Binotto MA, Guilherme L, Tanaka AC.
Rheumatic Fever.
Images Paediatr Cardiol 2002;11:12-25
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| Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Brazil |
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MeSH
rheumatic fever, streptococcus, rheumatic heart disease, arthritis, autoimmunity
Abstract
Rheumatic fever is an immunologically mediated inflammatory disease,
that occurs as a delayed sequel to group A streptococcal throat infection,
in genetically susceptible individuals. Chronic rheumatic heart disease
remains an important public health problem in developing countries. Aetiopathogenesis
and guidelines for the diagnosis, prevention and treatment of acute rheumatic
fever are reviewed.
Article
Introduction
Rheumatic fever (RF) is a multisystem, immunologically mediated inflammatory
disease, that occurs as a delayed sequel to group A streptococcal (GAS)
infection. Its subsequent complication, chronic rheumatic heart disease
(RHD), remains a major public health problem in developing countries.
Epidemiology
The epidemiology of RF in developed countries has changed dramatically
over the past decades. In developing areas, the prevalence is still high
at up to 24 per 1000 population.1 Rheumatic fever occurs most
frequently among children and adolescents between 5 and 18 years,2
coinciding with the age distribution of the highest prevalence of streptococcal
infections.
Aetiopathogenesis
The pathogenic mechanisms involved in the development of RF remain
unclear. However, it is evident that an abnormal humoral and cellular immune
response occurs. Antigenic mimicry between streptococcal antigens, mainly
M-protein epitopes and human tissues, such as heart valves, myosin and
tropomyosin, brain proteins, synovial tissue and cartilage has been proposed
as the triggering factor leading to autoimmunity in individuals with genetic
predisposition. 3 Several genetic markers of susceptibility
have been studied but no consistent association found.4 However,
associations with different HLA class II antigens have been observed in
several populations.5-13 Molecular mimicry was first demonstrated
by humoral immune response. Streptococcal antibodies cross-react with several
human tissues including heart, skin, brain, glomerular basement membrane,
striated and smooth muscles.14 The presence of CD4+ T cells
at lesions sites in the heart has been demonstrated, suggesting a direct
role of these cells in the pathogenesis of RHD.15,16 Infiltrating
T lymphocytes from heart lesions of severe RHD patients and peripheral
T lynphocytes were capable of recognising immunodominant myocardium M5
peptides and valve proteins. These results showed the significance of molecular
mimicry between beta hemolytic streptococci and heart tissue assessing
the T-cell repertoire leading to local tissue damage in RHD.17,18
Figure 1 illustrates the events that occur during the development of RF/RHD.
Figure 1: Schematic representation of the aetiopathogenic events
occurring during the development of carditis
Major Clinical Manifestations
Arthritis
Arthritis is the most common manifestation, present in 60-80% of patients.
19,20 Itu sually affects the peripheral large joints; small joints
and axial skeleton are rarely involved. Knees, ankles, elbows and wrists
are the most frequently affected. In addition to arthralgia, the joints
are red, warm and swollen. Arthritis is characteristically asymmetrical,
migratory, and very painful, although some patients may present mild joint
complaints. It usually resolves spontaneously at the most in 2 or 3 weeks.
Arthritis in ARF has an excellent response to salicylates.21
Approximately one third of patients with joint involvement reported
in a series of 786 cases of RF presented with "atypical" articular manifestations,
considered by some as a separate entity, i.e., post-streptococcal reactive
arthritis. It seems reasonable to include these manifestations as part
of the spectrum of RF.19,21 Secondary prophylaxis should be
recommended in these situations.
Carditis
Acute carditis was present in 50% of patients in a large recent series.
19 It is a pancarditis, but valvular involvement is the rule. The
commonest involved valve is the mitral, frequently associated with aortic
valve involvement. Right-sided heart valves are rarely affected.
On pathological examination, the valves are thickened and display rows
of small vegetations along their apposing surfaces (Figure 2). Myocarditis
is characterised by infiltration of mononuclear cells, vasculitis and degenerative
changes of the interstitial connective tissue.22 The pathognomonic
lesion is the Aschoff body in the proliferative stage, present in 30 to
40 per cent of biopsies of patients with acute RF.23 It is seen
mainly in the interstitial connective tissue of the myocardium, particularly
perivascularly (Figure 3).22 Inflammation of the valves consists
of oedema and mononuclear cell infiltration of the valvular tissue and
the chordae tendineae in the acute phase; fibrosis and calcification occur
with maintenance of the inflammatory process.22
Figure 2: Aortic valve showing active valvulitis. The valve
is slightly thickened and displays small vegetations – "verrucae"
Figure 3: Myocardial Aschoff body – the cells are large,
elongated, with large nuclei; some are multinucleate
The clinical picture includes high pulse rate, congestive heart failure,
arrhytmias and pericardial friction rubs. On the first attack, valvulitis
is suspected in the presence of a new apical systolic murmur of mitral
regurgitation (associated or not with an apical mid-diastolic murmur) and/or
a basal diastolic murmur of aortic regurgitation.24 Cardiomegaly
is noted on X-Ray (Figure 4) and on echocardiogram. Myocarditis and/or
pericarditis in the absence of valvular involvement is unlikely due to
acute RF.24 It is contentious if myocardial disfunction in acute
RF is valvular or myocardial in origin.25 In fact, in a subset
of patients, the initial presentation may be quite severe, with overt heart
failure, fever and toxaemia, making the differential diagnosis with infective
endocarditis very difficult, in particular in patients with recurrent rheumatic
heart disease.
