Mycolic acid-containing bacteria inactivate rifampicin in a variety of
ways such as glucosylation, ribosylation, phosphorylation and decolor
ization. These inactivations were found to be a species-specific pheno
mena in Nocardia and related taxa. Gordona, Tsukamurella and fast-grow
ing Mycobacterium modified rifampicin by ribosylation of the 23-OH gro
up of the antibiotic. Such ribosylation was not observed in Rhodococcu
s and Corynebacterium, but phosphorylation of the 21-OH group of rifam
picin was observed in one strain of Rhodococcus. Nocardia modified the
antibiotic by glucosylation (23-OH group) and phosphorylation, but ri
bosylation was not observed.