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Sex differences in vancomycin-resistant enterococci bloodstream infections—a systematic review and meta-analysis



Vancomycin-resistant enterococci (VRE) have emerged in the healthcare setting worldwide. Infections with these pathogens, i.e., bloodstream infections (BSI), are accompanied with an impaired patient outcome. Diverse factors comprising patient characteristics, therapeutic strategies, and infection control measures are positively or negatively associated with VRE BSI occurrence. However, whether sex-specific differences influence the frequency of VRE BSI is yet unknown.

The aim of this systematic review was to comprehensively summarize and analyze sex prevalence in VRE BSI patients.

Main text

A systematic search for relevant articles was conducted in PubMed and Web of Science. After screening for eligibility, data extraction from included articles and risk of bias assessment were processed. The prevalence of male/female sex in VRE BSI patients and 95% CI were calculated for each study and summarized as pooled estimated effect.

In total, nine articles met the inclusion criteria. Risk of bias assessment resulted in low (six studies) to moderate bias (three studies). The pooled prevalence of male patients suffering from VRE BSI was 59% resulting in a 1.4 male/female prevalence ratio.


Current literature suggests sex differences with male preference (59%) in the distribution of VRE BSI cases. Further primary studies should address the question of male-specific factors favoring the enhanced frequency of VRE BSI.


  • Sex differences play a role in the emergence of infectious diseases.

  • The overall prevalence of male patients suffering from VRE BSI is 59%.

  • Male/female ratio in VRE BSI is 1.4.


Since their first description in the 1980s [1, 2], vancomycin-resistant enterococci (VRE) have evolved to become some of the most relevant multidrug-resistant organisms (MDRO) worldwide as acknowledged by the World Health Organization [3]. VRE pose a particular challenge for healthcare settings, given their ability to survive in the environment [4, 5] as well as their higher nosocomial prevalence as compared to other MDRO [6]. Besides colonizing the gastrointestinal tract of their human host, VRE may cause, inter alia, abdominal, foreign body-associated, and bloodstream infections (BSI) [7]. Invasive VRE infections, especially BSI, are known to have a higher mortality than those caused by vancomycin-susceptible enterococci [8]. Among VRE associated with human disease, Enterococcus faecium (E. faecium) represents the most relevant species, accounting for over 93% of all VRE isolates in Europe in 2019 [9]. The detection of VRE in clinical samples has continuously increased in several regions [10]. In Europe, this information has been systematically collected and monitored by the European Centre for Disease Control and Prevention (ECDC) since 2015, analyzing the proportion of vancomycin resistance among E. faecium strains isolated from blood cultures as a benchmark for comparison between countries [11]. Starting at an average of 10.5% in ECDC’s first regional data analysis in 2015, this proportion has steadily increased over the last years, reaching 17.3% in 2018, with rising trends in over 20 of the 30 countries evaluated [11].

Several factors have been described to be significantly associated with VRE colonization and infection, including treatment with antibiotics, immunosuppression, and further pre-existing pathologies and treatments [12,13,14]. Regarding demographic characteristics, the incidence of VRE infections is higher in patients of older age [15, 16]. However, it is unclear whether an association exists between sex and the development of VRE infections. Sex differences in the occurrence of numerous infectious diseases have been conclusively described (Fig. 1), having been linked with hormonal and genetic factors that contribute to this phenomenon [17, 18]. Among others, these sex differences have been described to play a role in the composition of the gut microbiota [19] as well as in the occurrence of the gastrointestinal tract and BSI [17, 18], including those caused by other MDRO such as methicillin-resistant Staphylococcus aureus (MRSA) [20].

Fig. 1

Sex differences influencing the occurrence of infectious diseases

Given the increasing relevance of VRE as emerging MRO worldwide [10], we sought to assess the existence of sex differences in VRE BSI at our institution by analyzing patient data collected between 2015 and 2020. This showed a male bias in the occurrence of VRE bacteremia, with male patients accounting for 73% (n=45) of all cases of VRE BSI (n=71) in this period. Thereupon, we conducted a systematic review of evidence available in digital databases, focusing on bacteremia as indicator infection with the aim of facilitating comparability with current epidemiological data worldwide.

Main text

This systematic review with meta-analysis was planned and conducted according to the American Medical Association standards for meta-analysis of observational studies in epidemiology (MOOSE) [21] and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines [22].

