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Acute rheumatic fever, often believed to have been eradicated, has shown an increase in prevalence and virulence within the past few years. This article discusses current epidemiology, assessment findings, medical treatment, and nursing interventions for the child with rheumatic fever. Principles of prevention and implications for health teaching are included.
Sixty four children who presented with the initial attack of acute rheumatic fever and maintained continuous regular secondary prophylaxis, were followed up prospectively for 12.3 years (an observation period of 775 patient-years). The prevalence rate of rheumatic heart disease in the 29 children who had carditis in the initial attack and in the 35 children who had no carditis initially was 49 vs 0%, respectively. The overall prevalence rate of rheumatic heart disease was 20%. Mitral incompetence developed in 11 patients (17%), aortic incompetence in 2 (3%) and mitral stenosis in 2 (3%). None of the patients developed aortic stenosis. Two recurrences developed with a recurrence rate of 0.003 per patient per year. One patient needed cardiac surgery and there was no mortality. These data strongly suggest that continuous regular secondary prophylaxis can prevent or significantly reduce the development of mitral and aortic valve stenosis, the prevalence rate of rheumatic heart disease and mortality.
Rheumatic fever (RF) and rheumatic heart disease (RHD) are major public health problems in developing countries. A prospective study carried out in a large general hospital showed that carditis was the predominant feature in first attack and also the recurrence of RF but that recurrence was associated with more severe manifestations. Echocardiography picked up cases of subclinical carditis. Presence of congestive cardiac failure in association with carditis always led to chronic RHD. Recurrence occurred only when patient defaulted penicillin prophylaxis. The overall recurrence rate was 0.026 per patient.
OBJECTIVES: To investigate the progress of rheumatic fever (RF) and the predictors of severe chronic valvar disease. DESIGN: Patients prospectively followed up since their first attack of acute RF (ARF). SETTING: Universidade Federal de Minas Gerais, Brazil. PATIENTS: 258 children and adolescents who met the revised Jones criteria for RF. The follow up period ranged from 2-15 years. MAIN OUTCOME MEASURES: The presence and severity of mitral or aortic valvar disease were determined by both clinical and Doppler echocardiographic examinations. The variables associated with severe chronic valvar disease were initially identified by the Kaplan-Meier method and, later, by multivariate analysis. RESULTS: Doppler echocardiography of 258 patients studied showed that 186 (72.1%) developed chronic valvar disease and 41 (15.9%) progressed to severe chronic mitral or aortic lesions. Of 146 patients who developed carditis, 49 (33.6%) had a normal clinical examination in the chronic phase but only nine (6.2%) had normal Doppler echocardiographic findings--that is, 40 (27.4%) patients progressed to chronic subclinical valvar disease. Moderate or severe carditis, recurrences of ARF, and mother's low educational level were risk factors in predicting severe chronic valvar diseases. CONCLUSION: The increased risk of progressing to severe chronic valvar disease was associated with moderate or severe carditis, recurrences of ARF, and mother's low educational level. Hence, in a country such as Brazil, the options available for disease control are mainly primary and secondary prophylaxis.
BACKGROUND: The diagnosis of rheumatic fever is based on physical findings (major) and supporting laboratory evidence (minor) as defined by the Jones criteria. Rheumatic carditis is characterized by auscultation of a mitral regurgitant murmur. Doppler echocardiography, however, may detect mitral regurgitation when there is no murmur ("silent" mitral regurgitation), even in normal individuals. HYPOTHESIS: The hypothesis of this study was that physiologic mitral regurgitation can be differentiated from pathologic "silent" mitral regurgitation by Doppler echocardiography. METHODS: The study group consisted of 68 patients (2-27 years) with normal two-dimensional imaging and Doppler evidence of mitral regurgitation but no murmur. Patients with rheumatic fever (n = 37) met Jones criteria (chorea in 20, arthritis in 17). Patients without rheumatic fever (n = 31) were referred for innocent murmur (n = 7), abnormal electrocardiogram (n = 13), and chest pain (n = 11). Echoes were independently reviewed by two cardiologists blinded to the diagnosis. Pathologic mitral regurgitation was defined as meeting the following four criteria: (1) length of color jet > 1 cm, (2) color jet identified in at least two planes, (3) mosaic color jet, and (4) persistence of the jet throughout systole. Jet orientation was also noted. RESULTS: Using the above criteria, there was agreement in echo interpretation of pathologic versus physiologic mitral regurgitation in 67 of 68 patients (interobserver variability of 1.5%). Pathologic regurgitation was found in 25 (68%) patients with rheumatic fever but in only 2 (6.5%) patients without rheumatic fever (p < 0.001). The specificity of Doppler for detecting pathologic regurgitation was 94% with a positive predictive value of 93%. The color mitral regurgitant jet was posteriorly directed in all 25 patients with rheumatic fever. CONCLUSION: Pathologic "silent" mitral regurgitation of rheumatic fever can be distinguished from physiologic mitral regurgitation using strict Doppler criteria, particularly when the jet is directed posteriorly. These data support the use of Doppler echocardiography as a minor criterion for evaluating patients with suspected rheumatic fever.
