Rheumatic fever

MBBS, FCPS, MD, FACC, FESC, FRCP, FSCAI,
FCCP,FAPSC, FAPSIC, FAHA,FACP,FASE
Professor and Head of Cardiology
Colonel Malek Medical College , Manikganj.
For post-graduates
drtoufiq19711@yahoo.com27/8/2019
Post graduate version 2019

Rheumatic fever( RF) - a delayed autoimmune reaction in genetically predisposed individuals to group A, β-hemolytic,
streptococcal (GABHS) pharyngitis characterized by inflammation of several tissues that gives rise to typical
clinical characteristics including
• 1)Carditis/ valvulitis
• 2)Arthritis
• 3)Chorea
• 4)Erythema marginatum
• 5)Subcutaneous nodules
• Residual damage only in the heart
• Latent period of 3 weeks(1 – 5 wks) b/w GABHS infection & ARF
• 3%-6% of any population
Rheumatic fever
25.08.2019 drtoufiq1971@gmail.com
Introduction

•Acute rheumatic fever is a systemic disease of childhood ,often
recurrent that follows group A beta hemolytic streptococcal
infection
•It is a diffuse inflammatory disease of connective tissue
primarily involving heart, blood vessels, joints, subcutaneous
tissue and CNS
Rheumatic fever
Definition
drtoufiq1971@gmail.com

Etiology
•Acute rheumatic fever is a systemic disease of childhood, often
recurrent that follows group A beta hemolytic streptococcal
infection
•It is a delayed non-suppurative sequelae to URTI with GABH
streptococci.
•It is a diffuse inflammatory disease of connective tissue,
primarily involving heart, blood vessels, joints, subcutaneous
tissue and CNS
Rheumatic fever

Epidemiology
•Ages 5-15 yrs are most susceptible
•Rare <3 yrs
•Girls>boys
•Common in 3rd world countries
•Environmental factors-- over crowding, poor sanitation,
poverty,
•Incidence more during fall ,winter & early spring
Rheumatic fever

Pathogenesis
•Delayed immune response to infection with group
A beta- hemolytic streptococci.
•After a latent period of 1-3 weeks, antibody
induced immunological damage occur to heart
valves, joints, subcutaneous tissue & basal ganglia
of brain
Rheumatic fever

Group A Beta Hemolytic Streptococcus(GABHS)
•Strains that produces rheumatic fever - M types l, 3, 5,
6,18 & 24
•Pharyngitis- produced by GABHS can lead to- acute
rheumatic fever , rheumatic heart disease & post
strept. Glomerulonepritis
•Skin infection- produced by GABHS leads to post
streptococcal glomerulo nephritis only. It will not result
in Rh.Fever or carditis
Rheumatic fever

Features suggestive of GABHS infection
• Patient 5 to 15 years of age
• Presentation in winter or early spring
• Fever, Headache
• Sudden onset of sore throat
• Nausea, vomiting & abdominal pain; Pain with swallowing
• Beefy, swollen, red uvula
• Soft palate petechiae (“doughnut lesions”)
• Tender, enlarged anterior cervical nodes
• Tonsillopharyngeal erythema & exudates
Rheumatic fever

Features suggestive of GABHS infection
Redness & swelling
of throat & tonsils;
Beefy, swollen, red
uvula; Soft palate
petechiae
(“doughnut
lesions”)
Tonsillopharyngeal
erythema &
exudatesSore throat: fever,
white draining
patches on the
throat & swollen or
tender lymph glands
in the neck

10
Diagrammatic structure of the group A
beta hemolytic streptococcus
Capsule
Cell wall
Protein antigens
Group carbohydrate
Peptidoglycan
Cyto.membrane
Cytoplasmcytoplasm
……………………………………………
……...
Antigen of outer protein cell
wall of GABHS induces
antibody response in victim
which result in autoimmune
damage to heart valves,
sub cutaneous tissue,tendons,
joints & basal ganglia of brain

