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PubMed1990

Rheumatic fever and rubella immunity.

Anti-rubella IgG titer was estimated in 106 children: sixty five had acute rheumatic fever and 41 had either a history of rheumatic fever or a definite rheumatic heart disease. Their ages ranged from 6 to 16 years old (11.4 +/- 2.7 years). Sixty two were females and 44 were males. They were compared with 35 control normal subjects of both sexes with no history of rheumatic affection, aged 5 to 14 years (10.2 +/- 3.6 years). The results obtained showed a significantly (p less than 0.001) higher rubella IgG titer level in the controls (1066.5 +/- 8.3) as compared to the rheumatic cases (521.2 +/- 3.0). No differences were found in the rubella antibody titer between cases of acute rheumatic fever and those with history of rheumatic fever or rheumatic heart disease, nor between males and females in either cases or controls. We suggested that the low rubella IgG levels encountered in the rheumatic cases, make them more susceptible to rheumatic fever affection. In other words, a high immunity level against rubella might also produce an immunity against an agent, possibly related to rubella virus, with a specific role in the development of rheumatic fever. Vaccination against rubella could be worth a trial, for prevention of rheumatic fever.

Adolescent↗
PubMed1987

Acute rheumatic fever in western Pennsylvania and the tristate area.

Acute rheumatic fever is reported to have declined and perhaps be vanishing. Prompted by the occurrence of 17 cases of acute rheumatic fever in an 18-month period in 1985 and 1986, we reviewed the records of 243 children with acute rheumatic fever who were cared for at Children's Hospital of Pittsburgh or Mercy Hospital between 1965 and 1986. Acute rheumatic fever was diagnosed using the modified Jones criteria and cases were classified by major criteria as arthritis, arthritis and carditis, carditis alone, carditis and chorea, chorea alone, and arthritis and chorea. Among the 17 recent patients, 59% had carditis, 30% had chorea, and 24% had arthritis alone. The proportion of children who had particular major manifestations was similar in the last two decades and in 1985 to 1986. The recent children with acute rheumatic fever ranged in age from 6 to 13 years with a mean and median age of 10 years. There were 16 white children and one Asian child. Only four children lived in an urban setting. When demographic features of the children were contrasted with those in the previous two decades, a decrease in the proportion of children who lived in urban areas and who were black was noted. Four children had a history of preceding sore throat but only three sought medical care; nine children had no memorable illness and four had either a nonrespiratory illness or a respiratory infection without sore throat. This resurgence of rheumatic fever serves as a reminder that a diligent approach to the diagnosis and therapy of streptococcal infections remains essential.

Acute Disease↗
PubMed1995

Rapidly progressive glomerulonephritis complicating acute rheumatic fever.

A case of acute rheumatic fever and glomerulonephritis following streptococcal throat infection is presented. The coincidence of rheumatic fever and post-streptococcal glomerulonephritis is uncommon, but well recognised. This case is of additional interest since the nephritis was crescentic.

Acute Disease↗
PubMed1996

10-year educational programme aimed at rheumatic fever in two French Caribbean islands.

BACKGROUND: In less developed countries, rheumatic fever still occurs. We started a long-term educational programme in two French Caribbean islands that was directed at the public and at health-care workers to see whether we could reduce the incidence of rheumatic fever. METHODS: Our 10-year programme started in 1981 in Martinique and Guadeloupe, and was based in the community and in clinics and hospitals. The programme established a registry of all cases of primary and secondary rheumatic fever (diagnosed by Jones' modified criteria), with systematic hospital admission of children. We graded carditis as severe, mild, or subclinical, and acute glomerulonephritis was defined by oedema, proteinuria, and haematuria for less than 3 months. The educational part of the programme targeted the public and health-care workers, including doctors, with written information distributed in schools or via radio and television broadcasts or videotapes. For the public, the benign clinical presentation of the initial streptococcal infection was contrasted with the severity of later heart disease. FINDINGS: The first months of the programme led to a 10-20% increase in the number of rheumatic fever cases admitted to hospital, because of the renewed attention paid to the disease. Therefore we took 1982 as the baseline year. In 1982-83 the incidence of rheumatic fever was 19.6 per 100 000 inhabitants aged under 20 in Martinique, and 17.4 per 100 000 in Guadeloupe. In 100 Martinique children and 97 Guadeloupe children in 1982-83, 40 and 71% had carditis, respectively (severe in 10 and 32%). Rheumatic fever was preceded by symptomatic sore throat in 52 and 41% of cases, respectively. The disease was not seen in children with active streptococcal cutaneous infections. Disease frequency was highest in the poorest areas and families, a finding that persisted over time. The programme was associated with a progressive decline in the frequency of rheumatic fever: final reduction of 78% in Martinique and 74% in Guadeloupe. The frequency of carditis also fell. Apart from two outbreaks in one hospital, the frequency of acute glomerulonephritis also declined; 31% of cases had had sore throat, while 56% had skin infections. The cost of the programme during the 4 most intensive years was FFr 250 000 (US$ 44 500) in each island. The cost of childhood rheumatic fever, excluding late sequelae, was initially (in 1982) about FFr 7.8 million (US$ 1426 000). The cost fell to an average of Ffr 550 000 (US$ 100 000) per year in 1991-92. INTERPRETATION: A rapid decline in rheumatic fever incidence was achieved at modest cost. Such a programme needs to be continued because of the risk of disease resurgence.

