Comparative molecular analysis of community- or hospital-acquired methicillin-resistant Staphylococcus aureus - PubMed (original) (raw)

Comparative molecular analysis of community- or hospital-acquired methicillin-resistant Staphylococcus aureus

P D Fey et al. Antimicrob Agents Chemother. 2003 Jan.

Abstract

Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is a growing public health concern that has been associated with pediatric fatalities. It is hypothesized that the evolution of CA-MRSA is a recent event due to the acquisition of mec DNA by previously methicillin-susceptible strains that circulated in the community. This study investigated the genetic relatedness between CA-MRSA, hospital-associated MRSA (HA-MRSA), and nonmenstrual toxic shock syndrome (nmTSS) isolates. Thirty-one of 32 CA-MRSA isolates were highly related as determined by pulsed-field gel electrophoresis and spa typing yet were distinguishable from 32 HA-MRSA strains. The 31 related CA-MRSA isolates produced either staphylococcal enterotoxin B (n = 5) or C (n = 26), and none made TSS toxin 1. All CA-MRSA isolates tested contained a type IV staphylococcal cassette chromosome mec (SCCmec) element. In comparison, none of the HA-MRSA isolates (n = 32) expressed the three superantigens. Antibiotic susceptibility patterns were different between the CA-MRSA and HA-MRSA isolates; CA-MRSA was typically resistant only to beta-lactam antibiotics. Six of twenty-one nmTSS isolates were indistinguishable or highly related to the CA-MRSA isolates. MnCop, an nmTSS isolate obtained in Alabama in 1986, was highly related to the CA-MRSA isolates except that it did not contain an SCCmec element. These data suggest that CA-MRSA strains may represent a new acquisition of SCCmec DNA in a previously susceptible genetic background that was capable of causing nmTSS. CA-MRSA poses a serious health risk not only because it is resistant to the antibiotics of choice for community-acquired staphylococcal infections but also because of its ability to cause nmTSS via superantigen production.

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Figures

FIG. 1.

FIG. 1.

PFGE subtyping and dendrogram of CA-MRSA, HA-MRSA, and nmTSS isolates. A PFGE pattern seen in more than one isolate was given a letter-and-number designation (e.g., A1). PFGE groups are noted on the far right end of the tree. The spa type, spa profile, and SCC_mec_ type, if testing was performed, are shown on the right end of the figure.

FIG. 2.

FIG. 2.

Results of PFGE of a representative isolate from each CA-MRSA PFGE group (A1 to A8). Lanes: 1, REF607 (group A1); 2, REF571 (group A2); 3, C98-370 (group A3); 4, REF559 (group A4); 5, MnCop (group A5); 6, C99-193 (group A6); 7, REF553 (group A7); 8, REF1239 (group A8); 9, REF1247 (group A8); and 10, COL.

FIG. 3.

FIG. 3.

Results of PFGE and subsequent hybridization with mecA and gyrA DNA probes. (A) Lanes: 1, NCTC8325; 2, C99-459; and 3, MnCop. White arrows show bands in both C99-459 and MnCop that differentiate these strains by PFGE. (B) Hybridization with a mecA probe. Lanes: 1 and 1A, NCTC8325; 2 and 2A, MnCop; and 3 and 3A, C99-459. White arrows show bands that hybridize with a mecA probe in C99-459. (C) Hybridization with a gyrA probe. Lanes: 1 and 1A, NCTC8325; 2 and 2A, MnCop; and 3 and 3A, C99-459. White arrows show bands that hybridize with a gyrA probe in all three strains. Black arrows in panel A show the size of the _Sma_I bands in NCTC8325, which approximates the size of the bands that hybridize to gyrA in MnCop and both mecA and gyrA in C99-459.

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