Hepatic Fascioliasis Masquerading as Acute Appendicitis in a Child: A Case Report

Abstract

Background:

Fascioliasis is a neglected tropical disease caused by Fasciola species that can present with nonspecific abdominal symptoms and mimic surgical emergencies.

Case Presentation:

We report a 12-year-old Ethiopian boy who presented with right-sided abdominal pain, fever, and marked eosinophilia and was initially suspected to have acute appendicitis. Diagnostic laparoscopy revealed hepatic rather than appendiceal pathology. Imaging demonstrated subcapsular hepatic tracks, and serologic testing confirmed Fasciola species infection (most probably Fasciola gigantica in the Ethiopian context). Histopathology showed eosinophil-rich granulomatous hepatitis with helminthic structures. The patient was treated with triclabendazole and recovered completely.

Conclusion:

This case highlights the importance of considering parasitic infections such as fascioliasis in children presenting with atypical acute abdominal pain in endemic regions. Early use of imaging and serologic testing may prevent unnecessary surgical interventions and allow timely curative therapy.

Introduction

Fascioliasis is a zoonotic hepatobiliary infection caused by Fasciola species, food- and water-borne trematodes with worldwide distribution.^1,2 In sub-Saharan Africa, including Ethiopia, the predominant species is Fasciola gigantica, although species differentiation is often not possible in clinical practice. The disease is endemic in several regions of Africa, the Middle East, and Latin America, and pediatric cases continue to be reported from Ethiopia.^3,4 The World Health Organization (WHO) recognizes fascioliasis as a neglected tropical disease (NTD), underscoring the importance of heightened clinical awareness and timely diagnosis.

Human infection occurs through ingestion of metacercariae on contaminated aquatic plants or water. After ingestion, larvae migrate through the intestinal wall and peritoneum to invade the liver parenchyma, eventually reaching bile ducts where they mature. The acute hepatic phase (first 2-4 months) manifests with fever, right upper quadrant pain, malaise, and marked eosinophilia. The chronic biliary phase presents with obstructive symptoms and complications like cholangitis. Children experience more severe manifestations due to proportionally greater tissue damage from parasites in smaller livers. ⁵

Diagnosing acute fascioliasis is challenging because symptoms mimic common conditions such as viral hepatitis, liver abscess, or surgical emergencies like appendicitis. Cases have been misdiagnosed, leading to exploratory surgery before correct identification. Awareness of eosinophilia with hepatic lesions should prompt consideration of parasitic causes. ⁶ Early identification enables curative treatment and prevents complications such as biliary obstruction or pancreatitis. We present a pediatric case where hepatic fascioliasis initially mimicked acute appendicitis, and we discuss diagnostic challenges and management.

Case Presentation

A 12-year-old male from Addis Ababa presented with 1 week of migratory abdominal pain, low-grade fever, and malaise. Pain initially was diffuse but localized to the right side. Examination revealed right upper quadrant tenderness with mild guarding. McBurney’s point tenderness was minimal, though acute appendicitis was considered. The patient was afebrile and with normal vital signs.

Initial laboratory tests showed leukocytosis (19 000/mm³) with marked eosinophilia (55%, absolute count approximately 10 450/mm³). Inflammatory markers were elevated (CRP 40 mg/L). Liver enzymes were: AST 44 U/L, ALT 22 U/L, ALP 338 U/L. Total bilirubin was normal (0.8 mg/dL).

Abdominal ultrasound revealed multiple ill-defined hypoechoic lesions in the right hepatic lobe, some subcapsular, without gallstones or bile duct dilation. The appendix appeared unremarkable. Stool examinations for ova and parasites were negative, consistent with early-phase infection prior to biliary egg shedding. Serologic testing included an indirect hemagglutination assay (IHA) for Fasciola antibodies (titer 1:1024) and a commercially available DRG^® Fasciola IgG ELISA (DRG Instruments GmbH, Germany), performed according to the manufacturer’s instructions. The sensitivity and specificity of this ELISA test is proved to be 95.3% (95% CI, 82.9%-99.2%) and 95.7% (95%CI, 92.3%-97.5%). ⁷ Both tests were positive, confirming Fasciola infection. Because serologic assays cannot differentiate between F. hepatica and F. gigantica, and eggs were not detected for morphometric analysis during the acute phase, definitive species identification was not possible; however, F. gigantica is the most epidemiologically plausible cause in this setting.

• Laparoscopy: Before serologic confirmation, diagnostic laparoscopy was performed for suspected atypical appendicitis. The appendix was normal. Inspection of the liver revealed multiple whitish subcapsular nodules and tracks on the right lobe surface, with mild perihepatic inflammation but no pus (Supplemental Video 1). One indurated tract was biopsied. Laparoscopic findings were consistent with parasitic liver infection, and appendectomy was deferred.

