Acute Rheumatic Fever

2/20/2005

 

Question:  What is the clinical presentation of acute rheumatic fever in the current day?

 

<1> PMID: 16005340

Journal Article. Review.

Lancet. 366(9480):155-68, 2005 Jul 9-15.

Acute rheumatic fever.[see comment]. [Review] [204 refs]

<2> PMID: 15103230

Journal Article. Review.

International Archives of Allergy & Immunology. 134(1):56-64, 2004 May.

Rheumatic fever: from sore throat to autoimmune heart lesions. [Review] [55 refs]

<3> PMID: 15050943

Journal Article. Review.

The Lancet Infectious Diseases. 4(4):240-5, 2004 Apr.

Acute rheumatic fever: a chink in the chain that links the heart to the throat?[see comment]. [Review] [82 refs]

<4> PMID: 14743048

Journal Article.

Pediatric Infectious Disease Journal. 23(1):56-61, 2004 Jan.

Molecular characterization of Streptococcus pyogenes isolates collected during periods of increased acute rheumatic fever activity in Utah.

<5> PMID: 12735424

Case Reports. Journal Article. Review.

Netherlands Journal of Medicine. 61(2):57-61, 2003 Feb.

Cardiac failure following group A streptococcal infection with echocardiographically proven pericarditis, still insufficient arguments for acute rheumatic fever: a case report and literature update. [Review] [27 refs]

<6> PMID: 12417554

Congresses. Guideline. Practice Guideline.

Circulation. 106(19):2521-3, 2002 Nov 5.

Proceedings of the Jones Criteria workshop.

<7> PMID: 12387812

Journal Article. Review.

Best Practice & Research in Clinical Rheumatology. 16(3):481-94, 2002 Jul.

Rheumatic fever and post-streptococcal arthritis. [Review] [88 refs]

<8> PMID: 11564377

Journal Article. Review.

Current Rheumatology Reports. 3(5):445-52, 2001 Oct.

Rheumatic fever. [Review] [40 refs]

<9> PMID: 11512086

Historical Article. Journal Article. Review.

Clinical Infectious Diseases. 33(6):806-14, 2001 Sep 15.

Rheumatic fever in the 21st century. [Review] [66 refs]

<10> PMID: 10915082

Clinical Trial. Journal Article. Randomized Controlled Trial.

Journal of Infectious Diseases. 182(2):509-16, 2000 Aug.

Short-course antibiotic treatment of 4782 culture-proven cases of group A streptococcal tonsillopharyngitis and incidence of poststreptococcal sequelae.

<11> PMID: 10657336

Case Reports. Journal Article. Review.

BMJ. 320(7231):362-5, 2000 Feb 5.

Lesson of the week: difficulties in diagnosing acute rheumatic fever-arthritis may be short lived and carditis silent. [Review] [21 refs]

<12> PMID: 9877185

Editorial. Review.

Journal of Medical Microbiology. 47(8):655-7, 1998 Aug.

The changing face of rheumatic fever in the 20th century. [Review] [30 refs]

<13> PMID: 9676165

Journal Article. Review.

Canadian Journal of Cardiology. 14(6):807-10, 1998 Jun.

An easy method for detection of rheumatic antigen(s) in rheumatic fever/rheumatic heart disease patients by dot-ELISA. [Review] [20 refs]

<14> PMID: 9661932

Journal Article. Review.

Journal of Infection. 36(3):249-53, 1998 May.

Acute rheumatic fever. [Review] [12 refs]

<15> PMID: 9614827

Case Reports. Journal Article. Review.

CMAJ Canadian Medical Association Journal. 158(10):1335-6, 1998 May 19.

The disease that "bites the heart and licks the joints". [Review] [5 refs]

<16> PMID: 9606757

Journal Article. Review.

Rheumatic Diseases Clinics of North America. 24(2):237-59, 1998 May.

Rheumatic fever. The relationships between host, microbe, and genetics. [Review] [69 refs]

<17> PMID: 9287377

Journal Article. Review.

Rheumatic Diseases Clinics of North America. 23(3):545-68, 1997 Aug.

Acute rheumatic fever. Still a challenge. [Review] [144 refs]

<18> PMID: 9093263

Journal Article. Review.

Lancet. 349(9056):935-42, 1997 Mar 29.

Rheumatic fever.[see comment]. [Review] [49 refs]

<19> PMID: 8668953

Editorial. Review.

Scandinavian Journal of Rheumatology. 25(3):127-31; discussion 132-3, 1996.

Towards understanding the pathogenesis of rheumatic fever. [Review] [49 refs]

<20> PMID: 8571986

Journal Article. Review.

American Journal of the Medical Sciences. 311(1):41-54, 1996 Jan.

The reemergence of serious group A streptococcal infections and acute rheumatic fever. [Review] [92 refs]

<21> PMID: 7547107

Journal Article. Review.

Current Opinion in Rheumatology. 7(4):299-305, 1995 Jul.

Rheumatic fever and poststreptococcal reactive arthritis. [Review] [72 refs]

<22> PMID: 7795761

Journal Article.

