The class Trematoda (flukes) contains several species that are parasites of humans. The schistosomes (blood flukes) are of special biological and clinical importance and are dealt with elsewhere. More than 50 million people are infected by one or more species of the liver, lung, or intestinal fluke. Only the major liver and intestinal flukes are discussed in this chapter. These are Opisthorchis sinensis (the Chinese liver fluke, previously known as Clonorchis sinensis), Opisthorchis viverrini, Opisthorchis felineus (cat liver fluke), Fasciola hepatica (sheep liver fluke), and Fasciolopsis buski (the giant intestinal fluke).

Infection by these liver and intestinal flukes may produce hepatic, biliary, and intestinal complications that require surgical intervention.

Liver and intestinal flukes have common biological and morphological characteristics. They are digenetic hermaphrodites capable of infecting other mammalian species, which thus enlarges the reservoir of adult flukes from which human infection can occur. Human infection also depends on the epidemiology and abundance of the first intermediate hosts, which are usually freshwater or amphibious snails and of the second intermediate hosts, which are freshwater fish or vegetation.

The adult worm has a thick oval leaf shape with a glycocalyx tegument which may be covered with spines. Underlying the tegument is a layer of muscle fibres, the contraction of which can alter the shape of the fluke or move it along. An anterior or oral sucker leads to the digestive tract. There is also a ventral sucker; both are muscular organs of locomotion and attachment to host tissues. Each worm has male and female genital organs and produces operculated ova that are either self- or cross-fertilized.

The ova are passed in the host's faeces into water. The miracidia hatch either in the water or after being ingested by the snail intermediate host. Within the snail, each miracidium develops through the stages of sporocyst, redia, and daughter redia; the last multiplies asexually into thousands of free swimming cercariae which leave the snail. They reach the second intermediate host, either a freshwater fish or plant, and encyst as the metacercariae, the infective form.

A definitive host becomes infected by ingesting the metacercariae encysted on raw or undercooked fish or vegetables. The metacercariae excyst in the duodenum and advance into the biliary tracts or descend into the jejunum where the juvenile flukes mature within 3 to 5 months and begin oviposition.

Through their oral suckers, liver and intestinal flukes feed on blood, mucus, tissues, and intestinal contents of the host. It is estimated that each Fasciola ingests 0.2 ml of blood daily. The gastrodermal cells of the fluke secrete proteases that degrade globin into peptides and amino acids. Glucose, fructose, amino acids, and other nutrient molecules are directly absorbed by diffusion and active transport through the tegument.

Fasciola hepatica converts succinate to propionate as an energy-yielding process by recycling coenzyme A. The enzymes involved are vitamin B&sub1;&sub2;-dependent. This process may explain in part the tendency of many intestinal helminths to concentrate vitamin B&sub1;&sub2;, to the detriment of their hosts.

The miracidia and cercariae are free swimming larvae with limited life-span; they must locate the intermediate hosts or perish. In order to ensure transmission, their sensory-motor systems are genetically programmed to respond to a complex series of trigger cues specific to each stage of the life-cycle. These include tactic and kinetic responses to light, gravity, vibration, and chemoattractants. Together with high fecundity and chance, such behaviour ensures a high probability of contact between parasites and the intermediate hosts in endemic regions. A better understanding of this phenomenon would provide a more effective avenue for parasite control than would the indiscriminate use of molluscicides.

For the ingested metacercaria, the presence of bile salts and proteolytic enzymes indicates that the duodenum has been reached. Releaser responses vary among the flukes: Opisthorchis spp. find and traverse the sphincter of Oddi into the common bile duct; Fasciola perforates through the duodenum into the peritoneum and then locates and penetrates the liver to reach the bile ducts, while Fasciolopsis moves downstream to the jejunum.