Figure 4 : Chest radiograph of an 8 year old patient with acute
carditis before treatment
Figure 4b: Same patient after 4 weeks
The valvular lesions in RF often result in residual damage. Nevertheless,
in milder forms of rheumatic carditis patients may recover from valvulitis
without sequelae.1 In the first attack, the lesions are predominantly
regurgitant, due to ring dilatation, swollen cusps, chordal rupture or
papillary muscle dysfunction. In the chronic phase, obstructive lesions
are more frequent. Figures 5-7 depict aspects of the chronic valvar involvement
on echocardiography. Figures 8-10 show examples of the pathological presentation
of chronic rheumatic valve disease.
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Figure 5a: Two-dimensional color flow Doppler image of the left
ventricular inflow of a patient with mitral regurgitation in the four-chamber
view (top panel) and two-dimensional parasternal long-axis view (lower
panel), showing lack of apposition of the leaflets of the mitral valve
during systole (arrow)
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Figure 5b: Color flow Doppler study of a patient with aortic
regurgitation, as viewed from the parasternal long-axis view (top panel)
and two-dimensional four-chamber view, showing hypertrophy and dilatation
of the left ventricle (lower panel). LV = left ventricle; LA = left atrium;
RV = right ventricle; RA = right atrium; AO = aorta
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Figure 6a: Two-dimensional color flow Doppler study of the left
ventricular inflow of a patient with mitral stenosis
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Figure 6b: Pressure gradient half-time and mitral area is calculated
from the diastolic mitral orifice Doppler velocities signals (lower panel).
LV = left ventricle; LA = left atrium; RV = right ventricle; RA = right
atrium
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Figure 7: Two-dimensional parasternal long-axis view of a patient
with mitral stenosis, showing thickened valve cusps (arrow), with poor
leaflet separation in diastole. Left atrium is enlarged, with a thrombus
in the posterior aspect of it. Aortic valve is also stenotic
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Figure 8: Stenotic mitral valve seen from left atrium. Both
commissures are fused; the cusps are severely thickened. The left atrium
is huge. The valve is both incompetent and stenotic
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Figure 9: Opened stenotic mitral valve showing thickening distorted
cusps, adherent commissures with calcification and thrombus deposition,
and thickening, fusion and shortening of chordae tendinae
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Figure 10: Stenotic mitral valve seen from left atrium, showing
fusion of commissures, thickening and calcification of the cusps
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Sydenham’s chorea
Sydenham’s chorea is characterized by involuntary movements, specially
of the face and limbs, muscle weakness, disturbances of speech and gait.
Children usually exhibit concomitant psycologic dysfunction, especially
obsessive-compulsive disorder, increased emotional lability, hyperactivity,
irritablility and age-regressed behavior.26-28 It is usually
a delayed manifestation, and is often the sole manifestation of ARF. However,
chorea may occur in association with other major manifestations of RF,
particularly in the first attack.29 Evidence of a recent GAS
infection is often difficult to document. Most of the patients experience
resolution of the symptomatology after a few months.3,24 However,
a recurrence rate up to 32% has been described, despite the regular use
of secondary benzathine penicillin prophylaxis. Some believe that these
episodes represent exacerbations rather than distinct attacks of acute
RF.29,30
Subcutaneous nodules
Subcutaneous nodules are rarely seen and when present,
they are usually associated with severe carditis. They are painless, firm,
movable, measuring around 0.5 to 2 cm. They are usually located over extensor
surfaces of the joints, particularly knees, wrists and elbows (Figure 11).24
Figure 11: Subcutaneous nodule on the extensor surface of elbow
of a patient with acute RF
Erythema marginatum
This is an evanescent, erythematous, non-pruritic rash with pale centers
and rounded or serpiginous margins. Lesions occur mainly on the trunk and
proximal extremities and may be induced by application of heat (Figure
12).24 31
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Figure 12a: Erythema marginatum on the trunk, showing
erythematous lesions with pale centers and rounded or serpiginous margins
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Figure 12b: Closer view of erythema marginatum in the same patient
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Diagnosis
With the exception of Sydenham’s chorea, which has a latency period
of several months, the clinical manifestations of acute RF present after
about 3 weeks following the streptococcal throat infection. It usually
begins with nonspecific symptoms, such as fever, malaise and persistent
pallor.3
There is no specific clinical or laboratory test that establishes the
diagnosis of RF. Diagnosis is based on the revised Jones Criteria24
(Table 1). Arthritis, carditis, chorea, and less frequently, subcutaneous
nodules and erythema marginatum are major manifestations of RF. If supported
by evidence of preceding streptococcal infection, the presence of two major
