July 1988, Volume 38, Issue 7



Mohammad Imran  ( Department of Paediatrics, Postgraduate Medical Institute, Lady Reading Hospital, Peshawar. )
Amin Jan  ( Department of Paediatrics, Postgraduate Medical Institute, Lady Reading Hospital, Peshawar. )

Rheumatic fever is the commonest cause of heart disease in children over five years of age and the resulting rheumatic heart disease accounts for 20-30% of cardiovascular diseases in all age groups1. In the past few decades there has been a dramatic decline in its incidence and severity in Western world. It however, remains a serious and common health problem in almost all develop­ing countries2,3. Prevention of rheumatic fever (both primary and secondary) with the help of antibiotics is difficult and far from perfect, be­cause only one third of rheumatic fever patients give history of preceding sore throat, others have asymptomatic streptococcal infection. Only 0.3-3% of all patients with streptococcal sore throat develop rheumatic fever4 and a fraction of these consult the doctors even in developed coun­tries. This is because of the lack of awareness on the part of the patient (and doctor) that sore throat may lead to heart disease5. In order to prevent one case of acute rheumatic fever about 600 to 2000 cases of diagnosed streptococcal sore throats and about 1600 to 10,000 undia­gnosed sore throats will require treatment6. Similarly, prevention of recurrent attacks (secon­dary prevention) is not less cumbersome. It requires health education of the patient and family, constant vigilance and efforts. Although it may decrease the morbidity and mortality, it never eradicates the disease. The only solution of the whole problem is therefore, a safe and effec­tive Vaccine.
M.protein, a cell wall antigen and virulence factor of group. A streptococci, produces protec­tive antibodies when introduced into human beings. These antibodies are opsonic in character and provide type specific and long lasting immu­nity.7 The presence of hypersensitivity and! or toxicity to M. protein and the streptococcal antibodies which are cross reactive with human tissues8 indicated that M.Vaccine may cause rheumatic fever instead of ‘preventing it. This obstacle of immunotoxicity and cross reactivity was removed by separating M.protein from the non-type specific antigen (or M.associated protein)9,10 . Initial trials of 24 M. protein were successful. It was well tolerated and produced primary immune response without any toxicity in 10 out of 12 human volunteers11. The major problem is the presence of large number of sero­types of streptococci (70 or more). It is not feasible to produce a polyvalent vaccine containing more than 70 separate M. proteins. Therefore, prevalence studies are needed to know the main rheumatogenic serotypes in any community. Type 5,14 and 24 are the best knoWn serotypes found in Indian subcontinent, Saudi Arabia and Central and South America12, but these serotypes vary from place to place and from time to time.
Another solution of the problem will be a reduction in number of M. protein serotypes and making it easier for the host to acquire antibodies to the whole range. Although M. protein is gener­ally considered as strictly type specific, some degree of antigenic relationship among various.
M. Types has recently been reported9. This requires further confirmation because of its important implications in the development of vaccine. However, it should also be kept in mind that streptococci may not be the only agent res­ponsible for rheumatic fever. It has been suggested that coxsackie B4 virus is the cause of rheumatic fever13. Others believe that measles14 or rubel­la15 viruses may have primary or secondary role in the development of rheumatic fever.


1. Taranta, A. and Markowitz, M. Rheumatic fever. Lancaster, M.T.P.S. Press, 1981; p. 14.
2. Agarwal, B.L. Rheumatic heart disease unabated in developing countries. Lancet, 1981; 2:910.
3. Markowitz, M. The decline of rheumatic fever; role of medical intervention. Lewis W. Wanna make memorial lecture. J. Pediatr., 1985; 106:545.
4. Ilyas, M. Rheumatic fever; problem in prevention (editorial). JPMA., 1981; 31:239.
5. Julian, D.G. and Humphries, J.N. Preventive cardiology. London, Butterworths, 1983.
6. Davies, A.M., Halfon, S.T. and Ever Hadani, P. Prevention of rheumatic fever approaches to problems. Singapore Med. J., 1973; 14 : 142.
7. Stollerman, G.H. Rheumatic fever and strep­tococcal infection. New York, Grune and Stratton,1975.
8. Zabriskie, J.B. Rheumatic fever; the interplay between host, genetics, and microbe. Lewis, A. Conner memorial lecture. Circulation, 1985; 71: 1077.
9. Rotta, J. Biological Characteristics of Group—A streptococcus and the Pathogenesis of Rheumatic fever. Proceedings Ed, International Conference on rheumatic fever and rheumatic heart disease Otsu, Japan 1979, p.3.
10. Beachey, E.H. and Seyer, J.M. Studies of the Primary Antigenic structure of streptococcal M.       Protein Vaccines. Proceedings Ed, Inter­national Conference on rheumatic fever and rheumatic heart disease Otsu, Japan 1979, pp, 10-13.
11. Beachey, E.M. and Norton,W.L. The control of rheumatic fever. K.E.S.H. Med., 1982; 2:1.
12. Decline in rheumatic fever (editorial). Lancet, 1985; 2:647.
13. Burch, C.E. and Giles, T.D. The role of virus in production of heart disease. Am. J. Cardiol., 1972; 28: 231.
14. Row, P.C. Possible association of measles virus infection with rheumatic fever. N. Engi. J. Med., 1985;313 :580.
15. Wedum,B.G. Possible association between rubella vaccination and the decline in rheumatic fever. N. Engi. J. Med., 1985; 312 :991.

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