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The latest publications and resources from the END RHD CRE Team
End RHD CRE News & Events
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).
For Aboriginal Community Researchers Minitja Marawili and Yunutju Gondarra, the work of the END RHD CRE is deeply personal.
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.
Bacterial skin infections and scabies disproportionately affect children in resource-poor countries as well as underprivileged children in high-income countries. Atopic dermatitis is a common childhood dermatosis that predisposes to bacterial skin infection.
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.
Rheumatic heart disease is the largest contributor to cardiac-related mortality in children worldwide. Outcomes in endemic settings after its antecedent illness, acute rheumatic fever, are not well understood. We aimed to describe 3-5 year mortality, acute rheumatic fever recurrence, changes in carditis, and correlates of mortality after acute rheumatic fever.
Environmental factors including household crowding and inadequate washing facilities underpin recurrent streptococcal infections in childhood that cause acute rheumatic fever (ARF) and subsequent rheumatic heart disease (RHD).
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.