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Acanthamoeba granulomatous encephalitis is a rare disease that almost always proves fatal. Death occurs mainly due to neurological complications; however, the pathogenesis and pathophysiology associated with this disease remain incompletely understood. Haematogenous spread is a key step in the development of Acanthamoeba encephalitis, but it is not clear how circulating amoebae breakthrough the blood–brain barrier to gain entry into the central nervous system to produce the disease. This review of the literature describes the parasite factors and immune-mediated mechanisms involved in the blood–brain barrier dysfunction leading to neuropathogenesis.
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