Questions and Answers
What type of bacteria primarily causes acute rheumatic fever?
In acute rheumatic fever, the immune system correctly targets the streptococcal bacteria without attacking the body's tissues.
False
What is the approximate percentage of the population that produces cross-reactive antibodies in response to streptococcal infection?
3%
M proteins trigger the immune response and promote __________ in acute rheumatic fever.
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Which immune cells are primarily involved in the phagocytosis of bacteria?
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Match the following cytokines with their function:
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MHC Class II molecules present bacterial antigens to B cells.
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What role do macrophages play in the immune response during acute rheumatic fever?
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The release of __________ and __________ by tissue injury contributes to increased blood flow and permeability.
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Which of the following is NOT a cytokine released by activated T cells?
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What is the most common long-term effect of acute rheumatic fever?
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Pancarditis only affects the myocardium of the heart.
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What percentage of the population may develop autoimmune reactions due to molecular mimicry?
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Symptoms of syndenham's chorea may include uncontrolled jerky movements in the face, tongue, and ________.
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Match the following symptoms to their corresponding conditions:
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Which of the following is NOT a major criterion for diagnosing rheumatic fever?
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The mitral and aortic valves are commonly affected in rheumatic heart disease over time.
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What are the common symptoms of pancarditis?
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Cytokines activate ________ cells in lymph nodes, leading to their proliferation.
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Which of the following is a characteristic of Erythema marginatum?
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What mechanism causes the immune system to mistakenly target body tissues in acute rheumatic fever?
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Neutrophils are recruited solely for the destruction of body tissues during acute rheumatic fever.
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What type of proteins found on streptococcal bacteria are known to trigger the immune response?
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Activated T cells release various cytokines, including __________.
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Match the immune cells with their primary functions:
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Which cytokine modulates the immune response and aids in the function of B cells?
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Acute rheumatic fever is caused exclusively by a viral infection.
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Name the two key immune cells involved in the phagocytosis of bacteria during acute rheumatic fever.
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Inflammation during acute rheumatic fever is characterized by the release of __________ and __________.
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Which immune component enhances the permeability of capillaries during the immune response?
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Which of the following is a major criterion for diagnosing rheumatic fever?
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Pancarditis only affects the pericardium of the heart.
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What is a common skin manifestation associated with rheumatic fever?
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Antibodies can mistakenly attack self-proteins like ________, leading to autoimmune reactions.
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Match the following conditions with their associated details:
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Which of the following can be a long-term complication of rheumatic fever?
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Joint pain in rheumatic fever is often non-migratory.
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What is the primary purpose of antibodies in the immune response?
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Elevated ________ and ________ are inflammatory markers significant in diagnosing rheumatic fever.
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Which cytokine functions primarily in activating B cells?
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Which of the following is considered a major criterion for diagnosing rheumatic fever?
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Syndenham's chorea is characterized by controlled and coordinated movements.
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What type of inflammation involves all layers of the heart during rheumatic fever?
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The __________ is a common skin manifestation in rheumatic fever characterized by ring-like rashes.
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Match the following symptoms with their corresponding conditions:
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What is a common long-term effect of acute rheumatic fever?
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Post-streptococcal infection evidence is not necessary for diagnosing rheumatic fever.
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What type of joint involvement occurs in approximately 75% of rheumatic fever cases?
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Antibodies may mistakenly target __________ in the heart, resulting in pancarditis.
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Which of the following statements about molecular mimicry is true?
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What causes the immune system to target the body's own tissues in acute rheumatic fever?
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In acute rheumatic fever, neutrophils are primarily involved in the immune response by attacking body tissues.
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Name the key type of antibody response generated by 97% of the population after a streptococcal infection.
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Activated T cells release important signaling molecules known as __________.
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Match the cytokines with their role in the immune response:
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Which immune cells are responsible for presenting antigens to T cells?
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M proteins on streptococcal bacteria discourage the immune response in acute rheumatic fever.
