Pediatric Cysticercosis

Updated: Oct 17, 2016
  • Author: Delaram Ghadishah, MD; Chief Editor: Russell W Steele, MD  more...
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Cysticercosis, a tissue infection that involves larval cysts of the cestode Taenia solium (the human pork tapeworm), results from the ingestion of food (especially vegetables) and water contaminated with human feces that contain T solium eggs.

Although infections with Taenia tapeworm cysts may involve many parts of the body, the most common site of severe symptomatic infection is the CNS. See the image below.

Cysticercosis life cycle. Image courtesy of the Ce Cysticercosis life cycle. Image courtesy of the Centers for Disease Control and Prevention.

Neurocysticercosis, the most common parasitic disease of the CNS, is the most common cause of adult-onset epilepsy in many of the countries where the infection is endemic.



Cysticercosis, the intermediate form of T solium infection, is predominantly acquired by ingesting food or water contaminated with T solium eggs. Additionally, autoinfection may occur by means of fecal-oral contact and, theoretically, by reverse peristalsis in the small intestines of individuals infected with adult T solium worms.

In the stomach, oncospheres are liberated following digestion of the eggs' coats. Oncospheres invade and cross the intestinal wall, enter the bloodstream, and then migrate to and lodge in tissues throughout the body, where they produce small (0.2-0.5 cm) fluid-filled bladders containing a single juvenile-stage parasite (protoscolex).

Although the cysticerci may infect any organ of the body (most often the eye, skeletal muscle, and CNS), serious disease almost exclusively involves the CNS and heart.

Oncospheres that invade the brain may lodge in the brain parenchyma, subarachnoid space, ventricular space, or spinal cord. Cysticerci develop after 2 months and may or may not stimulate an appreciable inflammatory response.

In the brain parenchyma, cysticerci form a thin capsule of fibrous tissue that thickens with time. After several years, the parasite dies or is killed and is replaced by an astroglial and fibrous tissue granuloma that becomes calcified. The number of cysticerci present ranges from one to several hundred.

Cysts that grow in the sylvian fissure and in the subarachnoid space at the base of the skull may enlarge to 10-15 cm in diameter. Meningeal and spinal cord cysticercosis occurs if the oncospheres enter via the choroid plexus and hatch in the arachnoid membranes along the neural axis.

Cysts that develop in the subarachnoid space may cause an inflammatory response. Subsequent fibrosis of the arachnoid membranes may interfere with normal cerebral spinal fluid (CSF) resorption, resulting in hydrocephalus. Fourth ventricle cysts can create a subacute hydrocephalus via a valve-and-ball mechanism. However, head movement can suddenly increase the intracranial pressure (ICP).

With the exception of massive or obstructive disease, the cystic stages of most tapeworms do not provoke a strong immunologic response while they remain alive and intact. However, once the cysts die, the immune system recognizes them as foreign, and a vigorous immunologic response ensues. Seizures, hydrocephalus, blindness, strokes, meningitis, encephalitis, irreversible brain damage, myositis, and myocarditis may occur. Death may subsequently occur.




United States

Cysticercosis is not endemic to the United States, although domestic transmission has been documented from recent immigrants to the United States from highly endemic areas. [1] Historically, rates significantly decreased in the 1970s.

Since the 1970s, the number of cases of neurocysticercosis in the United States has increased, mainly because of the large number of immigrants from areas with endemic disease, such as Mexico, Central and South America, Africa, Asia, Spain, and Portugal. Americans without a travel history to such areas have developed neurocysticercosis, mainly because of exposure to a cohabitant with a T solium infection.

A review of hospitalization discharge data from the U.S. Nationwide Inpatient Sample for years 2003-2012 found that neurocysticercosis hospitalizations and hospital-associated charges for neurocysticercosis in the United States are greater than for all other neglected and tropical diseases combined, including malaria. Most hospitalizations were for management of seizures and obstructive hydrocephalus, with Hispanic young adult males at greatest risk. [2]  This study did not analyze outpatient visits or charges. 

About three quarters of patients hospitalized in the U.S. with neurocysticercosis were Hispanic in 2003-2012.

The number of hospitalizations and costs to the U.S. healthcare system is expected to increase due to immigration of persons from Latin America, Asia and sub-Saharan Africa. 


Disease is prevalent in areas with low socioeconomic status and poor hygiene and sanitation. Accurate estimation of the prevalence of cysticercosis is difficult because of the high prevalence of asymptomatic individuals. Overall, more than 2 million people are estimated to have adult tapeworm infection, and many more are infected with cysticercoids. Disease is prevalent in areas with poor hygiene and sanitation where pigs live in close proximity to people. 

Cysticercosis is endemic throughout Latin American, although it is rare in Chile, Argentina, and Uruguay. It is endemic in South Asia (especially India) as well as in sub-Saharan Africa.

Cysticercosis is absent in Arabic regions of Asia and Africa but is found in areas where pigs live in close proximity to humans. In Europe, cysticercosis is still endemic in Spain, Portugal, and some Eastern European countries but is rare in most other countries.


Worldwide, an estimated 50,000 people die from cysticercosis each year because of CNS or cardiac complications.


No racial predilection for cysticercosis is known.


The prevalence does not differ according to sex.


No known age-based differences in the frequency of cysticercosis have been reported. 


Prevention and Control

Cysticercosis was declared a potentially eradicable disease by the International Task Force for Disease Eradication in 1992.  Attempts at eradication and disease prevention have been limited to demonstration projects in targeted villages in endemic areas, and have had only limited and transitory effects.  Studies of disease eradication have shown that T. solium is extremely resistant to control in low-income countries. 

A study in an endemic region in northern Peru found that it was feasible to interrupt transmission of T. solium with prevention of human and porcine cysticercosis, but persistence of eradication requires intense and continuous measures that are costly and are currently not feasible in low-income countries. [3]