Archives of Pediatrics & Adolescent Medicine. 149(7):727-32, 1995 Jul.

Guideline maintenance and revision. 50 years of the Jones criteria for diagnosis of rheumatic fever.[see comment].

<23> PMID: 7993713

Journal Article. Review.

Current Opinion in Rheumatology. 6(5):537-43, 1994 Sep.

Infectious arthropathies and other rheumatologic manifestations of infectious diseases. [Review] [91 refs]

<24> PMID: 8107744

Journal Article. Review.

New England Journal of Medicine. 330(11):769-74, 1994 Mar 17.

Polyarthritis and fever. [Review] [52 refs]

<25> PMID: 8173648

Journal Article. Review.

Bulletin on the Rheumatic Diseases. 42(7):5-7, 1993 Nov.

Rheumatic fever: new insights into an old disease. [Review] [23 refs]

<26> PMID: 8502775

Journal Article. Review.

Rheumatic Diseases Clinics of North America. 19(2):333-50, 1993 May.

Acute rheumatic fever. [Review] [105 refs]

<27> PMID: 8416130

Journal Article. Review.

Cardiovascular Clinics. 23:3-23, 1993.

Acute rheumatic fever. [Review] [102 refs]

<28> PMID: 1344137

Journal Article. Review.

Heart Disease & Stroke. 1(6):391-4, 1992 Nov-Dec.

The resurgence of rheumatic fever. [Review] [9 refs]

<29> PMID: 1343439

Journal Article. Review.

Transactions of the American Clinical & Climatological Association. 104:15-23; discussion 23-5, 1992.

Acute rheumatic fever. [Review] [19 refs]

<30> PMID: 1480739

Journal Article. Review.

Quarterly Journal of Medicine. 84(305):641-58, 1992 Sep.

Rheumatic fever and rheumatic heart disease: the current status of its immunology, diagnostic criteria, and prophylaxis. [Review] [167 refs]

<31> PMID: 1404745

Guideline. Journal Article. Practice Guideline.

JAMA. 268(15):2069-73, 1992 Oct 21.

Guidelines for the diagnosis of rheumatic fever. Jones Criteria, 1992 update. Special Writing Group of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young of the American Heart Association.[see comment][erratum appears in JAMA 1993 Jan 27;269(4):476].

 

 

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16005340.ui or 15103230.ui or 15050943.ui or 14743048.ui or 12735424.ui or 12417554.ui or 12387812.ui or 11564377.ui or 11512086.ui or 10915082.ui or 10657336.ui or 9877185.ui or 9676165.ui or 9661932.ui or 9614827.ui or 9606757.ui or 9287377.ui or 9093263.ui or 8668953.ui or 8571986.ui or 7547107.ui or 7795761.ui or 7993713.ui or 8107744.ui or 8173648.ui or 8502775.ui or 8416130.ui or 1344137.ui or 1343439.ui or 1480739.ui or 1404745.ui or 1518750.ui or 1503878.ui or 1739046.ui or 1793538.ui or 1941847.ui or 1941846.ui or 1914256.ui or 1870652.ui or 1870080.ui or 4901868.ui

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PubMed recovery search string (copy and paste into PubMed search entry panel)

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16005340[PMID] OR 15103230[PMID] OR 15050943[PMID] OR 14743048[PMID] OR 12735424[PMID] OR 12417554[PMID] OR 12387812[PMID] OR 11564377[PMID] OR 11512086[PMID] OR 10915082[PMID] OR 10657336[PMID] OR 9877185[PMID] OR 9676165[PMID] OR 9661932[PMID] OR 9614827[PMID] OR 9606757[PMID] OR 9287377[PMID] OR 9093263[PMID] OR 8668953[PMID] OR 8571986[PMID] OR 7547107[PMID] OR 7795761[PMID] OR 7993713[PMID] OR 8107744[PMID] OR 8173648[PMID] OR 8502775[PMID] OR 8416130[PMID] OR 1344137[PMID] OR 1343439[PMID] OR 1480739[PMID] OR 1404745[PMID] OR 1518750[PMID] OR 1503878[PMID] OR 1739046[PMID] OR 1793538[PMID] OR 1941847[PMID] OR 1941846[PMID] OR 1914256[PMID] OR 1870652[PMID] OR 1870080[PMID] OR 4901868[PMID]

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<1>

Unique Identifier [PMID]: 16005340

Authors: Carapetis JR. McDonald M. Wilson NJ.

Institution: Centre for International Child Health, University of Melbourne Department of Paediatrics and Murdoch Children's Research Institute, Melbourne, Australia. jonathan.carapetis@rch.org.au

Title: Acute rheumatic fever.[see comment]. [Review] [204 refs]

Comments Comment in: Lancet. 2005 Oct 15-21;366(9494):1354-5; PMID: 16226606, Comment in: Lancet. 2005 Oct 15-21;366(9494):1355; author reply 1355-6; PMID: 16226607

 

Source: Lancet. 366(9480):155-68, 2005 Jul 9-15.