Pathogenetic pathway for ARF & RHD
strong correlation between progression
to RHD & HLA-DR class II alleles &
the inflammatory protein-encoding genes
MBL2 and TNFA
Common antigenic determinants are
shared between components of GAS
(M protein, protoplast membrane,
cell wall group A carbohydrate,
capsular hyaluronate) & specific
mammalian tissues (e.g., heart, brain,
joint)
certain M proteins
(M1, M5, M6, and
M19) share
epitopes with
human
tropomyosin &
myosin

Pathophysiology
Rheumatic fever

Rheumatic fever

First episode
or Recurrence
without
established
heart
disease: 2
major
criteria or 1
major & 2
minor criteria
& the
absolute
requirement
Recurrence
with
established
heart
disease: 2
minor criteria
and the
absolute
requirement
ARF & RHD

Key morphologic
features of acute
rheumatic heart
disease.

Carditis
Rheumatic fever
• Incidence varies from 50%-60%
• The clinical diagnosis of carditis in an index attack of RF is based on
• 1) Presence of significant murmurs (MR/AR)
• 2)Pericardial rub
• 3) Unexplained cardiomegaly with CHF.
• Common in young
• 80% of patients develop it within first 2 weeks of RF

Endocarditis/ Valvulitis
• Almost always associated with a murmur of valvulitis
• An universal finding in rheumatic carditis, whereas the presence of pericarditis
or myocarditis is variable.
• Valve involvments-
• 92 – 95% mitral valve involvement ( 70 – 75 % isolated MV)
• 20 – 25% aortic valve involvement( 5-8% isolated AV)
• MR – PSM in apex radiating to axilla > with grade 2 (MC FINDING IN CARDITIS)
• AR in the absence of MR is uncommon
Rheumatic fever

Rheumatic fever
• First attack of RF- apical holosystolic murmur of mitral regurgitation (with or without apical
MDM, Carey Coombs), or basal EDM
• Pt. with previous RHD- a definite change in the character of any of these murmurs or the
appearance of a new significant murmur
• Severe MR
• Associated with worst prognosis - fatal HF
• Incidence of chronic RHD 90%.
• Linear relationship between the severity of MR during the first episode of RF and subsequent RHD.

Pathogenesis of severe MR
• Valvulitis
• Mitral annular dilatation
• Leaflet prolapse with or without chordal elongation
• Chordal rupture
• Carey Coombs murmur
• MDM without presystolic accentuation
• Associated with severe MR
• Due to increased flow through diseased mitral valve
Rheumatic fever

During an episode of
ARF, valve changes can
be minor and are still
able to regress
After recurrent
episodes of ARF,
thickening of subvalvar
apparatus, chordal
thickening and
shortening and
progression to
permanent valve damage
is evident

26
Rheumatic heart
disease. Abnormal
mitral valve. Thick,
fused chordae

27
Another view of
thick and fused
mitral valves in
Rheumatic
heart disease

myocarditis
• Myocarditis is always associated with valvulitis
• New onset CMGLY and recent change in cardiac size - most specific sign
• No definite evidence of myocarditis!!
- No consistent elevation of cardiac biomarkers
- No evidence of systolic dysfunction
- CHF does not occur without significant valvular lesions
- Radionuclide studies failed to demonstrate significant myocardial staining
- Biopsy in acute RF failed to show cellular necrosis -inflammation was subepicardial, subendocardial and
perivascular
- Surgical valve replacement during RF and AHF reverted features of HF
- Aschoff nodules do not contain myocardial cells
Rheumatic fever

Pericarditis
Rheumatic fever
• 6 -15 % OF RF
• Diagnosed by typical pain & friction rub
• Always associated with rheumatic valvulitis
• May be associated with normal ECG
• May be associated with effusion but rarely causes constriction and tamponade
• Its presence denote severe carditis

Poly arthritis
• 66-75% of patients
• MC & most earliest manifestation
• Typically involves larger joints – knee, ankle, wrist, & elbow
• Involved joints - hot, red, swollen, and tender
• Migratory in nature
• Not deforming
• A dramatic response to small doses of salicylates
Rheumatic fever

• Synovial fluid in ARF usually has 10,000-100,000 WBC/mm3
• Exudative with normal glucose & neutrophil predominance
• Self limiting & normalizes by 2 – 4 wks
• Polyarthritis & sydenham’s chorea never occurs simultaneously
• Inverse relationship b/w the severity of arthritis & cardiac
involvement
Rheumatic fever
Poly arthritis

