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ACUTE RHEUMATIC FEVER
Ankita Manandhar
BAMS 23rd batch
Roll no: 04
INTRODUCTION
Acute rheumatic fever (ARF) is a multisystem
disease resulting from an autoimmune reaction to
infection with group A streptococcus.
Although many parts of a body may be affected
but almost all of the manifestations resolve
completely except cardiac valvular
damage[rheumatic heart disease (RHD)].
It is triggered by an immune-mediated delayed
response to infection with specific strains of group.
.
A streptococci that possess antigens which may
cross react with cardiac myosin and sarcolemmal
membrane protein.
It is major public health problem among children
and young adults in developing countries and most
important acquired heart disease in children.
DEFINITION
Acute rheumatic fever is an acute autoimmune
collagen disease occurs as a hypersensitivity
reaction to a group A beta hemolytic streptococcal
infection characterized by inflammatory lesions of
connective tissue and endothelial tissue affecting
heart, joint, blood vessels .
GLOBAL CONSIDERATIONS
ARF and RHD are disease of poverty common in
early twentieth century but it started decreasing in
developed countries.
This decline was attributable to improved living
conditions particularly less crowded and better
hygiene and introduction of antibiotics and
improved systems of medical care.
Recurrent outbreaks of ARF began in the 1980s in
Rocky Mountain States of the United States.
The disappearance of ARF in industrialized
countries during twentieth century was not
replicated in developing countries
Contd.
It has been estimated that between 15 and 19
million people worldwide are affected by RHD,
with approximately one-quarter of a million deaths
occurring each year.
Some 95% of ARF cases and RHD deaths now
occur in developing countries.
In Nepal, A total of six cases out of 4736 had
definite acute rheumatic fever (out of 13 suspected
cases) giving overall prevalence rate of 1.2 per
1000.
(Regmi PR, Pandey MR. Prevalence of rheumatic fever and rheumatic heart disease in
school children of Kathmandu city. Indian Heart J. 1997 Sep-Oct;49(5):518-20. PMID:
9505020.)
EPIDEMIOLOGY
It is common in children aged 5-14 years.
Rare in person aged >30 years
Both sexes are equally affected by ARF
But RHD most commonly affects females,
sometimes up to twice as frequently as males.
PATHOGENESIS
There is no direct invasion to the tissues by the microorganism but its an autoimmune
disease that involves antigen(Ag)-antibody(Ab) interaction.
↓
Group A Streptococcal(GAS) pharyngeal infection
↓
These antibodies cross react with human tissue because of the antigenic similarity
between streptococcal components and human connective tissues (Molecular mimicry)
↓
Immunologically mediated inflammation and damage(Autoimmune)to human tissue
which have antigenic similarity with streptococcal components like heart, joints, brains
(connective tissue) and subcutaneous tissue
↓
Rheumatic fever
CLINICAL FEATURES
There is a latent period of 1-5 weeks between the precipitating
group A streptococcal infection and appearance of clinical
features.
Heart involvement:
• About 60% cases of ARF progress to RHD.
• Valvular damage is the hallmark of rheumatic carditis.
• The mitral valve is almost always affected.
• Myocardial inflammation may affect electrical conduction
pathways, leading to P-R interval prolongation and softening of
the first heart sound.
.
Joint involvement:
• Polyarthritis affecting large joints most
commonly the knees, ankles, hips, and
elbows.
• Arthralgia
Syndeham’s Chorea:
• Abnormal involuntary, rapid ,jerky movements affect
particularly the head and upper limbs.
• They may be generalized or restricted to one side of the
body(hemi chorea)
,
Skin manifestation
• The classic rash of ARF is erythema marginatum,
which begins as pink macules that clear centrally ,
leaving a serpiginous spreading edge.
The rashes is evenest, appearing and disappearing before the
examiner’s eyes. It occurs usually on the trunk ,sometimes on
limbs ,but almost never on face
• Subcutaneous nodules occur as painless, small, mobile lumps
beneath skin overlying bony prominences, particularly of the
hands, feet, elbows, occupits and occasionally vertebrae.
DIAGNOSTIC EVALUATION
Medical history and Physical examination
Must have an infection with group A streptococcal
bacteria
Must have 2 major or 1 major and 2 major Jones
criteria
1.Major criteria-
• Carditis
• Polyarthritis
• Chorea
• Erythema marginatum
• Subcutaneous nodules
2. Minor criteria
• Arthralgia
• Hyperpyrexia
• High ESR
• High C-reactive protein
• Prolonged P-R interval
Electrocardiogram and Echocardiogram
Blood test-Antibodies to strep-bacteria in the blood.
[Anti streptolysin O (ASO)]
Inflammatory markers=increased ESR and C-reactive
protein
Throat swab =culture
Treatment
Antibiotic therapy: For treatment and prevention.
E.g. Penicillin 500mg (250mg for children)PO twice
daily ,Amoxicillin 50mg/kg daily for 10 days.
Anti-inflammatory agents: Salicylates and NSAIDS
for pain reliever, swelling, fever, inflammation
reducing aspirin, naproxen or corticosteroids like
predrisome in severe cases.
Anticonvulsants: Valproic acid, Carbamazepine
PREVENTION
Primary Prevention: Elimination of major risk
factors for streptococcal infection, particularly
overcrowded housing. Timely and complete
treatment of group A streptococcal sore throat with
antibiotics.
Secondary prevention: They should receive long
term penicillin prophylaxis to prevent recurrences.
The best antibiotics for secondary prophylaxis is
benzathine penicillin delivered every 4-2 week
considering the risk, age, last episode.
Tertiary prevention: Management of heart failure,
management of lesions, and treatment for
consequences of RHD including stroke, endocarditis
and arrhythmia.
.