Abstract: Acute rheumatic fever (ARF) and its chronic sequela, rheumatic heart disease (RHD), have become rare in most affluent populations, but remain unchecked in developing countries and in some poor, mainly indigenous populations in wealthy countries. More than a century of research, mainly in North America and Europe, has improved our understanding of ARF and RHD. However, whether traditional views need to be updated in view of the epidemiological shift of the past 50 years is still to be established, and improved data from developing countries are needed. Doctors who work in populations with a high incidence of ARF are adapting existing diagnostic guidelines to increase their sensitivity. Group A streptococcal vaccines are still years away from being available and, even if the obstacles of serotype coverage and safety can be overcome, their cost could make them inaccessible to the populations that need them most. New approaches to primary prevention are needed given the limitations of primary prophylaxis as a population-based strategy. The most effective approach for control of ARF and RHD is secondary prophylaxis, which is best delivered as part of a coordinated control programme. [References: 204]

Publication Type: Journal Article. Review.

 

<2>

Unique Identifier [PMID]: 15103230

Authors: Guilherme L. Kalil J.

Institution: Heart Institute-InCor, University of Sao Paulo School of Medicine, Sao Paulo, Brazil. luizagui@usp.br

Title: Rheumatic fever: from sore throat to autoimmune heart lesions. [Review] [55 refs]

 

Source: International Archives of Allergy & Immunology. 134(1):56-64, 2004 May.

Abstract: Molecular mimicry between streptococci and heart components has been proposed as the triggering factor leading to autoimmunity in rheumatic heart disease (RHD). In this review, we present data from cellular autoimmune responses, focusing on the interactions between HLA class II molecules, streptococcal peptides and heart tissue proteins and T-cell receptor (TCR) usage. HLA-DR7DR53 associated with DQ molecules seem to be related with the development of valvular lesions in severe RHD patients. DR7DR53 molecules were also involved in the recognition of an immunodominant M5 peptide in these patients. T cells infiltrating RHD hearts displayed several oligoclonal expansions. Intralesional T-cell clones presenting identical TCR-BVBJ AVAJ and -CDR3 sequences were able to recognize several antigens with little or low homology, showing an intramolecular degenerate pattern of antigen recognition. Peripheral blood mononuclear cells of rheumatic fever (RF) patients produced proinflammatory cytokines, and intralesional mononuclear cells from severe RHD patients produced predominantly Th1-type cytokines. These results illustrate the complex mechanisms leading to heart tissue damage in RF/RHD patients. Copyright 2004 S. Karger AG, Basel [References: 55]

Publication Type: Journal Article. Review.

 

<3>

Unique Identifier [PMID]: 15050943

Authors: McDonald M. Currie BJ. Carapetis JR.

Institution: Infectious Diseases and International Health Unit, Menzies School of Health Research and Charles Darwin University, Darwin, New Territories, Australia. malcolm@menzies.edu.au

Title: Acute rheumatic fever: a chink in the chain that links the heart to the throat?[see comment]. [Review] [82 refs]

Comments Comment in: Lancet Infect Dis. 2004 Nov;4(11):661; PMID: 15522676

 

Source: The Lancet Infectious Diseases. 4(4):240-5, 2004 Apr.

Abstract: Acute rheumatic fever (ARF) remains a major problem in tropical regions, resource-poor countries, and minority indigenous communities. It has long been thought that group A streptococcal (GAS) pharyngitis alone was responsible for acute rheumatic fever; this belief has been supported by laboratory and epidemiological evidence gathered over more than 60 years, mainly in temperate climates where GAS skin infection is uncommon. GAS strains have been characterised as either rheumatogenic or nephritogenic based on phenotypic and genotypic properties. Primary prevention strategies and vaccine development have long been based on these concepts. The epidemiology of ARF in Aboriginal communities of central and northern Australia challenges this view with reported rates of ARF and rheumatic heart disease (RHD) that are among the highest in the world. GAS throat colonisation is uncommon, however, and symptomatic GAS pharyngitis is rare; pyoderma is the major manifestation of GAS infection. Typical rheumatogenic strains do not occur. Moreover, group C and G streptococci have been shown to exchange key virulence determinants with GAS and are more commonly isolated from the throats of Aboriginal children. We suggest that GAS pyoderma and/or non-GAS infections are driving forces behind ARF in these communities and other high-incidence settings. The question needs to be resolved as a matter of urgency because current approaches to controlling ARF/RHD in Aboriginal communities have clearly been ineffective. New understanding of the pathogenesis of ARF would have an immediate effect on primary prevention strategies and vaccine development. [References: 82]

Publication Type: Journal Article. Review.

 

<4>

Unique Identifier [PMID]: 14743048

Authors: Miner LJ. Petheram SJ. Daly JA. Korgenski EK. Selin KS. Firth SD. Veasy LG. Hill HR. Bale JF Jr. The Post-Streptococcal Syndrome Stydy Team.

Institution: Department of Pediatrics, University of Utah Health Sciences Center, Salt Lake City, UT, USA.

Title: Molecular characterization of Streptococcus pyogenes isolates collected during periods of increased acute rheumatic fever activity in Utah.

 

Source: Pediatric Infectious Disease Journal. 23(1):56-61, 2004 Jan.

