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Fasciola hepatica in Ruminants

(Common liver fluke)


Lora R. Ballweber

, DVM, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University

Last full review/revision Aug 2014 | Content last modified Aug 2014
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Fasciola hepatica (30 × 2–12 mm and leaf-shaped) is distributed worldwide and has a broad host range, including people. Economically important infections are seen in cattle, sheep, alpacas, and llamas in three forms: chronic, which is rarely fatal in cattle but often fatal in sheep, alpacas, and llamas; subacute or acute, which is primarily in sheep, alpacas, and llamas, and often fatal; and in conjunction with “black disease” (see Infectious Necrotic Hepatitis in Animals Infectious Necrotic Hepatitis in Animals Infectious necrotic hepatitis is an acute toxemia primarily of sheep caused by Clostridium novyi type B. Death is sudden, often without clinical signs, and seems to be limited to animals infected... read more ), which is most common in sheep and usually fatal.

Eggs are passed in the feces, and miracidia develop within as little as 9–10 days (at 22°–26°C [71.6°–78.8°F]; little development occurs below 10°C [50°F]). Hatching only occurs in water, and miracidia are short-lived (~3 hr). Miracidia infect lymnaeid snails, in which asexual development and multiplication occur through the stages of sporocysts, rediae, daughter rediae, and cercariae. After 6–7 wk (or longer if temperatures are low), cercariae emerge from snails, encyst on aquatic vegetation, and become metacercariae. Snails may extend the developmental period by hibernating during the winter. Metacercariae may remain viable for many months unless they become desiccated.

After ingestion by the host, usually with herbage, young flukes excyst in the duodenum, penetrate the intestinal wall, and enter the peritoneal cavity, where they migrate to the liver. The time required for this transit can vary and results in delayed development rates, which affects the efficacy of some treatments because many are effective against flukes only later in their development. The young flukes penetrate the liver capsule and tunnel through the parenchyma for 6–8 wk, growing and destroying tissue. They then enter small bile ducts and migrate to the larger ducts and, occasionally, the gallbladder, where they mature and begin to produce eggs. The prepatent period is usually 2–3 mo, depending on the fluke burden. The minimal period for the completion of one entire life cycle is ~17 wk. Adult flukes may live in the bile ducts of sheep for years; most are shed from cattle within 5–6 mo.

Clinical Findings:

Fasciolosis ranges in severity from a devastating disease in sheep, alpacas, and llamas to an asymptomatic infection in cattle. The course usually is determined by the number of metacercariae ingested. Acute disease occurs 2–6 wk after the ingestion of large numbers of metacercariae (usually >2,000) over a short period. In sheep, acute fasciolosis occurs seasonally and is manifest by a distended, painful abdomen; anemia; and sudden death occurring 2–6 wk after infection. The acute syndrome can be complicated by concurrent infections with Clostridium novyi, resulting in “black disease” (clostridial necrotic hepatitis), although this is now less common due to vaccination against clostridial diseases. In subacute disease, large numbers (500–1,500) of metacercariae are ingested over longer periods of time; survival is longer (7–10 wk), even in cases with significant hepatic damage, but deaths occur due to hemorrhage and anemia. Chronic fasciolosis can be seen in all seasons but manifests primarily in late fall and winter. It occurs as a result of ingesting moderate numbers (200–500) of metacercariae over longer periods of time; signs include anemia, unthriftiness, submandibular edema, and reduced milk production, but even heavily infected cattle may show no clinical signs although their immunity to other pathogens (eg, Salmonella spp) may be reduced and reactions to the single intradermal test for tuberculosis modified. Heavy chronic infection is fatal in sheep, alpacas, and llamas.

Sheep do not appear to develop resistance to infection, and chronic liver damage is cumulative over several years. In cattle, a partial acquired resistance develops beginning 5–6 mo after infection.


Severity depends on the number of metacercariae ingested, the phase of development in the liver, and the species of host involved. During the first phase, immature, wandering flukes destroy liver tissue and cause hemorrhage. The second phase occurs when the flukes enter the bile ducts, where they ingest blood and damage the mucosa with their cuticular spines. 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. The damaged bile ducts become enlarged, or even cystic, and have thickened, fibrosed walls. In cattle but not sheep, the duct walls become greatly thickened and often calcified. Aberrant migrations occur more commonly in cattle, and encapsulated flukes may be found in the lungs. Mixed infections with Fascioloides magna can be seen in cattle.

Tissue destruction by wandering flukes may create a microenvironment favorable for activation of clostridial spores.


The oval, operculated, golden brown eggs (130–150 × 65–90 μm) 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 sedimentation may be required. Diagnosis can be aided by an ELISA (commercially available in Europe) that enables detection ~2–3 wk after infection and well before the patent period. Plasma concentrations of γ-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 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. Although molluscicides can be used to reduce lymnaeid snail populations, those that are available all have disadvantages 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. Other such chemicals are generally too expensive and have ecologically undesirable effects. 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; none are approved for alpacas and llamas), 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. Anthelmintic resistance by F hepatica to various compounds, including albendazole, clorsulon, and triclabendazole, has been demonstrated, further complicating control programs based only on anthelmintic usage. The timing of treatment is also important so that the pharmacokinetics of the drug used will result in the optimal removal of flukes—each flukicide has varying efficacy against different ages of fluke. Timing of treatments is 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 based on rainfall, evapotranspiration, number of wet days per month, and/or prevalence are used to predict the timing and severity of disease. 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.

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