Pediatric Cysticercosis

Updated: Oct 21, 2021
Author: Delaram Ghadishah, MD; Chief Editor: Russell W Steele, MD 


Practice Essentials

Cysticercosis is a tissue infection that involves larval cysts of the cestode Taenia solium (the human pork tapeworm). It 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 frequent cause of adult-onset epilepsy in many of the countries where the infection is endemic.

Signs and symptoms of cysticercosis

The clinical presentation depends on the number, location, and stage of the lesions, as well as the host immune response. In general, the following may be present:

  • Neurologic deficits
  • Seizures
  • Subcutaneous or ocular cysts

See Presentation for more detail.

Diagnosis of cysticercosis

Laboratory studies

The enzyme immunotransfer blot assay for the detection of serum and cerebrospinal fluid (CSF) antibodies to T solium is the antibody test of choice for cysticercosis.

The complement fixation test for the detection of antibodies in CSF is highly specific and sensitive.

Imaging studies

The diagnosis of neurocysticercosis is based primarily on computed tomography (CT) scanning or magnetic resonance imaging (MRI) results. Regardless of the neuroimaging modality, granulomas are the most common finding in patients with neurocysticercosis.

See Workup for more detail.

Management of cysticercosis

Medical treatment depends on the location of the cysts and the patient’s symptoms. Patients with live parenchymal cysts can be treated with either albendazole or praziquantel; however, corticosteroids and antiseizure medications are often required in addition. Those with nonviable (calcified) brain cysts should be treated only for their symptoms; anticonvulsants are used to treat seizures.

For cases that do not respond to medical therapy, shunt placement, removal of large solitary cysts for decompression, and the removal of mobile cysts that cause ventricular obstruction should be considered.

See Treatment and Medication for more detail.


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.


Cysticercosis is caused by the ingestion of T solium eggs. The human is the only definitive host of the adult pork tapeworm, which lives in the human intestinal tract and lays eggs that are shed in human feces. In the normal life cycle of the parasite, eggs shed in human feces are ingested by pigs, which then develop cysticerci in muscle tissue. Human infection with the adult tapeworm develops in people who ingest raw or poorly cooked pork that contains cysticerci. Note that human ingestion of pork does not result in the development of cysticercosis.

Contamination of water, fruits, and vegetables by human feces that contain eggs is usually the result of poor sanitation.

Untreated, adult T solium worms may cause autoinfection by means of fecal-oral ingestion and reverse peristalsis, but this is believed to be very uncommon.


United States statistics

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 US Nationwide Inpatient Sample for 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 United States with neurocysticercosis were Hispanic in 2003-2012.

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

International statistics

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.

In Madagascar, a population-based study by Carod et al investigated the prevalence of cysticercosis among schoolchildren (n = 1751) using the B158/B60 antigen enzyme-linked immunosorbent assay. They found that the overall prevalence based on antigen detection was 27.7% (95% CI, 10-37%).[3]

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.

Race-, sex-, and age-related demographics

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. 


The prognosis depends on the number and location of lesions, as well as the host response. Treatment with antihelminthics may result in radiologic improvement of CNS lesions, but this may or may not result in clinical improvement.


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


Complications of cysticercosis are numerous. They are most severe when they involve the CNS, visual, or cardiac system.

Permanent brain damage, seizures, strokes, hydrocephalus, and vague neurologic symptoms may result. Blindness often results from ocular cysticercosis, despite antiparasitic and surgical treatment. Muscle involvement may result in myositis and myocarditis.

Patient Education

Improved sanitation and hygiene are essential to the prevention of cysticercosis.

Use of toilets and proper disposal of human feces that may contain tapeworm eggs may eliminate transmission of infection. Avoid ingestion of unclean water. Proper cooking of pork may result in fewer T solium infections.

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.[4]




The clinical presentation of cysticercosis depends on the number, location, and stage of the lesions present, as well as the host immune response.

In general, the diagnosis of neurocysticercosis should be considered in any individual who is from or has traveled to an area where Taenia solium is endemic and who has new-onset partial seizures (with or without secondary generalization), behavioral disturbances, confusion, stupor, cognitive impairment, or signs of increased intracranial pressure (ICP).

Seizures are the presenting symptom in more than 70% of cases. The seizures frequently begin as simple or complex partial seizures but become generalized in 80% of cases.[5]

Parenchymal disease causes seizures and focal neurologic deficits.

Headache, vertigo, vomiting, papilledema, an altered level of consciousness, and gait disturbances may be present in patients with meningeal cysticercosis.