Abstract: BACKGROUND: Salt Lake City, Utah has seen a continuing resurgence of rheumatic fever (RF) since 1985. METHODS: emm genotyping and multilocus sequence typing of streptococcal isolates from periods of increased RF activity were performed. RESULTS: Multiple genotypes were present during 1985 and 1998, two peak years of RF activity, and in 1992, a year with reduced RF activity. emm3 and emm18.1 were present in 1985 and 1998, but not in 1992. Two other emm types, 12 and L28, were significantly elevated in 1998 (a peak RF year) over 1992 (a non-peak RF year). Allelic profiles for the emm3 and emm18.1 isolates exhibited clonality. CONCLUSIONS: During years of increased RF activity multiple emm types, including emm18.1 and emm3, were circulating in the community. During a year of decreased RF activity, emm3 and emm18.1 genotypes were absent. The clonality of the emm3 and emm18.1 types suggests that specific clones of both types are important in the resurgence of RF during these peak years. Two other genotypes, emm12 and emmL28, may also be associated with the persistence of RF in the Salt Lake City, UT area.

Publication Type: Journal Article.

 

<5>

Unique Identifier [PMID]: 12735424

Authors: Jansen TL. Joosten P. Brouwer J.

Institution: Department of Rheumatology, Medical Centre Leeuwarden, PO Box 888, 8901 BR Leeuwarden, the Netherlands. TJansen@znb.nl

Title: Cardiac failure following group A streptococcal infection with echocardiographically proven pericarditis, still insufficient arguments for acute rheumatic fever: a case report and literature update. [Review] [27 refs]

 

Source: Netherlands Journal of Medicine. 61(2):57-61, 2003 Feb.

Abstract: We recently encountered a 49-year-old female who developed fever due to group A streptococcal (GAS) bacteriaemia spreading to an abscess in the iliac muscle and a bacterial monarthritis of the right knee with a sterile arthritis of her left knee. Treatment was started with a six-week course of intravenous penicillin. She developed a mitral valve insufficiency and pericarditis on the tenth day of admission. In the third week heart failure developed with, on echocardiograph, a high output left ventricular failure without signs of valvulitis or myocarditis. Using a diuretic regimen she was recompensated. Because of the pericarditis with mitral valve insufficiency corticosteroids were given, which had a rapid beneficial effect. A discussion follows on the position of acute rheumatic fever versus post-streptococcal reactive arthritis in this clinical picture and the literature is updated. [References: 27]

Publication Type: Case Reports. Journal Article. Review.

 

<6>

Unique Identifier [PMID]: 12417554

Authors: Ferrieri P. Jones Criteria Working Group.

Title: Proceedings of the Jones Criteria workshop.

 

Source: Circulation. 106(19):2521-3, 2002 Nov 5.

Publication Type: Congresses. Guideline. Practice Guideline.

 

<7>

Unique Identifier [PMID]: 12387812

Authors: Hilario MO. Terreri MT.

Institution: Alameda dos Anapurus, 1370 ap 144, 04087-004 Sao Paulo, Brazil.

Title: Rheumatic fever and post-streptococcal arthritis. [Review] [88 refs]

 

Source: Best Practice & Research in Clinical Rheumatology. 16(3):481-94, 2002 Jul.

Abstract: Rheumatic fever resulting from group A beta-haemolytic Streptococcus infection continues to be a prevalent disease and an important cause of morbidity and mortality in developing countries. Molecular mimicry and CD4 T lymphocytes, interleukins and adhesion molecules play a crucial role in the pathogenesis of this disease. Arthritis, followed by carditis and chorea, are the main manifestations of the disease. Evidence of asymptomatic carditis has been increasing; however, abnormality identified by echo-Doppler evaluation is not considered as a criterion for diagnosis of rheumatic carditis. Benzathine penicillin is still the best therapeutic option for the treatment of streptococcal infection and secondary prophylaxis, due to its efficacy and low cost. [References: 88]

Publication Type: Journal Article. Review.

 

<8>

Unique Identifier [PMID]: 11564377

Authors: Rullan E. Sigal LH.

Institution: Department of Medicine, Division of Rheumatology, UMDNJ-Robert Wood Johnson Medical School, 1 Robert Wood Johnson Place, PO Box 19, MEB-484, New Brunswick, NJ 08903-0019, USA. rullaneu@UMDNJ.EDU

Title: Rheumatic fever. [Review] [40 refs]

 

Source: Current Rheumatology Reports. 3(5):445-52, 2001 Oct.

Abstract: Rheumatic fever is a multisystem inflammatory disease that occurs as a delayed sequel to group A streptococcal pharyngitis. It is less common than it was 50 years ago but is still a major cause of heart disease in developing areas of the world. The relationship between the site of infection, the type of causative organism, and susceptibility of the host is essential in the development of the disease. Its major clinical manifestations include carditis, migratory polyarthritis, chorea, erythema marginatum, and subcutaneous nodules. It can manifest as an acute febrile illness consisting of migratory polyarthritis involving the large joints, as carditis and valvulitis, or as Sydenham's chorea with involvement of the central nervous system. The disorder in its milder form resolves itself without sequelae. Carditis is the condition most associated with increased mortality and morbidity and may be fatal in its severe forms. Penicillin is the most appropriate primary and secondary prophylaxis. Anti- inflammatory agents provide symptomatic relief but do not prevent rheumatic heart disease. [References: 40]

Publication Type: Journal Article. Review.

