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Fasciolosis


Synonym(s): hepatic parasitic disease, hepatic infectious disease, liver fluke disease, fasciolhica, fasciola giganticoa, dicrocoelium dendriticum

Introduction

  • Cause: Fasciola hepatica (UK) and/or Fasciola gigantica infection.
  • Signs:
    • Light burdens can result in sub-clinical disease such as production losses.
    • Clinical signs may include weight loss, poor production, chronic diarrhea, anemia and sub-mandibular edema (bottle jaw).
  • Diagnosis: fecal sedimentation, fecal copro-antigen ELISA, serum or bulk milk serology and post-mortem.
  • Treatment: triclabendazole (all stages), closantel (limited stages), nitroxynil (limited stages), albendazole (adult stages), clorsulon (adult stages) and oxyclozanide (adult stages).
  • Prognosis: mortality low. Dependent upon magnitude of burden and extent of liver damage.

Geographic incidence

  • Worldwide distribution with particular significance in UK, Europe, North America, South America and the Caribbean. Also significant in parts of North Africa, Eastern Sub-Saharan Africa, the Middle East, Southern Asia and Australasia.
  • In the UK the distribution of Fasciola hepatica Fasciola hepatica infection in cattle has been historically recorded in the North West of England and Wales, Northern Ireland and Scotland; particularly the wetter West regions.
  • Recent serological studies demonstrate nearly 80% of dairy herds have been exposed to Fasciola hepatica infection with similar reports in other European countries.

Age predisposition

  • Cattle can be infected as soon as they start to graze and may be continually at risk throughout their lives whilst grazing affected herbage.
  • Cattle do not acquire protective immunity to the parasite.
Cattle of all ages are vulnerable, irrespective of prior exposure.

Public health considerations

  • The parasite is zoonotic.
  • The metacercariae stages may be ingested when affected raw herbage in ingested:
    • This is of particular significance in parts of South America, particularly Peru and Bolivia, along with parts of the Middle East and Asia, whereby the encysted stages may be ingested in soups and fresh teas.  
    • Occasional cases have been noted in Europe with consumption of un-washed watercress.

Cost considerations

  • Worldwide fasciolosis costs the global cattle industry approximately £2.5 billion (2017). These figures are primarily as a result of production losses.
  • In the UK:
    • F. hepatica infections cost the cattle industry an estimated £23 million per year due to production losses.
    • Bovine liver condemnations at slaughter cost an estimated at £3 million per annum (2017).
  • For beef cattle the economic impact on growth is estimated between £30-200 per animal. For dairy cattle a reduction in 0.7kg/milk per day in lactation.
  • In addition to diagnostic, treatment and surveillance costs, the subclinical effects on production include reduced milk production, growth rates and reproductive performance.
  • Fasciola infections modulate the host immune response to enable their survival. This leads to increased susceptibility to certain pathogens such as Salmonella dublin Salmonella spp, Clostridium novyii Clostridium spp and affects the diagnosis of Mycobacterium bovis Mycobacterium bovis positive cattle.

Pathogenesis

Predisposing factors

General

  • Risk of infection is dependent upon presence of the intermediate host at pasture and hospitable climatic conditions. Hence certain farms and pasture are likely to have a history of infection.
  • In general resting environmental stages, such as the eggs and metacercariae, require moist wet environments to survive. Such stages can over winter at pasture and become infective when temperatures increase (10-12°C/50-53.6°F).

Pathophysiology

  • Eggs are passed in the feces onto pasture and under the correct conditions develop into miracidia.
  • Miracidia are highly motile and locate obligate snail intermediate host such as G. trucatula .
  • Miracidia penetrate the snail intermediate host for asexual multiplication through sporocyst, redia to thousands of cercariae.
  • Cercariae exit the snail into the environment and rapidly attach to herbage and encyst into metacercariae; the infective form to definitive hosts such as cattle.
  • When cattle are grazing they ingest metacercariae which excyst in the lumen of the small intestine and penetrate into the abdomen to migrate towards the liver.
  • The pathogenesis caused by parenchymal migration of F. hepatica differs significantly between sheep and cattle:
    • In sheep, the migrating fluke cause acute hemorrhage and damage to the liver, seen as acute clinical disease.
    • In cattle, the specific syndrome of acute fasciolosis in rare. Although the migratory fluke inevitably cause some local pathology, there are only limited effects on health, appetite and growth.
  • Maturation occurs in the bile ducts, where the adults feed on blood and sexually reproduce to produce eggs.
  • It is the adults in the bile ducts that are responsible for the clinical disease seen in cattle.
  • The pathology caused by these adults is seen from around 25 weeks post-infection.
  • Typical lesions include:
    • Extensive fibrosis of the parenchyma, especially ventral lobe.
    • Enlarged bile ducts.
    • Fibrosis and calcification of bile ducts. It is this calcification that is believed to be responsible for limiting the life expectancy of F. hepatica adults within the host. The calcified bile ducts make feeding difficult.
  • Eggs are then passed intermittently from the bile ducts, via the gall bladder, into the small intestinal lumen into the faeces where they can be detected.

