Hepatobiliary fascioliasis: A neglected re-emerging threat, its diagnostic and management challenges

Abstract

Hepatobiliary fascioliasis is a neglected but re-emerging parasitic disease caused by Fasciola hepatica. Humans become infected by consuming contaminated water or aquatic plants, allowing the parasite to enter the digestive tract. From there, immature flukes penetrate the intestinal wall and migrate through the liver, triggering inflammation, fibrosis, and biliary complications. Over time, this can lead to cholangitis, biliary obstruction, and long-term liver damage. Due to its vague clinical symptoms and the limitations of current diagnostic methods, fascioliasis could be easily missed. Stool analysis is still used to detect eggs in diagnosis. However, this method is unreliable due to the inconsistency of the egg shedding. Also, serological tests are often linked to false positives due to the cross-reactions with other parasites. Imaging techniques such as ultrasound, computed tomography, and magnetic resonance imaging can reveal its complications, especially in the biliary phase, yet this is not specific. Molecular tests like polymerase chain reaction (PCR) have higher sensitivity and specificity and allow earlier diagnosis, but they are still not widely available, especially in low-resource settings. Triclabendazole is the only recommended medical treatment, yet it is not widely available. In addition, the emerging reports of resistance represent a potential threat in managing this infection. Other modalities could be needed in addition to triclabendazole, such as endoscopic retrograde cholangiopancreatography in patients with biliary complications. All the previously mentioned challenges necessitate the urgent need to make the newly developed diagnostic methods, such as PCR, available, especially in areas where fascioliasis is endemic. Additionally, new medical treatments and therapeutic options should be considered to provide a second line of management, particularly in light of emerging reports of resistance.

Key Words: Fascioliasis; Triclabendazole; Hepatobiliary; Parasitic infections; Flukes

Core Tip: In this review article, we discuss how hepatobiliary fascioliasis, a neglected parasitic disease caused by Fasciola hepatica. Current diagnostic methods, such as stool analysis and serological tests, are unreliable and often linked to false positives. Molecular tests like polymerase chain reaction are not widely available, and new treatments and therapeutic options are needed.

INTRODUCTION

Fascioliasis is a zoonotic parasitic infection caused by trematodes of the genus Fasciola, specifically Fasciola hepatica and Fasciola gigantica[1]. These liver flukes, or liver “termites” as we suggest to call, primarily infest the hepatic and biliary systems of various mammalian hosts, including humans and livestock, leading to significant pathological manifestations. Fasciola hepatica has a global distribution colonizing the five continents, while Fasciola gigantica is predominantly found in Africa and Asia. Transmission occurs via ingestion of water or aquatic vegetation contaminated with metacercariae, the infective larval stage of the parasite[2].

Fascioliasis is prevalent in regions characterized by extensive livestock farming and the presence of freshwater ecosystems that support the life cycle of the parasite. The disease is endemic in Latin America, Africa, Asia, and parts of Europe, where human cases are frequently reported[3].

An estimated 17 million cases of fascioliasis have been reported worldwide[3,4]. A recent meta-analysis revealed that the regions exhibiting the highest prevalence rates of fascioliasis are South America (9.0%) and Africa (4.8%)[5]. The global prevalence of fascioliasis was estimated to be 4.5%[5].

Hepatobiliary fascioliasis presents substantial public health challenges due to its capacity to induce severe hepatic and biliary complications[2]. Infected individuals may develop acute or chronic forms of the disease, with symptoms including hepatic inflammation, biliary duct obstruction, cholangitis, and secondary bacterial infections[2]. Chronic manifestations can result in fibrosis, cirrhosis, and long-term hepatic[6,7].

Fascioliasis has been documented in medical and veterinary literature for centuries, with early descriptions detailing liver fluke infestations in both humans and livestock. Historically, the disease was regarded primarily as a veterinary concern; however, its significance as a human infection has gained prominence in recent decades due to advancements in diagnostic methodologies and increased epidemiological surveillance[8]. The contemporary reemergence of fascioliasis underscores the necessity for intensified research, improved public health interventions, and the development of effective control strategies aimed at mitigating transmission and disease burden[2].

The reemergence of fascioliasis as a significant public health concern is attributed to factors such as climate change, modifications in agricultural practices, expansion of irrigation systems, and dietary changes that facilitate human exposure to infective stages[2]. An increase in the number of human infections has been documented in endemic regions, particularly in nations such as Egypt, Peru, Iran, Bolivia and Ecuador where the consumption of raw aquatic plants is customary[9,10].