Subcutaneous nodule
Rheumatic fever
• Rare
• 2-20%
• Freely mobile, painless
• 0.5 - 2 cm
• Occur in crops over bony prominences or
extensor tendons
• Common locations - elbow, wrist, knee,
ankle & achilles tendon

Erythema marginatum
Rheumatic fever
• 3-15%
• Erythematous, serpiginous, macular lesions
with pale centers that are not pruritic
• Multiple lesions primarily on the trunk or
proximal extremities,rarely on distal extremities
& never on face
• It occurs early in course of RF

Rheumatic fever
• Nonpainful , nonpruritic, blanches on pressure
• Accentuated by warming the skin.
• Not influenced by antiinflammatory therapy
• It is associated with carditis
• Nodules & marginatum can occur simultaneously
• It is also seen in sepsis, drug reactions , glomerulonephritis
Erythema marginatum

Chorea
Rheumatic fever
• Sydenham chorea , St.Vitus dance
• 5 - 36% of ARF
• Mc in females, rare > 20 yrs
• Isolated, frequently subtle, neurologic behavior disorder
• Emotional lability, incoordination, poor school performance, uncontrollable movements,
and facial grimacing
• Exacerbated by stress and disappears with sleep
• Seen occasionally unilateral

Rheumatic fever
• Long latent period
• Clinical maneuvers to elicit features of chorea include
• (1) demonstration of milkmaid’s grip (irregular contractions of the muscles of the hands
while squeezing the examiner’s fingers)
• (2) spooning & pronation of the hands when the patient’s arms are extended
• (3) wormian darting movements of the tongue upon protrusion
• (4) examination of handwriting to evaluate fine motor movements
• Do not cause permanent neurologic sequelae
Chorea

Sydenham’s Chorea
Rheumatic fever

Rheumatic fever
• Rheumatic chorea –marker of future carditis
•23% pure rheumatic chorea developed MS in 20 yr follow up
& 27% in 30 yr period
• Chorea is rarely associated with polyarthritis
• Inflammatory markers & ASO titres may be normal
Chorea

Minor manifestations
Rheumatic fever
• Arthralgia
• constitutes pain in one or more joints without evidence of inflammation, tenderness to touch, or limitation of motion.
• Arthralgia + monoarticular arthritis – suggestive of RF
• Fever
• Temperature >100.40 F rectally-diurnal variations are seen
• Children with mild carditis and pateints with chorea are afebrile
• Epistaxis seen in 4% of cases
• Abdominal pain
• 5% 0f cases - occurs before the appearance of major manifestation
• Pain usually epigastric or periumbilical & may mimic appendicitis

Rheumatic fever
• Those patients who develop extracardiac manifestation in the initial
attack , there is a less chance for carditis during recurrence whereas if
the initial attack is carditis there is a high chance of recurrent carditis
MIMETIC FEATURE OF RHEUMATIC FEVER

Rheumatic fever
POST STREPTOCOCCAL REACTIVE ARTHRITIS
• Relatively shorter latent period
( 7 to 10) days
• May be persistent or relapsing
• Slower response to aspirin
• Not associated with other
major manifestations
• Symmetric invlnt. of large , small
joints & axial skeleton
• Occ . causation by non GABHS
• Secondary prophylaxis for up to 1
year after the onset of their
symptoms (Class IIb,LOE C)

Rheumatic Pneumonia
Rheumatic fever
• An acute inflammatory pneumonitis has been described in patients with RF
• Presents as sudden onset respiaratory distress
• Associated with carditis
• CXR shows a hilar or patchy distribution
• Difficult to differentiate clinically with CHF
• Responds to steroids
• Uncertainity of its frequency and its existence as a distinct entity

Rheumatic fever
JACCOUD’S ARTHRITIS

JACCOUD’S ARTHRITIS
• Chronic postrheumatic fever arthritis
• Seen in patients with severe RHD & not associated with evidence of RF
• Recovery delayed & assoc. with stiffness of metacarpophalyngeal joints
• Characteristic deformity due to periarticular , fascial and tendon fibrosis
• Joint disease is inactive with normal ESR & negative RA factor
• Deformity characterized by flexion at the metcarpophalangeal joint with ulnar
deviation of 4th and 5th fingers & hyperextn of PIP
• Initially the deformity is correctable & not assoc with bone destruction
Rheumatic fever

