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An optimized, rapid method for creating markerless isogenic mutations that combines Gibson assembly cloning with a new temperature-sensitive plasmid, pLZts
Currently there are no diagnostic tests for ARF, and no treatments targeting immune responses to improve disease outcomes.
ARC is a global network of collaborators committed to reducing the burden of RHD in our lifetime.
A vaccine that prevents the initial attachment of Strep A to the tonsils would reduce the incidence of Strep throat and severe diseases that result.
Strep A causes over 775 million infections each year world-wide, including over 615 million cases of tonsil infection (Strep throat).
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.
Investigating what risk does underlying trimethoprim resistance pose for the development of cotrimoxazole-resistant skin infections.
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.
Pharyngitis, more commonly known as sore throat, is caused by viral and/or bacterial infections. Group A Streptococcus (Strep A) is the most common bacterial cause of pharyngitis. Strep A pharyngitis is an acute, self-limiting disease but if undertreated can lead to suppurative complications, nonsuppurative poststreptococcal immune-mediated diseases, and toxigenic presentations.
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.