Inactivation of the macrolide antibiotics erythromycin, midecamycin, and rokitamycin by pathogenic Nocardia species.
A survey of five Nocardia spp. with respect to susceptibility towards three macrolides (erythromycin, rokitamycin, and midecamycin) showed that the Nocardia spp. have different susceptibility profiles. Most of the resistance was due to the inactivation of the macrolides by phosphorylation, glycosylation, reduction, deacylation, or a combination thereof.
Yazawa
K
K
Research Center for Pathogenic Fungi and Microbial Toxicoses, Chiba University, Japan.
Mikami
Y
Y
Sakamoto
T
T
Ueno
Y
Y
Morisaki
N
N
Iwasaki
S
S
Furihata
K
K
D001711:Biotransformation; D004917:Erythromycin / Q000493:pharmacokinetics* / Q000494:pharmacology; D006031:Glycosylation; D008658:Inactivation, Metabolic; D007933:Leucomycins / Q000493:pharmacokinetics* / Q000494:pharmacology; D008826:Microbial Sensitivity Tests; D015644:Miocamycin / Q000031:analogs & derivatives* / Q000493:pharmacokinetics / Q000494:pharmacology; D009615:Nocardia / Q000187:drug effects* / Q000378:metabolism*; D010084:Oxidation-Reduction; D010766:Phosphorylation
D007933:Leucomycins; D015644:Miocamycin; D004917:Erythromycin; C026483:midecamycin; C033383:rokitamycin