The adult fluke in the bile duct must avoid being flushed out by the tides of bile encountered during the digestive cycles of the host. The ventral suckers of Fasciola hepatica respond to the host's gastrointestinal hormones: neuromuscular activities of the suckers increase to strengthen attachment in response to cholecystokinin (which contracts the gallbladder, relaxes the sphincter of Oddi, and increases bile flow) but relax in response to motilin, which is antagonistic to cholecystokinin. Fasciola hepatica also produces large quantities of proline by using an arginase enzyme system whose activity is four times that of the host and is not subject to end-product inhibition. Intraperitoneal infusion of proline in rats causes bile duct hyperplasia similar to that observed in the early phase of biliary fascioliasis. Thus, if proline has the same effect on the bile ducts of ruminants and humans, its synthesis would be a factor in pathogenesis.

The presence of the fluke causes an immune response which is multifactorial and differs according to the maturity of the fluke, the phase and site of infection, and host genetic factors. The outcome depends in part on the fluke's capacity for evasive action. Experiments with the metacercariae of Fasciola hepatica suggest that the dog and cat may have a natural resistance, whereas the sheep and goat have low or no resistance. Clinically, humans seem to occupy an intermediate position, showing some resistance to Fasciola. Most of the migrating juvenile flukes become trapped in the liver parenchyma and die without reaching the bile duct. In a few patients, the tissue reaction is of sufficient magnitude to eliminate all invading flukes, resulting in spontaneous cure, but the mechanism is not clear.

The tegument of the juvenile fluke is enveloped in a secreted glycocalyx that bears unique antigens and is continually replaced during the migration through the intestinal wall, peritoneum, and liver parenchyma. It is finally discarded only after the fluke enters the bile duct, where the overall concentration of immunoglublins is much lower than in serum. As a result of the antigenic changes of the glycocalyx, neither specific antibody plus complement, nor antibody-mediated eosinophil adherence is apparently able to damage the fluke's tegument. Thus, glycocalyx replacement appears to be a mechanism of evading antibody-mediated attack. In addition, excretory and secretory products of the adult fluke are toxic to lymphoid cells in vitro and prevent antibody-mediated adherence of peritoneal cells to juvenile flukes. A similar phenomenon in vivo would protect against any cell-based immune attack on the fluke. Infection by F. hepatica causes increased serum levels of IgG, IgM, and IgE in man. Total and specific IgE levels show a positive correlation with egg burden, age, clinical features, and the degree of eosinophilia. IgA levels are usually normal.

In animal experiments, calves infected with Schistosoma bovis and sheep infected with Schistosoma mansoni developed significant resistance to Fasciola hepatica. Common antigens have now been reported between S. mansoni and F. hepatica. Therefore, where both trematodes are endemic, some form of heterologous immunity might develop. It is not definitely known whether such a phenomenon occurs in man.

Infection of man with O. viverrini causes increased serum levels of both total and the parasite-specific IgG, IgA, and IgE. Analysis of the antibody levels in the serum and bile of patients with biliary obstruction suggests that the IgG and IgE in bile are derived entirely from the serum. Most of the IgA in bile is also derived from the serum, but IgA also appears to be synthesized locally within the hepatobiliary system. This may occur in response to soluble fluke antigens in the bile and reflects the importance of the IgA antibody in the human hepatobiliary system.

The role of the increased levels of parasite-specific antibodies in protective immunity is not clear. In endemic regions, multiple infections occur in adults during several years of eating infected raw fish. Egg output therefore increases over time, but reaches a plateau in patients older than 20 years and actually declines beyond the age of 50. The decline may be the consequence of parasite-associated mortality, but is more likely to reflect the slow development of concomitant immunity, whereby after several years of repeated infections, the host harbours a population of adult flukes and becomes relatively resistant to fresh infections.

The term Opisthorchiasis encompasses infection by all three Opisthorchis species, including infection by O. sinensis, (also known as Clonorchiasis).

