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Peirano G.,Calgary Laboratory Services | Peirano G.,University of Calgary | Costello M.,ACL Laboratories | Pitout J.D.D.,Calgary Laboratory Services | Pitout J.D.D.,University of Calgary
International Journal of Antimicrobial Agents | Year: 2010

This study was designed to characterise 30 non-duplicate extended-spectrum β-lactamase (ESBL)-producing Escherichia coli clinical isolates from the community in the Chicago metropolitan area collected during 2008. The majority of isolates (n=28) were recovered from urine and 2 isolates were from blood. Molecular characterisation was done using the following techniques: isoelectric focusing; polymerase chain reaction (PCR) and sequencing of blaESBL; PCR for plasmid-mediated quinolone resistance determinants; identification of ST131; phylogenetic grouping; and replicon typing. Genetic relatedness was determined by pulsed-field gel electrophoresis (PFGE) with XbaI and repetitive sequence-based PCR (rep-PCR) typing. Twenty-six (87%) of the ESBL-producing E. coli were positive for blaCTX-M genes (22 CTX-M-15 and 4 CTX-M-14), whilst the remaining 4 isolates produced SHV-2. Twenty-eight isolates (93%) were non-susceptible to ciprofloxacin and 16 (53%) were positive for aac(6')-Ib-cr. Overall, 16 (53%) of the ESBL-producers belonged to clonal complex ST131 that produced CTX-M-15 or CTX-M-14. Molecular characteristics of ST131 showed that it belonged to three distinct but related PFGE clones, was derived from phylogenetic group B2 and contained IncFII type plasmids. These results illustrate that E. coli clonal complex ST131 producing CTX-M-15, CTX-M-14, OXA-1, TEM-1 and aac(6')-Ib-cr has emerged as an important cause of community-onset urinary tract infections caused by ESBL-producing E. coli isolates in the Chicago area. © 2010 Elsevier B.V. and the International Society of Chemotherapy. Source

Rabs N.,Advocate Lutheran General Hospital | Wieczorkiewicz S.M.,Advocate Lutheran General Hospital | Costello M.,ACL Laboratories | Zamfirova I.,Russell Institute for Research and Innovation
American Journal of Infection Control | Year: 2014

Background Traditional antibiograms guide clinicians in selecting appropriate empiric antimicrobials, but they lack data on syndrome/disease- specific susceptibility, isolate location, polymicrobial infections, and patient risk factors. The aim of this study was to develop a urinary-specific antibiogram and to evaluate the impact of risk factors on antimicrobial susceptibility. Methods This retrospective descriptive study used culture and susceptibility data from January 1 to December 31, 2012. A urinary antibiogram specific for Escherichia coli (EC), Proteus mirabilis (PM), Klebsiella pneumoniae (KP), and Pseudomonas aeruginosa (PA) was developed. Urinary and standard antibiogram susceptibilities were compared. Urinary isolates were then stratified by risk factors - residence before admission, age, systemic antimicrobial use for ≤30 days, hospitalization for ≤ 30 days, and hospital unit - to determine the impact on antimicrobial susceptibility. Results There were 2,284 urinary isolate encounters. Overall antimicrobial susceptibility was increased, and the prevalence of extended-spectrum β-lactamase-producing isolates was significantly greater (KP, 14% vs 7% [P =.001]; EC, 13% vs 9% [P <.001]; PM, 18% vs 10% [P =.004]) in the urinary antibiogram vs the standard antibiogram. Health care facility residence had the greatest impact on susceptibility for all urinary isolates, especially on fluoroquinolone susceptibility for EC and PM. Conclusions Using a syndromic antibiogram and incorporating patient risk factors into susceptibility data may be more useful in guiding clinicians in selecting more appropriate empiric therapy. © 2014 by the Association for Professionals in Infection Control and Epidemiology, Inc. Published by Elsevier Inc. All rights reserved. Source

Munson E.,Technical Advisory Group | Munson E.,Wheaton Franciscan Laboratory | Munson E.,Marquette University | Block T.K.,Technical Advisory Group | And 23 more authors.
Wisconsin Medical Journal | Year: 2016

