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Complete heart block (CHB) during acute rheumatic fever is rarely reported. The Authors describe the case of a young woman with rheumatic relapse and CHB that required temporary and then, definitive cardiac stimulation.
In acute rheumatic heart disease, lysis of cardiac muscle fibres with or without retention of sarcolemma is found to be the most damaging feature in many cases. In deeper myocardium the cellular lysis often forms anastomosing clefts or sinus-like spaces between surviving muscle bundles and in the outer portion of myocardium cellular lysis may leave the sarcolemma more or less intact. From lysing cardiac muscle fibres there arise dedifferentiated cells with remarkable potentiality for regeneration. For the origin of these dedifferentiated cells, which are often indistinguishable from lymphocytes, no mitosis is seen in cardiac muscle cells. The successive stages of development of muscle cell from these dedifferentiated cells within the remaining or newly formed sarcolemma have been observed in this study. This study infers that the increased number of fibrous septa, when seen, denotes the tracks of previous muscle degeneration and subsequent replacement of it with incomplete muscle regeneration and fibrous tissue formation. In an area of muscle lysis the origin of Aschoff bodies from these dedifferentiated cells has been followed. Ashoff bodies arising in this was behave as an abortive and atypical growth of muscle fibres in a nodular fashion specific to rheumatic fever.
We determined the penicillin compliance rates in school year 1974-75 for 235 children with rheumatic fever through analysis of urine specimens collected at school. Patients relatively low on compliance during the first year of sampling were divided into two equal size groups for a second year sampling study. One-half (N = 44) of these second year study patients and their parents were readvised regarding the need for penicillin prophylaxis and one-half (N = 44) served as controls. We related eductional data, behavioral ratings, and family information to compliance rates in both study years. The overall compliance for the children during the initial sampling year was 64.6 per cent. Factors found to be significantly related to compliance in year one were: 1) male sex, 2) large sibship, 3) increased number of behavior problems, 4) relatively poor academic progress, 5) lower maternal educational level, and 6) recurrence of rheumatic fever. Compliance rates for reinforced patients did not differ significantly from controls during the second year sampling.
Lymphocyte cell-surface markers were examined in forty children with acute rheumatic fever (ARF) and twelve with acute post-streptococal glomerulonephritis (AGN) and compared to thirty-six normal controls of similar age. Cell-surface-marker studies included surface Ig using fluorescein-labelled F(ab)2 anti-F(AB')2, IgG aggregate binding cells, and EAC rosettes. T cells were identified both as 'active' rosettes and total E-binding cells. Proportions and absolute numbers of cells bearing surface Ig and Fc receptors were elevated in subjects with AGN (Pless than0-01-0-5), whereas proportions of cells producing EAC rosettes were diminished. Patients with acute rheumatic carditis or chorea showed a substantial elevation in proportions and numbers of active T-cell rosettes (Pless than0-01). Streptococcal antigen binding cells capable of forming rosettes with autologous cells coated with group A streptococcal membranes were elevated in the acute phase of both rheumatic fever and acute glomerulonephritis(Pless than0-01). The majority of such cells were removed by passage over insolubilized Ig-anti-IgG columns and appeared to be B cells.
Conditional logistic regression analysis of case-control study data showed that the following factors were significantly related to rheumatic fever occurrence: home dampness, change of place of residence during the last 5 years, low education of mother, body weight below normal, frequent sore throat and positive family history of rheumatic fever.
UNLABELLED: Plasma concentrations of inflammatory cytokines (IL-1 alpha, IL-1 beta, IL-6, IL-8 and TNF alpha) were determined by ELISA in 27 patients with acute rheumatic fever (RF), 12 with only arthritis (RFA) and 15 with rheumatic heart disease (RHD), before, during and after treatment. Altogether, significant increases in TNF alpha, IL-8 and IL-6 levels were observed in the acute phase as compared to the data found during and after treatment. No significant differences were observed for the other cytokines. Elevations of one or more of the inflammatory cytokines were observed in 9 of 12 patients with RFA, and 12 of 15 with RHD. Increase of TNF alpha (6/9) and IL-8 (5/9) levels were higher in RHD patients with cardiac failure. These cytokines were below the detection limits on day 7 of treatment in all 22 patients, except in two, and in all 10 days after treatment. CONCLUSIONS: These findings suggest that inflammatory cytokines, as TNF alpha, IL-8 and IL-6, may play a pathogenic role in rheumatic fever.