The life cycle of the three Opisthorchius species and the various disease syndromes they cause in humans are very similar. In many endemic regions, fish are raised in ponds where human and animal faeces are used as fertilizers. The prevalence of human infection with O. sinensis may be as high as 70 per cent in parts of southern China and Hong Kong. Neither the snail nor fish intermediate hosts are indigenous to Hong Kong but infected fish are imported from China daily for local consumption. In Korea, men eat raw fish at all-male parties and so are more often infected than women. In north-east Thailand, the prevalence of O. viverrini among snails is 1 per cent, but may reach 100 per cent in certain cyprinoid fish. In some locations 90 per cent of human adults are infected. In all endemic regions, infections begin in childhood but clinical disease usually becomes apparent during the third decade or later.

The metacercariae are ingested in a variety of raw fish preparations such as yue-shan and yue-shan chuk in China and Hong Kong, sashimi, sushi, and sunomono in Japan, and koi pla in Thailand. After excysting in the duodenum, the metacercariae travel through the ampulla of Vater into the common bile duct. There is no tissue-invasive phase. The juvenile flukes have narrow bodies and are thus able to swim far proximally within the intrahepatic ducts, where sexual maturation and oviposition occurs. Grossly dilated ducts may thus become visible just beneath Glisson's capsule. In massive infections, even the common bile duct and gallbladder and pancreatic ducts are filled with flukes.

Visitors to endemic regions who become infected with several metacercariae may develop acute symptoms similar to the Katayama fever of schistosomiasis, which may last 2 to 4 weeks. The syndrome comprises irregular high fever, painful hepatomegaly, anorexia, flatulence, and diarrhoea. There may be lymphadenopathy, leucocytosis, and eosinophilia. This syndrome is not common in residents of the region, who become symptomatic only after several years of accumulated infections.

The flukes may live up to 30 years in the bile ducts. They cause chronic irritation and injury to ductal epithelium by the mechanical activities of the suckers and by body movements, by the production of toxic metabolic products, by the immune reaction of the host, and by secondary bacterial infection. The extent of ductal injury is related to the number of flukes present and the duration of infection. Up to 20 000 flukes have been recovered from one patient.

Early changes include excessive mucin production, desquamation, inflammatory granulation, and repair with fibrosis and epithelial hyperplasia. Later, localized strictures and dilations of intrahepatic bile ducts lead to clubbing or cysts containing white bile or mucus. In late cases these sacs may coalesce into large multilocular or unilocular cysts of the liver. The wall is formed by the distended bile duct, with marked epithelial adenomatous hyperplasia.

Secondary infection with bacilli such as E. coli, which possess &bgr;-glucuronidase, causes deconjugation of bilirubin diglucuronide and the formation of calcium bilirubinate stones, with the ova and fragments of dead flukes as the nidus. The presence of bile duct strictures, bacterial infection, and gallstones is conducive to the development of recurrent pyogenic cholangitis. Such attacks may occur in infected persons even years after emigration to non-endemic regions of the world. Recurrent pyogenic cholangitis may lead to biliary cirrhosis, liver impairment, portal hypertension, or to fatal septicaemia. Other pathological changes of the liver reported in complicated opisthorchiasis, especially O. sinensis infection, are listed in Table 3 662. Chronic recurrent infections of the pancreatic duct are associated with periductal fibrosis, ductal dilatation, and foci of mucinous and squamous metaplasia.

Typhoid infection in a patient with chronic clonorchiasis often leads to the establishment of the Salmonella carrier state. The bacilli adhere to the surface of the fluke and replicate, and Salmonella is shed in the patient's bile and faeces, producing a source of virulent infection in the community.

