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Pediatric Cysticercosis Clinical Presentation

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

History

See the list below:

  • 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 T 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.[2]
  • 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.
  • Spinal neurocysticercosis can cause spinal cord compression, nerve root pain, transverse myelitis, or meningitis.
  • 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.
  • Ocular cysticercosis may decrease visual acuity because of retinal detachment, iridocyclitis, or floating cysticerci in the vitreous.[3]
  • 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.
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Physical

See the list below:

  • 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.
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Causes

See the list below:

  • 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.
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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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