Rheumatic fever natural history, complications, and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Lance Christiansen, D.O.; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S. [3]; Anthony Gallo, B.S. [4]
Overview
Natural History
If an individual develops rheumatic fever, they will experience the development of increased sensitization to Streptococcus pyogenes autoantigens. An infection by a virulent strain of Streptococcus pyogenes, at a later date, will likely cause an elevated, autoimmunological response and a recurrent case, probably a more severe case, of rheumatic fever will develop.
If an individual does not contract a Streptococcus pyogenes infection for five years or longer, his/her immunological/autoimmunological responsivness will naturally decrease and, therefore they are less likely to develop rheumatic fever if the individual contracts Streptococcal infection in the future.
The above natural phenomenon is the basis for the use of prophylactic penicillin therapy among individuals who are at risk for rheumatic fever. Providing individuals who have had rheumatic fever with Benzathine Penicillin G, 1,200,000 units every three weeks, or oral penicillin VK or G, 250mg twice daily, decreases the frequency of recurrent streptococcal infection and subsequent recurrent rheumatic fever. It is estimated that the recurrence rate of rheumatic fever is decreased by about 85% by providing prophylactic penicillin therapy. Recurrence rate of 0.2/patient/year follow-up was noted among those not receiving regular secondary prophylaxis in a series involving 120 children with initial rheumatic fever being followed-up for 6 years. While the recurrence rate among those receiving regular secondary prophylaxis was reported to be 0.005/patient/year follow-up[1].
Rheumatic fever if left untreated, may cause valvular diseases such as stenosis/regurgitation of mitral/aortic valves and myocarditis. This may lead to decreased cardiac output, pulmonary edema and ultimately cardiac failure. In a series where 497 children on treatment for rheumatic fever were followed over 10years, 19 children were reported to have died of rheumatic fever and rheumatic heart disease. Prognosis among those with pre-existing heart disease was poor[2].
Cardiac arrhythmias, systemic emboli and infective endocarditis are other possible complications of rheumatic carditis.
Complications
- Damage to heart valves (in particular, mitral stenosis and aortic stenosis)
- Infective endocarditis- Rheumatic heart disease is the most common cause for infective endocarditis in India[3][4], Turkey[5], Israel[6] and Lebanon[7] based on studies
- Cardiac failure
- Arrhythmias
- Systemic emboli leading to stroke. Approximately 3–7·5% of all strokes in developing countries have rheumatic heart disease as an underlying condition[8][9].
- Pericarditis
- Sydenham chorea
- Recurrence of rheumatic fever. Risk of recurrence is highest during the 5 years following an acute attack. Recurrence rate of 0.2/patient/year follow-up was noted among those not receiving regular secondary prophylaxis in a series involving 120 children with initial rheumatic fever being followed-up for 6 years. While the recurrence rate among those receiving regular secondary prophylaxis was reported to be 0.005/patient/year follow-up[1].
References
- ↑ 1.0 1.1 Majeed HA, Yousof AM, Khuffash FA, Yusuf AR, Farwana S, Khan N (1986). "The natural history of acute rheumatic fever in Kuwait: a prospective six year follow-up report". J Chronic Dis. 39 (5): 361–9. PMID 3700577.
- ↑ "The natural history of rheumatic fever and rheumatic heart disease. Ten-year report of a cooperative clinical trial of ACTH, cortisone, and aspirin". Circulation. 32 (3): 457–76. 1965. PMID 4284068.
- ↑ Garg N, Kandpal B, Garg N, Tewari S, Kapoor A, Goel P; et al. (2005). "Characteristics of infective endocarditis in a developing country-clinical profile and outcome in 192 Indian patients, 1992-2001". Int J Cardiol. 98 (2): 253–60. doi:10.1016/j.ijcard.2003.10.043. PMID 15686775.
- ↑ Khanal B, Harish BN, Sethuraman KR, Srinivasan S (2002). "Infective endocarditis: report of a prospective study in an Indian hospital". Trop Doct. 32 (2): 83–5. PMID 11931207.
- ↑ Heper G, Yorukoglu Y (2002). "Clinical, bacteriologic and echocardiographic evaluation of infective endocarditis in Ankara, Turkey". Angiology. 53 (2): 191–7. PMID 11952110.
- ↑ Borer A, Riesenberg K, Uriel N, Gilad J, Porath A, Weber G; et al. (1998). "Infective endocarditis in a tertiary-care hospital in southern Israel". Public Health Rev. 26 (4): 317–30. PMID 10641529.
- ↑ Kanafani ZA, Mahfouz TH, Kanj SS (2002). "Infective endocarditis at a tertiary care centre in Lebanon: predominance of streptococcal infection". J Infect. 45 (3): 152–9. PMID 12387770.
- ↑ Carapetis JR, Steer AC, Mulholland EK, Weber M (2005). "The global burden of group A streptococcal diseases". Lancet Infect Dis. 5 (11): 685–94. doi:10.1016/S1473-3099(05)70267-X. PMID 16253886.
- ↑ Kaul S, Sunitha P, Suvarna A, Meena AK, Uma M, Reddy JM (2002). "Subtypes of Ischemic Stroke in a Metropolitan City of South India (One year data from a hospital based stroke registry)". Neurol India. 50 Suppl: S8–S14. PMID 12665873.