PANDAS
•Pediatric autoimmune neuropsychiatric disorders
associated with streptococcal infections
•Autoimmune responses that cross-react with brain
tissue in response to a GAS infection
• Obsessive-compulsive & tic disorders
•No need of secondary prophylaxis (Class III, LOE
B).
Rheumatic fever

EVOLUTION OF JONES CRITERIA (ORGINAL JONES CRITERIA 1944)
Rheumatic fever
MAJOR MANIFESTATIONS MINOR
MANIFESTATION
1. CARDITIS
2. ARTHRALGIA
3. CHOREA
4. SUBCUTANEOUS NODULES
5.H/O OF PREVIOUS DEFINITIVE RF OR RHD
1.FEVER
2.ABDOMINAL PAIN
3.PRECORDIAL PAIN
4.RASHES( ERYTHEMA MARGINATUM)
5.EPISTAXIS
6.PULMONARY FINDINGS
7.LAB FINDINGS
A.ECG
B.MICROCYTIC ANAEMIA
C.ELEVATED TLC
D.RAISED ESR

MODIFIED JONES CRITERIA 1956
Rheumatic fever
MAJOR MANIFESTATION
1.CARDITIS
2.POLYARTHRITIS
3. CHOREA
4.SUBCUTANEOUS NODULES
5.ERYTHEMA MARGINATUM
1.FEVER
2.ARTHRALGIA
3.PROLONGED PR INTERVAL
4.INCREASED ESR,CRP OR
LEUKOCYTOSIS
5.PREVIOUS H/O OF RF OR RHD
6.EVIDENCE OF PRECEEDING BETA
HEMOLYTIC STREPTOCOCCAL

• REVISED CRITERIA OF 1965 WAS REVIEWED AND PUBLISHED AGAIN IN 1984
• INFERENCES MADE
• 1) Premature administration of antiinflammatory drugs may modify the clinical
picture
• 2) Usefulness of echo in distinguishing pt with MVP & BICUSPID VALVE from RHD
• 3) PR prolongation- not an indication of carditis nor does it corelate with
development of RHD
JONES CRITERIA WAS NOT DIAGNOSTIC-INDOLENTCARDITIS,RECURRENT RF,CHOREA
Rheumatic fever

JONES CRITERIA UPDATE 1992
Rheumatic fever
MAJOR MANIFESTATION MINOR MANIFESTATION
1.CARDITIS
2.POLYARTHRITIS
3. CHOREA
4.SUBCUTANEOUS NODULES
5.ERYTHEMA MARGINATUM
1.FEVER
2.ARTHRALGIA
3.PROLONGED PR INTERVAL
4.LAB FINDINGS
ELEVATED ACUTE PHASE
REACTANTS,INCREASED ESR,CRP
+
SUPPORTING EVIDENCE OF PRECEEDING STREPTOCOCCAL INFECTION,POSITIVE THROAT C/S FOR GROUP A STREPTOCOCCUS
OR RAPID ANTIGEN TEST,ELEVATED OR RISING STREPTOCOCCAL ANTIBODY TITRE

EVOLUTION OF JONES CRITERIA
Rheumatic fever

WHO 2002 – 2003
Rheumatic fever

LAB DIAGNOSIS OF ARF
• No gold standard diagnostic technique
• 1)THROAT C/S
• initially considered a gold standard for diagnosis of streptococcal infection
• LIMITATIONS
• 1) Difficult to differentiate a carrier from active infection
• 2) 1/3 of RF has no H/O preceeding pharyngeal infn.
• 3) Delay in getting culture report
Rheumatic fever

LAB DIAGNOSIS OF ARF
2)RAPID ANTIGEN TEST FROM THROAT SWAB
•Specificity is 95% & sensitivity 60 to 90%
3)STREPTOCOCCAL ANTIBODY TEST
•Antistreptolysin O (ASO)
•Anti DNAase B
•Anti hyaluronidase (AH)
•Streptozyme(SZ)
Rheumatic fever