The gravest complication of opisthorchiasis, well documented in infection with O. sinensis and O. viverrini, is mucin-secreting cholangiocarcinoma, which may be a terminal event. Areas endemic for opisthorchiasis consistently report a higher prevalence of cholangiocarcinoma and younger patients than non-endemic areas. Opisthorchis infections are more prevalent in patients with cholangiocarcinoma than in those without. The exact mechanism of carcinogenesis is unknown but in hamsters, experimental infection with O. viverrini acts as a promoter of bile duct carcinoma initiated by N-nitrosodimethylamine. Adenomatous hyperplasia and goblet cell metaplasia that occur in human infection may make the bile ducts more susceptible to otherwise subcarcinogenic doses of N-nitroso compounds and their precursors, derived either endogenously from macrophages activated by chronic fluke infections or exogenously from traditionally preserved foodstuffs such as salted fish, dried shrimp, or cured pork. In north-east Thailand, where O. viverrini infection is endemic, a combination of the tumour markers CA125 and CA19 - 9 was shown to be potentially useful in the early detection of cholangiocarcinoma in a population at very high risk for the tumour.

The majority of infected persons living in endemic areas have no symptoms. Moderate infection is associated with non-specific symptoms such as malaise, anorexia, flatulence, diarrhoea, and occasional biliary colic. Heavy infections due to several thousands of flukes in the bile ducts cause right upper quadrant pain, fever, tender hepatomegaly, and leucocytosis. Complications of the infection produce clinical syndromes similar to those occurring in similar non-parasitic conditions. Thus, in endemic areas, acute cholecystitis, pancreatitis, liver abscess, and pyogenic cholangitis must be suspected to be due to flukes. The differential diagnosis of obstructive jaundice and of hepatomegaly must include, for instance, recurrent pyogenic cholangitis in a febrile patient or cholangiocarcinoma in a non-febrile patient. Tender hepatomegaly without jaundice may result from large liver cysts or cholangiocarcinoma. Other possibilities should be given due consideration in compatible clinical settings.

In the Orient, the diagnosis of infection by liver flukes is usually suspected in all young adults presenting with a compatible clinical syndrome. The definitive diagnosis is made by the identification of ova or adult flukes. Ova may be found in the faeces, as may dead flukes after antihelminthic treatment. Both ova and adult flukes may be recovered in bile obtained by duodenal aspirate, endoscopic retrograde cholangiopancreatography, percutaneous transphepatic cholangiography, during common bile duct exploration, or at autopsy. Differentiation between the various Opisthorchis species is based on geographical location, characteristics of ova, and fluke morphology.

Immunological techniques for diagnosis based on complement fixation and enzyme-linked immunosorbent assays have been developed but are not generally available. New methods for diagnosis based on the detection of parasite DNA and antigens in faeces by dot-blot hybridization techniques are now being developed.

Abdominal ultrasonography and CT scan usually show dilated intrahepatic bile ducts without dilatation of the extrahepatic bile ducts. Sonograms may identify adult flukes as fusiform, weakly echogenic, non-shadowing casts which may be mobile, especially in the gallbladder. Both studies show dilated bile ducts filled with stones in patients with recurrent pyogenic cholangitis. Both identify cystic or solid masses in the liver such as cysts, abscesses, and tumours, and also show lobar atrophy. Endoscopic retrograde cholangiopancreatography shows dilated intrahepatic bile ducts and wavy filamentous filling defects, representing the flukes. Ductal irregularities due to epithelial proliferation are also shown, as are strictures and stones in those with recurrent pyogenic cholangitis. When endoscopic retrograde cholangiopancreatography is not possible, transhepatic cholangiography may provide similar information.

Hepatic arteriography is useful when a liver resection is planned. Cholangiocarcinoma is relatively avascular with encasement or displacement of the arteries, whereas hepatocellular carcinoma, which is also common in the Orient, shows florid vascularization.

All persons diagnosed as having opisthorchiasis should be treated since chronic infection, even of low intensity and asymptomatic, has the potential for serious complications such as recurrent pyogenic cholangitis and cholangiocarcinoma. The current drug of choice is praziquantel.

Patients with surgical and other complications, such as cholecystitis, cholangitis, and pancreatitis should be managed by standard surgical and endoscopic techniques. Endoscopic retrograde cholangiopancreatography and sphincterotomy may be adequate to extract the flukes, stones, and ova. Balloon dilatation of strictures may be attempted after sphincterotomy. Other patients may require cholecystectomy, common bile duct exploration, and evacuation of flukes and stones, followed by T-tube drainage.

