Abstract

INITIAL in vitro studies established that rifampicin, one of a group of rifamycin SV derivatives1,2, prohibits bacterial growth and phage replication by binding to a polypeptide component of the microbial DNA-dependent RNA polymerase3–7. The trachoma agent and related psittacosis-lymphogranuloma agents are also inhibited in vitro and in embryonated eggs by this drug8. Further studies have shown that rifampicin is active against a number of bacteria in vivo, both after parenteral and oral administration1,9,10. It also inhibits malaria in mice11 and trachoma in monkeys12,13 and is of special value in the treatment of human tuberculosis14–16. The low toxicity of the rifamycins in mammals17 has been attributed to the observed relative insensitivity of mammalian RNA polymerase to the rifamycins in vitro3,18.

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