Fasciola hepatica
Fasciola hepatica, also known as the common liver fluke or sheep liver fluke, is a parasitic flatworm that infects liver of various mammals, including humans. The disease caused by the fluke is called fascioliasis (also known as fasciolosis). F. hepatica is worldwide distributed and causes great economic losses in sheep and cattle.
Life cycle
In order to complete its life cycle, F. hepatica requires an aquatic snail as an intermediate host such as Galba truncatula, in which the parasite can reproduce asexually. 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 un-cooked foods such as water-cress. 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 5–6 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.
Disease biology
The effects of liver fluke are referred to as fascioliasis, and include anaemia, weight loss and sub-mandibular oedema. Diarrhea is only an occasional consequence of liver fluke. Liver fluke 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 Clostridium novyi type D.
Treatment
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.
Pathogenesis
The development of infection in definitive host is divided into two phases: the parenchymal (migratory) phase and the biliary phase. The parenchymal phase begins when excysted juvenile flukes penetrate the intestinal wall. After the penetration of the intestine, flukes migrate within the abdominal cavity and penetrate the liver or other organs. F. hepatica has a strong predilection for the tissues of the liver. Occasionally, ectopic locations of flukes such as the lungs, diaphragm, intestinal wall, kidneys, and subcutaneous tissue can occur. During the migration of flukes, tissues are mechanically destroyed and inflammation appears around migratory tracks of flukes. The second phase (the biliary phase) begins when parasites enter the biliary ducts of the liver. In biliary ducts, flukes mature, feed on blood, and produce eggs. Hypertrophy of biliary ducts associated with obstruction of the lumen occurs as a result of tissue damage.
Clinical Signs
The course of fasciolosis in humans has 4 main phases:
Incubation phase: from the ingestion of metacercariae to the appearance of the first symptoms; time period: few days to 3 months; depends on number of ingested metacercariae and immune status of host
Invasive or acute phase: fluke migration up to the bile ducts. This phase is a result of mechanical destruction of the hepatic tissue and the peritoneum by migrating juvenile flukes causing localized and or generalized toxic and allergic reactions.[25] The major symptoms of this phase are:
Fever: usually the first symptom of the disease; 40-42°C ,Abdominal pain ,Gastrointestinal disturbances: loss of appetite, flatulence, nausea, diarrhoea ,Urticaria ,Respiratory symptoms (very rare): cough, dyspnoea, chest pain, hemoptysis ,Hepatomegaly and splenomegaly ,Anaemia ,Jaundice
Latent phase: This phase can last for months or years. The proportion of asymptomatic subjects in this phase is unknown. They are often discovered during family screening after a patient is diagnosed.
Chronic or obstructive phase:
This phase may develop months or years after initial infection. Adult flukes in the bile ducts cause inflammation and hyperplasia of the epithelium. The resulting cholangitis and cholecystitis, combined with the large body of the flukes, are sufficient to cause mechanical obstruction of the biliary duct. In this phase, biliary colic, epigastric pain, fatty food intolerance, nausea, jaundice, pruritus, right upper-quadrant abdominal tenderness, etc., are clinical manifestations indistinguishable from cholangitis, cholecystitis and cholelithiasis of other origins. Hepatic enlargement may be associated with an enlarged spleen or ascites. In case of obstruction, the gall bladder is usually enlarged and edematous with thickening of the wall. Fibrous adhesions of the gall bladder to adjacent organs are common. Lithiasis of the bile duct or gall bladder is frequent and the stones are usually small and multiple.