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Pediatric Cysticercosis

  • Author: Delaram Ghadishah, MD; Chief Editor: Russell W Steele, MD  more...
 
Updated: Apr 03, 2012
 

Background

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.

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Pathophysiology

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.

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Epidemiology

Frequency

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.

Disease is prevalent in areas with low socioeconomic status and poor hygiene and sanitation.

International

An 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.

Cysticercosis is endemic throughout Latin American, although it is rare in Chile, Argentina, and Uruguay.

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.

Mortality/Morbidity

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

Race

No racial predilection for cysticercosis is known.

Sex

The prevalence does not differ according to sex.

Age

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

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Contributor Information and Disclosures
Author

Delaram Ghadishah, MD Physician, Emergency Department, Kaiser Permanente West Los Angeles Medical Center

Delaram Ghadishah, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Michael James Burns, MD, FACEP, FACP Health Science Clinical Professor, Department of Emergency Medicine, Department of Internal Medicine, Division of Infectious Diseases, University of California Irvine School of Medicine

Michael James Burns, MD, FACEP, FACP is a member of the following medical societies: Alpha Omega Alpha, American Geriatrics Society, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Phi Beta Kappa, Royal Society of Tropical Medicine and Hygiene, American College of Emergency Physicians, American College of Physicians, California Medical Association, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Martin Weisse, MD Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Glenn Fennelly, MD, MPH Director, Division of Infectious Diseases, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center; Clinical Associate Professor of Pediatrics, Albert Einstein College of Medicine

Glenn Fennelly, MD, MPH is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

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Cysticercosis life cycle. Image courtesy of the Centers for Disease Control and Prevention.
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. Image courtesy of Eric H. Kossoff, MD.
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-weighted MRI). Note the cyst in the fourth ventricle, causing obstructive hydrocephalus. Image courtesy of Fred Greensite, MD.
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 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 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.
 
 
 
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