Adolescent↗
PubMedDate not supplied

[Rheumatic fever in childhood--today].

Acute rheumatic fever in the young: a review of historical land marks and the current status of rheumatic fever are discussed. The follows are presented here: prevent-day epidemiology; the role of group A streptococcus and the reappearance of "rheumatogenic" serotypes; the host's susceptibility and the tantalizing possibility of a genetic basis; the basis of autoimmune pathogenesis (so-called molecular mimicry); the increasing diagnostic difficulties and the critical review of Jones criteria; the reassessment of primary prevention and the couvent possibility of a streptococcal vaccine.

Child↗
PubMedDate not supplied

[The system of complement in active rheumatic fever].

Pathogenesis of inflammation in acute rheumatic fever is still unknown. There is humoral immune response against streptococcal products and streptococcal infection plays a role in etiopathogenesis. When inflammation is due to humoral immune mechanisms, the serum Complement system is the most important mediator. We studied functional aspects of the Complement system in nine patients suffering acute rheumatic fever, all of them with clear humoral immune response against streptococcus. We could not show any abnormalities in Complement. Probably, inflammation during acute rheumatic fever depends on Complement independent mechanisms.

Complement System Proteins↗
PubMed2000

Cumulative incidence of rheumatic fever in an endemic region: a guide to the susceptibility of the population?

Aboriginal Australians in northern Australia are subject to endemic infection with group A streptococci, with correspondingly high rates of acute rheumatic fever and rheumatic heart disease. For 12 communities with good ascertainment, the estimated lifetime cumulative incidence of acute rheumatic fever was approximately 5.7%, whereas over the whole population, with less adequate ascertainment, the cumulative incidence was only 2.7%. The corresponding prevalences of established rheumatic heart disease were substantially less than the cumulative incidences of acute rheumatic fever, at least in part because of poor ascertainment. The cumulative incidence of acute rheumatic fever estimates the proportion of susceptible individuals in endemically exposed populations. Our figures of 2.7-5.7% susceptible are consistent with others in the literature. Such comparisons suggest that the major part of the variation in rheumatic fever incidence between populations is due to differences in streptococcal exposure and treatment, rather than to any difference in (genetic) susceptibility.

Acute Disease↗
PubMed1980

Plasmapheresis in treatment of rheumatic fever.

1. Three cases of rheumatic fever were treated with plasmapheresis. Improvement of abnormal clinical and laboratory findings of the patients was obtained by this procedure. 2. High levels of immune complexes, observed in the sera of patients with rheumatic fever, reduced markedly following plasmapheresis.

Adolescent↗
PubMed2000

Rheumatic fever--is it still a problem?

The incidence of rheumatic fever has declined in industrialized countries since the 1950s and now has an annual incidence of around 0.5 cases per 100,000 children of school age. In developing countries it remains an endemic disease with annual incidences ranging from 100 to 200 per 100,000 school-aged children and is a major cause of cardiovascular mortality. Interest in the pathogenesis of rheumatic fever was rekindled by outbreaks in the USA (1985-1987) and the rare cases still seen in industrialized countries. The current concept is that the disease results from the host's poorly adapted autoimmune response to group A beta-haemolytic streptococci. The risk of developing rheumatic fever following untreated tonsillopharyngitis is 1% in the civilian population. Knowledge of virulence factors has been greatly enriched by progress in molecular biology. One of the key elements is protein M, a surface protein on the bacterial wall which carries specific epitopes. Several serotypes which lead to rheumatic fever have been recognized among more than 80 identified serotypes. However, the reason why specific strains within a given serotype have increased rheumatogenic virulence remains unknown. The causal strain adheres to the oral and pharyngeal cells and then releases its degradation products. These products present antigenic determinants which cross-react with certain human tissues, particularly in cardiac valve tissue and myocardium. Diagnosis is now difficult owing to the low incidence. Late diagnosis can have serious consequences and acute rheumatic fever is a therapeutic emergency requiring immediate antibiotic and anti-inflammatory treatment. In most of Europe there is tacit agreement that all cases of pharyngitis and tonsillitis should be treated with antibiotics without identification of the causal agent despite the fact that only about 20% of the cases are caused by group A beta-haemolytic streptococci, and could lead to rheumatic fever.