 

<9>

Unique Identifier [PMID]: 11512086

Authors: Stollerman GH.

Institution: School of Medicine, Boston University, Boston, MA, USA. gstollerman@valley.net

Title: Rheumatic fever in the 21st century. [Review] [66 refs]

 

Source: Clinical Infectious Diseases. 33(6):806-14, 2001 Sep 15.

Abstract: In the first half of the twentieth century, the group A streptococcus (GAS) was established as the sole etiologic agent of acute rheumatic fever (ARF). In the century's latter half, the clinical importance of variation in the virulence of strains of GAS has become clearer. Although still obscure, the pathogenesis of ARF requires primary infection of the throat by highly virulent GAS strains. These contain very large hyaluronate capsules and M protein molecules. The latter contain epitopes that are cross-reactive with host tissues and also contain superantigenic toxic moieties. In settings where ARF has become rare, GAS pharyngitis continues to be common, although it is caused by GAS strains of relatively lower virulence. These strains, however, colonize the throat avidly and stubbornly. Molecularly distinct pyoderma strains may cause acute glomerulonephritis, but they are not rheumatogenic, even though they may secondarily colonize and infect the throat. Guidelines for the diagnosis, treatment, and prevention of GAS pharyngitis and ARF are reviewed with particular reference to the prevalence of the latter in the community. [References: 66]

Publication Type: Historical Article. Journal Article. Review.

 

<10>

Unique Identifier [PMID]: 10915082

Authors: Adam D. Scholz H. Helmerking M.

Institution: Department of Antimicrobial Therapy, Dr. v. Haunersches Children's Hospital, University of Munich, D-80337 Munich, Germany. D.Adam@kk-i. med.uni-muenchen.de.

Title: Short-course antibiotic treatment of 4782 culture-proven cases of group A streptococcal tonsillopharyngitis and incidence of poststreptococcal sequelae.

 

Source: Journal of Infectious Diseases. 182(2):509-16, 2000 Aug.

Abstract: A large-scale study with a 1-year follow-up was performed to compare 10 days of penicillin V with a short-course treatment (5 days) of other oral antibiotics in the treatment of group A beta-hemolytic streptococcus (GABHS) tonsillopharyngitis, to evaluate the efficacy and the incidence of poststreptococcal sequelae. The clinical response rates after completion of therapy were 94.5% in the 5-day group and 93.4% in the penicillin group (P<.001, equivalence test). The GABHS eradication rates were 83.3% in the 5-day group and 84.4% in the penicillin group (P=.022, equivalence test). Poststreptococcal sequelae were rare (5 patients) and did not occur in the context of this study. The efficacy of 5-day antibiotic regimens was equivalent to 10 days of penicillin V, but resolution of clinical symptoms was faster in the 5-day group (P<.001, Fisher's exact test). Recurrent tonsillopharyngitis occurs more frequently after treatment with penicillin (P=.03, Fisher's exact test).

Publication Type: Clinical Trial. Journal Article. Randomized Controlled Trial.

 

<11>

Unique Identifier [PMID]: 10657336

Authors: Williamson L. Bowness P. Mowat A. Ostman-Smith I.

Institution: Department of Rheumatology, Nuffield Orthopaedic Centre, Oxford OX3 7LD. d.williamson@ukonline.co.uk

Title: Lesson of the week: difficulties in diagnosing acute rheumatic fever-arthritis may be short lived and carditis silent. [Review] [21 refs]

 

Source: BMJ. 320(7231):362-5, 2000 Feb 5.

Publication Type: Case Reports. Journal Article. Review.

 

<12>

Unique Identifier [PMID]: 9877185

Authors: Stollerman GH.

Title: The changing face of rheumatic fever in the 20th century. [Review] [30 refs]

 

Source: Journal of Medical Microbiology. 47(8):655-7, 1998 Aug.

Publication Type: Editorial. Review.

 

<13>

Unique Identifier [PMID]: 9676165

Authors: Kumar D. Kaur S. Grover A. Singal PK. Ganguly NK.

Institution: Institute of Cardiovascular Sciences, Faculty of Medicine, University of Manitoba, Winnipeg. dkumar@sbrc.umanitoba.ca

Title: An easy method for detection of rheumatic antigen(s) in rheumatic fever/rheumatic heart disease patients by dot-ELISA. [Review] [20 refs]

 

Source: Canadian Journal of Cardiology. 14(6):807-10, 1998 Jun.

