Limits...
Global spread of vancomycin-resistant Enterococcus faecium from distinct nosocomial genetic complex.

Willems RJ, Top J, van Santen M, Robinson DA, Coque TM, Baquero F, Grundmann H, Bonten MJ - Emerging Infect. Dis. (2005)

Bottom Line: Evolutionary genetics, population structure, and geographic distribution of 411 VRE and vancomycin-susceptible Enterococcus faecium isolates, recovered from human and nonhuman sources and community and hospital reservoirs in 5 continents, identified a genetic lineage of E. faecium (complex-17) that has spread globally.This lineage is characterized by 1) ampicillin resistance, 2) a pathogenicity island, and 3) an association with hospital outbreaks.Preventing further spread of this epidemic E. faecium subpopulation is critical, and efforts should focus on the early disclosure of ampicillin-resistant complex-17 strains.

View Article: PubMed Central - PubMed

Affiliation: University Medical Center Utrecht, Utrecht, the Netherlands. r.willems@digd.azu.nl

ABSTRACT
Vancomycin-resistant enterococci (VRE) have caused hospital outbreaks worldwide, and the vancomycin-resistance gene (vanA) has crossed genus boundaries to methicillin-resistant Staphylococcus aureus. Spread of VRE, therefore, represents an immediate threat for patient care and creates a reservoir of mobile resistance genes for other, more virulent pathogens. Evolutionary genetics, population structure, and geographic distribution of 411 VRE and vancomycin-susceptible Enterococcus faecium isolates, recovered from human and nonhuman sources and community and hospital reservoirs in 5 continents, identified a genetic lineage of E. faecium (complex-17) that has spread globally. This lineage is characterized by 1) ampicillin resistance, 2) a pathogenicity island, and 3) an association with hospital outbreaks. Complex-17 is an example of cumulative evolutionary processes that improved the relative fitness of bacteria in hospital environments. Preventing further spread of this epidemic E. faecium subpopulation is critical, and efforts should focus on the early disclosure of ampicillin-resistant complex-17 strains.

Show MeSH

Related in: MedlinePlus

Relative abundance of complex-17 in various sampled categories and proportion increase explained by combined effect of 3 parameters. 0, animal surveillance samples; 1, human community surveillance samples; 2, human hospitalized patient samples; 3, human clinical samples; 4, hospital outbreak samples; amp, ampicillin resistance; PAI, pathogenicity island; gly, glycopeptide resistance.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3367597&req=5

Figure 2: Relative abundance of complex-17 in various sampled categories and proportion increase explained by combined effect of 3 parameters. 0, animal surveillance samples; 1, human community surveillance samples; 2, human hospitalized patient samples; 3, human clinical samples; 4, hospital outbreak samples; amp, ampicillin resistance; PAI, pathogenicity island; gly, glycopeptide resistance.

Mentions: When controlling for individual and combined effects of ampicillin resistance, presence of PAI, and vancomycin resistance, we can show that 1) the loglinear assumption holds for all effect parameters, and linear models describe the observed frequencies without substantial loss of goodness of fit; 2) individual genetic markers exert an independent and multiplicative effect; and 3) all genetic markers combined explain ≈48% of the category-specific abundance of complex-17 (Figure 2). The effect of vancomycin resistance did not increase the explanatory value of the model, owing to the fact that determinants for vancomycin resistance could be found in equal proportions within and outside of complex-17, likely a result of widespread horizontal transfer of vanA (Table 1). This finding suggests that the epidemiologic success of descendants of ST-17 that results in clinical infections and hospital epidemics was at least partly related to antimicrobial resistance and the presence of putative virulence genes. The fact that 126 of 128 isolates of complex-17 were resistant to ampicillin and only 77 of 139 isolates of complex-17 contain PAI (Table 1) suggests that E. faecium acquired ampicillin resistance first, which resulted in a selective advantage in hospitals, followed by the acquisition of PAI, which further facilitated transmission.


