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Taenia Solium (Pork Tapeworm) Infection and Cysticercosis

by Richard D. Pearson, MD

Taenia solium is an intestinal infection with adult tapeworms that follows ingestion of contaminated pork. Cysticercosis is infection with larvae of T. solium, which develops after ingestion of ova excreted in 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. Fewer 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 Taenia Saginata (Beef Tapeworm) Infection). However, humans may also act as intermediate hosts for T. solium larvae if they ingest T. solium eggs from human excreta (see Figure: Taenia solium life cycle. ). Or 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 reach 2 to 7 m in length and produce up to 1000 proglottids; each contains about 50,000 eggs.

Taenia solium life cycle.

Humans 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.

Taeniasis and cysticercosis occur worldwide. Cysticercosis is prevalent, and neurocysticercosis is a major cause of seizure disorders in Latin America. Cysticercosis is rare in Muslim countries. Infection in the US is most common among immigrants, but North Americans who have not traveled abroad have been infected by ingesting ova from immigrants harboring adult T. solium.

Symptoms and Signs

Intestinal infection

Humans infected with adult T. solium worms are asymptomatic or have mild GI complaints. They may see proglottids in their stool.


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 due to mass effect and inflammation induced by degeneration of cysticerci and release of antigens.

Depending on the location and number of cysticerci, 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 for ova and proglottids

  • CT and/or MRI and serologic testing for patients with CNS symptoms

Infection with adult T. solium worms can usually be diagnosed by microscopic examination of stool samples and identification of eggs and/or proglottids. However, T. solium eggs are present in 50% of stool samples from patients with cysticercosis. Cysticercosis is usually diagnosed when CT or MRI is done to evaluate neurologic symptoms. Scans may show solid nodules, cysticerci, 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).

Pearls & Pitfalls

  • T. solium eggs are present in 50% of stool samples from patients with cysticercosis.

Treatment

  • For intestinal infection: Praziquantel or niclosamide (outside the US)

  • For neurocysticercosis: Corticosteroids, anticonvulsants, and sometimes albendazole or praziquantel and/or surgery

Intestinal infection is treated with praziquantel 5 to 10 mg/kg po as a single dose to eliminate adult worms. Praziquantel should be used with caution in patients who also have neurocysticercosis because by killing cysts, praziquantel may trigger an inflammatory response associated with seizures or other symptoms. Alternatively, a single 2-g dose of niclosamide (not available in the US) is given as 4 tablets (500 mg each) that are chewed one at a time and swallowed with a small amount of water. For children, the dose is 50 mg/kg once.

Symptomatic neurocysticercosis is treated with corticosteroids (prednisone 60 mg po once/day or dexamethasone 6 mg po once/day) to reduce inflammation and symptoms and anticonvulsants to prevent seizures.

Anthelmintic treatment of neurocysticercosis is complicated, and consultation with an expert is recommended. Choice of treatment depends on the location, number, and stage of cysticerci, and clinical manifestations. 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, albendazole 400 mg po bid for 8 to 30 days is the drug of choice; praziquantel 33.3 mg/kg po tid on day 1 followed by 16.6 mg/kg po tid for 29 days is an alternative. Either prednisone or dexamethasone is given concurrently with the anthelminthic to reduce the inflammation that occurs in response to dying cysts in the brain. Neither albendazole nor praziquantel should be used in patients with ocular or spinal cord cysticerci.

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

Key Points

  • Ingestion of T. solium cysts may cause intestinal infection; ingestion of eggs may result in tissue cysts (cysticercosis), which are particularly problematic when in the brain.

  • Patients with neurocysticercosis may have seizures, signs of increased intracranial pressure, altered mental status, focal neurologic signs, or aseptic meningitis.

  • Diagnose infection with adult worms by microscopic examination of stool.

  • Diagnose neurocysticercosis by neuroimaging and serologic testing.

  • Give praziquantel for intestinal infection.

  • Consult an expert for neurocysticercosis; typically corticosteroids and anticonvulsants are given, and anthelmintics and/or surgery are sometimes used.

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