The pork tapeworm (T. solium) can cause two distinct forms of infection. The form that develops depends on whether humans are infected with adult tapeworms in the intestine or with larval forms in the tissues (cysticercosis). Humans are the only definitive hosts for T. solium; pigs are the usual intermediate hosts, although dogs, cats, and sheep may harbor the larval forms. The adult tapeworm generally resides in the upper jejunum. Its globular scolex attaches by both sucking disks and two rows of hooklets. The tapeworm, usually about 3 meters in length, may have as many as 1000 proglottids each of which produces up to 50,000 eggs. Groups of 3 to 5 proglottids generally are released and excreted into the feces, and the eggs in these proglottids are infective for both humans and animals. The eggs survive in the environment for several months After ingestion by the intermediate host (pig), eggs embryonate, penetrate the intestinal wall, and are carried to many tissues via systemic circulation, with a predilection for striated muscle of the neck, tongue, and trunk. Within 60 to 90 days, the encysted larval stage develops. These cysticerci can survive for long periods. Humans acquire infections that lead to intestinal tapeworms by ingesting undercooked pork containing cysticerci. Infections that cause human cysticercosis follow the ingestion of T. solium eggs, usually from fecally contaminated food. Autoinfection may occur if an individual with an egg-producing tapeworm ingests eggs derived from his or her own feces or if eggs pass by reflux from the intestine into the stomach. The growing larva in cysticercosis may provoke a series of inflammatory reactions including infiltration of neutrophils and eosinophils, lymphocytes, plasma cells, and at times giant cells, followed by fibrosis and necrosis of capsule with eventual caseation or calcification of the larva.

Intestinal infections with T. solium may be asymptomatic. Epigastric discomfort, nausea, a sensation of hunger, weight loss, and diarrhea are infrequent. Human cysticercosis may be seen in brain, meninges, liver, lungs, orbit and peritoneum, however it is rare in tongue muscle. Clinical symptoms vary according to the site of involvement. Dead cysts in brain can swell, causing surrounding nerve tissue reactions and manifests as space occupying lesions with headache, vomiting and seizures. These may be asymptomatic as in case of tongue or cheek.

The diagnosis of intestinal T. solium infection is made by the detection of eggs or proglottids in stool. For cysticercosis, definitive diagnosis requires examination of the cysticercus in an involved tissue, but a diagnosis often can be based on clinical presentation in conjunction with compatible results in radiographic studies, especially computed tomography (CT) and magnetic resonance imaging (MRI) and serologic tests. For soft tissue involvement, plain films may reveal multiple calcified “puffed-rice” lesions.

The management of cysticercosis can involve chemotherapy, surgery, and supportive medical treatment. Intestinal T. solium infection is treated with praziquantel. Asymptomatic patients with calcified soft tissue or neural lesions generally require no treatment. For symptomatic patients with neurocysticercosis, both praziquantel (50 mg/kg per day in three doses for 15 days) and albendazole (15 mg/kg per day in three doses for 8 to 28 days) are effective. Because both agents provoke inflammatory responses around dying cysticerci, patients receiving either drug should be hospitalized and given high doses of glucocorticoids during treatment. For ocular and spinal lesions, drug-induced inflammation may cause irreversible damage; thus, these lesions as well as those within the ventricles are best managed by surgical resection. Not all neurological deficits resolve after therapy, and some patients may require continued anticonvulsive treatment. Soft tissue lesion if causing problem or looking cosmetically bad should be surgically excised.

The major means of preventing infection is the adequate cooking of pork. The prevention of cysticercosis involves minimizing the opportunities for ingestion of fecally derived eggs by means of good personal hygiene, effective fecal disposal, and treatment and prevention of human intestinal infections.