Global spread of vancomycin-resistant Enterococcus faecium from distinct nosocomial genetic complex.

Willems RJ, Top J, van Santen M, Robinson DA, Coque TM, Baquero F, Grundmann H, Bonten MJ - Emerging Infect. Dis. (2005)

Relative abundance of complex-17 in various sampled categories and proportion increase explained by combined effect of 3 parameters. 0, animal surveillance samples; 1, human community surveillance samples; 2, human hospitalized patient samples; 3, human clinical samples; 4, hospital outbreak samples; amp, ampicillin resistance; PAI, pathogenicity island; gly, glycopeptide resistance.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3367597&req=5

Figure 2: Relative abundance of complex-17 in various sampled categories and proportion increase explained by combined effect of 3 parameters. 0, animal surveillance samples; 1, human community surveillance samples; 2, human hospitalized patient samples; 3, human clinical samples; 4, hospital outbreak samples; amp, ampicillin resistance; PAI, pathogenicity island; gly, glycopeptide resistance.
Mentions: When controlling for individual and combined effects of ampicillin resistance, presence of PAI, and vancomycin resistance, we can show that 1) the loglinear assumption holds for all effect parameters, and linear models describe the observed frequencies without substantial loss of goodness of fit; 2) individual genetic markers exert an independent and multiplicative effect; and 3) all genetic markers combined explain ≈48% of the category-specific abundance of complex-17 (Figure 2). The effect of vancomycin resistance did not increase the explanatory value of the model, owing to the fact that determinants for vancomycin resistance could be found in equal proportions within and outside of complex-17, likely a result of widespread horizontal transfer of vanA (Table 1). This finding suggests that the epidemiologic success of descendants of ST-17 that results in clinical infections and hospital epidemics was at least partly related to antimicrobial resistance and the presence of putative virulence genes. The fact that 126 of 128 isolates of complex-17 were resistant to ampicillin and only 77 of 139 isolates of complex-17 contain PAI (Table 1) suggests that E. faecium acquired ampicillin resistance first, which resulted in a selective advantage in hospitals, followed by the acquisition of PAI, which further facilitated transmission.

Bottom Line: Evolutionary genetics, population structure, and geographic distribution of 411 VRE and vancomycin-susceptible Enterococcus faecium isolates, recovered from human and nonhuman sources and community and hospital reservoirs in 5 continents, identified a genetic lineage of E. faecium (complex-17) that has spread globally.This lineage is characterized by 1) ampicillin resistance, 2) a pathogenicity island, and 3) an association with hospital outbreaks.Preventing further spread of this epidemic E. faecium subpopulation is critical, and efforts should focus on the early disclosure of ampicillin-resistant complex-17 strains.

View Article: PubMed Central - PubMed

Affiliation: University Medical Center Utrecht, Utrecht, the Netherlands. r.willems@digd.azu.nl

ABSTRACT
Vancomycin-resistant enterococci (VRE) have caused hospital outbreaks worldwide, and the vancomycin-resistance gene (vanA) has crossed genus boundaries to methicillin-resistant Staphylococcus aureus. Spread of VRE, therefore, represents an immediate threat for patient care and creates a reservoir of mobile resistance genes for other, more virulent pathogens. Evolutionary genetics, population structure, and geographic distribution of 411 VRE and vancomycin-susceptible Enterococcus faecium isolates, recovered from human and nonhuman sources and community and hospital reservoirs in 5 continents, identified a genetic lineage of E. faecium (complex-17) that has spread globally. This lineage is characterized by 1) ampicillin resistance, 2) a pathogenicity island, and 3) an association with hospital outbreaks. Complex-17 is an example of cumulative evolutionary processes that improved the relative fitness of bacteria in hospital environments. Preventing further spread of this epidemic E. faecium subpopulation is critical, and efforts should focus on the early disclosure of ampicillin-resistant complex-17 strains.

Show MeSH
Related in: MedlinePlus