Liver abscesses and liver cysts may be adequately treated by ultrasound-guided tube drainage. However, in the recent report of a Russian series, 17 of 34 patients had cysts of 5 cm diameter or greater and were operated upon either by excision of cyst wall and omentoplasty or by liver resection. The results were satisfactory over a period of 2 to 11 years. Liver resections and bilioenteric reconstructions may be appropriate in patients with complicated recurrent pyogenic cholangitis, and in well-selected candidates, liver resections may also be feasible for cholangiocarcinoma.

Attempts to control trematode infections by the control of the intermediate snail hosts have been generally unsuccessful. The new approach is to regard the control of food-borne parasitic zoonoses as a food-safety issue involving both a change in lifestyle and improved food technology. Thus, an innovative programme for the control of O. viverrini in Thailand is based on the combination of educating the community at large about the dangers of eating raw fish and treating all infected persons with praziquantel. Praziquantel is effective in killing the flukes, and probably decreases the susceptibility to cancer formation, but is unlikely to affect the course of already initiated carcinogenesis.

Human infection by the sheep liver fluke occurs mainly in temperate and subtropical countries with large sheep and cattle populations, among which infections are more common than in people. Clinical cases have been reported from more than 40 countries in the past two decades. In a collective review of 2594 persons with fascioliasis, more than half were reported from France, Portugal, Spain, Great Britain, and Tadjikistan. Other reports came from Cuba, Peru, Algeria, Egypt, and Australia. However, the total number of infected persons is unknown because light infections cause no symptoms.

Human infection is usually acquired by ingesting the metacercariae encysted on watercress prepared as a green salad. After excysting in the duodenum, the metacercariae burrow through the wall into the peritoneal cavity and travel along the parietes to the liver. They penetrate Glisson's capsule and eat through the parenchyma to enter the bile ducts where they attach with the suckers. This invasive phase takes 5 to 6 weeks. Maturation to adulthood occurs in the hepatic ducts, common bile ducts, and the gallbladder, where the adult fluke is confined at these sites by its relatively large body size (Table 1) 660. Oviposition begins 3 months after infection.

Some metacercariae develop in the peritoneal cavity, abdominal wall muscles, or subcutaneous fat, while others enter the blood circulation and are transported to widespread ectopic foci. In sheep, about 600 metacercariae invading the liver cause massive destruction known as ‘liver rot’ which is sufficient to kill the animal.

The development of symptoms depends on the number of metacercariae that have perforated the intestine to reach the liver, the number that eventually mature in the bile ducts and elsewhere, and the duration of infection.

Two weeks after infection, during the attack on Glisson's capsule by several metacercariae, subcapsular haematoma and haemoperitoneum may occur; in severe infestation this results in haemorrhagic shock requiring emergency laparotomy. There are patchy haemorrhages with hepatocyte necrosis, abscesses, and debris along the tracts, followed by reparative processes such as granulation tissue, regeneration, and fibrosis.

The patient complains of headache, anorexia, nausea and vomiting, pruritus, right hypochondrial pain, and high fever. There is tender hepatomegaly, urticaria, and marked eosinophilia. This may persist for 3 or 4 months.

Because of the size of the adult fluke in relation to the bile ducts, even light infections may sometimes cause transient biliary colic. Adult flukes attached to the ducts may eat through the wall into the parenchyma and vasculature, causing haemobilia. This manifests as haematemesis and melaena associated with epigastric pain, obstructive jaundice, and anaemia. Otherwise, a normocytic, hypochromic anaemia with eosinophilic bone marrow hyperplasia is more typical.