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What is the effect of histamine release during the immune response in acute rheumatic fever?
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The inflammatory markers elevated in rheumatic fever diagnosis include __________ and __________.
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What is a common complication of untreated acute rheumatic fever?
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What causes acute rheumatic fever?
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Molecular mimicry leads to the immune system correctly targeting only the bacteria.
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What is the main immune cell type involved in phagocytosis during acute rheumatic fever?
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Interleukin-2 primarily functions to activate ________ cells.
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Match the immune cells with their functions:
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Which of the following cytokines is involved in stimulating T cell activation?
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The presence of MHC Class II molecules is critical for the activation of CD4 T cells.
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What is the role of leukotrienes and prostaglandins in immune response?
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The condition known as ________ chorea is characterized by uncontrolled movements.
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Which immune response mechanism increases blood flow and permeability during acute rheumatic fever?
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Which of the following is a symptom of pancarditis?
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Pancarditis only involves the myocardium of the heart.
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What are two common long-term effects of acute rheumatic fever?
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Syndenham's chorea can cause uncontrolled movements in the face, tongue, and ________.
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Match the symptoms with their associated conditions:
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Which criteria are necessary for diagnosing rheumatic fever?
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Approximately 75% of rheumatic fever cases show non-migratory polyarthritis.
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What type of joint involvement is commonly seen in rheumatic fever?
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Antibodies may mistakenly target self-proteins like ________ in the heart.
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Evidence of a previous streptococcal infection is crucial for confirming a diagnosis of rheumatic fever.
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What is primarily responsible for the inflammatory response in acute rheumatic fever?
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MHC class II molecules are involved in presenting antigens to B cells.
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What percentage of the population generates antibodies that target the bacteria responsible for acute rheumatic fever?
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In acute rheumatic fever, antibodies can mistakenly target self-proteins like __________.
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Match the following cytokines with their primary functions:
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What is a common complication of acute rheumatic fever affecting the heart?
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Neutrophils primarily function by presenting antigens to T cells.
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What immune response component is released during tissue injury that increases blood flow and permeability?
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The immune system's incorrect targeting of body tissues in acute rheumatic fever is known as __________.
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What type of antibodies are responsible for cross-reactive responses in acute rheumatic fever?
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What is the primary function of antibodies in the immune response?
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Polyartritis is commonly a migratory type of arthritis in rheumatic fever.
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Which part of the heart is primarily affected by pancarditis?
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Syndenham's chorea is characterized by uncontrolled jerky movements in the face, tongue, and ________.
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Match the following symptoms with their corresponding descriptions:
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Which heart valves are commonly associated with rheumatic heart disease?
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Molecular mimicry is a mechanism that can cause the immune system to attack self-proteins.
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What is one major criterion used for diagnosing rheumatic fever?
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Evidence of a prior streptococcal infection can be determined through a ________ test.
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What is a key effect of cytokines in the immune response?
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Study Notes
Acute Rheumatic Fever Overview
- Acute rheumatic fever is an inflammatory condition that follows streptococcal pharyngitis, primarily caused by Group A beta-hemolytic Streptococcus bacteria, specifically Streptococcus pyogenes.
- It occurs when the immune system, after responding to streptococcal infection, mistakenly targets the body's own tissues.
Pathophysiology
- Antibody Response: 97% of the population generates antibodies that target the bacteria, while 3% produce cross-reactive antibodies that attack body tissues due to molecular mimicry.
- M Proteins: The streptococcal bacteria have M proteins that trigger the immune response and inflammation.
Immune Response Mechanism
- Injury and Inflammation: Tissue damage from the infection leads to the production of leukotrienes and prostaglandins, triggering mast cells to release histamines, causing vasodilation and increased capillary permeability.
- Increased Blood Flow & Permeability: Enhanced blood flow brings more immune cells to the infection site, while increased permeability allows immune components to exit capillaries and reach the tissues.
