Pamela Alatorre-Fernández1, Claudia Mayoral-Terán2, Consuelo Velázquez-Acosta3, Cecilia Franco-Rodríguez4, Karen Flores-Moreno2, Miguel Ángel Cevallos5, Yolanda López-Vidal2, Patricia Volkow-Fernández6. 1. Departmento de Enfermedades Infecciosas, Secretaría de Salud, Instituto Nacional de Cancerología, Mexico City, Mexico. 2. Programa de Inmunología Molecular Microbiana, Departamento de Microbiología y Parasitología, División de Investigación, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico. 3. Departamento de Enfermedades Infecciosas, Laboratorio de Microbiología, Secretaría de Salud, Instituto Nacional de Cancerología, Mexico City, Mexico. 4. Departamento de Farmacología Hospitalaria, Secretaría de Salud, Instituto Nacional de Cancerología, Mexico City, Mexico. 5. Programa de Genómica Evolutiva, Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, Mexico. 6. Departmento de Enfermedades Infecciosas, Secretaría de Salud, Instituto Nacional de Cancerología, Mexico City, Mexico. Electronic address: pvolkowf@gmail.com.
Abstract
BACKGROUND: Enterococcus faecium causes bloodstream infection (BSI) in patients with hematologic malignancies (HMs). We studied the clinical features and outcomes of patients with HM with vancomycin-sensitive E faecium (VSE) and vancomycin-resistant E faecium (VRE) BSI and determined the genetic relatedness of isolates and circumstances associated with the upsurge of E faecium BSI. METHODS: Case-control study of patients with HM and E faecium-positive blood culture from January 2008-December 2012; cases were patients with VRE and controls were VSE isolates. The strains were tested for Van genes by polymerase chain reaction amplification and we performed pulsed-field gel electrophoresis to determine genetic relatedness. RESULTS: Fifty-eight episodes of E faecium BSI occurred: 35 sensitive and 23 resistant to vancomycin. Mortality was 46% and 57%, attributable 17% and 40%, respectively. Early stage HM was associated with VSE (P = .044), whereas an episode of BSI within the 3 months before the event (P = .039), prophylactic antibiotics (P = .013), and vancomycin therapy during the previous 3 months (P = .001) was associated with VRE. The VanA gene was identified in 97% of isolates studied. E faecium isolates were not clonal. CONCLUSIONS: E faecium BSI was associated with high mortality. This outbreak of VRE was not clonal; it was associated with antibiotic-use pressure and highly myelosuppressive chemotherapy.
BACKGROUND:Enterococcus faecium causes bloodstream infection (BSI) in patients with hematologic malignancies (HMs). We studied the clinical features and outcomes of patients with HM with vancomycin-sensitive E faecium (VSE) and vancomycin-resistant E faecium (VRE) BSI and determined the genetic relatedness of isolates and circumstances associated with the upsurge of E faecium BSI. METHODS: Case-control study of patients with HM and E faecium-positive blood culture from January 2008-December 2012; cases were patients with VRE and controls were VSE isolates. The strains were tested for Van genes by polymerase chain reaction amplification and we performed pulsed-field gel electrophoresis to determine genetic relatedness. RESULTS: Fifty-eight episodes of E faecium BSI occurred: 35 sensitive and 23 resistant to vancomycin. Mortality was 46% and 57%, attributable 17% and 40%, respectively. Early stage HM was associated with VSE (P = .044), whereas an episode of BSI within the 3 months before the event (P = .039), prophylactic antibiotics (P = .013), and vancomycin therapy during the previous 3 months (P = .001) was associated with VRE. The VanA gene was identified in 97% of isolates studied. E faecium isolates were not clonal. CONCLUSIONS: E faecium BSI was associated with high mortality. This outbreak of VRE was not clonal; it was associated with antibiotic-use pressure and highly myelosuppressive chemotherapy.