This document discusses rheumatic fever and rheumatic heart disease. It notes that susceptibility to rheumatic fever is partly hereditary, with certain HLA alleles being associated with increased or decreased susceptibility. Initial damage is caused by streptococcal bacteria invading epithelial tissues, though not through molecular mimicry. Common symptoms include chorea, indolent carditis, and valvular damage, which is a hallmark of rheumatic heart disease. Prolonged PR interval and softening of the first heart sound may also be seen. While bed rest was once recommended, medications are now preferred to control symptoms, and antibiotics are given long-term to prevent recurrence.
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Acute rheumatic fever
3. Unfortunately such a decline was not replicated in developing countries,
where these diseases continue unabated.
7. Susceptibility to ARF is an
inherited characteristic鐚 with
44% concordance in monozygotic
twins compared to 12% in
dizygotic twins,
Heritability more recently
estimated at 60%.
HLA-DR7 and HLA-DR4鐚 appear
to be associated with
susceptibility鐚
other class II alleles have been
associated with protection (HLA-
DR5, HLA-DR6鐚 HLA-DR5 1,
HLA-DR52 and HLA-DQ )
8. .
Initial damage is due to
streptococcal invasion of
epithelial surfaces鐚
With binding of M
protein to type IV
collagen allowing it to
become immunogenic鐚
BUT NOT THROUGH THE
MECHANISM OF MOLECULAR
MIMICRY.
26. Myocardial inflammation may affect electrical
conduction pathways, leading to P-R interval
prolongation (first-degree atrio ventricular block or
rarely higher level block) and
softening of the first heart sound.
45. Traditional
recommendations
for long-term bed
rest, once the
cornerstone of
management鐚are
no longer widely
practiced.
Medications to control the
abnormal movements do
not alter the
duration or outcome of
chorea. Milder cases can
usually be managed
by providing a calm
environment. In patients
with severe chorea鐚
carbamazepine or sod i um
valproate is preferred to
haloperidol.