BACKGROUND: The incidence of acute rheumatic fever in New Zealand remains relatively high. Reliable early diagnosis of carditis is difficult and important in management. AIM: To determine if Doppler echocardiography contributed to the early diagnosis of carditis in acute rheumatic fever. METHODS: Forty-seven patients admitted to hospital with suspected acute rheumatic fever and 19 control patients, with a febrile illness due to a documented non-cardiac bacterial infection, were assessed two days and two weeks following admission. Presence or absence of clinical carditis was determined by a cardiologist unaware of the suspected diagnosis, from clinical examination, chest radiograph, electrocardiogram (ECG) and two dimensional echocardiogram. Doppler echocardiography was then performed and interpreted by a second cardiologist unaware of the diagnosis. After completion of the study the Jones criteria were applied, to categorise the patients with suspected acute rheumatic fever into four groups for the final diagnosis: no acute rheumatic fever, possible acute rheumatic fever, definite acute rheumatic fever without carditis, and definite acute rheumatic fever with carditis. RESULTS: In 19 patients with a final diagnosis of acute rheumatic fever and carditis at the baseline assessment carditis was detected by clinical assessment in 15 patients, compared with 19 patients with evidence of significant valve regurgitation by Doppler echocardiography. Following the two week assessment, all 19 patients had both clinical and Doppler evidence of carditis. Five patients with a final clinical diagnosis of possible acute rheumatic fever or definite acute rheumatic fever without carditis, had a Doppler abnormality detected. There was no clinical or Doppler abnormality in the febrile controls. CONCLUSIONS: Doppler echocardiography is more sensitive than clinical assessment in the detection of carditis in acute rheumatic fever, and can contribute to earlier diagnosis.
Rheumatic fever is a nonsuppurative sequelae to Group A streptococcal pharyngitis. Valvulitis resulting from cardiac involvement in this disease, is the main cause of morbidity in rheumatic fever. The study of rheumatic fever sera on cryostat sections of a variety of tissues using indirect immunofluorescence is described. A 95% incidence of smooth muscle antibody was found in 236 rheumatic fever sera, from 55 patients. Sera from hospital patients with a variety of diseases had an overall incidence of 12% for smooth muscle antibodies. The pattern and distribution of tissue staining strongly suggests that the smooth muscle antibodies described in rheumatic fever sera have antiactin specificity. This finding raises many questions concerning the immunopathogenesis and immunogenetics of rheumatic fever, and the pathogenesis of a number of diseases in which streptococci have not previously been considered.
