Hepatic Fascioliasis has a cosmopolitan distribution and most commonly found in North America, parts of Africa and Asia. In India, the disease has been reported from almost all over the country.
Aetiology
Commonly 3 species of liver fluke has been described from the country. Fasciola hepatica from the hilly areas of the country; Fasciola gigentica from planes of the country and is restricted to warmer regions and Fasciola jaksoni found in Assam and Kerala.
Epidemiology
lymnaeid mud snails are intermediate hosts and they release the infective form metacercaria, onto herbage. The availability of metacercariae is generally greatest in the late summer and autumn. But they do not survive under severe winter conditions.
The risk of hepatic fascioliasis is determined by the number of infected lymnaeid snails in the grazing area. The common species of lymnaeid snails in India are Lymnaea accumulate and Lymnaea auricularia. In general, the snails prefer nonacidic low laying swampy areas with slowly moving water, land with small streams, springs blocked drainage or spillages for example, water troughs may also be potentially hazardous infecting grounds. Snails burrow into the soil to survive dry periods and release cercariac when free water is present.
The main factors determining the timing and severity of hepatic fascioliasis are those that influence the number of metacercariae accumulating on herbage. In hot, dry regions, metacercariae die quickly, so infections are usually due to recent release of cercariae.
In particular, temperature and rainfall affect both the spatial and temporal abundance of snail hosts and the rate of development of fluke eggs larvae. Temperature above 10° C are necessary before the snail hosts will breed or before F. hepatica can develop within the snails. No development therefore takes place during the winter in most of the countries.
The clinical outcome of infection depends largely on the density of metacercariae on the garbage. This will be greatest when weather conditions have been favourable for snail production and survival. A high intake of metacercariae over a short time will produce acute disease; lower numbers over a larger period lead to chronic disease. F. hepatica can modulate the host immune response.
Hepatic fascioliasis is mainly economic importance in sheep or cattle but other species may provide a reservoir of infection. Fasciola hepatica may infest all domestic animals including Equidae and many wild species, but chronically infected sheep are the most important source of pasture contamination. Sheep and goats do not develop a strong protective immune response to F. hepatic and remain vulnerable throughout their lives. Cattle gain partial protection against reinfection.
Pathogenesis
Pathogenesis depends on the number of metacercariae ingested. The metacercariae penetrate through intestinal wall and reach peritoneal cavity. They migrate towards the liver through peritoneum and then migrate through liver parenchyma. There is very little pathogenesis produced during migratio through peritoneum and the main lesions are found in liver both in its parenchyma as well as in bile duct. Acute hepatic insufficiency and haemorrhage result.
Chronic hepatic fascioliasis develops only after flukes establish in the bile ducts. Here they cause cholangitis, biliary obstruction, fibrosis and a leakage of plasma protein across the epithelium resulting hypoalbuminemia.
The disease can be clearly differentiated into acute and chronic form. Acute form is comparatively rare form whereas chronic form is common form.
Clinical Findings
Acute fascioliasis: Acute fascioliasis in sheep most often occurs as sudden death with discharge of frothy blood through nostrils and anus confusing with anthrax. If the disease is observed clinically in sheep it is manifested by dullness, weakness, lack of appetite, pallor and oedema of the mucosae and conjunctiva, pain on pressure exerted over the area of liver and ultimately death within a period of 2-3 weeks.
Chronic fascioliasis: In chronic cases, symptoms start appearing only after the immature flukes in the parenchyma become quite mature. The animals become anaemic with rough and off coloured skin coat. The animals become lazy, mucous membranes become pale and the skin becomes dry. Subsequently oedema starts developing particularly below the mandibles and the condition known as ‘bottle jaw condition’. The course of the disease is often as long as 2-3 months in those which die; many survive but may remain in poor condition for longer periods. Cattle also loose weight specially if lactating; milk production falls and chronic diarrhoea may develop.
In cattle, most common symptoms are digestive disturbance, emaciation, constipation with animal feeling very difficulty in defaecation and followed by diarrhoea in extreme csaes.
