Fasciola Hepatica: a Review of the Economic Impact in Cattle and Considerations for Control

Veterinary Therapeutics • Vol. 2, No. 1, Winter 2001 Fasciola hepatica: A Review of the Economic Impact in Cattle and Considerations for Control Ray M. Kaplan, DVM, PhD Department of Medical Microbiology and Parasitology College of Veterinary Medicine University of Georgia Athens, Georgia 30602 I ABSTRACT opportunity to administer strategic treatments To understand the rationale behind recom- and still receive meaningful benefit is fairly mended control programs for liver flukes in large. To properly understand the rationale be- cattle, the economic impact and the complex hind recommended control programs, reason- life cycle of Fasciola hepatica need to be appre- able deviations that can be made from these ciated. Fluke-infected cattle rarely demonstrate recommendations, and issues pertaining to the clinical disease, but subclinical impairment of economic impact of fluke infections in cattle, feed efficiency, growth, and fertility can have the complex life cycle of liver flukes (Figure 1) an important impact on productivity. Al- needs to be appreciated. though the precise benefit from controlling liv- Liver fluke transmission is dependent on the er flukes is unknown due to the inherent vari- presence of its snail intermediate host; there- ability between studies, most investigations fore, the distribution of the parasite is limited demonstrate a considerable economic advan- to geographic areas where the appropriate snail tage to treatment. In addition, recent studies species is present. In the US, liver flukes are en- have demonstrated that liver flukes may cause zootic primarily in the Gulf coast and western a decrease in host fertility by altering normal states, where high annual rainfall, large areas of metabolism and/or balance of sex hormones. poorly drained pasture, and certain soil types This review focuses on these issues and how to provide suitable lymnaeid snail habitats.1 In best use available drugs to implement optimal addition, use of irrigated pastures, which is fluke control programs. common in the western US, may increase the distribution and prevalence of liver flukes. I INTRODUCTION Therefore, control of liver flukes is relevant Current recommendations for the control of only in areas where the parasite is enzootic or liver flukes (Fasciola hepatica) in cattle are when cattle are purchased from such areas. based on strategically timed treatments with This situation is somewhat different from that flukicidal drugs. The optimal timing of these of gastrointestinal nematodes, where control is treatments has been determined by studying almost always an important aspect of bovine the seasonal transmission dynamics of liver health programs in virtually all cattle-produc- flukes in numerous locations throughout the ing areas of the US. world. Because of the long time required to Adult liver flukes (Figure 2) reside in the bile complete the fluke life cycle, the window of ducts of host animals, and eggs are passed onto 40 R. M. Kaplan Figure 2. Adult liver flukes recovered from an infected bovine liver. Worms are large and leaf-shaped (approximately 1 cm × 3.5 cm). detritus while drinking contaminated water.2 The length of time that metacercariae survive on pasture primarily depends on available moisture. Under the hot and dry pasture conditions of coastal Texas during the summer, metacercariae were rapidly killed3; however, Figure 1. Liver fluke (Fasciola hepatica) life cycle. under conditions of high humidity, such as in Louisiana during the summer, metacercariae may survive for extended periods.4 the pasture in the feces. After a short period of Once ingested by a ruminant host, the development (usually 2 to 3 weeks), a miracid- metacercariae excyst, releasing juvenile flukes. ium hatches from the egg and attempts to find The juvenile flukes penetrate the wall of the and penetrate a snail intermediate host. The small intestine, migrate through the peritoneal parasite develops and replicates asexually in the cavity over a week’s time, and then penetrate snail over many weeks. Under optimal condi- through the liver capsule. Juvenile flukes mi- tions, parasite maturation within the snail to grate through the hepatic parenchyma for ap- the cercarial stage takes approximately 5 to 7 proximately 6 to 8 weeks before entering the weeks, and a single miracidium can develop bile ducts where they mature. Egg production into several hundred cercariae. Under wet con- can begin as early as 8 weeks after infection5; ditions, cercariae emerge from the snail and however, most infections do not become swim until they find and attach to vegetation. patent until after approximately 11 to 12 The cercariae then shed their tails and secrete a weeks.6 Thus, completion of the entire parasite protective coat, forming the encysted infective life cycle, from the time an egg is shed onto stage called metacercariae. Cattle become in- pasture until a newly infected animal reinfects fected primarily by ingesting the metacercarial the pasture with the next generation of fluke cysts on forage, but they also can become in- eggs, generally requires 18 to 24 weeks (4.5 to fected by ingesting cysts suspended on soil and 6 months). 