In this review, we aim to delineate the etiology, epidemiology, pathophysiology, diagnostic and management challenges of hepatobiliary fascioliasis, thereby informing effective public health strategies and guiding future research amid its global reemergence. Lifecycle Fasciola have a quite complex life cycle (Figure 1). In humans, fascioliasis commences with ingestion of metacercariae-contaminated vegetation, followed by excystation in the duodenum within an hour after ingestion. The immature flukes, or “termites” as we named after them, characterizing the behavior similar to termites, then penetrate the intestinal wall and appear in the abdominal cavity within two hours after ingestion, migrate to the liver within a six-day journey, migrate through the hepatic parenchyma for around six weeks feeding on hepatic parenchyma and eventually localize in the bile ducts, where they mature[2]. According to Valero et al[11], the prepatent period, which is the time from ingestion of infective stage-to-seeing the diagnostic stage in feces, is around 3-4 months. We observed that the liver fluke's invasion of the biliary system is analogous to termites infiltrating a tree's inner cavities. Just as termites create and occupy protective chambers within a tree-gradually compromising its structural integrity-we observed that the fluke establishes a niche within the bile ducts, progressively impairing the host’s hepatic function (Figure 2). This migratory phase underpins the acute inflammatory response, while the subsequent establishment in the biliary system precipitates chronic complications. During their migration through the hepatic parenchyma, the immature flukes mechanically disrupt tissue and provoke a localized inflammatory response. This invasive process results in tissue damage characterized by focal necrosis, hemorrhage, and subsequent fibrosis. Upon reaching the biliary system, the flukes mature and establish themselves within the bile ducts. Here, their presence incites chronic irritation, promotes ductal obstruction, and induces ongoing inflammatory processes that compromise biliary integrity and hepatic function[12]. Worth noting that adult flukes can survive in the hepatobiliary system for up to 10 years[13]. This represents the basis for the chronic and relapse pictures seen in some patients[13]. Fascioliasis is characterized by a multi-phasic clinical course that reflects the dynamic interplay between parasite migration, host tissue response, and chronic biliary alterations. In the invasive (acute) phase, the initial migration of liver “termites” through the hepatic parenchyma and peritoneum precipitates significant mechanical tissue destruction[14]. This destruction elicits a pronounced inflammatory response, manifesting as systemic and localized symptoms[14]. Patients typically present with fever, right upper quadrant or epigastric pain, and gastrointestinal disturbances including anorexia, nausea, flatulence, and diarrhea[14]. Additionally, respiratory symptoms such as cough, dyspnea, and even hemoptysis may occur, accompanied by allergic phenomena such as urticaria[14]. Subsequently, during the latent phase, the parasites complete their maturation and initiate oviposition, a period often marked by minimal or subclinical symptomatology[15]. This phase may persist for months or even years, with many infections remaining undiagnosed until incidental findings emerge during family screenings or routine investigations[15]. The transition to the chronic (biliary or obstructive) phase heralds more insidious but severe clinical manifestations (Figure 3). As adult flukes establish themselves within the bile ducts, their presence incites chronic inflammation, epithelial hyperplasia, and structural remodeling of the biliary system. The resultant pathological changes include cholangitis, cholecystitis, and mechanical bile duct obstruction[7,16]. Clinically, this phase is typified by recurrent biliary colic, epigastric pain, intolerance to fatty foods, and signs of obstructive jaundice such as pruritus and right upper quadrant tenderness. Moreover, prolonged infection predisposes to gallstone formation, with the potential for secondary bacterial infections, further compounding the clinical picture[7,16]. Laboratory investigations frequently reveal eosinophilia in fascioliasis patients, particularly during the acute phase of infection. However, clinical manifestations during the chronic biliary phase may present without accompanying eosinophilia in some cases[17,18]. Collectively, these stages underscore the progressive and multifaceted nature of fascioliasis, where acute inflammatory damage transitions into chronic biliary pathology, with significant implications for morbidity in affected populations.

