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- Patient - Rheumatic Fever (Oct. 18, 2026)
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What is rheumatic fever?
Rheumatic fever is an inflammatory disease affecting the heart, joints, central nervous system, and subcutaneous tissues, arising from an untreated streptococcal throat infection. It is most common in children aged 5–15.
The underlying cause is believed to be an autoimmune reaction, where antibodies attack the body's own tissues due to similarities between streptococcal proteins and human tissue. This can lead to tissue damage, especially in the heart, joints, and central nervous system.
Symptoms include fever, joint pain and inflammation, heart murmurs, and sometimes skin rashes or involuntary movements. Prompt treatment with antibiotics is essential to prevent heart damage, which can lead to long-term complications.
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What causes rheumatic fever to develop?
Rheumatic fever is an inflammatory disease affecting the heart, joints, central nervous system, and subcutaneous tissues. It arises following a throat infection caused by group A beta-hemolytic Streptococcus bacteria, such as untreated strep throat or scarlet fever.
The exact physiological factors aren't fully understood, but the prevailing theory suggests an autoimmune reaction where antibodies mistakenly target the body's own tissues. This is triggered by streptococcal protein components (antigens) that resemble molecules in human tissues. These antibodies then bind to self-antigens in the heart, joints, and central nervous system, causing tissue damage.
Risk factors include a family history of rheumatic fever, indicating a possible genetic predisposition, and socioeconomic factors like overcrowded, unsanitary conditions that facilitate Streptococcus transmission.
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Which parts of the body are most affected by rheumatic fever?
Rheumatic fever primarily affects the heart, joints, central nervous system, and subcutaneous tissues. Cardiac issues include heart murmurs, increased heart rate, and heart enlargement, potentially leading to permanent scarring of the heart valves and reduced life expectancy. Joint pain and inflammation are also typical. Other symptoms include skin nodules and rashes, nervous system issues (Sydenham chorea), abdominal pain, and weakness. The disease can range from mild to severe, sometimes causing cardiac failure.
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How does rheumatic fever damage the heart?
Rheumatic fever, a complication of untreated streptococcus A bacterial infections, primarily affects children and poses the greatest danger to the heart. The disease results from an autoimmune reaction, where antibodies attack the body's own tissues.
Inflammation of the heart (especially the valves) can lead to permanent scarring and contracture of the heart valves. The major damage occurs due to deformity of the heart valves from the initial or repeated attacks of acute illness, which may take years to become evident. The mitral valve is most frequently affected, followed by the aortic and tricuspid valves. This can cause valve insufficiency, leading to regurgitation, or stenosis, obstructing normal blood flow and burdening the heart. Resulting heart malfunction can cause shortness of breath and heart murmurs.
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What are the main symptoms of rheumatic fever?
Rheumatic fever, a rare inflammatory disease, arises as a complication of untreated streptococcus A bacterial infections, especially in children aged 5–15. The disease primarily endangers the heart, even though its name refers to joint involvement.
Key symptoms include fever, joint pain and inflammation, and signs of cardiac issues like heart murmurs, increased heart rate, and heart enlargement. Other symptoms can include skin nodules and rashes such as erythema marginatum, nervous system issues (Sydenham chorea), abdominal pain, nosebleeds, weakness, and loss of appetite and weight. The severity of rheumatic fever varies significantly, ranging from mild, unnoticed conditions to severe acute attacks that can lead to heart failure and death.
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How can rheumatic fever be prevented and treated?
Rheumatic fever, an inflammatory disease affecting the heart, joints, and central nervous system, arises from untreated strep throat or scarlet fever caused by group A beta-hemolytic Streptococcus bacteria.
Prevention is key, primarily through the use of penicillin to treat streptococcal infections. Both initial and recurrent attacks can be effectively prevented with penicillin. For those with damaged heart valves, continuous antibiotic treatment is necessary to prevent bacterial endocarditis.
Treatment focuses on managing symptoms. Aspirin and steroid hormones can alleviate inflammation. Surgery may be required to correct heart valve narrowing. Although there is no specific cure, antibiotics like penicillin or erythromycin are used to eradicate streptococci during an attack, while analgesics and anti-inflammatory medications treat acute symptoms.