41 Veterinary Therapeutics • Vol. 2, No. 1, Winter 2001 Although the life cycle of F. hepatica does not change, seasonal transmission profiles dif- fer for each geographic region. Therefore, in order to gain maximum benefit from treatment, fluke control programs must be de- signed based on knowledge of local parasite transmission patterns. In addition, such management-related factors as age and use-class of cattle, stocking rate, nutritional status, envi- ronmental stresses, and concomitant infection with gastrointestinal nematodes play an important role in determining the immune status of cattle and the ensuing risk of infection and Figure 3. Chronically infected bovine liver. Note fi- economic loss. Only three flukicidal products brosis and hemorrhage throughout the parenchyma are available for use in the US market, and all and bile ducts that are dilated, thickened, and calci- are extremely limited in their ability to kill the fied. Liver flukes also can be seen protruding from cut migrating stage of F. hepatica younger than 8 bile ducts. weeks. Only one product has >90% efficacy against the 8- to 12-week-old immature fluke, whereas the other two products kill only adult by migrating juvenile flukes.7 Alternatively, flukes with high efficacy. Therefore, timing chronic disease results from a combination of and frequency of treatments must be based on the partially resolved hepatic damage that fol- economic considerations. This review will fo- lows the acute phase and the blood sucking ac- cus on economic considerations so that the ra- tivities of the adult flukes within the bile ducts. tionale behind strategic drug treatment can be Clinical disease resulting from chronic infec- properly understood. In addition, current tion is uncommon in cattle; it is most fre- knowledge regarding the economic impact of quently seen in cattle younger than 2 years and liver flukes in stocker, cow-calf, and feedlot is characterized by weight loss, anemia, hy- cattle will be briefly reviewed. poproteinemia, eosinophilia, general depres- sion, and occasionally death.8 In response to I CLINICAL SIGNS AND PATHOLOGY the traumatic injury caused by the migrating On a herd basis, clinical signs of fluke infec- flukes, tracts of coagulative necrosis develop, tion are usually vague (i.e., reduced productiv- which result in a diffusely fibrotic hepatic ity) and can be difficult to discern from the ef- parenchyma containing hemorrhagic streaks fects of less-than-optimal management or and foci. These lesions can predispose cattle to other chronic disease conditions. From a clini- black disease (infectious necrotic hepatitis) and cal standpoint, bovine fascioliasis generally can bacillary hemoglobinuria due to Clostridium be considered a subclinical disease. When ex- novyi and C. haemolyticum, respectively. In the tremely high fluke burdens rapidly accumu- bile ducts, the adult flukes produce a mechan- late, however, outbreaks of acute or subacute ical irritation that causes cholangiohepatitis. bovine fascioliasis can occur. In these situa- This leads to dilation, thickening, and exten- tions, clinical disease is caused by extensive sive fibrosis of the duct wall, resulting in steno- damage to the hepatic parenchyma produced sis and calcification (Figure 3). 42 R. M. Kaplan TABLE 1. Comparison of Flukicidal Drugs Currently Available in the US Clorsulon Clorsulon + Ivermectin Albendazole Dose 7 mg/kg 2 mg/kg + 0.2 mg/kg 10 mg/kg Kills Adult Flukes * Yes (> 99%) Yes (97% – 99%) Yes (76% – 92%) Kills Immature Flukes* Yes (85% – 95%) No No (8–12 weeks) Kills Juvenile Flukes No No No (0–8 weeks) Route of Administration Oral drench Subcutaneous injection Oral drench Kills Nematodes No Yes Yes Kills Cestodes No No Yes Kills Ectoparasites No Yes No *See text for references regarding drug efficacy. I HOST IMMUNITY adult stages (>99%) and also kills immature Over time, cattle may develop a partially flukes (8 to 12 weeks) with fairly high efficacy protective immune response to F. hepatica. The (85% to 95%)9–11; however, clorsulon only kills interaction of such factors as age of the host, flukes and has no effect against other parasites. innate resistance of the host, previous exposure The combination product of clorsulon plus of the host, and present level of parasite expo- ivermectin (2 mg/kg clorsulon, 0.2 mg/kg iver- sure determine the degree

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