Taeniasis solium is infection with adult worms that follows ingestion of contaminated pork. Cysticercosis is infection with larvae of Taenia solium from ova in human feces. Adult worms may produce mild GI symptoms or passage of a motile segment in the stool. Symptoms with cysticercosis are usually absent unless larvae invade the CNS, which can cause seizures and various other neurologic signs. Neurocysticercosis may be recognized on brain imaging studies. Less than half of patients with neurocysticercosis have adult T. solium in their intestines and thus eggs or proglottids in their stool. Adult worms can be eradicated with praziquantel. Treatment of symptomatic neurocysticercosis is with corticosteroids, anticonvulsants, and, in some situations, albendazole or praziquantel. Surgery may be required.

Etiology and Pathophysiology

Humans infected with adult T. solium worms are asymptomatic or have mild GI complaints. The presentation, diagnosis, and management are similar to beef tapeworm infection (see above). However, humans may also act as intermediate hosts for T. solium larvae if they ingest T. solium eggs from human excreta. It has also been postulated that if an adult tapeworm is present in the intestine, gravid proglottids may be passed retrograde from the intestine to the stomach, where oncospheres (immature form of the parasite) may hatch and migrate to subcutaneous tissue, muscle, viscera, and CNS.

Cysticercosis is prevalent, and neurocysticercosis is a major cause of epilepsy in Latin America, Africa, Southeast Asia, and Eastern Europe. Infection in the US is most common in immigrants from those areas but has occurred in North Americans who have not traveled abroad; they have apparently been infected through exposure to immigrants harboring adult T. solium.

Symptoms, Signs, and Diagnosis

Viable cysticerci in most organs cause minimal or no tissue reaction, but death of the cysts in the CNS can elicit an intense tissue response. Thus, symptoms often do not appear for years after infection. Infection in the brain may result in severe symptoms, resulting from mass effect and inflammation after degeneration of the cysticercus.

Patients may present with seizures, signs of increased intracranial pressure, hydrocephalus, focal neurologic signs, altered mental status, or aseptic meningitis. Cysticerci may also infect the spinal cord, muscles, subcutaneous tissues, and the eye. Substantial secondary immunity develops after larval infection.

Eggs are present in ≤ 50% of stool samples from patients with cysticercosis. Diagnosis is usually made when CT or MRI is performed to evaluate neurologic symptoms. Scans may show solid nodules, cysts, calcified cysts, ring-enhancing lesions, or hydrocephalus. Enzyme-linked immunosorbent assay (ELISA) and other serologic assays can be performed to identify antibodies, but many infected people are negative. Infection with adult T. solium worms can usually be diagnosed from stool samples.

Treatment

Corticosteroids (prednisone 60 mg po once/day or dexamethasone 6 mg once/day) and anticonvulsants should be administered to patients with symptomatic neurocysticercosis to reduce inflammation and symptoms. The treatment of choice for cerebral cysticercosis is controversial. Not all patients respond to treatment, and not all patients must be treated (cysts may already be dead and calcified, or the inflammatory response to treatment may be worse than the disease). Albendazole 400 mg po bid for 8 to 14 days is the drug of choice; praziquantel 20 to 35 mg/kg po tid for 30 days can also be used. Neither albendazole nor praziquantel should be used in patients with ocular or spinal cord involvement.

Surgery may be necessary for obstructive hydrocephalus (due to intraventricular cysticerci), infection of the 4th ventricle, and spinal and ocular cysticercosis.

Intestinal infection is treated with praziquantel 5 to 10 mg/kg as a single dose to eliminate adult worms.

Last full review/revision November 2005