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Vancomycin-resistant Enterococcus

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Vancomycin-resistant Enterococcus
Other names: Hospital acquired infection - VRE[1] , Vancomycin-resistant enterococci
  • Top:SEM micrograph of vancomycin-resistant enterococci

  • Bottom:Twenty-year trend percent vancomycin-resistant enterococci among Enterococcus sp. bloodstream infections [2]
SpecialtyMicrobiology
SymptomsFever,chills[3]
ComplicationsEndocarditis,colitis,osteomyelitis,sepsis,pneumonia[4]
Diagnostic methodRoutine cultures(determine species and drug susceptibilities)[4]
Differential diagnosisBacterial sepsis,hospital-acquired infections,infective endocarditis,pyogenic hepatic abscesses,septic arthritis[4]
PreventionScreen with peri-rectal swab[5]
TreatmentLinezolid [6]
Frequency5,400 deaths U.S.(2017)[3]

Vancomycin-resistant Enterococcus, or vancomycin-resistant enterococci (VRE), are bacterial strains of the genus Enterococcus that are resistant to the antibiotic vancomycin.[7]VRE can spread via contact with contaminated surfaces or and person-to-person.[3]

VRE infections are treated with antibiotics other than vancomycin; healthcare providers select the antibiotic based on laboratory tests[3]

Signs and symptoms

The presentation of Vancomycin resistant Enterococcus may indicate:[3][8]

Complications

Osteomylitis


Among the possible complications an individual may have due to Vancomycin-resistant Enterococcus are the following:[4]

  • Sepsis

Cause

To become vancomycin-resistant, vancomycin-sensitive enterococci typically obtain new DNA in the form of plasmids or transposons which encode genes that confer vancomycin resistance.[9] This acquired vancomycin resistance is distinguished from the natural vancomycin resistance of certain enterococcal species including E. gallinarum and E. casseliflavus/flavescens.[10][11]

Risk factors

In terms of the risk factors of Vancomycin-resistant Enterococcus we find the following:[12]

  • Older individuals
  • Currently in the hospital(taking antibiotics for long time)
  • Long-term illnesses or weak immune systems

Mechanism

Vancomycin resistance in enterococci is based on the modification of the D-Ala-D-Ala terminal AA's[13]

Six different types of vancomycin resistance are shown by enterococcus: Van-A, Van-B, Van-C, Van-D, Van-E and Van-G.[14] The significance is that Van-A VRE is resistant to both vancomycin and teicoplanin,[15]

Van-B VRE is resistant to vancomycin but susceptible to teicoplanin,[16][17] 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.[18]

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.[19][20]

Diagnosis

Image of a cluster of paired, or diplococcal, vancomycin-resistant Enterococcus (VRE) bacteria.

Once the individual has VRE, it is important to ascertain which strain.[21] The determination is done via routine culture to narrow down exact species and drug susceptibilities[4]

In terms of the sample it depends on the type of infection(urine or wound samples).Should the organism tests positive in the laboratory for VRE, then it must be determined which antibiotics will be effective via further analysis.[22]

Differential diagnosis

In terms of the DDx we find that the following is done:[23]

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.[5]

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 National Committee for Clinical Laboratory Standards (NCCLS) 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.[5][24]

Treatment

Linezolid

Ceftriaxone (a third generation cephalosporin) use is a risk factor for colonization and infection by VRE, and restriction of cephalosporin usage has been associated with decreased VRE infection and transmission in hospitals.[25]

Lactobacillus rhamnosus GG (LGG), a strain of L. rhamnosus, was used successfully for the first time to treat gastrointestinal carriage of VRE.[26]

In the US, linezolid is commonly used to treat VRE.[6]

Epidemiology

Map showing regional distribution of VRE in Ethiopia[27]

High-level vancomycin-resistant E. faecalis and E. faecium are clinical isolates first documented in the 1980s.[28]

In the United States, vancomycin-resistant E. faecium was associated with 4% of healthcare-associated infections reported to the Centers for Disease Control and Prevention National Healthcare Safety Network from January 2006 to October 2007.[29]

