. Infection is often asymptomatic.

Wildlife population impacts: While pathogenicity is generally considered to be low, experimental infections in mice and rats have documented hepatic failure and mortality with host survival rate reduced by up to ten percent. The host inflammatory response can vary widely and due to the severity of some lesions observed in experimental studies, it is suggested that hepatic capillariasis could be a population-limiting factor.

References:

• Borucinska, JD, Nielsen, SW. 1993. Hepatic capillariasis in muskrats (Ondatra zibethicus). J Wildl Dis: 29(3):518–520, https://doi.org/10.7589/0090-3558-29.3.518.
• Fuehrer, H-P. 2014. An overview of the host spectrum and distribution of Calodium hepaticum (syn. Capillaria hepatica): part 1 – Muroidea. Parasitol Res: 113:619–640, https://doi.org/10.1007/s00436-013-3691-x.
• Spratt DM, Singleton GR. 2001. Hepatic Capillariasis. In: Parasitic Diseases of Wild Mammals, 2^nd edition. Samuel WM, Pybus MJ, Kocan AA, editors. Iowa State University Press, Ames, pp. 365–379, https://doi.org/10.1002/9780470377000.ch14.