FROM ENVIRONMENTAL RESERVOIRS TO NEURAL DEVASTATION: A COMPREHENSIVE REVIEW ON THE BRAIN-EATING AMOEBA NAEGLERIA FOWLERI, ITS PATHOPHYSIOLOGY, HOST–PATHOGEN INTERACTIONS, AND THERAPEUTIC CHALLENGES
Yash Srivastav, Shankar Gavaroji, Tanmay Ghosh, Deepika Singh, Rohini Armo, Vivek, Harish Nath, Swapnil Dattatray Darade, Varaganti Sai Chitra Prathyusha*
ABSTRACT
Background: Naegleria fowleri, commonly known as the “brain-eating amoeba,” is a free-living thermophilic protozoan responsible for a rapidly progressive and almost universally fatal infection known as primary amoebic meningoencephalitis (PAM). Despite being rare, the disease poses a severe public health concern due to its high mortality rate, diagnostic challenges, and limited therapeutic efficacy. Global climate change, increasing freshwater exposure, and inadequate awareness have contributed to the amoeba’s growing ecological persistence and sporadic outbreaks. Objective: This review aims to provide a comprehensive overview of N. fowleri—encompassing its environmental reservoirs, morphological transitions, molecular mechanisms of neuroinvasion, host–pathogen interactions, clinical manifestations, diagnostic advancements, therapeutic interventions, and emerging research directions—to highlight critical gaps and future challenges in managing PAM. Methods: A systematic literature review was conducted using scientific databases including PubMed, Scopus, ScienceDirect, and Google Scholar (2010–2025). Peer-reviewed research articles, reviews, case studies, and epidemiological reports focusing on N. fowleri pathophysiology, host immune responses, diagnostic tools, and treatment strategies were analyzed and synthesized thematically. Results: N. fowleri exists in three morphologic stages—trophozoite, flagellate, and cyst—enabling it to survive diverse environmental conditions. The infection initiates through nasal exposure to contaminated warm freshwater, allowing amoebae to traverse the olfactory epithelium and invade the central nervous system. The pathogen secretes proteolytic enzymes, disrupts the blood–brain barrier, and induces extensive neural tissue necrosis accompanied by intense inflammatory responses.
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