|Scolex of Taenia solium|
Taenia solium, also called the pork tapeworm, is a cyclophyllid cestode in the family Taeniidae. It infects pigs and humans in Asia, Africa, South America, parts of Southern Europe and pockets of North America. In the larval stage, it causes cysticercosis, which is a major cause of seizures in humans. Like all cyclophyllid cestodes, T. solium has four suckers on its scolex ("head"). T. solium also has two rows of three hooks.
T. solium , commonly known as tapeworm, is a triploblastic aceolomate. It is normally 2 to 3 m in length, but can become very large, over 50 m long in some situations.
T. solium has a very similar life cycle to Taenia saginata. Cysticerci have three morphologically distinct types. The common one is the ordinary "cellulose" cysticercus, which has a fluid-filled bladder 0.5 cm to 1.5 cm in length and an invaginated scolex. The intermediate form has a scolex, while the "racemose" has no evident scolex but is believed to be larger and much more dangerous. They are 20 cm in length and have 60 ml of fluid, and 13% of patients might have all three types in the brain. Humans are usually infected through eating infected pork, fostering adult tapeworms in the intestine, and passing eggs through feces, but autoinfection is also possible. In that case, a cysticercus (a larva sometimes called a "bladder worm") develops in the human, who acts as an intermediate host. This happens if eggs get to the stomach, usually as a result of contaminated hands, but also due to retroperistalsis. Cysticerci often occur in the central nervous system, which can cause major neurological problems, such as hydrocephalus, paraplegy, meningitis, convulsions and even death. The condition of having cysticerci in one's body is called cysticercosis.
Eggs can be diagnosed only to the family level, but if a proglottid's uterus is stained with India ink, the number of visible uterine branches can help identify the species; unlike the Taenia saginata uteri, T. solium uteri have only five to 10 uterine branches on each side.
Infection with T. solium adults is treated with niclosamide, which is one of the most popular drugs for adult tapeworm infections, as well as for fluke infections. As cysticercosis is a major risk, it is important to wash one's hands before eating and to suppress vomiting if a patient may be infected with T. solium. If neurocysticercosis occurs, the drug of choice is either albendazole or praziquantel. These drugs damage the parasites' skin internally, causing it to disintegrate and is then removed by the host's immune system.
Infection may be prevented with proper disposal of human feces around pigs, cooking meat thoroughly and/or freezing the meat at −10°C for 5 days. Most cases occur because infected food handlers contaminate the food.
Life cycle 
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 containing eggs, 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 sequelae 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 scolices. 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.
Ingestion of T. solium eggs or proglottid rupture within the host intestine can cause larvae to migrate into host tissue and cause cysticercosis. This is the most frequent and severe disease caused by T. solium. In symptomatic cases, a wide spectrum of symptoms may be expressed, including headaches, dizziness and occasional seizures. In more severe cases, dementia or hypertension can occur due to perturbation of the normal circulation of cerebrospinal fluid. (Any increase in intracranial pressure will result in a corresponding increase in arterial blood pressure, as the body seeks to maintain circulation to the brain.) The severity of cysticercosis depends on location, size and number of parasite larvae in tissues, as well as the host immune response. Other symptoms include sensory deficits, involuntary movements, and brain system dysfunction. In children, ocular location of cysts is more common than cystation in other locations of the body. Heavy infection with T. solium can lead to neurocysticercosis, which can lead to epilepsy, seizures, lesions in the brain, blindness, tumor-like growths, and low eosinophil levels.
Diagnosis requires biopsy of the infected tissue and examination of feces. T. solium eggs and proglottids found in feces diagnoses taeniasis and not cysticercosis. Cysticercosis is diagnosed primarily on confirming the presence of hooks on the scolex of T. solium. Radiological tests, such as X-ray, CT scans which demonstrate "ring-enhancing brain lesions", and MRIs, can also be used to detect diseases. X-rays are used to identify calcified larvae in the subcutaneous and muscle tissues, and CT scans and MRIs are used to find lesions in the brain.
Praziquantel (PZQ) is the drug of choice for the treatment of T. solium infection. Some consider niclosamide to be the drug of choice for all types of tapeworms. For cysticercosis,treatment with albendazole combined with steroids reduces the inflammation. Surgical intervention may be necessary to treat central nervous system lesions. Albendazole appears to be more effective and a safe drug for neurocysticercosis.
Prevention and control 
The best way to avoid getting tapeworms is to not eat undercooked pork. Moreover, a high level of personal hygiene and prevention of fecal contamination of pig foods also plays a major role in prevention.
T. solium is found worldwide, but is more common in cosmopolitan areas. 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. Cysticercosis is often seen in areas where poor hygiene allows for contamination of food, soil or water supplies. Prevalence rates in the United States have shown immigrants from Mexico, Central and South America and Southeast Asia account for most of the domestic cases of cysticercosis. Taeniasis and cysticercosis are very rare in predominantly Muslim countries, as Islam forbids the consumption of pork. Human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human tapeworm carrier via gravid proglottids, so can occur in populations that neither eat pork nor share environments with pigs, although the completion of the life cycle can occur only where humans live in close contact with pigs and eat pork.
In 1990 and 1991, four unrelated members of an Orthodox Jewish community in New York City developed recurrent seizures and brain lesions, which were found to have been caused by T. solium. In keeping with their religion, none of the patients ate pork; additionally, none had any history of recent foreign travel. Several immediate family members of these four patients with seizures were found to have cysticercus antibodies. The families of the four patients had all employed housekeepers from Latin American countries, and one of the housekeepers tested positive for cysticercus antibodies, leading to the conclusion that the housekeepers were the most likely source of the infections.
See also 
- Rabiela, MT; Rivas, A; Flisser, A (November 1989). "Morphological types of Taenia solium cysticerci". Parasitology Today 5 (11): 357–359. doi:10.1016/0169-4758(89)90111-7. PMID 15463154.
- Garcia HH, Pretell EJ, Gilman RH, Martinez SM, Moulton LH, Del Brutto OH, Herrera G, Evans CA, Gonzalez AE, Cysticercosis Working Group in Peru. (2004). "A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis". N Engl J Med. 350 (3): 249–258. doi:10.1056/NEJMoa031294. PMID 14724304.
- Matthaiou DK, Panos G, Adamidi ES, Falagas ME. (2008). "Albendazole versus Praziquantel in the Treatment of Neurocysticercosis: A Meta-analysis of Comparative Trials". In Carabin, Hélène. PLoS Negl Trop Dis. 2 (3): e194. doi:10.1371/journal.pntd.0000194. PMC 2265431. PMID 18335068.
- Flisser A. (May 1988). "Neurocysticercosis in Mexico". Parasitology Today 4 (5): 131–137. doi:10.1016/0169-4758(88)90187-1. PMID 15463066.
- Dworkin, Mark S. (2010). Outbreak Investigations Around the World: Case Studies in Infectious Disease. Jones and Bartlett Publishers. pp. 192–196. ISBN 978-0-7637-5143-2. Retrieved August 9, 2011.
- Schantz, Peter M. et al.; Moore, Anne C.; Muñoz, José L.; Hartman, Barry J.; Schaefer, John A.; Aron, Alan M.; Persaud, Deborah; Sarti, Elsa et al. (September 3, 1992). "Neurocysticercosis in an Orthodox Jewish Community in New York City". New England Journal of Medicine 327 (10): 692–695. doi:10.1056/NEJM199209033271004. Retrieved August 9, 2011.
- Taenia solium Genome Project - UNAM
- Cysticercosis at DPD
- Taeniasis at Stanford
- Taenia solium at Bioweb
- Parasites in Humans