Fasciola hepatica in a New Zealander Traveler

Authors


Mei L. Kang, MBChB, MRCP, Infectious Diseases Division, Department of Internal Medicine, Singapore General Hospital, Outram Road, Singapore 169608. E-mail: mlkang98@yahoo.com

Abstract

Fascioliasis is a reemerging zoonosis endemic in many parts of the world. Reports of imported fascioliasis by migrants into nonendemic countries are common, but tourists and business travelers are rarely afflicted. Here, we report a case of a New Zealander traveler who acquired the infection on a business trip.

Case report

A 39-year-old Caucasian male from New Zealand presented to the Travelers Health and Vaccination Centre in Singapore in December 2005 for investigations of eosinophilia, intermittent fever, and mild right upper abdominal pain. He first developed fever during a business trip to Hong Kong in November 2005. He was admitted to a local hospital and received empirical treatment with mebendazole and doxycycline. His fever defervesced and he was discharged, but no final diagnosis was made.

His second episode of fever occurred 1 month later in Singapore and he presented to our center. On examination, no abnormalities were found except for a mildly tender hepatomegaly of 2 cm. His liver function tests were normal. He had eosinophilia (white blood count 6.8 × 109/L, eosinophils 16%) and otherwise normal blood count. Two stool studies were negative for ova, cysts, and parasites. Within a week after his presentation, he developed increasingly right upper quadrant pain and was admitted.

The patient had an extensive travel history. He had grown up in a sheep farm in New Zealand but had been a resident in Singapore for the past 7 years. He travels frequently in his job as an information technology consultant and had visited Pakistan, India, China, Australia, and California in the past year. Each trip lasted 2 to 3 weeks; he stayed in business hotels belonging to international chains and ate nearly all his meals at hotel restaurants.

His abdominal ultrasound revealed a complex cystic lesion in the right lobe of liver, with a size of 10 × 6.7 × 5.0 cm (Figure 1). Radiologically, the differential diagnoses include hydatid disease, cholangiocarcinoma, hemorrhagic cyst, and hepatic abscess. Magnetic resonance imaging (MRI) showed that the lesion was hyperintense on T1-weighted images and hypointense on T2-weighted images, consistent with hemorrhagic contents (Figure 2). Magnetic resonance cholangiopancreatography suggested segmental focal intrahepatic ductal dilatation with proteinous mucinous contents.

Figure 1.

Abdominal ultrasound showing complex cystic lesion in the right lobe of the liver.

Figure 2.

T1-weighted magnetic resonance images showing a hyperintense lesion corresponding to the cystic mass seen in abdominal ultrasound.

As a malignant lesion was suspected, the patient underwent an exploratory laparotomy and right hepatectomy. Intraoperatively, the external surface of the liver appeared normal, and there was no lymphadenopathy. Cut sections of the resected right liver revealed multiple serpiginous abscesses involving 9 × 4 cm of the liver parenchyma (Figure 3). The largest abscess measured 3 cm in maximum dimension. No worms or intrahepatic gallstones were noted.

Figure 3.

Resected right lobe of the liver with multiple serpiginous abscesses within liver parenchyma.

Histological examination of the abscesses showed necrotizing granulomatous inflammation with Charcot-Leyden crystals, prominent eosinophilic infiltrate, and surrounding fibrosis. Degenerate ova without internal structures were noted within the necrotic exudates (Figure 4). They were collapsed and distorted in appearance, with well-defined thin refractile wall. No refractile hooklets or protoscolices suggestive of hydatid disease were identified. The adjacent portal tracts were expanded by a mixed inflammatory infiltrate including eosinophils. There was also evidence of ductular proliferation and cholangitis.

Figure 4.

Histological finding: necrotizing granulomatous inflammation with Charcot-Leyden crystals, eosinophilic infiltrates, and surrounding fibrosis, and degenerate ova without internal structures were noted within necrotic exudates.

The specimen was sent to Mount Sinai Hospital in Toronto, Canada, and ova of Fasciola hepatica were identified. Postoperatively, the patient had no additional episodes of fever, and his eosinophil count normalized. He received a single dose of triclabendazole.

