Prevalence of vancomycin-resistant enterococcus in Africa in one health approach: a systematic review and meta-analysis.
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ABSTRACT:
SUBMITTER: Alemayehu T
PROVIDER: S-EPMC7688635 | biostudies-literature | 2020 Nov
REPOSITORIES: biostudies-literature
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Prevalence of vancomycin-resistant enterococcus in Africa in one health approach: a systematic review and meta-analysis.
Alemayehu Tsegaye T Hailemariam Mengistu M
Scientific reports 20201125 1
Vancomycin-resistant enterococci are a global challenge currently as reported by the World Health Organization. It is also important to recognize that combating antimicrobial resistance needs to recognize the interconnections between people, animals, plants and their shared environment in creating public health, the so-called One Health approach. Although the presence of VRE has been described in many regions of the world, there is a lack of comprehensive data indicating their prevalence of in A ...[more]
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Project description:BACKGROUND:The emergence of Vancomycin resistant enterococci (VRE) poses a major public health problem since it was first reported. Although the rising rates of VRE infections are being reported elsewhere in the worldwide; there is limited national pooled data in Ethiopia. Therefore, this study was aimed to estimate the pooled prevalence of VRE and antimicrobial resistance profiles of enterococci in Ethiopia. METHODS:Literature search was done at PubMed, EMBASE, Google scholar, African Journals online (AJOL) and Addis Ababa University repository following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline. Both published and unpublished studies reporting the prevalence of VRE until June 30, 2019 were included. Data were extracted using Microsoft Excel and copied to Comprehensive Meta-analysis (CMA 2.0) for analysis. Pooled estimate of VRE was computed using the random effects model and the 95% CIs. The level of heterogeneity was assessed using Cochran's Q and I2 tests. Publication bias was checked by visual inspection of funnel plots and Begg's and/or Egger's test. RESULTS:Twenty studies fulfilled the eligibility criteria and found with relevant data. A total of 831 enterococci and 71 VRE isolates were included in the analysis. The pooled prevalence of VRE was 14.8% (95% CI; 8.7-24.3; I2 = 74.05%; P < 0.001). Compared to vancomycin resistance, enterococci had higher rate of resistance to Penicillin (60.7%), Amoxicillin (56.5%), Doxycycline (55.1%) and Tetracycline (53.7%). Relatively low rate of resistance was found for Daptomycin and Linezolid with a pooled estimate of 3.2% (95% CI, 0.5-19.7%) and 9.9% (95% CI, 2.8-29.0%); respectively. The overall pooled multidrug resistance (MDR) rate of enterococci was 60.0% (95% CI, 42.9-75.0%). CONCLUSION:The prevalence of VRE and drug resistant enterococci are on the rise in Ethiopia. Enterococcal isolates showed resistance to one or more of the commonly prescribed drugs in different or the same drug lines. Multidrug resistant (MDR) enterococci were also found. Although the rates were low, the emergence of resistance to Daptomycin and Linezolid is an alarm for searching new ways for the treatment and control of VRE infections. Adherence to antimicrobial stewardship, comprehensive testing and ongoing monitoring of VRE infections in the health care settings are required.
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Project description:Vancomycin-resistant Enterococcus (VRE) is a leading cause of hospital-acquired infections and continues to spread despite widespread implementation of pathogen-targeted control guidelines. Commensal gut microbiota provide colonization resistance to VRE, but the role of gut microbiota in VRE acquisition in at-risk patients is unknown. To address this gap in our understanding, we performed a case-control study of gut microbiota in hospitalized patients who did (cases) and did not (controls) acquire VRE. We matched case subjects to control subjects by known risk factors and "time at risk," defined as the time elapsed between admission until positive VRE screen. We characterized gut bacterial communities using 16S rRNA gene amplicon sequencing of rectal swab specimens. We analyzed 236 samples from 59 matched case-control pairs. At baseline, case and control subjects did not differ in gut microbiota when measured by community diversity (P = 0.33) or composition (P = 0.30). After hospitalization, gut communities of cases and controls differed only in the abundance of the Enterococcus-containing operational taxonomic unit (OTU), with the gut microbiota of case subjects having more of this OTU than time-matched control subjects (P = 0.01). Otherwise, case and control communities after the time at risk did not differ in diversity (P = 0.33) or community structure (P = 0.12). Among patients who became VRE colonized, those having the Blautia-containing OTU on admission had lower Enterococcus relative abundance once colonized (P = 0.004). Our results demonstrate that the 16S profile of the gut microbiome does not predict VRE acquisition in hospitalized patients, likely due to rapid and profound microbiota change. The gut microbiome does not predict VRE acquisition, but it may be associated with Enterococcus expansion, suggesting that these should be considered two distinct processes.IMPORTANCE The Centers for Disease Control and Prevention estimates that VRE causes an estimated 54,000 infections and 539 million dollars in attributable health care costs annually. Despite improvements in hand washing, environmental cleaning, and antibiotic use, VRE is still prevalent in many hospitals. There is a pressing need to better understand the processes by which patients acquire VRE. Multiple lines of evidence suggest that intestinal microbiota may help some patients resist VRE acquisition. In this large case-control study, we compared the 16S profile of intestinal microbiota on admission in patients that did and did not subsequently acquire VRE. The 16S profile did not predict subsequent VRE acquisition, in part due to rapid and dramatic change in the gut microbiome following hospitalization. However, Blautia spp. present on admission predicted decreased Enterococcus abundance after VRE acquisition, and Lactobacillus spp. present on admission predicted Enterococcus dominance after VRE acquisition. Thus, VRE acquisition and domination may be distinct processes.
