Merck Manual: Trematode (Fluke) Infections

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Merck Manual

 

 

Trematode (Fluke) Infections

 

Schistosomiasis is by far the most important trematode infection.

About 500 million people are at risk of infection, which is spreading

as new dams are built in endemic areas. However, numerous trematodes

other than schistosomes parasitize humans and readily infect travelers

to endemic areas. Because the adults of these other trematodes are

hermaphroditic (in contrast to schistosomes), infections are generally

long-lasting. Only the early stages of larval development occur in

snails and other mollusks; the infectious larval stages develop in

fish or crustaceans or on aquatic vegetation, which must be ingested

to cause infection.

SCHISTOSOMIASIS

(Bilharziasis)

 

Infection with blood flukes of the genus Schistosoma, which may cause

chronic disease of the intestine, liver, and GU tract.

Etiology and Pathogenesis

 

Adult worms live and copulate within the veins of the mesentery or the

bladder. Some eggs penetrate the intestinal or bladder mucosa and are

passed in feces or urine. Eggs hatch in fresh water, liberating

miracidia that multiply in snails and produce thousands of cercariae.

These penetrate human skin within a few minutes after exposure and

transform into schistosomula. Schistosomula develop into sexually

active adult worms in the intestinal veins or in the venous plexus of

the GU tract, depending on the species. Eggs appear in the feces or

urine 1 to 3 mo after cercarial penetration. Estimates of the adult

worm life span range from 3 to 37 yr.

 

S. haematobium affects primarily the GU system and is widely

distributed over the African continent; smaller foci are present in

the Middle East and India. S. mansoni is widespread in Africa and is

the only species in the Western Hemisphere (in Brazil, Surinam,

Venezuela, and on some Caribbean islands). S. japonicum is present

only in Asia, mainly in China and the Philippines. S. mekongi causes

intestinal schistosomiasis in Laos and Cambodia; S. intercalatum in

Central Africa. Transmission of schistosomiasis cannot occur within

the USA and Canada because the snails that act as intermediary hosts

are absent. However, the disease may be present in travelers and

immigrants from endemic areas.

Symptoms and Signs

 

Schistosome dermatitis may occur in previously sensitized persons,

causing a pruritic papular rash where the cercariae penetrated the

skin (see also Dermatitis Caused by Animal Schistosomes, below). Acute

schistosomiasis (Katayama fever) may occur 2 to 4 wk after heavy

exposure. Manifestations of acute schistosomiasis are more common and

usually more severe in visitors than in native residents of endemic

areas. Symptoms include fever, chills, nausea, abdominal pain,

malaise, myalgia, urticarial rashes, and marked eosinophilia.

Occasionally, eggs lodge aberrantly in the CNS and cause transverse

myelitis or seizures.

 

Chronic schistosomiasis results mostly from host responses to eggs

retained in tissues. Early on, abscesses in the intestinal mucosa

caused by S. mansoni or S. japonicum may ulcerate and produce bloody

diarrhea; as the lesions progress, focal fibrosis, strictures,

fistulas, and papillomatous growths may develop. With S. haematobium,

ulcerations in the bladder wall may cause dysuria, hematuria, and

frequency. Over time, chronic cystitis develops; strictures may lead

to hydroureter and hydronephrosis; papillomatous masses in the bladder

are common and may become malignant; and secondary bacterial infection

of the GU tract and persistent Salmonella septicemia are common.

 

Granulomatous reactions to eggs of S. mansoni and S. japonicum in the

liver produce a diffuse nodular periportal cirrhosis (pipestem

fibrosis). Liver cell function usually is not seriously compromised,

but damage to the circulation results in sometimes severe portal

hypertension. Hematemesis is common and can be fatal. Portal

hypertension also shunts the eggs to the lungs, where they produce

focal obliterative arteritis and granulomas, which may cause pulmonary

hypertension and cor pulmonale.

Diagnosis

 

Eggs are found in the stool (S. japonicum, S. mansoni, S. mekongi, S.

intercalatum) or urine (S. haematobium), but repeated stool

examinations using concentration techniques may be necessary.

Prognosis and therapy differ with the species. If the clinical picture

is compatible with schistosomiasis but no eggs are found on repeated

examination of urine or feces, the intestinal or bladder mucosa should

be biopsied for eggs.