Key Immune Cells Involved
-
Neutrophils and Macrophages:
- Neutrophils are recruited for phagocytosis of bacteria, utilizing lysosomes to degrade bacterial components.
- Macrophages also engulf bacteria and present antigens using MHC class II molecules.
Antigen Presentation
- MHC Class II Molecules: Formed by macrophages upon activation, presenting bacterial antigens to T cells.
- T Cell Activation: CD4 T cells interact with MHC II molecules, using their T cell receptors (TCR) to recognize specific antigens.
Cytokine Release
- Activated T cells release various cytokines, including:
- Interleukin-1: Stimulates T cell activation.
- Interleukin-2, 4, 5: Further modulate the immune response, aiding in the function of B cells and the entire immune system.
Clinical Implications
- Understanding the immunopathogenesis is crucial for diagnosing and managing acute rheumatic fever and its potential long-term effects, such as rheumatic heart disease.### Cytokines and Immune Response
- Cytokines activate B cells in lymph nodes, leading to their proliferation and differentiation into plasma cells.
- Plasma cells are equipped with extensive rough endoplasmic reticulum for antibody production.
- Antibodies target antigens, enhancing phagocytosis, activating natural killer cells, and promoting inflammation to combat bacteria.
Molecular Mimicry and Autoimmunity
- Approximately 3% of the population may develop autoimmune reactions due to molecular mimicry, particularly in children aged 5-15, and in impoverished or overcrowded settings.
- Antibodies designed to target Group A beta-hemolytic streptococcal bacteria may mistakenly attack similar self-proteins, such as:
- Keratin in the skin, leading to specific skin lesions.
- Ganglioside proteins in the basal ganglia, contributing to Syndenham's chorea.
- Proteins like laminin, tropomyosin, and actin in the heart, resulting in pancarditis.
- Vimentin in synovial joints, potentially leading to migratory polyarthritis.
Pancarditis
- Pancarditis involves inflammation of all heart layers due to antibody interactions.
- Common symptoms include friction rub during auscultation, signaling pericarditis and sharp chest pain.
- Myocardium damage can lead to fibrinoid necrosis and Ashoff bodies, indicating serious tissue injury.
- Chronic inflammation and necrosis risk congestive heart failure due to impaired myocardial contractility.
Endocardial Effects
- Rheumatic fever can cause damage to heart valves, leading to vegetations and valvular dysfunction over time.
- Commonly affected valves are mitral and aortic, resulting in stenosis or regurgitation.
- Severe cases may lead to subacute bacterial endocarditis, introducing serious complications.
Central Nervous System Impacts
- CNS-related damage occurs in structures like the lentiform nucleus and caudate nucleus, disrupting motor control.
- This can manifest as Syndenham's chorea, characterized by uncontrolled jerky movements in the face, tongue, and limbs.
Joint Involvement
- About 75% of rheumatic fever cases display polyarthritis, affecting large synovial joints, particularly the hips and shoulders.
- The arthritis can be migratory and is different from typical joint pain.
Skin Manifestations
- Erythema marginatum presents as concentric ring-like rashes on extremities and trunk.
- Subcutaneous nodules form due to collagen deposits on extensor surfaces like wrists and elbows.
Diagnosis: Jones Criteria
- Diagnosis of rheumatic fever requires either:
- Two major criteria, or
- One major and two minor criteria.
- Major criteria include:
- Polyarthritis (joints)
- Pancarditis (heart involvement)
- Subcutaneous nodules
- Erythema marginatum
- Syndenham's chorea.
- Minor criteria include:
- Fever, arthralgia (joint pain), prolonged PR interval, and elevated inflammatory markers (CRP and ESR).
Post-Streptococcal Infection Evidence
- Evidence of a prior streptococcal infection is necessary; methods include:
- Rapid antigen test.
- Positive culture and sensitivity.
- Elevated anti-streptolysin O titers.
