David G. Baker, in The Laboratory Rat (Second Edition), 2006
2. Calodium hepaticum
Description and lifecycle. Calodium hepaticum, formerly known as Capillaria hepatica, is a member of the order Enoplida, and is therefore phylogenetically related to Trichinella spiralis, Trichuris sp., and Trichosomoides crassicauda. Adult worms are slender. The eggs are brownish, barrel-shaped, and possess a thick double wall, of which the outer one is distinctly pitted. At each end of the egg there is a plug (operculum) that does not bulge beyond the outline of the outer wall.
Calodium hepaticum has a direct lifecycle but may involve a transport host. The natural host acquires the infection by ingesting infective embryonated eggs in the environment. These hatch in the cecum, and the larvae penetrate the intestinal mucosa and enter the portal vein. Larvae reach the liver, where they mature within 3 weeks. The adult worms live for short periods but deposit large numbers of unembryonated eggs in the liver (Figs. 13-5 and 13-6). These eggs do not develop but may remain viable in the liver for many months. When the infected mammal is eaten by a carnivorous animal, eggs are then discharged and passed out in the feces. Alternatively, cannibalism and carcass decomposition may release eggs into the environment (Farhang-Azad, 1977). Eggs embryonate in the environment, and become infective in 2 to 6 weeks under suitable conditions.
Hosts. C. hepaticum is commonly
found in the liver of wild rats and,
less frequently, in mice,
squirrels, muskrats, hares, beavers, dogs, pigs, nonhuman primates, and rarely, in man. The infection rate is often very high in wild rats. Ceruti and coworkers (2001) reported a prevalence of 36% of 47 wild rats, Conlogue and coworkers (1979) found 82% of 86 wild rats infected, and lastly, Luttermoser (1936) found 86% of 2,500 wild rats infected.
Diagnosis. Final diagnosis is based on the demonstration of parasites or eggs in the liver. Parasite eggs are only found in the rat feces after cannibalism of other infected rats. However, this is uncommon.Pathobiology. Although the parasite has low pathogenicity in rats, infection can result in hepatomegaly and liver damage.
Accumulations of eggs in the liver are usually visible as irregular yellow-gray spots or streaks on the surface. Histologically, the liver architecture is distorted by granulomatous foci. Adult parasites and/or eggs may be observed in the central portion of the lesions, which consist of an amorphous center with parasites surrounded by eosinophils, plasma cells, macrophages, epithelioid cells, and multinucleated giant cells. In more advanced stages, there are extensive areas of septal fibrosis, containing large numbers of eggs (Santos et al., 2001). In fact, the C. hepaticum-rat system has been developed as a valuable model for testing antifibrotic drugs (de Souza et al., 2000).
Clinical symptoms. Infection with C. hepaticum is generally asymptomatic. It can be anticipated that heavily infected rats may experience anorexia, malaise, and other signs compatible with hepatic dysfunction.
Treatment. Both mebendazole and ivermectin have been shown to eliminate early larval stages of C. hepaticum and to reduce fecundity of adult worms (El Gebaly et al., 1996). However, unless infected colonies are highly valuable, they should be culled.
Prevention and control. C. hepaticum infection should not occur in well-managed laboratory rat colonies. Rodent feed and bedding stocks should be protected from contamination with feces from other animals, particularly that of feral dogs.