Capillaria hepatica infection
The liver parenchyma shows spindle-shaped eosinophilic eggs surrounded by eosinophilic inflammatory infiltrates and epithelioid granuloma (original magnification ×200). Figure B shows spindle-shaped eosinophilic eggs with shells, radial striations, and visible polar body, containing granular eosinophilic debris (original magnification ×1000), consistent with Capillaria hepatica. Figure C reveals crescent-shaped, degenerated adult worms of C. hepatica showing longitudinal bacillary bands, vacuolated intestine, and convoluted gonads surrounded by intense eosinophilic inflammation in liver parenchyma (original magnification ×400). The outer cuticle is not appreciated because the worms are degenerated.
A review of history revealed that the child played with stray cats and had pica. He was given 10 mg/kg of oral albendazole for 16 weeks and 1 mg/kg of oral prednisolone for the first 2 weeks to prevent paradoxical inflammatory response. Thereafter, prednisolone was tapered and stopped. Pyrexia, liver size, AEC, and liver enzymes normalized at 24 hours, 72 hours, 4 months, and 5 months, respectively. At 12 months of follow-up, the child is asymptomatic.
Capillaria hepatica is a rare nematodal invasive parasitosis where humans are the dead-end host; the main lifecycle occurs between rodents and their predators. Adult worms live, mate, and lay noninfective unembryonated eggs in rodent livers. Embryogenesis occurs only after contact with the soil in two settings: 1) the rodent is eaten by the predator and the unembryonated eggs are released in the predator's feces or 2) carcass disintegration after natural death of the rodent. Humans incidentally ingest the infective embryonated eggs by soil to mouth transmission. They hatch in the human intestine and the larvae migrate through the portal vein into the liver where they mature into adult worms. In the liver, the cycle continues with the adult worms mating and laying eggs. This elicits intense inflammation with systemic symptoms. 1 In the index case, we hypothesize that the toddler with pica would have come in contact with soil in the vicinity of the stray cats. This soil would have initially contained the feline feces with unembryonated eggs that later underwent embryogenesis. The triad of fever, hepatomegaly, and eosinophilia is the hallmark and characteristic liver histology clinches the diagnosis. Duration of anthelminthic therapy should be guided by AEC response. 2,3
References
1. Wright K.A. Observation on the life cycle of Capillaria hepatica with a description of the adult. Can J Zool. 1961;39:167-82.
2. Berger T. Degrémont A. Gebbers J.O. et al. Hepatic capillariasis in a 1-year-old child. Eur J Pediatr. 1990;149:333-633.
3. Choe G. Lee H.S. Seo J.K. et al. Hepatic capillariasis: first case report in the Republic of Korea. Am J Trop Med Hyg. 1993;48:610-25.
