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The current status of rheumatic fever is reviewed and the reasons for its decline in the United States are explored. Continuation of primary prevention efforts is recommended or there could be a resurgence of this disease. The need for further research continues because rheumatic fever is still a major health problem for much of the world's population.
The incidence of rheumatic fever in the population of Rochester, Minnesota, during the years 1935 through 1978 was determined by means of the medical records-linkage system of the Rochester Epidemiology Program Project. The annual age-adjusted incidence rate per 100,000 population for all episodes of rheumatic fever was 9.7, comprising 7.0 for initial attacks and 2.7 for recurrent attacks. There was a marked decline over time: incidence rates of initial episodes decreased from 13.6 in 1935-1949 to 8.2 in 1950-1964 and 2.7 in 1965-1978; and rates of recurrent attacks decreased even more--from 7.0 to 3.2 and 0.3 in the same intervals. There was also a secular trend in the clinical manifestations of rheumatic fever, as the proportion of initial episodes with carditis increased from 23% in 1935-44 to 52% in 1965-1978.
The public health importance of rheumatic fever is not directly related to its prevalence but is a complex function of many factors, such as incidence, prevalence, mortality, disability, and cost to the community, all relative to the importance of other diseases. Although the prevalence is low and still decreasing in developed countries, rheumatic fever is the commonest form of heart disease in many developing countries. Advances in the bacterial and serological characterization of group A streptococci are reviewed in this Memorandum, with emphasis on the nature of the structural elements of the cell wall. Microbiological methods play an important role in the diagnosis and control of rheumatic fever and up-to-date information is given concerning methods of isolation and grouping and of typing. Methods of assessing streptococcal activity in the host, in particular the different antibody responses found in relation to different pathological conditions, are discussed, as are the improvements required in laboratory services to enable them to carry out these duties adequately. Current concepts concerning the pathogenesis of rheumatic fever are reviewed together with differences in the epidemiology related to the different sites of infection and the problems of carriership. The Memorandum is also concerned with the methods of prevention and treatment, including prevention of recurrences, control of the disease in communities, and strategies for nationwide control.
A case of rheumatic fever with severe heart involvement, in which articular rheumatoid-like features involving both hands appeared many years after clinical onset, is described. After reviewing the articular sequelae of rheumatic fever and describing the clinical features of each form, the authors point out the main differences between rheumatic fever and rheumatoid arthritis, and diagnose Jaccoud's arthritis.
Serum immunoglobulin A (IgA) was markedly increased in 80% of 50 patients with acute rheumatic fever in Trinidad in contrast to 20% of 63 patients with acute glomerulonephritis, whereas serum IgG was increased in nearly all of both groups. Since total antibody to M-associated protein (MAP) (assessed by complement fixation) is the only antibody as yet consistently found to be of higher titer in patients with acute rheumatic fever than in patients with acute glomerulonephritis in Trinidad, it was measured and the titers were related to serum levels of IgA. The titers of total antibody to MAP were greater than or equal to 40 in 58% of the rheumatic fever patients, 43% of the nephritis patients, and 8% of well school-children. However, its presence in rheumatic fever patients did not correlate directly with amounts of serum IgA present (r = 0.0507). Moreover, titers of total antibody to MAP related equally well to enzyme-linked immunosorbent assay indicated amounts of IgG antibody (r = 0.3939) and IgA antibody (r = 0.3054) to MAP in rheumatic fever patients but not in nephritis patients (r = 0.0301 for IgA antibody and 0.6909 for IgG antibody to MAP), whereas they related best to IgM antibody to MAP in the school-children (r = 0.4204).
The alteration of cellular reactivity was investigated in 20 patients with rheumatic fever at the first rheumatic attack or in relapse with confirmed heart damage. The results obtained by studying in parallel ESR, the ASLO titer, IDR to streptococci and the degree of leukocyte migration inhibition proved that the onset of rheumatic attack was preceded by a deep disturbance of the cellular immunity. The migration inhibition values were between 50 and 60% (as compared with 10% in the normal controls) in over 85% of the patients investigated. It is emphasized that the selection of cases of streptococcal angina should be made very carefully and that sometimes it is necessary to use a more specific method for the detection of rheumatic fever in its preclinical stage.