Developed Countries↗
PubMed1991

Antibodies to N-acetylglucosamine and heparin in acute and remission phases of rheumatic fever.

The etiology of acute rheumatic fever (ARF) is believed to involve an immunological response to group A streptococcal antigens. Antibodies to group A carbohydrate (A-CHO) have been reported in ARF and rheumatic heart disease patients. As N-acetylglucosamine (GlcNAc) units form the major immunodominant regions in A-CHO antigens, we investigated levels of antibodies to GlcNAc and heparin (with repeated sequences of GlcNAC) in rheumatic fever (RF) patients. Serum samples from 26 acute cases (ARF), 18 remission cases and 17 normal healthy subjects were analyzed for IgG and IgM levels of antibodies to GlcNAc and heparin. High titres of IgG antibodies to heparin and GlcNAc were observed in the ARF group in comparison with controls (p less than 0.0025 and 0.0125 respectively). There was no difference in the levels of IgM antibodies. Remission group demonstrated low titres of IgG to heparin and GlcNAc (p less than 0.01 and 0.0125 respectively) in comparison with ARF group. Heparin antibodies of IgM class was comparatively lower in remission group (p less than 0.005). While the role of these antibodies in different phases of RF needs to be investigated, we conclude that GlcNAc antibodies do not play any role in the pathogenesis of RF or rheumatic heart disease.

Acetylglucosamine↗
PubMed1986

Association of class II human histocompatibility leukocyte antigens with rheumatic fever.

The association of class I and II HLA antigens with rheumatic fever and its manifestations was examined in 72 patients, including 48 blacks and 24 Caucasians. No significant association was found between class I antigens and rheumatic fever. In contrast, HLA-DR2 and HLA-DR4 phenotypes were encountered in a significantly higher frequency in black and Caucasian patients with rheumatic fever, respectively, compared with the control populations (P less than 0.005). The most significant association (P less than 0.005) of these DR antigens with a major manifestation of rheumatic fever was found for mitral insufficiency. In addition, a significant association was encountered between persistent elevation of antibody to the group A streptococcal carbohydrate and HLA-DR4 in Caucasian patients (P less than 0.04) or HLA-DR2 in the black patients (P less than 0.001). The frequency of HLA-DR2/4 heterozygotes among patients with rheumatic fever did not differ significantly from controls. These findings support the concept of a genetically determined susceptibility to rheumatic fever and, particularly, to rheumatic heart disease. The association of the clinical manifestations of rheumatic fever and the immune hyperresponsiveness to a streptococcal antigen could be ascribed to a disease-associated immune-response gene which is in linkage disequilibrium with the DR2 and DR4 alleles of HLA-DR locus on chromosome six.

Alleles↗
PubMed1983

Clinical-echocardiographic correlations in acute rheumatic fever.

Thirty-three children with acute rheumatic fever were studied using echocardiography to characterize heart involvement in this disease. Among 26 subjects with a first episode of acute rheumatic fever, 18 had a clinical diagnosis of carditis and six had heart failure. Heart failure usually resulted from valvular incompetence rather than from myocardial failure in these patients. Conversely, among seven subjects with recurrent rheumatic fever, five had a clinical diagnosis of carditis and four had heart failure. Severe left ventricular dysfunction noted on echocardiography probably contributed significantly to the appearance of heart failure in two of these four subjects. Ten patients were initially believed not to have carditis: a diagnosis of mitral valvulitis was made in two of these ten on the basis of the results of the echocardiographic examination. Echocardiography, which provides important information on the cardiac status of patients with acute rheumatic fever, may help in assessing the prognosis and may be useful in the therapy of these patients.

Adolescent↗
PubMedDate not supplied

[Levels of total hemolytic complement, C3, C4 and antibodies against the myocardium in rheumatic fever].

The levels of the hemolytic complement (UH 50%), C3, C4 and the antibodies against myocardium and against the antigenic fractions of myocardium precipitated with ammonium sulphate were studied in 8 patients with active rehumatic fever (ARF), 28 with inactive rheumatic fever (IRF) and 26 people without cardiopaties (NI). The UH 50% was low in 2 out of 36 patients with rheumatic fever (RF). C3 was normal and C4 low in 12.5% of the ARF patients. C3 had subnormal values in 25% and C4 in 33% of IRF patients, this last value had a stadistic significant decrease with respect to the values of C4 in normal people. The 36 patients with RF had antibodies against the myocardium and also against the heart antigenic fractions precipitated with 10% ammonium sulphate. 11.5% of the normal group had anti-myocardial antibodies and none had antibodies against the fractions. The levels of anti-streptolysin-O and C-reactive protein were higher in the ARF group than in the patients with IRF or the normal people. The participation of the hemolytic complement, the anti-myocardium antibodies, the anti-streptococcus antibodies and the cytophilic activity in the etiopathogeny of rheumatic fever is discussed.

