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PubMed2001

Rheumatic fever in a high incidence population: the importance of monoarthritis and low grade fever.

AIMS: To describe the clinical features of rheumatic fever and to assess the Jones criteria in a population and setting similar to that in many developing countries. METHODS: The charts of 555 cases of confirmed acute rheumatic fever in 367 patients (97% Aboriginal) and more than 200 possible rheumatic fever cases from the tropical "Top End" of Australia's Northern Territory were reviewed retrospectively. RESULTS: Most clinical features were similar to classic descriptions. However, monoarthritis occurred in 17% of confirmed non-chorea cases and 35% of unconfirmed cases, including up to 27 in whom the diagnosis was missed because monoarthritis is not a major manifestation. Only 71% and 25% of confirmed non-chorea cases would have had fever using cut off values of 38 degrees C and 39 degrees C, respectively. In 17% of confirmed non-chorea cases, anti-DNase B titres were raised but antistreptolysin O titres were normal. Although features of recurrences tended to correlate with initial episodes, there were numerous exceptions. CONCLUSIONS: Monoarthritis and low grade fever are important manifestations of rheumatic fever in this population. Streptococcal serology results may support a possible role for pyoderma in rheumatic fever pathogenesis. When recurrences of rheumatic fever are common, the absence of carditis at the first episode does not reliably predict the absence of carditis with recurrences.

Adolescent↗
PubMed2006

Low rates of streptococcal pharyngitis and high rates of pyoderma in Australian aboriginal communities where acute rheumatic fever is hyperendemic.

BACKGROUND: Acute rheumatic fever is a major cause of heart disease in Aboriginal Australians. The epidemiology differs from that observed in regions with temperate climates; streptococcal pharyngitis is reportedly rare, and pyoderma is highly prevalent. A link between pyoderma and acute rheumatic fever has been proposed but is yet to be proven. Group C beta-hemolytic streptococci and group G beta-hemolytic streptococci have also been also implicated in the pathogenesis. METHODS: Monthly, prospective surveillance of selected households was conducted in 3 remote Aboriginal communities. People were questioned about sore throat and pyoderma; swab specimens were obtained from all throats and any pyoderma lesions. Household population density was determined. RESULTS: From data collected during 531 household visits, the childhood incidence of sore throat was calculated to be 8 cases per 100 person-years, with no cases of symptomatic group A beta-hemolytic streptococci pharyngitis. The median point prevalence for throat carriage was 3.7% for group A beta-hemolytic streptococci, 0.7% for group C beta-hemolytic streptococci, and 5.1% for group G beta-hemolytic streptococci. Group A beta-hemolytic streptococci were recovered from the throats of 19.5% of children at some time during the study. There was no seasonal trend or correlation with overcrowding. Almost 40% of children had pyoderma at least once, and the prevalence was greatest during the dry season. In community 1, the prevalence of pyoderma correlated with household crowding. Group C and G beta-hemolytic streptococci were rarely recovered from pyoderma lesions. CONCLUSIONS: These data are consistent with the hypothesis that recurrent skin infections immunize against throat colonization and infection. High rates of acute rheumatic fever were not driven by symptomatic group A beta-hemolytic streptococci throat infection. Group G and C beta-hemolytic streptococci were found in the throat but rarely in pyoderma lesions.

Adolescent↗
PubMed1989

Recurrence of rheumatic fever after valve replacement.

While recurrence of rheumatic fever is common, recurrence after valve replacement has not been reported. A 15-year-old Ethiopian boy returned from America after mitral valve replacement in May 1986. He did not take antibiotic prophylaxis and, in February 1987, had recurrent rheumatic fever. The literature on recurrence of rheumatic fever and prophylaxis is reviewed. Monthly injections of benzathine penicillin have been shown to be the most effective drug to prevent rheumatic fever recurrences. It is recommended that patients with rheumatic heart disease in the developing world should take prophylaxis for life.

Adolescent↗
PubMed2004

Acute rheumatic fever in children: recognition and treatment.