Overview of Acute Rheumatic Fever
- Acute rheumatic fever is an inflammatory condition developing after streptococcal pharyngitis, mainly caused by Group A beta-hemolytic Streptococcus (Streptococcus pyogenes).
- Occurs when the immune system mistakenly attacks the body's own tissues following a streptococcal infection.
Pathophysiology
- Approximately 97% of individuals produce antibodies against streptococcus, while 3% generate cross-reactive antibodies due to molecular mimicry.
- M proteins on streptococcal bacteria instigate immune responses and inflammation.
Immune Response Mechanism
- Tissue injury triggers production of leukotrienes and prostaglandins, activating mast cells to release histamines.
- Increased blood flow and capillary permeability allow immune cells to access affected tissues.
Key Immune Cells Involved
- Neutrophils are essential for phagocytosis, utilizing lysosomes to degrade bacteria.
- Macrophages engulf bacteria and present antigens through MHC class II molecules.
Antigen Presentation
- MHC class II molecules are formed by activated macrophages to present bacterial antigens to T cells.
- CD4 T cells recognize specific antigens via their T cell receptors (TCR) in conjunction with MHC II.
Cytokine Release
- Activated T cells secrete cytokines, such as:
- Interleukin-1, stimulating further T cell activation.
- Interleukin-2, 4, and 5, which help in the modulation of the immune response.
Clinical Implications
- Understanding the immunopathogenesis aids in the diagnosis and management of acute rheumatic fever and its long-term consequences like rheumatic heart disease.
Cytokines and Immune Response
- Cytokines stimulate B cells in lymph nodes to proliferate and differentiate into antibody-producing plasma cells.
- Antibodies enhance phagocytosis, activate natural killer cells, and promote inflammation against bacteria.
Molecular Mimicry and Autoimmunity
- Around 3% may experience autoimmune reactions due to molecular mimicry, especially in children aged 5-15, or in crowded, impoverished conditions.
- Antibodies can mistakenly attack self-proteins such as:
- Keratin, causing specific skin lesions.
- Ganglioside proteins, leading to Syndenham's chorea.
- Heart proteins, resulting in pancarditis.
- Vimentin in synovial joints, leading to migratory polyarthritis.
Pancarditis
- Involves inflammation of all heart layers caused by antibody interactions.
- Symptoms include friction rub and sharp chest pain, indicating pericarditis.
- Myocardial damage may lead to fibrinoid necrosis and Ashoff bodies, worsening heart function and risking congestive heart failure.
Endocardial Effects
- Rheumatic fever can damage heart valves, causing vegetations and dysfunction, primarily affecting the mitral and aortic valves.
- Severe damage may result in subacute bacterial endocarditis.
Central Nervous System Impacts
- Damage to structures like the lentiform nucleus and caudate nucleus can disrupt motor control.
- Symptoms include Syndenham's chorea, characterized by involuntary movements of the face, tongue, and limbs.
Joint Involvement
- Polyarthritis occurs in about 75% of rheumatic fever cases, typically affecting large synovial joints like the hips and shoulders.
- Arthritis may be migratory and presents differently from standard joint pain.
Skin Manifestations
- Erythema marginatum appears as concentric ring-like rashes on the trunk and extremities.
- Subcutaneous nodules develop from collagen deposits on extensor surfaces, such as wrists and elbows.
Diagnosis: Jones Criteria
- Diagnosis requires either two major criteria or one major and two minor criteria.
- Major criteria include polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, and Syndenham's chorea.
- Minor criteria involve fever, arthralgia, prolonged PR interval, and elevated inflammatory markers (CRP and ESR).
Post-Streptococcal Infection Evidence
- Evidence of previous streptococcal infection is needed, which can be confirmed by:
- Rapid antigen tests.
- Positive culture and sensitivity results.
- Elevated anti-streptolysin O titers.