Neurocysticercosis can present with nearly any type of focal neurologic deficit. Persons with arachnoiditis can present with stroke syndromes due to occlusion of small and medium size intracranial arteries.  Arachnoiditis can produce entrapment of cranial nerves resulting in extraocular muscle palsies, hearing loss, facial nerve palsy.  Spinal neurocysticercosis can cause spinal cord compression, nerve root pain, focal extremity weakness and sensory deficits, transverse myelitis, or meningitis.[6]

Intraventricular neurocysticercosis (5-10% of all cases) is associated with hydrocephalus and acute, subacute, or intermittent signs of increased ICP without localizing signs. The lateral ventricles are less likely to become obstructed, whereas the fourth ventricle most commonly becomes obstructed. Hydrocephalus develops from the intense and widespread immune response in the subarachnoid space.

Neurocysticercosis-associated inflammation is more severe in children and women than in adult men. Children are more likely to have single, enhancing nodules.

Cysticercoid encephalitis is seen in children and presents with altered mental status associated with seizures and raised intracranial pressure. These patients usually have hundreds of small, viable, or degenerating cysts, with a diffuse inflammatory reaction. 

Ocular cysticercosis may decrease visual acuity because of retinal detachment, iridocyclitis, or floating cysticerci in the vitreous.[7]

Heavy infections in skeletal or heart muscle may result in myositis or carditis, respectively.

Rarely, cysticerci may obstruct small terminal arteries or cause a vasculitis, leading to a cerebral infarction.

Children with an acute infection that is massive may present with signs and symptoms of fulminant encephalitis.

Intellectual deterioration due to extensive frontal lobe disease may simulate dementia or parkinsonism.

Chronic basilar meningitis is associated with many forms of neurocysticercosis. In addition to signs of meningeal irritation, increased ICP due to inflammation, edema, or an obstructing cyst may be present.

A study that evaluated 81 cases of neurocysticercosis from 1980-2013 in five centers in Italy and Spain found that when comparing pediatric cases to adult cases, pediatric cases were more likely to have eosinophilia, to have other parasitic infections, and to be asymptomatic.[8]

Physical Examination

Findings vary depending on the number, location, and local effects of cysticerci, as well as on the host response. In general, neurologic deficits, seizures, and subcutaneous or ocular cysts may be present. Cysts may be palpable under the skin. The features of the history assist in focusing the physical examination.





Laboratory Studies

The enzyme immunotransfer blot assay for the detection of serum and cerebrospinal fluid (CSF) antibodies to T solium is the antibody test of choice for cysticercosis. It is available through the Centers for Disease Control and Prevention. The test is more sensitive with serum than with CSF specimens. Serum antibody testing has a sensitivity and specificity of more than 90%. The serum antibody assay results are often negative in children with solitary parenchymal lesions or old calcified disease, and results are usually positive in patients with multiple inflamed lesions.

The complement fixation (CF) test for the detection of anticysticercus antibodies in CSF is highly specific and sensitive. The CF test results are negative in the absence of active forms of the parasite. Results may remain positive for several months following successful treatment. Antibody may be demonstrated in the CSF but not in the serum of patients with parenchymal or ventricular neurocysticercosis.

The use of both the enzyme immunotransfer blot assay and the CF test increases the probability of antibody detection.

Cysticercosis may result in CSF eosinophilia.

Imaging Studies

The diagnosis of neurocysticercosis is primarily based on CT scanning or MRI results.[9] See the images below.

MRI of 6-year-old boy from Peru with single right MRI of 6-year-old boy from Peru with single right frontal cyst (coronal image). Image courtesy of Eric H. Kossoff, MD.
Axial image MRI of same patient as in Media file 2 Axial image MRI of same patient as in Media file 2. Image courtesy of Eric H. Kossoff, MD.
CT scan of intraparenchymal cysticercosis with les CT scan of intraparenchymal cysticercosis with lesions in different stages. Lesions that are breaking down demonstrate peripheral enhancement after intravenous contrast injection, whereas lesions without peripheral enhancement are intact. Typical residual calcification from an old focus of infection is observed in the left occipital lobe. Image courtesy of Fred Greensite, MD.
Racemose (extraparenchymal) cysticercosis (T1-weig Racemose (extraparenchymal) cysticercosis (T1-weighted MRI). Note the cyst in the fourth ventricle, causing obstructive hydrocephalus. Image courtesy of Fred Greensite, MD.
Racemose cysticercosis (T1-weighted MRI). Note clu Racemose cysticercosis (T1-weighted MRI). Note cluster of cysts anterior to the pons and inferior to the hypothalamus in a different patient. Image courtesy of Fred Greensite, MD.
Racemose cysticercosis (same patient as in Media f Racemose cysticercosis (same patient as in Media file 6). Note the enhancing margin of the cysts in the suprasellar cistern and in the left sylvian fissure after gadolinium injection (T1-weighted MRI). Image courtesy of Fred Greensite, MD.
Racemose cysticercosis (same patient as in Media f Racemose cysticercosis (same patient as in Media files 6-7). Coronal image (postgadolinium T1-weighted MRI) posterior to the slice in Media file 7. Cysts in this slice (below the hypothalamus) do not have enhancing margins. Also, unlike intraparenchymal lesions, scolexes are typically not identified in the cysts of racemose cysticercosis. Image courtesy of Fred Greensite, MD.

