Minocycline resistance in Staphylococcus aureus: effect on phage susceptibility

Abstract

Tetracycline-resistant strains of Staphylococcus aureus are minocycline sensitive, with the exception of strains susceptible to phages of the 83A/84/85 complex and some methicillin-resistant strains of other phage types. Strains of the 83A/84/85 complex yield mutants with increased minocycline resistance. Transduction of minocycline resistance into the susceptible strain RN 450 was obtained with donor strains possessing either markers for both extrachromosomal tetracycline resistance (tet) and chromosomal tetracycline + minocycline resistance (tmn R), or only for chromosomal tmn R resistance. The chromosomal marker was differentiated from the extrachromosomal marker by the lack of detectable extrachromosomal deoxyribonucleic acid after transfer into strain RN 450, transfer into a rec(+) strain, lack of transfer into rec(-) acceptor strain, and cotransduction with chromosomal determinants for guanine biosynthesis. Both chromosomal and extrachromosomal tetracycline resistance can be induced by tetracycline. Induction by tetracycline of chromosomal tetracycline resistance resulted in simultaneous induction of minocycline resistance. The mutation toward increased minocycline resistance (tmn --> tmn R) is a regulatory mutation toward constitutivity or semiconstitutivity. Constitutive resistance is dominant in tmn R/tet diploids. Transfer of the tet marker does not affect the phage susceptibility of the acceptor strain. The tmn R marker, originating from donor strains of the 83A/84/85 complex, renders strain RN 450 resistant to several typing phages, with the exception of phages of the 83A/84/85 complex. This could possibly account for the phage typing patterns of minocycline-resistant staphylococci.