The liver flukes Fasciola hepatica and gigantica are parasitic infections that affect humans and animals—cattle, sheep, and goats—in all inhabited areas where they are raised, on all continents, and in over eighty countries. People acquire the disease by eating raw vegetables such as watercress that have been contaminated by one of thirty species of snails, the intermediate hosts.

The cycle begins with the adult fluke releasing eggs from its residence in the host’s bile ducts. The eggs pass into the intestines and are discharged in the feces near a pond or stream. There, the eggs hatch in the water and become “embryonated” as free-swimming ciliated Fasciola larvae called miracidia. These miracidia seek out an intermediate host, a snail, and bore themselves into its tissues.

In the snail’s body, the miracidium undergoes a cycle to transform itself into a cercarial larva. These larvae, in turn, leave the snail and attach themselves to aquatic plants, encysting themselves into metacercarial cysts. The primary hosts, humans or animals, become infected by eating these metacercarial cysts from contaminated vegetation.

In the duodenum of their primary hosts, humans or animals, the metacercarial cysts “excyst” themselves, bore their way through the gut wall into the peritoneum, and from there bore themselves into the liver and settle in the bile ducts, maturing into adult flukes. These can live for 5–10 years in a mammalian host. Early symptoms may consist of fever, abdominal pain, and sometimes allergic reactions as the flukes migrate through the liver. A chronic phase may develop when adult flukes inhabiting the bile ducts cause inflammation, fibrosis, and potential obstruction. Symptoms may include intermittent pain, jaundice, and anemia.

The history of liver flukes stretches back centuries. They were known to ancient civilizations and in the Middle Ages were first described by the French shepherd Jean de Brie (1379), who noted liver flukes in sheep and their association with wet pastures. The great taxonomist Carl Linnaeus described in 1758 the parasite and named it Fasciola hepatica in his work Systema Naturae.

The complex life cycle of Fasciola gradually unraveled throughout the 19th century. In 1881, Rudolf Leuckart discovered that snails served as intermediate hosts, and in 1882 Algernon Thomas demonstrated how sheep become infected by ingesting encysted larvae on grass. Francisco Pizarro Jiménez in Cuba in 1856 first documented the first human case. By the early 20th century, fascioliasis was recognized as a significant zoonotic disease capable of infecting both animals and humans. The 20th century saw the spread of fascioliasis to new regions, often through the movement of livestock. Diagnosis typically involves detecting eggs in stool samples or identifying antibodies in blood tests. Imaging techniques like ultrasound or CT scans can reveal liver damage or the presence of adult flukes. A drug called Bithionol was introduced in the 1960s but had significant side effects. Triclabendazole, discovered in the 1970s and approved for human use in 1997, revolutionized treatment due to its efficacy and safety profile. In areas where triclabendazole resistance has emerged, alternatives like nitazoxanide may be used. Prevention focuses on improving sanitation, properly washing vegetables, and implementing veterinary control measures in livestock. Public health education about the risks of consuming raw aquatic plants is crucial in endemic areas. In 1995, the World Health Organization officially recognized human fascioliasis as a significant public health problem. The complete genome of Fasciola hepatica was sequenced in 2015, opening new avenues for research.