Search the site

Skin Microbiome

The skin is home to an array of bacteria, fungi and viruses, which together make up the skin microbiome. We explore how the skin microbiome can contribute to healthy skin.

What risk does underlying trimethoprim resistance pose for the development of cotrimoxazole-resistant skin infections

Investigating what risk does underlying trimethoprim resistance pose for the development of cotrimoxazole-resistant skin infections.

Longitudinal surveillance of group A streptococcal pharyngitis and impetigo in remote Western Australian school children informs acute rheumatic fever prevention

The prevalence of impetigo and pharyngitis - which are both superficial group A streptococcus (GAS) infections that precede acute rheumatic fever - is poorly defined. Guidelines recommend the early diagnosis of both infections to prevent ARF; however, screening to enable the concurrent detection of these infections in high-risk populations has rarely been performed.

Macrophage infectivity potentiator protein, a peptidyl prolyl cis-trans isomerase, essential for Coxiella burnetii growth and pathogenesis

Coxiella burnetii is a Gram-negative intracellular pathogen that causes the debilitating disease Q fever, which affects both animals and humans. The only available human vaccine, Q-Vax, is effective but has a high risk of severe adverse reactions, limiting its use as a countermeasure to contain outbreaks. Therefore, it is essential to identify new drug targets to treat this infection.

Describing skin health and disease in urban-living Aboriginal children: co-design, development and feasibility testing of the Koolungar Moorditj Healthy Skin pilot project

Indigenous children in colonised nations experience high rates of health disparities linked to historical trauma resulting from displacement and dispossession, as well as ongoing systemic racism. Skin infections and their complications are one such health inequity, with the highest global burden described in remote-living Australian Aboriginal and/or Torres Strait Islander (hereafter respectfully referred to as Aboriginal) children. Yet despite increasing urbanisation, little is known about the skin infection burden for urban-living Aboriginal children.

A pilot study to develop assessment tools for Group A Streptococcus surveillance studies

Group A Streptococcus (GAS) causes pharyngitis (sore throat) and impetigo (skin sores) GAS pharyngitis triggers rheumatic fever (RF) with epidemiological evidence supporting that GAS impetigo may also trigger RF in Australian Aboriginal children. Understanding the concurrent burden of these superficial GAS infections is critical to RF prevention. This pilot study aimed to trial tools for concurrent surveillance of sore throats and skins sore for contemporary studies of RF pathogenesis including development of a sore throat checklist for Aboriginal families and pharynx photography.

Standardization of epidemiological surveillance of group A Streptococcal cellulitis

Cellulitis is an acute bacterial infection of the dermis and subcutaneous tissue usually found complicating a wound, ulcer, or dermatosis. This article provides guidelines for the surveillance of cellulitis.

Roadmap to incorporating group A Streptococcus molecular point-of-care testing for remote Australia: a key activity to eliminate rheumatic heart disease

Jonathan Asha Dylan Rosemary Janessa Jeffrey Carapetis AM Bowen Barth Wyber Pickering Cannon AM MBBS FRACP FAFPHM PhD FAHMS BA MBBS DCH FRACP PhD

Penicillin G concentrations required for prophylaxis against Group A Streptococcus infection evaluated using a hollow fibre model and mathematical modelling

Acute rheumatic fever (ARF), an autoimmune reaction to Group A Streptococcus (Streptococcus pyogenes; Strep A) infection, can cause rheumatic heart disease (RHD). New formulations of long-acting penicillins are being developed for secondary prophylaxis of ARF and RHD.

Host-dependent resistance of Group A Streptococcus to sulfamethoxazole mediated by a horizontally-acquired reduced folate transporter

Described antimicrobial resistance mechanisms enable bacteria to avoid the direct effects of antibiotics and can be monitored by in vitro susceptibility testing and genetic methods. Here we describe a mechanism of sulfamethoxazole resistance that requires a host metabolite for activity.