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Etiopathogenesis of Rheumatic fever
By Spandana Rallapalli
Pediatrics 1st year PG
“Disease of the poverty”
• Agent – Group A Beta hemolyticus Streptococci
Rheumatogenic strains 1,3,5,6,18,29.
• Host – 5-15 years, F=M, Sequelae F>M, Susceptible to
HLA class II.
• Environment- Overcrowded,Developing,Inadequate
hygiene.
Conceptual relationship between Streptococci and Rheumatic fever
Almost all the cases of rheumatic fever are preceded by
pharyngitis; but not all the cases of pharyngitis succeded by
rheumatic fever(<3%)
Pharyngitis – sublinical or symptomatic.
Average time duration : 3 weeks
• M protein – virulent factor - inhibit complement – prevents phagocytosis.
• Antibodies + M protein ( weakest structures ) = destruction of M protein by
macrophages.
• Streptolysin O – Oxygen labile/Antigenic
• Streptolysin S – Oxygen stable/ Non antigenic.
• Streptokinase – Fibrin degradation.
• Pyrogenic exotoxin – Superantigen – B cells – release autoreactive antibodies
– superstimulation of T cells – rekease inflammatory cyokines.
• Anti C5a peptidase,Hyaluronidase,DNAase.
• Cytokines – thalamus - precipitate fever - many patients joints were inflamed
– so this name.
Cytotoxic theory
• GAS toxin is involved cytotoxic for
mammalian cardiac cells e.g
streptolysin O, inability to explain the
substantial latent period between
pharyngitis & onset of acute
rheumatic fever.
Immunologic theory
The antigenicity of GAS cellular &
extracellular epitopes & their
immunologic crossreactivity with cardiac
antigenic epitopes- molecular
mimicry.Common epitopes & specific
mammalian tissues
“Licks the joint, bites the heart”
Summary
• Rheumatic fever is multisystem , immune mediated , acute inflammation
which is non suppurative, which develops 2-4 weeks after pharygitis by beta-
hemolyticus streptococci lancefied A with rheumatogenic strains.

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  • 1. Etiopathogenesis of Rheumatic fever By Spandana Rallapalli Pediatrics 1st year PG
  • 2. “Disease of the poverty” • Agent – Group A Beta hemolyticus Streptococci Rheumatogenic strains 1,3,5,6,18,29. • Host – 5-15 years, F=M, Sequelae F>M, Susceptible to HLA class II. • Environment- Overcrowded,Developing,Inadequate hygiene.
  • 3. Conceptual relationship between Streptococci and Rheumatic fever
  • 4. Almost all the cases of rheumatic fever are preceded by pharyngitis; but not all the cases of pharyngitis succeded by rheumatic fever(<3%) Pharyngitis – sublinical or symptomatic. Average time duration : 3 weeks
  • 5.
  • 6. • M protein – virulent factor - inhibit complement – prevents phagocytosis. • Antibodies + M protein ( weakest structures ) = destruction of M protein by macrophages. • Streptolysin O – Oxygen labile/Antigenic • Streptolysin S – Oxygen stable/ Non antigenic. • Streptokinase – Fibrin degradation. • Pyrogenic exotoxin – Superantigen – B cells – release autoreactive antibodies – superstimulation of T cells – rekease inflammatory cyokines. • Anti C5a peptidase,Hyaluronidase,DNAase. • Cytokines – thalamus - precipitate fever - many patients joints were inflamed – so this name.
  • 7.
  • 8. Cytotoxic theory • GAS toxin is involved cytotoxic for mammalian cardiac cells e.g streptolysin O, inability to explain the substantial latent period between pharyngitis & onset of acute rheumatic fever. Immunologic theory The antigenicity of GAS cellular & extracellular epitopes & their immunologic crossreactivity with cardiac antigenic epitopes- molecular mimicry.Common epitopes & specific mammalian tissues “Licks the joint, bites the heart”
  • 9. Summary • Rheumatic fever is multisystem , immune mediated , acute inflammation which is non suppurative, which develops 2-4 weeks after pharygitis by beta- hemolyticus streptococci lancefied A with rheumatogenic strains.