Autoantibodies↗
PubMedDate not supplied

Coxsackie virus infections in rheumatic fever.

The close relationship between Group A beta Hemolytic Streptococci (GABS) and rheumatic fever is a well established one. However, the concept of the streptococcus as the sole etiologic agent of the rheumatic heart disease (RHD) has been challenged over the past years. Since coxsackievirus group B (CVB) has long been proposed as a cause of acquired valvular disease simulating rheumatic fever, we attempted in this study to document infections with this group of viruses in patients with rheumatic fever. We obtained blood samples from 106 patients with old (quiescent) rheumatic fever/rheumatic heart disease [group I], 94 patients with acute rheumatic fever (ARF) [group II], and 74 normal matched controls. We tested for the presence of neutralizing antibodies to the 6 serotypes of CVB by a micro neutralization test. We have found that infection with CVB, especially types B2 and B4, was common in the studied population. Forty-two percent of normal individuals had evidence of infection with any of the 6 serotypes of CVB. Patients of group I had significantly more frequent infections with CVB 2. Patients in group II had significantly more frequent infections with CVB 2 and CVB 6. There was no clear correlation between such infections and the clinical course of rheumatic fever. There was no difference in the incidence of CVB infections between patients with definite ARF, and patients with suspected ARF. We set a low order association between rheumatic fever and infection with CVB types B2 and B6. We emphasize the importance of pursuing the investigation of the role of CVB in relation to RHD.

Adolescent↗
PubMed1984

[Brucellosis and rheumatic fever].

Brucellosis and Acute Rheumatic Fever can not be verified by only clinical manifestations and the pattern of joint involvement. Four patients presented below had high fever, sweats, severe arthralgia and swelling of one or multiple joints, elevated sedimentation rate and positive C - reactive protein test and even leukocytosis. Therefore they were treated with anti - rheumatic drugs for 4 to 7 days after onset till brucellosis was considered or its specific tests became positive.

Adolescent↗
PubMed1989

Reappearance of rheumatic fever.

Even though incompletely understood, much of the information about the epidemiology and pathogenesis of rheumatic fever has become available only in the last few decades, a time when there have been significant fluctuations in rheumatic fever and rheumatic heart disease in the United States. The precise roles of the bacteria, the human host, and the environment and their interrelationships require more study. Determining their roles and defining the pathogenesis can have important practical application. If one could identify a susceptible population, if one could identify the serotypes and/or strains of group A streptococci that are more dangerous (rheumatogenic) and if one could identify the reason for an abnormal immune response, vaccines might be made with specific protective components of the group A streptococci and administered only to known susceptible individuals. Providing optimal public health programs to control a disease that still is a major problem in a large segment of the world's population is the goal. It is quite clear from the resurgence of acute rheumatic fever in the United States in the mid-1980s that antibiotics alone are not the answer to rheumatic fever control. If antibiotics are not completely effective in a country such as the United States, they cannot be expected to be effective in many of the developing countries of the world where primary health care delivery is even more difficult. Intensified efforts to understand the pathogenetic mechanisms responsible for the development of rheumatic fever should be undertaken. In the meantime, the preventive methods that are available should be vigorously applied.

Developing Countries↗
PubMed1981

Rheumatic fever in Nigerian children: a prospective study.

The initial attack of acute rheumatic fever is hardly ever diagnosed in our environment. Most cases of acute rheumatic fever are seen during recurrent illness when cardiac damage is already severe and death from cardiac failure common. In the absence of effective primary prophylaxis against rheumatic fever in the foreseeable future it is important to find every case of acute rheumatic fever at the first attack, as on this would depend effective secondary prophylaxis and, hopefully, reduction of the morbidity and mortality rates. A prospective study was set up to achieve this aim. All cases suspected of having rheumatic fever among children seen at the Lagos University Teaching Hospital over a period of five years were subjected to the Jones' diagnostic criteria for diagnosis, and grouped into "Initial illness" and "Recurrent illness" groups. Twenty-one cases of acute rheumatic fever were diagnosed during the period, out of which ten (47.6%) were in the initial stage of the illness. There was a direct relationship between the severity of cardiac involvement and delay in recognition of the condition. It was concluded that efforts aimed at prompt recognition of the initial illness would be rewarding in minimising cardiac morbidity and mortality.

Child↗