Fasciolosis is a parasitic worm infection caused by the common liver fluke Fasciola hepatica as well as by Fasciola gigantica. 


It is a plant-borne trematode zoonosis.


A tropical disease.


An emerging disease: the World Health Organization (WHO) has estimated that 2.4 million people are infected with Fasciola, and a further 180 million are at risk of infection.



Occurs in Europe, Africa, the Americas as well as Oceania.



Its main host is ruminants such as cattle and sheep, but can affect humans.


F. hepatica is found throughout the world, with an estimated 2.4 million-17,000,000 persons infected.



Most often results from the consumption of freshwater plants such as watercress and water chestnuts, to which the infective metacercariae attach themselves.


Most cases in the US are diagnosed in immigrants and returning travels.



Phases of disease (4):



an initial incubation phase of between a few days up to three months with little or no symptoms.



acute phase which may manifest with: fever, malaise, abdominal pain, gastrointestinal symptoms, urticaria, anemia, jaundice, and respiratory symptoms.



latent phase with less symptoms 



chronic or obstructive phase months to years later.



The  chronic state the disease causes inflammation of the bile ducts, gall bladder and may cause gall stones as well as fibrosis.



Metacercariae ingested by humans then emerge from the cyst  within 2-24 hours in the intestine, and migrate into the peritoneal cavity as immature  flukes.



After 48 hours the larvae penetrate the liver capsule and in over a period of seven weeks the immature flukes migrate through the liver, resulting in necrosis and eosinophilic infiltration.


During the larval stage, immature larva they do not release eggs, and the clinical signs of right upper quadrant abdominal pain, weight loss and fever, as well as eosinophilia results from inflammatory response to the migrating larvae.


In the chronic, or biliary stage adult flukes release eggs in the hepatic in common bile duct and this latent stage can last for decades and may be characterized by biliary obstruction, ascending cholangitis, acute pancreatitis, or mucosal erosion and hemobilia.


Urticaria is seen in 20-25% of cases during acute infection.



It is unknown whether fasciolosis is associated with increased cancer risk.



As many as half of infected patients display no symptoms.


In endemic areas infection is most common in children.



Diagnosis is difficult because the worm eggs are often missed in fecal studies.



Diagnostic methods: 


fecal examination, parasite-specific antibody detection, or radiological diagnosis, as well as laparotomy. 



With fecal exam the worm eggs can seldom be detected in the chronic phase of the infection. 



Eggs appear in the feces first between 9–11 weeks post-infection. 



Most immunodiagnostic tests detect infection with very high sensitivity, and as concentration drops after treatment, it is a very good diagnostic method.



The size of the parasite, as adult F. hepatica: 20–30 × 13 mm (0.79–1.18 × 0.51 inches) or adult F. gigantica: 25–75 × 12 mm (0.98–2.95 × 0.47 inches), fasciolosis is concerning, as the amount of symptoms depend on how many worms and what stage the infection is in. 



Death rates are significant in both cattle (67.55%) and goats (24.61%),[8] but generally low among humans.



Treatment with triclabendazole is effective against the adult worms as well as various developing stages.



Secondary bacterial infection can cause cholangitis and can be treated with antibiotics, and toxemia may be treated with prednisolone.



Infections occur  by eating watergrown plants, primarily wild-grown watercress in Europe or morning glory in Asia, 


 by drinking contaminated water with floating young fasciola or when using utensils washed with contaminated water.



Human infection is rare, even if the infection rate is high among animals. 



High rates of human infection have been found in Bolivia, Peru and Egypt.



No vaccine is available.



Preventative measures:  treating and immunization of  livestock, which are required to host the live cycle of the worms. 



Illness has 4 main phases:



Incubation phase



Invasive or acute phase



Latent phase



Chronic or obstructive phase.



Incubation phase is the time from the ingestion of metacercariae to the appearance of the first symptoms; few days to 3 months; dependent on number of ingested metacercariae and immune status of host.



Invasive or acute phase: fluke migration up to the bile ducts. 



There is mechanical destruction of the hepatic tissue and the peritoneum by migrating juvenile flukes.



In the invasive or acute phase, localized and or generalized toxic and allergic reactions to the flukes occur.



In the invasive or acute phase symptoms include, 






Abdominal pain



Gastrointestinal disturbances: loss of appetite, flatulence, nausea, diarrhea.






Respiratory symptoms, cough, dyspnea, chest pain, hemoptysis



Hepatomegaly and splenomegaly












Latent phase: This phase can last for months or years. 



Chronic or obstructive phase:



This phase may develop months or years after initial infection. 



Adult flukes in the bile ducts cause inflammation and cholangitis, cholecystitis, and mechanical obstruction of the biliary duct. 



In this phase, biliary colic, epigastric pain, fatty food intolerance, nausea, jaundice, pruritus, right upper-quadrant abdominal tenderness may occur.



Hepatomegaly, splenomegaly or ascites may occur.



The gall bladder is usually enlarged and edematous, and stones in the bile duct or gall bladder is frequent.



Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress.



After ingestion, metacercariae excyst in the duodenum  following ingestion and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adults.



The maturation process from metacercariae into adult flukes takes approximately 3 to 4 months. 



