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# *Fasciola hepatica* ## Life Cycle * Adult in Biliary Passages * Eggs in Feces (Yolk Mass) * Penetrates Liver * Burrows Through Intestinal Wall * 33 Days * Ingested by Host * Metacercaria on water plants - bark or free floating * Cercaria swarming (Seasonal - Aug. and Sep)...

# *Fasciola hepatica* ## Life Cycle * Adult in Biliary Passages * Eggs in Feces (Yolk Mass) * Penetrates Liver * Burrows Through Intestinal Wall * 33 Days * Ingested by Host * Metacercaria on water plants - bark or free floating * Cercaria swarming (Seasonal - Aug. and Sep) * Enters snail - *Lymnaea truncatal* (21 *Lymnaea* spp) * Larval Stages - 32-54 days * Sporocyst-Mother Redia * Daughter Redia-Cercaria (temperature dependent) * Deposited in Water * 9 to 15 Days Development in Water * Miracidium Free ## *Fasciola hepatica* Life Cycle * Eggs passed in the feces of the mammalian host develop and hatch releasing motile ciliated miracidia. * This takes nine days at optimal temperatures of 22-26°C and little development occurs below 10°C. * The liberated miracidium has a short life span and must locate a suitable snail within three hours. * In the infected snails, development proceed through the sporocyst and redial stages to the final stage in the intermediate host, the cercariae; these are shed from the snail as motile forms which attach themselves to firm surfaces, such as grass blades, and encyst there to form the infective metacercariae. * It takes a minimum of 6-7 weeks for completion of development from miracidium to metacercaria, although under unfavorable circumstances a period of several months is required. * Infection of a snail with one miracidium can produce over 600 metacercariae. ## *Fasciola hepatica* Life Cycle * Metacercariae ingested by the snail host encyst in the small intestine, migrate through the gut wall, cross the peritoneum and penetrate the liver capsule. * The young flukes tunnel through the parenchyma for 6-8 weeks, then enter the small bile ducts where they migrate to the larger ducts and occasionally gall bladders. **The life cycle of *F. hepatica* is therefore 17-18 weeks** * The longevity of *F. hepatica* in untreated sheep may be years, in cattle it is usually less than one year. ## *Fasciola hepatica* Life Cycle * Since *L. truncutula* is the most widespread and important species involved in the transmission of *F. hepatica*. * *L. truncutula* is a small snail , the adults being about 1 cm in length . * The shell is usually dark brown and has a turreted appearance , being coiled in a series of spiral whorls. When held with the turret upright and the aperture facing the observer , the latter is approximately half the length of the snail and is on the right hand side , and there are four and a half whorls. * The snails are amphibious and although they spend hours in shallow water , they periodically emerge onto surrounding mud. They are capable of withstanding summer drought or winter freezing fur several months by respectively aestivating or hibernating deep in the mud. * Optimal conditions include a slightly acid pH environment and a slowly moving water medium to carry away waste products. They feed mostly on algae and the optimum temperature range for development is 15-22°C; below 5°C development ceases ## *Fasciola hepatica* Epidemiology There are three main factors influencing the production of the large numbers of metacercariae necessary for outbreaks of fasciolosis: 1. Availability of the intermediate host 2. Temperature 3. Moisture ## *Fasciola hepatica* Pathogenesis and Clinical Signs * These vary according to the phase of parasitic development in the liver and the species of host involved. * Essentially the pathogenesis is two-fold; the first phase occurs during migration in the liver parenchyma and is associated with liver damage and haemorrhage. * The second occurs when the parasite is in the bile ducts, and results from the hacmatophagic activity of the adult flukes and from damage to the biliary mucosa by their cuticular spines. * Fasciolosis may be acute, sub-acute or chronic. * The acute disease occurs 2-6 weeks after the ingestion of large numbers of metacercariae, usually over 2000 and is due to the severe hemorrhage which results when the young flukes. migrating in the liver parenchyma, rupture blood vessels. Damage to the liver parenchyma is also severe. * At necropsy the liver is enlarged, haemorrhagic and honeycombed