Page 147 - Clinical Pearls in Cardiology

Heart Disease and Fever 135

12. What is the role of streptococcal infection in acute
rheumatic fever and acute post-streptococcal
glomerulonephritis?
Acute rheumatic fever and acute post-streptococcal
glomerulonephritis are nonsuppurative complications
of streptococcal infection. The organ systems involved
in acute rheumatic fever and acute post-streptococcal
glomerulonephritis (i.e. the heart and kidney respectively)
are not directly invaded by the microorganism.
Both the post-streptoccocal disorders are actually
immunologically-mediated. Some of the group A
streptococcal proteins (antigens) structurally mimic
some of the normal cardiac and renal tissue proteins
in humans. This, in turn, triggers an inappropriate
immunological response against these normal cardiac
and renal tissue proteins, leading to rheumatic fever and
glomerulonephritis.
13. Why is streptococcal pyoderma not associated with
rheumatic fever?
Molecular mimicry is the hallmark of the pathogenesis
of both acute rheumatic fever and acute post-infectious
glomerulonephritis. This mimicry between the cardiac
or renal proteins and the group A streptococcal proteins
trigger an inappropriate host immunological response
against the cardiac and renal tissues, in the event of
a group A streptococcal infection. The cardiac tissue
proteins have resemblance to the proteins present in
certain strains of streptococci causing only pharyngeal
infection (like type 12 strain), whereas the renal tissue
proteins have resemblance to the proteins present
in strains of streptococci causing either pharyngeal
or cutaneous infection (like type 49 strain). Hence
post-infectious glomerulonephritis can follow either a