Fasciolosis Synonyms : Liver fluke disease, liver rot, pipe stem liver. It is characterized by both acute and chronic form of disease caused by large fluke parasitic in the bile ducts liver mammals characterized by loss of appetite, debility, jaundice, anemia, and bottle jaw.
Etiology The disease is caused by Fasciola hepatica and F.gigantica.the common parasite is F.gigantica but in the upper hill region F.hepatica may be recovered from the liver. Its leaf shaped, broader anteriorly than posteriorly with anteriorly cone shaped projection fallowed by pair of broad shoulders.
Fascioliasis is caused by T rematode worms F. gigantica F. hepatica
Epidemiology The parasite has cosmopolitan’s distribution but more common at places where water lodging remains for many months. F.gigantica is found in Asia, Africa, Australia, and India and F.hepatica is found in European country and South and North America, high altitude of Asia and Africa.
In India fasciola is mainly caused by F.gigantica but F.hepatica also present at high altitude and hilly area. A. P. W. Thomas discovered this trematode in 1883. Fluke occur in the bile duct of sheep, goat, ox and other ruminants, pigs, rabbit, elephants, horse, dog, cat, kangaroo and man. Disease is more common in cattle and buffalo and sheep. In case of horse and man, these fluke are present in lungs. However in goat, horse and pig the incidence of disease is low.
It is transmitted through the snail of Lymnea Spp. ( L.trunneculata , L.aunculata ). Â
The Fasciola Life Cycle
Pathogenesis Life cycle of parasite is indirect. Eggs come faeces and hatch in the environment to release to the miracidium that penetrate inside the snail and undergoes asexual reproduction to develop sporocyst and radiae . They leave snail in 5-8 weeks from the time of infection in the form of cercariae. Cercariae immediately convert in metacercariae. Which may survive for 4-6 months depending about humidity.
Metacercarie are ingested by definitive host and excyst in small intestine . Immature larvae penetrate the lumen and come in peritoneal cavity than goes to liver capsule to damage liver parenchyma during movement, where it live and migrate at places for 6-8 weeks then reaches to bile ducts. By the time it become mature and start laying eggs. During migration of larvae damage parenchyma take place. Adult parasite sucks blood and it hinders in normal flow of bile to disturb the digestion.
Hepatic damage and loss of enzyme production also contribute the pathogenesis by disturbing the digestion.
Clinical findings Disease of entity can be divided into an acute and chronic form . Acute Acute form mostly encounters in sheep and occurs after 5-6 weeks of ingestion. It occurs because of liver parenchyma damage by moving immature fluke causing traumatic hepatitis. The liver is very much enlarged and become inefficient to cause anorexia and distended abdomen with painful to touch due to hepatitis
There is hypoprotenemia leading to edema of dependent parts. Sometimes rupture of liver capsule and hemorrhage into the peritoneal cavity may occur. In acute cases the animal dies suddenly with blood stained froth appearing at the nostril and anus.
Sub-acute This type of disease occurs in all species of animals. In sheep and cattle weight loss, pale mucus membrane and submandibular edema are commonly observed.
Chronic Chronic form mostly occur in cattle and buffalo. There are digestive disturbances such as sometimes constipation and other time diarrhea. There is marked decrease in milk yield, anaemia weight loss, lack of vigor, paler mucus membrane, anorexia, and edema of dependent part and edema in intermandibular space called as bottle-jaw. Skin becomes dry and wool brittles and falling out in patches. Prostration occurs in severely affected animals
The chronic phase affects liver function
Necropsy findings Necropsy is characterized by appearance of damaged and swollen of liver, sub scapular hemorrhage, calcification of bile duct (clay- pipe like appearance) and presence of large, leaf-like fluke in bile ducts and liver.
Diagnosis Although history and symptoms provide clue , confirmation can be made by faecal examination for detection of typically elliptical eggs , having less distinct embryonic mass, operculum and yellow in colour . Hematology will reveal hypercytic, normochromic , anaemia and eosinophilia . Serological test like double immunodifusion , ELISA , AGPT are also helpful in diagnosis. Necropsy finding clearly elucidate adult parasite in the bile ducts.
Fascioliasis is usually diagnosed by finding eggs in the feces
Treatment Carbon tetrachloride, hexachloroethane , hexachlorophene, brotianide , and nitroxynilare old drugs with several side effects so presently not in use. Now-a-days following medicines are in commonly being used.
Refoxanide @ 7,5 mg/kg body weight Clioxanide @ 20-40 mg/kg body weight Dianiphenenthial @ 100 mg/kg body weight Oxylozanide @ 10 mg/kg body weight Albendazole @ 15 mg/kg body weight Fendendazole @ 20 mg/kg body weight Closental @ 10 mg/kg body weight Triclalbendazole @ 12 mg/kg body weight
Control Control of the disease can be achieved by regular prophylactic treatment at least two times in a year during months of February- March and September-October. Therapeutic treatment as and when required should be carried out to minimize the chance of spread of disease to other contact animals. Management practices particularly in aspect of hygiene should be regularly monitored.
If possible attempt should be made for disruption of meracedia , as it may be most suitable aspect of disease control. Control of snails may be achieved by CuSO4, other molluscicide and by the ducks that feed on snails. Vaccination are been tried but still at experimental stage.
Conclusion Fasciolosis is a common fluke infestation of domestic animal that causes heavy production losses. An intermediate host, snail is required for compilation of life-cycle. Disease is clinically manifested by loss of appetite, weight, jaundice, anaemia , and reduce milk yield. Regular deworming decreases the burden of disease in domestic animals.