Fasciola gigantica

Fasciola gigantica is a parasitic flatworm of the class Trematoda, which causes tropical fascioliasis. It is regarded as one of the most important single platyhelminth infections of ruminants in Asia andAfrica. Estimates of infection rates are as high as 80-100% in some countries.

Distribution Fasciola gigantica causes outbreaks in tropical areas of southern Asia, Southeast Asia, and Africa.[1] The geographical distribution ofFasciola gigantica overlaps with Fasciola hepatica in many African and Asian countries and sometimes in the same country, although in such cases the ecological requirement of the flukes and their snail host are distinct.[1] Infection is most prevalent in regions with intensive sheep and cattle production.[1] In Egypt Fasciola gigantica exist in domestic animals since the times of the pharaohs.[1] ]Life cycle The life cycle of Fasciola gigantica is as follows: eggs (transported with feces) eggs hatchs miracidium miracidium infect snail intermediate host (parthenogenesis in 24 hours) sporocyst redia daughter redia cercaria (gets outside the snail and forms sporocyst) metacercaria infection of the host adult stage produces eggs. Intermediate hosts As with other trematodes, Fasciola develop in a molluscan intermediate host. Species of the freshwater snails from the family Lymnaeidaeare well known for their role as intermediate hosts in the life cycle of Fasciola gigantica; however, throughout the years an increasing number of other molluscan intermediate hosts of Fasciola gigantica have been reported.[1] There are many ecological factors affecting snail populations including temperature, light, hydrogen ion concentration (pH), vegetation, depth of water, current of the water, chemical composition of the soil, and snail population competition.[1] It has been reported that the Lymnaeid intermediate hosts of Fasciola gigantica are distinguishable from those of Fasciola hepatica, both morphologically and as to habitat requirement. [1] The species of Fasciola can become adapted to new intermediate hosts under certain conditions at least based on laboratory trials.[1] It has been reported that the most

important intermediate host for Fasciola gigantica is Radix auricularia. [1] However,Lymnaea rufescens and Lymnaea acuminata are the host snails in the Indian Subcontinent; Radix rubiginosa and Radix natalensis are the hosts in Malaysia and in Africa respectively; and the synonymous Lymnaea cailliaudi is the intermediate host in east Africa.[1] There is some evidence, at least based on laboratory trails, that the species of Fasciola can become adapted to new hosts, either amphibious or aquatic, under certain conditions.[1] The Australian Lymnaea tomentosa (host of Fasciola hepatica) was shown to be receptive to miracidia of Fasciola gigantica from East Africa, Malaysa and Indonesia.[1] Radix natalensis is considered to be the essential intermediate host for Fasciola gigantica based on field and experimental studies in Egypt.[1] Cercarial production from Radix natalensis experimentally infected with Fasciola gigantica is affected by the species of definitive host from which the eggs are obtained, as well as the different laboratory conditions.[1] Another lymnaeid, Galba truncatula, may play a role in transmitting this parasite in Egypt, as it was found naturally infected with Fasciola gigantica.[1] At the level of intermediate hosts ofFasciola gigantica, the conditions are thus favorable in Egypt to transmit fascioliasis.[1] Other species in the family Lymnaeidae are serving as naturally or experimentally intermediate hosts of Fasciola gigantica and they include: Austropeplea ollula, [2] Austropeplea viridis,[2] Radix peregra,[2] Radix auricularia,[2] Radix natalensis,[2] Radix luteola,[2] Radix rubiginosa,[2] Pseudosuccinea columella[2] and Galba truncatula.[2] Hosts Fasciola gigantica is a causative agents (together with Fasciola hepatica) of fascioliasis in ruminants and in humans worldwide.[1] The parasite infects cattle and buffalo and can also be seen regionally in goats, sheep, and donkeys. ]Infection Main article: Fasciolosis Infection with Fasciola spp. occurs when metacercariae are accidentally ingested on raw vegetation.[1] The metacercariae exist in thesmall intestine, and move through the intestinal wall and peritoneal cavity to the liver where adults mature in the biliary

