Trend of clinical vancomycin-resistant enterococci isolated in a regional Italian hospital from 2001 to 2018

Fioriti, Simona; Simoni, Serena; Caucci, Sara; Morroni, Gianluca; Ponzio, Elisa; Coccitto, Sonia Nina; Brescini, Lucia; Cirioni, Oscar; Menzo, Stefano; Biavasco, Francesca; Giovanetti, Eleonora; Brenciani, Andrea; Vignaroli, Carla

doi:10.1007/s42770-020-00360-8

Cited by 9 publications

(6 citation statements)

References 21 publications

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“…Our results highlighted that vanB 2 -VREfm and nearly half of VSEfm analyzed were from the hospital-associated (HA) ST117/CC17 or CladeA1 [ 22 ]. These STs are frequently associated with nosocomial outbreaks in Europe [ 23 , 24 , 25 ] and have also been reported in Italian hospitals [ 26 ], along with the other HA-STs that were detected here (ST78, ST916, ST80, and ST780).…”

Section: Discussionsupporting

confidence: 73%

Occult Vancomycin-Resistant Enterococcus faecium ST117 Displaying a Highly Mutated vanB2 Operon

et al. 2023

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Rare information is available on clinical Enterococcus faecium encountered in Sardinia, Italy. This study investigated the antimicrobial susceptibility profiles and genotypic characteristics of E. faecium isolated at the University Hospital of Sassari, Italy, using the Vitek2 system and PCR, MLST, or WGS. Vitek2 revealed two VanB-type vancomycin-resistant Enterococcus faecium (VREfm) isolates (MICs mg/L = 8 and ≥32) but failed to detect vancomycin resistance in one isolate (MIC mg/L ≤ 1) despite positive genotypic confirmation of vanB gene, which proved to be vancomycin resistant by additional phenotypic methods (MICs mg/L = 8). This vanB isolate was able to increase its vancomycin MIC after exposure to vancomycin, unlike the “classic” occult vanB-carrying E. faecium, becoming detectable by Vitek 2 (MICs mg/L ≥ 32). All three E. faecium had highly mutated vanB2 operons, as part of a chromosomally integrated Tn1549 transposon, with common missense mutations in VanH and VanB2 resistance proteins and specific missense mutations in the VanW accessory protein. There were additional missense mutations in VanS, VanH, and VanB proteins in the vanB2-carrying VREfm isolates compared to Vitek2. The molecular typing revealed a polyclonal hospital-associated E. faecium population from Clade A1, and that vanB2-VREfm, and nearly half of vancomycin-susceptible E. faecium (VSEfm) analyzed, belonged to ST117. Based on core genome-MLST, ST117 strains had different clonal types (CT), excluding nosocomial transmission of specific CT. Detecting vanB2-carrying VREfm isolates by Vitek2 may be problematic, and alternative methods are needed to prevent therapeutic failure and spread.

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Section: Discussionsupporting

confidence: 73%

Occult Vancomycin-Resistant Enterococcus faecium ST117 Displaying a Highly Mutated vanB2 Operon

et al. 2023

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“…In recent publications from the neighbouring countries Germany [27][28][29] and Italy [30], molecular characterisation of local vancomycin-resistant E. faecium isolates failed to detect this new clone.…”

Section: Discussionmentioning

confidence: 99%

“…To our knowledge, this was also the first documented outbreak with this ST in Europe. In recent publications from the neighbouring countries Germany [ 27 - 29 ] and Italy [ 30 ], molecular characterisation of local vancomycin-resistant E. faecium isolates failed to detect this new clone.…”

Section: Discussionmentioning

confidence: 99%

Nosocomial outbreak of vancomycin-resistant Enterococcus faecium (VRE) ST796, Switzerland, 2017 to 2020

et al. 2022

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A large clonal outbreak caused by vancomycin-resistant Enterococcus faecium (VRE) affected the Bern University Hospital group from the end of December 2017 until July 2020. We describe the characteristics of the outbreak and the bundle of infection prevention and control (IPC) measures implemented. The outbreak was first recognised when two concomitant cases of VRE bloodstream infection were identified on the oncology ward. During 32 months, 518 patients in the 1,300-bed hospital group were identified as vanB VRE carriers. Eighteen (3.5%) patients developed an invasive infection, of whom seven had bacteraemia. In 2018, a subset of 328 isolates were analysed by whole genome sequencing, 312 of which were identified as sequence type (ST) 796. The initial IPC measures were implemented with a focus on the affected wards. However, in June 2018, ST796 caused another increase in cases, and the management strategy was intensified and escalated to a hospital-wide level. The clinical impact of this large nosocomial VRE outbreak with the emergent clone ST796 was modest. A hospital-wide approach with a multimodal IPC bundle was successful against this highly transmissible strain.

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“…All isolates were tested by PCR for the presence of vanA and vanB genes, the most common glycopeptide resistance genes, as previously described [ 26 ].…”

Section: Methodsmentioning

confidence: 99%

Genetic analysis of vancomycin-variable Enterococcus faecium clinical isolates in Italy

Coccitto,

Cinthi,

Simoni

et al. 2024

Eur J Clin Microbiol Infect Dis

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Purpose To investigate the occurrence of vancomycin-variable enterococci (VVE) in a hospital in central Italy. Methods vanA positive but vancomycin-susceptible Enterococcus faecium isolates (VVE-S) were characterized by antibiotic susceptibility tests, molecular typing (PFGE and MLST), and WGS approach. The reversion of VVE-S to a resistant phenotype was assessed by exposure to increasing vancomycin concentrations, and the revertant isolates were used in filter mating experiments. qPCR was used to analyze the plasmid copy number. Results Eleven putative VVE-S were selected. WGS revealed two categories of vanA cluster plasmid located: the first type showed the lack of vanR, the deletion of vanS, and an intact vanH/vanA/vanX cluster; the second type was devoid of both vanR and vanS and showed a deletion of 544-bp at the 5′-end of the vanH. Strains (n = 7) carrying the first type of vanA cluster were considered VVE-S and were able to regain a resistance phenotype (VVE-R) in the presence of vancomycin, due to a 44-bp deletion in the promoter region of vanH/vanA/vanX, causing its constitutive expression. VVE-R strains were not able to transfer resistance by conjugation, and the resistance phenotype was unstable: after 11 days of growth without selective pressure, the revertants were still resistant but showed a lower vancomycin MIC. A higher plasmid copy number in the revertant strains was probably related to the resistance phenotype. Conclusion We highlight the importance of VVE transition to VRE under vancomycin therapy resulting in a potential failure treatment. We also report the first-time identification of VVE-S isolates pstS-null belonging to ST1478.

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Trend of clinical vancomycin-resistant enterococci isolated in a regional Italian hospital from 2001 to 2018

Cited by 9 publications

References 21 publications

Occult Vancomycin-Resistant Enterococcus faecium ST117 Displaying a Highly Mutated vanB2 Operon

Occult Vancomycin-Resistant Enterococcus faecium ST117 Displaying a Highly Mutated vanB2 Operon

Nosocomial outbreak of vancomycin-resistant Enterococcus faecium (VRE) ST796, Switzerland, 2017 to 2020

Genetic analysis of vancomycin-variable Enterococcus faecium clinical isolates in Italy

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