Cysticercosis (Pork Tapeworm Infection)

Updated: Jun 07, 2023
  • Author: Joseph Adrian L Buensalido, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Cysticercosis is an increasingly common medical problem in the United States, especially in the Southwest and other areas where large populations migrated from endemic areas and among populations that often travel to these areas.

Cysticercosis is a tissue infection with the cysticercus, or larval, stage of Taenia solium (pork tapeworm) that results from ingestion of T solium eggs. The clinical syndromes caused by T solium are categorized as either cysticercosis (cysts in various tissues including the brain) or taeniasis (intestinal tapeworm infection).

Cysticercosis can involve skeletal muscles, subcutaneous tissues, eyes, the central nervous system (CNS), and other tissues. Neurocysticercosis refers to CNS infection with T solium. Neurocysticercosis, which is probably the most common parasitic infestation of the CNS, has gained increased recognition in the last 2 decades because of the development of MRI and CT scanning in the United States and in countries where neuro cysticercosis is endemic.

Neurocysticercosis is further divided into parenchymal and extraparenchymal disease. Parenchymal disease is characterized by infection with cysticerci within the brain parenchyma. Extraparenchymal disease develops when cysticerci migrate to the CSF of the ventricles, cisterns, and subarachnoid space or within the eyes or spinal cord.



When humans ingest undercooked pork that contains cysticerci of T solium, the scolex evaginates from the cyst and develops into an intestinal tapeworm (taeniasis). The tapeworm grows to a length of up to 10 meters and has hundreds of proglottids. Mature proglottids contain approximately 50,000 eggs each. Free eggs or whole proglottids are released periodically into the stool of the carrier and can survive in the environment for many months.

When pigs ingest the proglottids or eggs, the eggs hatch, penetrate the pigs' intestinal wall, and spread to skeletal muscle, especially the neck, tongue, and trunk. There, the larvae mature into encysted cysticerci over 2-3 months. The cysticerci suppress the host inflammatory response and can survive in tissues for months to years. The life cycle is completed when humans ingest inadequately cooked pork that contains viable cysticerci.

This cycle of cysts in pigs and tapeworms in humans can be broken if a human ingests eggs excreted in the feces of a human carrier of the pork tapeworm. Humans are an accidental host of the larval stage and develop cysticercosis similar to that in pigs. These cysticerci have tropism for neural tissue and migrate to the brain, although they can also be found in skeletal muscle. Thus, cysticercosis is a foodborne infection and can be acquired in the absence of pork consumption. [1]

Humans can be infected with eggs through fecal-oral transmission or possibly through autoinfection. Fecal-oral contamination usually occurs via infected food handlers via ingestion of fruit and vegetables fertilized with contaminated human waste. The eggs are sticky and often can be found under the fingers of tapeworm carriers. Thus, even populations who do not eat pork can develop cysticercosis. The egg-containing feces can contaminate water supplies in endemic areas. If the water is used to irrigate fruits and vegetables, eggs are ingested with the contaminated food. Therefore, people who have never visited endemic countries also can develop infection.

Cysticerci are able to survive in the human brain by disarming host defenses. The cysticercus secretes prostaglandins and other compounds (paramyosin, taeniastatin, sulfated polysaccharides) that inhibit or divert complement activation and cytokine production, resulting in only minimal host inflammation around the viable cysticercus. In addition, humoral antibodies do not kill the mature metacestode. Taeniastatin and other poorly defined factors may interfere with lymphocyte proliferation and macrophage function, inhibiting normal cellular immune defenses. The clinical manifestations commonly result when an inflammatory response develops around a degenerating cysticercus after it has died.

Over a period of years, the parasite may lose its ability to control the host defenses. Consequently, an inflammatory response leads to degeneration of the cysticercus. An inflammatory response that occurs in the CNS parenchyma causes seizures typical of parenchymal neurocysticercosis. As the degeneration continues, the parasite becomes encased in a granuloma, which either resolves or leads to scarring and calcification. In rare cases, patients with numerous parenchymal cysticerci develop a diffuse cerebral edema termed cysticercal encephalitis. Pathologically, cysticercal encephalitis may progress to meningoencephalitis, granulomatous meningitis, focal granulomas or abscess, hydrocephalus, ependymitis, or arteritis.

Approximately 10-20% of patients with neurocysticercosis present with extraparenchymal disease, often with concomitant parenchymal disease. Subarachnoid neurocysticercosis may form in the gyri of the cerebral convexities or in the fissures of the brain, especially the sylvian fissures. These forms of neurocysticercosis are associated with parenchymal inflammation and resemble parenchymal disease in manifestations and pathogenesis.

In severe cases, cysticerci in the sylvian fissures may enlarge to several centimeters in diameter and cause mass effects. Cysticerci can form in the ventricles of the brain, where they can cause hydrocephalus by blocking the outflow of CSF. Obstructive hydrocephalus may also be caused by associated ependymitis. If cysticerci form in the basal cisterns, they can cause basilar arachnoiditis. Arachnoiditis may result in communicating hydrocephalus or vasculitis. Involvement of the arteries may lead to lacunar infarctions or, occasionally, large-vessel strokes.