Abstract: BACKGROUND: Various monoclonal antibodies developed against human B cell alloantigen have different positivity in different population groups around the world. Thus, monoclonal antibody D8/17, found to be 100% specific for rheumatic fever/rheumatic heart disease (RF/RHD) patients from New York, identified only 62% to 68% in the north Indian population. PATIENTS AND METHODS: A battery of monoclonal antibodies against B cell alloantigen was developed in Indian RF/RHD patients. A total of 50 patients and 25 controls were studied. RESULTS: These antibodies, named PG-12A, -13A and -20A, demonstrate more specificity in north Indian patients. In dot-ELISA, these antibodies correctly show the presence of the marker in 84% of RHD and 90% of recurrence of rheumatic activity patients. CONCLUSIONS: It is suggested that different alloantigens are expressed in the north Indian population. This standardized dot-ELISA is low cost and simple to use, and has a very high percentage of sensitivity, specificity and positive predictive value for this population. [References: 20]

Publication Type: Journal Article. Review.

 

<14>

Unique Identifier [PMID]: 9661932

Authors: Hutchison SJ.

Institution: Cardiology Department, District NHS Trust, Nevill Hall Hospital, Abergavenny, UK.

Title: Acute rheumatic fever. [Review] [12 refs]

 

Source: Journal of Infection. 36(3):249-53, 1998 May.

Publication Type: Journal Article. Review.

 

<15>

Unique Identifier [PMID]: 9614827

Authors: Hoey J.

Title: The disease that "bites the heart and licks the joints". [Review] [5 refs]

 

Source: CMAJ Canadian Medical Association Journal. 158(10):1335-6, 1998 May 19.

Publication Type: Case Reports. Journal Article. Review.

 

<16>

Unique Identifier [PMID]: 9606757

Authors: Gibofsky A. Kerwar S. Zabriskie JB.

Institution: Hospital for Special Surgery, Cornell University Medical College, New York, New York, USA.

Title: Rheumatic fever. The relationships between host, microbe, and genetics. [Review] [69 refs]

 

Source: Rheumatic Diseases Clinics of North America. 24(2):237-59, 1998 May.

Abstract: 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. [References: 69]

Publication Type: Journal Article. Review.

 

<17>

Unique Identifier [PMID]: 9287377

Authors: da Silva NA. Pereira BA.

Institution: Department of Pediatrics, Faculdade de Medicina, Universidade Federal de Goias, Goitania-Goias, Brazil.

Title: Acute rheumatic fever. Still a challenge. [Review] [144 refs]

 

Source: Rheumatic Diseases Clinics of North America. 23(3):545-68, 1997 Aug.

Abstract: At the end of the 20th century, after an apparent decline, acute rheumatic fever (ARF) now constitutes a great challenge for developed and developing countries. It is caused by a group A beta-hemolytic Streptococcus upper airways infection, but the exact pathogenetic mechanisms are not yet clear. The role of the immune system in the pathogenesis of ARF is understood better than genetic host factors. ARF can mimic many other diseases, and the diagnosis is based on clinical criteria. It is still overdiagnosed and underdiagnosed in different settings. Penicillin has greatly contributed to the reduction in the incidence and recurrence of this disease. Current schemes of prophylaxis, however, present many problems, and failures are common. Future efforts to reduce the burden of this disease should induce public health measures the vaccine strategies. [References: 144]

Publication Type: Journal Article. Review.

 

<18>

Unique Identifier [PMID]: 9093263

Authors: Stollerman GH.

Institution: Department of Medicine, Boston University, USA.

Title: Rheumatic fever.[see comment]. [Review] [49 refs]

Comments Comment in: Lancet. 1997 Jun 7;349(9066):1700; PMID: 9186408

 

Source: Lancet. 349(9056):935-42, 1997 Mar 29.

Publication Type: Journal Article. Review.

 

<19>

Unique Identifier [PMID]: 8668953

Authors: Carapetis JR. Currie BJ. Good MF.

Title: Towards understanding the pathogenesis of rheumatic fever. [Review] [49 refs]

 

Source: Scandinavian Journal of Rheumatology. 25(3):127-31; discussion 132-3, 1996.

Abstract: Acute rheumatic fever results from an immunological response to group A streptococcal infection, but the exact nature of this response, and of the underlying host and organism characteristics, continues to evade researchers. Earlier models of rheumatic fever pathogenesis emphasised the importance of humoral immunity, but more recent work suggests that cellular immunity may play a primary role. Greater understanding of these disease mechanisms is allowing researchers to move towards the development of a vaccine for rheumatic fever. [References: 49]

Publication Type: Editorial. Review.

 

<20>

Unique Identifier [PMID]: 8571986

Authors: Bronze MS. Dale JB.

Institution: University of Tennessee, Memphis, USA.

Title: The reemergence of serious group A streptococcal infections and acute rheumatic fever. [Review] [92 refs]

 

Source: American Journal of the Medical Sciences. 311(1):41-54, 1996 Jan.

Abstract: Acute rheumatic fever and life-threatening group A streptococcal infections have reemerged during the past 15 years to once again become a serious health threat in the developed countries of the world. Reports of outbreaks of acute rheumatic fever in many parts of this country and others have shattered the complacency that the health-care community had acquired related to this devastating sequela of streptococcal pharyngitis. Invasive streptococcal infections, often associated with loss of limbs of life despite optimal antibiotic therapy, have underscored the potential virulence of these organisms. A new clinical entity, streptococcal toxic shock syndrome, has emerged as a consequence of the new invasive strains of group A streptococci. In this article, the authors summarize the recent changes in the epidemiology of group A streptococcal infections and rheumatic fever and review the potential reasons for the increased virulence of these organisms. In addition, they discuss prospects for a streptococcal M protein vaccine designed to control these infections and their sequelae. [References: 92]

Publication Type: Journal Article. Review.