T cell lines were established from both valvular specimens and peripheral blood lymphocytes from seven patients with well documented rheumatic heart disease. These cell lines were stimulated with either PHA or streptococcal antigens. Proliferation assays revealed that both valvular and peripheral blood T cell lines reacted to cell wall (CW) and cell membrane (CM) antigens obtained from rheumatic fever associated group A streptococci and not to nephritogenic strains. None of the cell lines reacted to M protein, myosin or other mammalian cytoskeletal proteins. The unique reactivity of rheumatic fever T cell lines only to cellular structures obtained from rheumatogenic strains suggests that these lines react to epitopes specific for antigens obtained from these strains.
The clinical and laboratory data for an 8 year old girl with abdominal pain as a presenting manifestation of acute rheumatic fever are reported. An abdominal investigation with ultrasonography carried out at the same time showed free peritoneal fluid. These findings support the proposal that the abdominal pain classically described in acute rheumatic fever is one of the manifestations of the inflammatory process. It is suggested that in patients with abdominal pain, fever, and increased erythrocyte sedimentation rate in whom the diagnosis is not clear, an abdominal investigation with ultrasonography could be helpful in establishing the correct diagnosis.
BACKGROUND: People with a history of rheumatic fever (RF) are at high risk of recurrent attacks and of developing rheumatic heart disease following a streptococcal throat infection. Giving penicillin to these people can prevent recurrent attacks of RF and subsequent rheumatic heart disease. However, there is no agreement on the most effective method of giving penicillin. OBJECTIVES: To assess the effects of different penicillin regimens and formulations for preventing streptococcal infection and RF recurrence. SEARCH STRATEGY: We searched the Controlled Trials Register (Cochrane Library Issue 2, 2001), Medline (January 1966-July 2000), Embase (January 1985-July 2000), reference lists of articles, and contacted experts in the field. SELECTION CRITERIA: Randomised and quasi-randomised studies comparing: (i) oral with intramuscular penicillin; and (ii) 2- or 3-weekly with 4-weekly intramuscular penicillin in patients with previous RF. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed trial quality and extracted data. MAIN RESULTS: Six studies were included (1,707 patients). Data were not pooled because of clinical and methodological heterogeneity of the trials. Four trials (1,098 patients) compared intramuscular with oral penicillin and all showed that intramuscular penicillin was more effective in reducing RF recurrence and streptococcal throat infections than oral penicillin. One trial (360 patients) compared 2-weekly with 4-weekly intramuscular penicillin. Penicillin given every 2 weeks was better at reducing RF recurrence (relative risk (RR) 0.52, 95% confidence interval (CI): 0.33-0.83) and streptococcal throat infections (RR 0.60, 95% CI: 0.42-0.85). One trial (249 patients) showed that 3-weekly intramuscular penicillin injections reduced streptococcal throat infections (RR 0.67, 95% CI: 0.48-0.92) compared with 4-weekly intramuscular penicillin. CONCLUSIONS: Intramuscular penicillin seemed to be more effective than oral penicillin in preventing RF 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 trials and the use of outdated formulations of oral penicillin.
A large outbreak of streptococcal sore throat in a Royal Air Force Training Camp resulted in five cases of rheumatic fever among the 16- to 18-year-old apprentices, and one case in a 33-year-old airman. The most prevalent type of group A streptococcus isolated from throat swabs was M-type 5 and there was serological evidence that at least four of the rheumatic fever (R.F.) cases were due to this type.Among the patients with uncomplicated throat infection the anti-streptolysin O (ASO) and anti-deoxyribonuclease B (anti-DNAase B) responses were in general rather low, even where there was evidence of protective antibody against type 5. However, a combination of the results of the ASO and anti-DNAase B tests gave an estimate of the extent of streptococcal infection 15-25% higher than did either test alone.The titres of antibody to M-associated protein (MAP) were >/= 60 in all the R.F. patients, and in about 50% of the other patients with ASO titres >/= 200. This figure is unusually high compared with data from several other outbreaks of streptococcal infection due to different serotypes and also greatly exceeds comparable figures for cases of sporadic sore throat and acute glomerulonephritis.
A closed population of juveniles was studied to follow-up manifestations of primary rheumatic fever. In line with other unfavourable factors, the onset of the disease within the first 6 months of the observation was due to cross streptococcal infection (foci of chronic nasopharyngeal infection were detected in 68.6% examinees, rheumatism debut after acute nasopharyngeal infection was in 91.0% patients). Persistence of streptococci was established in many blood counts in immunofluorescence reaction in 88.2% patients in acute disease, in more patients with lingering rheumatic process. Clinical manifestations include, aside from arthritis and rheumocarditis, frequent thyroid and gastrointestinal lesions. It is thought valid to raise the dose and duration of administration of penicillin in patients with primary rheumatic fever as it eradicates chronic infection foci, prevents recurrences, reduces the number of patients with a lingering course of the disease, with recurrences and valvular defects of the heart.
