Liver Fluke Factsheet

Liver fluke disease in cattle and sheep is caused by the leaf shaped parasite Fasciola hepatica. This parasite migrates across the gut in affected animals to the liver where it causes severe liver damage and consequent production losses. The disease is on the increase in many parts of the UK and certainly in the North West. As a practice, we have seen a rise in the number of farms where liver fluke has become an increasing issue, including farms where liver fluke has never previously been diagnosed.

Liver fluke has a complicated 2 host life cycle involving the water snail Lymnea truncatula, in which the larval stages develop and multiply, and a mammalian host in which the adults live.

In mammals, the adult flukes live in the bile ducts of the liver and in the gall bladder. They lay massive numbers of eggs which are then passed out in the hosts' faeces onto pasture. At temperatures above 10
ºC a larval stage starts to develop in this egg and will hatch out after approximately 2-4 weeks. This larval stage in wet conditions will then swim to and penetrate a water snail. This snail is found on any wet/poorly drained land, adjacent to water courses and ponds, wheel tracks, standing water, etc. After penetration of this snail this larval stage then develops through further stages over the next 6 to 8 weeks, and multiplies in number to hundreds, if not thousands of the next larval stage, which are then released from the snail, develop into infective cysts and these then attach to and sit on herbage and are infective to mammals. This not only includes sheep and cattle, but wildlife hosts including deer and hares.


Under optimum conditions these infective cysts can survive on pasture for up to 1 year, but prolonged periods of freezing and dry weather will kill them. This life cycle is then completed when these cysts are ingested by grazing livestock. Following ingestion the cysts pass through to the small intestine where they hatch as immature fluke and migrate through the gut wall, across the body cavity, and into the liver. These immature fluke then migrate over a period of 8 – 10 weeks through the liver to the bile ducts and gall bladder where they mature into egg laying adults.


The severity of disease seen depends on the numbers of infective cysts ingested and the time period over which they are ingested for.

  • Where a large number of infected cysts are ingested over a short period of time, usually in autumn/early winter, commonly after a prolonged wet summer, when there is optimal infection of snails, acute disease is seen. Following migration of large numbers of fluke through the liver, the liver becomes severely damaged and haemorrhage as a result of this leads to sudden death of animals. Less severely affected animals will be anaemic, and can have a 'bottle jaw' appearance and/or a swollen abdomen. Deaths typically occur before fluke have developed into adults and eggs are seen in the faeces. Therefore diagnosis relies on post-mortem examination or blood samples to confirm liver damage.

  • If the infection is picked up over a more prolonged period, there is damage to the liver tissue and also the presence of adult flukes in the bile ducts and sub-acute disease is seen. Typically animals show rapid weight loss and poor condition during mid to late winter with deaths occurring in the absence of treatment.

  • If low to moderate numbers of infective cysts are ingested over a long period of time then chronic disease is seen. This is the most common presentation of liver fluke in cattle and sheep and is most commonly seen in winter/spring or early summer. These animals have an accumulation of adult fluke in the bile ducts and gall bladder and show a progressive loss of body condition. This can also be accompanied by anaemia and affected animals may also have a 'bottle jaw' appearance due to fluid retention under the jaw.


Traditionally these are the times when these stages of the disease are seen. This is because the snail is very much temperature and moisture dependent. The snail traditionally becomes infected in spring/early summer, and in a wet season these snails then shed massive numbers of infective larvae onto herbage in late summer/autumn with disease being seen from autumn onwards. If the season is relatively dry then a combination of fewer snails, and reduced hatching of fluke will lead to lower levels of autumn infection on herbage.


However the pattern of disease is changing, probably due to changing climatic conditions. Disease is also now seen as a result of snails becoming infected by fluke larvae in late summer and autumn. Due to low winter temperatures these infected snails become inactive and lie dormant until the following spring. The following spring larvae are then capable of emerging and developing to infective cysts which attach to vegetation and are infective to sheep and cows, leading to disease being seen in spring and early summer.


As previously mentioned diagnosis of acute disease is either by post mortem examination or by taking blood samples and demonstrating liver damage. Diagnosis of both sub-acute and chronic disease can be made by either post-mortem examination, blood samples to show liver damage, or examination of faeces with fluke eggs being present. However the presence of fluke eggs in faeces does not give an accurate indication of the burden of infection. Also eggs deposited by adult fluke in the bile ducts tend to be released sporadically, so a negative sample is not always negative, and it is possible for fluke eggs to be seen in faeces for some time after successful treatment with a flukicide giving a false positive result.


Liver fluke control relies on the strategic use of flukicides and, where practical, avoidance of grazing wet areas and land adjacent to ponds and water courses. The flukicides available show a broad spectrum of activity, with triclabendazole based products having efficacy against all stages of liver fluke, and benzimadazole based products only being effective against adult fluke, with no efficacy against immature fluke. Benzimadazole based products are therefore not suitable where cattle and sheep are being exposed to acute infection. Other products which are also useful are products containing clorsulon, nitroxynil and closantel. These drugs are effective against adult fluke and late immature fluke, but have poor efficacy against early immature fluke.


Because treatment of liver fluke can be complex it is recommended that your vet is contacted to discuss the most appropriate treatment schedule for your farm. However a typical dosing schedule would be:

  • Dose adult cattle and sheep in spring to remove fluke burdens and reduce the deposition of fluke eggs onto the pasture.

  • Where stock are winterred outside all sheep and cattle should be dosed in autumn and again in winter with a flukicide which is effective against immature fluke. Following particularly wet summers dosing intervals may need to be reduced and fluke treatment started from late September onwards, with the frequency of treatment depending on the efficacy against immature fluke.

  • Cattle and sheep which are to be housed should be treated in autumn, and again at housing with a product which will kill both adult and immature flukes. These animals should then be treated again following housing, as not all very immature flukes will be killed. When this post – housing treatment is done depends on the efficacy of the flukicide used at housing against immature fluke.

  • Livestock bought in from areas where there is a known high incidence of fluke should be treated before they join the flock/herd with a flukicide effective against immature stages.


When deciding on products to treat liver fluke it is also important to be aware of withdrawal periods of the product chosen. Some products have a long withdrawal period and are, for example, unsuitable for fattening lambs which are nearly fit. Also there are no products licensed for lactating dairy cows. Dairy cows can therefore only be treated in the dry period before calving. It is also important that products used are used correctly, and not over used, to reduce the risk of resistance developing. There is recently the emergence of resistance to triclabendazole based products in some parts of the country which is concerning as it is in a number of leading flukicides, it has the broadest spectrum of activity against all the stages of liver fluke, and is the drug of choice in treatment of livestock in acute outbreaks.