 

Serologic tests are highly sensitive and specific. Serum levels of

antigen can be used to assess worm burdens and monitor treatment

efficacy. MRI or ultrasonography may detect periportal fibrosis and

calcified eggs in the liver, the intestinal wall, or the bladder and

ureter.

Prevention and Treatment

 

Scrupulously avoiding contact with contaminated water prevents

infection. Adult residents of endemic areas are more resistant to

reinfection than children, suggesting the possibility of acquired

immunity. Vaccine development is under way.

 

Currently three drugs are used for treatment. Single-day oral

treatment with praziquantel (20 mg/kg bid for S. haematobium and S.

mansoni; 20 mg/kg tid for S. japonicum and S. mekongi) is recommended.

However, it does not affect developing schistosomula and thus may not

abort an early infection. Side effects are generally mild and include

some abdominal pain, diarrhea, headache, and dizziness. A

drug-resistant strain has developed. Oxamniquine is effective only

against S. mansoni. African strains are more resistant to this drug

than South American strains and require larger doses (30 mg/kg/day po

for 1 or 2 days vs. 15 mg/kg once). Oxamniquine-resistant cases have

been observed. Metrifonate is useful only for S. haematobium. It is

widely used in endemic areas because of low cost. Metrifonate is given

in 3 doses, each 2 wk apart. Certain antiparasitic drugs may have

limited availability; manufacturers can be contacted to locate local

suppliers.

 

Patients should be examined for living eggs 3 and 6 mo after

treatment. Retreatment is indicated if egg excretion has not decreased

markedly. Antigen-detection tests may supplant quantitative egg counts

as tools to monitor chemotherapy.

DERMATITIS CAUSED BY ANIMAL SCHISTOSOMES

(Swimmers' Itch; Clam Diggers' Itch)

 

Cercariae of some animal parasites can penetrate the skin. Although

the cercariae do not develop in humans, humans become sensitized and

may develop pruritic maculopapular skin lesions at the site of repeat

penetration. Skin lesions may be accompanied by a systemic febrile

response that runs for 5 to 7 days and resolves spontaneously.

 

Saltwater schistosome dermatitis (clam diggers' itch) is found on all

Atlantic, Gulf, Pacific, and Hawaiian coasts. It is very common in

muddy flats off Cape Cod. Freshwater schistosome dermatitis (swimmers'

itch) is common in lakes of northern Michigan, Wisconsin, and Minnesota.

PARAGONIMIASIS

(Oriental Lung Fluke; Endemic Hemoptysis)

 

Infection with Paragonimus westermani and related species, which may

cause lung disease mimicking tuberculosis.

Etiology and Pathogenesis

 

P. westermani is the main cause. Eggs passed in sputum or in feces

develop for 2 to 3 wk in fresh water before miracidia hatch. The

miracidia invade snails; larvae develop and multiply and eventually

emerge as cercariae. Cercariae penetrate crabs or crayfish and encyst

to form metacercariae. Humans become infected by eating raw, pickled,

or poorly cooked crustaceans. The metacercariae excyst in the

digestive tract, penetrate the intestinal wall into the peritoneum,

migrate to and through the diaphragm into the pleural cavity, enter

lung tissue, encyst, and develop into hermaphroditic adult worms.

Worms may also develop in the brain, liver, lymph nodes, skin, and

spinal cord. Adults may persist for 20 to 25 yr.

 

The most important endemic areas are in the Far East, principally

Korea, Japan, Taiwan, the highlands of China, and the Philippines.

Endemic foci also exist in West Africa and in parts of South and

Central America.

Symptoms and Signs

 

In light infections, most damage is to the lungs. Heavier infections

usually involve other organs; about 25 to 45% of all extrapulmonary

infections affect the CNS. Manifestations of pulmonary infection

develop slowly and include dyspnea, chronic cough, chest pain, and

hemoptysis. X-rays may show a diffuse infiltrate, nodules and annular

opacities, cavitations, lung abscesses, pleural effusion, and

pneumothorax. The clinical picture resembles and is often confused

with TB. Cerebral infections mimic and present as a space-occupying

tumor, often within a year after the onset of pulmonary disease.

Seizures, aphasia, paresis, and visual disturbances are common.

Migratory allergic skin lesions similar to those of cutaneous larva

migrans are common in infections with P. skriabini but also occur with

other species.