with the tracts of migrating flukes. * The surface particularly over the ventral lobe is frequently covered with a fibrinous exudate. * Subcapsular hemorrhage are common and these may rupture so that a quantity of blood-stained fluid is often present in the abdominal cavity. * Outbreaks of acute fasciolosis are generally presented by sudden deaths usually during autumn and early winter especially in sheep. * On examination of the remainder of the flock, one may find some sheep with weak, with pale mucus membranes, palpable enlarged livers with abdominal pain and ascitis. * Some times these outbreaks are complicated with concurrent infections with *Clostridium novyi* resulting in 'Black disease', although this is less common nowadays because of widespread vaccination against clostridial diseases. * It is presented as a rapid and severe haemorrhagic anaemia with hypoalbuminaemia, and if untreated, can result in a high mortality rate. * However it is not so rapidly fatal as the acute condition and affected sheep may show clinical signs for 1-2 weeks prior to death; these include a rapid loss of condition, a marked pallor of the mucous membranes, and an enlarged and palpable liver. * Submandibular or facial oedema and ascites may be present. * Chronic fasciolosis, which is seen mainly in late winter and early spring, is the most common form of the disease. * It occurs 4-5 months after the ingestion of moderate numbers, 200- 500, of metacercariae. * The principal pathogenic effects arc anemia and hypoalbuminaemia and more than 0.5ml blood per fluke can be lost into the bile ducts each day. * Additional loss of plasma proteins occurs by leakage through the hyperplastic biliary mucosa and the pathogenic effect is exacerbated if the sheep is on a low plane of nutrition. * In necropsy the liver has an irregular outline and is pale and firm, the ventral lobe being most affected and reduced in size. The liver pathology is characterized by hepatic fibrosis, hyper plastic cholangitis, egg's granuloma may be present. * In the subacute disease, metacercariae are ingested over a longer period and while some have reached the bile ducts where they cause a cholangitis, others are still migrating causing lesions less severe, but similar to those of the acute disease; thus the liver is enlarged with numerous necrotic or haemorrhagic tracts visible on the surface and in the substance. * Subcapsular hemorrhage s are usually evident but rupture of these is rare. * This form of the disease occurs 6-10 weeks after ingestion of approximately 500-1500 metacercariae, also appears in the late autumn and winter. * Although acute and subacute disease may occasionally occur under conditions of heavy challenge, especially in young calves, the chronic form of the disease is by far the most important, and as in sheep, is seen in the late winter and early spring. * The pathogenesis is similar to that in sheep but has the added features of calcification of the bile ducts and enlargement of the gallbladder. * Aberrant migration of the flukes is more common in cattle and encapsulated parasites are often seen in the lungs. * On reinfection of adult cows, migration to the foetus has been recorded resulting in prenatal infection. * In heavy infections, where anemia and hypoalhuminaemia are severe, submandibular oedema frequently occurs. * With smaller fluke burdens, the clinical effect is minimal and the loss of productivity is difficult to differentiate from inadequate nutrition. * It must be emphasized that diarrhoea is not a feature of bovine fasciolosis unless it is complicated hy the presence of *Ostertagia* spp. Combined infection with these two parasites has been referred lo as the fasciolosis /ostertagiosis complex. * Fasciola infections may cause a loss of production in milking cows during winter. * Clinically, these are difficult to detect since the fluke burdens are usually low and anaemia is not apparent. The main effects are a reduction in milk yield and quality, particularly of the solids-not-fat component. ## * Fasciola hepatica* Diagnosis * This is based primarily on clinical signs, seasonal occurrence, prevailing weather patterns, and a previous history of fasciolosis on the farm or the identification of snail habitats. * While diagnosis of ovine fasciolosis should present few problems, especially when a postmortem examination is possible, diagnosis of bovine fasciolosis can sometimes prove difficult. * In this