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rheumatic fever, inflammatory disease of the heart, joints, central nervous system, and subcutaneous tissues that develops after a throat infection with group A beta-hemolytic Streptococcus bacteria, including untreated scarlet fever or strep throat. Prevention is possible with penicillin, but specific treatment is not available. Rheumatic fever is particularly important because of the heart disease, which includes vascular damage, that may ensue. The illness occurs chiefly in children and young adults, with a peak incidence between ages 5 and 15.
Symptoms
When a streptococcal throat infection goes untreated, most patients recover without complications. Approximately 1 percent, however, develop rheumatic fever. The onset of the disease is most often characterized by the sudden occurrence of fever and joint pain and inflammation several days to six weeks after the streptococcal infection. Signs of cardiac involvement include heart murmurs, increased pulse (heart rate), and heart enlargement. Inflammation of the heart muscle and supporting structures may lead to a permanent scarring and contracture of the heart valves and a marked decrease in life expectancy.
Other symptoms of rheumatic fever include nodules beneath the skin and skin rashes, the most typical of which is erythema marginatum; Sydenham chorea, a nervous system manifestation marked by emotional instability and purposeless, involuntary movements of the arms and legs; abdominal pain; nosebleeds; weakness; and loss of appetite and body weight. Generally, the clinical symptoms, severity, and aftereffects of an attack of rheumatic fever are highly variable, ranging from a condition so mild as to go unnoticed to a severe acute attack associated with cardiac failure and death.
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Diagnosis and treatment
During the course of rheumatic fever, the streptococcal organism may no longer be demonstrable in cultures of the throat or other infected body areas, but blood titres of antibodies against the streptococcus, such as antistreptolysin O, are high. All the numerous types of group A beta-hemolytic Streptococcus appear capable of inducing rheumatic fever in susceptible individuals, infection with one type confers no immunity against the others, and individuals who have experienced one attack of rheumatic fever are especially prone to subsequent attacks. Both the initial and recurrent attacks can be effectively prevented with penicillin.
Symptomatic treatment of the condition includes the use of salicylates such as aspirin or one of the steroid hormones. Surgery may be advocated to relieve the narrowing of the openings of the heart valves. Rheumatic fever patients must receive antibiotics on a regular basis for the remainder of their lives because their damaged heart valves predispose them to the development of bacterial endocarditis.
Suspected role of autoimmunity and risk factors
The underlying physiological factors that are responsible for rheumatic fever are not clear. Most authorities favour the theory that the disease results from an autoimmune reaction, involving the production of antibodies that attack the body’s own tissues. The autoimmune reaction is thought to be triggered by certain protein components of the streptococci, known as antigens, the structure of which resembles that of molecules found in human tissue (“self antigens”). Because of this resemblance, the antibodies that recognize streptococcal antigens may mistakenly react with similarly shaped antigens of certain cells of the body—such as those of the heart, joints, and central nervous system. By binding to these self antigens, the antibodies cause the tissue damage characteristic of rheumatic fever.
Various risk factors have been identified for rheumatic fever, among them family history of the disease and socioeconomic factors. Persons with a family history of rheumatic fever may have a genetic predisposition that increases their chances of developing the disease. In terms of socioeconomic factors, rheumatic fever is sometimes referred to as a disease of poverty, because of the notably high risk for developing the disease in persons living in overcrowded unsanitary conditions. Such conditions provide the foundation for the rapid transmission of Streptococcus. The strain of Streptococcus can also be a factor in determining whether a person will develop rheumatic fever.
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Historical developments and epidemiological considerations
Since the mid-20th century the incidence and severity of rheumatic fever and other streptococcal infections, such as scarlet fever, have declined precipitously in the developed countries. This decline has occurred independently of the use of penicillin and other drugs. Research suggests that the historical decline in rheumatic fever likely was due to vast improvements in living conditions that occurred in the mid-20th century in more-developed countries. This idea is supported by the fact that rheumatic fever in the 21st century persists mainly in less-developed parts of the world, where poor nutrition, poor living conditions, and limited access to health care are common. Rheumatic fever also remains a serious concern for certain indigenous populations, particularly those of Australia and New Zealand.