• Pathology Report: Microscopic examination of the hepatic biopsy revealed hepatic parenchyma with necrotizing granulomatous inflammation characterized by central zones of coagulative necrosis surrounded by palisading epithelioid histiocytes, with a dense mixed inflammatory infiltrate predominantly composed of eosinophils admixed with lymphocytes, plasma cells, and neutrophils. Multiple multinucleated giant cells of foreign body type were identified within and at the periphery of the granulomas. Helminthic larval structures consistent with Fasciola species (most probably Fasciola gigantica in the Ethiopian context) were observed within areas of necrosis and inflammatory infiltrate. The surrounding hepatic parenchyma showed preserved hepatocyte architecture with mild portal tract expansion. Special stains (Ziehl-Neelsen) were negative for acid-fast bacilli, excluding mycobacterial infection. The constellation of necrotizing eosinophil-rich granulomas with helminthic structures in the clinical context of marked peripheral eosinophilia and positive serology was diagnostic of hepatic fascioliasis (Figures 1 and 2).

• Treatment and Outcome: The patient received triclabendazole 10 mg/kg twice, 12 hours apart (two 500 mg doses), with food. No significant side effects occurred apart from mild transient abdominal discomfort. By Day 5, pain markedly improved. Eosinophil count fell to 8% by Day 10 (from 35% on admission). The patient was discharged in good condition. Follow-up ultrasound (1 month) showed resolution of lesions with faint residual scars. Repeat ELISA titer (3 months) declined fourfold, indicating successful treatment. The family received counseling on preventing reinfection by avoiding raw aquatic vegetables and boiling water.

Figure 1.

Eosinophil rich inflammation with central necrosis with palisading epitheloid cells (20×).

Figure 2.

Scattered Charcot-Leyden crystals (40×).

Discussion

This case illustrates how hepatic fascioliasis can mimic acute appendicitis in children. The initial presentation with fever, right-sided abdominal pain, leukocytosis, and elevated liver enzymes prompted a broad differential. ⁸ Bacterial liver abscess was considered, but marked eosinophilia was atypical for pyogenic abscess and prompted parasitic investigation. Acute cholecystitis or cholangitis could cause right upper quadrant pain but would not explain migratory liver tracts on imaging. Viral hepatitis typically causes diffuse hepatic inflammation with jaundice and very high transaminases, not focal lesions or eosinophilia. Hydatid disease (Echinococcal cysts) presents with well-defined cystic masses with septations, unlike the ill-defined subcapsular tracks seen here. The possibility of atypical appendicitis was entertained, but laparoscopy ruled it out and revealed liver lesions, underscoring the need to consider unusual etiologies in acute abdomen cases with anomalous features like eosinophilia or abnormal liver imaging. ⁹

In sub-Saharan Africa, including Ethiopia, Fasciola gigantica is the predominant species and is mainly transmitted by the widely distributed lymnaeid snail Radix natalensis. Although F. hepatica has been reported in Ethiopia, including areas near Addis Ababa, these reports lack molecular confirmation and are largely based on animal infections, sometimes associated with imported livestock. ⁴ In areas where Galba/Fossaria snails are absent, transmission may involve introduced vectors such as Pseudosuccinea columella, which primarily maintains animal fascioliasis but can also transmit F. gigantica. Because serologic assays cannot differentiate between F. hepatica and F. gigantica, and eggs were not detected in this acute-phase patient, definitive species identification was not possible. Nevertheless, infection by F. gigantica is the most epidemiologically plausible explanation, and its clinical presentation is indistinguishable from that of F. hepatica.^4,5,8 Misclassification between the 2 species in human cases is well documented due to reliance on serology without molecular confirmation and overlapping clinical, radiologic, and laboratory features. ⁶ Large-scale epidemiological data further demonstrate that F. gigantica readily infects humans, including children, and can produce widespread transmission comparable to that attributed to F. hepatica. ⁸ Accordingly, the present case most likely represents F. gigantica infection, although confirmation was not possible because stool examination during the acute phase did not reveal eggs for morphometric differentiation. The clinical timing also supports this interpretation, as the acute hepatic phase of F. gigantica is typically longer than that of F. hepatica.^10,11

