eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Amebic Meningoencephalitis

Author: Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Contributor Information and Disclosures

Updated: Jan 21, 2009

Introduction

Background

The free-living amebae Naegleria fowleri,1 Acanthamoeba species, and Balamuthia mandrillaris2 cause extremely rare and sporadic CNS infections, which were first described in 1965. Typically, N fowleri produces primary amebic meningoencephalitis (PAM), which is clinically indistinguishable from acute bacterial meningitis. The other amebae cause granulomatous amebic encephalitis (GAE), which is a more subacute or chronic infection. The presentation of GAE can mimic a brain abscess, aseptic or chronic meningitis, or CNS malignancy.

Pathophysiology

Although it is ubiquitous in most soils and environments, N fowleri can also be found in warm, particularly stagnant, freshwater.3 PAM is an exceptionally uncommon result of CNS invasion of the typically healthy host by N fowleri, following the very common exposure to the amebae. Especially in warmer months and climates, children younger than 2 years frequently carry the organism asymptomatically in their noses and throats. During a period of a few days to 2 weeks after swimming, diving, bathing, or playing in warm, usually stagnant, freshwater, the N fowleri amebae migrate through the cribriform plate, along the fila olfactoria and blood vessels, and into the anterior cerebral fossae, where they cause extensive inflammation, necrosis, and hemorrhage.

In contrast, GAE apparently results from either acanthamebic keratoconjunctivitis, which is the uncommon spread of the amebae from the cornea into the CNS, or from hematogenous spread of all of these ubiquitous organisms (eg, Acanthamoeba species, Balamuthia species) from primary inoculation sites in the lungs or skin into the CNS, where abscesses and focal granulomatous infections result. These infections often occur in hosts who are debilitated or otherwise immunocompromised; however, GAE may also affect previously healthy hosts.

Frequency

United States

PAM and GAE are both extremely rare but continue to be reported. PAM is more common in warmer regions and in the warmer months of spring and summer. From 1937-2007, 121 cases (0-8 per year) were reported.

International

More than 440 cases have been reported; although rare, cases of PAM and GAE have been reported worldwide, reflecting the ubiquity of the organisms. Most reports come from the United States, Australia, and Europe; this frequency is likely because of identification and reporting bias. In addition, a predominance of cases occurs in warmer climes and during warmer seasons of the year.

Mortality/Morbidity

These infections are nearly uniformly fatal. Only 5 survivors of PAM have been reported;4 this represents approximately 3% of reported cases. The high mortality rate is likely because of the difficulty of diagnosis and poor-to-marginal response to therapy. In most individuals with PAM or GAE, diagnosis is made after their deaths.

Race

PAM and GAE demonstrate no particular ethnic or racial predilection.

Sex

The male-to-female ratio of PAM is 2:1; the male-to-female ratio of GAE is 5:1.

Age

PAM has been reported in infants as young as 4 months and is most commonly observed in the first 3 decades of life. Although persons of all ages are affected by GAE, this infection appears to occur more commonly in individuals at the extremes of age.

Clinical

History

The history seldom helps to differentiate amebic meningoencephalitis from other CNS diseases.

  • Primary amebic meningoencephalitis (PAM)
    • PAM commonly affects children and young adults who have previously been healthy.
    • This disease occurs more often during the warmer months of the year and in warmer climates.
    • Patients with PAM may have a history of swimming, diving, bathing, or playing in warm, generally stagnant, freshwater during the previous few days to 2 weeks.
    • Rarely, patients with PAM may experience disordered smell or taste.
    • Most often, the symptoms of PAM are indistinguishable from acute bacterial meningitis.
    • Acute onset of PAM occurs over hours to 1-2 days.
    • Symptoms of PAM include high fever, headache, photophobia, stiff neck, nausea, and vomiting.
    • Additional symptoms include confusion, somnolence, seizures, and coma.
    • Infection may rapidly progress.
  • Granulomatous amebic encephalitis (GAE)
    • GAE affects individuals of all ages, although very young or very old persons may be more susceptible.
    • Persons with debility or immunocompromise may be more susceptible to GAE.
    • GAE occurs throughout the year because the causative organisms are ubiquitous.
    • Individuals with GAE may have keratoconjunctivitis or a skin ulcer or lesion.
    • A subacute or chronic presentation of GAE lasting days or weeks is most common.
    • GAE must be differentiated from brain abscess or tumor and aseptic or chronic meningitis.
    • Typical symptoms include low-grade fever and focal neurologic signs, including cranial nerve palsies, hemiplegia, ataxia, aphasia, diplopia, and seizures.
    • Patients with GAE may exhibit behavioral changes, stiff neck, signs of increasing intracranial pressure (ICP), stupor, or coma.
    • Progression varies; occasionally, patients survive for weeks or months.

