Vancomycin-resistant Enterococcus

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Vancomycin-resistant Enterococcus
Other namesVancomycin-resistant enterococci
SEM micrograph of vancomycin-resistant enterococci
SpecialtyMicrobiology
PreventionScreen with peri-rectal swab[1]
TreatmentLinezolid [2]

Vancomycin-resistant Enterococcus, or vancomycin-resistant enterococci (VRE), are

resistant to the antibiotic vancomycin.[3]

Mechanism of acquired resistance

Vancomycin

Six different types of vancomycin resistance are shown by enterococcus: Van-A, Van-B, Van-C, Van-D, Van-E and Van-G.[4] The significance is that Van-A VRE is resistant to both vancomycin and teicoplanin,[5] Van-B VRE is resistant to vancomycin but susceptible to teicoplanin,[6][7] and Van-C is only partly resistant to vancomycin.

The mechanism of resistance to vancomycin found in enterococcus involves the alteration of the peptidoglycan synthesis pathway.[8]

The D-alanyl-D-lactate variation results in the loss of one hydrogen-bonding interaction (four, as opposed to five for D-alanyl-D-alanine) being possible between vancomycin and the peptide. The D-alanyl-D-serine variation causes a six-fold loss of affinity between vancomycin and the peptide, likely due to steric hindrance.[9][10]

To become vancomycin-resistant, vancomycin-sensitive enterococci typically obtain new DNA in the form of

transposons which encode genes that confer vancomycin resistance.[11] This acquired vancomycin resistance is distinguished from the natural vancomycin resistance of certain enterococcal species including E. gallinarum and E. casseliflavus/flavescens.[12][13]

Diagnosis

Once the individual has VRE, it is important to ascertain which strain.[14]

Screening

Screening for VRE can be accomplished in a number of ways. For inoculating peri-rectal/anal swabs or stool specimens directly, one method uses bile esculin azide agar plates containing 6 μg/ml of vancomycin. Black colonies should be identified as an enterococcus to species level and further confirmed as vancomycin resistant by an MIC method before reporting as VRE.[1]

Vancomycin resistance can be determined for enterococcal colonies available in pure culture by inoculating a suspension of the organism onto a commercially available brain heart infusion agar (BHIA) plate containing 6 μg/ml vancomycin. The Clinical and Laboratory Standards Institute (CLSI) recommends performing a vancomycin MIC test and also motility and pigment production tests to distinguish species with acquired resistance (vanA and vanB) from those with vanC intrinsic resistance.[1] Detection of vancomycin resistance by the use of PCR targeting vanA and vanB can also be performed.[15][16]

Treatment of infection

Linezolid

L. rhamnosus, was used successfully for the first time to treat gastrointestinal carriage of VRE.[18] In the US, linezolid is commonly used to treat VRE.[2] The combination of daptomycin and ampicillin is another option to treat VRE infections, especially for bacteremia.[19] For invasive vancomycin-resistant E. faecalis infections, both ampicillin-ceftriaxone and ampicillin-gentamicin combinations have been used successfully, with the latter specifically showing success in treating endocarditis.[20] If the VRE strain is vanB, teicoplanin and dalbavancin are suitable therapeutic options.[21] Another antibiotic often used as off-label salvage therapy in systemic VRE infections is oritavancin, a semisynthetic glycopeptide that has demonstrated synergic activity with fosfomycin.[22]

History

High-level vancomycin-resistant

Other regions have noted a similar distribution, but with increased incidence of VRE. For example, a 2006 study of nosocomial VRE revealed a rapid spread of resistance among enterococci along with an emerging shift in VRE distribution in the Middle East region, such as Iran. Treatment failures in enterococcal infections result from inadequate information regarding glycopeptide resistance of endemic enterococci due to factors such as the presence of VanA and VanB. The study from Iran reported the first case of VRE isolates that carried VanB gene in enterococcal strains from Iran. This study also noted the first documented isolation of nosocomial E. raffinosus and E. mundtii in the Middle East region.[29]

See also

References

  1. ^ a b c "Vancomycin-resistant Enterococci (VRE) and the Clinical Laboratory". Centers for Disease Control and Prevention. Retrieved 21 May 2017. Public Domain This article incorporates text from this source, which is in the public domain.
  2. ^
    PMID 24247127
    .
  3. ^ "Vancomycin-resistant Enterococci (VRE) in Healthcare Settings". VRE in Healthcare Settings - HAI. CDC. Retrieved 2015-06-09.
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  13. ^ "VRE and the Clinical Laboratory - HAI". Healthcare-associated Infections. CDC. Retrieved 2015-06-09.
  14. PMID 30020605
    . Retrieved 27 March 2022.
  15. . The LightCycler instrument (Roche Diagnostics Corporation) is used to detect vanA and vanB using a rapid real-time PCR assay(Figure 3). This method is more sensitive and faster (~3.5 vs >72 hours) than culture for detecting VRE colonization.47 The assay detects the presence of genes associated with vancomycin resistance in enterococci, vanA and vanB.
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  24. . The first reports of vancomycin-resistant enterococci (later classified as VanA type of resistance) involved strains of E. faecium that were resistant to vancomycin and teicoplanin (another glycopeptide) and that were isolated from patients in France and England in 1986. Vancomycin-resistant E. faecalis, subsequently classified as VanB type, was recovered from patients in Missouri in 1987.
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  26. ^ "Diseases and Organisms in Healthcare Settings". Healthcare-associated Infections (HAIs). CDC. Retrieved 2015-06-09.
  27. PMID 23115435
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  29. ^ Fathollahzadeh B, Hashemi FB, Emaneini M, Aligholi M, Nakhjavani FA (2006). "Frequency of Vancomycin-Resistant Enterococci from Three Hospitals in Iran". Daru. 14 (3): 141–146. Archived from the original (PDF) on 2016-03-04. Retrieved 2015-12-30.

Further reading

External links