IMPLICATION OF COHESIVE BINDING OF A MACROLIDE ANTIBIOTIC, ROKITAMYCIN, TO RIBOSOMES FROM Staphylococcus aureus

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In a previous paper we reported that rokitamycin (RKM) which killed some types of RKM-susceptible staphylococci bound cohesively to ribosomes obtained from such bacteria whereas other macrolides such as erythromycin and josamycin, which are generally known to be bacteriostatic, bound to these ribosomes only reversibly. From this observation, we speculated that such cohesive binding of RKM to certain ribosomes probably resulted in cell killing (ENDOU, K. et al., FEMS Microbiology Letters, 72: 93-96, 1990). However, this speculation was based only on circumstantial evidence and we did not show directly that reversible binding of RKM to ribosomes from other strains would bring about bacteriostasis only. A clinically isolated strain, Staphylococcus aureus S704, was found to be susceptible to RKM, mycinamicin and tylosin as well as lincosamide and streptogramin type B antibiotics but not to other macrolides (erythromycin, josamycin, rosamicin, etc.). RKM showed bacteriostatic, but not bactericidal activity, on the strain. Determinant(s) responsible for the bacteriostatic phenotype was transferred into strain NCTC8325 using bacteriophage 80L2; the obtained transductant was referred to as strain 8325MMT7. The drug bound reversibly, not cohesively, to the ribosomes from both strains S704 and 8325MMT7, confirming our earlier hypothesis that rokitamycin can cause bacteriostasis or cell death depending upon whether it binds reversibly or cohesively to the ribosomes of a given strain.