A-Z Index × Submit A-Z Index × Submit A-Z Index Search Dropdown × Submit Facebook Twitter LinkedIn Syndicate Emerging Infectious Disease journal ISSN: 1080-6059 Disclaimer: Early release articles are not considered as final versions. Any changes will be reflected in the online version in the month the article is officially released.
Amebic meningoencephalitis (AME) is a highly fatal central nervous system infection caused by various free-living amebae. We describe epidemiology of AME cases from Kerala, India, during January 1–November 11, 2025, and identify behavioral risk factors associated with PCR-confirmed Acanthamoeba spp. infection through a matched case–control study. We identified 159 AME case-patients, of which 67 (42.1%) tested positive for Acanthamoeba spp. amebae. Most AME cases were reported from 4 districts, peaking during the monsoon and postmonsoon periods. Exposure to natural water bodies for swimming or bathing and using nonchlorinated water for domestic purposes were associated with AME. History of maxillofacial injury or nasal surgery with subsequent exposure to natural water bodies and washing ulcers or skin lesions in natural water bodies were associated with higher odds of disease. Targeted risk communication about safe water practices and routine chlorination of domestic water sources can reduce AME risk in affected communities.
Amebic meningoencephalitis (AME) is a collection of rare but frequently fatal infections of the central nervous system caused by various free-living amebae (FLA). Such infections include primary amebic meningoencephalitis (PAM), caused by Naegleria fowleri amebae, and granulomatous amoebic encephalitis (GAE), caused by different species of Acanthamoeba , Balamuthia mandrillaris , and Sappinia spp. amebae ( 1 , 2 ). PAM typically manifests as an acute, rapidly progressive meningoencephalitis, whereas GAE usually manifests as a subacute or chronic encephalitic illness. The clinical manifestations of PAM are indistinguishable from those of bacterial meningitis, whereas GAE can mimic brain abscess, encephalitis, or meningitis. PAM and GAE are associated with high mortality rates; case-fatality rates >90% have been reported globally ( 3 , 4 ).
N. fowleri amebae infect susceptible persons when contaminated water enters the nasal cavity; trophozoites can penetrate the olfactory mucosa, cross the cribriform plate, and invade the olfactory bulb, leading to parenchymal inflammation and tissue damage ( 5 , 6 ). The trophozoites of Acanthamoeba spp. amebae can enter the body through the eyes, nasal passages, or ulcerated or broken skin ( 7 , 8 ). Ocular exposure can cause severe keratitis ( 9 ); entry through the respiratory tract or broken skin can cause hematogenous spread to the central nervous system ( 10 , 11 ). Swimming or diving in warm fresh water like hot springs, lakes, rivers, and ponds are the primary risk factors for N. fowleri infection, although other water sources, including tap water, have been implicated ( 12 ). Environmental risk factors for Acanthamoeba GAE include exposure to contaminated soil, dust, freshwater sources, and untreated water systems. Because Acanthamoeba is ubiquitous in natural and manmade environments, inhalation of airborne cysts or contamination of skin lesions can result in infection, particularly in susceptible persons ( 13 – 15 ).
In the state of Kerala, India, 45 cases of AME were reported during 2016–2024, including 15 deaths (33% case-fatality rate).…