 

<21>

Unique Identifier [PMID]: 7547107

Authors: Gibofsky A. Zabriskie JB.

Institution: Hospital for Special Surgery-Cornell University Medical College, New York, New York, USA.

Title: Rheumatic fever and poststreptococcal reactive arthritis. [Review] [72 refs]

 

Source: Current Opinion in Rheumatology. 7(4):299-305, 1995 Jul.

Abstract: 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. [References: 72]

Publication Type: Journal Article. Review.

 

<22>

Unique Identifier [PMID]: 7795761

Authors: Shiffman RN.

Institution: Center for Medical Informatics, Yale School of Medicine, New Haven, Conn., USA.

Title: Guideline maintenance and revision. 50 years of the Jones criteria for diagnosis of rheumatic fever.[see comment].

Comments Comment in: Arch Pediatr Adolesc Med. 1995 Jul;149(7):725-6; PMID: 7795760

 

Source: Archives of Pediatrics & Adolescent Medicine. 149(7):727-32, 1995 Jul.

Abstract: OBJECTIVE: To understand better the factors that led to revisions of the Jones criteria, a widely used diagnostic guideline for diagnosis of rheumatic fever. DESIGN: The original publication of the Jones criteria and the four revisions were examined to identify changes. A computer software maintenance paradigm was applied, and modifications were categorized as corrective (error correction), perfective (enhancements in response to user needs), or adaptive (responses to new knowledge). RESULTS: Modifications of the Jones criteria were primarily corrective and perfective. Disease characteristics, originally characterized as major manifestations, were subsequently categorized as minor manifestations and vice versa. Twenty years after the initial publication, a requirement was added to enhance specificity (evidence for antecedent streptococcal infection). Descriptions of rheumatic manifestations became more detailed over time to eliminate ambiguous definitions and provide information to help clinicians decide about borderline cases. This emphasis on corrective and perfective maintenance contrasts with an expectation that adaptive changes would predominate, as with most knowledge-based systems. In fact, despite 50 years of technologic and methodologic advances in medicine, only echocardiography and new antibody testing contributed new knowledge that bears on the diagnosis of rheumatic fever. CONCLUSIONS: Corrective and perfective maintenance can be avoided by making effective use of knowledge that exists at the time a guideline is published. Despite the apparent durability of the Jones criteria, carefully structured, evidence-based guidelines should require less corrective and perfective maintenance. Adaptive maintenance can be anticipated if the quality of evidence or the level of consensus that supports each recommendation is explicitly recorded.

Publication Type: Journal Article.

 

<23>

Unique Identifier [PMID]: 7993713

Authors: Nocton JJ.

Institution: Children's Hospital of Wisconsin, Milwaukee.

Title: Infectious arthropathies and other rheumatologic manifestations of infectious diseases. [Review] [91 refs]

 

Source: Current Opinion in Rheumatology. 6(5):537-43, 1994 Sep.

Abstract: Infectious agents have been implicated in the pathogenesis of many rheumatologic diseases. In most of these diseases, including those in which specific organisms are known to play a role, the details of pathogenesis remain incompletely defined. Recent studies have aimed to isolate bacterial and viral pathogens from patients with rheumatic diseases, efforts have been made to further define the host immune response to infection, and there have been attempts to develop improved methods of diagnosis and treatment of infectious diseases affecting the musculoskeletal system. This review discusses recent studies on the association of infection with illnesses affecting the joints and musculoskeletal system, with an emphasis on the rheumatic diseases of childhood. [References: 91]

Publication Type: Journal Article. Review.

 

<24>

Unique Identifier [PMID]: 8107744

Authors: Pinals RS.

Institution: Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick.

Title: Polyarthritis and fever. [Review] [52 refs]

 

Source: New England Journal of Medicine. 330(11):769-74, 1994 Mar 17.

Publication Type: Journal Article. Review.

 

<25>

Unique Identifier [PMID]: 8173648

Authors: Gibofsky A. Zabriskie JB.

Institution: Division of Rheumatic Diseases, Hospital for Special Surgery, Cornell University Medical College, NY.

Title: Rheumatic fever: new insights into an old disease. [Review] [23 refs]

 

Source: Bulletin on the Rheumatic Diseases. 42(7):5-7, 1993 Nov.

Publication Type: Journal Article. Review.

 

<26>

Unique Identifier [PMID]: 8502775

Authors: Amigo MC. Martinez-Lavin M. Reyes PA.

Institution: Rheumatology Service, Instituto Nacional de Cardiologia Ignacio Chavez, Mexico City, Mexico.

Title: Acute rheumatic fever. [Review] [105 refs]

 

Source: Rheumatic Diseases Clinics of North America. 19(2):333-50, 1993 May.

