Plasmid-Mediated Resistance to Gentamicin in
            <i>Staphylococcus aureus</i>

Wood, Douglas; Carter, Mary Jo; Best, Gary K.

doi:10.1128/aac.12.4.513

Cited by 25 publications

(15 citation statements)

References 14 publications

(11 reference statements)

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“…Many of these determinants are thought to be of chromosomal origin (18), and some occur as such in other recent MR S. aureus isolates (4,32). The Melbourne isolates differ from these, however, with respect to the total number of resistance determinants carried by the chromosome, being only rivalled, perhaps, by recently described strains from France (8), and by the addition to the chromosome of genes for penicillinase production and resistance to heavy-metal ions, which are frequently reported as being located on plasmids (4,15,19,40). It is possible that these loci, which may be transposable (33), have undergone translocation to the chromosome in these recent Melbourne strains, and our evidence suggests that a similar process might now be occurring with the aminoglycoside determinant(s).…”

Section: Resultsmentioning

confidence: 99%

Analysis of plasmids in nosocomial strains of multiple-antibiotic-resistant Staphylococcus aureus

Lyon¹,

May²,

Skurray³

1983

Antimicrob Agents Chemother

117

119

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Nosocomial infections caused by Staphylococcus aureus strains resistant to methicillin and multiple antibiotics have reached epidemic proportions in Melbourne, Australia, over the past 5 years. Plasmid analysis of representative clinical isolates demonstrated the presence of three classes of plasmid DNA in most strains. Resistance to gentamicin, kanamycin, and tobramycin was usually mediated by an 18-megadalton plasmid but could also be encoded by a related 22-megadalton plasmid. Two distinguishable plasmids of 3 megadaltons each endowed resistance to chloramphenicol, and the third class consisted of small plasmids, each approximately 1 megadalton in size, with no attributable function. An extensive array of resistance determinants, including some which have usually been associated with a plasmid locus, were found to exist on the chromosome. Evidence that resistance to gentamicin, kanamycin, and tobramycin is chromosomally encoded in some clinical isolates suggests that this determinant may have undergone genetic translocation onto the staphylococcal chromosome.

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Section: Resultsmentioning

confidence: 99%

Analysis of plasmids in nosocomial strains of multiple-antibiotic-resistant Staphylococcus aureus

Lyon¹,

May²,

Skurray³

1983

Antimicrob Agents Chemother

117

119

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“…The difficulty experienced by several groups of workers in transducing gentamicin resistance might be explained if gen-r passed spontaneously between cells in vivo but its phage component tended to be lost in culture. On entry into the recipient cell, the genes determining gentamicin resistance would survive only if they became integrated into the chromosome or into a plasmid-as presumably had occurred in the cultures described by de Saxe and Porthouse (1979) and possibly others (Soussy et al, 197%;Wood, Carter, and Best, 1977). If such loci have a low probability of inclusion into prophages during induction or propagation, transduction would be difficult.…”

Section: Discussionmentioning

confidence: 99%

“…Gentamicin resistance in S. aureus is attributable to the production of inactivating enzymes (Bint et al, 1977;Dowding, 1977;Scott et al, 1978), as is usually the case with plasmid-mediated resistance. Plasmid DNA has been identified in gentamicin-resistant strains by Soussy et al (197%) and by Wood, Carter and Best (1977), but in neither case was it established that this DNA was responsible for the resistance, because the plasmid DNA was not isolated after transduction of the trait. Although transduction of gentamicin resistance has been achieved by a few workers, the frequencies have been low (Porthouse et al, 1976;Bint et al, 1977), and several others have been unable to transduce the resistance at all (e.g., Naidoo and Noble, 1978;Greenhood et al, 1979).…”

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confidence: 99%

Transfer of Gentamicin Resistance Between Cultures of Staphylococcus Aureus in Nutrient Broth, Serum and Urine

Lacey

Lord

1980

Journal of Medical Microbiology

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“…Most clinical isolates of S. aureus resistant to particular aminoglycosides have normal colonial morphology and possess plasmids directing the production of specific aminoglycoside-inactivating enzymes (4,15,20,25,26,33). The aminoglycoside-resistant strain described in this study is not of this type.…”

mentioning

confidence: 90%

Single and Combination Antibiotic Therapy of Staphylococcus aureus Experimental Endocarditis: Emergence of Gentamicin-Resistant Mutants

Miller

Wexler

Steigbigel

1978

Antimicrob Agents Chemother

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The efficacy of nafcillin and gentamicin used alone and in combination at doses giving serum concentrations comparable to those achieved in patients was studied in rabbits with experimental Staphylococcus aureus endocarditis. The organism used was a penicillinase-producing, methicillin-susceptible, clinical isolate. The addition of gentamicin to nafcillin significantly increased the rate of killing of organisms in valvular vegetations, compared to the effect of nafcillin alone. Gentamicin alone delayed mortality but was not effective in reducing the bacterial populations of the vegetations. Bacteremia persisted in the animals treated with gentamicin alone, in contrast to the groups treated with nafcillin or the combination. Selection of a subpopulation of aminoglycoside-resistant small-colony variants occurred in animals treated with gentamicin alone. This variant was subsequently employed in the rabbit model and produced endocarditis, metastatic infection, and bacteremia comparable to those caused by the parent strain. Animals with infection produced by the variant died later than animals infected by the parent strain. Nafcillin was equally effective in reducing the population of both parent and variant strains in vitro and in therapy of the infected animals. Population studies showed the variant to be a mutant emerging at a rate of 1.9 X 10-7. It was shown to differ from the parent strain in coagulase and hemolysin production, colonial morphology, and aminoglycoside susceptibility, but was similar by light and electron microscopy and in phage type, pigmentation of colonies, deoxyribonuclease production, mannitol fermentation, and growth rate.In vitro time-kill studies with blood culture isolates of penicillinase-producing, methicillinsusceptible S. aureus have demonstrated that gentamicin at a concentration of 5 ,ug/ml is rapidly bactericidal and reduces the bacterial population at a rate greater than that achieved by nafcillin at 20 jig/ml (N. H. Steigbigel, J. I.Casey, and B. J. Heeter, Clin. Res. 21:976, 1973). The initial rate of killing at a lower concentration of gentamicin (0.5 ,ug/ml) was similar to that obtained with 5 ,ug/ml but was associated with the later overgrowth, in each of 24 strains tested, of a small-colony variant which showed increased resistance when rechallenged with aminoglycosides. The combination of nafcillin and gentamicin (0.5 yg/ml) demonstrated the initial rapid killing without the subsequent emergence of the variant strain. Studies using a high inoculum of organisms, 109 colony-forming units (CFU) per ml, demonstrated that gentamicin alone or in combination with nafcillin was significantly active, whereas nafcillin alone did not decrease the population. The relevance of these in vitro observations was studied in a model of S. aureus endocarditis in rabbits.This study was presented in part at the 16th Interscience Conference on Antimicrobial Agents and Chemotherapy, October, 1976

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Plasmid-Mediated Resistance to Gentamicin in Staphylococcus aureus

Cited by 25 publications

References 14 publications

Analysis of plasmids in nosocomial strains of multiple-antibiotic-resistant Staphylococcus aureus

Analysis of plasmids in nosocomial strains of multiple-antibiotic-resistant Staphylococcus aureus

Transfer of Gentamicin Resistance Between Cultures of Staphylococcus Aureus in Nutrient Broth, Serum and Urine

Single and Combination Antibiotic Therapy of Staphylococcus aureus Experimental Endocarditis: Emergence of Gentamicin-Resistant Mutants

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