Resistance Pattern and Genetics of Erythromycin-resistant Mutants of Streptococcus pyogenes

Malke, Horst

doi:10.1099/00221287-64-3-353

Journal of General Microbiology

1970

DOI: 10.1099/00221287-64-3-353

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Resistance Pattern and Genetics of Erythromycin-resistant Mutants of Streptococcus pyogenes

Horst Malke¹

Abstract: S U M M A R YSingle-step erythromycin-resistant strains of Streptococcus pyogenes 561 88 fell into two classes: whereas class A mutants were sensitive to lincomycin and carried mutations transducible by phage A 25, class B mutations conferred lincomycin cross-resistance and failed to be transducible under the conditions employed. Recombination and cotransduction experiments allowed the assigning of at least 10 of 13 class A mutations to the same linkage group. From interclass crosses recombinants emerged at fr… Show more

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Cited by 15 publications

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“…Sedimentation analyses of CCC DNA from S. faecalis DS-5. Fractions[9][10][11][12] in the gradient of Fig.1were dialyzed against 0.015 M NaCl-0.0015 M Na citrate, pH 7.4. "C-labeled 23S ColEl DNA, serving as a…”

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Characterization of Three Plasmid Deoxyribonucleic Acid Molecules in a Strain of Streptococcus faecalis : Identification of a Plasmid Determining Erythromycin Resistance

et al. 1974

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Three plasmids designated α, β, and γ, distinguishable by their molecular weights (6, 17, and 34 million, respectively) were isolated from Streptococcus faecalis strain DS-5 (ATCC 14508). Derivatives of this strain “cured” for erythromycin resistance lacked the β-plasmid. In the parent strain the β-plasmid was estimated to be present to the extent of one to two copies per chromosomal genome equivalent whereas the α- and γ-plasmids were about nine and five copies, respectively.

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Characterization of Three Plasmid Deoxyribonucleic Acid Molecules in a Strain of Streptococcus faecalis : Identification of a Plasmid Determining Erythromycin Resistance

et al. 1974

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“…S. pyogenes strain SM60 was used throughout (MALKE 1970 a). Derivatives of SMBO carrying chromosomal markers for erythromycin (eryA) or lincomycin resistance (ZinA) were obtained by A25-mediated transduction, using appropriate mutants of 56188 as donors (MALKE 1970b(MALKE , 1972a. The ERLl plasmid was introduced into these strains by transduction with P13 234mo (MALKE 1974).…”

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Interaction of chromosomal mutations to erythromycin resistance with plasmid‐mediated resistance to erythromycin and lincomycin in Streptococcus pyogenes

Malke

1977

J of Basic Microbiology

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Structural alterations of the bacterial ribosome resulting in resistance to antibiotics which inhibit protein synthesis can be brought about by chromosomal and plasmidlinked genes. The biochemical mechanism of plasmid-determined resistance to macrolides, lincosamides and streptogramin B (MLS) antibiotics in staphylococci and streptococci involves methylation of a specific sequence of 23 S ribosomal RNA, which blocks the binding of the drugs to the ribosome (review: WEISBLUM 1975 (MALKE 1972 b). The availability of plasmid and chromosomal determinants for erythromycin and lincomycin resistance in group A streptococci prompted an investigation of whether there exist any interactive relationships between these determinants. The experimental approach consisted in introducing the ERLl plasmid into a number of strains carrying mutations to erythromycin or lincomycin resistance isolated i n vitro and measuring the resulting changes in the level of resistance.The composition of horse serum-based liquid and solid media has been described elsewhere (MALKE 1973). Erythromycin and lincomycin were from VEB JENAPHARM, Jena and The UPJOHN Co., Kalamazoo, Mich., respectively. S. pyogenes strain SM60 was used throughout (MALKE 1970 a). Derivatives of SMBO carrying chromosomal markers for erythromycin (eryA) or lincomycin resistance (ZinA) were obtained by A25-mediated transduction, using appropriate mutants of 56188 as donors (MALKE 1970b(MALKE , 1972a. The ERLl plasmid was introduced into these strains by transduction with P13 234mo (MALKE 1974). Since the chromosomal mutations mediated relatively low levels of drug resistance (see Tab. l), transductants carrying E R L l could readily be selected by challenging erythromycin or lincomycin concentrations ranging from 10 t o 100 pg/ml. The minimal inhibitory concentrations (MIC) of erythromycin and lincomycin for the various strains were determined by the tube dilution method using serum broth containing serial doubling concentrations of the drugs and an inoculum of about 5 x lo4 colony-forming units/ml. The MIC of an antibiotic is defined as the lowest drug concentration preventing visible growth after overnight incubation a t 37 "C. I n general, extended incubation for 40 to 70 hr led to a doubling of the MIC values.

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Transductional analysis of resistance to lincomycin and erythromycin in Streptococcus pyogenes

Malke¹

1972

J of Basic Microbiology

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From the group A streptococcal strain 56188, mutants were selected for resistance t o lincomycin. Among these, two distinguishable classes occurred: whereas mutations assigned to the ZinA locus did not change the susceptibility to erythromycin and were transducible by phage A25, class B mutations conferred erythromycin cross-resistance and failed to be transducible under the conditions employed. Corresponding findings have previously been made concerning the properties of mutants selected for resistance to erythromycin.By two-point transduction crosses, the eryA and ZinA loci were placed in the same linkage group, as defined by cotransfer with phage A25. A common feature of mutants carrying both an eryA and a ZinA mutation was the slower growth compared to that of the parental strains bearing either mutation alone. This interaction among eryA and ZinA mutations proved to be strongest in certain combinations which were phenotypically unrecognizable because the resultant strains failed to develop colonies under the conditions used. On the other hand, the mutations of the established double mutants did not interact with respect to their effect on the resistance characteristics of the strains, which were the simple addition of the effects of the single mutations. Both the linkage relationships and the phenotypic properties of the eryA and ZinA mutations suggested that they might occur in genes coding for ribosomal proteins.Mutations carried out by the B classes of the erythromycin-resistant and lincomycin-resistant strains appeared to be located outside the eryA ZinA linkage group in region@), the function of which is unknown.

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Resistance Pattern and Genetics of Erythromycin-resistant Mutants of Streptococcus pyogenes

Cited by 15 publications

References 5 publications

Characterization of Three Plasmid Deoxyribonucleic Acid Molecules in a Strain of Streptococcus faecalis : Identification of a Plasmid Determining Erythromycin Resistance

Characterization of Three Plasmid Deoxyribonucleic Acid Molecules in a Strain of Streptococcus faecalis : Identification of a Plasmid Determining Erythromycin Resistance

Interaction of chromosomal mutations to erythromycin resistance with plasmid‐mediated resistance to erythromycin and lincomycin in Streptococcus pyogenes

Transductional analysis of resistance to lincomycin and erythromycin in Streptococcus pyogenes

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