Abstract: The diagnosis of acute rheumatic fever has become difficult. A growing number of diseases that were not recognized in the past could fulfill its diagnostic criteria. We emphasize its changing incidence, current knowledge of its pathogenesis, and lesser known clinical features such as pneumonitis, encephalitis and glomerulonephritis. [References: 105]

Publication Type: Journal Article. Review.

 

<27>

Unique Identifier [PMID]: 8416130

Authors: Burge DJ. DeHoratius RJ.

Title: Acute rheumatic fever. [Review] [102 refs]

 

Source: Cardiovascular Clinics. 23:3-23, 1993.

Abstract: During the first half of this century rheumatic fever was a common disease with significant morbidity and mortality in the United States. In the 1980s, when many clinicians were hoping this disease was a disease of the past, anxieties were renewed when outbreaks were reported in several areas around the country. Although the etiology still eludes us, insight has been gained. Environmental and genetic factors are believed to play a role in the epidemiology of this disease. Additionally, the implicated organism, the group A streptococcus, has many strains, and differences in its many proteins may determine their potential for rheumatic fever. The mechanisms leading to disease are not clear, but the streptococcus has been implicated as a source of antigens with cross-reactivity with human tissues and has been shown to modify immune mechanisms. Clinical aspects are briefly reviewed and physicians are reminded to consider rheumatic fever as a diagnostic possibility in the appropriate settings. [References: 102]

Publication Type: Journal Article. Review.

 

<28>

Unique Identifier [PMID]: 1344137

Authors: Wald ER.

Institution: Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh, PA 15213-2583.

Title: The resurgence of rheumatic fever. [Review] [9 refs]

 

Source: Heart Disease & Stroke. 1(6):391-4, 1992 Nov-Dec.

Publication Type: Journal Article. Review.

 

<29>

Unique Identifier [PMID]: 1343439

Authors: Sergent JS.

Institution: St. Thomas Hospital, Vanderbilt University, Nashville, Tennessee.

Title: Acute rheumatic fever. [Review] [19 refs]

 

Source: Transactions of the American Clinical & Climatological Association. 104:15-23; discussion 23-5, 1992.

Abstract: A funny thing has happened on our way to the elimination of rheumatic fever from the United States. It is quite clear that, at least in some areas, rheumatic fever has made a dramatic resurgence. Although all the factors accounting for this are not clearly understood, there are several obvious conclusions that must be drawn: 1. Rheumatic fever is no longer the province of the poor and overcrowded. 2. Clinical manifestations, as embodied in the Jones criteria, may have changed somewhat over the years. 3. New insights into the genetics and immunology of rheumatic fever may lead to a vaccine and/or effective therapy in the future. 4. Rheumatic fever will continue to occur unless and until we resume an aggressive approach to the treatment and prophylaxis of pharyngitis, probably utilizing benzathine penicillin as our primary drug. [References: 19]

Publication Type: Journal Article. Review.

 

<30>

Unique Identifier [PMID]: 1480739

Authors: Haffejee I.

Institution: Department of Paediatrics and Child Health, Faculty of Medicine, University of Natal, Durban, South Africa.

Title: Rheumatic fever and rheumatic heart disease: the current status of its immunology, diagnostic criteria, and prophylaxis. [Review] [167 refs]

 

Source: Quarterly Journal of Medicine. 84(305):641-58, 1992 Sep.

Publication Type: Journal Article. Review.

 

<31>

Unique Identifier [PMID]: 1404745

Authors: Anonymous.

Title: Guidelines for the diagnosis of rheumatic fever. Jones Criteria, 1992 update. Special Writing Group of the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease of the Council on Cardiovascular Disease in the Young of the American Heart Association.[see comment][erratum appears in JAMA 1993 Jan 27;269(4):476].

Comments Comment in: JAMA. 1993 Apr 28;269(16):2084; PMID: 8468752

 

Source: JAMA. 268(15):2069-73, 1992 Oct 21.

Abstract: The Jones Criteria for guidance in the diagnosis of acute rheumatic fever were first published by T. Duckett Jones, MD, in 1944 and have been revised over the years by the American Heart Association. The current guidelines are an update of these criteria. For the first time, the guidelines are designed to establish the initial attack of acute rheumatic fever. Major manifestations, minor manifestations, and supporting evidence of antecedent group A streptococcal infection are discussed. These updated guidelines expand on the available tools to diagnose streptococcal pharyngitis and clarify the available antibody tests for detecting antecedent group A streptococcal infection. At the present time echocardiography without accompanying auscultatory findings is insufficient to be the sole criterion for valvulitis in acute rheumatic fever. Finally, this article addresses overdiagnosis of rheumatic fever and lists exceptions to the Jones Criteria, including recurrent attacks in individuals with a history of rheumatic fever.

Publication Type: Guideline. Journal Article. Practice Guideline.

 

 

 

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Emory University School of Medicine

2005 Edition

Participating Faculty:  Carlos Del Rio MD  / Joyce Doyle MD / Lorenzo Difrancesco MD / Erich Folch MD / Alicia Hidron  MD  

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