manifestations or one major and two minor manifestations indicates a high
probability of acute RF. The two exceptions to this requirement are Sydenham’s
chorea and indolent carditis. Other manifestations include arthralgia,
serositis and involvement of the kidneys and lungs.3
Table 1: Guidelines for the diagnosis of initial attack of rheumatic
fever (Jones Criteria, 1992 Update).24
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| Major manifestations |
Minor manifestations |
| Carditis |
Fever |
| Polyarthritis |
Arthralgia |
| Sydenham’s chorea |
Elevated acute phase reactants |
| Erythema marginatum |
Prolonged PR interval |
| Subcutaneous nodules |
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* plus supporting evidence of preceding GAS infection
Differential diagnosis
The differential diagnosis is extensive because of the lack of specificity
of many of the clinical and laboratory findings in RF and also the unavailability
of a laboratory test to confirm the diagnosis. Several diseases need to
be considered. Table 2 includes those more often presenting clinical difficulties
to the clinician. Juvenile rheumatoid arthritis (JRA) and other connective
tissue diseases often should be considered. The articular involvement in
JRA usually lasts longer than in RF. It is generally polyarticular and
symmetrical, typically affecting the small joints of the hands. Patients
complain of increased pain in the morning or after long periods of immobility.
Arthritis of the cervical spine occurs in about half of the cases but is
also quite frequent in acute RF.3
Table 2: Differential diagnosis of rheumatic fever
Juvenile rheumatoid arthritis
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Systemic lupus erythematosus
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Infective endocarditis
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Reactive arthritis
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Sickle cell disease
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Drug reactions
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Other connective tissue diseases
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Septicaemia
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Leukaemia
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Gonoccocal arthritis
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Tuberculosis
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Lyme disease
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Serum sickness
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Cardiac involvement presents primarily as pericarditis therefore infective
endocarditis should be considered in patients with recurrent RF presenting
with persistent fever of unknown origin. Sometimes the differential diagnosis
can be difficult, especially in those presenting with a more severe clinical
presentation. Splenomegaly, vascular and immmunologic phenomena, demonstration
of vegetations on echocardiogram and positive blood cultures are indicative
of infective endocarditis. Gallium-67 cardiac scintigraphy can be helpful
in this setting.
Systemic lupus erythematosus (SLE) shares clinical characteristics with
acute RF. Arthralgia and transient arthritis are common. SLE affects multiple
organs, including kidney, central nervous system, skin, and blood. Diagnosis
is made on clinical grounds and confirmed by serologic studies.32
Laboratory studies
Acute phase reactants are useful in helping to recognize acute RF and
also to exclude other diseases. C-reactive protein and erythrocyte sedimentation
rates are helpful in monitoring inflammatory activity.24
Laboratory evidence of a preceding GAS infection should be sought, either
by demonstration of GAS in the throat by culture or rapid streptoccocal
antigen test, or using streptococcal antibody tests. Elevated or rising
titers of antistreptolysin O (ASO) occur in more than 80% of patients with
acute GAS pharyngitis.24 There is a remarkable response during
the acute phase of RF. The test specificity has been shown to be 93% with
ASO titers above 960 IU/ml.33
Prolonged P-R interval relative to heart rate is a nonspecific finding,
present in more than one third of the patients. Low-voltage QRS complexes
and ST segment changes may be found in the presence of pericarditis and
pericardial effusion.3
Endomyocardial biopsy is invasive and does not appear to provide additional
diagnostic information where there is a clinical consensus about the diagnosis
of RF, with a diagnostic sensitivity in one relatively large study of 27%.
It should be limited to clinical investigation.23,34
Cardiac scanning scintigraphy has been shown to be a reliable method
distinguishing acute from chronic, inactive RHD and also in the follow-up
of active carditis (Figure 13). 35-37
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Figure 13: Gallium-67 scintigraphy of the myocardium, showing
on left, a positive study, with hypercaptation on the heart projection
and, on the right, a negative study
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The role of echocadiography to diagnose valvulitis without auscultatory
findings has been debated.34,38-41 At present, subauscultatory
valve regurgitation is not considered a diagnostic criterion for RF.24
Treatment
Prevention
Prevention of initial attacks of RF (primary prevention) requires the
eradication of GAS from the pharynx. Table 3 shows the currently recommended
treatment schedules.42 Emphasis should be given to the need
of eradication of GAS as part of the treatment of acute RF.