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Project description:BackgroundVancomycin-resistant Enterococci (VRE) represent a critical medical and public health concerns due to their association with serious nosocomial infections and a high risk of mortality. We aimed to reveal the pooled prevalence of VRE and antimicrobial resistance profiles among enterococci clinical isolates in Egypt.MethodsA PubMed, Scopus, Google Scholar, and Web of Science literature search was carried out in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline. Only published studies documenting the prevalence of VRE between 2010 and 2022 were included. Using the random effects model and the 95% confidence intervals, the pooled estimate of VRE was calculated by MedCalc Version 20.113. Cochran's Q and I2 tests were used to evaluate the degree of heterogeneity, and publication bias was examined by visually examining the funnel plot and its associated tests (Begg's and Egger's tests).ResultsThe pooled prevalence of VRE among enterococci clinical isolates in Egypt was estimated to be 26% (95% CI 16.9 to 36.3). E. faecalis had a greater pooled prevalence than E. faecium, with 61.22% (95% CI 53.65 to 68.53) and 32.47% (95% CI 27 to 38.2), respectively. The VanA gene is more frequent than the VanB gene among VRE, with a pooled prevalence of 63.3% (95% CI 52.1 to 73.7) and 17.95% (95% CI 7.8 to 31), respectively. The pooled resistance rate of linezolid was substantially lower than that of ampicillin and high-level gentamicin (HLG) 5.54% (95% CI 2.33 to 10%), 65.7% (95% CI 50.8 to 79.2%), and 61.1% (95% CI 47.4 to 73.9), respectively.ConclusionThe prevalence of VRE is alarmingly high in Egypt. It is imperative that antimicrobial stewardship activities and infection control programs are strictly adhered to and implemented to prevent further escalation of the problem.
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Project description:VanD type Enterococcus faecium 10/96A is constitutively resistant to vancomycin and to low levels of teicoplanin by nearly exclusive synthesis of peptidoglycan precursors terminating in D-alanyl-D-lactate (L. M. Dalla Costa, P. E. Reynolds, H. A. Souza, D. C. Souza, M. F. Palepou, and N. Woodford, Antimicrob. Agents Chemother. 44:3444-3446, 2000). A G(184)S mutation adjacent to the serine involved in the binding of D-Ala1 in the D-alanine:D-alanine ligase (Ddl) led to production of an impaired Ddl and accounts for the lack of D-alanyl-D-alanine-containing peptidoglycan precursors. The sequence of the vanD gene cluster revealed eight open reading frames. The organization of this operon, assigned to a chromosomal location, was similar to those in other VanD type strains. The distal part encoded the VanH(D) dehydrogenase, the VanD ligase, and the VanX(D) dipeptidase, which were homologous to the corresponding proteins in VanD-type strains. Upstream from the structural genes for these proteins was the vanY(D) gene; a frameshift mutation in this gene resulted in premature termination of the encoded protein and accounted for the lack of penicillin-susceptible D,D-carboxypeptidase activity. Analysis of the translated sequence downstream from the stop codon, but in a different reading frame because of the frameshift mutation, indicated homology with penicillin binding proteins (PBPs) with a high degree of identity with VanY(D) from VanD-type strains. The 5' end of the gene cluster contained the vanR(D)-vanS(D) genes for a putative two-component regulatory system. Insertion of ISEfa4 in the vanS(D) gene led to constitutive expression of vancomycin resistance. This new insertion belonged to the IS605 family and was composed of two open reading frames encoding putative transposases of two unrelated insertion sequence elements, IS200 and IS1341.
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