VICTOR AUGUSTO CAMARINHA DE CASTRO LIMA
Projetos de Pesquisa
Unidades Organizacionais
LIM/49 - Laboratório de Protozoologia, Hospital das Clínicas, Faculdade de Medicina
4 resultados
Resultados de Busca
Agora exibindo 1 - 4 de 4
- Colistin-resistant Klebsiella pneumoniae co-harboring KPC and MCR-1 in a Hematopoietic Stem Cell Transplantation Unit(2019) HIGASHINO, Hermes Ryoiti; MARCHI, Ana Paula; MARTINS, Roberta Cristina Ruedas; BATISTA, Marjorie Vieira; PERDIGAO NETO, Lauro Vieira; LIMA, Victor Augusto Camarinha de Castro; ROSSI, Flavia; GUIMARAES, Thais; LEVIN, Anna Sara; ROCHA, Vanderson; COSTA, Silvia Figueiredo
- Phenotypic and genotypic characteristics of a carbapenem-resistant Serratia marcescens cohort and outbreak: describing an opportunistic pathogen(2022) PRADO, Gladys; MENDES, Elisa Teixeira; MARTINS, Roberta Cristina Ruedas; PERDIGAO-NETO, Lauro Vieira; FREIRE, Maristela Pinheiro; MARCHI, Ana Paula; CORTES, Marina Farrel; LIMA, Victor Augusto Camarinha de Castro; ROSSI, Flavia; GUIMARAES, Thais; LEVIN, Anna Sara; COSTA, Silvia FigueiredoSerratia marcescens is an emerging opportunistic pathogen with high genetic diversity. This article describes the microbiological characteristics of isolates and the risk factors for infections caused by carbapenem-resistant S. marcescens. A retrospective study of patients colonized (n=43) and infected (n= 20) with carbapenem-resistant S. marcescens over a 3-year period was conducted. Polymerase chain reaction for carbapenemase genes and molecular typing of all available strains was performed. Forty-two isolates were analysed, including three environmental samples identified during an outbreak. Thirty-five carbapenem-resistant S. marcescens carried bla KPC-2, one isolate was bla(NDM)-positive and four isolates carried bla(OXA)-101. The genomes were grouped into three clusters with 100% bootstrap; three patterns of mutations on ompC and ompF were found. The strains carried virulence genes related to invasion and haemolysis, and the environmental strains presented fewer mutations on the virulence genes than the clinical strains. Multi-variate analysis showed that previous use of polymyxin (P= 0.008) was an independent risk factor for carbapenem-resistant S. marcescens infection. This study highlighted that bla KPC-2 in association with ompC or ompF mutation was the most common mechanism of resistance in the study hospital, and that previous use of polymyxin was an independent risk factor for carbapenem-resistant S. marcescens. There was a predominant clone, including the environmental isolates, suggesting that crosstransmission was involved in the dissemination of this pathogen.
- Genetic description of VanD phenotype vanA genotype in vancomycin-resistant Enterococcus faecium isolates from a Bone Marrow Transplantation Unit(2022) MARCHI, Ana Paula; PERDIGAO NETO, Lauro Vieira; CORTES, Marina Farrel; LIMA, Victor Augusto Camarinha de Castro; MARTINS, Roberta Cristina Ruedas; FRANCO, Lucas Augusto Moyses; ROSSI, Flavia; ROCHA, Vanderson; LEVIN, Anna S.; COSTA, Silvia FigueiredoBackground Vancomycin-resistant Enterococcus faecium (VREfm) is an important agent of hospital-acquired infection. VanA phenotype is characterized by resistance to high levels of vancomycin and teicoplanin and is encoded by the vanA gene, whereas VanD phenotype is characterized by resistance to vancomycin and susceptibility or intermediate resistance to teicoplanin; however, some isolates carry a VanD phenotype with a vanA genotype, but there are many gaps in the knowledge about the genetic mechanisms behind this pattern. Objective To characterize the genetic structure, clonality, and mobile genetic elements of VRE isolates that display a VanD-vanA phenotype. Results All vanA VRE-fm isolates displayed minimum inhibitory concentration (MIC) for vancomycin > 32 mu g/mL and intermediate or susceptible MIC range for teicoplanin (8-16 mu g/mL). The isolates were not clonal, and whole-genome sequencing analysis showed that they belonged to five different STs (ST478, ST412, ST792, ST896, and ST1393). The absence of some van complex genes were observed in three isolates: Ef5 lacked vanY and vanZ, Ef2 lacked vanY, and Ef9 lacked orf1 and orf2; moreover, another three isolates had inverted positions of orf1, orf2, vanR, and vanS genes. IS1542 was observed in all isolates, whereas IS1216 in only five. Moreover, presence of other hypothetical protein-encoding genes located downstream the vanZ gene were observed in six isolates. Conclusion VRE isolates can display some phenotypes associated to vanA genotype, including VanA and VanB, as well as VanD; however, further studies are needed to understand the exact role of genetic variability, rearrangement of the transposon Tn1546, and presence of insertion elements in isolates with this profile.
- Colistin-resistant Enterobacteriaceae infections: clinical and molecular characterization and analysis of in vitro synergy(2017) CARRILLHO, Claudia M. D. de Maio; GAUDERETO, Juliana J.; MARTINS, Roberta Cristina Ruedas; LIMA, Victor Augusto Camarinha de Castro; OLIVEIRA, Larissa M. de; URBANO, Mariana R.; PEROZIN, Jamile S.; LEVIN, Anna Sara; COSTA, Silvia F.We described 27 polyclonal colistin-resistant Enterobacteriaceae (MIC 4-16 mu g/mL) infections (12 pneumonia, 12 urinary tract infection (UTI), two Bacteremia, and one skin/soft tissue infection) in which 74% harbored KPC. The isolates were polyclonal, 6 STs were identified and the colistin resistance was due to chromosome mutations. Eight patients with UTI received monotherapy, and combination therapy was given to 19 patients. Overall mortality was 37%. In vitro synergy using time-kill assay was observed in 14 of 19 (74%) isolates tested; the synergistic effect was observed for almost all isolates for the combination of three drugs: colistin, amikacin, and tigecycline. The Kaplan-Meier survival curve showed no significant difference comparing combination therapy with 2, 3, or more drugs and risk factors associated with death were dialysis and shock. These findings reinforce the fact that colistin in combination with other classes of drugs can be useful in treating infections caused by colistin-resistant CRE.