Beyond Brain-Eating Amoebas: Current Insights into Naegleria fowleri Identification, Prevalence, and Treatment
DOI:
https://doi.org/10.71320/bcs.0011Keywords:
Meningoencephalitis, Molecular Diagnosis, Naegleria fowleri, Miltefosine, Amphotericin B.Abstract
Naegleria fowleri, commonly known as the “brain-eating amoeba,” is an opportunistic, free-living protozoan responsible for primary amoebic meningoencephalitis (PAM), a rare but almost invariably fatal infection of the central nervous system. This thermophilic amoeba thrives in warm freshwater environments such as lakes, hot springs, and poorly maintained swimming pools. It can survive under high temperatures, making it more prevalent in regions with warm climates and developed countries, including Australia, Europe, and the United States. This review summarizes current evidence on the global prevalence, clinical presentation, diagnostic challenges, and treatment strategies related to N. fowleri infections. Epidemiological data indicate that approximately 26.4% of global freshwater sources contain Naegleria species, with the highest prevalence recorded in the Americas at 33.2%. Infected individuals typically present with acute symptoms such as severe headache, high fever (101–105°F), neck stiffness, seizures, altered mental status, and coma, with disease progression often resulting in death within one to two weeks of symptom onset. Despite advances in supportive care and antimicrobial therapy, the case fatality rate remains over 90%. Conventional diagnostic methods include microscopy, culture, serology, imaging, and molecular techniques such as real-time PCR; however, delays in diagnosis often hamper timely treatment. Therapeutic regimens traditionally involve a combination of antifungal and antimicrobial agents, including amphotericin B, azoles, azithromycin, and miltefosine. Although amphotericin B is considered the gold standard due to its potent amoebicidal activity at concentrations as low as 0.01 μg/ml, its poor solubility and high toxicity can cause significant adverse effects such as nephrotoxicity, hematologic complications, and systemic symptoms like headache, vomiting, and fever. Additionally, in vitro studies have shown that N. fowleri may develop resistance to miltefosine at concentrations up to 40 μg/ml. This review underscores the critical need for early and accurate diagnostic tools, safer and more effective therapeutic alternatives, and greater public awareness to prevent exposure and improve patient survival. Further research is urgently required to develop novel treatment options and reduce the devastating impact of this neglected but deadly pathogen.
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