The cestode (tapeworm) Taenia solium (pork tapeworm) is the main cause of human cysticercosis. In addition, the larval stage of other Taenia species (e.g., multiceps, serialis, brauni, taeniaeformis, crassiceps) can infect humans in various sites of localization including the brain, subcutaneous tissue, eye, or liver.
Cysticercosis is an infection of both humans and pigs with the larval stages of the parasitic cestode, Taenia solium. This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier . Pigs and humans become infected by ingesting eggs or gravid proglottids . Humans are infected either by ingestion of food contaminated with feces, or by autoinfection. In the latter case, a human infected with adult T. solium can ingest eggs produced by that tapeworm, either through fecal contamination or, possibly, from proglottids carried into the stomach by reverse peristalsis. Once eggs are ingested, oncospheres hatch in the intestine , invade the intestinal wall, and migrate to striated muscles, as well as the brain, liver, and other tissues, where they develop into cysticerci. In humans, cysts can cause serious sequellae if they localize in the brain, resulting in neurocysticercosis. The parasite life cycle is completed, resulting in human tapeworm infection, when humans ingest undercooked pork containing cysticerci . Cysts evaginate and attach to the small intestine by their scolex . Adult tapeworms develop, (up to 2 to 7 m in length and produce less than 1000 proglottids, each with approximately 50,000 eggs) and reside in the small intestine for years .
Taenia solium is found worldwide. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Taeniasis and cysticercosis are very rare in Muslim countries. It is important to note that human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human T. solium tapeworm carrier, and thus can occur in populations that neither eat pork nor share environments with pigs.
The symptoms of cysticercosis are caused by the development of cysticerci in various sites. Of greatest concern is cerebral cysticercosis (or neurocysticercosis), which can cause diverse manifestations including seizures, mental disturbances, focal neurologic deficits, and signs of space-occupying intracerebral lesions. Death can occur suddenly. Extracerebral cysticercosis can cause ocular, cardiac, or spinal lesions with associated symptoms. Asymptomatic subcutaneous nodules and calcified intramuscular nodules can be encountered.
The definitive diagnosis consists of demonstrating the cysticercus in the tissue involved. Demonstration of Taenia solium eggs and proglottids in the feces diagnoses taeniasis and not cysticercosis. While suggestive, it does not necessarily prove that cysticercosis is present. Persons who are found to have eggs or proglottids in their feces should be evaluated serologically since autoinfection, resulting in cysticercosis, can occur.
Antibody detection provides a useful adjunct in specific diagnosis.
Infections are generally treated with antiparasitic drugs in combination with antiinflammatory drugs. Surgery is sometimes necessary to treat infection in the eyes, cases that are not responsive to drug treatment, or to reduce brain edema. Not all cases of cysticercosis are treated and the use of albendazole and praziquantel is controversial.