Fascioliasis is a food-borne zoonosis caused either by F. hepatica, distributed worldwide, or by Fasciola gigantica, whose distribution is restricted to Africa and Asia. Definitive hosts, mainly livestock but also humans, become infected through the ingestion of metacercariae in food, especially freshwater plants or water.1 Highly endemic areas for human fascioliasis include the Near East (mainly Iran and Türkiye), Pakistan, Egypt and the Andean region in Latin America. In Europe, France, Spain and Portugal are considered endemic areas, although sporadic cases have been reported in almost all countries.2 Here, we present a case of a 66-year-old German woman presenting with subacute fever, nocturnal sweats, fatigue and weight loss with onset two months after an extended journey to Uzbekistan and Tajikistan. While the clinical examination was unremarkable, laboratory investigations showed eosinophilia of up to 13.000/μl, leucocytosis, elevated IgG and IgE levels, slightly elevated C-reactive protein, as well as moderately elevated liver enzymes with cholestatic pattern. On ultrasound, a hypodense lesion in the right lobe of the liver was observed. Magnetic resonance imaging (MRI) showed irregular, garland-like liver lesions with dynamic progression on follow-up (Figure 1). Histopathological examination of ultrasound-guided biopsy of the main lesion revealed an eosinophilic, granulomatous abscess. Serological screening for tissue invasive helminths showed a positive result for F. hepatica in the enzyme-linked immunoassay with confirmation in the immunofluorescence antibody test. Serology for toxocariasis, filariasis and echinococcosis was negative. Amplification and Sanger sequencing of the cytochrome c oxidase subunit 1 (COX-1) mitochondrial gene from the biopsy material identified the species F. hepatica and confirmed the suspected diagnosis of fascioliasis.3 The patient was treated with 10 mg/kgBW/d triclabendazole for two days and amoxicillin/clavulanic acid due to suspicion of secondary cholangitis. Symptoms subsided within two weeks and eosinophils decreased rapidly. At follow-up after four months, a complete regression of the liver lesions on ultrasound and normalization of eosinophils, inflammation markers and liver enzymes were observed.

(A) Ultrasound and MRI at initial presentation, showing a hypoechogenic, irregular lesion in segment VI of the liver. (B) Follow-up MRI two months later in two axial planes revealing dynamic progression with irregular, garland-shaped lesions and a new central lesion, while the initial lesion in segment VI is in regression.
Figure 1

(A) Ultrasound and MRI at initial presentation, showing a hypoechogenic, irregular lesion in segment VI of the liver. (B) Follow-up MRI two months later in two axial planes revealing dynamic progression with irregular, garland-shaped lesions and a new central lesion, while the initial lesion in segment VI is in regression.

Fasciola hepatica is one of the most widespread parasites worldwide. The clinical course of human fascioliasis can be divided into an invasive or acute phase, which lasts about two to four months, and a chronic or obstructive phase, which lasts for months or years.2 During the acute phase, serological tests are used for diagnosis.4 As in our case, eosinophilia is one of the most striking laboratory finding in this stage of the disease. Sequencing of COX-1, a gene commonly used for the identification of helminths, from biopsy material can help to confirm the diagnosis in unclear cases. Confirmation of the diagnosis by microscopic detection of eggs in stool is only possible after the prepatent period of 3–4 months elapsed.1 Due to the discontinuous excretion of eggs, multiple stool examinations are often necessary.

Fascioliasis is rare in travellers.5 The GeoSentinel surveillance network reported only 14 cases among 42.173 ill returning travellers between 2007 and 2011.6 However, fascioliasis should be considered as a differential diagnosis in travellers with hypereosinophilia, B symptoms and hepatic lesions on imaging. Triclabendazole remains the drug of choice with cure rates ranging from 92–100%.1 This drug is often neither regionally available nor approved for use in humans, but can be requested directly from the WHO. Second-line options such as nitazoxanide, albendazole or bithionol can be considered if triclabendazole is not at hand or if treatment fails after repeated administration of triclabendazole.2 Endoscopic retrograde cholangiopancreatography may be needed in cases of biliary obstruction.

Author contributions

Lukas Rohloff (Conceptualization [equal], Visualization [equal], Writing—original draft [equal]), Veronika Neumayr (Conceptualization [equal], Visualization [equal], Writing—original draft [equal]), Maura Concu (Writing—review & editing [equal]), Marie-Therese Ruf (Writing—review & editing [equal]), Robert Thimme (Writing—review & editing [supporting]), Annerose Serr (Writing—review & editing [supporting]), and Siegbert Rieg (Writing—review & editing [equal])

Funding

None.

Disclosure

None.

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Author notes

Lukas Rohloff and Veronika Neumayr contributed equally

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