Figure 1  Immature eggs are discharged in the biliary ducts and passed in the stool (1). Eggs become embryonated in freshwater over approximately 2 weeks (2); embryonated eggs release miracidia (3), which invade a suitable snail intermediate host (4). In the snail, the parasites undergo several developmental stages (sporocysts 4a, rediae 4b, and cercariae 4c). The cercariae are released from the snail (5) and encyst as metacercariae on aquatic vegetation or other substrates. Humans and other mammals become infected by ingesting metacercariae-contaminated vegetation (e.g., watercress) (6). After ingestion, the metacercariae excyst in the duodenum (7) and penetrate through the intestinal wall into the peritoneal cavity. The immature flukes then migrate through the liver parenchyma into biliary ducts, where they mature into adult flukes and produce eggs (8). In humans, maturation from metacercariae into adult flukes usually takes about 3-4 months; development of F. gigantica may take somewhat longer than F. hepatica. Source: CDC-DPDx-Fascioliasis[12].

Figure 2 The termite's analogy illustration. We suggest calling the liver flukes the liver “termites” emphasizing the inhabitation and damage to the biliary tract and hepatic parenchyma.

Figure 3  Flowchart of mechanisms of liver and bile duct involvement and how they lead to symptoms.

Diagnostic challenges

Traditional diagnostic approaches for fascioliasis include serological assays and stool examinations. Serological tests, such as enzyme-linked immunosorbent assays (ELISA), are commonly employed to detect antibodies against Fasciola spp. in serum, intradermal, or stool samples, offering relatively high sensitivity, particularly during the early invasive phase when eggs are not yet detectable in stool samples[19]. However, these assays may encounter specificity issues due to potential cross-reactivity with antibodies against other helminths. Conversely, stool examinations involve the microscopic identification of characteristic Fasciola eggs, serving as a direct method for diagnosing chronic infections[11]. Although stool examination provides definitive evidence of infection, its diagnostic sensitivity is notably reduced during the acute stage of the disease, and intermittent egg shedding can further complicate accurate detection. A variety of techniques, ranging from simple direct smears to various concentration methods, can be employed. Egg concentration has been successfully achieved using both flotation and sedimentation techniques. However, sedimentation techniques have demonstrated greater accuracy and sensitivity compared to flotation methods[20]. The diagnostic utility of fasciolid egg size is fraught with challenges. Traditionally, egg size thresholds-approximately 150 μm in length and 90 μm in width-have been employed to differentiate Fasciola hepatica (smaller eggs) from Fasciola gigantica (larger eggs). However, substantial variability in egg dimensions has been documented, influenced by geographical differences and the species of the definitive host, as demonstrated by studies in livestock[21,22]. The presence of intermediate forms and genetic hybrids further complicates matters, as these forms exhibit overlapping morphological characteristics that blur the conventional size distinctions. Notably, in human infections, recent computer image analysis studies have revealed that F. hepatica eggs tend to be larger while F. gigantica eggs are smaller than those observed in animals, resulting in overlapping measurement ranges that render differential diagnosis unreliable[19,23]. Consequently, reliance on classic egg size parameters in human samples may lead to erroneous diagnostic conclusions, underscoring the need for revised measurement standards in parasitological guides and clinical practice. In addition to detecting eggs through stool analyses, adults and eggs may also be identified using other invasive techniques. These include obtaining duodenal fluid, duodenal and biliary aspirates, as well as surgical procedures such as laparotomy, cholecystectomy, and sphincterotomy. Furthermore, histological examination of liver or other organ biopsy samples can also reveal their presence. Serological detection of Fasciola-specific antibodies demonstrates high diagnostic sensitivity, particularly during the acute phase when stool microscopy remains negative. ELISA platforms exhibit > 95% sensitivity and specificity, with validated targets including excretory-secretory (E/S) antigens, cathepsin proteases, and the immunodominant 27 kDa protein[24-26]. The United States Centers for Disease Control and Prevention provides serologic diagnosis of fascioliasis via an immunoblot assay detecting IgG antibodies against the recombinant FhSAP2[27,28]. Serological tests, while sensitive, may produce false-positive results in areas where multiple helminth infections are endemic, thereby limiting their specificity. Moreover, the window period between infection and seroconversion can delay diagnosis. The current diagnostic practices for fascioliasis are constrained by several limitations (Table 1)[29-33]. In response to these limitations, emerging diagnostic techniques are being developed to enhance early and accurate detection of fascioliasis. Molecular methods, particularly polymerase chain reaction (PCR) assays, have shown promise in detecting minute quantities of parasite DNA in clinical specimens, thus offering a more sensitive and specific alternative to traditional methods. PCR-based assays have been developed not only to detect Fasciola DNA with high sensitivity during early infection but also to differentiate between Fasciola hepatica and Fasciola gigantica. This differentiation is critical in endemic regions where both species-and even their hybrid forms-coexist, yet conventional clinical, pathological, stool microscopy, and immunological methods fail to distinguish them. Simple and rapid PCR-RFLP assays (using enzymes such as Ava II and Dra II) have been successfully employed to discriminate between the two pure species by targeting a conserved 28S rRNA gene fragment[34]. However, these assays, along with other PCR-based methods like duplex PCR and TaqMan real-time PCR, are limited in detecting hybrid forms due to the wide introgression capacity between the species[35]. As a result, DNA marker sequencing-targeting markers such as ITS-1, ITS-2, cox1, and nad1-remains the definitive approach for both haplotyping pure species and identifying hybridization events[35,36]. A novel isothermal PCR technique-recombinase polymerase amplification-was developed for field application in resource-limited settings. This innovative assay achieved 88% sensitivity and 100% specificity in detecting Fasciola spp. DNA in human stool samples[37]. Additionally, radiologic imaging modalities are being explored to overcome the shortcomings of traditional invasive techniques such as endoscopic retrograde cholangiopancreatography (ERCP)[38,39]. A study reported a case where Initial imaging suggested choledocholithiasis, but ERCP uncovered live Fasciola larvae in the bile duct, later confirmed by stool analysis[39]. Although ERCP has primarily been utilized for therapeutic purposes due to its invasiveness, imaging approaches-such as high-resolution ultrasonography, computed tomography (CT), and magnetic resonance imaging-could have a diagnostic potential, offering non-invasive means to visualize hepatic and biliary involvement associated with fascioliasis[17,40]. During the acute hepatic phase, contrast-enhanced CT typically demonstrates pathognomonic hypoattenuating, serpiginous subcapsular tracts. However, radiographic manifestations exhibit heterogeneity and may additionally include non-enhancing parenchymal lesions, nodular formations, hepatosplenomegaly, and regional lymphadenopathy[41].