BACKGROUND: People with a history of rheumatic fever are at high risk of recurrent attacks of rheumatic fever and developing rheumatic heart disease following a streptococcal throat infection. Giving penicillin to these people can prevent recurrent attacks of rheumatic fever and subsequent rheumatic heart disease. However, there is no agreement on the most effective method of giving penicillin. OBJECTIVES: To assess the effects of penicillin compared to placebo and the effects of different penicillin regimens and formulations for preventing streptococcal infection and rheumatic fever recurrence. SEARCH STRATEGY: We searched the Controlled Trials Register (Cochrane Library Issue 2, 2001), MEDLINE (1997 to July 2000), EMBASE (1998 to July 2000), reference lists of articles and we contacted experts in the field. SELECTION CRITERIA: Randomised and quasi-randomised studies comparing (i) penicillin with control, (ii) oral with intramuscular penicillin (iii) 2- or 3-weekly with 4-weekly intramuscular penicillin in patients with previous rheumatic fever. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed trial quality and extracted data. MAIN RESULTS: Nine studies were included (n=3008). Data were not pooled because of heterogeneity. Overall, the methodological quality of included studies was poor. Three trials (n= 1301) compared penicillin with control. Only one of three studies showed that penicillin reduced rheumatic fever recurrence (RR 0.45, 95% CI 0.22 to 0.92) and streptococcal throat infection (RR 0.84, 95% CI 0.72 to 0.97). Four trials (n=1098) compared intramuscular with oral penicillin and all showed that intramuscular penicillin reduced rheumatic fever recurrence and streptococcal throat infections compared to oral penicillin. One trial (n= 360) compared 2-weekly with 4-weekly intramuscular penicillin. Penicillin given every two-weeks was better at reducing rheumatic fever recurrence (RR 0.52, 95% CI 0.33 to 0.83) and streptococcal throat infections (RR 0.60, 95% CI 0.42 to 0.85). One trial (n= 249) showed 3-weekly intramuscular penicillin injections reduced streptococcal throat infections (RR 0.67, 95% CI 0.48 to 0.92) compared to 4-weekly intramuscular penicillin. REVIEWER'S CONCLUSIONS: Intramuscular penicillin seemed to be more effective than oral penicillin in preventing rheumatic fever recurrence and streptococcal throat infections. Two-weekly or 3-weekly injections appeared to be more effective than 4-weekly injections. However, the evidence is based on poor quality of trials.
Acute rheumatic fever (ARF) and associated rheumatic heart disease are serious sequelae after infection with group A Streptococcus (Strep A). Autoantibodies are thought to contribute to pathogenesis, with deeper exploration of the autoantibody repertoire needed to improve mechanistic understanding and identify new biomarkers. Phage immunoprecipitation sequencing (PhIP-Seq) with the HuScan library (>250,000 overlapping 90-mer peptides spanning the human proteome) was utilized to analyze autoreactivity in sera from children with ARF, uncomplicated Strep A pharyngitis, and matched healthy controls. A global proteome-wide increase in autoantigen reactivity was observed in ARF, as was marked heterogeneity between patients. Public epitopes, common between individuals with ARF were rare, and comprised less than 1% of all enriched peptides. Differential analysis identified both unknown and previously identified ARF autoantigens, including PPP1R12B, a myosin phosphatase complex regulatory subunit expressed in cardiac muscle, and members of the collagen protein family, respectively. Pathway analysis found antigens from the disease-relevant processes encompassing sarcomere and heart morphogenesis were targeted. In sum, PhIP-Seq has substantially expanded the spectrum of autoantigens in ARF, and reveals the rarity of public epitopes in the disease. It provides further support for the role of epitope spreading in pathogenesis and has identified PPP1R12B as an enriched autoantigen.
In acute rheumatic fever, various types of myocardial degeneration and subsequent transformation of the damaged muscle fibers into a variety of cells, classified and unclassified, are described from microscopic examination of autopsy specimens. This study suggests that in the origin of Aschoff bodies, the diagnostic feature of rheumatic fever, there are three different pathways (Types A, B and C) for cytogenesis of Aschoff cells from altered muscle fibers. Type A cytogenesis takes place through the stage of Anitschkow myocytes of cardiac muscle origin (McDONALD 1963), and the Type B pathway, through the stage of dedifferentiated cells arising in lysing cardiac muscle fibers. These dedifferentiated cells with capacity for regeneration of regular cardiac muscle fibers (McDONALD 1975), show abortive or atypical development of muscle cells through the Aschoff cell stage. The Type C cytogenesis of Aschoff cells takes place through direct transformation of cardiac muscle fibers which show central hyalinization of myoplasm and changes in nuclei from normal to single or multinucleated large vesicular forms. The fibrinoid material of Aschoff bodies is shown to be the product of muscle origin. The mechanism of formation of fibrous scars in the myocardium and fibrous thickening of subendocardium are explained on the basis of fibrous transformation of cardiac muscle. Altered muscle fibers have been shown to give rise to cells which simulate inflammatory cells and others which cannot be classified.
