A Paradigm Shift for Rheumatic Heart Disease: Role of Group G Streptococcus

Acute rheumatic fever and rheumatic heart disease (ARF/RHD) have long been described as autoimmune sequelae of Streptococcus pyogenes or group A streptococcal (GAS) infection characterised by inflammatory changes to heart, joint, brain, blood vessel and skin tissue. ARF/RHD is considered to be triggered by antibody and T-cell responses against immunodominant GAS virulence factors including M-protein, that cross-react with host tissue proteins. Repeat exposures to GAS perpetuate the autoimmune process leading to permanent cardiac damage. However, in some ARF/RHD endemic regions, there is low carriage of GAS were correspondingly high carriage of Streptococcus dysgalactiae subspecies equisimilis (SDSE), also known as β-hemolytic groups C and G streptococci (GCS/GGS). This has led to the suggestion that SDSE might also have the potential to initiate or exacerbate ARF/RHD. We have discovered using an appropriate model that GGS does indeed cause both myocarditis and valvulitis, hallmarks of ARF/RHD. Remarkably the histological, immunological and functional changes in the hearts of animals exposed to GGS are identical to those exposed to GAS. Furthermore, antibody cross-reactivity to cardiac myosin and collagen I were comparable in both GGS and GAS exposed animals providing further evidence that GGS can induce and/or exacerbate ARF/RHD.

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15th International Scientific Conference

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