Search strategy and inclusion/exclusion criteria

Queries of literature were performed with the help of the electronic databases PubMed and Web of Science until May 2020 using the following combination of search terms to identify relevant articles: ((‘vancomycin resistant enterococci’) OR (‘vancomycin resistant enterococcus’) OR VRE) AND ((‘blood stream infection’) OR (‘bacteremia’) OR (‘bacteraemia’)) AND (male OR female OR sex OR gender). The literature search was conducted by two authors (CC and SK), with discrepancies resolved via discussion. Search results were limited to English language articles with a start date on 01/01/2015. Articles were included if they were conducted in hospitalized patients suffering from VRE BSI with an assumingly balanced sex ratio. Articles were excluded if they did not contain original peer-reviewed research (e.g., case reports, review articles, letters, etc.) and if no balanced sex ratio in patients could be assumed (e.g., veteran hospital studies, obstetric patients’ cohort).

Data extraction and risk of bias assessment

After determination of the study selection, two investigators independently extracted the following characteristics: the first author’s last name, year of publication, study origin, patient clientele, sample size, VRE BSI sample size, and prevalence of VRE BSI among observed male and female patients. To assess the risk of bias and quality of the included studies, we used the Cochrane risk of bias tool for prognosis studies QUIPS, which grades studies on a scale from high risk to low risk of bias due to study participation, study attrition, prognostic factor measurement, outcome measurement, study confounding, and statistical analysis and reporting. For each factor, 1 score point was assigned, resulting in a maximum of 6 points if no bias was detected. For partial bias, 0.5 points and for reliable bias 0 points were assigned, respectively.

Statistical analysis

Proportions and 95% CI were calculated for each study, with VRE BSI being the outcome variable and male sex representing the exposure. The pooled proportion was estimated using a random effects model with DerSimonian and Laird as variance estimator. Statistical inconsistency test I2 was used to assess inter-study heterogeneity, which was assumed at I2 > 50%. All the analyses were made using the software R version 3.6.3 (R Foundation for Statistical Computing, Vienna, Austria). Visualization of data was performed using the forest-plot package of the same software.


The literature screening process revealed nine articles [23,24,25,26,27,28,29,30,31], which were included for quantitative synthesis of data and are discussed in this review. Figure 2 summarizes the full screening and inclusion procedure. Included articles comprise cohort [23], cross-sectional [23], chart review [25], and case-control studies [27, 29], mostly with retrospective nature of conducted analyses from eight different countries. All admitted patients were considered in six of nine studies. In three studies [24, 26, 31], the analyzed population was limited due to age and/or underlying diagnoses. Further characteristics from each study can be extracted from Table 1.

Fig. 2

Systematic review flow chart

Table 1 Characteristics of included studies

Risk of bias assessment revealed five studies with 6 points [25, 27,28,29,30], indicating no risk of bias. The minimum score achieved was 4 points in two of the included studies, indicating a moderate risk of bias according to the chosen QUIPS tool. Details of the risk of bias assessment can be gathered from Table 2.

Table 2 Risk of bias assessment

All the nine selected studies contributed to the statistical analysis. As there was a borderline heterogeneity in selected studies (I2 = 48% [0%;76%]; p=0.05), a random effects model was employed. In a single study [23], sex ratio favors female patients for VRE BSI. All other eight studies revealed a gender bias towards male sex (Table 1, Fig. 2). The pooled effect size revealed 59% patients suffering from VRE BSI to be of male sex resulting in a pooled prevalence male/female ratio of 1.4 (Fig. 3).

Fig. 3

Forest plot displaying included articles


VRE are worldwide spread MDRO that thrive in healthcare settings and can cause severe invasive infections such as bacteremia. The evidence analyzed in this study indicates sex differences with male preference (59%) in the distribution of VRE BSI cases. This is in accordance with data collected during a 5-year period at our own institution, a university hospital with 1500 beds. Furthermore, epidemiological trends observed in the German federal state in which our hospital is located, a region with over 20 million inhabitants, show that 61% of all patients with VRE bacteremia between 2016 and 2019 were male (Correa-Martínez et al., unpublished data).

Sex differences have been previously reported in population-based studies on BSI caused by several pathogens, including Staphylococcus aureus (male bias) [20, 32] and Escherichia coli (female bias) [32, 33]. Besides socioeconomic, behavioral, and other contextual factors that could contribute to this phenomenon, certain biological determinants are considered to play a role in the sex differences observed in infectious diseases on the epidemiological level (Fig. 1). These include genetic and hormonal factors.

