Fasciola hepatica, also known as the common liver fluke or sheep liver fluke, is a parasitic flatworm of the class Trematoda, phylum Platyhelminthes that infects the livers of various mammals, including humans. The disease caused by the fluke is called fascioliasis (also known as fasciolosis). F. hepatica is distributed worldwide, and causes great economic losses in sheep and cattle. It has been known as an important parasite of sheep and cattle for hundreds of years. Because of its size and economic importance, it has been the subject of many scientific investigations and may be the best known of any trematode species.

Morphology

Fasciola hepatica is one of the largest flukes of the world, reaching a length of 30mm and a width of 13mm. It is leaf shaped, pointed posteriorly and wide anteriorly, although the shape varies somewhat. The oral sucker is small but powerful and is located at the end of a cone-shaped projection at the anterior end. The acetabulum is larger than the oral sucker and is anterior. The tegument is covered with large, and scalelike spines. The intestinal ceca are highly dendritic and extend to near the posterior end of the body. The testes are large and greatly branched, arranged in tandem behind the ovary. The smaller, dendritic ovary lies on the right side, coiling between the ovary and the preacetabular cirrus pouch. Vitelline follicles are extensive, filling most of the lateral body and becoming confluent behind the testes.

Life cycle

To complete its life cycle, F. hepatica requires a freshwater snail as an intermediate host, such as Galba truncatula, in which the parasite can reproduce asexually.

Species in the family Lymnaeidae that serve as naturally or experimentally intermediate hosts of Fasciola hepatica include: Austropeplea tomentosa,^[1] Austropeplea ollula,^[1] Austropeplea viridis,^[1] Radix peregra,^[1] Radix lagotis,^[1] Radix auricularia,^[1] Radix natalensis,^[1] Radix rubiginosa,^[1] Omphiscola glabra,^[1] Lymnaea stagnalis,^[1] Stagnicola fuscus,^[1] Stagnicola palustris,^[1] Stagnicola turricula,^[1] Pseudosuccinea columella,^[1] Lymnaea viatrix,^[1] Lymnaea neotropica,^[1] Fossaria bulimoides,^[1] Lymnaea cubensis,^[1] Lymnaea sp. from Colombia,^[1] Galba truncatula,^[1] Lymnaea cousini,^[1] Lymnaea humilis,^[1] Lymnaea diaphana,^[1] Stagnicola caperata^[1] and Lymnaea occulta.^[1]

Adult hepatica lives in bile passages of the liver of many kinds of mammals, especially ruminants. Humans are occasionally infected. In fact, fascioliasis is one of the major causes of hypereosinophilia in France. The flukes feed on the lining of biliary ducts. Their eggs are passed out of the liver with bile and into the intestine to the voided with feces. If they fall into water, eggs will complete their development into miracidia and hatch in 9 to 10 days during warm weather. Colder water retards their development. On hatching, miracidia have 24 hours in which a find a suitable snail host. Mother sporocysts produce first generation rediae, which in turn produce daughter rediae that develop in snail's digestive gland. From the snail, minute cercariae emerge and swim through pools of water in pasture, and encyst as metacercariae on near-by vegetation. From here, the metacercariae are ingested by the ruminant, or in some cases, by humans eating uncooked foods such as watercress. Contact with low pH in the stomach causes the early immature juvenile to begin the process of excystment. In the duodenum, the parasite breaks free of the metacercariae and burrows through the intestinal lining into the peritoneal cavity. The newly excysted juvenile does not feed at this stage, but once it finds the liver parenchyma after a period of days, feeding will start. This immature stage in the liver tissue is the pathogenic stage, causing anaemia and clinical signs sometimes observed in infected animals. The parasite browses on liver tissue for a period of up to six weeks, and eventually finds its way to the bile duct, where it matures into an adult and begins to produce eggs. Up to 25,000 eggs per day per fluke can be produced, and in a light infection, up to 500,000 eggs per day can be deposited onto pasture by a single sheep.

Epidemiology

Infection begins when metacercaria infected aquatic vegetation is eaten or when water containing metacercariae is drunk. Humans are often infected by eating watercress. Human infections occur in parts of Europe, northern Africa, Cuba, South America, and other locales. It is one of the most important disease agents of domestic stock throughout the world and shows promise of remaining so for years to come.

Pathology

Little damage is done by juveniles penetrating the intestinal wall and the capsule surrounding the liver but much necrosis results from migration of flukes through the liver parenchyma. During this time, they feed on liver cells and blood. Anemia sometimes results from heavy infections. Worms in bile ducts cause inflammation and edema, which in turn stimulate production of fibrous tissue in the walls of these ducts. Thus thickened, the ducts can handle less bile and are less responsive to needs of the liver. Back pressure causes atrophy of liver parenchyma, with concomitant cirrhosis and possibly jaundice. In heavy infections the gall bladder is damaged, and walls of the bile ducts are eroded completely.

Disease biology

Egg of F. hepatica

In the United Kingdom, F. hepatica is a frequent cause of disease in ruminants, most commonly between March and December. Cattle and sheep are infected when they consume the infectious stage of the parasite from low-lying, marshy pasture. The effects of liver flukes are referred to as fascioliasis, and include anaemia, weight loss and submandibular oedema; diarrhoea is only an occasional consequence. Liver fluke infestation is diagnosed by yellow-brown eggs in the faeces. They are not distinguishable from the eggs of Fascioloides magna, although the eggs of F. magna are very rarely passed in sheep, goats or cattle.

A serious consequence of the liver damage caused by fascioliasis is that latent Clostridium novyi spores can be activated by the low oxygen conditions in the damaged tracts the parasite forms in the liver; this can lead to "black disease", caused by Clostridium novyi type B or immune-mediated haemolytic anaemia (IMHA) leading to haemoglobinuria caused by C. novyi type D.

Diagnosis and Treatment

Slide showing its internal organs

Specific diagnosis depends on finding eggs in the stool. A false record can result when the patient has eaten infected liver and egg passes through the feces. Daily examination during a liver free diet will unmask the false diagnosis. An enzyme linked immunosorbent assay (ELISA) test is available as well. ELISA tests are available commercially and can detect anti-hepatica antibodies in serum and milk, but new ones, especially intended for use on fecal samples are being developed.Proteases secreted by F.hepatica also have been used experimentally in immunizing antigens. Several drugs are effective in chemotherapy of fascioliasis, both in humans and in domestic animals. One of these, rafoxanide, apparently acts by uncoupling oxidative phosphorylation in the fluke. The drug of choice in the treatment of fasciolosis is triclabendazole, a member of the benzimidazole family of anthelmintics. The drug works by preventing the polymerization of the molecule tubulin into the cytoskeletal structures, microtubules. However, resistance of F. hepatica to triclabendazole has already been recorded in Australia^[2] and Ireland.^[3] Artemether has been shown to be effective in a rat model of fascioliasis.^[4]

See also

List of parasites (human)

References

http://www.stanford.edu/class/humbio103/ParaSites2001/fascioliasis/Fasciola.htm

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