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Amebic Meningoencephalitis

  • Author: Robert W Tolan, Jr, MD; Chief Editor: Russell W Steele, MD  more...
Updated: Nov 17, 2015


Amebic meningoencephalitis, an extremely rare and sporadic central nervous system (CNS) infection, is caused by free-living amoebae; specifically, Naegleria fowleri[1] and Balamuthia mandrillari s ,[2] as well as species of Acanthamoeba and Sappinia. (See Etiology.)[3]

Typically, N fowleri produces primary amebic meningoencephalitis (PAM), which is clinically indistinguishable from acute bacterial meningitis. The other amoebae 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. (See Etiology, Presentation, and Workup.)



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 of patients to therapy. In most individuals with PAM or GAE, the diagnosis is made postmortem. (See Presentation, Workup, Treatment, and Medication.)

Depending on the extent of CNS injury, complications vary among the rare survivors of these infections.

Linam et al presented a survivor of amebic meningoencephalitis in North America. The authors conclude that the patient's survival most likely resulted from a variety of factors including early identification and treatment, use of a combination of antimicrobial agents (including miltefosine), and management of elevated intracranial pressure based on the principles of traumatic brain injury.[5]

Patient education

For patient education resources, see the Brain and Nervous System Center, as well as Brain Infection.



Primary meningoencephalitis

Although it is ubiquitous in most soils and environments, N fowleri can also be found in warm freshwater, particularly if the water is stagnant.[6] Exposure to the amoeba is very common. Children younger than 2 years frequently carry the organism asymptomatically in their nose and throat, especially in warmer months and climates.

PAM is an exceptionally uncommon result of CNS invasion of the typically healthy host by N fowleri. During a period of a few days to 2 weeks after swimming, diving, bathing, or playing in warm, usually stagnant, freshwater, the N fowleri amoebae 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.[7]

Case reports have detailed rare infection following ritual ablution with tap water that involves taking water into the nostrils.[8, 9] Similarly, sinus irrigation with contaminated tap (or other) water using neti pots (or other such devices) has resulted in PAM.[10]

Granulomatous amebic encephalitis

In contrast to PAM, GAE apparently results from either acanthamebic keratoconjunctivitis, via an uncommon phenomenon in which amoebae spread from the cornea to the CNS, or from the hematogenous spread of the ubiquitous organisms that cause GAE (B mandrillaris and Acanthamoeba and Sappinia species) from primary inoculation sites in the lungs or skin to 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 healthy hosts.



Occurrence in the United States

PAM and GAE are extremely rare but continue to be reported.[11] PAM is more common in warmer regions and in the warmer months of spring and summer. However, it has been reported as far north as Minnesota.[12] From 1937-2007, 121 cases (0-8 per year) were reported. Approximately 60 cases of Balamuthia GAE have been reported since 1975.[13] Those caused by Sappinia are even more rare.[3]  Cope et al reported the first PAM death associated with culturable N. fowleri in tap water from a US treated drinking water system.[14]

International occurrence

Although rare, cases of PAM and GAE have been reported worldwide, reflecting the ubiquity of the organisms.[15] More than 125 cases of Balamuthia GAE have been reported since 1975.[13] Most reports come from the United States, Australia, and Europe, although this is likely because of identification and reporting bias. Balamuthia infection in South America has been increasingly recognized.[16] In addition, a predominance of cases occurs in warmer climates and during warmer seasons of the year.

Sex- and age-related demographics

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

Contributor Information and Disclosures

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 Society for Microbiology, American Society of Tropical Medicine and Hygiene, American Academy of Pediatrics, Phi Beta Kappa, American Medical Association, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Physicians for Social Responsibility

Disclosure: Received honoraria from Novartis for speaking and teaching.

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.


Michael D Nissen, MBBS, 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, 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.

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.

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.

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