Acute rheumatic fever (ARF) is still an important disease of the pediatric and adult age. The increased number of cases described in the literature in the last 10 years brought us to evaluate the ARF cases diagnosed in a Pediatric Teaching Hospital in the period 1988-1997. Most of the children with ARF presented with joint involvement even if patients with cardiac disease or chorea minor were numerous. About 50% of our patients with ARF did not refer a history of a febrile tonsillopharyngitis in the 15-60 days before the presentation of ARF. The remaining patients have had a preceding pharyngitis not adequately treated. In none of the subjects a throat swab positive for group A beta hemolytic streptococci was available. These results confirm the importance of the correct diagnosis and treatment of streptococcal pharyngitis but suggest that ARF can develop without any outstanding clinical evidence of streptococcal infection.
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Several areas in the United States have experienced significant outbreaks of acute rheumatic fever. Reasons for the reappearance of acute rheumatic fever are incompletely understood but may relate to changes in the organism. Fortunately, however, GABHS has remained exquisitely susceptible to penicillin. Given the resurgence in cases of acute rheumatic fever, the practicing physician needs to be vigilant in diagnosing and ensuring adequate treatment of acute streptococcal pharyngitis. In addition, acute rheumatic fever must be considered in a patient who presents with a new onset murmur, a migratory polyarthritis, chorea, or a rash suggestive of erythema marginatum.
One hundred and fourty-eight rheumatic fever patients and 444 controls matched by age, sex and place of residence, were interviewed about socio-economic and some other variables. Socio-economic factors recognized as risk factors for rheumatic fever (flat dampness, more than 2 persons per room, sleeping in bed with other person, low education of mother and undernourishment) were of lesser importance for persons with frequent sore throat in comparison to persons without frequent sore throat. According to the results obtained it seems that there is positive connection between host's propensity to clinical manifestation of throat infection and manifestation of rheumatic fever. The lesser susceptibility the more additional factors are needed for Rheumatic Fever to occur. The relative importance of socio-economic factors in rheumatic fever occurrence depends on host's susceptibility to infection.
Case records of hospitalized children (age 4 to 18 years) with acute rheumatic fever on Oahu, HI, were reviewed for the 4-year period from Oct 1, 1980, to Sept 30, 1984. Ninety-eight cases met the modified Jones criteria. The overall incidence of rheumatic fever was 13.4 hospitalized children per 100,000 children per year and that for recurrent attacks was 2.5. Of the 98 with rheumatic fever, 73 had polyarthritis, 33 had carditis, and ten had chorea. Polynesian/part-Polynesian children accounted for 76 of the 98 cases. The incidence of rheumatic fever in Hawaiian/part-Hawaiian was 18.0 and for Samoan children was 206 hospitalized children per 100,000 per year. The relative risks were 7.7 and 88 times that of the white children, respectively. Rheumatic fever continues to cause significant morbidity in children in Hawaii, especially in Polynesian children.
Acute rheumatic fever is a nonsuppurative sequela of upper respiratory tract infection with group A streptococci. We describe our recent experience with the diagnosis and management of 3 cases of acute rheumatic fever to highlight the delays that may arise in the diagnosis of this condition. In adults, febrile polyarthritis is the most common presentation of acute rheumatic fever. Increased awareness on the part of the physician is necessary to ensure both prompt and accurate diagnosis of this cause of febrile polyarthritis.
During the last 30 years, acute rheumatic fever has been a curiosity in Norway, and only five cases have been reported to MSIS (National Notification System for Infectious Diseases, Norway) in the 1990s. Even so, during the period 1990 to 1992 99 patients were discharged from Norwegian hospitals with the diagnosis acute rheumatic fever. Could the increase in the number of group A-streptococci in the last years have led to a corresponding increase in the incidence of acute rheumatic fever? If so, could such an increase have escaped our attention? We present an updated review of acute rheumatic fever and the case of a young soldier.
BACKGROUND: The arthritis of rheumatic fever is very responsive to treatment with salicylates, but there are many adverse reactions, especially hepatotoxicity, due to aspirin (acetylsalicylic acid) therapy. These side-effects change the course and duration of rheumatic fever. Other non-steroidal anti-inflammatory drugs may be equally effective, although no reports are available. METHODS: We studied 72 patients with rheumatic fever who were admitted to Dr Sami Ulus Children's Hospital between 1995 and 1999. Twenty patients with arthritis were treated with tolmetin (25 mg/kg per day; group I) and 52 patients with arthritis and/or mild carditis were put on aspirin therapy (75-100 mg/kg per day) for 4-6 weeks (group II). Arthritis had disappeared at the same time in both the aspirin and tolmetin groups (P = 0.675). RESULTS: The erythrocyte sedimentation rates of patients upon admission, at the first week and at the end of therapy were not different in the two groups (P > 0.05). No adverse effect of tolmetin therapy was observed, whereas side-effects of salicylate were observed in 19 patients (36.5%) in the aspirin group. Hepatotoxicity, gastric irritation and salicylism were found in 16, four and three patients, respectively. Renal toxicity and Reye syndrome were not demonstrated. Because of these side-effects of aspirin, therapy had to be stopped for 10-20 days and the duration of hospitalization in this group was lengthened unnecessarily. CONCLUSION: Tolmetin was safe and effective treatment for arthritic rheumatic fever patients without carditis. Tolmetin can be used particularly in patients who cannot tolerate aspirin.