context, routine haemalological tests and examination of feces for fluke eggs are useful and may be supplemented by two other laboratory tests. * The first is the estimation of plasma levels of enzymes released by damaged liver cells. Two enzymes are usually measured Glutamate dehydrogenase (GLDH) which levels become elevated within the first few weeks of infection. The other, gamma glutaniyltranspeptidase (GGT) elevation of this enzyme takes place mainly after the flukes reach the bile ducts and raised levels are maintained for a longer period. * The second is the detection of antibodies against components of flukes, the ELISA and the passive haemagglutination test being the most reliable. ## *Fasciola hepatica* Treatment * The older drugs such as carbon tetrachloride, hexachlorethane and hexachlorophene are still used in some countries, but these have been largely replaced by more efficient and less toxic compounds. * Until recently, treatment was not highly successful due to the inefficiency of the older drugs against the early parenchymal stages. * However, efficient drugs are now available and the one of choice is triclabendazole which removes all developing stages over one week old. Other drugs are rafoxanide, closantel and nitroxynil, which will remove flukes over lour weeks old. * A single dose of triclabendazole accompanied with a move to fluke-free pasture or a well drained, recently cultivated field should be adequate treatment. * However treatment with rafoxanide, closantel or nitroxvnil a second dose of treatment may be necessary 2-3 weeks after moving to fluke-free ground. * Where sheep cannot be moved to clean ground, treatment should be repeated at three weekly intervals until six weeks after deaths have ceased. * The drugs recommended for acute fasciolosis can be used against older flukes responsible for subacute fasciolosis. * Movement to fluke-free pasture is again advisable following treatment, and where this is not possible treatment should be repeated at four and eight weeks to eliminate maturing flukes. * Outbreaks of chronic fasciolosis can be successfully treated with a single dose of any of a range of drugs (rafoxanide, nitroxynil. brotianide, closantel, oxyclozanide and triclabendazole) and following treatment, the anaemia usually regresses within 2-3 weeks. The roundworm anthelmintics, albendazole and netobimin are also effective against adult flukes albeit at increased dosage rates. * At present there is only one drug, namely triclabendazole, which will remove the early parenchymal stages. * Apart from triclabendazole, the two drugs most commonly used for subacute or chronic fasciolosis are rafoxanidc and nitroxynil and several others, such as clorsulon and niclofolan, are also marketed in some countries; albendazole is also effective. * In lactating cows, where the milk is used for human consumption, the above drugs are either banned or have extended withdrawal periods in most countries. An exception is oxyclozanide which is licensed for use in actating heifer ## *Fasciola hepatica* Control * Control may be approached in two ways: * A- by reducing populations of the intermediate snail host 1. Proper drainage system 2. Molluscicide (copper sulphate) * B- or by using anthelmintics. * The prophylactic use of fluke anlhelmintics is aimed to: * (I) Reducing pasture contaminatinn by fluke eggs at a time most suitable for then development, i.e. April to August. * (2) Removing fluke populations at a time of heavy hurdens or at a period of nutritional and pregnancy stress. # *Fascioloides magna* * This is primarily a parasite of deer which can infect other ruminants. * It is found in North America and central and SW Europe. * Transmitted by *Lymnaea* species this very large fluke measures up to 10 cm and has no anterior cone. * In deer and cattle, the parasite can cause hepatic damage on reaching the liver, but it rapidly becomes encapsulated by the host reaction and clinical effects are minimal. * But in sheep this response is negligible and the damage of liver can be sever or even fatal; because of the sheep rearing is difficult in areas where the parasite is prevalent. # Family DICROCOELIDAE * These trematodes are small. lancet-like flukes occurring in the biliary and pancreatic ducts of vertebrates. * Miracidia are present in the eggs when they are passed in the feces; there is no redial stage during development in the snail. # *Dicrocoelium dendriticum* * **Hosts**: Sheep, cattle, deer and rabbits * **Intermediate hosts**: * Land snails of many genera * Brown Ants, of genus *Formica* * **Site**: Bile ducts & gall bladder. * **Distribution**: Worldwide * **Species**: *Dicrocoelium dendriticum* ## *Dicrocoelium dendriticum* Identification * **Gross**: * There is no possibility of confusion with other flukes in the bile ducts of ruminants as *Dicrocoelium* is 1.0 cm long, distinctly lanceolate and semitransparent. * **Microscopic**: * The gut is simple, consisting of two branches and resembles a tuning fork. Behind the ventral sucker the testes lie in tandem with the ovary immediately posterior. * There are no spines on the cuticle (*cf Farciola*). The egg is small, 45 x 30 µm, dark brown and operculated usually with a flattened side. It contains a miracidium when passed in the feces. ## *Dicrocoelium dendriticum* Life Cycle * The egg does not hatch until ingested by the first intermediate host, the land snail, in which two generations of sporocysts develop which then produce cercariae. * Cercariae are extruded in masses cemented together by slime. This phase of development takes at least three months. * The slime balls of cercariae are ingested by ants in which they develop to metacercariac mainly in the body cavity and occasionally the brain. * The presence of a brain lesion in the ant, induced by metacercariae, impels the ant to climb up and remain on the tips of the herbage, thus increasing the chance of ingestion by the final host. This phase in the ant is completed in just over one month in summer temperatures. * In the final host, the metacercariae hatch in the small intestine and the young flukes migrate up the main bile duct and thence to the smaller ducts in the liver. * There is no parenchymal migration and the prepatent period is 10-12 weeks. * The flukes are long-lived and can survive in the final host for several years. # *Eurytrema* * The fluke *Eurytrema pancreaticum* is found in the pancreatic ducts of ruminants in parts of Asia, Brazil and Venezuela. * Like *D. dendriticum* it has two consecutive intermediate hosts, a land snail followed by a grasshopper or tree cricket. * Infection of the final host is by ingestion of the grasshopper and migration of the fluke from the small intestine to the final site in the pancreatic duct. * Heavy infections are reported as causing fibrosis and atrophy of the pancreas. * At present there is no known effective treatment. # *Paramphistomum* * **Hosts**: Ruminants * **Intermediate hosts**: Water snails; principally *Planorbis* and *Bulinus* * **Site**: Adults in the rumen and reticulum, immature stages in the duodenum. ## *Paramphistomum* Identification * **Gross**: The adults are small, conical, maggot-like fluke about 1 cm long. One sucker is visible at the tip of the cone and the other at the base. The larval stages are less than 5.0 mm, fresh specimens having a pink colour. * **Microscopic**: The egg resembles that of *F. hepatica* being large and operculate, but is clear rather than yellow. ## *Paramphistomum* Life Cycle * Development in the snail intermediate host is similar to that of *Fasciola* and under favorable conditions (26-30°C) can be completed in four weeks. After ingestion of encysted metacercariae with herbage, development in the final host occurs entirely in the alimentary tract. * Following excystment in the duodenum the young flukes attach and feed there for about six weeks before migrating forward to the forestomachs where they mature. * The prepatent period is between 7 and 10 weeks. ## *Paramphistomum* Species * There are at least 14 specics of which *Paramphistomum cervi* and *P. microbothrium* are the most common. * Distribution: Worldwide. They are of little veterinary significance in Europe and America, but are occasionally the cause of disease in the tropics and subtropics. * Other genera and species: * *Cotylophoron* and *Ceylonocotyle* which are responsible for outbreaks of paramphistomosis in buffalo and cattle in Asia and cattle in Australasia and the southern USA. * *Gastrodiscus* has a high prevalence in the small and large intestine of equines in the tropics and * *Homologaster* in the large intestine of ruminants in some parts of Asia. * Another genus, *Gigantocotyle* occurs in the bile ducts of buffaloes in the Middle and far East. # Family PARAMPHISTOMATIDAE * Adult paramphistomes arc mainly parasitic in the forestomachs of ruminants, although a few species occur in the