Timecourse

  • In total the pre-patent period (PPP) in cattle is 10-12 weeks, in temperate climates, and 4-7 weeks in the obligate snail intermediate host.
  • Extent of pathological damage caused by F. hepatica Fasciola hepatica infection, and subsequent degree of clinical disease, is dependent upon intensity of infection and parasite burden.
  • Chronic, rather than acute, disease is the most common manifestation of fasciolosis in cattle.  
  • Chronic inflammation can result in parasites being unable to feed and may limit the extent of parasite burden over time.
  • In some cases, especially where cattle have been exposed to light burdens, the liver may regenerate where no re-infection occurs.

Epidemiology

  • Presence of the intermediate snail hosts are vital for development and transmission of F. hepatica in the UK:
    • Fresh water mud snails (Lymnaeidae) are the intermediate hosts of F. hepatica worldwide. 
    • Galba truncatula (the dwarf pond snail) is the most common snail intermediate host in the UK and most of Europe.
    • Other species of snail host have localised importance in other countries.
  • In the UK, along with much of Northern and Western Europe, risk period for cattle is later summer early autumn for clinical and subclinical disease. Warmer southern Europe and other countries may have less seasonal exposure to F. hepatica with infections occurring all year round depending upon suitable environmental conditions.
  • Primary transmission can occur with eggs being shed on pasture, hatching to miracidia to infect snails, to release of cercariae and form metacercariae on herbage in one grazing season from spring to autumn (May-October) in the UK. Although disease is not seen until winter or early spring due to the 10-12 week development from juveniles to adults within the definitive host.
  • Peak numbers of metacercariae are found at pasture between August-October although they can be present on pasture all year round.
  • Eggs can survive on pasture over the winter in the UK to hatch and infect snails the following spring. Intermediate stages can also survive whilst the snail host is hibernating over the winter months for reactivation the following spring.
  • Passage of eggs onto pasture from definitive hosts is dependent upon parasite burden, frequency of eggs release from the gall bladder and composition of fecal matter in the host.
  • Spreading slurry, from infected cattle, can contaminate pasture with F. hepatica eggs that can establish infection if a suitable intermediate host is present.  
  • Metacercariae can survive for short periods on preserved forage and be infective to cattle.
  • Due to absence of the correct climatic conditions, in combination with presence of suitable snail intermediate host species, F. gigantica Fasciola gigantica lifecycles are not currently supported in the UK.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Moazeni M & Ahmadi A (2016) Controversial aspects of the life cycle of Fasciola hepatica. Exp Parasitol 169, 81-89 PubMed.
  • Mazeri S, Sargison N, Kelly R F, Bronsvoort B M & de C Handel I (2016) Evaluation of the performance of five diagnostic tests for Fasciola hepatica infection in naturally infected cattle using a Bayesian no gold standard approach. PLoS One 11 PubMed.
  • Knubben-Schweizer G & Torgerson P R (2015) Bovine fasciolosis: Control strategies based on the location of Galba truncatula habitats on farms. Vet Parasitol 208, 77-83 PubMed.
  • Howell A, Baylis M, Smith R, Pinchbeck G & Williams D (2015) Epidemiology and impact of Fasciola hepatica exposure in high-yielding dairy herds. Prev Vet Med 121, 41-48 PubMed.
  • Khan M K, Sajid M S, Riaz H, Ahmad N E, He L, Shahzad M, Hussain A, Khan M N, Iqbal Z & Zhao J (2013) The global burden of fasciolosis in domestic animals with an outlook on the contribution of new approaches for diagnosis and control. Parasitol Res 112, 2421-2430 PubMed.
  • McCann C M, Baylis M & Williams D J L (2010) The development of linear regression models using environmental variables to explain the spatial distribution of Fasciola hepatica infection in dairy herds in England and Wales. Int J parasitol 40, 1021-1028 PubMed.
  • Piedrafita D, Spithill T W, Smith R E & Raadsma H W (2010) Improving animal and human health through understanding liver fluke immunology. Parasite Immunol 32, 572-581 PubMed.
  • Charlier J, De Meulemeester L, Claerebout E, Williams D & Vercruysse J (2008) Qualitative and quantitative evaluation of coprological and serological techniques for the diagnosis of fasciolosis in cattle. Vet Parasitol 153, 44-51 PubMed.
  • Mas-coma S (2003) Human fasciolosis: Epidemiological patterns in human endemic areas of South America, Africa and Asia. Europe 1-11 PubMed.
  • Mitchell G (2002) Update on fasciolosis in cattle and sheep. In Pract 24, 378-385 VetMedResource.

Other sources of information

  • NOAH & VMD (2020) Joint Statement from the National Office of Animal Health (NOAH) and the Veterinary Medicines Directorate (VMD) on the Use of Flukicides in Dairy Cattle. Website: www.noah.co.uk (pdf download).
  • Control of Worms Sustainably (2013) Control of Liver and Rumen Fluke in Cattle. Website: www.cattleparasites.org.uk (pdf download).
  • Scott P R, Penny C D & Macrae I M (2011) Cattle Medicine. Manson Publishing, UK.
  • Andrews A H, Blowey R W, Boyd H & Eddy R G (2004) Bovine Medicine: Diseases and Husbandry of Cattle. 2nd edn. Blackwell Science Ltd, UK. Website: www.semanticscholar.org (pdf download).
  • Dalton J P (1999) Ed. Fasciolosis. CABI Publishing, UK.

Organisation(s)

  • Royal (Dick) School of Veterinary Studies, University of Edinburgh, UK. Website: www.ed.ac.uk/vet.