Background: Antimicrobial resistance presents a threat to quality patient care. Knowledge of local antibacterial susceptibility patterns can guide clinicians in empiric antibacterial administration and assist pharmacists and infectious disease physicians in development of appropriate therapeutic pathways. Methods: To characterize Wisconsin antibacterial susceptibility patterns and elucidate geographic or temporal variation in antibacterial resistance, a retrospective, observational analysis of antibiogram data was performed. Seventy-two members of the Wisconsin Clinical Laboratory Network (WCLN) submitted antibiograms describing clinically significant isolates tested in calendar year 2013 to the WCLN Laboratory Technical Advisory Group. Results: In the context of commonly reported antibacterial agents, data were compiled for approximately 75,800 isolates of Escherichia coli; 13,300 Klebsiella pneumoniae; 6300 Proteus mirabilis; 2800 Enterobacter cloacae; 8400 Pseudomonas aeruginosa; 30,000 S aureus; 11,200 coagulasenegative Staphylococcus spp; and 13,800 Enterococcus spp. P mirabilis isolates from northern Wisconsin were more likely to demonstrate resistance than those in the southern region. In contrast, P aeruginosa isolates from southern Wisconsin had decreased susceptibility to a number of agents when compared to other regions. Temporal trending in decreased E coli and P mirabilis susceptibility to fluoroquinolones and trimethoprim-sulfamethoxazole was observed. Increased methicillin-resistant Staphylococcus aureus (MRSA) rates were observed in northwest and southeast Wisconsin. In general, northeast Wisconsin exhibited less frequency of antibacterial resistance. Conclusions: Geographic variation exists with respect to antibacterial resistance, particularly in areas of Wisconsin adjacent to large population centers of neighboring states. Antibacterial surveillance in Wisconsin is indicated on a regular basis to assess emerging trends in antibacterial resistance. Existing WCLN infrastructure allows for such investigations. © 2016 Wisconsin Medical Society. Source

Peirano G.,University of Calgary | Van Der Bij A.K.,Center for Infectious Disease Control | Freeman J.L.,Auckland District Health Board | Freeman J.L.,University of Auckland | And 5 more authors.
Antimicrobial Agents and Chemotherapy | Year: 2014

We designed a study to describe the characteristics of sequence type 131 (ST131) lineages, including the H30-Rx sublineage, among a global collection of extended-spectrum β-lactamase (ESBL)-producing Escherichia coli isolates from 9 countries collected from 2000 to 2011. A total of 240 nonrepeat isolates from Canada, the United States, Brazil, the Netherlands, France, the United Arab Emirates (UAE), India, South Africa, and New Zealand were included. Established PCR, sequencing, and typing methods were used to define ST131 lineages, H30 and H30-Rx phylogenetic groups, gyrA and parC mutations, virotypes, and plasmid-mediated quinolone resistance determinants. The majority of the isolates produced CTX-M-15 with aac(6′)-lb-cr, belonged to phylogenetic group B2, and were positive for the H30 lineage with the gyrA1AB and parC1aAB mutations. ST131 showed 15 distinct pulsotypes; 43% of the isolates belonged to four pulsotypes, with a global distribution. Seventy-five percent of the ST131 isolates belonged to H30-Rx; this sublineage was present in all the countries and was associated with multidrug resistance, blaCTX-M-15, aac(6′)-lb-cr, and virotypes A and C. The H41 lineage was negative for the ST131 pabB allele-specific PCR. The multidrug-resistant H30-Rx sublineage poses an important public health threat due to its global distribution, association with virotype C, and high prevalence among ST131 isolates that produce CTX-M-15. Copyright © 2014, American Society for Microbiology. All Rights Reserved. Source

Aldinger K.A.,University of Chicago | Aldinger K.A.,University of Southern California | Kogan J.,Cincinnati Childrens Hospital Medical Center | Kogan J.,ACL Laboratories | And 10 more authors.
American Journal of Medical Genetics, Part A | Year: 2013

The 22q13.3 deletion causes a neurodevelopmental syndrome, also known as Phelan-McDermid syndrome (MIM #606232), characterized by developmental delay and severe delay or absence of expressive speech. Two patients with hemizygous chromosome 22q13.3 telomeric deletion were referred to us when brain-imaging studies revealed cerebellar vermis hypoplasia (CBVH). To determine whether developmental abnormalities of the cerebellum are a consistent feature of the 22q13.3 deletion syndrome, we examined brain-imaging studies for 10 unrelated subjects with 22q13 terminal deletion. In seven cases where the availability of DNA and array technology allowed, we mapped deletion boundaries using comparative intensity analysis with single nucleotide polymorphism (SNP) microarrays. Approximate deletion boundaries for three additional cases were derived from clinical or published molecular data. We also examined brain-imaging studies for a patient with an intragenic SHANK3 mutation. We report the first brain-imaging data showing that some patients with 22q13 deletions have severe posterior CBVH, and one individual with a SHANK3 mutation has a normal cerebellum. This genotype-phenotype study suggests that the 22q13 deletion phenotype includes abnormal posterior fossa structures that are unlikely to be attributed to SHANK3 disruption. Other genes in the region, including PLXNB2 and MAPK8IP2, display brain expression patterns and mouse mutant phenotypes critical for proper cerebellar development. Future studies of these genes may elucidate their relationship to 22q13.3 deletion phenotypes. © 2012 Wiley Periodicals, Inc. Source

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