CT scanning is more readily available and less expensive but is less sensitive than MRI in the depiction of inflammation around a cyst.

MRI better depicts cysts in the ventricles and spinal cord because it delineates the membranes of the parasite and the differences in the signal intensities of the fluids and tissues of the cysticercus. The protoscolex may even be visible within the cyst on MRI; it is a pathognomonic sign of cysticercosis.

Regardless of the neuroimaging modality, granulomas are the most common finding in patients with neurocysticercosis.

Parenchymal cysts with inflammation appear as ring enhancement on neuroimages.

The presence of hydrocephalus on a CT scan finding may suggest intraventricular cysts, which are otherwise difficult to detect because the cyst fluid often has the same density as that of CSF.

The most common findings in children are a solitary parenchymal cyst with or without contrast enhancement and numerous calcifications.

Plain radiography may reveal calcifications in muscle or brain that are consistent with cysticercosis, but these are more often nondiagnostic in children than in adults. On images, cysticerci can be mistaken for calcified tuberculomas, toxoplasmosis, or CNS tumors.



Medical Care

Medical treatment of cysticercosis depends on the location of the cysts and the patient's symptoms. Patients with live parenchymal cysts can be treated with either albendazole or praziquantel, but corticosteroids and antiseizure medications are often required in addition. Consultation with a physician (neurologist or infectious diseases specialist) experienced in treating neurocysticercosis is recommended prior to planning a course of antiparasitic drug treatment.[10] Many authorities consider albendazole to be preferred over praziquantel because of its higher eradication rate of parenchymal brain cysts.

For treatment of neurocysticercosis, albendazole is orally administered at a dose of 15 mg/kg/d divided into 2 daily doses for 8-30 days (not to exceed 800 mg/d in children or 400 mg twice daily in adults). This regimen can be repeated if necessary. Praziquantel orally administered at a single dose of 5-10 mg/kg is highly effective in eradicating adult tapeworm infection. However, when this drug is used to treat neurocysticercosis, much higher doses and a longer duration of treatment is required. For neurocysticercosis, praziquantel is orally administered at a dose of 50-100 mg/kg/d divided into three daily doses for 30 days.

Patients with nonviable (calcified) brain cysts should be treated only for their symptoms; anticonvulsants are used to treat seizures. Seizures most often recur for months and may indefinitely recur. Anticonvulsant medications must be continued until cysts have resolved and until the patient is seizure free for 1-2 years.

No consensus has been reached regarding the role of antiparasitic drugs in patients with parenchymal cysts and inflammation (depicted as ring enhancement on neuroimages).

Although taeniacidal drugs that may hasten radiologic resolution of cysts are available, treatment may worsen the inflammation and, thus, precipitate complications or death.

Coadministration of corticosteroids (eg, dexamethasone, prednisone) is recommended to decrease the adverse effects of antiparasitic treatment.

In all patients with multiple cysts and associated cerebral edema (cysticercal encephalitis), antiparasitic therapy should be deferred until the cerebral edema is controlled by corticosteroid therapy. In addition, antiparasitic drug therapy may cause permanent damage if used to treat ocular or spinal cysts, even when combined with corticosteroids. A careful ocular examination to rule out ocular cysts should be performed prior to initiating antiparasitic drug treatment.

Surgical Care

For cases that do not respond to medical therapy, shunt placement, removal of large solitary cysts for decompression, and the removal of mobile cysts that cause ventricular obstruction should be considered.

Intraventricular cysts and hydrocephalus usually require surgical therapy and, often, the placement of intraventricular shunts. Adjunctive chemotherapy with antiparasitic agents and corticosteroids can reduce the rate of subsequent shunt failure.

Neuroendoscopy may be used to remove certain ventricular cysts. Spillage of cyst contents during surgery is not associated with parasite dissemination, as it is with echinococcosis. Very large cysts that cause a mass effect may require surgical debridement.

Ocular cysticercosis is treated with surgical excision of the cysts. The outcome is often poor. Thus, enucleation is frequently required. Treatment with antiparasitic drugs is contraindicated in ocular cysticercosis because the inflammatory response may worsen the outcome.


Consultation with a neurologist should be considered to recommend anticonvulsant medications and further neurologic assessment is indicated in patients with seizures or neurologic deficits.

Consultation with a neurosurgeon may be indicated in patients with acute hydrocephalus or large intracerebral cysts with a mass effect, in those with suspected cysts in the ventricular system, or in those with spinal cysts.