Overview of Acute Rheumatic Fever
- Acute rheumatic fever is an inflammatory condition developing after streptococcal pharyngitis, mainly caused by Group A beta-hemolytic Streptococcus (Streptococcus pyogenes).
- Occurs when the immune system mistakenly attacks the body's own tissues following a streptococcal infection.
Pathophysiology
- Approximately 97% of individuals produce antibodies against streptococcus, while 3% generate cross-reactive antibodies due to molecular mimicry.
- M proteins on streptococcal bacteria instigate immune responses and inflammation.
Immune Response Mechanism
- Tissue injury triggers production of leukotrienes and prostaglandins, activating mast cells to release histamines.
- Increased blood flow and capillary permeability allow immune cells to access affected tissues.
Key Immune Cells Involved
- Neutrophils are essential for phagocytosis, utilizing lysosomes to degrade bacteria.
- Macrophages engulf bacteria and present antigens through MHC class II molecules.
Antigen Presentation
- MHC class II molecules are formed by activated macrophages to present bacterial antigens to T cells.
- CD4 T cells recognize specific antigens via their T cell receptors (TCR) in conjunction with MHC II.
Cytokine Release
- Activated T cells secrete cytokines, such as:
- Interleukin-1, stimulating further T cell activation.
- Interleukin-2, 4, and 5, which help in the modulation of the immune response.
Clinical Implications
- Understanding the immunopathogenesis aids in the diagnosis and management of acute rheumatic fever and its long-term consequences like rheumatic heart disease.
Cytokines and Immune Response
- Cytokines stimulate B cells in lymph nodes to proliferate and differentiate into antibody-producing plasma cells.
- Antibodies enhance phagocytosis, activate natural killer cells, and promote inflammation against bacteria.
Molecular Mimicry and Autoimmunity
- Around 3% may experience autoimmune reactions due to molecular mimicry, especially in children aged 5-15, or in crowded, impoverished conditions.
- Antibodies can mistakenly attack self-proteins such as:
- Keratin, causing specific skin lesions.
- Ganglioside proteins, leading to Syndenham's chorea.
- Heart proteins, resulting in pancarditis.
- Vimentin in synovial joints, leading to migratory polyarthritis.
Pancarditis
- Involves inflammation of all heart layers caused by antibody interactions.
- Symptoms include friction rub and sharp chest pain, indicating pericarditis.
- Myocardial damage may lead to fibrinoid necrosis and Ashoff bodies, worsening heart function and risking congestive heart failure.
Endocardial Effects
- Rheumatic fever can damage heart valves, causing vegetations and dysfunction, primarily affecting the mitral and aortic valves.
- Severe damage may result in subacute bacterial endocarditis.
Central Nervous System Impacts
- Damage to structures like the lentiform nucleus and caudate nucleus can disrupt motor control.
- Symptoms include Syndenham's chorea, characterized by involuntary movements of the face, tongue, and limbs.
Joint Involvement
- Polyarthritis occurs in about 75% of rheumatic fever cases, typically affecting large synovial joints like the hips and shoulders.
- Arthritis may be migratory and presents differently from standard joint pain.
Skin Manifestations
- Erythema marginatum appears as concentric ring-like rashes on the trunk and extremities.
- Subcutaneous nodules develop from collagen deposits on extensor surfaces, such as wrists and elbows.
Diagnosis: Jones Criteria
- Diagnosis requires either two major criteria or one major and two minor criteria.
- Major criteria include polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, and Syndenham's chorea.
- Minor criteria involve fever, arthralgia, prolonged PR interval, and elevated inflammatory markers (CRP and ESR).
Post-Streptococcal Infection Evidence
- Evidence of previous streptococcal infection is needed, which can be confirmed by:
- Rapid antigen tests.
- Positive culture and sensitivity results.
- Elevated anti-streptolysin O titers.