Cysticerci may be located in the spinal subarachnoid space and the spinal cord medulla. Medullary cysticerci may cause cord compression or other symptoms related to their location. Ocular cysticercosis is generally intravitreal or subretinal. Skeletal muscle cysticerci are common but usually cause only minor local symptoms unless they are present in overwhelming numbers. Subcutaneous cysticerci manifest as painless, palpable, cystic lesions. CNS parenchymal cysticerci may be present in patients with suspected extraparenchymal or extra-CNS disease.




United States

Approximately 2,000 patients are hospitalized for neurocysticercosis each year in the United States. [2] Most occur among Latin American immigrants in locations such as California, Arizona, and Texas. Less frequently, cysticercosis is observed in immigrants from other areas, including India, Asia, and Africa. A small number of cases of cysticercosis develop in people born in the United States who have traveled to areas in which the infection is endemic. These travelers are often the children of immigrants. Locally acquired infection is rare and is associated with contact with a tapeworm carrier. All tapeworm carriers acquire infection from areas of endemic disease.

In a mortality study using data from the National Center for Health Statistics from 1990 to 2002; 62% of patients with cysticercosis had emigrated from Mexico. [3]


An estimated 50-100 million people are infected with cysticercosis worldwide. This is probably an underestimate since many infections go undiagnosed. The World Health Organization (WHO) estimates suggest 2.56-8.30 million cases of neurocysticercosis globally. [2] Neurocysticercosis is one of the leading causes of adult-onset seizures worldwide. CT scanning and MRI of the brain have greatly improved the diagnosis of neurocysticercosis.

Areas of endemic disease include Central and South America, India, China, Southeast Asia, and sub-Saharan Africa. [4] Studies in Latin America and India have noted adult-onset seizures in approximately 2% of the population, with as many as half due to neurocysticercosis. In Latin America, the seroprevalence rate ranges from 4.9-24%. In India, the estimated prevalence is similar. Rural China and Korea have lower infection rates. The seroprevalence in certain rural South American communities is as high as 10-25%. [5] The estimated true prevalence of human taeniasis and cysticercosis in rural Vietnam is as high as 13% for each. [6] There is also an indication that cysticercosis and taeniasis are present across eastern European countries. [7]


Neurocysticercosis is the most frequent preventable cause of epilepsy worldwide and is estimated to cause 30% of all epilepsy cases in endemic countries. In 2015, the WHO’s Foodborne Disease Burden Epidemiology Reference Group identified T solium as a leading cause of death from foodborne diseases, resulting in a considerable total of 2.8 million disability-adjusted life-years. Neurocysticercosis was found to be responsible for 10% of newly onset seizures in one Los Angeles, California, emergency department. [8] Overall, among patients who presented to emergency departments with newly onset seizure, neurocysticercosis was found to be responsible for 2.1-5.7% of cases. [9]

A total of 221 deaths were attributed to cysticercosis in the United States from 1990-2002. [3]

Although some patients die of status epilepticus in areas with poor access to medical care, mortality due to parenchymal disease is rare. With modern medical and surgical care, mortality due to extraparenchymal disease is also unusual. However, without aggressive surgical management, hydrocephalus is potentially life-threatening. Even with shunting procedures, subarachnoid cysticercosis is associated with a high 10-year fatality rate.


Immigrants from countries where T solium is endemic are more likely to be infected. While most of these immigrants are Hispanic and some are Asian, prevalence rates appear to be related more to exposure than to genetic predisposition.

Nearly 75% of all hospitalized patients in the United States with neurocysticercosis were Hispanic. [10]


Cysticercal encephalitis, a severe form of cysticercosis, is more common in children and young females. The cause is unknown.

US hospitalizations were more common among males. [10]

No other sex predisposition has been noted.


Patients with cysticercosis are typically aged 10-40 years. However, cases have been described in every age group.

People aged 20-44 years were at an increased risk for hospitalizations in the United States. [10]



Most patients with parenchymal cysticercosis either remain asymptomatic or develop a self-limited seizure disorder.

Among patients who develop intracerebral calcifications, most have recurrent seizures unless treated with anticonvulsants. If treated with anticonvulsants, the seizures are generally easily controlled.

Ventricular neurocysticercosis usually requires shunting. Neurosurgery may be complicated by focal neurologic damage. Shunt revisions are often needed unless patients are treated with corticosteroids or antiparasitic drugs. However, even with treatment, some still require subsequent revision. Prior to the use of corticosteroids and antiparasitic drugs, subarachnoid disease was associated with a 90% 10-year fatality rate, even with shunting. With current management, fatalities appear to be rare.

Good evidence indicates that, once infected, patients are immune to reinfection.


Patient Education

Patients and their family members should be educated on how to decrease the source of egg carriers by emphasizing improvement in sanitation, separation of pigs from humans, and food-preparation hygiene in endemic areas.

Family members should be screened and queried about symptoms suggestive of tapeworm infection, such as passing proglottids. They should be treated if symptoms are present.

Family members should also be screened.

Patients with seizures and their families should know proper seizure first-aid.

Patients who have had seizures should know about possible driving restrictions, which, in the United States, vary from state to state.

Patients who have received a VP shunt should be educated about the signs and symptoms of elevated ICP (possible shunt failure) and meningitis (secondary infection of indwelling hardware).

For excellent patient education resources, please see eMedicineHealth's Infections Center.