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.

Keywords: Fascioliasis; Flukes; Hepatobiliary; Parasitic infections; Triclabendazole.

Figure 1

Life cycle of Fasciola spp. 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.

Figure 4

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