Summer can be hot, and many people cool down by jumping in nearby lakes and rivers. However, that’s also where millions of microbes like to play: as reported by multiple news outlets, the third 2011 US death has now been attributed to what the popular press has dubbed “the brain-eating amoeba.”
This “amoeba,” actually a protist called Naegleria fowleri, has been known to medicine since 1965. It belongs to a completely different biological branch from the true amoebas (I won’t go into all the biological background here, but Jennifer Frazier over at The Artful Amoeba has much more to say). This organism’s M.O. sounds like a cross between kuru (a brain-destroying prion disease)and flesh-eating bacteria. When a victim inhales freshwater containing N. fowleri, the organism attacks nasal membranes, working its way up towards the brain. Infected patients’ symptoms mimic those of encephalitis or meningitis, delaying proper drug treatment, while the protist quite literally consumes their nerve tissues.
Sound gruesome? Well, so are the existing therapies to fight it – the CDC Naegleria fact sheet discloses no current best treatment. The infected often receive amphotericin B, an antifungal known to have toxicity issues, in combination with an antibiotic (minocycline, or azithromycin). These combination therapies may improve the overall infection survival rate, but targets for small-molecule inhibition have been sorely lacking.
One promising biological lead to conquering N. fowleri does exist: the Nfa-1 gene. This gene produces proteins that impact the structure of the protist’s food cups, the organs used to digest tissue. A 2011 study indicated that chlorpromazine, an antipsychotic developed in the 1950s, inhibits Nfa-1 gene expression, and a 2008 test showed 75% survival of mice treated with chlorpromazine. Researchers hope this legacy drug can be further optimized to discover new N. fowleri treatments.
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