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AbstractObjective:Describe the epidemiological and molecular characteristics of an outbreak of Klebsiella pneumoniaecarbapenemase (KPC)–producing organisms and the novel use of a cohorting unit for its control.Design:Observational study.Setting:A 566-room academic teaching facility in Milwaukee, Wisconsin.Patients:Solid-organ transplant recipients.Methods:Infection control bundles were used throughout the time of observation. All KPC cases were intermittently housed in a cohorting unit with dedicated nurses and nursing aids. The rooms used in the cohorting unit had anterooms where clean supplies and linens were placed. Spread of KPC-producing organisms was determined using rectal surveillance cultures on admission and weekly thereafter among all consecutive patients admitted to the involved units. KPC-positive strains underwent pulsed-field gel electrophoresis and whole-genome sequencing.Results:A total of 8 KPC cases (5 identified by surveillance) were identified from April 2016 to April 2017. After the index patient, 3 patients acquired KPC-producing organisms despite implementation of an infection control bundle. This prompted the use of a cohorting unit, which immediately halted transmission, and the single remaining KPC case was transferred out of the cohorting unit. However, additional KPC cases were identified within 2 months. Once the cohorting unit was reopened, no additional KPC cases occurred. The KPC-positive species identified during this outbreak included Klebsiella pneumoniae, Enterobacter cloacaecomplex, and Escherichia coli. blaKPCwas identified on at least 2 plasmid backbones.Conclusions:A complex KPC outbreak involving both clonal and plasmid-mediated dissemination was controlled using weekly surveillances and a cohorting unit.

OBJECTIVETo describe the investigation and control of a rare cluster of Klebsiella pneumoniaecarbapenemase–producing Citrobacter freundiiin a hospital in southern Florida.METHODSAn epidemiologic investigation, review of infection prevention procedures, and molecular studies including whole genome sequencing were conducted.RESULTSAn outbreak of K. pneumoniaecarbapenemase–3-producing C. freundiiwas identified at a tertiary hospital in Florida in 2014. Of the 6 cases identified, 3 occurred in the same intensive care unit and were caused by the same clone. For 2 of the 3 remaining cases, the isolates had low carbapenem minimum inhibitory concentrations and were unrelated by whole genome sequencing. As a response to the outbreak, supplementary environmental cleaning was implemented, including closure and terminal cleaning of the unit where the 3 cases clustered, in addition to the infection control bundle already in place at the time. No further cases were identified after these additional interventions.CONCLUSIONSAlthough C. freundiiis not a species that commonly demonstrates carbapenem resistance, our findings suggest that carbapenemase-producing C. freundiimay be underdetected even when active surveillance is in place and has a potential to cause hospital outbreak.Infect Control Hosp Epidemiol2017;38:320–326

Carbapenem-nonsusceptible Citrobacterspp. (CNSC) are increasingly recognized as health care-associated pathogens. Information regarding their clinical epidemiology, genetic diversity, and mechanisms of carbapenem resistance is lacking. We examined microbiology records of adult patients at the University of Pittsburgh Medical Center (UMPC) Presbyterian Hospital (PUH) from 2000 to 2018 for CNSC, as defined by ertapenem nonsusceptibility. Over this time frame, the proportion of CNSC increased from 4% to 10% (P?=?0.

OXA-232 is an OXA-48-group class D β-lactamase that hydrolyzes expanded-spectrum cephalosporins and carbapenems at low levels. Clinical strains producing OXA-232 are sometimes susceptible to carbapenems, making it difficult to identify them in the clinical microbiology laboratory.

We report patient-to-patient transmission of Enterobacter hormaecheiisolates with reduced susceptibility to ceftazidime-avibactam due to production of KPC-40, a variant of KPC-3 with a two-amino-acid insertion in the Ω-loop region (L167_E168dup). The index patient had received a prolonged course of ceftazidime-avibactam therapy, whereas the second patient had not received the agent and still became colonized with the KPC-40-producing strain.

Meropenem-vaborbactam is a new agent with the potential to treat carbapenem-resistant Enterobacteriaceae(CRE) infections. We describe the in vitroactivity of meropenem-vaborbactam against representative CRE genotypes and laboratory-engineered Escherichia coliisolates harboring mutant blaKPCgenes associated with ceftazidime-avibactam resistance.

Acinetobacter baumanniiis a prevalent nosocomial pathogen with a high incidence of multidrug resistance. Treatment of infections due to this organism with colistin, a last-resort antibiotic of the polymyxin class, can result in the emergence of colistin-resistant strains.

ABSTRACTFosfomycin maintains activity against most Escherichia coliclinical isolates, but the growth of E. colicolonies within the zone of inhibition around the fosfomycin disk is occasionally observed upon susceptibility testing. We aimed to estimate the frequency of such nonsusceptible inner colony mutants and identify the underlying resistance mechanisms. Disk diffusion testing of fosfomycin was performed on 649 multidrug-resistant E. coliclinical isolates collected between 2011 and 2015. For those producing inner colonies inside the susceptible range, the parental strains and their representative inner colony mutants were subjected to MIC testing, whole-genome sequencing, reverse transcription-quantitative PCR (qRT-PCR), and carbohydrate utilization studies. Of the 649 E. coliclinical isolates, 5 (0.8%) consistently produced nonsusceptible inner colonies. Whole-genome sequencing revealed the deletion of uhpTencoding hexose-6-phosphate antiporter in 4 of the E. coliinner colony mutants, while the remaining mutant contained a nonsense mutation in uhpA. The expression of uhpTwas absent in the mutant strains with uhpTdeletion and was not inducible in the strain with the uhpAmutation, unlike in its parental strain. All 5 inner colony mutants had reduced growth on minimal medium supplemented with glucose-6-phosphate. In conclusion, fosfomycin-nonsusceptible inner colony mutants can occur due to the loss of function or induction of UhpT but are rare among multidrug-resistant E. coliclinical strains. Considering that these mutants carry high biological costs, we suggest that fosfomycin susceptibility of strains that generate inner colony mutants can be interpreted on the basis of the zone of inhibition without accounting for the inner colonies.

ABSTRACTmcr-1was initially reported as the first plasmid-mediated colistin resistance gene in clinical isolates of Escherichia coliand Klebsiella pneumoniaein China and has subsequently been identified worldwide in various species of the family Enterobacteriaceae. mcr-1encodes a phosphoethanolamine transferase, and its expression has been shown to generate phosphoethanolamine-modified bis-phosphorylated hexa-acylated lipid A in E. coli. Here, we investigated the effects of mcr-1on colistin susceptibility and on lipopolysaccharide structures in laboratory and clinical strains of the Gram-negative ESKAPE (Enterococcus faecium, Staphylococcus aureus, K. pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacterspecies) pathogens, which are often treated clinically by colistin. The effects of mcr-1on colistin resistance were determined using MIC assays of laboratory and clinical strains of E. coli, K. pneumoniae, A. baumannii, and P. aeruginosa. Lipid A structural changes resulting from MCR-1 were analyzed by mass spectrometry. The introduction of mcr-1led to colistin resistance in E. coli, K. pneumoniae, and A. baumanniibut only moderately reduced susceptibility in P. aeruginosa. Phosphoethanolamine modification of lipid A was observed consistently for all four species. These findings highlight the risk of colistin resistance as a consequence of mcr-1expression among ESKAPE pathogens, especially in K. pneumoniaeand A. baumannii. Furthermore, the observation that lipid A structures were modified despite only modest increases in colistin MICs in some instances suggests more sophisticated surveillance methods may need to be developed to track the dissemination of mcr-1or plasmid-mediated phosphoethanolamine transferases in general.