Indian Journal of Pathology and Microbiology
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Year : 2016  |  Volume : 59  |  Issue : 1  |  Page : 124-125
Hepatic capillariasis: A rare parasitic infection

Department of Pathology, Seth G. S. Medical College, Mumbai, Maharashtra, India

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Date of Web Publication9-Mar-2016

How to cite this article:
Yadav SC, Sathe PA, Ghodke RK. Hepatic capillariasis: A rare parasitic infection. Indian J Pathol Microbiol 2016;59:124-5

How to cite this URL:
Yadav SC, Sathe PA, Ghodke RK. Hepatic capillariasis: A rare parasitic infection. Indian J Pathol Microbiol [serial online] 2016 [cited 2021 Oct 25];59:124-5. Available from: https://www.ijpmonline.org/text.asp?2016/59/1/124/174878

Capillaria hepatica discovered in 1893 by Bankroft is a nematode of family Trichocephalidea and class Trichuroidea, similar to Trichuris trichiura. The parasite primarily infects the rodents with rare cases of human infections. Approximately 90% of the rats are infected with Capillaria species. This explains the global distribution of sporadic cases of C. hepatica. Humans are the accidental host with <50 cases reported worldwide. From India, till date only 2 cases have been reported. We, hereby, report the third case of C. hepatica in a 2-year-old male child. [1],[2],[3]

A 2-year-old male child complained of fever of unknown origin since 3 months and abdominal distention since 1-month. There was no history of jaundice, loose motions, vomiting or passing worms in the stools. On examination, he had pallor and clubbing. Abdominal distension was noticed over the right hypochondrium. Hematologic investigations showed hemoglobin -7.2 g%, total leukocyte count -39700/mm 3 , differential leukocyte count -67% eosinophils, 23% lymphocytes, and 10% polymorphs and platelet count -4.2 lakh/mm 3 . Bone marrow examination did not reveal any abnormality. Stool routine microscopy and culture was negative. With a clinical impression of hepatosplenomegaly with ascites possibly due to Budd-Chiari malformation or hematolymphoid malignancy or parasitic infestation, a liver biopsy was performed. Histology revealed preserved lobular architecture. Many discrete and confluent granulomas surrounded by abundant eosinophilic infiltrate were identified in the portal areas. The center of the granulomas showed many spherical or oval structures with radial striations and an eosinophilic shell resembling C. hepatica [Figure 1] Some of these structures showed polar bodies. A final histopathological diagnosis of parasitic hepatitis secondary to C. hepatica infection was given. The patient was subsequently started on thioalbendazole for 3 months, to which, he responded completely.
Figure 1: (a) Low power view showing dense inflammatory infiltrate with discrete and confluent granulomas in the portal area. The center of the granuloma shows parasite. (b) High power view shows spherical or oval structures with radial striations and an eosinophilic shell resembling Capillaria hepatica

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C. hepatica also known as Calodium hepaticum is an extremely rare infection of human with nonspecific symptoms and are frequently misdiagnosed. The typical triad of this infection is persistent fever, hepatomegaly, and leukocytosis with eosinophilia. Pica is an important presenting complaint and this explains why parasitic infections occur in children. Anemia and hypergammaglobulinemia could be the other presenting features. [1],[2],[4]

The life cycle of C. hepatica requires a single host. The liver of the host contains both the adult worm and the ova. The worms and the ova remain in the liver of the host and are released in the soil after the decay of carcass or discharge in the feces of the carnivorous predator who has fed upon the infected mammal. Humans do not discharge them in their excreta. The eggs become embryonated in the soil. On ingestion by second host by feco-oral contamination, or geophagy, they reach the intestine of second host and migrate via the walls of intestines and through the portal vein, reach the liver where they grow into adult forms. [1],[2] C. hepatica induces granuloma formation in the liver parenchyma. Multifocal discrete and confluent necrotizing eosinophilic granulomas surrounded by dense mononuclear cells and eosinophils are seen. Both adult worms and eggs are seen scattered in the liver parenchyma in advanced cases. However, in very early cases, there may be only immature worms without eggs. The adult worms disappear over a period of time and induce multifocal fibrosis. [4] Although the pathogenesis of fibrosis is not well established, it is assumed that slow and continuous release of disintegrated products from the encapsulated worm activate the Kupffer cells, which then promotes fibrosis in the liver. [3]

A typical C. hepatica is slender in shape with a narrow anterior part and gradual swelling of the posterior part. The esophagus is long occupying half of the female body and one third of the male body. The eggs of C. hepatica resemble those of Trichuris trichiura, but differ in size. The C. hepatica egg is about 48-66 µm × 28-36 µm, and has numerous minipores in its outer shell. [3] These worms are identified by the presence of the stichosome, a glandular structure surrounding the esophagus. The stichosome is composed of a row of distinctive cells, the stichocytes. This is the hallmark characteristic of C. hepatica. [1]

The differential diagnosis includes accidental tissue infestation by nematodes including Toxocara cati, Toxocara canis, Fasciola hepatica, and visceral larva migrans. Liver biopsy remains the cornerstone of diagnosis, but serological testing by indirect immunofluorescence assay is also recommended for diagnostic and screening purpose. [2] Treatment includes thiobendazole, albendazole, or ivermectin.

C. hepatica can cause serious liver disorders in humans with high mortality. Unexplained fever with eosinophilia and hepatomegaly should warrant a prompt and aggressive work-up to look for liver lesions and to rule out this infection. The patient can present with nonspecific complaints and the diagnosis can be missed easily. Hence, C. hepatica should be kept in the differential diagnosis in children with chronic fever and eosinophilia.

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There are no conflicts of interest.

   References Top

Sawamura R, Fernandes MI, Peres LC, Galvão LC, Goldani HA, Jorge SM, et al. Hepatic capillariasis in children: Report of 3 cases in Brazil. Am J Trop Med Hyg 1999;61:642-7.  Back to cited text no. 1
Nabi F, Palaha HK, Sekhsaria D, Chiatale A. Capillaria hepatica infestation. Indian Pediatr 2007;44:781-2.  Back to cited text no. 2
Li CD, Yang HL, Wang Y. Capillaria hepatica in China. World J Gastroenterol 2010;16:698-702.  Back to cited text no. 3
Klenzak J, Mattia A, Valenti A, Goldberg J. Hepatic capillariasis in Maine presenting as a hepatic mass. Am J Trop Med Hyg 2005;72:651-3.  Back to cited text no. 4

Correspondence Address:
Subhash C Yadav
Department of Pathology, Seth G.S. Medical College, Mumbai - 400 012, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.174878

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