Development of Resistance to Ciprofloxacin, Rifampin, and Mupirocin in Methicillin-Susceptible and -Resistant
            <i>Staphylococcus aureus</i>
            Isolates

Schmitz, Franz‐Josef; Fluit, Ad C.; Häfner, D.; Beeck, Andreas; Perdikouli, Mirella; Boos, Mechthild; Scheuring, Sibylle; Verhoef, J.; Köhrer, Karl; Eiff, Christof von

doi:10.1128/aac.44.11.3229-3231.2000

Cited by 45 publications

(32 citation statements)

References 14 publications

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“…Two strains (221 SCV and 927 SCV ) produced growth revertants (designated 221 REV and 927 REV ) at rates of 1.76 ϫ 10 Ϫ6 and 1.21 ϫ 10 Ϫ6 per cell per generation, respectively, as assessed by fluctuation analysis (22). These rates are consistent with expected values for the reversion of a point mutation and are similar to other data in the literature reported for reversion of SCV strains (26,27). Sanger DNA sequencing confirmed that the revertant strains had a wild-type allele of the cognate men gene.…”

Section: Isolation Of S Aureus Scvssupporting

confidence: 80%

Identification of Point Mutations in Clinical Staphylococcus aureus Strains That Produce Small-Colony Variants Auxotrophic for Menadione

et al. 2014

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Staphylococcus aureus small-colony variants (SCVs) are implicated in chronic and relapsing infections that are difficult to diagnose and treat. Despite many years of study, the underlying molecular mechanisms and virulence effect of the small-colony phenotype remain incompletely understood. We sequenced the genomes of five S. aureus SCV strains recovered from human patients and discovered previously unidentified nonsynonymous point mutations in three genes encoding proteins in the menadione biosynthesis pathway. Analysis of genetic revertants and complementation with wild-type alleles confirmed that these mutations caused the SCV phenotype and decreased virulence for mice.

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Section: Isolation Of S Aureus Scvssupporting

confidence: 80%

Identification of Point Mutations in Clinical Staphylococcus aureus Strains That Produce Small-Colony Variants Auxotrophic for Menadione

et al. 2014

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“…Our data provide some insight into the epidemiology of these strains, as none of the isolates were USA300 and none of the patients were inpatients known to have received mupirocin ointment in the previous year. Studies have shown that the spontaneous mutation rate to mupirocin that results in low-level resistance is lower than the rates that result in resistance to ciprofloxacin and rifampin (18). A recent study found a coassociation between chlorhexidine resistance and low-level mupirocin resistance in hospitalized patients who had been decolonized with mupirocin and failed eradication (13).…”

Section: Discussionmentioning

confidence: 99%

Molecular Epidemiology of Methicillin-Resistant Staphylococcus aureus Isolates from Patients Newly Identified as Nasal Carriers

Weir¹,

Fram²,

Berg³

et al. 2012

J Clin Microbiol

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We aimed to determine whether additional molecular and microbiological evaluations of methicillin-resistant Staphylococcus aureus (MRSA) isolated from patients newly identified as nasal carriers were useful for control strategies and whether longitudinal testing during the same or repeat hospitalization changed MRSA status. Nasal swabs from patients positive by Xpert MRSA PCR and not known to be colonized in the previous year were cultured for S. aureus. Isolates were tested for resistance to a variety of antibiotics, including high-level mupirocin resistance (HLMR) and low-level mupirocin resistance (LLMR) and the presence of genes mecA and mupA and those for Panton-Valentine leukocidin (PVL), USA300, and USA400. Repeat nasal screens during the 6-month study were tested for continued presence of MRSA. Among 130 patients, cultures revealed MRSA in 85 (65.4%), methicillin-susceptible S. aureus in 19 (14.6%), and no growth in 26 (20%). MRSA isolates were USA300 positive in 13/85 (15.3%) and LLMR in 8/85 (9.4%) patients. No isolates were HLMR or mupA positive. mecA dropout was detected in 9/130 (6.9%) patients. The rate of subsequent MRSA infections in USA300-positive versus -negative patients was not different. MRSA nasal status remained concordant in 69/70 (98.6%) patients who had follow-up testing. The findings do not support expanding MRSA surveillance to include routine detection of genes for USA300, PVL, or mupA, all of which were either of low frequency or not significantly associated with MRSA infection risk in our population of newly identified nasal carriers. Repeat nasal screening for MRSA during the same or subsequent hospitalizations over 6 months could also be deferred, reducing costs associated with screening.

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“…A previous study has shown that inactivation of mutS in S. aureus RN4220 led to a hypermutator phenotype (28). It has also been suggested that hypermutable S. aureus might exist in naturally occurring populations (5,40). Although the study by O'Neill and Chopra (28) failed to detect any strong mutator strain in a large collection of clinical isolates, we recently detected a high proportion of hypermutable S. aureus among strains isolated from cystic fibrosis (CF) patients (33).…”

mentioning

confidence: 85%

Role of mutS and mutL Genes in Hypermutability and Recombination in Staphylococcus aureus

Prunier¹,

Leclercq²

2005

J Bacteriol

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The mutator phenotype has been linked in several bacterial genera to a defect in the methyl-mismatch repair system, in which the major components are MutS and MutL. This system is involved both in mismatch repair and in prevention of recombination between homeologous fragments in Escherichia coli and has been shown to play an important role in the adaptation of bacterial populations in changing and stressful environments. In this report we describe the molecular analysis of the mutS and mutL genes of Staphylococcus aureus. A genetic analysis of the mutSL region was performed in S. aureus RN4220. Reverse transcriptase PCR experiments confirmed the operon structure already reported in other gram-positive organisms. Insertional inactivation of mutS and mutL genes and complementation showed the role of both genes in hypermutability in this species. We also designed an in vitro model to study the role of MutS and MutL in homeologous recombination in S. aureus. For this purpose, we constructed a bank of S. aureus RN4220 and mutS and mutL mutants containing the integrative thermosensitive vector pBT1 in which fragments with various levels of identity (74% to 100%) to the S. aureus sodA gene were cloned. MutS and MutL proteins seemed to have a limited effect on the control of homeologous recombination. Sequence of mutS and mutL genes was analyzed in 11 hypermutable S. aureus clinical isolates. In four of five isolates with mutated or deleted mutS or mutL genes, a relationship between alterations and mutator phenotypes could be established by negative complementation of the mutS or mutL mutants.

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Development of Resistance to Ciprofloxacin, Rifampin, and Mupirocin in Methicillin-Susceptible and -Resistant Staphylococcus aureus Isolates

Cited by 45 publications

References 14 publications

Identification of Point Mutations in Clinical Staphylococcus aureus Strains That Produce Small-Colony Variants Auxotrophic for Menadione

Identification of Point Mutations in Clinical Staphylococcus aureus Strains That Produce Small-Colony Variants Auxotrophic for Menadione

Molecular Epidemiology of Methicillin-Resistant Staphylococcus aureus Isolates from Patients Newly Identified as Nasal Carriers

Role of mutS and mutL Genes in Hypermutability and Recombination in Staphylococcus aureus

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