Poster Presentation 20th Lancefield International Symposium on Streptococci and Streptococcal Diseases 2017

Group G streptococcus induces autoimmune mediated carditis in the Lewis rat model of Rheumatic Heart Disease (#160)

Suchandan Sikder 1 , Natasha L Williams 1 , Alanna E Sorenson 1 , Md Abdul Alim 1 , Miranda E Vidgen 2 , Nicole J Moreland 3 , Catherine M Rush 1 , Robert S Simpson 4 , Brenda L Govan 1 , Robert E Norton 5 , Madeleine W Cunningham 6 , David J McMillan 2 , Kadaba S Sriprakash 7 , Natkunam Ketheesan 1
  1. James Cook University, Townsville, QLD, Australia
  2. INFLAME Biomedical Research Cluster, University of the Sunshine Coast, Maroochydore, QLD, Australia
  3. School of Medical Sciences, University of Auckland, Auckland, New Zealand
  4. Paediatric Intensive Care Services , The Townsville Hospital, Townsville, QLD, Australia
  5. Microbiology and Pathology, The Townsville Hospital, Townsville, QLD, Australia
  6. Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma, USA
  7. Bacterial Pathogenesis Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia

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. Both antibody and T cell responses against immunodominant GAS virulence factors including M protein, cross-react with host tissue proteins triggering an inflammatory response leading to permanent heart damage. However, in some ARF/RHD endemic regions, throat carriage of GAS is low. As Streptococcus dysgalactiae subspecies equisimilis (SDSE), also known as β-hemolytic groups C and G streptococci (GCS/GGS) also express M-protein, we postulated that streptococci other than GAS may have the potential to initiate or exacerbate ARF/RHD. Using a model initially developed to investigate the uniquely human disease of ARF/RHD, we have now discovered that Streptococcus dysgalactiae or group G streptococcus (GGS) does indeed cause both myocarditis and valvulitis, hallmarks of ARF/RHD. Remarkably the histological, immunological and functional changes in the hearts of rats exposed to GGS are identical to those exposed to GAS.  Furthermore, antibody cross-reactivity to cardiac myosin was comparable in both GGS and GAS exposed animals providing additional evidence that GGS can induce and/or exacerbate ARF/RHD.