Physical

Physical examination seldom helps to differentiate amebic meningoencephalitis from other CNS diseases. Findings outside the neurologic examination are exceptional.

  • PAM
    • Patients may experience abnormal smell or taste.
    • Other signs of PAM include high fever, photophobia, stiff neck, mental status changes, and seizures.
    • PAM infection may progress rapidly to evidence of increased ICP and cerebral herniation.
    • Rarely, myocarditis may occur, although amebae are not present in the myocardium.
  • GAE
    • Individuals with GAE may have low-grade fever, photophobia, or stiff neck. Focal neurologic findings, such as cranial nerve palsies, hemiplegias, aphasias, ataxias, or diplopia, may be observed in addition to seizures, which may be focal.
    • Individuals with GAE may demonstrate signs of elevated ICP and cerebral herniation.
    • Keratoconjunctivitis, primarily in people who wear contact lenses, or skin lesions may rarely occur.

Causes

  • PAM
    • Exposure to and carriage of free-living amebae appears to be common.
    • Although the cause is unclear, CNS invasion is exceptionally rare.
    • The protozoologic basis for CNS tropism remains to be fully elucidated.
    • Individuals with frequent exposure to warm, often stagnant, freshwater (eg, persons swimming in freshwater lakes, ponds, and pools during the summer months) are most at risk of infection with PAM.
  • GAE
    • Exposure to and carriage of free-living amebae appears to be common.
    • Although the cause is unclear, hematogenous spread of GAE to the CNS from eye, skin, or lung portals of entry is exceptionally rare.
    • The protozoologic basis for CNS tropism remains to be fully elucidated.
    • The basis for the observed male preponderance in CNS infection is uncertain.
    • Hosts who are debilitated and immunocompromised appear to be most at risk, although hosts who are healthy can become infected as well.

More on Amebic Meningoencephalitis

Overview: Amebic Meningoencephalitis
Differential Diagnoses & Workup: Amebic Meningoencephalitis
Treatment & Medication: Amebic Meningoencephalitis
Follow-up: Amebic Meningoencephalitis
References
Further Reading
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Further Reading

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Keywords

amebic meningoencephalitis, acanthamebic keratoconjunctivitis, Acanthamoeba, aphasia, aseptic meningitis, ataxia, bacterial meningitis, Balamuthia mandrillaris, central nervous system infection, CNS infection, cerebral herniation, cranial nerve palsies, diplopia, encephalitis, Entamoeba histolytica, granulomatous amebic encephalitis, GAE, hemiplegias, intracranial pressure, ICP, leptomyxid meningitis, meningitis, myocarditis, Naegleria fowleri, photophobia, primary amebic meningoencephalitis, PAM, Sappinia diploidea

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Contributor Information and Disclosures

Author

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Medical Editor

Michael D Nissen, MBBS, BMedSc, FRACP, FRCPA, Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital
Michael D Nissen, MBBS, BMedSc, FRACP, FRCPA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Royal Australasian College of Physicians, and Royal College of Pathologists of Australasia
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
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Managing Editor

Martin Weisse, MD, Program Director, Associate Professor, Department of Pediatrics, West Virginia University
Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

CME Editor

David Pallares, MD, Clinical Assistant Professor, Department of Pediatrics, Division of Allergy and Immunology, University of Louisville
David Pallares, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology
Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
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, and Southern Medical Association
Disclosure: None None None

 
 
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