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Acute rheumatic fever: a chink in the chain that links the heart to the throat?

McDonald, Malcolm I., Currie, Bart J. and Carapetis, Jonathan R. (2004). Acute rheumatic fever: a chink in the chain that links the heart to the throat?. Lancet Infectious Diseases,4(4):240-245.

Document type: Journal Article
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Title Acute rheumatic fever: a chink in the chain that links the heart to the throat?
Author McDonald, Malcolm I.
Currie, Bart J.
Carapetis, Jonathan R.
Journal Name Lancet Infectious Diseases
Publication Date 2004
Volume Number 4
Issue Number 4
ISSN 1473-3099   (check CDU catalogue open catalogue search in new window)
Start Page 240
End Page 245
Total Pages 6
Place of Publication London, England, UK
Publisher The Lancet Publishing Group
Field of Research 1102 - Cardiovascular Medicine and Haematology
HERDC Category C1 - Journal Article (DEST)
Abstract Acute rheumatic fever (ARF) remains a major problem in tropical regions, resource-poor countries, and minority indigenous communities. It has long been thought that group A streptococcal (GAS) pharyngitis alone was responsible for acute rheumatic fever; this belief has been supported by laboratory and epidemiological evidence gathered over more than 60 years, mainly in temperate climates where GAS skin infection is uncommon. GAS strains have been characterised as either rheumatogenic or nephritogenic based on phenotypic and genotypic properties. Primary prevention strategies and vaccine development have long been based on these concepts. The epidemiology of ARF in Aboriginal communities of central and northern Australia challenges this view with reported rates of ARF and rheumatic heart disease (RHD) that are among the highest in the world. GAS throat colonisation is uncommon, however, and symptomatic GAS pharyngitis is rare; pyoderma is the major manifestation of GAS infection. Typical rheumatogenic strains do not occur. Moreover, group C and G streptococci have been shown to exchange key virulence determinants with GAS and are more commonly isolated from the throats of Aboriginal children. We suggest that GAS pyoderma and/or non-GAS infections are driving forces behind ARF in these communities and other high-incidence settings. The question needs to be resolved as a matter of urgency because current approaches to controlling ARF/RHD in Aboriginal communities have clearly been ineffective. New understanding of the pathogenesis of ARIF would have an immediate effect on primary prevention strategies and vaccine development.
Keywords group-a streptococci
yarrabah aboriginal community
acute glomerulonephritis
molecular epidemiology
distinct classes
northern Australia
Oceanic Ancestry Group
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