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disease
Epidemiology
Prevalence in (1937)western countries 45/1000 children dropped to 2.9/100000 in
the late 1960s.
In India, the prevalence was 6-11/1000
(padmavathi,1978).
In south india a study done by Dr.Koshy et
el in 1981 showed the prevalence of
rheumatic fever and heart disease was
4.9/1000 in a survey in school children.
Etiology
Rheumatic fever follows 2-4weeks after a
Group A streptococcal infection of the
throat and not of the skin.
The infection can be identified in about
25% by bacteriological and in over 90% by
serological methods.
Individuals with vigorous antibody
response develop rheumatic fever with
greater frequency.
Mammalian tissue
component
Streptococcal hyaluronic
acid
Mammalian hyaluronicacid
& protein polysaccharide
Glycoproteins of heart
valves.
Sarcolemma of cardiac and
skeletal muscles.
Sarcolemma of cardiac and
skeletal muscles.
Group A carbohydrate
Protein cell wall
Protein of cell menbrane
Glycoprotein of the
cell membrane
Antigen of the cell
membrane
Glycoprotein of the
glomerular
basement
membrane
Histocompatibility
antigen.
Minor
Fever
Arthralgia
Prolonged PR
interval on ECG
Increased
ESR,leukocytois or
CRP.
Essential criteria
Evidence of recent streptococcal
infection elevated streptococcal
antibodies.
Positive throat culture for group A
streptococcus.
Diagnosis
2 major or 1 major and two minor
criteria indicate high probability of
acute rheumatic process.
These criteria are guidelines not
meant to substitute clinician s
judgement .
On examination
Apical murmur- pan systolic murmur of the
mitral regurgitation is heard. It is soft and
are transmitted to the axilla.
The intensity and duration of the murmur
can wane and may disappear towards
recovery.
The development of the low pitched apical
mid diastolic murmur (carey coombs)
murmur which is attributed to mitral
valvulitis helps to confirm the organic
significance of MR murmur.It tend to
disappear during recovery.
Natural history
TOMPKIN et el 1972 reported that about
2/3rd of patients with mitral regurgitation or
AR became free of murmurs within 5-10
years.
Mitral stenosis did not develop in any
patient who was on regular penicillin
prophylaxis.
New valvular lesions do not develop
usually in the absence of recurrences,
even in the patient who had carditis as an
initial attack but old valvar lesions may
evolve further.