New understanding of the group A Streptococcus pathogenesis cycle

Tart, Anne H.; Walker, Mark J.; Musser, James M.

doi:10.1016/j.tim.2007.05.001

Cited by 105 publications

(99 citation statements)

References 74 publications

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“…These include simple pharyngitis (> 600 million cases per year) and impetigo (> 100 million cases per year), but also life-threatening invasive infections such as necrotizing fasciitis, bacteremia, and toxic shock syndrome (> 600,000 cases and 163,000 deaths per year) (1). Over the past two decades there have been numerous reports of a resurgence in GAS invasive disease of increasing severity in Western countries (2,3). Additionally, in developing nations, the epidemiology of GAS disease is less well-described, and GAS infection remains endemic in many areas (4).…”

Section: Introductionmentioning

confidence: 99%

M protein‐mediated plasminogen binding is essential for the virulence of an invasiveStreptococcus pyogenesisolate

Sanderson-Smith¹,

Dinkla²,

Cole³

et al. 2008

FASEB j.

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MJ, M protein mediated plasminogen binding is essential for the virulence of an invasive Streptococcus pyogenes isolate, The FASEB Journal, 22(8), 2008, 2715-2722 M protein mediated plasminogen binding is essential for the virulence of an invasive Streptococcus pyogenes isolate AbstractThe human protease plasmin plays a crucial role in the capacity of the group A streptococcus (Streptococus pyogenes; GAS) to initiate invasive disease. The GAS strain NS88.2 was isolated from a case of bacteremia from the Northern Territory of Australia, a region with high rates of GAS invasive disease. Mutagenesis of the NS88.2 plasminogen binding M protein Prp was undertaken to examine the contribution of plasminogen binding and cell surface plasmin acquisition to virulence. The isogenic mutant NS88.2prp was engineered whereby four amino acid residues critical for plasminogen binding were converted to alanine codons in the GAS genome sequence. The mutated residues were reverse complemented to the wildtype sequence to construct GAS strain NS88.2prpRC. In comparison to NS88.2 and NS88.2prpRC, the NS88.2prp mutant exhibited significantly reduced ability to bind human plasminogen and accumulate cell surface plasmin activity during growth in human plasma. Utilising a humanised plasminogen mouse model of invasive infection, we demonstrate that the capacity to bind plasminogen and accumulate surface plasmin activity plays an essential role in GAS virulence. ABSTRACTThe human protease plasmin plays a crucial role in the capacity of the group A streptococcus (Streptococus pyogenes; GAS) to initiate invasive disease. The GAS strain NS88.2 was isolated from a case of bacteremia from the Northern Territory of Australia, a region with high rates of GAS invasive disease. Mutagenesis of the NS88.2 plasminogen binding M protein Prp was undertaken to examine the contribution of plasminogen binding and cell surface plasmin acquisition to virulence.The isogenic mutant NS88.2prp was engineered whereby four amino acid residues critical for plasminogen binding were converted to alanine codons in the GAS genome sequence. The mutated residues were reverse complemented to the wildtype sequence to construct GAS strain NS88.2prpRC. In comparison to NS88.2 and NS88.2prpRC, the NS88.2prp mutant exhibited significantly reduced ability to bind human plasminogen and accumulate cell surface plasmin activity during growth in human plasma. Utilising a humanised plasminogen mouse model of invasive infection, we demonstrate that the capacity to bind plasminogen and accumulate surface plasmin activity plays an essential role in GAS virulence.

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Section: Introductionmentioning

confidence: 99%

M protein‐mediated plasminogen binding is essential for the virulence of an invasiveStreptococcus pyogenesisolate

Sanderson-Smith¹,

Dinkla²,

Cole³

et al. 2008

FASEB j.

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“…The Gram-positive bacterium group A Streptococcus (GAS, S. pyogenes) is a major human pathogen causing the ubiquitous infections of pharyngitis and impetigo and, less commonly, life-threatening invasive diseases including streptococcal toxic shock-like syndrome and necrotizing fasciitis [1]. Repeated GAS infections may trigger a suite of non-suppurative immune sequelae including acute rheumatic fever, rheumatic heart disease and acute post-streptococcal glomerulonephritis [1].…”

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confidence: 99%

“…Repeated GAS infections may trigger a suite of non-suppurative immune sequelae including acute rheumatic fever, rheumatic heart disease and acute post-streptococcal glomerulonephritis [1]. Globally, GAS causes ~700 million human infections each year, resulting in over 500,000 deaths [2].…”

mentioning

confidence: 99%

Conserved anchorless surface proteins as group A streptococcal vaccine candidates

et al. 2012

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“…It produces a wide variety of diseases, ranging from mild skin and throat infections (impetigo and pharyngitis) to systemic and life threatening infections (streptococcal toxic shock syndrome and necrotizing fasciitis). [1][2][3] A conservative estimate of 500,000 deaths per year globally due to GAS infections has been calculated, making this bacterium one of the top 10 infectious causes of mortality. 3 If left untreated, GAS throat and skin infections can lead to complications involving the heart and kidneys (rheumatic heart disease and glomerulonephritis, respectively), so prompt antibiotic treatment is imperative.…”

Section: Introductionmentioning

confidence: 99%