F 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 and sheep in 3 forms: chronic, which is rarely fatal in cattle but often fatal in sheep; subacute or acute, which is primarily in sheep and often fatal; and in conjunction with “black disease” (infectious necrotic hepatitis, see Hepatic Disease in Large Animals: Infectious Necrotic Hepatitis), which is most common in sheep and usually fatal.
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, where they travel to the liver. The time required for this transit can vary and results in delayed development rates and efficacy of some treatments that affect flukes only later in their development. 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.
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, 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.
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 F magna can be seen in cattle.
Tissue destruction by wandering flukes may create a microenvironment favorable to 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 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 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. 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. 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), 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 flukes—each 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 based on rainfall and temperature 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.
Last full review/revision March 2012 by Stuart M. Taylor, PhD, BVMS, MRCVS, DECVP