Table 1 Challenges in fascioliasis diagnostics and emerging techniques.

Method		Strengths	Challenges	Emerging solutions/comments
Stool analysis		Direct detection of eggs in stool samples confirms active infection	Does not allow the differentiation between F. gigantica and F. hepatica due to morphological similarities, delay in detection (only positive 3-4 months post-infection), intermittent egg output, low or absent egg shedding in light infections, chronic cases, ectopic infections, or false positives from ingested infected liver tissue	Necessitates alternative or adjunct diagnostic methods due to limited sensitivity in early and complex cases
Serology	Serological tests using excretory/secretory Antigens[29,30]	ELISA-based tests using purified or recombinant antigens (e.g., cysteine proteinases produced in yeasts[29] or in E. coli[30]) offer high sensitivity and specificity, particularly for F. hepatica and F. gigantica	May suffer from cross-reactivity with antibodies against other helminths; delayed seroconversion in the acute phase; cannot differentiate between species in regions where both coexist	Recombinant antigens produced in yeast or E. coli have been successfully incorporated into ELISA protocols, improving diagnostic performance
	MM3 coproantigen-detection test[31]	Provides high sensitivity and specificity; suitable for large-scale screening, early detection in chronic infections, and monitoring treatment outcomes	Limited in its ability to quantify fluke burden on its own, which is crucial for determining appropriate treatment doses and assessing disease intensity	The use of a new preservative/diluent (CoproGuard™) has enhanced coproantigen extraction and antigen stability, potentially improving the test's diagnostic yield[32]
	Commercial F. hepatica IgG ELISA[26]	High sensitivity and high negative predictive value, making it useful for ruling out infection when combined with a compatible clinical history	Exhibits a low positive predictive value and lacks correlation with egg output, necessitating confirmation with additional diagnostic methods to avoid misclassification, particularly in areas with potential cross-reactive helminth infections	Considered promising for individual diagnosis and large-scale epidemiological studies, provided it is supplemented by other diagnostic tests to confirm positive results
	SeroFluke Lateral Flow Test[33]	Offers maximal specificity and sensitivity; applicable to both serum and whole-blood samples; user-friendly and suitable for point-of-care testing in both hospital settings and endemic regions	While promising, further validation is required to fully assess its performance across diverse clinical settings and to ensure its reliability in routine diagnostic practice	Represents a significant step forward in rapid, field-friendly diagnostics, potentially addressing the shortcomings of more invasive or technically demanding methods