ducts of the liver.[1]Eggs are passed through the bile ducts into the intestine where they are then passed in the feces.[1] Identification Despite the importance to differentiate between the infection by either fasciolid species, due to their distinct epidemiological, pathological and control characteristics, there is, unfortunately, neither a direct coprological (excretion-related) nor an indirect immunological test available for their diagnosis.[1] The specific differentiation can only be made by either a morphological study of adult flukes or by molecular tools.[1] Toxicology The chloroform extract of the leaves of Pycnanthus angolensis (Myristicaceae) and the methanol extracts of the leaves and stem of the same plant exhibited considerable anthelmintic activities in vitro against Fasciola gigantica.[3] [edit]References This article incorporates CC-BY-3.0 text from references.[1][3] 1. ^ a b c d e f g h i j k l m n o p q r s t u v w Soliman M. F. M. (2008). "Epidemiological

review of human and animal fascioliasis in Egypt". The Journal of Infection in Developing Countries 2(3): 182-189. abstract. PDF 2. ^ a b c d e f g h i Correa C. A., Escobar J. S., Durand P., Renaud F., David P., Jarne P., Pointier J.-P. & Hurtrez-Bousss S. (2010). "Bridging gaps in the molecular phylogeny of the Lymnaeidae (Gastropoda: Pulmonata), vectors of Fascioliasis". BMC Evolutionary Biology 10: 381.doi:10.1186/1471-2148-10-381. 3. ^ a b Onocha P. & Otunla E. (2008). "Biological activities of extracts of Pycnanthus angolensis (Welw.) Warb". African Journal of Traditional, Complementary and Alternative medicines, Abstracts of the world congress on medicinal and aromatic plants, Cape Town, November 2008. abstract [edit]Further reading Le T. H., De N. V., Agatsuma T., Blair D., Vercruysse J., Dorny P., Nguyen T. G. & McManus D. P. (2007). "Molecular confirmation that Fasciola gigantica can undertake aberrant migrations in human hosts". J. Clin. Microbiol. 45(2): 648650. PubMed,doi:10.1128/JCM.01151-06

Meemon K., Grams R., Vichasri-Grams S., Hofmann A., Korge G., Viyanant V., Upatham E. S., Habe S. & Sobhon P. (2004). "Molecular cloning and analysis of stage and tissue-specific expression of cathepsin B encoding genes from Fasciola gigantica. Mol. Biochem. Parasitol. 136(1): 1-10.

Spithill T. M., Smooker P. M. & Copeman D. B. (1999). "Fasciola gigantica: epidemiology, control, immunology and molecular biology". In: Dalton J. P. (ed.) Fasciolosis. CABI Publishing, Oxin, UK. 465-525.

Eggs passed in the feces develop into miracidia in ~2-4 wk, depending on temperature, and hatch in water. Miracidia infect lymnaeid snails, in which development and multiplication occur through the stages of sporocysts, rediae (sometimes daughter rediae), and cercariae. After ~2 mo (or longer if temperatures are low), cercariae emerge from snails and encyst on aquatic vegetation. Snails may extend the period by hibernating during the winter. Encysted cercariae (metacercariae) may remain viable for many months unless they become desiccated.

