7 results match your criteria: "Austin Centre for Infection Research (ACIR)[Affiliation]"

In-vitro activity of avermectins against Mycobacterium ulcerans.

PLoS Negl Trop Dis

March 2015

Department of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria, Australia.

Mycobacterium ulcerans causes Buruli ulcer (BU), a debilitating infection of subcutaneous tissue. There is a WHO-recommended antibiotic treatment requiring an 8-week course of streptomycin and rifampicin. This regime has revolutionized the treatment of BU but there are problems that include reliance on daily streptomycin injections and side effects such as ototoxicity.

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Antibiotics and Staphylococcus aureus--more than meets the MIC.

J Mol Med (Berl)

February 2014

Austin Centre for Infection Research (ACIR), Infections Diseases Department, and Department of Microbiology, Austin Health, Heidelberg, Melbourne, Australia,

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The importance of regulatory RNAs in Staphylococcus aureus.

Infect Genet Evol

January 2014

Architecture et Réactivité de l'ARN, Université de Strasbourg, CNRS, IBMC, Strasbourg, France. Electronic address:

RNA molecules with regulatory functions in pathogenic bacteria have benefited from a renewed interest these two last decades. In Staphylococcus aureus, recent genome-wide approaches have led to the discovery that almost 10-20% of genes code for RNAs with critical regulatory roles in adaptive processes. These RNAs include trans-acting RNAs, which mostly act through binding to target mRNAs, and cis-acting RNAs, which include regulatory regions of mRNAs responding to various metabolic signals.

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Unlabelled: Nosocomial outbreaks of vancomycin-resistant Enterococcus faecium (VREfm) are thought to occur by transmission of VREfm between patients, predicting that infection control interventions will limit cross-transmission. Despite implementation of such strategies, the incidence of VREfm infections continues to rise. We aimed to use genomics to better understand the epidemiology of E.

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Population genetics and the evolution of virulence in Staphylococcus aureus.

Infect Genet Evol

January 2014

Department of Microbiology, Monash University, Clayton, Victoria 3800, Australia; Department of Infectious Diseases, The Alfred Hospital, Melbourne, Victoria 3181, Australia; Division of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, MA, USA. Electronic address:

Staphylococcus aureus is one of the most important human pathogens, causing life-threatening infection in the community and hospital setting. The population genetics of S. aureus and the evolution of virulence is the focus of this review.

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The evolution of vancomycin intermediate Staphylococcus aureus (VISA) and heterogenous-VISA.

Infect Genet Evol

January 2014

Department of Microbiology and Immunology, University of Melbourne, Victoria, Australia; Department of Microbiology, Monash University, Wellington Rd, Clayton, Victoria, Australia.

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).

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