Table 3: Primary prevention of rheumatic fever.42
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| Agent |
Therapeutic scheme |
| Benzathine
penicillin G |
600,000 U for patients
< 27Kg; 1,200,000 U
for patients > 27kg, IM (once)
or |
| Penicillin V |
Children: 250mg 2-3 times daily, PO (10 d)
Adolescents: 500mg 2-3 times daily, PO (10 d) |
| For individuals allergic to penicillin: |
| Erythromycin:
Estolate
Ethylsuccinate |
20-40mg/kg/d 2-4 times daily, PO (10 d)
or
40mg/kg/d 2-4 times daily, PO (10 d)
(maximum 1g/d) |
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The following are unsuitable: sulfonamides, trimetroprim, tetracyclines
and chloranphenicol.
Antibiotic prophylaxis is the safest way to prevent recurrent attacks
of acute RF and is recommended for patients with well-documented RF. The
recommendations from the Committee on Rheumatic Fever, Endocarditis, and
Kawasaki Disease of the Council on Cardiovascular Disease in the Young
of the American Heart Association are shown on Table 4.42
Table 4: Secondary prevention of rheumatic fever.42
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| Agent |
Therapeutic Scheme |
| Benzathine
penicillin G |
1,200,000 U every 4 weeks*, IM
or |
| Penicillin V |
250mg twice daily, PO
or |
| Sulfadiazine |
500mg once daily for patients < 27kg; 1g
once daily for patients > 27kg, PO |
| For individuals allergic to penicillin
and sulfadiazine: |
| Erythromycin |
250mg twice daily, PO |
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*In high-risk situations, administration every 3 weeks is recommended.
Arthritis
Salicylates remain the first-line drugs in the treatment of arthritis.
The response is usually excellent. Treatment should be started at 80 to
100 mg/kg/day (maximum, 4g daily) for 3-4 weeks. Naproxen (10-15mg/kg/day,
bid) is an alternative drug, with very good response. Other nonsteroidal
antiinflammatory drugs also can be used.
Carditis
Moderate to severe carditis is usually an indication for cortiscoteroids
although efficacy in reducing sequelae has not been proven so far. Albert
at al. performed a meta-analysis of the literature on the treatment of
rheumatic carditis, comparing corticosteroids and salicylates in preventing
valvular damage. It seems clear that corticosteroids are superior to salicylates
in rapidly resolving acute manifestations, but the advantage of the former
in preventing a pathologic murmur at 1 year posttreatment was not statistically
significant. 43 Prednisone, 2mg/kg/day (maximum, 60mg/day) is
used for two weeks and after that, the dose is gradually tapered, reducing
20 to 25% of the previous dose every week. Some advocate the concomitant
use of salicylates to avoid rebound. In severe carditis, therapy may be
initiated with intravenous methylprednisolone.44,45 Intravenous
immunoglobulin seems not to alter the extent and severity of carditis or
decrease chronic morbitidy. 46
Heart failure usually responds to steroids. Bed rest is always recommended
and should be planned on an individual basis. Diuretics and vasodilators
may be used in patients with more severe haemodynamic decompensation. Digoxin
should be used with caution because of the risk of toxicity in the presence
of active myocarditis.47 Surgical treatment in the acute stage
should be considered when clinical therapy is ineffective to control cardic
failure. Valve repair, although technically more difficult, is the first
choice for younger patients.48
Chorea
Treatment with haloperidol (initial dose of 0.5 to 1mg/kg/day, maximum,
5mg/day) 49 or valproic acid (15-20 mg/kg/day)50
51are helpful in decreasing the severity of involuntary movements
but may not improve the behavioral symptoms. Carbamazepine has also been
suggested as a first-line treatment for Sydenham’s chorea.52
Alternatively, phenobarbital also may be used, 5-7mg/kg/day, tid. Treatment
is usually maintained for 8-12 weeks. Intravenous immunoglobulin therapy
has been suggested.26
Acknowledgements
The authors would like to acknowledge the assistance of Dr. Clovis
Artur Almeida da Silva, from the Department of Paediatrics, Rheumatology
Unity (director), University of Sao Paulo Medical School, who provided
invaluable help with the illustrations and suggestions on the text. We
would also like to thank Prof. Maria de Lourdes Higuchi, director of the
Laboratory of Pathology, Heart Institute (InCor), University of Sao Paulo
Medical School, for the pictures on the pathological specimens.
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Contact information
InCor
Dr. Maria Angelica Binotto
Rua Monte Alegre, 220/401
CEP 05014-000
Sao Paulo, SP
Brazil
Phone/Fax ++55 11 38715368
conangelica@incor.usp.br
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