After ingestion by the host, usually with herbage, young flukes are released in the duodenum, penetrate the intestinal wall, and enter the peritoneal cavity. The young flukes penetrate the liver capsule and wander in the parenchyma for several weeks, growing and destroying tissue. They usually enter the bile ducts 6-8 wk after ingestion, mature, and begin to produce eggs. The prepatent period is usually 2-3 mo, depending on the fluke burden. Adult flukes may live in the bile ducts of sheep for years; most are shed from cattle within 5-6 mo. Prenatal infections have been reported in cattle. Clinical Findings: Fasciolosis ranges in severity from a devastating disease in sheep to an asymptomatic infection in cattle. The course usually is determined by the number of metacercariae ingested over a short period. In sheep, acute fasciolosis occurs seasonally and is manifest by a distended, painful abdomen; anemia; and sudden death. Deaths can occur within 6 wk of infection. The acute syndrome must be differentiated from black disease. In subacute disease, survival is longer (7-10 wk), even in cases with significant hepatic damage, but deaths occur due to hemorrhage and anemia. Chronic fasciolosis is seen in all seasons; signs include anemia, unthriftiness, submandibular edema, and reduced milk secretion, but even heavily infected cattle may show no clinical signs. Heavy chronic infection is fatal in sheep. Sheep do not appear to develop resistance to infection, and chronic liver damage is cumulative over several years. In cattle, there is evidence of reduced susceptibility after fibrosis of liver tissues and calcification of bile ducts.

Immature, wandering flukes destroy liver tissue and cause hemorrhage. In acute fasciolosis, damage is extensive; the liver is enlarged and friable with fibrinous deposits on the capsule. Migratory

tracts can be seen, and the surface has an uneven appearance. In chronic cases, cirrhosis develops. Mature flukes damage the bile ducts, which become enlarged, or even cystic, and have thickened, fibrosed walls. In cattle, the duct walls become greatly thickened and often calcified. Flukes may be found in aberrant sites, eg, lungs. Mixed infections with Fasciola magna can be seen in cattle. Tissue destruction by wandering flukes may create a microenvironment favorable to activation of clostridial spores. Diagnosis: The oval, operculated, golden brown eggs, 130-150 65-90 m, must be distinguished from those of paramphistomes (rumen flukes), which are larger and clear. Eggs of F hepatica cannot be demonstrated in feces during acute fasciolosis. In subacute or chronic disease in cattle, the number varies from day to day, and repeated fecal examination may be required. Diagnosis can be aided by an ELISA (commercially available in Europe) that enables diagnosis ~2-3 wk after infection and well before the prepatent period. Plasma concentrations of glutamyltransferase, which are increased with bile duct damage, are also helpful during the late maturation period when flukes are in the bile ducts. At necropsy, the nature of the liver damage is diagnostic. Adult flukes are readily seen in the bile ducts, and immature stages may be squeezed or teased from the cut surface. Control: Control measures for F hepatica ideally should involve removal of flukes in affected animals, reduction of the intermediate host snail population, and prevention of livestock access to snail-infested pasture. In practice, only the first of these is used in most cases. While molluscicides can be used to reduce lymnaeid snail populations, those that are available all have drawbacks that restrict their use. Copper sulfate, if applied before the snail population multiplies each year, is effective but toxic to sheep, which must be kept off treated pasture for 6 wk after application. Prevention of livestock access to snail-infested pasture is frequently impractical because of the size of the areas involved and the consequent expense of erecting adequate fencing. Several drugs are available to treat infected ruminants, including

triclabendazole, clorsulon (cattle and sheep only), albendazole, netobimin, closantel, rafoxanide, and oxyclozanide. Not all are approved in all countries (eg, only clorsulon and albendazole are approved in the USA), and most have long withdrawal periods before slaughter if used in meat-producing animals and before milk from treated livestock can be used for human consumption. The timing of treatment is also important so that the pharmacokinetics of the drug used will result in the optimal removal of flukeseach flukicide has varying efficacy against different ages of fluke. Traditionally, some treatments are determined by local epidemiologic factors and additional treatments by unusually suitable conditions for parasite multiplication. For example, in the Gulf Coast states of the USA, cattle should be treated before the fall rainy season and again in the late spring. In northwestern USA and in northern Europe, cattle should be treated at the end of the pasture season and, if not housed, again in late January or February. In European countries with large susceptible sheep populations, computerized prediction systems are used to determine the likely prevalence of F hepatica infections. In areas where heavy infections are expected, sheep may require treatment in September or October, January or February, and again in April or May to reduce both the chances of acute or chronic infections and the output of fluke eggs for development of future disease.

