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Rheumatic fever is a complex and important medical condition that connects infectious disease with autoimmune problems. It is an inflammatory disease that can develop after an infection with group A Streptococcus bacteria, usually after strep throat or scarlet fever. Unlike most infections, where the bacteria directly harm the body, rheumatic fever happens when the immune system mistakenly attacks healthy tissues while trying to fight the bacteria. This mistake affects connective tissues, especially in the heart, joints, skin, and nervous system. The main concern is that rheumatic fever can cause lasting damage to the heart valves, leading to rheumatic heart disease.
To understand rheumatic fever, it helps to look at what happens on a microscopic level. Group A Streptococcus bacteria have a cell wall with special proteins, especially the M protein, which helps them avoid the immune system. The M protein and some other parts of the bacteria look very similar to proteins found in human tissues, like those in the heart, joints, and brain. This similarity, called molecular mimicry, causes the immune system to attack both the bacteria and the body’s own tissues. This reaction leads to inflammation and the symptoms of rheumatic fever. Usually, these problems start 2 to 4 weeks after the original throat infection, so patients may think they are better before symptoms appear.
Not everyone who gets strep throat will develop rheumatic fever. Only a small number of people with untreated strep throat have this complication, which suggests that genetics plays a big role. Certain genetic markers, especially those related to the immune system, make some people more likely to get rheumatic fever. This is why the disease can run in families, not because it is directly inherited, but because the tendency for a strong immune reaction is passed down. Rheumatic fever is most common in children aged 5 to 15, which matches the ages when strep throat is most common in schools. While the disease is now rare in wealthier countries, it is still a major cause of heart problems in children and young adults in many developing areas.
The definition of rheumatic fever is broad because it is a multisystem disorder. It is classified as a nonsuppurative sequel, meaning it does not result in pus formation in the affected organs. Instead, the inflammation is sterile. In the joints, this manifests as a fleeting but painful arthritis. In the brain, it causes a temporary disruption of motor control. In the skin, it produces distinctive rashes and nodules. However, the heart remains the central concern. Inflammation can affect all three layers of the heart: the pericardium (the outer sac), the myocardium (the muscle), and the endocardium (the inner lining). This condition, known as pancarditis, is the disease’s unique signature. The inflammation of the endocardium is particularly devastating because it involves the heart valves. Unlike the joints, which heal completely, the heart valves can suffer permanent scarring, thickening, and deformity. This potential for irreversible cardiac injury defines the disease’s severity and dictates the urgency of medical intervention.
Historically, rheumatic fever was a widespread scourge, often feared as much as polio or tuberculosis. Before the antibiotic era, it was the primary cause of valvular heart disease in young people. The decline of the disease in the mid-20th century is one of the great success stories of public health, driven by improved living conditions, less overcrowding, and the introduction of penicillin. However, the bacteria are constantly evolving. Different strains of group A Streptococcus have varying degrees of rheumatogenic potential, meaning some strains are more likely to trigger the autoimmune reaction than others. Modern medicine defines the disease not just by the clinical symptoms but by the ongoing interaction between these bacterial strains and human immunity. It is a disease that requires constant vigilance because, as long as group A Streptococcus exists in the community, the potential for rheumatic fever remains. At Liv Hospital, we view the condition through this lens of historical diligence and modern immunological science to provide comprehensive care
Because there is no single diagnostic test that can definitively identify rheumatic fever, the medical community relies on a set of clinical classifications known as the Jones Criteria. First established in 1944 and periodically revised to reflect current epidemiology, these criteria define the disease based on combinations of major and minor manifestations. Major manifestations are specific symptoms like carditis, arthritis, chorea, erythema marginatum, and subcutaneous nodules. Minor manifestations include fever, joint pain without swelling, and elevated inflammatory markers in the blood. For a diagnosis to be made, there must be evidence of a preceding streptococcal infection plus the presence of two major criteria, or one major and two minor criteria. This strict definition helps clinicians distinguish rheumatic fever from other autoimmune diseases or viral infections that may mimic its symptoms, ensuring that patients are not misdiagnosed and subjected to unnecessary treatments.
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Rheumatic fever is caused by an autoimmune reaction to a prior infection with group A Streptococcus bacteria, where the body creates antibodies that mistakenly attack its own tissues.
No, rheumatic fever is not an active bacterial infection. It is the inflammatory aftermath of a bacterial infection that has usually cleared from the throat by the time rheumatic symptoms appear.
It is most common in school-aged children, specifically those between 5 and 15 years old, due to the high rate of strep throat transmission in schools and playgrounds.
The inflammation in the joints and skin usually heals without a trace, but the inflammation in the heart can cause permanent scarring of the valves, leading to rheumatic heart disease.
The term rheumatic refers to the pain and stiffness in joints and muscles, which are prominent symptoms, combined with the high fever that typically accompanies the acute phase of the illness.
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