The Neuropathogenesis of Acanthamoeba encephalitis : Barriers to Overcome

Acanthamoeba is an opportunistic protist pathogen that is ubiquitously distributed in the environment. It is known to produce a sight-threatening, extremely painful keratitis and granulomatous encephalitis [1-4]. Acanthamoeba encephalitis is a fatal brain infection with a case fatality of more than 90%, despite advances in antimicrobial chemotherapy and supportive care. This is partly due to our incomplete understanding of the pathogenesis and pathophysiology of Acanthamoeba infections. At present, the treatment of Acanthamoeba encephalitis is a hit and miss, where a mixture of drugs is administered and even then the prognosis remains extremely poor. No single drug has shown to be effective against this devastating infection indicating an urgent need for improved antimicrobial chemotherapy and/or alternative strategies for therapeutic interventions. Here, we attempt to elucidate the mechanisms of parasite entry into the central nervous system (CNS) leading to granulomatous encephalitis-associated complications.