Acute rheumatic fever (ARF) is an inflammatory disease of the heart, joints, CNS, and subcutaneous tissue that develops after a pharyngeal infection by one of the group A beta-hemolytic streptococci (Streptococcus pyogenes). The pathogenesis of the disease remains an enigma and specific treatment is not available, yet prevention of initial and recurrent attacks is possible by penicillin treatment. Rheumatic fever is especially important because of the heart disease that usually ensues; as succinctly stated by Lasegue many years ago, rheumatic fever "licks the joints and bites the heart", a statement that holds true today. Rheumatic fever is no longer a significant health problem in most socioeconomically advanced countries but it still causes 25-40% of all cardiovascular disease in the world, including tropical countries where it was once believed to be rare. In many countries it causes more hospital admissions than congenital heart conditions.ARF and rheumatic heart disease - with high associated morbidity, cost, and mortality - are largely preventable. Importantly, recurrences of rheumatic fever with their increased likelihood of more severe carditis are inexpensively preventable. Primary prevention has been achieved innovatively in some countries, for example, Costa Rica, and more conventionally in some developed countries. Treatment of the acute episode controls symptoms and may limit cardiac damage.

Acute Disease↗
PubMed2005

Two unusual presentations of acute rheumatic fever.

Patients with acute rheumatic fever sometimes present with atypical signs and symptoms. In these circumstances, the Jones criterions may not be sufficient to make a clinical diagnosis. We describe here two patients with unusual presentations, highlighting that, both in regions where the disease is endemic, or where it is seen only sporadically, physicians should be more alert and careful in making the diagnosis.

Abdominal Pain↗
PubMed1975

Acute rheumatic fever in adults.

Acute rheumatic fever (ARF) in 53 adults was characterized by a severe, febrile migratory polyarthritis involving primarily large joints in the lower extremities, with evidence of an antecedent streptococcal infection. Carditis, present in only eight (15%) of the adults, was mild and transient. The characteristic abnormality in laboratory findings was an erythrocyte sedimentation rate (Westergren) greater than 100 mm/hr. Response to high-dose aspirin therapy was prompt and dramatic in all patients. Mild andevanescent abnormalities of both renal function and hepatic function (not aspirin-mediated) were detected in 51% and 64%, respectively. A common disorder in San Antonio, ARF has distinctive symptoms. It can be readily diagnosed and promptly treated. In the adult, it is almost exclusively a syndrome of events severe but transient in the joints, and mild and transient in the heart, kidneys, and liver.

Acute Disease↗
PubMed1984

M-associated protein antibodies in patients with rheumatic fever.

Sequential serum samples obtained from 50 rheumatic fever subjects and from control individuals matched for time, age and geographical location were tested for antibodies against the M-associated protein antigens, MAP I and MAP II. Antibody titres were determined by the complement fixation test with a partially-purified extract of Streptococcus pyogenes serotype M30 as the MAP I antigen and an acid extract of serotype M48 as the MAP II antigen. Titres of MAP I antibody exceeded those of MAP II antibody in all but six rheumatic fever subjects. Anti-MAP I titres in excess of 40 were significantly more common in rheumatic fever subjects than in matched controls (p less than 0.001) or matched subjects with a diagnosis of acute post-streptococcal glomerulonephritis (p less than 0.01). Peak MAP I titres were present at the time of admission to hospital in the sera of 40 of the 50 rheumatic fever subjects. In the remainder peak titres occurred within 10 days. Antibody titres were maintained for a mean of 10.3 weeks before declining. Changes in MAP antibody titres were independent of changes in antistreptolysin O and anti-DNAase B titres. Normal children aged between 6 and 15 had higher MAP antibody titres than 2-5-year-old children. Rheumatic fever subjects had significantly higher mean titres of MAP I antibody than matched controls in each age group.

Acute Disease↗
PubMed1975

Rheumatic fever in adult patients.

A study of rheumatic fever in adult patients (diagnosed according to the Jones revised criteria; Circulation 36: 664, 1965) was performed by examining 26 patients during the acute phase of the disease, and by re-examining 22 of them from 6 months to 64 months later (mean 33 months). Polyarthritis and carditis were the most common major manifestations. 23 patients had polyarthritis and 3 monoarthritis. 18 patients had signs of acute cardiac involvement. Carditis appeared to be rather benign: at the acute stage no patient developed congestive heart failure or any other serious complication. Five patients had erythema marginatum, but we saw no chorea or subcutaneous nodules. Of the 22 patients examined in the follow-up study, 4 had persistent signs of cardiac involvement and 15 showed chronic joint manifestations. Yersinia enterocolitica infection was by far the most difficult differential diagnostic problem, since polyarthritis and carditis associated with this enteric infection were very similar to those in patients with rheumatic fever. Current literature on rheumatic fever and the results of this series suggest that the diagnostic criteria of rheumatic fever (Jones) should be re-evaluated, at least in industrial countries.

