Taeniasis solium is infection with adult Taenia solium worms that follows ingestion of contaminated pork, resulting in intestinal infection. Cysticercosis is infection with larvae of T. solium, which develop from ova excreted with human feces. Adult worms may cause mild GI symptoms or passage of a motile segment in the stool. Cysticercosis is usually asymptomatic unless larvae invade the CNS, resulting in neurocysticercosis, 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.

Presentation, diagnosis, and management of intestinal infection with the adult T. solium tapeworm are similar to those of beef tapeworm infection (see Cestodes (Tapeworms): Taeniasis Saginata). However, humans may also act as intermediate hosts for T. solium larvae if they ingest T. solium eggs from human excreta (see Fig. 1: Cestodes (Tapeworms): Taenia solium life cycle. ). Another theory is 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 enclosed in an embryonic envelope) may hatch and migrate to subcutaneous tissue, muscle, viscera, and the CNS.

Adult tapeworms may reside in the small bowel for years. They may be 2 to 7 m long and produce < 1000 proglottids; each contains about 50,000 eggs.

Fig. 1
Taenia solium life cycle. Humans may develop intestinal infection with adult worms after ingestion of contaminated pork or may develop cysticercosis after ingestion of T. solium eggs (making humans intermediate hosts). 1. Humans ingest raw or undercooked pork containing cysticerci (larvae). 2. After ingestion, cysts evaginate, attach to the small intestine by their scolex, and mature into adult worms in about 2 mo. 3. Adult tapeworms produce proglottids, which become gravid; they detach from the tapeworm and migrate to the anus. 4. Detached proglottids, eggs, or both are passed from the definitive host (human) in feces. 5. Pigs or humans become infected by ingesting embryonated eggs or gravid proglottids (eg, in fecally contaminated food). Autoinfection may occur in humans if proglottids pass from the intestine to the stomach via reverse peristalsis. 6. After eggs are ingested, they hatch in the intestine and release oncospheres, which penetrate the intestinal wall. 7. Oncospheres travel through the bloodstream to striated muscles and to the brain, liver, and other organs, where they develop into cysticerci. Cysticercosis can result.

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

Symptoms and Signs

Humans infected with adult T. solium worms are asymptomatic or have mild GI complaints.

Cysticercosis: Viable cysticerci (larval form) 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 (cerebral cysticercosis) may result in severe symptoms, resulting from mass effect and inflammation induced by degeneration of cysticerci and release of antigens.

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 eyes. Substantial secondary immunity develops after larval infection.

Diagnosis

• Microscopic examination of stool
• Imaging and serologic testing for patients with CNS symptoms

T. solium eggs are present in ≤ 50% of stool samples from patients with cysticercosis. Diagnosis is usually made when CT or MRI is done to evaluate neurologic symptoms. Scans may show solid nodules, cysts, calcified cysts, ring-enhancing lesions, or hydrocephalus. The CDC's (Centers for Disease Control and Prevention's) immunoblot assay (using a serum specimen) is highly specific and more sensitive than other enzyme immunoassays (particularly when > 2 CNS lesions are present; sensitivity is lower when only a single cyst is present). Infection with adult T. solium worms can usually be diagnosed using stool samples.

Treatment

• For intestinal infection: PraziquantelSome Trade Names
  BILTRICIDE
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• For cysticercosis: Corticosteroids, anticonvulsants, and sometimes surgery

Intestinal infection is treated with praziquantelSome Trade Names
BILTRICIDE
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5 to 10 mg/kg po as a single dose to eliminate adult worms.

Corticosteroids (prednisoneSome Trade Names
DELTASONE
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60 mg po once/day or dexamethasoneSome Trade Names
DECADRON
DEXASONE
HEXADROL
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6 mg once/day) and anticonvulsants should be given to patients with symptomatic neurocysticercosis to reduce inflammation and symptoms.

The anthelmintic 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). When anthelmintic treatment is used, albendazoleSome Trade Names
ALBENZA
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400 mg po bid for 8 to 30 days is the drug of choice; praziquantelSome Trade Names
BILTRICIDE
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33.3 mg/kg po tid on day 1 followed by 16.6 mg/kg po tid for 29 days can also be used. Neither albendazoleSome Trade Names
ALBENZA
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nor praziquantelSome Trade Names
BILTRICIDE
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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.

Last full review/revision December 2009 by Richard D. Pearson, MD

Content last modified February 2012