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Group A streptococcal (GAS) pharyngitis has traditionally been considered the sole precursor of acute rheumatic fever (ARF). Evidence from Australia, however, suggests that GAS skin infections may contribute to the pathogenesis of ARF.
Households are known to be high-risk locations for the transmission of communicable diseases. Numerous modelling studies have demonstrated the important role of households in sustaining both communicable diseases outbreaks and endemic transmission, and as the focus for control efforts. However, these studies typically assume that households are associated with a single dwelling and have static membership.
The majority of Australian Aboriginal and Torres Strait Islander (hereafter referred to as “Aboriginal”) people live in urban centres. Otitis media (OM) occurs at a younger age, prevalence is higher and hearing loss and other serious complications are more common in Aboriginal than non-Aboriginal children. Despite this, data on the burden of OM and hearing loss in urban Aboriginal children are limited.
Prevalence of impetigo (skin sores) remains high in remote Australian Aboriginal communities, Fiji, and other areas of socio-economic disadvantage. Skin sore infections, driven primarily in these settings by Group A Streptococcus (GAS) contribute substantially to the disease burden in these areas. Despite this, estimates for the force of infection, infectious period and basic reproductive ratio-all necessary for the construction of dynamic transmission models-have not been obtained.
BK polyomavirus infection in transplanted kidneys that leads to BK virus–associated nephropathy (BKVAN) is an important cause of allograft loss and has limited treatment options. Recent data suggest that BK viremia affects approximately 10% of people within the first 12 months following kidney transplantation. Among recipients with BKVAN, the overall risk of allograft loss is substantially increased, estimated to be 50% within 5 years of diagnosis.
A summary of the literature regarding the use of adjunctive protein synthesis inhibitors for toxin suppression in the setting of S. aureus infections is presented