Rheumatic fever is a catastrophic illness in many parts of the world, particularly in developing nations, where the incidence has been estimated to be between 10 and 15 million new cases each year. In the United States, rheumatic fever had become a rarity, having virtually disappeared by the mid 1960s. Of increasing concern, however, was the abrupt rise in the incidence of rheumatic fever in the United States in the mid 1980s, with reported "outbreaks" in middle-class communities in five cities and two military camps. Recently, a number of cases of poststreptococcal reactive arthritis have been reported. On close examination, however, these are most likely alternate clinical presentations of rheumatic fever. It is widely accepted that rheumatic fever occurs following an overactive immune response by a genetically susceptible host to oropharyngeal infection with group A beta-hemolytic streptococci. Nevertheless, details of pathogenesis at a level allowing more effective intervention remain obscure. The question of pathogenesis holds a deep interest, because rheumatic fever is one of the few autoimmune diseases with a known infectious etiology.
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Recurrent acute rheumatic fever and rheumatic heart disease can be prevented by antibiotic intervention. We report the case of genetically identical twins, one of whom had overt rheumatic fever, received penicillin prophylaxis and did not have rheumatic heart disease. The other must have had inapparent rheumatic fever, received no chemotherapy prophylaxis and proceeded to develop rheumatic heart disease. A greater clinical and laboratory vigilance is required for the diagnosis of acute rheumatic fever in the asymptomatic identical twin of a patient with rheumatic fever. This case provides further evidence of a genetic predisposition to rheumatic fever and demonstrates the continued value of penicillin in the prophylaxis of acute rheumatic fever. It emphasises the need to maintain the integrity of preventive programmes against rheumatic fever worldwide. Studies which explore the HLA and other genetic linkages with rheumatic fever should be encouraged.
In recent years, rheumatic fever seems to have decreased but rheumatic heart disease with latent onset appears to persist in similar frequency. Measurement of AH along with ASO is required in rheumatic heart disease with latent onset, for more definite diagnosis, therapy and suggestion for the mode of living. For the diagnosis of rheumatic fever in acute stage, serological reactions for hemolytic streptococcus other than ASO should be done along with ASO. In our cases, ASO titer was high in 84.5% of cases, but either ASO or AH titer was elevated indicating positive reaction for hemolytic streptococcus in 100% of cases.
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The apparent fall of rheumatic fever incidence in developed countries and in Yugoslavia is one of the reasons of negligence of the diagnosis of this disease. This fall was associated with mild forms of rheumatic fever (arthritis and mild forms of carditis are the main manifestations) where the beginning resembled other rheumatic disease. Consequently the problem of diagnosis of rheumatic fever is complicated. The early diagnosis of rheumatic fever is very important for the course of the disease, because appropriate measures (secondary prophylaxis) can prevent recurrence and severe rheumatic heart defects. The other disease recent increase of rheumatic fever incidence in the United States is the warning to other countries.
We evaluated the efficacy and safety of naproxen (10-20 mg/kg/d) for the treatment of arthritis and fever related to rheumatic fever in 19 children. Fever and arthritis resolved within a median of 1 day of beginning treatment (range, 1-2 and 1-30 days, respectively). The sole patient with prolonged arthritis had small joint involvement. No gastrointestinal, dermatologic, liver, or renal side effects were observed. None of the patients developed carditis over the following 6 months. Naproxen appears to be effective for the treatment of arthritis and fever related to rheumatic fever and is well tolerated.
Rheumatic fever is no longer a significant health problem in socioeconomically advanced countries, but it still causes 25% to 40% of all cardiovascular disease in the rest of the world, including tropical countries where it was once believed to be rare. Differences in clinical manifestations may have obscured the rheumatic fever syndrome in the past, but there is reason to believe that the incidence of the disease has increased with urbanization. In any event, carditis is severe and frequently leads to advanced heart disease. Rheumatic fever is, to a large extent, preventable. Obstacles to effective prevention programs are discussed.