In heavy infections, mechanical irritation by the suckers and injury by the spines on the fluke's body, combined with fluke metabolites such as proline, cause inflammation, hyperplasia, and desquamation of ductal epithelium. Together with fibrosis, these changes lead to thickening and dilatation mainly of the extrahepatic bile ducts. The gallbladder is enlarged and oedematous with thickened walls and contains multiple small stones, with or without blood clots and fibrin plugs. Secondary bacterial infections result in acute cholecystitis or empyema, choledocholithiasis, and cholangitis. At this stage the patient presents with right upper quadrant pain and obstructive jaundice, fever, and chills. There is tender hepatomegaly, eosinophilia, and liver function tests are abnormal. On account of the longevity of the fluke, episodic attacks of cholangitis may occur.

Occasionally, fascioliasis causes acute pancreatitis, which may also be recurrent. This has been ascribed to the blockage of the pancreatic duct at the ampulla of Vater by either the ova or dead adult flukes from the common bile duct. The patient complains of recurrent epigastric pain radiating to the back. Serum amylase levels are usually elevated.

During the acute invasive phase, some metacercariae fail to reach the liver. In an outbreak of acute invasive fascioliasis in the United Kingdom in 1970, only 20 (71 per cent) of the 28 patients subsequently passed eggs in their faeces, indicating that many flukes perished in other tissues without reaching the bile ducts.

Ectopic fascioliasis frequently manifests as painful migratory subcutaneous nodules, which may be mistaken for infected sebaceous cysts. Excision and microscopic examination shows a fluke trapped in a zone of intense eosinophilic reaction surrounded by haemorrhage, fat necrosis, and some of its own ova. Such lesions have been found in the stomach, caecum, appendix, pancreas, spleen, orbit, brain, heart, lungs, pleura, and the epididymis.

A syndrome comprising oedema and bleeding of the pharynx with acute odynophagia and laryngeal obstruction known as ‘halzoun’ in Lebanon and ‘marrara’ in the Sudan was formerly thought to be caused by the ingestion of juvenile fasciola flukes in the raw liver of sheep or goat. The syndrome is now considered to be more likely due to the nymphs of the pentostomid, linguatula serrata (tongue worm), or to leeches such as Limnatis nilotica.

The definitive diagnosis of fascioliasis depends on the identification of the eggs in faeces or duodenal aspirates. Dead flukes expelled after antihelminthic therapy or live flukes recovered during endoscopic retrograde cholangiopancreatography and sphincterotomy or during common bile duct exploration, can also be identified.

During the invasive phase before oviposition and in ectopic fascioliasis, serological tests such as indirect haemagglutination, complement fixation, and countercurrent immunoelectrophoresis tests are quite useful, but they show cross-reactivity with other trematodes. The enzyme-linked immunosorbent assay may be more specific. Abdominal ultrasound and CT scans can detect subcapsular haematoma and often show hypodense lesions during liver invasion. CT may also show tortous linear peripheral lesions. During the chronic biliary phase, ultrasound shows extrahepatic bile duct dilatation with irregular wall thickening. Live flukes appear as oval mobile bodies without acoustic shadowing, especially in the gallbladder. Endoscopic retrograde cholangiopancreatography (ERCP) performed to relieve cholangitis usually shows bile duct dilatation with linear crescent-shaped defects in the common bile duct. Liver biopsy sometimes demonstrates the fluke within the parenchyma.

During the acute invasive phase, differential diagnosis includes other causes of fever and tender hepatomegaly such as viral hepatitis and amoebic or pyogenic liver abscess. The combination of hepatomegaly, eosinophilia, and elevated serum alkaline phosphatase, and a positive serological test should suggest the correct diagnosis in a patient who gives the history of recent consumption of watercress salad.

The syndrome of acute abdominal pain with haemoperitoneum and shock is a surgical emergency requiring laparotomy. At laparotomy, subcapsular haematoma with multiple haemorrhagic points in the liver are clues to the diagnosis. Metacercariae may be identified in the haemoperitoneum. During the chronic biliary phase, cholecystitis and cholangitis often require laparotomy and the diagnosis of fascioliasis may first be made during the operation. Ectopic fascioliasis is often diagnosed only after excision and histological examination.