The eggs after fertilization stay in the uterus for some time which later rich the bile duct, then in the intestine of the host and finally pass out with the faces. Under suitable conditions, the eggs are hatched into ciliated larvae, which swim in search of suitable host and enter in its pulmonary sac. After 8 days miracidium forms sporocyst from which 3 to 8 rediae larvae are formed. Now these rediae enter the liver of the snail and produce more rediae parthenogenetically. From each daughter rediae the other larval form id formed. The cercaria larva, which is provided with slender tail, sucker and intestine, burrows the snail and comes out of the snails body. Now it starts swimming, attaches itself with grasses, loses its tail gets encysted and forms the metacercariae which enters the alimentary canal of the sheep at the time of water drinking or grazing the grasses. In the alimentary canal of sheep cyst gets dissolved and metacercariae reach the liver by burrowing the alimentary canal of the sheep. First they damage the liver tissues and then enter the bile duct and get matured. Disease: The infection of liver fluke cause the rotting of sheeps liver. A number of diseases viz., anemia, diarrhea, dysentery, eosinophilia and ulcers have been noticed in the liver fluke-infested sheep. The production of both the quality and quantity of leather, meat and wool from the sheep is badly affected due to infection of fasciola hepatica.

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

Liver Fluke Fasciola Hepatica

Life-cycle of the liver fluke Epidemiology Fascioliasis: liver fluke disease Acute fascioliasis Sub-acute fascioliasis Chronic fascioliasis Diagnosis

Treatment Related Products

Life-cycle of the liver fluke Top The life cycle of the Fasciola hepatica (liver fluke) is shown in Figure 1. The adult fluke, which live in the bile ducts, produce eggs which are pass the faeces (a). When the eggs separate from the faecal material in wet areas, under optimal conditions they will hatch, releasing the larvae or mi (b). The miracidia invade the lymnaeid snails in which they develop and multiply as sporocyst, rediae and cercariae (c). The tadpole like cercaria the snails (d) and swim until they encyst on vegetation, forming metacercariae (e), which are the infective stage of the fluke.

The entire cycle of the liver fluke in the snails takes 2 - 3 months under favourable conditions in the field. If ingested by sheep, cattle or other hos including man (f), the metacercariae excyst in the small intestine and the released immature flukes penetrate the intestinal wall and enter the abd cavity. The young fluke penetrate the liver capsule and migrate through the liver tissue for 6 to 7 weeks before entering the bile ducts to become fluke (g). The fluke reach sexual maturity and commence egg production 8 to 10 weeks after infection. Figure 1: Life Cycle of Fasciola Hepatica.

Epidemiology Top The two primary requirements for the establishment of liver fluke are a suitable snail (intermediate host) and a suitable environment. In Australia, Lymnaea tomentosa, an indigenous freshwater snail, is the most important intermediate host. Ideal situations for the environmental stages of the cycle are slow-moving streams with marshy banks, irrigation channels, seepage areas, etc.

The eggs produced by adult fluke pass out in the hosts faeces into wet areas. They hatch when temperatures increase above 10 C (typically fro September to May). The larvae (miracidia) invade a suitable snail (Lymnaea spp) and develop and multiply. One miracidium hatching from a fluk can produce up to 4,000 infective cysts (metacercariae). These cysts attach to grass and other vegetation. The host is infected when this vegeta ingested.

Adult fluke can survive for many years in the livers of infected sheep; the adult fluke lays between 20 000 and 50 000 eggs per day over a long p The rate of egg production is responsible for the degree of pasture contamination and thus greatly influences the epidemiology of the disease.

