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The END RHD CRE is producing a costed, step-wise strategy to end rheumatic heart disease (RHD) as public health priority in Australia.

RHD in Australia

Rheumatic heart disease (RHD) is a preventable,devastating condition that disproportionately affects Aboriginal and Torres Strait Islander Australians.

The Cost of Inaction on Rheumatic Heart Disease

Aboriginal and Torres Strait Islander communities have some of the highest rates of rheumatic heart disease (RHD) in the world. This report outlines

Rheumatic Heart Disease Endgame Strategy: what does it mean to community?

Across Australia, more than 5,000 Aboriginal and Torres Strait Islander people are currently living with rheumatic heart disease (RHD) or its precursor, acute rheumatic fever (ARF).

Visit from On Track Watch Community Researchers helps build a pathway of looking at two different cultures

For Aboriginal Community Researchers Minitja Marawili and Yunutju Gondarra, the work of the END RHD CRE is deeply personal.

Laqueisha's story: living with RHD

Laqueisha was just five years old when she was diagnosed with rheumatic heart disease and sent on a 5,000km return trip to Perth for major heart surgery.

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.

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.