The gold standard for diagnosing fascioliasis is finding Fasciola eggs in stool, but this is often negative in early-phase infection before bile duct maturation. ¹² Serologic tests (IHA and ELISA) are critical for acute diagnosis, with reported sensitivity and specificity often exceeding 95%. ⁷ However, ELISA cannot reliably distinguish active from resolved infection, as antibody titers may remain positive for months after treatment, limiting its usefulness for post-treatment monitoring. The laboratory profile in our patient, characterized by marked eosinophilia, elevated inflammatory markers, and mild to moderate elevation of liver enzymes with disproportionate alkaline phosphatase elevation, aligns with biochemical patterns described in acute fascioliasis. Experimental and clinical data have shown that F. gigantica may induce a more pronounced inflammatory and biochemical response during the hepatic migratory phase compared with F. hepatica, which is consistent with the findings observed in this case. ¹¹

Imaging also played a pivotal role. Ultrasound findings of clustered subcapsular hepatic lesions with linear extension (“tunnel tract” lesions) are highly suggestive of migratory Fasciola. ¹³ Similar radiologic patterns have been documented as radiographic hallmarks of acute fascioliasis. In ambiguous cases, advanced imaging can raise suspicion and direct serologic testing. Laparoscopic visualization and histopathology provided additional confirmation in our patient. Historically, some cases were only diagnosed during surgery or biopsy for presumed tumors or abscesses. Fortunately, increasing availability of noninvasive serology and awareness of imaging signs can spare patients unnecessary invasive procedures by yielding earlier diagnosis. ¹⁴

Triclabendazole is the treatment of choice for fascioliasis in adults and children, with excellent activity against Fasciola species at all life stages. ¹⁵ The standard WHO regimen is 10 mg/kg with food, with some experts advising a second dose 12 hours later for heavy infections or to ensure clearance. Triclabendazole has a high cure rate (greater than 90%) and is well tolerated in children aged 6 years and older.^15,16 Our patient responded very well with rapid symptom resolution. In our setting, the drug was obtained via the national tropical disease program, reflecting increasing access in endemic countries. Although triclabendazole remains the treatment of choice, emerging resistance has been increasingly reported, particularly in endemic regions, highlighting the need for careful use, treatment monitoring, and ongoing surveillance.

In endemic regions, coinfections with other helminths or protozoa have been documented in patients with fascioliasis, reflecting shared environmental exposures such as contaminated water sources, agricultural practices, and close contact with livestock. Multiparasitism may modify clinical presentation, laboratory findings, and inflammatory responses, potentially complicating diagnosis. In hepatic presentations, concomitant infections such as hydatid disease or bacterial abscess must be carefully excluded through imaging and laboratory evaluation. Awareness of overlapping transmission pathways and immunologic interactions is therefore essential when assessing hepatic lesions in hyperendemic settings. ¹⁷

With timely diagnosis and appropriate therapy, the prognosis of pediatric fascioliasis is excellent. In endemic settings, misdiagnosis as a surgical emergency remains a significant risk. Similar Ethiopian cases and reports from other regions demonstrate variable presentations and frequent initial suspicion of appendicitis or other acute abdominal conditions.^18,19 These findings highlight the importance of applying structured clinical and diagnostic methods, including careful evaluation of eosinophilia, appropriate serologic testing, and recognition of characteristic imaging features, to differentiate hepatic fascioliasis from surgical diseases. ²⁰ Early recognition using these approaches can help avoid unnecessary surgical interventions and allow prompt curative treatment.

Limitations

This report has several limitations inherent to single-patient case studies. First, as a single case report, the findings cannot be generalized to broader populations and should be interpreted primarily as a clinical observation rather than evidence of causal relationships. Second, the retrospective nature of the report limits the completeness of available clinical data and follow-up information. Third, although histopathological findings supported the diagnosis of hepatic fascioliasis, additional confirmatory investigations such as serologic testing or molecular diagnostic methods were not available, which may limit the diagnostic certainty. Finally, the lack of long-term follow-up data restricts the ability to fully assess the long-term clinical outcomes and response to treatment. Despite these limitations, this case highlights an unusual presentation of hepatic fascioliasis mimicking acute appendicitis and underscores the importance of considering parasitic infections in the differential diagnosis in endemic regions.

Conclusion

Fascioliasis should be considered in children presenting with acute abdominal pain, particularly in endemic regions where eosinophilia and hepatic lesions are present. Early recognition through careful evaluation of eosinophilia, targeted serologic testing, and characteristic imaging findings is essential for timely diagnosis, effective treatment with triclabendazole, and avoidance of unnecessary surgical interventions in patients with atypical acute abdomen. A structured diagnostic approach can help distinguish parasitic hepatic disease from surgical emergencies, while public health measures, including livestock control and health education, remain crucial for reducing transmission in endemic areas.