intestine of ruminants, pigs and horses. * Their shape is not typical of the trematodes, being conical rather than flat. All require a water snail as an intermediate host. There are several genera of which *Paramphistomum* is the most common and wide spread. ## *Paramphistomum* Pathogenesis * Any pathogenic effect is associated with the intestinal phase of the infection. The young flukes are plug feeders and this results in severe erosions of the deuodenal mucosa. * In heavy infections these cause an enteritis characterized by oedema, hemorrhage and ulceration. * At necropsy the young flukes can be seen as clusters of brownish pink parasites attached to the deuodenal mucosa and occasionally jejunum and abomasum. * The adult parasites in forestomachs are well tolerated, even when many thousands are present and feeding on the wall of the rumen or reticulum ## *Paramphistomum* Clinical Signs * In heavy duodenal infections, the most obvious sign is diarrhoea accompanied by anorexia and intense thirst. * Sometimes in cattle, there is rectal haemorrhage following a period of prolonged straining. * Mortality in acute outbreaks can be as high as 90%. ## *Paramphistomum* Epidemiology * Paramphistomosis often depends for its continuous endemicity on permanent water masses, such as lakes and ponds, from which snails are dispersed into previously dry areas by flooding during heavy rains. * Paramphistomes eggs deposited by animals grazing these areas hatch and infect snails. Subsequent production of cercariae often coincides with receding water levels making them accessible to grazing ruminants. * In other areas, the situation is complicated by the ability of the snails to aestivate on dry pastures and become reactivated on the return of rainfall. * A good immunity develops in cattle, and outbreaks are usually confined to young stock. * However, adults continue to harbour low burdens of adult parasites and are important reservoirs of infection for snails. * In contrast, sheep and goats are relatively susceptible throughout their lives. ## *Paramphistomum* Diagnosis * This is based on the clinical signs usually involving young animals in the herd and a history of grazing around snail habitats during a period of dry weather. * Fecal examination is of a little value since the disease occurs during the prepatent period. * Confirmation can be obtained by a postmortem examination and recovery of the small flukes from the duodenum. ## *Paramphistomum* Treatment & Control * Resorantel and oxyclozanide are considered the anthelmintics of choice against both immature and adult rumen flukes in cattle and sheep. * As in *Fasciola* the best control is achieved by providing a piped water supply to troughs and preventing access of the animals to natural water. * Even then snails may gain access to watering troughs and regular application of a molluscicide at source or manual removal of snails may be necessary. # Heterophyes *heterophyes* * Geographical Distribution: Egypt, Palestine, Far East. * Habitat: Small intestines. * **Intermediate Host** * First: Snail. * Second: Fish. * Reservoir Host: Piscivores and birds. * Infective form: Metacercaria. * Mode of Infection: Ingestion. ## *Heterophyes heterophyes* Life Cycle * Adult in Small Intestine * Becomes Adult (7- 8 days) * Ingested by Host * Metacercaria in gills, under scales of Fish - (Mullet *Mugil cephalus*) * Deposited in Brakish Water * Egg in feces (Fully developed) miracidium * Egg Ingested by snail * Snail *Pirenella conica* * Larval stages 21-28 days * Sporocyst-Mother Redia-Daughter Redia-Cercaria ## *Heterophyes heterophyes* Identification * Adult: * Size: 1.0 to 1.7 mm long by 0.3 to 0.7 mm wide (very small). * Shape: Gourd-like. * Color: Grayish. * Intestinal Ceca: Straight. * Centered Acetabulum gonotyl is present * Retractile sucker-like structure. * Armed with hooklets. * Egg: * Size: 30 x 15 μ (small, 12 end to end per HPF), resemble ova of the *Opisthorchis* sp. * Shape: Vaselike. * Color: Yellowish-brown. * Operculum: Present, pronounced. * Content: Miracidium. # ECHINOSTOMES * **Common name**: Spiny fluke. * **Geographical Distribution**: Asia. * **Pathogenesis**: Heavy infections induce catarrhal inflammations; necrosis of mucosa. * **Habitat**: Small intestines. * **Intermediate Host** * First: Snail. * Second: Clam or snail. * **Reservoir Host**: Dogs , cats , rats , and birds. * **Infective Form**: Metacercaria. * **Mode of Infection**: Ingestion.