A P Marchi1, L V Perdigão Neto1, R C R Martins1, C F Rizek1, C H Camargo2, L Z Moreno3, A M Moreno3, M V Batista4, M S Basqueira5, F Rossi6, U Amigo4, T Guimaraes7, A S Levin1, S F Costa8. 1. Laboratório de Investigação Médica, Bacteriologia-LIM-54, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil; Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil. 2. Centro de Bacteriologia, Instituto Adolfo Lutz, São Paulo, Brazil. 3. Faculdade de Medicina Veterinária e Zootecnia, Departamento de Medicina Veterinária Preventiva e Saúde Animal Universidade de São Paulo, São Paulo, Brazil. 4. Bone Marrow Transplant Unit, Hospital das Clinicas, Universidade de São Paulo, São Paulo, Brazil. 5. Laboratório de Investigação Médica, Parasitologia-LIM-46, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil. 6. Hospital das Clínicas da Faculdade de Medicina, Universidade de São Paulo, Divisão de Laboratório Central Serviço de Microbiologia Clínica, São Paulo, Brazil. 7. Infection Control Committee, Hospital das Clinicas, University of São Paulo, São Paulo, Brazil. 8. Laboratório de Investigação Médica, Bacteriologia-LIM-54, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil; Tropical Medicine Institute, University of São Paulo, São Paulo, Brazil. Electronic address: costasilviaf@ig.com.br.
Abstract
BACKGROUND: Vancomycin-resistant enterococci (VRE) are an important agent of colonization and infection in haematology patients. However, the role of virulence on VRE colonization and infection is controversial. AIM: To characterize the lineage, virulence and resistance profile of VRE infection and colonization isolates; as well as their impact on outcome of haematology patients using a regression logistic model. METHODS: Eighty-six isolates (80 Enterococcus faecium and six E. faecalis) from 76 patients were evaluated. Polymerase chain reaction for resistance and virulence genes, and pulsed-field gel electrophoresis and whole genome sequencing of the major clusters, were performed. Bivariate and multivariate analyses were carried out to evaluate the role of virulence genes on outcome. FINDINGS: All isolates harboured the vanA gene. Regarding the virulence genes, 96.5% of isolates were positive for esp, 69.8% for gelE and asa1 genes. VRE infection isolates were more virulent than colonization isolates and harboured more often the gelE gene (P = 0.008). Infections caused by VRE carrying asa1 gene resulted more frequently in death (P = 0.004), but only the predominant clone remained as protector in the multivariate model. The E. faecium strains were assigned to seven STs (ST78, ST412, ST478, ST792, ST896, ST987, ST963) that belonged to CC17. The E. faecalis sequenced belonged to ST9 (CC9). CONCLUSION: E. faecium was predominant, and infection isolates were more virulent than colonization isolates and harboured more often the gene gelE. Infections caused by VRE carrying the asa1 gene appeared to be associated with a fatal outcome.
BACKGROUND:Vancomycin-resistant enterococci (VRE) are an important agent of colonization and infection in haematology patients. However, the role of virulence on VRE colonization and infection is controversial. AIM: To characterize the lineage, virulence and resistance profile of VRE infection and colonization isolates; as well as their impact on outcome of haematology patients using a regression logistic model. METHODS: Eighty-six isolates (80 Enterococcus faecium and six E. faecalis) from 76 patients were evaluated. Polymerase chain reaction for resistance and virulence genes, and pulsed-field gel electrophoresis and whole genome sequencing of the major clusters, were performed. Bivariate and multivariate analyses were carried out to evaluate the role of virulence genes on outcome. FINDINGS: All isolates harboured the vanA gene. Regarding the virulence genes, 96.5% of isolates were positive for esp, 69.8% for gelE and asa1 genes. VRE infection isolates were more virulent than colonization isolates and harboured more often the gelE gene (P = 0.008). Infections caused by VRE carrying asa1 gene resulted more frequently in death (P = 0.004), but only the predominant clone remained as protector in the multivariate model. The E. faecium strains were assigned to seven STs (ST78, ST412, ST478, ST792, ST896, ST987, ST963) that belonged to CC17. The E. faecalis sequenced belonged to ST9 (CC9). CONCLUSION: E. faecium was predominant, and infection isolates were more virulent than colonization isolates and harboured more often the gene gelE. Infections caused by VRE carrying the asa1 gene appeared to be associated with a fatal outcome.
Authors: Ana Paula Marchi; Lauro Vieira Perdigão Neto; Marina Farrel Côrtes; Victor Augusto Camarinha de Castro Lima; Roberta Cristina Ruedas Martins; Lucas Augusto Moyses Franco; Flavia Rossi; Vanderson Rocha; Anna S Levin; Silvia Figueiredo Costa Journal: Braz J Microbiol Date: 2021-10-31 Impact factor: 2.476
Authors: Lindsay A Rogers; Kayla Strong; Susan C Cork; Tim A McAllister; Karen Liljebjelke; Rahat Zaheer; Sylvia L Checkley Journal: Front Public Health Date: 2021-06-10
Authors: Daragh Hill; Paula M O'Connor; Eric Altermann; Li Day; Colin Hill; Catherine Stanton; R Paul Ross Journal: Sci Rep Date: 2020-08-10 Impact factor: 4.379