Overview of Acute Rheumatic Fever
- Acute rheumatic fever is an inflammatory condition developing after streptococcal pharyngitis, mainly caused by Group A beta-hemolytic Streptococcus (Streptococcus pyogenes).
- Occurs when the immune system mistakenly attacks the body's own tissues following a streptococcal infection.
Pathophysiology
- Approximately 97% of individuals produce antibodies against streptococcus, while 3% generate cross-reactive antibodies due to molecular mimicry.
- M proteins on streptococcal bacteria instigate immune responses and inflammation.
Immune Response Mechanism
- Tissue injury triggers production of leukotrienes and prostaglandins, activating mast cells to release histamines.
- Increased blood flow and capillary permeability allow immune cells to access affected tissues.
Key Immune Cells Involved
- Neutrophils are essential for phagocytosis, utilizing lysosomes to degrade bacteria.
- Macrophages engulf bacteria and present antigens through MHC class II molecules.
Antigen Presentation
- MHC class II molecules are formed by activated macrophages to present bacterial antigens to T cells.
- CD4 T cells recognize specific antigens via their T cell receptors (TCR) in conjunction with MHC II.
Cytokine Release
- Activated T cells secrete cytokines, such as:
- Interleukin-1, stimulating further T cell activation.
- Interleukin-2, 4, and 5, which help in the modulation of the immune response.
Clinical Implications
- Understanding the immunopathogenesis aids in the diagnosis and management of acute rheumatic fever and its long-term consequences like rheumatic heart disease.
Cytokines and Immune Response
- Cytokines stimulate B cells in lymph nodes to proliferate and differentiate into antibody-producing plasma cells.
- Antibodies enhance phagocytosis, activate natural killer cells, and promote inflammation against bacteria.
Molecular Mimicry and Autoimmunity
- Around 3% may experience autoimmune reactions due to molecular mimicry, especially in children aged 5-15, or in crowded, impoverished conditions.
- Antibodies can mistakenly attack self-proteins such as:
- Keratin, causing specific skin lesions.
- Ganglioside proteins, leading to Syndenham's chorea.
- Heart proteins, resulting in pancarditis.
- Vimentin in synovial joints, leading to migratory polyarthritis.
Pancarditis
- Involves inflammation of all heart layers caused by antibody interactions.
- Symptoms include friction rub and sharp chest pain, indicating pericarditis.
- Myocardial damage may lead to fibrinoid necrosis and Ashoff bodies, worsening heart function and risking congestive heart failure.
Endocardial Effects
- Rheumatic fever can damage heart valves, causing vegetations and dysfunction, primarily affecting the mitral and aortic valves.
- Severe damage may result in subacute bacterial endocarditis.
Central Nervous System Impacts
- Damage to structures like the lentiform nucleus and caudate nucleus can disrupt motor control.
- Symptoms include Syndenham's chorea, characterized by involuntary movements of the face, tongue, and limbs.
Joint Involvement
- Polyarthritis occurs in about 75% of rheumatic fever cases, typically affecting large synovial joints like the hips and shoulders.
- Arthritis may be migratory and presents differently from standard joint pain.
Skin Manifestations
- Erythema marginatum appears as concentric ring-like rashes on the trunk and extremities.
- Subcutaneous nodules develop from collagen deposits on extensor surfaces, such as wrists and elbows.
Diagnosis: Jones Criteria
- Diagnosis requires either two major criteria or one major and two minor criteria.
- Major criteria include polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, and Syndenham's chorea.
- Minor criteria involve fever, arthralgia, prolonged PR interval, and elevated inflammatory markers (CRP and ESR).
Post-Streptococcal Infection Evidence
- Evidence of previous streptococcal infection is needed, which can be confirmed by:
- Rapid antigen tests.
- Positive culture and sensitivity results.
- Elevated anti-streptolysin O titers.
Overview of Acute Rheumatic Fever
- Acute rheumatic fever is an inflammatory condition developing after streptococcal pharyngitis, mainly caused by Group A beta-hemolytic Streptococcus (Streptococcus pyogenes).