ASO TEST
• Significant antibody response defined as a
rise in titre > 2 dilution increments b/w acute
phase and convalescent phase
• Serum samples obtained 2 to 4 week
intervals
• ASO Titre of > 240 todd units in adults & >
320 todd units in children> 5 yrs is elevated
• Appears 7 to 10 days after the infection with
peak detection at 2 & 3 weeks after the onset
of RF
Rheumatic fever

ASO TEST
• All cases of suspected ARF should have elevated serum streptococcal serology
demonstrated.
• If the initial titre is above ULN, there is no need to repeat serology.
• If the initial titre is below the ULN for age, testing should be repeated 10–14 days
later.
Rheumatic fever

ANTI DNASe B
• Anti DNAse B titers begin to rise 1 to 2
weeks and peak 6 to 8 weeks after
infection
• Antidnase 1:60 in preschool, 1:480 in
school age, 1:340 in adult( NORMAL TITRE)
• Single antibody test-( only ASO) -80-85%
• Multiple antibody test-(ASO +ANTIDNase
B)-95-100%
Rheumatic fever

LAB INVESTIGATION
•1) B CELL MARKER
• D8/17 monoclonal antibody - 90 to 100% of all patients
with RF
•Mode of inheritence - Autosomal recessive
•2) CRP, ESR
Rheumatic fever

ECG CHANGES IN ARF
• 1) Persistent sinus tachycardia & an elevated sleeping pulse rate are signs of carditis
• 2)Sinus bradycardia
3) PR prolongation
• Seen in 20- 30% of cases
• Proposed theory – due to vagal overactivity,myocardial inflmmation
• No correlation with carditis and future development of RHD
• 4) High grade AV block ,CHB
• 5) pericarditis
• 6) QT prolongation
Rheumatic fever

ECHOCARDIOGRAPHY
•CHARACTERISTIC CHANGES IN
RHEUMATIC MITRAL VALVULITIS
•CHORDAL ELONGATION
•ANNULAR DILATION
•AML PROLAPSE
•POSTEROLATERAL JET OF MR
Rheumatic fever

SUBCLINICALCARDITIS/ ECHOCARDITIS
• Patients with suspected acute
rheumatic carditis have no
clinical murmurs but have
documented regurgitation on
echocardiography
• Prevalence 0 to 53%
Rheumatic fever

ECHOCARDIOGRAPHY
• ADVANTAGES
• 1)Superior sensitivity in detecting rheumatic carditis
• 2) Avoids misdiagnosis
• DISADVANTAGES
-Overdiagnosis of physiological valvular regurgitation as an organic dysfn.
-Echocardiographic facilities not widely available
-Ability to detect the recurrence of subclinical carditis not clear
Rheumatic fever

WHO ECHO CRITERIA FOR CLINICAL CARDITIS
• 0: Nil, including physiological or trivial regurgitant jet <1.0 cm, narrow, small, of short
duration, early systolic at mitral valve or early diastolic at aortic valve.
• 0+: Very mild regurgitant jet, more than 1.0cm, wider, localized immediately above or below
the valve, throughout systole at the mitral valve or diastole at the aortic valve (clinically, no
murmur audible).
• 1+: Mild regurgitant jet.
• 2+: Moderate regurgitant jet, longer and at a wider area.
• 3+: Moderately severe regurgitant jet, reaching the entire left atrium (MR) or left ventricle
(AR).
• 4+: Severe regurgitant jet, diffusely into the enlarged LA, with systolic backward ﬂow into
pulmonary veins (mitral valve); markedly enlarged LV ﬁlled with regurgitant jets (aortic
valve).
Rheumatic fever

WHO CRITERIA FOR SUBCLINICAL CARDITIS
Rheumatic fever

OUTCOME OF SUBCLINICAL CARDITIS
Rheumatic fever

WORLD HEART FEDERATION CRITERIA 2012 FOR RHD
Rheumatic fever

WHF CRITERIA
Rheumatic fever

MORPHOLOGIC FEATURES OF RHD
Rheumatic fever

Echocardiography in Acute Rheumatic fever
Rheumatic fever

EXCESSIVE LEAFLET TIP MOTION
Rheumatic fever

RESTRICTED MV LEAFLET MOTION
NORMAL RHD
World Heart Federation criteria for echocardiographic diagnosis of rheumatic heart disease—an evidence-based guideline
NATURE REVIEWS | CARDIOLOGY VOLUME 9 | MAY 201