A particular characteristic of the XX genotype is the inactivation of parts of the X chromosomes. The resulting mosaicism leads to a transcriptional silencing of genes encoding chromosomal immune defects such as the X-linked chronic granulomatous disease and the X-linked Wiskott-Aldrich syndrome [34]. Moreover, the X chromosome also encodes microRNAs bearing an important immunoregulatory function [35].

The influence of sex steroid hormones on the immune response has been well documented [17, 34]. While higher levels of anti-inflammatory cytokines such as IL-10 have been detected in females with sepsis, pro-inflammatory cytokines IL-6 and TNF-α seem to predominate in males [36, 37]. Inflammation and tissue injury might also be enhanced by testosterone through stimulation of neutrophil activation [38]. However, estrogen has also been found to promote inflammatory responses, enhancing natural killer (NK) cell cytotoxicity and inducing the production of IL-1, Il-6, and TNFα [39, 40]. Furthermore, testosterone may induce immunosuppression by decreasing the expression of the major histocompatibility complex (MHC) class II and the toll-like receptor 4 (TLR4) on immune cells [40, 41]. Taken together, data indicate that sex hormones decisively influence immunity not by inducing a sex-specific pro- or anti-inflammatory effect, but rather by affecting the balance between both states in response to infectious agents. The immune homeostasis regulation seems to be more effective in females, as shown by the higher rate of splenocyte proliferation and production of IL-2 and IL-3 observed in animal models [42]. This leads to the belief that male immune response to sepsis can be more pronounced and prolonged, potentially inducing systemic damage more often than in females.

Female enhanced protection against microorganisms has been documented, as in the case of estrogen-driven, innate antibody-mediated immunological responses supporting clearance of enteropathogenic Escherichia coli from the bloodstream in animal models [43]. However, complex interactions between sex-specific and pathogen-specific immune responses may ultimately be decisive for outcomes in infection [44].

Perspectives and significance

Although current evidence points towards a male bias in VRE bacteremia, data is scattered and systematic assessment of evidence regarding this phenomenon is lacking. Our review constitutes a first comprehensive approach to the evidence available on the sex distribution of VRE bacteremia, highlighting consistent sex differences among published studies with male patients developing this condition significantly more frequently than female patients do.

The evidence reviewed in this work does not allow to establish causality. It rather indicates a significant association between male sex and occurrence of VRE bacteremia, a condition that can partially be favored by confounders such as underlying pathologies or antibiotic administration that predispose for susceptibility. The establishment of causal relationships through the characterization of causal (e.g., immunomodulatory) pathways and other factors involved warrants further epidemiological and biomedical research.

Sex differences regarding the outcomes of VRE BSI and possible discrepancies with the observed male predominance in the development of VRE bacteremia constitute a further research topic, considering evidence indicating a higher female mortality in spite of a lower incidence of MRSA BSI [45, 46].

In light of the growing challenges posed by VRE to healthcare systems worldwide, evidence on sex differences of invasive VRE infections constitutes valuable information at the clinical, epidemiological, and policymaking levels.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.


  1. 1.

    Leclercq R, Derlot E, Duval J, Courvalin P. Plasmid-mediated resistance to vancomycin and teicoplanin in Enterococcus faecium. N Engl J Med. 1988;319(3):157–61.

    CAS  Article  PubMed  Google Scholar 

  2. 2.

    Uttley AH, Collins CH, Naidoo J, George RC. Vancomycin-resistant enterococci. Lancet. 1988;1(8575-6):57–8.

    CAS  Article  PubMed  Google Scholar 

  3. 3.

    Tacconelli E, Carrara E, Savoldi A, Harbarth S, Mendelson M, Monnet DL, et al. Discovery, research, and development of new antibiotics: the WHO priority list of antibiotic-resistant bacteria and tuberculosis. Lancet Infect Dis. 2018;18(3):318–27.

    Article  PubMed  Google Scholar 

  4. 4.

    Ford CD, Lopansri BK, Gazdik MA, Webb B, Snow GL, Hoda D, et al. Room contamination, patient colonization pressure, and the risk of vancomycin-resistant Enterococcus colonization on a unit dedicated to the treatment of hematologic malignancies and hematopoietic stem cell transplantation. Am J Infect Control. 2016;44(10):1110–5.

    Article  PubMed  Google Scholar 

  5. 5.