- Occurs when the immune system mistakenly attacks the body's own tissues following a streptococcal infection.
Pathophysiology
- Approximately 97% of individuals produce antibodies against streptococcus, while 3% generate cross-reactive antibodies due to molecular mimicry.
- M proteins on streptococcal bacteria instigate immune responses and inflammation.
Immune Response Mechanism
- Tissue injury triggers production of leukotrienes and prostaglandins, activating mast cells to release histamines.
- Increased blood flow and capillary permeability allow immune cells to access affected tissues.
Key Immune Cells Involved
- Neutrophils are essential for phagocytosis, utilizing lysosomes to degrade bacteria.
- Macrophages engulf bacteria and present antigens through MHC class II molecules.
Antigen Presentation
- MHC class II molecules are formed by activated macrophages to present bacterial antigens to T cells.
- CD4 T cells recognize specific antigens via their T cell receptors (TCR) in conjunction with MHC II.
Cytokine Release
- Activated T cells secrete cytokines, such as:
- Interleukin-1, stimulating further T cell activation.
- Interleukin-2, 4, and 5, which help in the modulation of the immune response.
Clinical Implications
- Understanding the immunopathogenesis aids in the diagnosis and management of acute rheumatic fever and its long-term consequences like rheumatic heart disease.
Cytokines and Immune Response
- Cytokines stimulate B cells in lymph nodes to proliferate and differentiate into antibody-producing plasma cells.
- Antibodies enhance phagocytosis, activate natural killer cells, and promote inflammation against bacteria.
Molecular Mimicry and Autoimmunity
- Around 3% may experience autoimmune reactions due to molecular mimicry, especially in children aged 5-15, or in crowded, impoverished conditions.
- Antibodies can mistakenly attack self-proteins such as:
- Keratin, causing specific skin lesions.
- Ganglioside proteins, leading to Syndenham's chorea.
- Heart proteins, resulting in pancarditis.
- Vimentin in synovial joints, leading to migratory polyarthritis.
Pancarditis
- Involves inflammation of all heart layers caused by antibody interactions.
- Symptoms include friction rub and sharp chest pain, indicating pericarditis.
- Myocardial damage may lead to fibrinoid necrosis and Ashoff bodies, worsening heart function and risking congestive heart failure.
Endocardial Effects
- Rheumatic fever can damage heart valves, causing vegetations and dysfunction, primarily affecting the mitral and aortic valves.
- Severe damage may result in subacute bacterial endocarditis.
Central Nervous System Impacts
- Damage to structures like the lentiform nucleus and caudate nucleus can disrupt motor control.
- Symptoms include Syndenham's chorea, characterized by involuntary movements of the face, tongue, and limbs.
Joint Involvement
- Polyarthritis occurs in about 75% of rheumatic fever cases, typically affecting large synovial joints like the hips and shoulders.
- Arthritis may be migratory and presents differently from standard joint pain.
Skin Manifestations
- Erythema marginatum appears as concentric ring-like rashes on the trunk and extremities.
- Subcutaneous nodules develop from collagen deposits on extensor surfaces, such as wrists and elbows.
Diagnosis: Jones Criteria
- Diagnosis requires either two major criteria or one major and two minor criteria.
- Major criteria include polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, and Syndenham's chorea.
- Minor criteria involve fever, arthralgia, prolonged PR interval, and elevated inflammatory markers (CRP and ESR).
Post-Streptococcal Infection Evidence
- Evidence of previous streptococcal infection is needed, which can be confirmed by:
- Rapid antigen tests.
- Positive culture and sensitivity results.
- Elevated anti-streptolysin O titers.
Overview of Acute Rheumatic Fever
- Acute rheumatic fever is an inflammatory condition developing after streptococcal pharyngitis, mainly caused by Group A beta-hemolytic Streptococcus (Streptococcus pyogenes).
