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  • Author: Nancy F Crum-Cianflone, MD, MPH; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
Updated: Nov 30, 2015


The free-living amoebae that cause human infections include Acanthamoeba, Naegleria, Balamuthia mandrillaris, and Sappinia diploidea. All 4 genera cause CNS infections that are frequently fatal. These amoebae are distinct from other pathogenic protozoa. They all have a free-living existence, have no human carrier state (which is important in disease transmission), have a limited relationship with the spread of infection and poor sanitation, and involve no insect vector.[1]

Pathogenic species Acanthamoeba among humans includeAcanthamoeba castellanii, Acanthamoeba polyphaga, Acanthamoeba culbertsoni, Acanthamoeba palestinensis, Acanthamoeba astronyxis, Acanthamoeba hatchetti, Acanthamoeba rhysodes, Acanthamoeba divionensis, Acanthamoeba healyi,andAcanthamoeba griffini. The life cycle consists of 2 stages: a trophozoite (which is 14-40 µm in diameter) and a cyst (which has a double-layered wall with a diameter of 12-16 µm).

Acanthamoeba was first established as a cause of human disease in the 1970s. This genus causes 3 clinical syndromes: granulomatous amebic encephalitis (GAE), disseminated granulomatous amebic disease (eg, skin, sinus, and pulmonary infections), and amebic keratitis. Individuals who develop GAE or disseminated disease are usually immunocompromised, whereas those with amebic keratitis are usually immunocompetent. Disseminated disease and GAE carry a poor prognosis, and treatment strategies are not well defined; Acanthamoeba keratitis is a sight-threatening disease that carries a favorable prognosis when diagnosed and treated early in the disease course.



Acanthamoeba keratitis occurs in patients who sustain minor corneal trauma; this is usually associated with wearing contact lenses. Amoebae can be introduced through environmental exposures, including swimming while wearing contact lenses or using contaminated contact lens solutions, especially homemade solutions. Rare reports cite radial keratotomy preceding this infection.[2, 3]

GAE usually develops after hematogenous spread of the amoebae from pulmonary or skin lesions to the CNS. Alternatively, amoebae may enter via the olfactory epithelium.

Disseminated disease may begin in the sinuses, skin, or lungs and disseminate from these locations to other sites, including the brain, leading to GAE.


Acanthamoeba are ubiquitous organisms and have been isolated from soil, water (including natural and treated water), air, and dust. Most persons appear to have been exposed to this organism during their lifetime, as 50-100% of healthy people have serum antibodies directed against Acanthamoeba; studies have also demonstrated that this amoeba can be cultured from the pharyngeal area of healthy persons. Acanthamoeba has caused disease worldwide, including in the United States, Europe, Australia, Africa, and South America.

Acanthamoeba keratitis typically develops in otherwise healthy persons, with over 1,300 cases described in the literature. Most cases occur in people who wear contact lenses. Keratitis has been associated with wearing nondisposable contact lenses, using homemade sodium chloride solution to clean the lenses, and wearing lenses while swimming. An outbreak was described in 2005-2007 involving a multipurpose contact solution.[4] The isolation of Acanthamoeba from swimming pool water is not unusual. The bacteriologic quality of the water does not correlate with the presence of Acanthamoeba in swimming pools. Acanthamoeba cysts are very resistant to chlorine. A higher percentage of isolates from swimming pools have been shown to be pathogenic than those isolated from natural fresh water.

Despite the widespread existence of Acanthamoeba, GAE usually occurs among immunocompromised persons, including those with AIDS, transplant recipients (eg, bone marrow transplants), patients with cancer receiving chemotherapy, and those with systemic lupus erythematosus, steroid use, diabetes mellitus, malnutrition, or liver disease. Children who are malnourished, but otherwise healthy, are also at increased risk. Likewise, persons with disseminated disease without CNS involvement are usually immunocompromised; this condition is most common among patients with AIDS who have low CD4 counts (eg, < 200 cells/µL). In unusual cases, disseminated disease develops in immunocompetent children and adults. The incidence of GAE and disseminated disease appears to be rising, likely mirroring the increased number of persons worldwide who are living with immunocompromising conditions. To date, more than 100 cases of GAE have been described.




United States

Keratitis cases substantially increased in the 1980s with the introduction of disposable soft contact lenses.[5] Some evidence shows that the rate has subsequently declined, especially with the introduction of multipurpose cleaning solutions. The estimated rate of Acanthamoeba keratitis is 1 per 250,000 people in the United States, although rates vary among studies: from 1.65-2.01 per million population up to 1 per 10,000 people who wear contact lenses.[6]

GAE and disseminated Acanthamoeba disease are very rare, but rates may be increasing given the rising number of persons living with immunocompromising conditions. More than 100 cases of GAE have been described to date.


Acanthamoeba can cause keratitis, GAE, and disseminated disease worldwide. Data on the incidence rates of these infections internationally are not available since it is not a reportable disease.


Keratitis is a local infection that does not lead to systemic infection or death but may be complicated by cataracts, hypopyon, and increased intraocular pressure and may threaten sight.

GAE carries a very high mortality rate (nearly 100%). Survivors of GAE have been described; these patients were treated with combination antimicrobial therapies. Disseminated disease also carries a high mortality rate, but it is lower than GAE if CNS involvement does not occur.

Contributor Information and Disclosures

Nancy F Crum-Cianflone, MD, MPH Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Naval Medical Center at San Diego

Nancy F Crum-Cianflone, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Richard B Brown, MD, FACP Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine

Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

David Hall Shepp, MD Program Director, Fellowship in Infectious Diseases, Department of Medicine, North Shore University Hospital; Associate Professor, New York University School of Medicine

David Hall Shepp, MD is a member of the following medical societies: Infectious Diseases Society of America

Disclosure: Received salary from Gilead Sciences for management position.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthor William B. Harley, MD, to the development and writing of this article.

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