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| Vancomycin-resistant Staphylococcus aureus | |
|---|---|
 | |
| Scanning electron micrograph (SEM) shows astrain ofStaphylococcus aureus bacteria taken from avancomycin-intermediateStaphylococcus aureus (VISA) culture. | |
| Specialty | Microbiology |
| Diagnostic method | Disk diffusion[1] |
| Treatment | Beta-lactam antibiotic (in combination)[2] |
Vancomycin-resistantStaphylococcus aureus (VRSA) are strains ofStaphylococcus aureus that have acquired resistance to theglycopeptide antibioticvancomycin.[3] Bacteria can acquire resistance genes either by random mutation or through the transfer of DNA from one bacterium to another. Resistance genes interfere with the normal antibiotic function and allow bacteria to grow in the presence of the antibiotic.[4] Resistance in VRSA is conferred by the plasmid-mediatedvanA gene and operon.[5] Although VRSA infections are uncommon, VRSA is often resistant to other types of antibiotics and a potential threat to public health because treatment options are limited.[6] VRSA is resistant to many of the standard drugs used to treatS. aureus infections. Furthermore, resistance can be transferred from one bacterium to another.[5]
Vancomycin-resistantStaphylococcus aureus was first reported in the United States in 2002.[5] To date, documented cases of VRSA have acquired resistance through uptake of avancomycin resistance gene cluster fromEnterococcus (i.e.VRE).[7] The acquired mechanism is typically thevanA gene and operon from a plasmid inEnterococcus faecium orEnterococcus faecalis.[5]
This mechanism differs from strains ofvancomycin-intermediateStaphylococcus aureus (VISA), which appear to develop elevated MICs to vancomycin through sequential mutations resulting in a thicker cell wall and the synthesis of excess amounts ofD-ala-D-ala residues.[8]
The diagnosis of vancomycin-resistantStaphylococcus aureus (VRSA) is performed by performing susceptibility testing on a singleS. aureus isolate to vancomycin. This is accomplished by first assessing the isolate'sminimum inhibitory concentration (MIC) using standard laboratory methods, includingdisc diffusion,gradient strip diffusion, andautomated antimicrobial susceptibility testing systems.[1] Once the MIC is known, resistance is determined by comparing the MIC with established breakpoints.[9]
Resistant or "R" designations are assigned based on agreed upon values called breakpoints. Breakpoints are published bystandards development organizations such as the U.S.Clinical and Laboratory Standards Institute, theBritish Society for Antimicrobial Chemotherapy and theEuropean Committee on Antimicrobial Susceptibility Testing.
When theminimum inhibitory concentration of vancomycin is> 2 µg/mL, alternative antibiotics should be used. The approach is to treat with at least one agent to which the bacteria known to be susceptible byin vitro testing. The agents that are used includedaptomycin,linezolid,telavancin,ceftaroline, andquinupristin–dalfopristin. For people withmethicillin-resistantStaphylococcus aureus (MRSA)bacteremia in the setting of vancomycin failure the Infectious Diseases Society of America recommends high-dosedaptomycin, if the isolate is susceptible, in combination with another agent (e.g.,gentamicin,rifampin,linezolid,trimethoprim/sulfamethoxazole, or abeta-lactam antibiotic).[2]
Three classes of vancomycin-resistantS. aureus have emerged that differ in vancomycinsusceptibilities: vancomycin-intermediateS. aureus (VISA), heterogeneous vancomycin-intermediateS. aureus (hVISA), and high-level vancomycin-resistantS. aureus (VRSA).[10]
Vancomycin-intermediateS. aureus (VISA) (/ˈviːsə/ or/viːaɪɛseɪ/) was first identified inJapan in 1996[11] and has since been found in hospitals elsewhere inAsia, as well as inthe United Kingdom,France, theU.S., andBrazil. It is also termed GISA (glycopeptide-intermediateStaphylococcus aureus), indicating resistance to all glycopeptide antibiotics. These bacterial strains present a thickening of the cell wall, which is believed to reduce the ability of vancomycin to diffuse into the division septum of the cell required for effective vancomycin treatment.[12]
High-level vancomycin resistance inS. aureus has rarely been reported.[13]In vitro andin vivo experiments reported in 1992 demonstrated that vancomycin resistance genes fromEnterococcus faecalis could be transferred bygene transfer toS. aureus, conferring high-level vancomycin resistance toS. aureus.[14] Until 2002 such a genetic transfer was not reported for wildS. aureus strains. In 2002, a VRSA strain (/ˈvɜːrsə/ or/viːɑːrɛseɪ/) was isolated from a patient in Michigan.[15] The isolate contained themecA gene formethicillin resistance. VancomycinMICs of the VRSA isolate were consistent with the VanA phenotype ofEnterococcus species, and the presence of thevanA gene was confirmed bypolymerase chain reaction. The DNA sequence of the VRSAvanA gene was identical to that of avancomycin-resistant strain ofEnterococcus faecalis recovered from the same catheter tip. ThevanA gene was later found to be encoded within atransposon located on aplasmid carried by the VRSA isolate. This transposon, Tn1546, confersvanA-type vancomycin resistance in enterococci.[16]
As of 2019, 52 VRSA strains have been identified in the United States, India, Iran, Pakistan, Brazil, and Portugal.[17]
The definition of hVISA according to Hiramatsu et al. is a strain of Staphylococcus aureus that gives resistance to vancomycin at a frequency of 10−6 colonies or even higher.[18]