Consultation with an infectious diseases or tropical medicine specialist should be considered when planning antiparasitic drug treatment in patients suspected to have live parenchymal cysts.

Consultation with an ophthalmologist to rule out intraocular cysts should be considered prior to initiating antiparasitic drug treatment.

Diet and Activity


No special diet is indicated. Good sanitation is essential to prevent the spread of the disease.


No limitations are necessary, unless activity is limited by the patient's symptoms.



Medication Summary

Specific recommendations for treatment of neurocysticercosis remain controversial. Treatment depends on disease presentation. Observation, symptomatic treatment, antiparasitic treatment, and/or surgery may play a role.

Medical therapy may include antihelminthic medications (to reduce cysts) or anticonvulsant medications. Antihelminthic medications work only in noncalcified lesions and may not decrease long-term morbidity associated with cysticercosis. Initially, they may worsen the patient's condition because of the inflammatory response to the dying or dead cyst. Additionally, medical therapy may convert quiescent parenchymal lesions to active ones or may worsen ventricular, ocular, or spinal disease. Corticosteroids should be started 2-3 days before the initiation of antihelminthic drugs and continued during their use to decrease the inflammatory response to the dying cysts. In cases with evidence of hydrocephalus or ventricular or spinal disease, a ventricular shunt should be placed before medical therapy is initiated.

If one drug is not successful, a second drug may be used in a sequential manner. This treatment may eliminate more than 95% of the parenchymal cysticerci.

Albendazole is the drug of choice. Repeated courses of albendazole have been shown to be of benefit in patients who had a positive response to an initial course. Therapy for 1 week may be as beneficial as a 4-week course of therapy.

Antihelminthic agents

Class Summary

These are used to eradicate cysts in noncalcified brain lesions. Parasite biochemical pathways are different from those of the human host; thus, toxicity is directed to the parasite, egg, or larvae. The mechanism of action varies within the drug class. Antiparasitic actions may include the following:

- Inhibition of microtubules, which causes irreversible block of glucose uptake

- Inhibition of tubulin polymerization

- Depolarizing neuromuscular blockade

- Cholinesterase inhibition

- Increased cell membrane permeability, which results in intracellular calcium loss

- Vacuolization of the schistosome tegument

- Increased cell membrane permeability to chloride ions caused by alternations in the chloride channels

Albendazole (Albenza)

Broad-spectrum antihelminthic. It is cysticidal and destroys approximately 85% with a single course. Administer for 8-30 d with a fatty meal to improve absorption.

Praziquantel (Biltricide)

Cysticidal agent that destroys approximately 75% of cysts with a single course. Increases cell membrane permeability in susceptible worms, resulting in loss of intracellular calcium, massive contractions, and paralysis of musculature. Causes vacuolization and disintegration of the schistosome tegument, followed by attachment of phagocytes to the parasite and death. Tabs should be swallowed whole with some liquid during meals. Bitter taste can cause nausea or vomiting if tabs are held in the mouth.

Niclosamide (Niclocide)

Used in the treatment of adult worms. No longer commercially available in the United States. Not absorbed and does not provoke an inflammatory response to cysticerci. Inhibits mitochondrial oxidative phosphorylation and glucose uptake in the parasite.



Further Care

Further outpatient care

Treat seizures with anticonvulsant medications. Follow-up with a neurologist is recommended for patients with numerous lesions or seizures. Follow-up with an ophthalmologist is recommended for patients with visual lesions or complications.

Further inpatient care

Monitor patients with cysticercosis for anticonvulsant levels or signs of toxicity. Monitor with serial neurologic examinations and initiate corticosteroid therapy if cerebral edema is present. Place a ventriculoperitoneal shunt if acute hydrocephalus develops. Brain surgery may be recommended for a mass effect, and ocular surgery may be recommended for the removal of cysts.

Inpatient and outpatient medications

The following medications may be indicated:

  • Anticonvulsant medications as indicated

  • Corticosteroids for cerebral edema due to inflammation

  • Antihelminthic medications if indicated


Transfer patients if specialized care, such as that provided by a neurosurgeon or ophthalmologist, is needed.


Avoid areas and countries with poor hygiene.

Persons traveling to developing countries with high rates of endemic cysticercosis should avoid ingestion of unboiled or nonpurified water or ice cubes and should also avoid eating uncooked pork or vegetables and fruits that cannot be peeled.

All family members of an index patient with cysticercosis, as well as persons handling their food, should be examined for signs of disease or evidence of adult worm infection.

Persons known to have the adult T solium tapeworm should be immediately treated and should exercise care in handwashing to prevent contamination with feces.

Examine the stool of food handlers who have recently emigrated from countries with endemic disease for T solium eggs and proglottids.

Raw or undercooked pork should not be eaten, as this may result in infection with the adult tapeworm.