BACKGROUND: Acute rheumatic fever (ARF) remains the leading cause of acquired heart disease in children worldwide. No therapeutic agent has been shown to alter the clinical outcome of the acute illness. Immunological mechanisms appear to be involved in the pathogenesis of ARF. Intravenous immunoglobulin (IVIG), a proven immunomodulator, may benefit cardiac conditions of an autoimmune nature. We investigated whether IVIG modified the natural history of ARF by reducing the extent and severity of carditis. METHODS AND RESULTS: This prospective, double-blind, randomized, placebo-controlled trial evaluated IVIG in patients with a first episode of rheumatic fever, stratifying patients by the presence and severity of carditis before randomization. Patients were randomly allocated to receive 1 g/kg IVIG on days 1 and 2 and 0.4 g/kg on days 14 and 28, or they received a placebo infusion. Clinical, laboratory, and echocardiographic evaluation was performed at 0, 2, 4, 6, 26, and 52 weeks. Fifty-nine patients were treated, of whom 39 had carditis (including 4 subclinical) and/or migratory polyarthritis (n=39). There was no difference between groups in the rate of normalization of the erythrocyte sedimentation rate or acute-phase proteins at the 6-week follow-up. On echocardiography, 59% in the IVIG group and 69% in the placebo group had carditis at baseline. There was no significant difference in the cardiac outcome, including the proportion of valves involved, or in the severity of valvar regurgitation at 1 year. At 1 year, 41% of the IVIG and 50% of the placebo group had carditis. CONCLUSIONS: IVIG did not alter the natural history of ARF, with no detectable difference in the clinical, laboratory, or echocardiographic parameters of the disease process during the subsequent 12 months.
The clinical features of the first attack acute rheumatic fever in 32 adults are described in a prospective study. Classical migratory polyarthritis occurred in 11 patients whilst the arthritis in the remaining 21 was additive in type, rapidly becoming symmetrical. The lower limb joints were involved more frequently than those of the upper limb. Mild transient carditis was present in only one patient. All patients showed evidence of antecedent streptococcal infection but none had chorea, subcutaneous nodules or erythema marginatum. The disease ran a benign course so that the sensitivity of the modified Jones criteria for adult rheumatic fever needs re-evaluation. Rheumatic fever is still a significant health problem in Iraq and should always be considered in the differential diagnosis of acute polyarthritis in adults.
In spite of general complacency about first-degree heart block in acute rheumatic fever, abnormal conduction with dysrhythmias, occasional complete heart block, and, rarely, Stokes-Adams attacks are important early signs of acute rheumatic fever and may precede other signs. Every person with episodic fainting is entitled to an ECG, and frequent ECGs are imperative in any case of rheumatic fever with signs of arrhythmias. Changing atrioventricular block necessitates continuous monitoring for dysrhythmias. A 13-year-old boy who appeared with Stokes-Adams attacks secondary to acute rheumatic fever was successfully treated by temporary pacing.
Thirty-seven cases of streptococcal rheumatic fever in adults (20 women and 17 men; mean age 33 years) are reported. Only 3 patients had a history of previous rheumatic fever. In 73% of the cases untreated sore throat had occurred 8 to 30 days before the condition developed. Throat swabs taken during the rheumatic attack were positive for Streptococcus haemolyticus in only 5 out of 22 patients. The joints most commonly affected were those of the lower limbs and the symptoms were severe; in 2 out of 3 patients other joints were subsequently involved. Five patients had stable mitral regurgitation of undetermined duration, with systolic murmur. ECG abnormalities were noted in 7 patients, including 5 with prolongation of the PR interval and 2 with moderate elevation of the ST segment; these abnormalities regressed in all cases. No specific skin lesions were observed. The streptococcal infection was associated with a rise in antistreptolysins in 73% of the cases, a rise in antistreptokinases in 80% and a rise in both types of antibodies in 97%. Response to antibiotics and anti-inflammatory drugs was satisfactory in all cases. Cure was achieved within less than one month in 57% of the patients, but the condition lasted three years in 3 patients.