Acute Disease↗
PubMed1991

NADPH oxidase activity in the monocytes and neutrophils of patients with rheumatic fever.

The enzyme NADPH oxidase is involved in the production of oxygen free radicals. We measured its activity in neutrophils and monocytes obtained from patients with acute rheumatic fever, chronic rheumatic heart disease, acute streptococcal pharyngitis and normal controls. Follow up studies were made at 15 days, 3 months and 6 months. Streptococcal membrane antigen, carbohydrate antigens and latex were used to stimulate the oxidative activity in the neutrophils and monocytes. These three agents caused a significant increase in the enzyme activity of the phagocytes of patients with acute rheumatic fever and chronic rheumatic heart disease (p less than 0.001) but not in acute pharyngitis. Maximal NADPH oxidase enzyme activity was observed in patients with acute rheumatic fever. During the follow-up, there was a significant decline in the enzymatic activity in patients with acute rheumatic fever but not in those with chronic rheumatic heart disease. Enzymatic activity was greater when the phagocytic cells were triggered with membrane as compared to carbohydrate antigen and latex in all the groups and at all intervals. The enzymatic response of neutrophils and monocytes was similar although the magnitude of the NADPH oxidase activity was significantly higher in neutrophils than in monocytes.

Adult↗
PubMed1987

Pneumonia associated with acute rheumatic fever.

Pulmonary involvement in acute rheumatic fever is rare. Clinical and laboratory findings in rheumatic pneumonia are non-specific. Most of the cases of rheumatic pneumonia described in recent years have had a fulminant course often resulting in death. Autopsy findings are suggestive of but not specific for rheumatic pneumonia. In this article a case of pneumonia associated with acute rheumatic fever is described. Pneumonia and carditis occurred simultaneously in a 10-year-old boy treated without steroids, which resulted in recovery. The clinical spectrum of rheumatic pneumonia can range from mild to fulminant.

Acute Disease↗
PubMed1956

Rheumatic fever in Southern California; problems related to diagnosis.

Rheumatic fever occurs in native of Southern California and is a cause of death. The incidence of streptococcosis in Los Angeles is approximately equal to that in three other major cities in the United States where rheumatic fever is known to occur commonly. Manifestations of rheumatic fever may range from mild to severe. It is suggested that a greater percentage of patients in Southern California have symptoms of rheumatic fever that are more mild. Differentiation between prolonged, uncomplicated streptococcosis and rheumatic fever is a major problem. The judicious use of a battery of tests, acute phase reactants, on the same blood sample will frequently help to establish the diagnosis in borderline situations so common to Southern California.

California↗
PubMedDate not supplied

Autoimmune mechanisms in the pathogenesis of rheumatic fever.

The etiologic agent of acute rheumatic fever is the group A streptococcus; however, its role in the pathogenesis of this disease is not well understood. Epidemiologic and immunologic evidence suggests that there is a population at risk and that the nature of the host response to streptococcal antigens and the physicochemical nature of the streptococcal antigens all play a significant role in determining the natural history of the disease process. Furthermore, the genetic control of the interaction of the host with the streptococci is clearly involved in a set of events--as yet obscure--that result in acute rheumatic fever. Neither antibody-mediated nor cell-mediated hypersensitivity reactions have been demonstrated in vivo or in vitro that wholly reproduce the characteristics of this disease. Additional studies of the regulation of the immune response and of human immunogenetics are essential for gaining further insight into the pathogenesis of acute rheumatic fever.

Animals↗
PubMedDate not supplied

[Rheumatic fever in the 80s].

Two contradictory changes related to rheumatic fever existed in the 80's. A constant, almost dramatic fall of rheumatic fever incidence occurred in the second half of the 80's. This fact was explained by improvement of living conditions and way of life, as well as by a developed health service. But, unexpectedly, a sudden rise of rheumatic fever incidence occurred in many states of the United States of America in that period. The medical experts were reminded that similar danger might also be expected in other countries. This increase of rheumatic fever incidence was followed by severe forms of the disease. In the 80's intensive epidemiologic, microbiologic and molecular researches of the beta haemolytic streptococcus A and parallel genetic investigations of the population with rheumatic fever, were undertaken. The aim of these studies was to discover the rheumatogenic factor in the streptococcus and to differentiate it from the immunogenic one, as well as to detect the genetic factor in the sick people. In this way these findings would be the best contribution to the knowledge of the pathogenesis of rheumatic fever and to a more efficacious protection (vaccination).

Humans↗