    Suleyman G, Alangaden G, Bardossy AC. The role of environmental contamination in the transmission of nosocomial pathogens and healthcare-associated infections. Curr Infect Dis Rep. 2018;20(6):12.

    Article  PubMed  Google Scholar 

  6. 6.

    Erb S, Frei R, Dangel M, Widmer AF. Multidrug-resistant organisms detected more than 48 hours after hospital admission are not necessarily hospital-acquired. Infect Control Hosp Epidemiol. 2017;38(1):18–23.

    Article  PubMed  Google Scholar 

  7. 7.

    Agudelo Higuita NI, Huycke MM. Enterococcal disease, epidemiology, and implications for treatment. In: Gilmore MS, Clewell DB, Ike Y, Shankar N, editors. Enterococci: from commensals to leading causes of drug resistant infection. Boston: Massachusetts Eye and Ear Infirmary; 2014.

    Google Scholar 

  8. 8.

    DiazGranados CA, Zimmer SM, Klein M, Jernigan JA. Comparison of mortality associated with vancomycin-resistant and vancomycin-susceptible enterococcal bloodstream infections: a meta-analysis. Clin Infect Dis. 2005;41(3):327–33.

    Article  Google Scholar 

  9. 9.

    European Centre for Disease Prevention and Control. Surveillance Atlas of Infectious Diseases 2019 [Available from:].

    Google Scholar 

  10. 10.

    Pfaller MA, Cormican M, Flamm RK, Mendes RE, Jones RN. Temporal and geographic variation in antimicrobial susceptibility and resistance patterns of enterococci: results from the SENTRY Antimicrobial Surveillance Program, 1997-2016. Open Forum Infect Dis. 2019;6(Suppl 1):S54–s62.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  11. 11.

    European Centre for Disease Prevention and Control (ECDC). Surveillance of antimicrobial resistance in Europe 2018. Stockholm: European Centre for Disease Prevention and Control; 2019. Available from:

    Google Scholar 

  12. 12.

    Zacharioudakis IM, Zervou FN, Ziakas PD, Rice LB, Mylonakis E. Vancomycin-resistant enterococci colonization among dialysis patients: a meta-analysis of prevalence, risk factors, and significance. Am J Kidney Dis. 2015;65(1):88–97.

    CAS  Article  Google Scholar 

  13. 13.

    Papadimitriou-Olivgeris M, Drougka E, Fligou F, Kolonitsiou F, Liakopoulos A, Dodou V, et al. Risk factors for enterococcal infection and colonization by vancomycin-resistant enterococci in critically ill patients. Infection. 2014;42(6):1013–22.

    CAS  Article  PubMed  Google Scholar 

  14. 14.

    Pan SC, Wang JT, Chen YC, Chang YY, Chen ML, Chang SC. Incidence of and risk factors for infection or colonization of vancomycin-resistant enterococci in patients in the intensive care unit. PloS One. 2012;7(10):e47297.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  15. 15.

    Tacconelli E, Cataldo MA. Vancomycin-resistant enterococci (VRE): transmission and control. Int J Antimicrobial Agents. 2008;31(2):99–106.

    CAS  Article  Google Scholar 

  16. 16.

    Diekema DJ, Hsueh PR, Mendes RE, Pfaller MA, Rolston KV, Sader HS, et al. The microbiology of bloodstream infection: 20-year trends from the sentry antimicrobial surveillance program. Antimicrob Agents Chemother. 2019;63(7):e00355-19.

  17. 17.

    Vázquez-Martínez ER, García-Gómez E, Camacho-Arroyo I, González-Pedrajo B. Sexual dimorphism in bacterial infections. Biol Sex Differ. 2018;9(1):27.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  18. 18.

    Schurz H, Salie M, Tromp G, Hoal EG, Kinnear CJ, Möller M. The X chromosome and sex-specific effects in infectious disease susceptibility. Hum Genomics. 2019;13(1):2.

    Article  PubMed  PubMed Central  Google Scholar 

  19. 19.

    Gomez A, Luckey D, Taneja V. The gut microbiome in autoimmunity: Sex matters. Clin Immunol. 2015;159(2):154–62.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  20. 20.

    Allard C, Carignan A, Bergevin M, Boulais I, Tremblay V, Robichaud P, et al. Secular changes in incidence and mortality associated with Staphylococcus aureus bacteraemia in Quebec, Canada, 1991-2005. Clin Microbiol Infect. 2008;14(5):421–8.