VRE can be carried by healthy people who have come into contact with the bacteria, usually in a hospital[30] (nosocomial infection),[31] although it is thought that a significant percentage of intensively farmed chickens also carry VRE.[32]

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.[33]

See also

References

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  2. Diekema, Daniel J.; Hsueh, Po-Ren; Mendes, Rodrigo E.; Pfaller, Michael A.; Rolston, Kenneth V.; Sader, Helio S.; Jones, Ronald N. (July 2019). "The Microbiology of Bloodstream Infection: 20-Year Trends from the SENTRY Antimicrobial Surveillance Program". Antimicrobial Agents and Chemotherapy. 63 (7). doi:10.1128/AAC.00355-19.
  3. 3.0 3.1 3.2 3.3 3.4 "Vancomycin-resistant Enterococci (VRE) Basics". Vancomycin-resistant Enterococci (VRE). 28 June 2024. Archived from the original on 11 September 2024. Retrieved 10 September 2024.
  4. 4.0 4.1 4.2 4.3 4.4 Levitus, Matthew; Rewane, Ayesan; Perera, Thomas B. (2024). "Vancomycin-Resistant Enterococci". StatPearls. StatPearls Publishing. Archived from the original on 2023-05-16. Retrieved 2024-09-06.
  5. 5.0 5.1 5.2 "Vancomycin-resistant Enterococci (VRE) and the Clinical Laboratory". Centers for Disease Control and Prevention. Archived from the original on 14 April 2019. Retrieved 21 May 2017. Public Domain This article incorporates text from this source, which is in the public domain.
  6. 6.0 6.1 Balli, Eleni P.; Venetis, Chris A.; Miyakis, Spiros (2014). "Systematic Review and Meta-Analysis of Linezolid versus Daptomycin for Treatment of Vancomycin-Resistant Enterococcal Bacteremia". Antimicrobial Agents and Chemotherapy. 58 (2): 734–739. doi:10.1128/AAC.01289-13. ISSN 0066-4804. PMC 3910884. PMID 24247127.
  7. "Vancomycin-resistant Enterococci (VRE) in Healthcare Settings". VRE in Healthcare Settings - HAI. CDC. Archived from the original on 2019-05-18. Retrieved 2015-06-09.
  8. Professional Guide to Signs and Symptoms. Lippincott Williams & Wilkins. 28 March 2012. ISBN 978-1-4511-5250-0. Archived from the original on 14 September 2024. Retrieved 14 September 2024.Google books offers no page #
  9. Gould, Dinah; Brooker, Christine (2008-08-20). Infection Prevention and Control: Applied Microbiology for Healthcare. Palgrave Macmillan. ISBN 9781137045928.{{cite book}}: CS1 maint: url-status (link)
  10. Monticelli J, et al. (2018). "Clinical management of non-faecium non-faecalis vancomycin-resistant enterococci infection. Focus on Enterococcus gallinarum and Enterococcus casseliflavus/flavescens". J Infect Chemother. 24 (4): 237–246. doi:10.1016/j.jiac.2018.01.001. PMID 29396199.
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  17. Grayson, M. Lindsay; Crowe, Suzanne M.; McCarthy, James S.; Mills, John; Mouton, Johan W.; Norrby, S. Ragnar; Paterson, David L.; Pfaller, Michael A. (2010-10-29). Kucers' The Use of Antibiotics Sixth Edition: A Clinical Review of Antibacterial, Antifungal and Antiviral Drugs. CRC Press. ISBN 9781444147520. Archived from the original on 2021-12-11. Retrieved 2021-11-25.
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  19. Meziane-Cherif, Djalal; Saul, Frederick A.; Haouz, Ahmed; Courvalin, Patrice (2012). "Structural and Functional Characterization of VanG d-Ala:d-Ser Ligase Associated with Vancomycin Resistance in Enterococcus faecalis♦". The Journal of Biological Chemistry. 287 (45): 37583–37592. doi:10.1074/jbc.M112.405522. ISSN 0021-9258. PMC 3488035. PMID 22969085.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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