The adult flukes, Fasciola hepatica measuring up to 30 mm by 13 mm, and F. gigantica measuring up to 75 mm reside in the large biliary ducts.



Fasciolosis is caused trematodes F. hepatica and F. gigantica. 



Adult flukes of both species localized to the bile ducts of the liver or gallbladder. 



F. hepatica measures 2 to 3 cm and has a cosmopolitan distribution.



F. gigantica measures 4 to 10 cm in length and the distribution of the species is limited to the tropics and has been recorded in Africa, the Middle East, Eastern Europe and south and eastern Asia.



F. hepatica infection in humans is determined by the presence of the intermediate snail hosts, domestic herbivorous animals, climatic conditions and the dietary habits of man.



Sheep, goats and cattle are considered the predominant animal reservoirs. 



Cattle, sheep, pigs and other domesticated herbivores such as donkeys and llamas are the definitive hosts from which fasciola eggs are released to form ciliated swimming miracidia, which can infect the intermediate host, snails. 



Infected snails release their cer arias that form cysts on freshwater plants.



Humans are infected by ingestion of aquatic plants that contain the infectious cercariae.



Several species of aquatic vegetables act as vehicles of human infection. 



In Europe, Nasturtium officinale (common watercress), Nasturtium silvestris, Rorippa amphibia (wild watercress), Taraxacum dens leonis (dandelion leaves), Valerianella olitoria (lamb’s lettuce), and Mentha viridis (spearmint) were reported as a source of human infections.[5] 



Humans can be infected by drinking of fresh untreated water containing cercariae.



Intermediate hosts of F. hepatica are mostly freshwater snails from family Lymnaeidae.



Ectopic locations of flukes include the lungs, diaphragm, intestinal wall, kidneys, and subcutaneous tissue.



Tissues are mechanically destroyed by flukes and inflammation appears around migratory flukes. 



In the second phase, the biliary phase, begins when parasites enter the biliary ducts of the liver. 



Flukes mature n the biliary tree and feed on blood, and produce eggs. 



Hypertrophy of biliar ducts associated with obstruction of the lumen occurs 



As result of tissue damage biliary ducts hypertrophy and obstruct.



Diagnosis can be made with immunodiagnostic tests that detect infection and have a sensitivity above 90% during all stages of the diseases. 



Antibody concentration quickly drops post treatment and no antibodies are present one year after treatment.



The diagnosis is usually achieved by findings of the fluke eggs in stool, and immunologically by ELISA and Western blot. 



Examination of stools are generally not adequate for diagnosis because infected humans have  clinical presentation long before eggs are found in the stools.


Stool can be examined with the presence of eggs in the biliary stage of disease.


Stool samples testing for ova and parasites is uninformative early in the course of infection.


Eggs are characteristically yellow brown, ovoid and large. 


Eggs are released sporadically in chronic fascioliasis and multiple stool examinations are required for an accurate diagnosis.


Ova are present only in the biliary stage which occurs 2-4 months after infection of the infected metacerariae.



In many human infections, the fluke eggs are often not found in the faeces, even after multiple faecal examinations.



The eggs of F. hepatica, F. gigantica and Fasciolopsis buski are morphologically indistinguishable.



The ELISA and enzyme-linked immunoelectrotransfer blot, also called Western blot, are the most important methods in diagnosis of F. hepatica infection. 


In chronic fascioliasis ultrasound can show moving parasites or crescent shaped contents in the biliary tract.


Is acute infection nonspecific liver nodules can be seen, and portal lymph node enlargement can also be seen on CT scan or MRI.



Eosinophilia, elevation of liver enzymes support the diagnosis.



Ultrasonography and xray of the abdominal cavity, biopsy of liver, and gallbladder can also be used.



For prevention strict control of the growth and sale of watercress and other edible water plants is important. 



Protection  comes by not eating raw watercress and other water plants, especially from endemic grazing areas.



Travelers to areas with poor sanitation should avoid food and water that might be contaminated 



Vegetables that might have been irrigated with polluted water, should be thoroughly cooked.



The drug of choice in the treatment of fasciolosis is triclabendazole, a member of the benzimidazole family of anthelmintics.



Triclabendazole prevents  the polymerization of the molecule tubulin into the cytoskeletal structures, microtubules.



Case reports of nitazoxanide and bithionol being used successfully have been reported.



Clorsulon and albendazole are approved for use in the treatment of domestic animals.



Closantel, nitroxynil, and oxyclozanide should only be used to treat subacute and chronic infections. 



Triclabendazole is effective at killing flukes of any age with acute infections, but for flukes that have remained in the body for long periods of time resistance develops.



Animal fasciolosis occurs  in countries with high cattle and sheep production.



Human fasciolosis occurs, excepting Western Europe, in developing countries,only in areas where suitable conditions for intermediate hosts exist.



Fasciolosis has been reported from: Europe, America, Asia, Africa and Oceania, and the incidence of human cases has been increasing in 51 countries of the five continents.



France is an human endemic area. 



In North America, the disease is very sporadic. 



Andean countries are considered to be the area with the highest prevalence of human fasciolosis in the world. 



The highest prevalence  is distributed in communities living in the Nile Delta.



In Asia, the most human cases were reported in Iran.



Triclabendazole (Fasinex) is the most common drug due to its high efficacy against adult as well as juvenile flukes. 







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