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Related Concept Videos

Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies01:22

Rheumatic Heart Disease II: Clinical Manifestations and Diagnostic Studies

The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
Tonsillitis I: Introduction01:30

Tonsillitis I: Introduction

Tonsillitis is inflammation of the tonsils, which are two lymphoid tissue masses at the back of the throat. This condition can cause discomfort and irritation in the throat.
Etiology
Three primary contributing factors have been identified.
Rheumatic Heart Disease III: Medical Management01:21

Rheumatic Heart Disease III: Medical Management

Rheumatic heart disease (RHD) management can be divided into two main strategies: prevention and long-term management.Primary PreventionPrimary prevention focuses on timely diagnosis and management of group A streptococcal pharyngitis to prevent acute rheumatic fever. The most widely used antibiotic for treating this condition is intramuscular benzathine penicillin G.Acute Rheumatic Fever TreatmentThe primary treatment goal for a patient diagnosed with acute rheumatic fever is to suppress the...
Endocarditis I: Introduction01:25

Endocarditis I: Introduction

Introduction:Endocarditis is the infection of the endocardium, the inner lining of the heart and its valves. When the heart muscle is involved, the condition is termed myocarditis, while an infection of the outer lining is called pericarditis. Infective endocarditis (IE) primarily affects the endocardium, where pathogens adhere to the valves or lining, forming vegetation that can lead to severe complications. Infective endocarditis occurs when microorganisms, usually bacteria from other body...
Rheumatic Heart Disease IV: Nursing Management01:20

Rheumatic Heart Disease IV: Nursing Management

AssessmentA comprehensive assessment is essential in managing a patient with rheumatic heart disease (RHD). Begin with obtaining a detailed medical history, including recent streptococcal infections, a history of rheumatic fever, or previously diagnosed rheumatic heart disease. Assess the patient for symptoms such as fever, chest pain, widespread joint pain (arthralgia), tachycardia, pericardial friction rub, muffled heart sounds, heart murmurs, peripheral edema, subcutaneous nodules, and...

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Related Experiment Video

Updated: May 22, 2026

Visualization of Streptococcus pneumoniae within Cardiac Microlesions and Subsequent Cardiac Remodeling
08:25

Visualization of Streptococcus pneumoniae within Cardiac Microlesions and Subsequent Cardiac Remodeling

Published on: April 7, 2015

Streptococcus and rheumatic fever.

Madeleine W Cunningham1

  • 1Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. madeleine-cunningham@ouhsc.edu

Current Opinion in Rheumatology
|May 24, 2012
PubMed
Summary
This summary is machine-generated.

Group A Streptococcus infections can trigger autoimmune responses targeting heart valves and brain cells. Molecular mimicry involving the N-acetyl-beta-D-glucosamine epitope explains cross-reactivity in rheumatic fever and Sydenham chorea.

Related Experiment Videos

Last Updated: May 22, 2026

Visualization of Streptococcus pneumoniae within Cardiac Microlesions and Subsequent Cardiac Remodeling
08:25

Visualization of Streptococcus pneumoniae within Cardiac Microlesions and Subsequent Cardiac Remodeling

Published on: April 7, 2015

Area of Science:

  • Immunology
  • Rheumatology
  • Neurology

Background:

  • Rheumatic fever and Sydenham chorea are autoimmune sequelae of Group A Streptococcus infections.
  • Pathogenesis involves cross-reactive autoantibodies and T cells targeting host tissues.

Purpose of the Study:

  • To review current hypotheses on the pathogenesis of rheumatic fever and Group A Streptococcus-induced autoimmune sequelae.
  • To explore the role of molecular mimicry in targeting heart valves and brain cells.

Main Methods:

  • Analysis of human monoclonal antibodies from patients with rheumatic heart disease and Sydenham chorea.
  • Investigation of T cell reactivity against streptococcal antigens and cardiac/neuronal proteins.

Main Results:

  • Cross-reactive autoantibodies target Group A Streptococcus carbohydrate (N-acetyl-beta-D-glucosamine) and host antigens like laminin, cardiac myosin, gangliosides, and dopamine receptors.
  • Evidence suggests a two-hit hypothesis involving antibody attack and T cell infiltration in heart valve pathogenesis.
  • T cells cross-reactive with streptococcal M protein and cardiac myosin were identified.
  • Antibodies in Sydenham chorea target N-acetyl-beta-D-glucosamine and neuronal cell surface/intracellular antigens, including tubulin.

Conclusions:

  • Pathogenic mechanisms in rheumatic heart disease and Sydenham chorea share a common streptococcal epitope (N-acetyl-beta-D-glucosamine).
  • Molecular mimicry involves targeting extracellular antigens (laminin, gangliosides, dopamine receptors) while recognizing intracellular biomarkers (cardiac myosin, tubulin).
  • Antibody binding to cell surface antigens mediates valve damage and neuropsychiatric symptoms.