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Acanthamoeba encephalitis exhibits broad spectrum of neuropathology depending on the localization of the lesions. Natural infection is associated with haematogenous spread leading to Acanthamoeba entry into the brain, most likely via the blood-brain barrier, although blood-cerebrospinal fluid barrier has also been suggested as a possible route. Experimental infection is induced by intranasal injection of parasites, followed by amoebae invasion of the central nervous system via the olfactory neuroepithelium route. The precise mechanism of entry and the factors that influence amoebae entry into the central nervous system are not fully understood. The development of strategies to combat this fatal infection requires an understanding of the interactions between Acanthamoeba and the central nervous system.