Discussion

This is a case report of F hepatica in a Western traveler. Fascioliasis is primarily an infection of livestock such as cattle and sheep, caused by the flat, brown liver fluke Fasciola hepaticus. Humans are accidental hosts and acquire the infection via consumption of aquatic vegetation (commonly watercress) or water contaminated by the metacercaria of the parasite. Fascioliasis is a reemerging disease and is now endemic in many parts of the world including Turkey, Peru, France, China, and parts of Southeast Asia. Cases of fascioliasis have been reported in nonendemic countries, mainly imported by migrants or travelers from endemic regions.1–3

Two phases of the disease have been described. The acute phase occurs 1 to 3 months following ingestion of metacercaria and corresponds to the migration of larvae through the liver to the bile ducts. This stage is manifested clinically by fever, urticaria, eosinophilia, right upper quadrant pain, and hepatomegaly. There may be considerable destruction of the liver with necrosis and abscess formation.4 Granulomata and a mixed inflammatory infiltrate can be seen on histology. The chronic phase begins when the parasites reach the bile ducts, mature, and begin to lay eggs. The chronic phase may persist for years and is often asymptomatic. Occasionally, however, adult worms or eggs may obstruct the extrahepatic bile ducts and cause cholestasis, cholangitis, or even pancreatitis.5 On microscopy, the bile ducts may show fibrotic thickening, epithelial hyperplasia, and even biliary cirrhosis. Whole eggs are not commonly seen due to their large size; rather, they appear collapsed or distorted.6 During the chronic phase, parasite ova may be excreted in the stools.

Diagnosis of fascioliasis by stool examination, however, is hindered by the late and intermittent nature of egg laying by F hepaticus. Serological testing with enzyme-linked immunosorbent assay is the cornerstone of diagnosis, with reported sensitivity and specificity of up to 95 and 100%, respectively.7 Radiological imaging may be useful for diagnosis and follow-up. The characteristic radiological features of hepatic fascioliasis are clusters of microabscesses arranged in tract-like fashion (burrow tract), subcapsular location of the hepatic lesions, and slow evolution of the lesion on follow-up examinations.8 Sonographically, the lesions may appear as focal areas of increased echogenicity, multiple nodular or irregular lesions of variable echogenicity, or a complex mass. Gallbladder and common duct abnormalities are also frequently seen. Despite the parasite’s large size (3.0 × 1.5 cm), the detection rate of F hepatica by ultrasound is disappointingly low.9 On MRI, diverse signal intensity may be demonstrated,10 attributable to the traumatic hepatitis caused by the migration of the worm in the liver. Patients presenting with biliary tract obstruction are also investigated and treated with endoscopic retrograde cholangiopancreatography, which allows visualization and removal of flukes.5,11

In nonendemic areas with limited experience with fascioliasis, the diagnosis may be delayed. We did not suspect fascioliasis in this business traveler, who visited restaurants and hotels of high hygienic standards on his travels. Retrospectively, he recalled consumption of raw watercress on a few occasions. Given his childhood in a sheep farm and ultrasonic findings of cysts, we initially considered echinococcosis. However, the large size of the lesion and MRI features were not typical of hydatid disease. The radiological findings were also not typical for fascioliasis, where typically smaller lesions have been described.10 Stool investigations were not helpful as he was in the hepatic phase of infection. We were further hampered by the lack of serological tests locally for parasitic infections.

Similar to reported cases in which surgeries were performed on patients with fascioliasis,12 our patient underwent right hepatectomy because of increasing pain and concerns of malignancy. This was, in retrospect, unnecessary, as the treatment of choice for fascioliasis is a single dose of triclabendazole at 10 mg/kg. This drug has been shown to be well tolerated and to achieve a cure rate of up to 79%.13 Though the resected liver indicated a parasitic infection, we had difficulty identifying the parasite from the degenerate shells, and the diagnosis of fascioliasis was made only after an opinion from an expert from Toronto. Treatment was further delayed in this patient for a month as we had to import triclabendazole from overseas. Despite recommendations by the World Health Organization as a first-line treatment since 1998,14 triclabendazole is not freely available in many countries, including Singapore.

This case illustrates that fascioliasis is not limited to endemic countries or migrants from endemic countries. Travelers and tourists may be at risk regardless of the quality of their accommodations and meals, though fascioliasis is still relatively rare among this population.15 Limited experience with this condition and lack of diagnostic serologies in nonendemic countries often lead to delayed diagnosis or misdiagnosis. Treatment may be further hampered by the nonavailability of optimal antiparasitic drugs in many countries.

Acknowledgments

We thank Professor Robert Riddel, Dr Mary Anne Harrington, and Dr Ian Crandell, Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Canada, and Dr Lynne Goh, Dr Jean Ho, and Dr Timothy Barkham, Department of Pathology and Laboratory Medicine, Tan Tock Seng Hospital.

Declaration of interests

The authors state that they have no conflicts of interest.

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