Management challenges

The development of effective fascioliasis treatments has included the evaluation of various antiparasitic agents, as summarized in Table 2. Among these, the World Health Organization (WHO) identifies triclabendazole as the antiparasitic agent of choice for fascioliasis, demonstrating efficacy against both immature and mature stages of Fasciola spp[42]. Triclabendazole is benzimidazole drug that interferes with the parasite’s β-tubulin polymerization balance leading to inhibition of protein synthesis[43]. Triclabedazole is deemed safe. Extensive global clinical experience and available safety data support the drug's favorable safety profile. However, canine studies identified potential QTc prolongation at supratherapeutic doses. Current prescribing guidelines recommend caution in patients with preexisting QTc prolongation or those concurrently using other QT-prolonging medications[44]. Standard treatment regimens with triclabendazole typically involve a single or double-dose administration, tailored to parasite load and clinical severity at 10 mg/kg after a meal separated by 12-24 hours. Some studies reported cure rates between 75% and 100% using a single dose of triclabendazole 10 mg/kg[43,45,46]. Two randomized studies, with poor methodological designs, reported no difference in effectiveness between single-dose and multiple-dose regimens[45,47]. Existing evidence indicates that administering two doses of triclabendazole at 10 mg/kg may be more effective than a single-dose regimen[48]. Dosage adjustments are made based on patient-specific factors such as age, hepatic function, and the risk of reinfection, ensuring optimized therapeutic outcomes. In many endemic regions, limited access to triclabendazole poses a significant challenge. Furthermore, the emergence of triclabendazole-resistant fascioliasis is a growing concern. Extensive use in livestock has led to widespread resistance in cattle and sheep, raising the risk of transmitting resistant infections to humans[49]. Notably, treatment failures have been documented in human cases form Tureky, Peru, Portugal, Chile, and The Netherlands[50-54], with some patients continuing to shed eggs despite high-dose regimens[52]. While resistance mechanisms do not involve the same ß-tubulin mutations seen in other helminths[55,56], alterations in drug uptake and detoxification pathways are suspected[57-59]. Additionally, Nitazoxanide, 500 mg twice a day for a week in adults, has been proposed as an alternative treatment for Fasciola infections, especially in the chronic stage of infection[60]. However, evidence on its efficacy is conflicting. While some studies report success rates as high as 94%[61], others show significantly lower efficacy, with some cases failing treatment altogether[52]. Due to these inconsistencies, nitazoxanide cannot be recommended as a reliable therapeutic option. Novel antiparasitic compounds are currently under investigation, aiming to provide effective alternatives. Poor water solubility of triclabendazole may limit its organ concentration and efficacy. Flores-Ramos et al[62] developed a prodrug (MFR-5) that is vastly more water-soluble and stable, achieving high fasciolicidal activity in animal models. Adjunctive therapies, including surgical interventions and endoscopic procedures, play a critical role in managing complications such as biliary obstruction (Figure 4). These therapies are essential in cases where pharmacological treatment alone is insufficient to alleviate structural complications. Endoscopic intervention, particularly ERCP, can be extremely helpful in such cases, as revealed by Bahcecioglu et al[63]. The authors reported the use of ERCP to manage 36 patients in the biliary phase of fasciola, achieving a high success rate and safety profile. The complexity of hepatobiliary fascioliasis, particularly in advanced or refractory cases, underscores the necessity for a multidisciplinary management approach. Coordinated care involving hepatologists, infectious disease specialists, surgeons, and interventional radiologists ensures that both the parasitic infection and its systemic complications are comprehensively addressed, ultimately enhancing patient outcomes.

Figure 4  Viable Fasciola spp. Specimens retrieved from the gallbladder during endoscopic retrograde cholangiopancreatography.

Table 2 Summary of antiparasitic medications, including dosages and treatment regimens.

