Flukes are parasitic flatworms that infect various parts of the body (eg, blood vessels, gastrointestinal tract, lungs, liver) depending on the species.
Although > 30 species of Paragonimus exist and 10 have been reported to infect humans, P. westermani is the most frequent cause of disease.
The most important endemic areas are in the Far East, principally Korea, Japan, Taiwan, the highlands of China, and the Philippines.
Endemic foci with other Paragonimus species exist in West Africa and in parts of South and Central America. P. kellicotti has caused human infection in North America.
Eggs passed in sputum or feces develop for 2 to 3 weeks in freshwater before miracidia (first larval stage) hatch. The miracidia invade snails; there, they develop, multiply, and eventually emerge as cercariae (free-swimming larvae). Cercariae penetrate freshwater crabs or crayfish and encyst to form metacercariae. Humans become infected by eating raw, pickled, or poorly cooked crustaceans. Metacercariae excyst in the human gastrointestinal tract, penetrate the intestinal wall, and move into the peritoneal cavity, then through the diaphragm into the pleural cavity; they enter lung tissue, become encapsulated, and develop into hermaphroditic adult worms, which produce eggs. Adult worms grow to about 7.5 to 12 mm by 4 to 6 mm. From the lungs, eggs exit the body in sputum that is coughed up and spit out or swallowed and passed in stool.
Worms may also reach the brain, liver, lymph nodes, skin, and spinal cord and develop there. However, in these organs, the life cycle cannot be completed because the eggs have no way to exit the body. Adult flukes may persist for 20 to 25 years.
Other hosts include pigs, dogs, and a variety of feline species.
During invasion and migration of the flukes, diarrhea, abdominal pain, fever, cough, urticaria, hepatosplenomegaly, pulmonary abnormalities, and eosinophilia may develop.
During the chronic phase, the lungs are damaged most, but other organs may be involved. Manifestations of pulmonary infection develop slowly and include chronic cough, chest pain, hemoptysis, and dyspnea; the clinical picture resembles and is often confused with tuberculosis.
Cerebral infections manifest as space-occupying lesions, often within a year after the onset of pulmonary disease. Seizures, aphasia, paresis, and visual disturbances occur.
Migratory allergic skin lesions similar to those of cutaneous larva migrans are common in infections with P. skrjabini but also occur with other species.
Diagnosis of paragonimiasis is by identifying the characteristic large operculated eggs in sputum or stool. 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. Concentration techniques increase sensitivity.
Serologic tests to detect antibodies are useful in light infections and in the diagnosis of extrapulmonary paragonimiasis.
X-rays provide ancillary information but are not diagnostic; chest x-rays and CT may show a diffuse infiltrate, nodules, annular ring shadow lesions, cavitations, linear opacities, lung abscesses, pleural effusion, and/or pneumothorax.
Praziquantel 25 mg/kg orally 3 times a day for 2 days is the drug of choice for paragonimiasis.
Triclabendazole is an acceptable treatment in areas where it is available; dosage is 10 mg/kg orally once postprandially or, for severe infections, 2 doses of 10 mg/kg given postprandially 12 hours apart.
Praziquantel is used to treat extrapulmonary infections, but multiple courses may be required.
For cerebral infections, a short course of corticosteroids may be given with praziquantel to reduce the inflammatory response induced by dying flukes.
Surgery may be needed to excise skin lesions or, rarely, brain cysts.
The best prevention is to avoid eating raw or undercooked freshwater crabs and crayfish from endemic waters.
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