To the Editors:
Hepatic capillariasis is a neglected, but serious, hepatic disease with a worldwide distribution caused by the nematode Calodium hepaticum.1–4
The nematode has a monoxenous life cycle and can infect any mammalian liver but mainly affects rodents, while humans are an accidental host.1,3,4 Infection occurs after ingestion of embryonated eggs from contaminated soil. The larvae hatch in the intestine, migrate, mature, and mate in the liver parenchyma, with hundreds unembryonated eggs laid.1,5 The eggs remain viable in the liver and are released into the environment after death of the host.3,4 In the soil, the eggs reach the infective stage.3,5 Poor sanitation and living conditions predispose to infection.1,5 There is a higher incidence in children attributable to higher soil-to-hand-to-mouth contact. Pica is an additional risk, particularly when presenting as geophagia.1
A 3-year-old Afghan girl born in Belgium and living in an asylum seeker center was referred for persistent high fever and abdominal pain. A history of pica was present. Pallor, weakness, and hepatomegaly were observed on clinical examination. Blood tests revealed elevated C-reactive protein (151 mg/L), ALT (360 IU/L), AST (207 IU/L), IgM levels (13.05 g/L), microcytic anemia (8.3 g/dL), and eosinophilia (12,750/µL). Stool cultures were negative. Abdominal ultrasound examination showed hepatosplenomegaly with ascites. FibroScan revealed minor fibrosis with a stage F1. Serology for Fasciola hepatica and Toxocara canis was positive. Liver biopsy revealed adult nematodes and eggs. The child was treated with triclabendazole (10 mg/kg/day) for 2 days then albendazole (50 mg/kg/day) and methylprednisolone (1 mg/kg/day) for 5 days. She responded well. Twenty days after treatment, she presented with a relapse. A review of the liver biopsy identified the diagnostic features of C. hepaticum (Fig. 1). This diagnosis was confirmed by PCR on the liver tissue. The positive Fasciola and Toxocara serologic tests were determined to be cross-reactions. Albendazole course was continued for 100 days (25 mg/kg/day) and corticosteroids (1 mg/kg/day) for 50 days followed by degressive weaning with positive clinical and biological response.
FIGURE 1.
A: Liver tissue showing granuloma formation around Calodium hepaticum eggs. The granulomata were nodules with sizes between 1 mm to 3.5 × 2.0 cm containing eggs and worms or necrotic materials and nucleic debris surrounded by a rim of diverse inflammatory cells. Liver tissue outside the granulomata appears healthy. B: Transverse section of recurved necrotic adult female; midbody (left; 115 µM at widest point) and anterior (right; 45 × 27 µM). The BB and thick Cu are visible, as are a necrotic Ov and St. C: Two eggs in longitudinal (left; 41 µM long) and transverse (right; 36 × 27 µM) section. The external envelop contains numerous minipores and is thinner than the internal envelop with SS between them. A PP may be seen in 1 egg. Hematoxylin and eosin stain. BB indicates bacillary bands, Cu, cuticle, Ov, ovary, PP, polar plug, SS, sagittal striations, St, stichocyte.
The clinical presentation of hepatic capillariasis is nonspecific. Prolonged fever, anemia, hepatomegaly, eosinophilia, hyperglobulinaemia and elevated levels of liver enzymes are usually present.1,2,5 Clinical, biochemical and radiological correlation may assist in diagnosis but definitive diagnosis requires liver biopsy.1,2,5 The parasite and its eggs are undetectable in feces.1,2 Serological detection of antibodies to C. hepaticum may be useful but is limited by antigen availability1 and the absence of a commercially available test.2 Antibodies to C. hepaticum can cross-react in serological tests for Toxocara,5 Schistosoma, and Dirofilaria immitis.1,5
Clinical prognosis is defined by the intensity of infestation and ranges from mild to severe or fatal.2,5 Survival rates increases with early diagnosis.1
Treatment consists of a combination of corticosteroids and anthelmintics.1,2,5
Hepatic capillariasis is rare, but should be taken into account in a child presenting with persistent fever, hepatomegaly and eosinophilia. Currently, biopsy remains the cornerstone of diagnosis. The development of serological tests would be beneficial to early diagnosis and treatment, which improves prognosis.
Footnotes
The authors have no funding or conflicts of interest to disclose.
V.A. and S.G. have contributed equally to this article.
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REFERENCES
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