    CAS  Article  PubMed  Google Scholar 

  21. 21.

    Stroup DF, Berlin JA, Morton SC, Olkin I, Williamson GD, Rennie D, et al. Meta-analysis of observational studies in epidemiology: a proposal for reporting. Meta-analysis Of Observational Studies in Epidemiology (MOOSE) group. JAMA. 2000;283(15):2008–12.

    CAS  Article  PubMed  Google Scholar 

  22. 22.

    Moher D, Liberati A, Tetzlaff J, Altman DG. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. PLoS Med. 2009;6(7):e1000097.

    Article  PubMed  PubMed Central  Google Scholar 

  23. 23.

    Chen CH, Lin LC, Chang YJ, Chang CY. Clinical and microbiological characteristics of vancomycin-resistant Enterococcus faecium bloodstream infection in Central Taiwan. Medicine (Baltimore). 2017;96(49):e9000.

    Article  PubMed  PubMed Central  Google Scholar 

  24. 24.

    Ford CD, Gazdik MA, Lopansri BK, Webb B, Mitchell B, Coombs J, et al. Vancomycin-resistant Enterococcus colonization and bacteremia and hematopoietic stem cell transplantation outcomes. Biol Blood Marrow Transplant. 2017;23(2):340–6.

    Article  PubMed  Google Scholar 

  25. 25.

    Xie O, Slavin MA, Teh BW, Bajel A, Douglas AP, Worth LJ. Epidemiology, treatment and outcomes of bloodstream infection due to vancomycin-resistant enterococci in cancer patients in a vanB endemic setting. BMC Infect Dis. 2020;20(1):228.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  26. 26.

    Ye JJ, Shie SS, Cheng CW, Yang JH, Huang PY, Wu TS, et al. Clinical characteristics and treatment outcomes of vancomycin-resistant Enterococcus faecium bacteremia. J Microbiol Immunol Infect. 2018;51(6):705–16.

    CAS  Article  PubMed  Google Scholar 

  27. 27.

    Johnstone J, Chen C, Rosella L, Adomako K, Policarpio ME, Lam F, et al. Patient- and hospital-level predictors of vancomycin-resistant Enterococcus (VRE) bacteremia in Ontario, Canada. Am J Infect Control. 2018;46(11):1266–71.

    Article  PubMed  Google Scholar 

  28. 28.

    Ryan L, O'Mahony E, Wrenn C, FitzGerald S, Fox U, Boyle B, et al. Epidemiology and molecular typing of VRE bloodstream isolates in an Irish tertiary care hospital. J Antimicrob Chemother. 2015;70(10):2718–24.

    CAS  Article  PubMed  Google Scholar 

  29. 29.

    Gouliouris T, Warne B, Cartwright EJP, Bedford L, Weerasuriya CK, Raven KE, et al. Duration of exposure to multiple antibiotics is associated with increased risk of VRE bacteraemia: a nested case-control study. J Antimicrob Chemother. 2018;73(6):1692–9.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  30. 30.

    Kramer TS, Remschmidt C, Werner S, Behnke M, Schwab F, Werner G, et al. The importance of adjusting for enterococcus species when assessing the burden of vancomycin resistance: a cohort study including over 1000 cases of enterococcal bloodstream infections. Antimicrob Resist Infect Control. 2018;7(1):133.

    Article  PubMed  PubMed Central  Google Scholar 

  31. 31.

    Bae KS, Shin JA, Kim SK, Han SB, Lee JW, Lee DG, et al. Enterococcal bacteremia in febrile neutropenic children and adolescents with underlying malignancies, and clinical impact of vancomycin resistance. Infection. 2019;47(3):417–24.

    CAS  Article  PubMed  Google Scholar 

  32. 32.

    Uslan DZ, Crane SJ, Steckelberg JM, Cockerill FR 3rd, St Sauver JL, Wilson WR, et al. Age- and sex-associated trends in bloodstream infection: a population-based study in Olmsted County, Minnesota. Arch Intern Med. 2007;167(8):834–9.

    Article  PubMed  Google Scholar 

  33. 33.

    Laupland KB, Gregson DB, Church DL, Ross T, Pitout JD. Incidence, risk factors and outcomes of Escherichia coli bloodstream infections in a large Canadian region. Clin Microbiol Infect. 2008;14(11):1041–7.

    CAS  Article  PubMed  Google Scholar 

  34. 34.

