The belief that the outcome of bacterial meningitis is improved by controlling the intracerebral inflammatory response and, in particular, inflammation associated with antimicrobial-induced bacterial death is longstanding. The potential for antimicrobial treatment to cause paradoxical clinical harm was first recognised more than more than 100 years ago by Herxheimer and Krause and Jarisch when they noted fever, flushing, and hypotension after the treatment of syphilis with mercury. This reaction became termed the Jarisch-Herxheimer reaction. Similar reactions were reported by Reilly and colleagues4 in the 1950s, after patients received high doses of antibiotics for typhoid, and were caused by the sudden liberation of endotoxin from the bacterial cell wall. Reilly cautioned that the natural desire is to hit the disorder hard and fast, but that this approach should be resisted and that less aggressive antibiotic treatment might improve outcomes.
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