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ACUTE RHEUMATIC FEVER.pptx

  • 1. ACUTE RHEUMATIC FEVER Ankita Manandhar BAMS 23rd batch Roll no: 04
  • 2. INTRODUCTION Acute rheumatic fever (ARF) is a multisystem disease resulting from an autoimmune reaction to infection with group A streptococcus. Although many parts of a body may be affected but almost all of the manifestations resolve completely except cardiac valvular damage[rheumatic heart disease (RHD)]. It is triggered by an immune-mediated delayed response to infection with specific strains of group.
  • 3. . A streptococci that possess antigens which may cross react with cardiac myosin and sarcolemmal membrane protein. It is major public health problem among children and young adults in developing countries and most important acquired heart disease in children.
  • 4. DEFINITION Acute rheumatic fever is an acute autoimmune collagen disease occurs as a hypersensitivity reaction to a group A beta hemolytic streptococcal infection characterized by inflammatory lesions of connective tissue and endothelial tissue affecting heart, joint, blood vessels .
  • 5. GLOBAL CONSIDERATIONS ARF and RHD are disease of poverty common in early twentieth century but it started decreasing in developed countries. This decline was attributable to improved living conditions particularly less crowded and better hygiene and introduction of antibiotics and improved systems of medical care.
  • 6. Recurrent outbreaks of ARF began in the 1980s in Rocky Mountain States of the United States. The disappearance of ARF in industrialized countries during twentieth century was not replicated in developing countries
  • 7. Contd. It has been estimated that between 15 and 19 million people worldwide are affected by RHD, with approximately one-quarter of a million deaths occurring each year. Some 95% of ARF cases and RHD deaths now occur in developing countries.
  • 8. In Nepal, A total of six cases out of 4736 had definite acute rheumatic fever (out of 13 suspected cases) giving overall prevalence rate of 1.2 per 1000. (Regmi PR, Pandey MR. Prevalence of rheumatic fever and rheumatic heart disease in school children of Kathmandu city. Indian Heart J. 1997 Sep-Oct;49(5):518-20. PMID: 9505020.)
  • 9. EPIDEMIOLOGY It is common in children aged 5-14 years. Rare in person aged >30 years Both sexes are equally affected by ARF But RHD most commonly affects females, sometimes up to twice as frequently as males.
  • 10. PATHOGENESIS There is no direct invasion to the tissues by the microorganism but its an autoimmune disease that involves antigen(Ag)-antibody(Ab) interaction. ↓ Group A Streptococcal(GAS) pharyngeal infection ↓ These antibodies cross react with human tissue because of the antigenic similarity between streptococcal components and human connective tissues (Molecular mimicry) ↓ Immunologically mediated inflammation and damage(Autoimmune)to human tissue which have antigenic similarity with streptococcal components like heart, joints, brains (connective tissue) and subcutaneous tissue ↓ Rheumatic fever
  • 11. CLINICAL FEATURES There is a latent period of 1-5 weeks between the precipitating group A streptococcal infection and appearance of clinical features. Heart involvement: • About 60% cases of ARF progress to RHD. • Valvular damage is the hallmark of rheumatic carditis. • The mitral valve is almost always affected. • Myocardial inflammation may affect electrical conduction pathways, leading to P-R interval prolongation and softening of the first heart sound.
  • 12. . Joint involvement: • Polyarthritis affecting large joints most commonly the knees, ankles, hips, and elbows. • Arthralgia Syndeham’s Chorea: • Abnormal involuntary, rapid ,jerky movements affect particularly the head and upper limbs. • They may be generalized or restricted to one side of the body(hemi chorea)
  • 13. , Skin manifestation • The classic rash of ARF is erythema marginatum, which begins as pink macules that clear centrally , leaving a serpiginous spreading edge. The rashes is evenest, appearing and disappearing before the examiner’s eyes. It occurs usually on the trunk ,sometimes on limbs ,but almost never on face • Subcutaneous nodules occur as painless, small, mobile lumps beneath skin overlying bony prominences, particularly of the hands, feet, elbows, occupits and occasionally vertebrae.
  • 14. DIAGNOSTIC EVALUATION Medical history and Physical examination Must have an infection with group A streptococcal bacteria Must have 2 major or 1 major and 2 major Jones criteria
  • 15. 1.Major criteria- • Carditis • Polyarthritis • Chorea • Erythema marginatum • Subcutaneous nodules
  • 16. 2. Minor criteria • Arthralgia • Hyperpyrexia • High ESR • High C-reactive protein • Prolonged P-R interval
  • 17. Electrocardiogram and Echocardiogram Blood test-Antibodies to strep-bacteria in the blood. [Anti streptolysin O (ASO)] Inflammatory markers=increased ESR and C-reactive protein Throat swab =culture
  • 18. Treatment Antibiotic therapy: For treatment and prevention. E.g. Penicillin 500mg (250mg for children)PO twice daily ,Amoxicillin 50mg/kg daily for 10 days. Anti-inflammatory agents: Salicylates and NSAIDS for pain reliever, swelling, fever, inflammation reducing aspirin, naproxen or corticosteroids like predrisome in severe cases. Anticonvulsants: Valproic acid, Carbamazepine
  • 19. PREVENTION Primary Prevention: Elimination of major risk factors for streptococcal infection, particularly overcrowded housing. Timely and complete treatment of group A streptococcal sore throat with antibiotics. Secondary prevention: They should receive long term penicillin prophylaxis to prevent recurrences. The best antibiotics for secondary prophylaxis is benzathine penicillin delivered every 4-2 week considering the risk, age, last episode.
  • 20. Tertiary prevention: Management of heart failure, management of lesions, and treatment for consequences of RHD including stroke, endocarditis and arrhythmia.
  • 21. .