ECHO AS A SCREENING TEST
• N=2170, Simplified echo criteria vs reference echo criteria
• When compared with the reference criteria, the simplified approach yields a
maximum sensitivity of 73% for case detection, with a positive predictive value of 92%.
Screening for rheumatic heart disease: evaluationof a simplified echocardiography-based approach
Mariana Mirabel; European Heart Journal – Cardiovascular Imaging:FEB2012
25.08.2019

ENDOMYOCARDIAL BIOPSY
• Aschoff nodules or histiocytic aggregates considered diagnostic of rheumatic
myocarditis
• Sensitivity 43% ,specificity of 100%
• Myocyte degeneration usually without lymphocytic infiltration and frequently
without Aschoff nodules.
• Does not provide additional diagnostic information
• Not recommended
Rheumatic fever

Treatment
• Step I - primary prevention (eradication of streptococci)
• Step II - anti inflammatory treatment (aspirin,steroids)
• Step III- supportive management & management of complications
• Step IV- secondary prevention (prevention of recurrent attacks)
Rheumatic fever

STEP I: Primary Prevention of Rheumatic Fever (Treatment of Streptococcal Tonsillopharyngitis)
Agent Dose Mode Duration
Benzathine penicillin G 600 000 U for patients Intramuscular Once
27 kg (60 lb)
1 200 000 U for patients >27 kg
or
Penicillin V Children: 250 mg 2-3 times daily Oral 10 d
(phenoxymethyl penicillin) Adolescents and adults: 500 mg 2-3 times daily
For individuals allergic to penicillin
Erythromycin: 20-40 mg/kg/d 2-4 times daily Oral 10 d
Estolate (maximum 1 g/d)
or
Ethylsuccinate 40 mg/kg/d 2-4 times daily Oral 10 d
(maximum 1 g/d)
TREATMENT OF RF

Step II: Anti inflammatory treatment
Arthritis only Aspirin 75-100
mg/kg/day,give as 4
divided doses for 6
weeks
(Attain a blood level 20-
30 mg/dl)
Carditis Prednisolone 2-2.5
mg/kg/day, give as two
divided doses for 2
weeks
Taper over 2 weeks &
while tapering add
Aspirin 75 mg/kg/day
for 2 weeks.
Continue aspirin alone
100 mg/kg/day for
another 4 weeks

TREATMENT OF RF
Rheumatic fever

TREATMENT OF RF
Rheumatic fever
1)TREATMENT OF GABHS 1) ORAL PENCILLIN V 500MG B.D -10DAYS
2) INJ BENZATHINE PENCILLIN 12LAKH UNITS
3)ERYTHROMYCIN 250MG Q.I.D - 10 DAYS
2)TREATMENT OF ARTHRITIS 1)ASPIRIN ONCE DIAGNOSIS IS CONFIRMED WITH
100MG/KG FOR 2 WEEKS AND THEN GRADUALLY
TAPERED TO 60 -80 MG/KG FOR ANOTHER 4 WKS
2) NAPROXEN ALTERNATIVE
3) TREATMENT OF CARDITIS 1)NO CHF- ONLY ASPIRIN
2) CHF- STEROIDS AT A DOSE 2MG/KG FOR 4 WEEKS
TO BE OVERLAPPED WITH ASPIRIN WHEN IT IS TAPERED
3) ANTIFAILURE eg. Diuretics ,Ace, beta blockers,digoxin

TREATMENT OF RF
Rheumatic fever
TREATMENT OF SKIN LESIONS NO SPECIFIC TREATMENT
TREATMENT OF CHOREA 1) REASSURANCE & SEDATION
2) NSAID & STEROID HAVE NO ROLE
3) HALOPERIDOL
4) CARBAMZEPINE & VALPROATE –REFRACTORY CASES
5) IVIG & PLASMAPHERESIS-NO BENEFIT
SURGERY 1) PT WITH REFRACTORY CARDITIS
2) IDEAL AFTER THE ACUTE INFLAMMATION SETTLES
3) VALVE REPLACEMENT BETTER THAN VALVE REPAIR
4) IF MORPHOLOGIC EVIDENCE OF INFLAMMATION
REPAIR MAY CAUSE INCREASED REOPERATION