Diagnosis
(i) History: To support diagnosis accurate account should be taken for grazing history and the seasonably of fascioliasis in that locality.
(ii) Clinical symptoms
(iii) Clinical pathology: In acute fascioliasis there is a severe normochromic anaemia, eosinophilia and a severe hypoalbuminemia. Serum enzymes are elevated. Increase in aspartate aminotransferase can result.
In subacute and chronic disease weight loss is associated with a severe hypochromic, macrocytic anaemia, hypoalbuminemia and hyperglobulinaemia. Serum glutamyl transpeptidase concentration is raised by the activities of adult F. hepatica in bile ducts.
(iv) In can be confirmed by finding of eggs in the faeces. In case of acute infection, by post mortem lesions characteristic hepatic lesions, since the animals harbour immature parasites and there is very little chance of getting eggs in the faeces.
(v) Serological test such as enzyme linked immunosorbent assay has shown promise, particularly for the diagnosis of infection in cattle. A rise in antibody can be detected by 2 weeks after infection and keeps rising until 6 weeks.
Differential Diagnosis
- Haemonchosis
- Infectious necrotic hepatitis
- Anthrax
- Johne’s disease
- Other internal parasitism including parasitic gastroenteritis in sheep and ostertagiosis in cattle.
Treatment
Treatment of acute fascioliasis requires selection of a product highly effective against the juveniles those damage the liver parenchyma. For chronic disease, a compound active against the adult fluke is required.
1. Triclabendazole is specific compound for use against F. hepatica in sheep and cattle.
Dose: Sheep 10 mg/kg, Cattle 12 mg/kg
Higher doses are required for the control of F. gigentica in buffalo.
It is highly effective against all stages of fluke from 2 days old in sheep and 2 weeks in cattle and is the drug of choice in outbreaks of acute fluke disease.
It has been used with success in horses and donkeys (12 mg/kg) but is not licensed for this purpose.
Fluke populations resistent to triclabendazole have developed following intensive control regimes in a few instances.
2. Oxyclozanide is used only in cattle and has a significant effect against the adult fluke but is inactive against immature forms.
Dose: 10-15 mg/kg orally
3. Rafoxanide is found to be 98-99% effective @ 7.5 mg/kg B. wt.
4. Nitroxynil @ 10 mg/kg subcutaneously for 3 alternate days has good efficacy against adult flukes.
5. Albendazoles @ 7.5 mg/kg in sheep and 10 mg/kg in cattle is effective against adult fluke.
6. Closantel will kill the majority of flukes older than 4 weeks in sheep @ 10 mg/kg.
Control
Preventive measures are required in endemic areas as fascioliasis can cause death without warning causes significant production losses.
(1) By controlling snails
- Use of molluscicide: A number of chemicals are used as molluscicides and this method is known as chemical control. Common chemicals used are copper sulphate, Sodium pentachlorophenate but they may be potentially hazardous to man, livestock and environment. Safer and more selective low involvement molluscicides such as N-tritylmorpholine has been developed.
- Biological control: In this type of control the predator is used which eat on snails such as duck. Some arthropod larvae also eat on cercariae.
- Physical destruction: This is done by collecting the snails physically and then destroying them.
(2) By controlling animals from picking up infection by not allowing them to graze near water holdings particularly during late summer when grazing grounds become dried and after monsoon when the population of snails is at the peak.
(3) Livestock on heavily contaminated land may be protected from acute fascioliasis by taking advantage of the interval between the ingestion of metacercariae and the onset of the disease. Treatment during this period with a product effective against young flukes will eliminate migrating parasites before they cause serious liver damage.
(4) Reduction of pasture contamination with metacercariae will reduce future risk. To achieve this, adult fluke should be eliminated by using specific drugs from the bile ducts of all grazing stock in spring and early summer. This prevents egg excretion and minimizes the numbers of snail-seeking miracidia at this crucial stage of epidemiological cycle.
Vaccines for F. hepatica are under trial. Immune responses to successful vaccination strategies are qualitatively different from those induced by natural infection.