A 15-year-old boy developed an annular erythematous skin rash, fever, knee pain, syncope, and was found to be in complete heart block requiring temporary transvenous pacing. His recovery was complete following therapy with high dose steroids, aspirin, and IV ceftriaxone followed by oral penicillin. Serologic tests documented diagnostic levels of antibodies to Borrelia burgdorferi as well as to Group A streptococcal DNase B. Diagnoses of both Lyme disease and rheumatic fever are based on clinical presentation and serologic confirmation. Our patient had a clinical presentation compatible with either diagnosis and serologic test results suggestive of infection by both B burgdorferi and Group A streptococci. The patient's management was aimed at preventing complications of both diseases, since clinicians involved with the patient's case could not agree on the most likely diagnosis. We present this case to emphasize the following: both rheumatic fever and Lyme disease should be considered in patients presenting with annular skin rashes and complete heart block; serologic studies may be confusing in both Lyme disease and rheumatic fever since neither is entirely sensitive nor specific and efforts should be made to document the causative organism by appropriate cultures, biopsies, and stains when possible; and improved immunoserologic testing for Lyme disease, in particular, is highly needed.
For the assessment of the situation after streptococcal infection and thus for prevention of rheumatic fever and glomerulonephritis more simple and rapid serological tests are needed. The principle of indirect haemagglutination seems particularly suited for this purpose. A rapid slide test (streptozyme) for the simultaneous detection of antibodies against five streptococcal enzymes in capillary blood or serum was compared to four monospecific tests: latex-Asl, Antistreptolysin-O (ASL-O), antistreptokinase and anti NADase. Several lots of test kits and more than four hundred sera of adults and children with and without suspected rheumatic fever were tested. The number of falsely negative and falsely positive results was small as compared to single monospecific tests. Additional positive reactions were obtained when the ASL-O was within the normal range, but the titer against several exoenzymes were elevated, or, when the antibodies against a single exoenzyme were extremely strong. The precision of the polyvalent test may not be quite as high as if three monospecific tests are applied, It is however sufficient. Thus it seems unrealistic to require the performance of at least three monospecific tests under the present epidemiological conditions.
Human monoclonal antibodies were produced by fusion of peripheral blood lymphocytes from a patient with acute rheumatic fever, with the HGPRT-non-secreting murine (Balb-c) cell line SP2/0Ag14. Heterohybridomas were selected by screening against rheumatic fever-associated group A streptococci using an ELISA, and against paraffin wax-embedded human heart sections using an immunoperoxidase technique. Two human IgM monoclonal antibodies were selected for further analysis by Western blotting and ELISA. Both antibodies demonstrated multispecificity by immunoblotting and ELISA. One of the monoclonals bound to 48 kD and 83 kD bands common to group A streptococcal and heart antigen preparations. Both human monoclonal antibodies bound to a 43 kD constituent band common to human heart and sarcolemma membrane extract. Inhibition studies performed using a competitive solid phase immunoassay confirmed shared epitopes between group A streptococci and human heart. The significance of these monoclonal antibodies to the pathogenesis of rheumatic fever is uncertain.
Recent investigation has delineated some of the bacterial and host factors that may play a role in the pathogenesis of rheumatic fever. Continuing studies support the role of antibodies to crossreactive antigens in human tissues and the group A streptococcal cell in inducing tissue damage associated with this disease. Several specific epitopes have now been defined that are common to the crossreactive antigens. Data from recent outbreaks of rheumatic fever in the USA suggest that mucoid group A streptococcal strains, belonging to serotypes M1, M3, M5, M6 and M18 may have accounted for these outbreaks. While these strains are thought to be rheumatogenic, the exact characteristic(s) that renders them so is yet to be determined.
How do we make sense of the process of disease definition when the tools for "framing" a pathophysiologic reality and the reality to be framed may have both been changing? The sudden emergence of rheumatic fever at the end of the eighteenth century was the result of distinct biological changes that led to cardiac damage. But the identification of the disease also depended on the ability of clinicians to diagnose it in the absence of easily observable cardiac symptoms. Clinicians were able to appreciate the alteration of rheumatism into rheumatic fever through assimilation of technological changes (the stethoscope and autopsy), refinements in clinical thinking (the "typical case"), and the concentration of patients in hospitals where they were treated by physicians who were medical leaders and educators.
Acute rheumatic fever is a delayed, nonsuppurative sequela of a pharyngeal infection with the group A streptococcus. The onset of the disease is usually characterized by an acute febrile illness; however, there may be chronic involvement of the heart and/or central nervous system. The article explores the relationship between the initial infection and host-microbial interactions that may be operative in disease pathogenesis.
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