PRIMORDIAL PREVENTION
•(i) Improvement in socio-economic status
• (ii) Prevention of overcrowding
• (iii) Improving nutritional status
• (iv) Availability of prompt medical care
•(v) Public education regarding
Rheumatic fever

PRIMARY PREVENTION
Rheumatic fever

TREATMENT
• Post treatment throat cultures 2 to 7 days after completion of therapy
are indicated:
• If patient remain symptomatic
• Whose symptoms recur
• Patients who have had RF and are therefore at unusually high risk for
recurrence
• TREATMENT FAILURE
• A second course of therapy in asymptomatic individuals should be considered
only for those with previous RF themselves or in members of their families.
• Treatment required if symptomatic
• May require other drugs – clindamycin, rifampicin,amoxclav
Rheumatic fever

TREATMENT OF CARRIERS
•Chronic streptococcal carriers (defined as individuals with
positive throat cultures for GAS without clinical findings or
immunologic response to GAS antigens) usually do not need
to be identified or treated with antibiotics
Rheumatic fever

SECONDARY PROPHYLAXIS
Rheumatic fever

WHO 2002 CRITERIA FOR SECONDARY PROPHYLAXIS
Rheumatic fever
PATIENT WITHOUT PROVEN CARDITIS FOR 5 YEARS AFTER THE LAST
ATTACK, OR UNTIL 18 YEARS OF
AGE WHICHEVER IS LONG
PATIENT WITH CARDITIS
(MILD MITRAL REGURGITATION,
HEALED CARDITIS)
FOR 10 YEARS AFTER THE LAST ATTACK,
OR AT LEAST UNTIL 25 YEARS OF AGE
WHICHEVER IS LONGER
MORE SEVERE VALVULAR DISEASE LIFELONG
AFTER VALVE SURGERY. LIFELONG

National Heart Foundation of Australiaand the Cardiac Society of Australia and New
ZealandDiagnosis and managementof acute rheumatic feverand rheumatic heart diseasein
AustraliaAn evidence-based review;june 2006

COMPARISION OF GUIDELINES
Rheumatic fever

Recurrence
• Oral agents are more appropriate for patients at lower risk for rheumatic fever
recurrence
• Accordingly, some physicians may consider switching patients to oral prophylaxis
when they have reached late adolescence or young adulthood and have
remained free of rheumatic attacks for at least 5 years (Class IIb, LOE C).
Rheumatic fever

RECURRENCE RISK OF ANTIBIOTICS
Rheumatic fever

META-ANALYSIS OF SECONDARY PREVENTION
Rheumatic fever

ANTISTREPTOCOCCAL VACCINE
• Components of GAS used in vaccine development
• 1)M- protein
• 2)GAS C5a peptidase, a major surface virulence factor
• 3) Fibronectin binding protein sfb1
• 4) Chimeric peptide J8 from the conserved region of the M- protein
• M protein vaccines-less likely to succeed
• 1) Heterogeneous distribution of strains- varies from place to place and keeps changing even within a closed
community in a short period.
• 2) On the basis of emm typing of M-protein more than 250 strains of GAS can cause infection and provide only
strain-specific immunity.
• 3) GAS has a strong tendency for mutation
Rheumatic fever

Prognosis
• Rheumatic fever can recur whenever the individual experience new
GABH streptococcal infection, if not on prophylactic medicines
• Good prognosis for older age group & if no carditis during the initial
attack
• Bad prognosis for younger children & those with carditis with valvular
lesions
Rheumatic fever

SUMMARY
• Rheumatic fever is more of a clinical diagnosis but nowadays echo & doppler also has a role
• No gold standard diagnostic test
• No entity as rheumatic myocarditis
• Duration of prophylaxis depends on the high risk factors
• Injectable pencillin is better than oral pencillin
• School & community based programme required for primary prophylaxis
Rheumatic fever

Rheumatic fever

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