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Full-Text Articles in Comparative and Laboratory Animal Medicine

An Epidemiologic Study Of Antimicrobial Resistance Of Staphylococcus Species Isolated From Equine Samples Submitted To A Diagnostic Laboratory, Ronita Adams, Jackie Smith, Stephan Locke, Erica Phillips, Erdal Erol, Craig N. Carter, Agricola Odoi Feb 2018

An Epidemiologic Study Of Antimicrobial Resistance Of Staphylococcus Species Isolated From Equine Samples Submitted To A Diagnostic Laboratory, Ronita Adams, Jackie Smith, Stephan Locke, Erica Phillips, Erdal Erol, Craig N. Carter, Agricola Odoi

Veterinary Science Faculty Publications

Background

Antimicrobial resistance limits traditional treatment options and increases costs. It is therefore important to estimate the magnitude of the problem so as to provide empirical data to guide control efforts. The aim of this study was to investigate the burden and patterns of antimicrobial resistance (AMR) among equine Staphylococcus samples submitted to the University of Kentucky Veterinary Diagnostic Laboratory (UKVDL) from 1993 to 2009. Retrospective data of 1711 equine Staphylococcus samples submitted to the UKVDL during the time period 1993 to 2009 were included in the study. Antimicrobial susceptibility testing, that included 16 drugs, were performed using cultures followed …


Biochemical And Mutational Analysis Of The Histidine Residues Of Staphylococcal Enterotoxin A., M Hoffman, M Tremaine, J Mansfield, M Betley Mar 1996

Biochemical And Mutational Analysis Of The Histidine Residues Of Staphylococcal Enterotoxin A., M Hoffman, M Tremaine, J Mansfield, M Betley

Manuscripts, Articles, Book Chapters and Other Papers

The goal of this study was to examine the role of histidine residues in the biological activities of staphylococcal enterotoxin A (SEA). Carboxymethylated SEA was unable to stimulate murine T-cell proliferation but was resistant to monkey stomach lavage fluid degradation, suggesting that native conformation was intact. Site-directed mutagenesis of the histidine residues of SEA was subsequently performed. SEA-H44A (SEA with histidine 44 replaced with alanine), SEA-H44D, SEA-H50A, SEA-H50D, SEA-H114A, SEA-H114D, SEA-H187A, and SEA-H187D retained superantigen and emetic activities, whereas SEA-H225A and SEA-H225D were defective in the ability to stimulate T-cell proliferation. These mutants were unable to compete with SEA for …