The definitive treatment of uncomplicated acute fascioliasis is by means of specific antihelminthics. Bithionol is currently the drug of choice. In a recent Egyptian series, a cure rate of 100 per cent was recorded in 14 adults with acute fascioliasis treated with bithionol. Praziquantel is not effective against Fasciola hepatica.

In complicated fascioliasis, abdominal emergencies such as haemoperitoneum and hypovolaemic shock, haemobilia, and cholangitis require a standard surgical approach, including resuscitation with intravenous fluids and blood transfusion, antibiotics, nasogastric tube suction and irrigation, followed by a laparotomy. The procedures indicated may include cholecystectomy with common bile duct exploration and removal of obstructing flukes. When the diagnosis of haemobilia has been confirmed by hepatic arteriogram, selective catheter embolization may suffice, failing which a liver resection may be required.

Infection with Fasciola is of low overall prevalence. Although cholangitis may result from obstruction of the common bile duct by the large flukes, recurrent pyogenic cholangitis is not associated with infection by this fluke; chronic fascioliasis, unlike chronic opisthorchiasis, is not associated with cholangiocarcinoma. Death due to fascioliasis is uncommon. However, fatalities do occur among patients who sustain massive haemobilia and in those with severe liver damage.

Human infection by the giant intestinal fluke, fasciolopsiasis, is most common in regions where both the domestic pig and water plants are cultivated, as in eastern China and Thailand. The dog serves as a reservoir in Bangladesh. Ova in the faeces of infected dogs, pigs, and humans wash into the ponds. The miracidia hatch and attack planorbid snails. The cercariae emerging from the snails encyst on the stems, leaves and pods of water plants such as water-caltrop, -chestnut, -bamboo, -cress, and -morning glory. When pigs or people, especially children, ingest the raw vegetables, the metacercariae excyst and attach themselves to the duodenal or jejunal mucosa and develop into adult worms in about 90 days, when oviposition begins.

The suckers cause local inflammation, ulceration, bleeding, and abscess formation. A few worms cause no symptoms. When hundreds or thousands are present, some spread up into the stomach and others down into the ileum and colon. They cause epigastric pain similar to that of duodenal ulcer. There is also profuse mucous diarrhoea containing undigested food.

Children with large worm burdens may become toxic from absorption of fluke metabolites. Hypoalbuminaemia results from malabsorption and possible protein-losing enteropathy resulting in oedema and ascites. Vitamin B&sub1;&sub2; deficiency has been noted occasionally.

On account of its relatively large size, attachment of several worms within a short segment of bowel may cause partial or complete intestinal obstruction, which may be fatal if unrelieved. In endemic regions the differential diagnosis of intestinal obstruction always includes fasciolopsiasis.

The large eggs are easy to identify in the stool. An adult worm may occasionally be expelled in the stool. Duodenal aspirate may recover both ova and fluke. Uncomplicated fasciolopsiasis is treated with praziquantel 25 mg/kg body weight orally, three doses in 1 day.

When intestinal obstruction is present, a nasogastric tube is inserted and intravenous fluid replacement is begun. Praziquantel is given through the nasogastric tube. The drug paralyses the flukes and loosens their attachments to the bowel wall. They are carried into the colon and the obstruction is relieved.

Rarely, surgical relief may be required. Resuscitation is begun and praziquantel is given via the nasogastric tube. During laparotomy, the drug is milked down to the location of the flukes. Subsequently the worms can be massaged into the colon, failing which enterotomy and extraction of the worms is required.

Control of Fasciola hepatica and Fasciolopsis buski

The use of lavatories and of chemical fertilizers, together with modern techniques of livestock management, is likely to break the transmission of the parasites. Human infection can also be avoided by proper cleansing and cooking of water plants and their products before eating them.

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