- Occurs when the immune system mistakenly attacks the body's own tissues following a streptococcal infection.
Pathophysiology
- Approximately 97% of individuals produce antibodies against streptococcus, while 3% generate cross-reactive antibodies due to molecular mimicry.
- M proteins on streptococcal bacteria instigate immune responses and inflammation.
Immune Response Mechanism
- Tissue injury triggers production of leukotrienes and prostaglandins, activating mast cells to release histamines.
- Increased blood flow and capillary permeability allow immune cells to access affected tissues.
Key Immune Cells Involved
- Neutrophils are essential for phagocytosis, utilizing lysosomes to degrade bacteria.
- Macrophages engulf bacteria and present antigens through MHC class II molecules.
Antigen Presentation
- MHC class II molecules are formed by activated macrophages to present bacterial antigens to T cells.
- CD4 T cells recognize specific antigens via their T cell receptors (TCR) in conjunction with MHC II.
Cytokine Release
- Activated T cells secrete cytokines, such as:
- Interleukin-1, stimulating further T cell activation.
- Interleukin-2, 4, and 5, which help in the modulation of the immune response.
Clinical Implications
- Understanding the immunopathogenesis aids in the diagnosis and management of acute rheumatic fever and its long-term consequences like rheumatic heart disease.
Cytokines and Immune Response
- Cytokines stimulate B cells in lymph nodes to proliferate and differentiate into antibody-producing plasma cells.
- Antibodies enhance phagocytosis, activate natural killer cells, and promote inflammation against bacteria.
Molecular Mimicry and Autoimmunity
- Around 3% may experience autoimmune reactions due to molecular mimicry, especially in children aged 5-15, or in crowded, impoverished conditions.
- Antibodies can mistakenly attack self-proteins such as:
- Keratin, causing specific skin lesions.
- Ganglioside proteins, leading to Syndenham's chorea.
- Heart proteins, resulting in pancarditis.
- Vimentin in synovial joints, leading to migratory polyarthritis.
Pancarditis
- Involves inflammation of all heart layers caused by antibody interactions.
- Symptoms include friction rub and sharp chest pain, indicating pericarditis.
- Myocardial damage may lead to fibrinoid necrosis and Ashoff bodies, worsening heart function and risking congestive heart failure.
Endocardial Effects
- Rheumatic fever can damage heart valves, causing vegetations and dysfunction, primarily affecting the mitral and aortic valves.
- Severe damage may result in subacute bacterial endocarditis.
Central Nervous System Impacts
- Damage to structures like the lentiform nucleus and caudate nucleus can disrupt motor control.
- Symptoms include Syndenham's chorea, characterized by involuntary movements of the face, tongue, and limbs.
Joint Involvement
- Polyarthritis occurs in about 75% of rheumatic fever cases, typically affecting large synovial joints like the hips and shoulders.
- Arthritis may be migratory and presents differently from standard joint pain.
Skin Manifestations
- Erythema marginatum appears as concentric ring-like rashes on the trunk and extremities.
- Subcutaneous nodules develop from collagen deposits on extensor surfaces, such as wrists and elbows.
Diagnosis: Jones Criteria
- Diagnosis requires either two major criteria or one major and two minor criteria.
- Major criteria include polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, and Syndenham's chorea.
- Minor criteria involve fever, arthralgia, prolonged PR interval, and elevated inflammatory markers (CRP and ESR).
Post-Streptococcal Infection Evidence
- Evidence of previous streptococcal infection is needed, which can be confirmed by:
- Rapid antigen tests.
- Positive culture and sensitivity results.
- Elevated anti-streptolysin O titers.
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Description
This quiz provides an overview of acute rheumatic fever, an inflammatory condition that follows streptococcal infections. It covers the underlying pathophysiology, the immune response mechanisms involved, and the specific triggers of the inflammatory reactions. Test your knowledge on this important health topic.