The epidemiology of the disease is also influenced by the grazing habits of the animals. Animals grazing in wet marshy areas, favoured by the flu snail, are more likely to become infected. Typically, long, wet seasons are associated with a higher rate of infection. However, sheep are more lik ingest large numbers of cysts during dry periods following a wet season. This is due to a reduction in available pasture, forcing the animals to gra swampy areas or in areas where the water has receded, thus exposing them to vegetation heavily infected with metacercariae.

Fascioliasis: liver fluke disease Top Fascioliasis is the disease caused by liver fluke (Fasciola hepatica). Sheep and cattle are most commonly affected and sheep are more suscepti the disease than cattle. Horses, deer and goats may also be infected by liver fluke; humans are also occasionally infected.

Acute fascioliasis Top Acute fascioliasis occurs as an outbreak of disease following a massive but relatively short-term intake of metacercariae. This high intake is often result of certain seasonal and climatic conditions combined with a lack of appropriate fluke control measures. It typically occurs when stock are f to graze in heavily contaminated wet areas as a result of over-stocking and/or drought. Animals suffering from acute fascioliasis may display no signs prior to death; some may display abdominal pain and discomfort and may develop jaundice. Death usually results from blood loss due to haemorrhage in the liver caused by the migration of the immature fluke through the liver.

Sub-acute fascioliasis Top Sub-acute fascioliasis is characterised by anaemia, jaundice and ill-thrift. The migrating fluke cause extensive tissue damage, haemorrhage and particular, liver damage. The result is severe anaemia, liver failure and death in 8-10 weeks.

Chronic fascioliasis Top Chronic fascioliasis is the most common clinical syndrome associated with liver fluke infection in sheep and cattle. It occurs when the parasites r the hepatic bile ducts. The principle effects are bile duct obstruction, destruction of liver tissue, hepatic fibrosis (scarring) and anaemia.

The onset of clinical signs is slow. Animals become gradually anaemic and inappetent, as the adult fluke become active within the bile ducts; sig include dependent oedema or swelling under the jaw (bottle jaw). Affected animals are reluctant to travel. Death eventually occurs when anaem becomes severe. Additional stress upon anaemic animals, such as droving, may lead to collapse and death. Cattle typically present with signs o loss, anaemia and chronic diarrhoea.

Chronic fascioliasis provides the right environment in the liver for the germination of the spores of the bacterium, Clostridium novyi Type B, which Black disease. Vaccines against C.novyi are available and should be given to all animals, particularly those at risk of fascioliasis.

Diagnosis Top Fascioliasis should be considered when there are cases of death, anaemia, chronic diarrhoea or ill thrift in sheep or cattle grazing on fluke-prone country. In the live animal, chronic fascioliasis is indicated by the presence of fluke eggs in a faecal sample (faecal samples may be sent to a veterinary laboratory for diagnosis).

A dead animal can be quickly diagnosed by the presence of mature or immature fluke in the liver; the autopsy will also identify any other conditio may be contributing to the problem.

Treatment Top The treatment recommended will depend upon the nature of disease. Some of the available anthelmintics are not effective against immature fluk so are not recommended in acute fluke outbreaks. In addition, they are less efficient for the strategic control of fascioliasis.

At least 2 treatments annually with Flukare S or C are required on sheep and beef properties where liver fluke occurs. The initial dose should be administered in spring to remove any fluke that have been present in the animals during the winter. This is followed by a second dose in early su to remove fluke picked up during the spring. A third treatment, in autumn, may be required on properties heavily infested with liver fluke.

Closicomb is registered for use in sheep and it is a suitable rotational product to be used with Flukare S, to delay the onset of resistance. Closico kill a high proportion of fluke aged 4 weeks and is highly effective against fluke aged 6 weeks or older. The very early immature fluke will be reta their development and egg production will not commence for several weeks, thus reducing the level of pasture contamination. Ask your veterinarian to develop a programme that is specific and appropriate for your property. For further information please read the NSW Agriculture factsheet on liver fluke disease in sheep and cattle.