Diagnosis

 

Diagnosis is made by identifying the characteristic large operculated

eggs in sputum or feces. Occasionally, eggs may be found in pleural or

peritoneal fluid. Eggs may be difficult to find, because they are

released intermittently and in small numbers. X-rays provide ancillary

information but are not diagnostic. Serodiagnostic tests may assist in

the diagnosis of extrapulmonary infections and help in monitoring

treatment.

Prevention and Treatment

 

The best prevention is to avoid eating raw or undercooked freshwater

crabs and crayfish. Praziquantel (25 mg/kg po tid for 2 days) cures 80

to 100% of pulmonary infections and is the drug of choice. Bithionol

(30 to 50 mg/kg/day po on alternate days for 10 to 15 doses) is

equally effective and cheaper but has more side effects. The same

drugs can be used to treat extrapulmonary infections, but multiple

courses may be required for cure. Surgery may be needed to excise skin

lesions or, rarely, brain cysts.

CLONORCHIASIS

(Oriental Liver Fluke)

 

Infection with Clonorchis sinensis, which may cause chronic liver disease.

Etiology and Pathogenesis

 

The adult worms of C. sinensis live in the bile ducts. Eggs are passed

in the stool, and cercariae released from infected snails infect a

variety of freshwater fish. Humans become infected by eating raw,

dried, salted, or pickled fish containing encysted metacercariae. The

latter are released in the duodenum, enter the common bile duct, and

migrate to smaller intrahepatic ducts (or occasionally the gallbladder

and pancreatic ducts), where they mature into adult worms in about 1

mo. The adults may live >= 20 yr.

 

Clonorchis is endemic in the Far East, especially in Korea, Japan,

Taiwan, and southern China, and is found elsewhere among immigrants

and in fish imported from endemic areas in the Orient.

Symptoms and Signs

 

Light infections are usually asymptomatic. Clinical cases occur mainly

in adults, when the worm load accumulates to > 500. Initial signs

include fever, chills, epigastric pain, tender hepatomegaly, mild

jaundice, and eosinophilia. Later, diarrhea becomes common; chronic

cholangitis may progress to portal fibrosis in heavy infections.

Portal fibrosis may be associated with portal hypertension, cirrhosis,

and atrophy of liver parenchyma. Jaundice is usually caused by biliary

obstruction due to a mass of flukes or stone formation. Other

complications include cholangiocarcinoma, suppurative cholangitis, and

chronic pancreatitis.

Diagnosis

 

Diagnosis is confirmed by finding eggs in the feces or duodenal

contents. The eggs are difficult to distinguish from those of

Metagonimus, Heterophyes, and Opisthorchis. Alkaline phosphatase and

bilirubin levels may be elevated; eosinophilia varies. A plain

abdominal x-ray occasionally shows intrahepatic calcification.

Percutaneous transhepatic cholangiography often shows dilation of

peripheral intrahepatic bile ducts. Adult worms look like round

filling defects. In acute symptomatic disease, liver scan is usually

negative but may show multiple areas of diminished uptake.

Prevention and Treatment

 

Freshwater fish should be thoroughly cooked and not eaten raw,

pickled, or wine-soaked. Praziquantel (25 mg/kg po tid for 2 days) is

highly effective. Biliary obstruction may require surgery.

FASCIOLIASIS

 

Infection with Fasciola hepatica, the liver fluke of sheep and cattle.

 

Human fascioliasis occurs in Europe, Africa, China, and South America

but is rare in the USA. Infection is acquired by eating contaminated

watercress. The adult flukes mature in the bile ducts and cause

biliary tract obstruction and liver damage. Treatment is with

bithionol (30 to 50 mg/kg po on alternate days for 10 to 15 doses).

OPISTHORCHIASIS

 

Infection with Opisthorchis, which resembles clonorchiasis.

 

Two species of Opisthorchis cause human disease, which is acquired by

eating raw or undercooked fish that contains infectious metacercariae.

Opisthorchiasis occurs in Eastern and Central Europe, Siberia, and

parts of Asia, such as Thailand and Cambodia. Treatment is as for

clonorchiasis.

FASCIOLOPSIASIS

 

Infection with the fluke Fasciolopsis buski.

 

F. buski is present in the intestine of pigs in many parts of Asia.

Human infection is acquired by eating plants, such as water chestnuts,

bearing infectious metacercariae. The adult worms attach to and

ulcerate the mucosa of the proximal small intestine, thereby

simulating peptic ulcer disease. Treatment is as for clonorchiasis.