    Jaillon S, Berthenet K, Garlanda C. Sexual dimorphism in innate immunity. Clin Rev Allergy Immunol. 2019;56(3):308–21.

    CAS  Article  PubMed  Google Scholar 

  35. 35.

    Fischer J, Jung N, Robinson N, Lehmann C. Sex differences in immune responses to infectious diseases. Infection. 2015;43(4):399–403.

    CAS  Article  PubMed  Google Scholar 

  36. 36.

    Wang HE, Shapiro NI, Griffin R, Safford MM, Judd S, Howard G. Inflammatory and endothelial activation biomarkers and risk of sepsis: a nested case-control study. J Crit Care. 2013;28(5):549–55.

    CAS  Article  PubMed  Google Scholar 

  37. 37.

    Mencacci A, Leli C, Cardaccia A, Meucci M, Moretti A, D’Alo F, et al. Procalcitonin predicts real-time PCR results in blood samples from patients with suspected sepsis. PloS One. 2012;7(12):e53279.

    CAS  Article  PubMed  PubMed Central  Google Scholar 

  38. 38.

    Maser E, Xiong G, Grimm C, Ficner R, Reuter K. 3alpha-Hydroxysteroid dehydrogenase/carbonyl reductase from Comamonas testosteroni: biological significance, three-dimensional structure and gene regulation. Chem Biol Interact. 2001;130-132(1-3):707–22.

    CAS  Article  Google Scholar 

  39. 39.

    Sorachi K, Kumagai S, Sugita M, Yodoi J, Imura H. Enhancing effect of 17 beta-estradiol on human NK cell activity. Immunol Lett. 1993;36(1):31–5.

    CAS  Article  PubMed  Google Scholar 

  40. 40.

    Miller L, Hunt JS. Sex steroid hormones and macrophage function. Life Sci. 1996;59(1):1–14.

    CAS  Article  PubMed  Google Scholar 

  41. 41.

    Mayr S, Walz CR, Angele P, Hernandez-Richter T, Chaudry IH, Loehe F, et al. Castration prevents suppression of MHC class II (Ia) expression on macrophages after trauma-hemorrhage. J Appl Physiol (1985). 2006;101(2):448–53.

    CAS  Article  Google Scholar 

  42. 42.

    Zellweger R, Wichmann MW, Ayala A, Stein S, DeMaso CM, Chaudry IH. Females in proestrus state maintain splenic immune functions and tolerate sepsis better than males. Crit Care Med. 1997;25(1):106–10.

    CAS  Article  PubMed  Google Scholar 

  43. 43.

    Zeng Z, Surewaard BGJ, Wong CHY, Guettler C, Petri B, Burkhard R, et al. Sex-hormone-driven innate antibodies protect females and infants against EPEC infection. Nat Immunol. 2018;19(10):1100–11.

    CAS  Article  PubMed  Google Scholar 

  44. 44.

    McClelland EE, Smith JM. Gender specific differences in the immune response to infection. Arch Immunol Ther Exp (Warsz). 2011;59(3):203–13.

    Article  PubMed  Google Scholar 

  45. 45.

    Smit J, Lopez-Cortes LE, Kaasch AJ, Sogaard M, Thomsen RW, Schonheyder HC, et al. Gender differences in the outcome of community-acquired Staphylococcus aureus bacteraemia: a historical population-based cohort study. Clin Microbiol Infect. 2017;23(1):27–32.

    CAS  Article  Google Scholar 

  46. 46.

    Tacconelli E, Foschi F. Does gender affect the outcome of community-acquired Staphylococcus aureus bacteraemia? Clin Microbiol Infect. 2017;23(1):23–5.

    CAS  Article  Google Scholar 

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CC performed the formal analysis, was a major contributor in writing the manuscript, reviewed, and edited the manuscript. FS analyzed and interpreted internal prevalence data, reviewed, and edited the manuscript. SK conceptualized the present investigation, performed the formal analysis, curated the data, was a major contributor in writing the manuscript, reviewed, and edited the manuscript. All authors read and approved the final manuscript.

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Correspondence to Stefanie Kampmeier.

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Correa-Martínez, C.L., Schuler, F. & Kampmeier, S. Sex differences in vancomycin-resistant enterococci bloodstream infections—a systematic review and meta-analysis. Biol Sex Differ 12, 36 (2021).

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  • Vancomycin-resistant enterococci
  • VRE
  • Bloodstream infection
  • Bacteremia
  • epidemiology
  • Sex differences