LIFE - CYCLE
The life cycle of liver fluke is indirect because one or two intermediate hosts are usually involved before invasion of the definitive hosts. The life cycle of Fasciola is very similar to that of paramphistomes while Archibald reported that Liver fluke does not only have an alternation of generations but also an alternation of hosts.
The host which produced the fertilized eggs (i.e. sexual generation) is usually a vertebrate but the intermediate host is always a Mollusc:-Lymnae natalensis which is truly aquatic and Lymnae truncatula which is amphibious, for Fasciola gigantica and Fasciola hepatica respectively. In some cases, A 2nd intermediate host is required which is usually either an arthropod or one of the lower vertebrates.
Reports has it that the amphibious intermediary liver fluke hosts usually allow the evolution of the liver fluke larval forms which as a result of clonal multiplication inside the snail from one Miracidium entering the snail, up to 300 - 1772 Cercariae may be produced. The eggs of the liver fluke which lives in the intestinal tract of the definitive host (bovine) are either coughed up and discharged in the sputum or swallowed and then voided in the faeces.
Under the right conditions of moisture and warmth, the eggs hatch into larvae (the Miracidia), which is ciliated and swims actively through the water in search of an appropriate Molluscan host (snail). When it approaches a mollusc of the correct species, it turns and makes straight for it. If it strikes a soft portion of the mollusc, it attaches itself by means of glandular secretions and digests its way into the tissues of its victim. The entrance may be by way of the gills or through the head or foot. The Miracidium soon reaches a lymph channel and gradually migrate towards the apical end of the mollusc. During this period it loses its cilia and change into a simple sac-like creature (the Sporocysts).
The Sporocyst which is the early stage of liver fluke may undergo several changes into Redia → Sporocyst (again) → Cercaria/Metacercaria. When the cercaria matures, they escape from their parents either by rupturing the wall or through the birth pore and vigorously work their way through the enveloping host tissue and eventually lie freely in the cavity between the mollusc and its shell. The cercaria or metacercaria swims about by means of tail, but may also attach itself either to the surface film of the water or lie in the mud at the bottom.
The Cercaria of liver fluke must affect an entrance into the bovine, usually within 24 hours or else it dies. It usually penetrates the bovine host passively (while haemoparasites do so actively), that is, it encysts either on a plant, which is then subsequently grazed by Cattle.
When Cattle ingest the Cercaria during grazing, then the young parasite as reported, after emerging from the cyst in the intestine, penetrate the peritoneal cavity and goes into the liver and feed on the liver parenchyma for a period of 6-7 weeks and thereafter penetrate into the bile duct where it becomes mature, lay eggs and the cycle continue- as shown below.
Nine (9) years later, Anon (1974) reported that in Britain, the loss to the farmer due to Livers condemned at meat inspection because of liver fluke was said to be at least £ 50 million per annum.Hammond (1965) noted that in Africa, Asia, tropical and sub-tropical areas Liver fluke have been identified as a major source of loss of production in domestic animals.
ECONOMIC IMPORTANCE LIVER FLUKE
Report has it that Liver fluke is the most widespread and most destructive parasitic disease of farm animals in the Phillippines with incidence rates of 34.61-100% in endemic areas- and liver weight was found to be higher in infected than in non-infected animals. This is because of the necrotic and calcified lesions due to the compensatory hypertrophy of liver parenchyma caused by infection. Where an infection has been observed, liver fluke infection in growing cattle has been shown to depress live weight gain in the livestock by between 0.07kg/week and 1.2 kg/week depending on the size of the fluke burden.
Estimation has it that Nigerian cattle had mean burdens of 30 flukes and that each fluke reduced the annual liveweight gain by about 200g. Liver fluke investigation reported an average burden of 30 flukes in an abattoir survey in Nigeria. In the same year, also found out that N32, 421, 200 was the annual loss due to liver fluke infection in bovine, Ovis and Caprines in Nigeria.
Chadler and Read (1982) observed that liver fluke causes a greater damage in young cattle causing them to become unthrifty, emaciated and may die under severe condition. It is also on record that the loss caused by not being able to sell livers for human consumption is calculated using the estimated number of cattle livers condemned annually due to Liver fluke X weight of each liver X price per unit weight. The effect of liver fluke infection on the rate of weight gains in growing cattle (Dairy or Beef) was also suggested as:- Minimum decrease in weight gain of 0.1kg/week, average decrease in weight gain of 0.05kg/week and a minimum value of 1.0kg/week (Asanji and Williams, 1984).
Aliyara and Ayanwale (1999) also revealed that 3.72% of Cattle liver and 4.27% of Sheep liver in Nigeria were condemned due to liver - fluke infestation while in Kenya, Kithuka et al. (2002) reported that the total economic loss incurred by the country between 1990-1999 (10 year period) due to condemnation of infected livers was US $2.6 million approximately and that the total annual economic losses during that period ranges from approximately US $0.2 - 0.3 million. Mazhar (2002), also stated that the economic losses due to the condemnation of 250,000 Cattle fluke-infected Livers cost US $140,000, which represents 15% of the livers inspected at the abattoirs in the state of Rio Grande do sul in Southern Brazil and that approximately nine dollars are lost per animal due to reduce weaning weight during slaughter.
According to a report by Sandra and Maria, the sub-clinical and chronic disease usually results in decrease production of meat, milk, wool, 2 bacterial infections, fertility problems and great expenses with anthelmintics in Brazil.
Liver fluke research stated that interference by parasites generally have resulted in significant impediment to achieving efficient immunization of animals against bacterial and viral disease. He further stated that despite repetitive treatment using efficient drugs, the prevalence of the parasites have remained high.
Unfortunately the awareness of farmers in many countries concerning this economically important parasite is low. In Switzerland for instance, 72.2% of the farmers are ignorant of the Liver fluke in their animals. For the last forty 40 years the presence of anti “f2” antibodies in humans has been considered as a serological evidence for the liver fluke (Biguet and Coll. 1962 and 1965; Capron and Coll. 1964).
The persistence of liver fluke disease was confirmed by Pritchard et al. (2005) who stated that liver fluke infection was found to cause weight loss, diarrhoea, decreased milk yield and occasionally death in East Anglia during the winter of 2001-2003.