Drug	Mechanism of action	Dose	Comments
Triclabendazole	Binds to β-tubulin, inhibiting microtubule formation, leading to impaired motility and disruption of vital processes in the parasite	For patients ≥ 6 years: Two doses of 10 mg/kg administered 12 hours apart (alternatively, a single 10 mg/kg dose has been used)	Taken orally with food to improve absorption. It is the drug of choice for fascioliasis, with extensive clinical experience supporting its efficacy against both immature and mature stages. FDA-approved for use in patients aged six and older. Caution is advised in patients with preexisting QTc prolongation. Resistance has been documented in some cases
Nitazoxanide	Inhibits the pyruvate: Ferredoxin oxidoreductase (PFOR) enzyme-dependent electron transfer reaction essential for anaerobic energy metabolism	For adults: 500 mg orally twice daily for 7 days	Proposed as an alternative, especially for chronic infection. However, conflicting evidence on its efficacy (ranging from as high as 94% to as low as 36%) limits its recommendation as a reliable therapeutic option
Praziquantel	Increases calcium ion permeability in parasite membranes, causing muscle contraction and paralysis	Once considered as an alternative, praziquantel is now contraindicated for fascioliasis due to insufficient efficacy against Fasciola species
Bithionol	Disrupts oxidative phosphorylation, impairing energy metabolism in parasites	A halogenated phenol formerly used as primary therapy for fascioliasis in the United States; it has been discontinued
Emetine/Dehydroemetine	Inhibits protein synthesis by interfering with the elongation step in translation	Discontinued because of inadequate efficacy and safety issues
Metronidazole	Undergoes reduction in anaerobic organisms to form reactive nitro radicals that damage DNA and other critical biomolecules
Albendazole	Binds to β-tubulin, inhibiting microtubule polymerization, leading to impaired glucose uptake and energy depletion in parasites
Niclofolan	Disrupts energy metabolism by uncoupling oxidative phosphorylation in parasite mitochondria
Chloroquine	Inhibits DNA and RNA biosynthesis and causes degradation of ribosomes in parasites
Hexachloro-para-xylol	Disrupts parasite metabolism through oxidative damage and interference with enzymatic processes
Artemisinin derivatives (artesunate/artemether)	Activated by heme iron to produce free radicals that alkylate and damage parasite proteins and membranes

Public health implications

The resurgence of fascioliasis is influenced by a confluence of environmental, socioeconomic, and ecological factors. Climate change, including increased rainfall and rising temperatures, has expanded the habitats of intermediate snail hosts, facilitating the transmission of Fasciola spp[64]. Additionally, intensified agricultural practices, such as irrigation expansion and livestock farming, contribute to environmental contamination, thereby sustaining the parasite's life cycle[65]. Socioeconomic determinants, including sanitation and restricted access to clean water, further exacerbate transmission, particularly in rural and peri-urban areas[3]. Effective control requires a multifaceted approach, treatment of livestock with anthelmintic drugs, integrating improved water resource management, snail control strategies, and agricultural policies that mitigate contamination risks[8,66]. Public awareness and education are pivotal in reducing fascioliasis transmission. Knowledge dissemination regarding risk factors, such as the consumption of raw or contaminated aquatic vegetation, is essential in high-risk communities. Community engagement and participatory education models foster local ownership of disease control strategies, ultimately improving compliance with preventive measures[10]. Additionally, environmental sustainability policies play a crucial role in controlling transmission by promoting ecological balance and sustainable agricultural practices[64]. The WHO endorses mass drug administration (MDA) to reduce human fascioliasis prevalence in endemic countries. National health authorities must implement standardized treatment protocols and ensure the equitable distribution of antiparasitic drugs such as triclabendazole[67]. Bolivia, Egypt, Peru, and Vietnam have implemented various control strategies-including diagnosis-and-treatment campaigns, school-based programs, and MDA-though most are now inactive[42]. Egypt’s school- and village-based screen-and-treat initiative reduced prevalence from 6% to 1% over seven years. Peru piloted a school-based MDA program in the Northern Highlands but did not expand it nationally. Bolivia sustained a decade-long MDA program near Lake Titicaca, administering fixed 250 mg triclabendazole doses annually to all residents in hyperendemic areas, regardless of age or weight[42,68,69].

CONCLUSION

Fascioliasis is a globally neglected zoonotic disease with significant health impacts. Its complex pathophysiology complicates diagnosis and management, yet timely treatment remains essential. Triclabendazole is the only recommended drug, but emerging resistance threatens control efforts.

To combat fascioliasis, investment in research, diagnostics, and alternative treatments is crucial. Strengthening global health policies, public health infrastructure, and interdisciplinary collaboration will be key to reducing transmission and disease burden. A comprehensive multi-disciplinary, sustained approach is necessary to prevent its reemergence in endemic regions.