T. Duckett Jones, MD, first published these criteria in 1944. They have been periodically revised by the American Heart Association in collaboration with other groups. According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection. Exceptions are chorea and indolent carditis, each of which by itself can indicate rheumatic fever.
- Migratory polyarthritis: a temporary migrating inflammation of the large joints, usually starting in the legs and migrating upwards.
- Carditis: inflammation of the heart muscle which can manifest as congestive heart failure with shortness of breath, pericarditis with a rub, or a new heart murmur.
- Subcutaneous nodules: painless, firm collections of collagen fibers over bones or tendons. They commonly appear on the back of the wrist, the outside elbow, and the front of the knees.
- Erythema marginatum: a long lasting rash that begins on the trunk or arms as macules and spreads outward to form a snake like ring while clearing in the middle. This rash never starts on the face and it is made worse with heat.
- Sydenham's chorea (St. Vitus' dance): a characteristic series of rapid movements without purpose of the face and arms. This can occur very late in the disease.
- Arthralgia: Joint pain without swelling
- Raised Erythrocyte sedimentation rate or C reactive protein
- ECG showing features of heart block, such as a prolonged PR interval
- Supporting evidence of Streptococcal infection: elevated or rising Antistreptolysin O titre or DNAase., producing the symptoms of rheumatic fever.
Group A ''streptococcus pyogenes'' has a cell wall composed of branched polymers which sometimes contain "''M proteins''" that are highly antigenic. The antibodies which the immune system generates against the "''M proteins''" may cross react with cardiac myofiber protein myosin,heart muscle glycogen and smooth muscle cells of arteries, inducing cytokine release and tissue destruction. However, the only proven cross reaction is with perivascular connective tissue. This inflammation occurs through direct attachment of complement and Fc receptor-mediated recruitment of neutrophils and macrophages. Characteristic Aschoff bodies, composed of swollen eosinophilic collagen surrounded by lymphocytes and macrophages can be seen on light microscopy. The larger macrophages may become Aschoff giant cells. Acute rheumatic valvular lesions may also involve a cell-mediated immunity reaction as these lesions predominantly contain T-helper cells and macrophages.
In acute RF, these lesions can be found in any layer of the heart and is hence called pancarditis. The inflammation may cause a serofibrinous pericardial exudates described as “bread-and-butter” pericarditis, which usually resolves without sequelae. Involvement of the endocardium typically results in fibrinoid necrosis and verrucae formation along the lines of closure of the left-sided heart valves. Warty projections arise from the deposition, while subendothelial lesions may induce irregular thickenings called MacCallum plaques.
Chronic rheumatic heart disease is characterized by repeated inflammation with fibrinous resolution. The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion and shortening and thickening of the tendinous cords.
Screening school-aged children for sore throats also aid in prevention.
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