Rheumatic fever
Rheumatic fever is defined as an inflammatory disease caused by the Group A streptococcus bacterium. The infection develops two to three weeks after a Group A streptococcal infection such as scarlet fever and strep throat. Rheumatic fever may involve the heart, skin, joints and the central nervous system. It is characterized by an exudative and proliferative inflammation of the connective tissue. Its signs and symptoms are similar to rheumatism. That is why it was named as rheumatic fever. Rheumatic fever is believed to be caused by antibody cross-reactivity. This cross-reactivity is a Type II hypersensitivity reaction and is known as molecular mimicry. One beta-streptococcal serotype is directly linked to acute rheumatic fever. There is strong evidence that the M protein in certain streptococci subtypes is responsible for antigenicity.
Rheumatic fever is common worldwide and is responsible for many cases of damaged heart valves. It affects children between the ages of 6 to 15. There is no sex predilection, although mitral valve prolapse and Sydenham chorea occur more often in females than in males. Clinical trials suggest that there is a genetic susceptibility to the development of the disease. Clinical studies also reveal that non-group A streptococci never cause the disease. In the United States, disease prevalence is associated with socioeconomic status, with higher incidence in overcrowded areas. The disease’s overall incidence is decreasing in developed nations but is still prevalent in less developed countries. It is a major problem in countries with limited resources and in communities with minority indigenous populations.
The diagnosis of rheumatic fever can be made in the presence of two major criteria, or one major criterion and two minor criteria, along with the evidence of streptococcal infection. The following are the major diagnostic criteria: migratory polyarthritis, carditis, erythema marginatum and Sydenham’s chorea. The subcutaneous nodules are described as edematous, fragmented collagen fibers. They are painless nodules found on the exterior surface of the wrists, elbows and knees. The skin rashes may be eruptions on the trunk and upper part of the legs or arms or eruptions that look ring-shaped or snake-like. The rash is serpiginous and long lasting. The manifestations of Sydenham chorea include emotional instability, muscle weakness, and quick, uncoordinated jerky movements that mostly affect the face, hands and feet. The onset of Sydenham chorea, also known as St. Vitus dance, may be delayed for several months and may stop when the patient is sleeping. Minor criteria include fever, arthralgia, raised erythrocyte sedimentation rate (ESR) or C reactive protein, leukocytosis, electrocardiogram (ECG) showing features of heart block, previous episode of rheumatic fever or inactive heart disease, and elevated or rising Antistreptolysin O titer or DNAse. Other signs and symptoms include nose bleeds and abdominal pain. Possible complications of rheumatic fever include endocarditis, arrhythmias, pericarditis and heart failure.
Treatment of the infection is centered on the reduction of inflammation using anti-inflammatory drugs such as corticosteroids or aspirin. The drug of choice is aspirin. It is given at high doses of 100 mg/kg/day. Steroids are prescribed when the heart is already involved. Antibiotics such as penicillin, sulfadiazine or erythromycin are given to people with positive cultures for strep throat. The disease may return if patients failed to take low dose antibiotics continually, especially during the first three to five years after the first episode of the disease. The recurrence of the disease may cause heart complications of long-term and of severe magnitude. Disease relapse is prevented by stopping the acute infection and prophylaxis with antibiotics. The American Heart Association suggests daily or monthly prophylaxis with antibiotics. Another preventive strategy is the screening of school-aged children for sore throats.
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