Fitness Cost of SCC
            <i>mec</i>
            and Methicillin Resistance Levels in
            <i>Staphylococcus aureus</i>

Ender, Miriam; McCallum, Nadine; Adhikari, Rajan P.; Berger‐Bächi, Brigitte

doi:10.1128/aac.48.6.2295-2297.2004

Cited by 147 publications

(128 citation statements)

References 13 publications

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“…MRSA strains that have been passaged to high-level vancomycin resistance and have retained methicillin resistance have converted to homotypic methicillin resistance (n ϭ 7; data not shown). Therefore, it may be that the mecA-associated fitness cost is a result of the conversion to the homotypic expression of methicillin resistance and not a direct consequence of increasing resistance to vancomycin, as previously shown by Ender et al (19). The conversion from heterotypic to homotypic methicillin resistance is not well understood.…”

Section: Discussionmentioning

confidence: 92%

“…Ender et al found an inverse correlation between oxacillin resistance levels and growth rate by competing strains with heterotypic and homotypic expression of oxacillin resistance (19). Also, Katayama et al have shown that a naïve methicillinsensitive S. aureus strain did not tolerate the introduction of plasmid-borne, unregulated mecA, as mecA was often mutated or deleted to circumvent the expression of PBP 2a (28).…”

Section: Discussionmentioning

confidence: 99%

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Spontaneous Deletion of the Methicillin Resistance Determinant, mecA , Partially Compensates for the Fitness Cost Associated with High-Level Vancomycin Resistance in Staphylococcus aureus

Noto¹,

Fox²,

Archer

2008

Antimicrob Agents Chemother

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Treatment of infections caused byStaphylococcus aureus is often confounded by the bacterium's ability to develop resistance to chemotherapeutic agents. Methicillin-resistant S. aureus (MRSA) arises through the acquisition of staphylococcal chromosomal cassette mec (SCCmec), a genomic island containing the methicillin resistance determinant, mecA. In contrast, resistance to vancomycin can result from exposure to the drug, a mechanism that is not dependent upon a gene acquisition event. Here we describe three MRSA strains that became resistant to vancomycin during passage in the presence of increasing concentrations of the drug. In each case two derivative strains were isolated, one that had lost mecA and one that retained mecA during passage. Strain 5836VR lost mecA by the site-specific chromosomal excision of SCCmec, while the other two strains (strains 3130VR and VP32) deleted portions of their SCCmec elements in a manner that appeared to involve IS431. Conversion to vancomycin resistance caused a decrease in the growth rate that was partially compensated for by the deletion of mecA. In mixed-culture competition experiments, vancomycin-resistant strains that lacked mecA readily outcompeted their mecA-containing counterparts, suggesting that the loss of mecA during conversion to vancomycin resistance was advantageous to the organism.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Spontaneous Deletion of the Methicillin Resistance Determinant, mecA , Partially Compensates for the Fitness Cost Associated with High-Level Vancomycin Resistance in Staphylococcus aureus

Noto¹,

Fox²,

Archer

2008

Antimicrob Agents Chemother

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“…Previous studies have shown that the relative fitness of hospital-acquired MRSAs carrying the type I SCCmec element is reduced (Ender et al, 2004), whereas strains containing the smaller type IV element were not affected (Lee et al, 2007). It has also been shown in vancomycin-resistant MRSA strains containing the type II SCCmec element that deletion of mecA compensated for some of the fitness costs associated with becoming vancomycin resistant, suggesting that mecA is also costly (Noto et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Offsetting virulence and antibiotic resistance costs by MRSA

et al. 2010

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The prevalence of diverse MRSA (methicillin-resistant Staphylococcus aureus) types in both hospital and community settings is a major health problem worldwide. Here we compare hospitalacquired MRSAs with large type II SCCmec elements with those prevalent in both hospital and community settings with smaller type IV SCCmec elements. We find that the type II but not the type IV SCCmec element causes the bacteria to reduce their levels of costly toxin expression. We compare the relative growth rates of these MRSA types and show that the type II SCCmec carrying MRSAs are more affected than those carrying type IV elements and from this we hypothesize that offsetting the costs associated with antibiotic resistance and toxin expression is why the type II are confined to hospital environments where antibiotic use, the prevalence of immunocompromised individuals and vector-mediated transmission is high. In contrast, those MRSAs that are also successful in the community can maintain their high levels of toxin expression due to a lower fitness burden associated with the smaller SCCmec element.

