Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/11731
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dc.contributor.authorHowden, Benjamin P-
dc.contributor.authorPeleg, Anton Y-
dc.contributor.authorStinear, Timothy P-
dc.date.accessioned2015-05-16T01:21:25Z
dc.date.available2015-05-16T01:21:25Z
dc.date.issued2013-04-06-
dc.identifier.citationInfection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases 2013; 21(): 575-82en_US
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/11731en
dc.description.abstractResistance to new antimicrobials is generally recognized in Staphylococcus aureus soon after they are released for clinical use. In the case of vancomycin, which was first released in the 1950s, resistance was not reported until the mid 1990s, with the description of vancomycin-intermediate S. aureus (VISA), and heterogenous-VISA (hVISA). Unraveling the complex genetic and cell wall structural changes conferring low-level vancomycin resistance in S. aureus has proved challenging. However the recent advances in high throughput whole-genome sequencing has played a key role in determining the breadth of bacterial chromosomal changes linked with resistance. Diverse mutations in a small number of staphylococcal regulatory genes, in particular walKR, graRS, vraSR and rpoB, have been associated with hVISA and VISA. Only a small number of these mutations have been experimentally proven to confer the resistance phenotype and some of these only partially contribute to resistance. It also appears that the evolution of VISA from VSSA is a step-wise process. Transcriptomics studies, and analysis of host pathogen interactions, indicate that the evolution of vancomycin-susceptible S. aureus to VISA is associated not only with antibiotic resistance, but with other changes likely to promote persistent infection. These include predicted alterations in central metabolism, altered expression of virulence associated factors, attenuated virulence in vivo, and alterations in susceptibility to host innate immune responses, together with reduced susceptibility to other antibiotics. In fact, current data suggests that hVISA and VISA represent a bacterial evolutionary state favoring persistence in the face of not only antibiotics, but also the host environment. The additional knowledge of staphylococcal biology that has been uncovered during the study of hVISA and VISA is significant. The present review will detail the current understanding of the evolutionary process in the generation of hVISA and VISA, and explore the diverse additional changes that occur in these strains.en_US
dc.language.isoenen
dc.subject.otherEvolutionen
dc.subject.otherStaphylococcus aureusen
dc.subject.otherVISAen
dc.subject.otherVancomycin resistanceen
dc.subject.otherhVISAen
dc.subject.otherEvolution, Molecularen
dc.subject.otherGenetic Variationen
dc.subject.otherGenome, Bacterialen
dc.subject.otherHigh-Throughput Nucleotide Sequencingen
dc.subject.otherHumansen
dc.subject.otherPhenotypeen
dc.subject.otherStaphylococcal Infections.epidemiology.microbiologyen
dc.subject.otherStaphylococcus aureus.geneticsen
dc.subject.otherVancomycin Resistanceen
dc.subject.otherVirulence Factors.genetics.metabolismen
dc.titleThe evolution of vancomycin intermediate Staphylococcus aureus (VISA) and heterogenous-VISA.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleInfection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseasesen_US
dc.identifier.affiliationDivision of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, MA, United Statesen_US
dc.identifier.affiliationInfectious Diseasesen_US
dc.identifier.affiliationDepartment of Infectious Diseases, The Alfred Hospital, Melbourne, Australiaen_US
dc.identifier.affiliationDepartment of Microbiology, Monash University, Wellington Rd, Clayton, Victoria, Australiaen_US
dc.identifier.affiliationDepartment of Microbiology and Immunology, University of Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationMicrobiologyen_US
dc.identifier.doi10.1016/j.meegid.2013.03.047en_US
dc.description.pages575-82en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/23567819en
dc.type.contentTexten_US
dc.type.austinJournal Articleen
local.name.researcherHowden, Benjamin P
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptInfectious Diseases-
crisitem.author.deptMicrobiology-
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