Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/11731
Title: The evolution of vancomycin intermediate Staphylococcus aureus (VISA) and heterogenous-VISA.
Authors: Howden, Benjamin P;Peleg, Anton Y;Stinear, Timothy P
Affiliation: Austin Centre for Infection Research (ACIR), Infectious Diseases Department, Austin Health, Heidelberg, Victoria, Australia; Microbiology Department, Austin Health, Heidelberg, Victoria, Australia; Department of Microbiology and Immunology, University of Melbourne, Victoria, Australia; Department of Microbiology, Monash University, Wellington Rd, Clayton, Victoria, Australia. Electronic address: benjamin.howden@austin.org.au.
Department of Microbiology, Monash University, Wellington Rd, Clayton, Victoria, Australia; Division of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, MA, United States; Department of Infectious Diseases, The Alfred Hospital, Melbourne, Australia.
Department of Microbiology and Immunology, University of Melbourne, Victoria, Australia; Department of Microbiology, Monash University, Wellington Rd, Clayton, Victoria, Australia.
Issue Date: 6-Apr-2013
Citation: Infection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases 2013; 21(): 575-82
Abstract: Resistance 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.
Internal ID Number: 23567819
URI: http://ahro.austin.org.au/austinjspui/handle/1/11731
DOI: 10.1016/j.meegid.2013.03.047
URL: http://www.ncbi.nlm.nih.gov/pubmed/23567819
Type: Journal Article
Subjects: Evolution
Staphylococcus aureus
VISA
Vancomycin resistance
hVISA
Evolution, Molecular
Genetic Variation
Genome, Bacterial
High-Throughput Nucleotide Sequencing
Humans
Phenotype
Staphylococcal Infections.epidemiology.microbiology
Staphylococcus aureus.genetics
Vancomycin Resistance
Virulence Factors.genetics.metabolism
Appears in Collections:Journal articles

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