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“…Resistance-associated MGEs provide an advantage only in the presence of antibiotics. Otherwise, they can even be disadvantageous [17,18]. Thus, for such an element it is necessary to ensure its maintenance in the absence of selective pressure, e.g., if an antibiotic therapy was discontinued.…”

mentioning

confidence: 99%

“…Thus, for such an element it is necessary to ensure its maintenance in the absence of selective pressure, e.g., if an antibiotic therapy was discontinued. It can evolve to cause no or only minimal disadvantage in the absence of antibiotics, as it is the case for SCCmec type IV [17,18], to impose a selective pressure by itself [19] or, alternatively, to encode a factor conferring a selective advantage independently of the presence of antibiotics. Since experimental data show an influence of PSM-mec on virulence and/or biofilm formation [2,20], its presence might be a key factor for the evolutionary success (i.e., the pandemic spread and abundance) of SCCmec II and III elements and their host strains such as ST239-MRSA-III and ST5/ST225-MRSA-II.…”

mentioning

confidence: 99%

Distribution of SCCmec-associated phenol-soluble modulin in staphylococci

Monecke

Engelmann

Archambault

et al. 2012

Molecular and Cellular Probes

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Please cite this article as: Monecke S, Engelmann I, Archambault M, Coleman DC, Coombs GW, Cortez de Jäckel S, Pelletier-Jacques G, Schwarz S, Shore AC, Slickers P, Ehricht R, Distribution of SCCmecassociated phenol-soluble modulin in staphylococci, Molecular and Cellular Probes (2012), doi: 10.1016/ j.mcp.2012 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AB547236.1) and S. vitulinus (AB546780.1).The aim of this study was to screen staphylococcal isolates for the presence of PSM-mec in order to obtain more data on its distribution. 102 S. aureus isolates and 38 coagulase-negative staphylococci were genotyped using DNA microarrays (StaphyType, Alere Technologies GmbH, Jena, Germany, [7,9]). This allowed characterising their SCCmec elements [10]. In addition, SCCmec elements of some isolates have previously been studied comprehensively [11,12]. PCR primers pr_psmMEC_02 (5'-CGAAAGCCTGAATGCAAGTCT-3') and pr_psmMEC_03(5'-GGATTTCACTGGTGTTATTACAAGC-3') were used to detect PSM-mec. Reaction conditions included an initial denaturation (2 min at 96°C) followed by 35 cycles (20 sec at 96°C, 20 sec at 70°C and 20 sec at 72°C). A second PCR covered a region spanning from xylR to PSMmec (pr_psmMEC_02 and pr_xylR_04, 5'-AAGCGTCATCTTCTCATTTAGTTGA-3') and a third PCR covered the region from PSM-mec to mecR1 (pr_mecR_01, 5'-CCAGAAAGTAAACAACGATATTCACC-3' and pr_psmMEC_03). Both reactions comprised denaturation (2 min at 96°C) followed by 35 cycles (20 sec at 96°C, 20 sec at 55°C and 70 sec at The results are summarised in Table 1 vitulinus. The presence of PSM-mec did not depend on the host species, and was found in isolates from humans, dogs, cats, goats, cattle, pigs and turkeys. PSM-mec was absent in SCCmec types I, IIC, IIE, IV, V or XI and in SCC elements lacking the mec complex. Some isolates, including CC12-MRSA, WA-MRSA-59, harboured SCCmec elements comprising mecR1 but lacking xylR.These strains were PSM-mec-negative.There was no evidence for alternative locations of PSM-mec. Isolates lacking SCCmec elements, or harbouring SCCmec types I, IIC, IIE, IV and V were PSM-mec-negative regardless of clonal complex or species affiliation. A PCR covering the region from xylR to PSM-mec using primers pr_psmMEC_02/pr_xylR_04 yielded results which were in all cases but one in accordance with the PSM-mec PCR. In a PSM-mec-positive CC5-MRSA, xylR was absent, and primer pair pr_psmMEC_02/pr_xylR_04 did not yield a result.Results of a third PCR (pr_psmMEC/pr_mecR_01) differed from those of the other two PCRs by yielding negative results for ST8-MRSA-IIA or -IID, and for deletion variants of this strain. This can be attrib...

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Fitness Cost of SCC mec and Methicillin Resistance Levels in Staphylococcus aureus

Cited by 147 publications

References 13 publications

Spontaneous Deletion of the Methicillin Resistance Determinant, mecA , Partially Compensates for the Fitness Cost Associated with High-Level Vancomycin Resistance in Staphylococcus aureus

Spontaneous Deletion of the Methicillin Resistance Determinant, mecA , Partially Compensates for the Fitness Cost Associated with High-Level Vancomycin Resistance in Staphylococcus aureus

Offsetting virulence and antibiotic resistance costs by MRSA

Distribution of SCCmec-associated phenol-soluble modulin in staphylococci

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