RESUMO
An atypically large outbreak of Elizabethkingia anophelis infections occurred in Wisconsin. Here we show that it was caused by a single strain with thirteen characteristic genomic regions. Strikingly, the outbreak isolates show an accelerated evolutionary rate and an atypical mutational spectrum. Six phylogenetic sub-clusters with distinctive temporal and geographic dynamics are revealed, and their last common ancestor existed approximately one year before the first recognized human infection. Unlike other E. anophelis, the outbreak strain had a disrupted DNA repair mutY gene caused by insertion of an integrative and conjugative element. This genomic change probably contributed to the high evolutionary rate of the outbreak strain and may have increased its adaptability, as many mutations in protein-coding genes occurred during the outbreak. This unique discovery of an outbreak caused by a naturally occurring mutator bacterial pathogen provides a dramatic example of the potential impact of pathogen evolutionary dynamics on infectious disease epidemiology.
Assuntos
Infecções por Flavobacteriaceae/microbiologia , Flavobacteriaceae/genética , Genoma Bacteriano/genética , Taxa de Mutação , Virulência/genética , Proteínas de Bactérias/genética , DNA Glicosilases/genética , Surtos de Doenças , Flavobacteriaceae/patogenicidade , Infecções por Flavobacteriaceae/epidemiologia , Humanos , Filogenia , Análise de Sequência de DNA , Wisconsin/epidemiologiaRESUMO
Carbapenem-resistant Enterobacteriaceae (CRE) are multidrug-resistant gram-negative bacilli that can cause infections associated with high case fatality rates, and are emerging as epidemiologically important health care-associated pathogens in the United States (1). Prevention of CRE transmission in health care settings is dependent on recognition of cases, isolation of colonized and infected patients, effective use of infection control measures, and the correct use of antibiotics. The use of molecular technologies, including polymerase chain reaction (PCR) testing, pulsed-field gel electrophoresis (PFGE), and whole genome sequencing (WGS), can lead to detection of transmission events and interruption of transmission. In Wisconsin, acute care and critical access hospitals report laboratory-identified CRE to the Wisconsin Division of Public Health (WDPH), and clinical laboratories submit CRE isolates to the Wisconsin State Laboratory of Hygiene (WSLH) for molecular testing. During February-May 2015, a total of 49 CRE isolates from 46 patients were submitted to WSLH. On June 8, WSLH informed WDPH of five carbapenemase-producing CRE isolates with closely related PFGE patterns identified among four inpatients at two hospitals in southeastern Wisconsin. An investigation revealed a high degree of genetic relatedness among the patients' isolates, but did not identify the mechanism of transmission between the two facilities. No breaches in recommended practices were identified; after reviewing respiratory care procedures, no further cases were identified. Routine hospital- and laboratory-based surveillance can detect and prevent health care transmission of CRE.
