Rheumatic fever is an inflammatory disease that can develop after an untreated or poorly treated Streptococcus pyogenes infection, commonly known as strep throat or scarlet fever. It mainly affects the heart, joints, skin, and brain. The condition occurs when the immune system, while fighting the strep bacteria, mistakenly attacks the body’s own tissues. This happens because some of the bacterial proteins look similar to those found in human tissues, a process known as molecular mimicry. Although rheumatic fever itself cannot spread between people, the strep infection that causes it can be passed on through droplets from coughing or sneezing.
Rheumatic fever remains a serious health problem in many developing countries, where access to timely diagnosis and antibiotics is limited. The World Health Organization (WHO) estimates that about 470,000 new cases occur worldwide each year, and that rheumatic heart disease (RHD), a long-term complication of the fever, affects over 40 million people and causes more than 300,000 deaths annually, mostly among children and young adults in low- and middle-income nations. In contrast, rheumatic fever is now rare in wealthier countries thanks to better healthcare, sanitation, and the widespread use of antibiotics.
Typical symptoms include fever, tiredness, and joint pain that moves from one joint to another. Some patients develop small lumps under the skin or a ring-shaped rash called erythema marginatum. The disease can also affect the brain, leading to Sydenham’s chorea, a condition that causes involuntary, jerky movements of the face, hands, and feet, especially in children. When the heart is involved, a condition called rheumatic carditis, symptoms may include chest pain, shortness of breath, rapid heartbeat, or heart murmurs. Repeated or severe attacks can cause permanent damage to the heart valves, most often the mitral and aortic valves, leading to chronic rheumatic heart disease.
The best way to prevent rheumatic fever is through early and complete antibiotic treatment of strep throat. The preferred treatment is benzathine penicillin G, given as a single injection, or penicillin V taken by mouth for ten days. People allergic to penicillin may be treated with azithromycin, erythromycin, or clarithromycin. If rheumatic fever develops, treatment focuses on removing any remaining bacteria, reducing inflammation, and easing symptoms. Aspirin and other pain-relieving drugs like naproxen are used to treat joint pain and swelling, while corticosteroids such as prednisone may be given if the heart is severely inflamed.
Long-term care is important to prevent recurrence. This usually involves monthly penicillin injections for at least five to ten years, or longer if heart damage is present. People with rheumatic heart disease may also need medications like diuretics (to reduce fluid buildup), beta-blockers and ACE inhibitors (to improve heart function), and anticoagulants (to prevent blood clots). In severe cases, heart valve repair or replacement surgery may be required.
Historical Background
Rheumatic fever was once one of the leading causes of heart disease and death among children and young adults across the world. The condition was first recognized in the early 19th century, when physicians began noting the link between fever, painful joints, and later heart complications. The term “rheumatic” originates from the Greek word rheuma, meaning “flow” or “stream,” a reference to the migratory nature of the joint pain that characterizes the disease.
Before the discovery of antibiotics, rheumatic fever was a major public health problem in both industrialized and developing nations. In the early 20th century, hospitals in Europe and North America recorded thousands of cases annually, with mortality rates as high as 30% in severe cases. It was particularly common among children living in overcrowded and impoverished conditions, where streptococcal throat infections spread easily through respiratory droplets. The disease often left survivors with chronic heart valve damage, leading to lifelong disability or early death from rheumatic heart disease (RHD).
The causal relationship between rheumatic fever and Streptococcus pyogenes infections was established in the 1930s and 1940s following advances in bacteriology and immunology. Researchers demonstrated that untreated strep throat could trigger an autoimmune response, explaining why symptoms often appeared weeks after recovery from the initial infection. The introduction of penicillin in the 1940s transformed the management of strep throat and dramatically reduced the incidence of rheumatic fever in high-income countries. By the 1980s, widespread antibiotic use, improved sanitation, and better healthcare access had brought the incidence in countries such as the United States, Canada, and the United Kingdom to below 1 case per 100,000 population.
Despite this progress, rheumatic fever has not disappeared globally. It remains a persistent health challenge in low- and middle-income countries (LMICs), where socioeconomic inequalities, limited access to healthcare, and poor living conditions facilitate the spread of streptococcal infections. According to the World Health Organization (WHO), rheumatic fever and its complications still cause over 300,000 deaths annually. The Global Burden of Disease Study (2019) estimated that more than 40 million people live with rheumatic heart disease worldwide, and about 470,000 new cases of rheumatic fever are diagnosed each year.
In the pre-antibiotic era, rheumatic fever accounted for up to half of all deaths from heart disease in individuals under 40 years of age in industrialized nations. Today, the same trend persists in many low-resource settings. For example, in sub-Saharan Africa, the prevalence of rheumatic heart disease among school-aged children is estimated at 5 to 15 cases per 1,000, compared to less than 0.1 per 1,000 in high-income countries. In some Pacific Island nations, such as Fiji and Samoa, rates exceed 30 per 1,000, making rheumatic heart disease one of the leading causes of death among young adults.
Epidemiology
Rheumatic fever primarily affects children between the ages of 5 and 15 years, as this group is most likely to contract untreated strep throat infections. The disease is rare in infants and uncommon in adults, largely because older individuals have developed partial immunity through repeated exposure to the bacteria.
Globally, the incidence and prevalence of rheumatic fever and rheumatic heart disease vary significantly across regions. In high-income countries, such as those in North America and Western Europe, incidence rates have fallen below 1 case per 100,000 population. In contrast, low- and middle-income countries continue to report 10 to 100 cases per 100,000 population annually, reflecting disparities in healthcare access and social determinants of health.
The highest burden of rheumatic fever and RHD is found in sub-Saharan Africa, South Asia, the Middle East, and the Pacific Islands. For instance:
- In Africa, the WHO estimates that up to 300,000 children develop rheumatic fever each year, with RHD responsible for 1.5% to 3% of all hospital admissions.
- In India, approximately 25,000 new cases of rheumatic fever occur annually, and RHD affects nearly 2 million people.
- In the Pacific region, countries such as Fiji, Tonga, and Samoa record some of the highest prevalence rates in the world, with up to 30 per 1,000 school-aged children affected.
- Even within high-income countries, Indigenous and marginalized populations remain disproportionately affected. For example, in Australia, the incidence among Aboriginal and Torres Strait Islander communities reaches up to 100 times higher than that of the non-Indigenous population.
Rheumatic fever continues to be a major cause of preventable cardiovascular disease in children and young adults. The Global Rheumatic Heart Disease Registry (REMEDY) found that patients in developing countries are typically diagnosed 10–15 years younger than those in wealthier nations, often with more advanced valve damage at the time of diagnosis. Mortality rates remain high: up to 12% of children with severe carditis die within the first episode, and recurrent infections significantly increase the risk of heart failure and early death.
The persistence of rheumatic fever is closely linked to poverty, overcrowding, and limited access to healthcare, factors that increase the spread of streptococcal infections and hinder timely treatment. Effective control depends on primary prevention (treating strep throat early with antibiotics) and secondary prevention (long-term prophylaxis to prevent recurrence).
Causes of Rheumatic Fever
Rheumatic fever develops as a delayed immune reaction following an infection by a specific bacterium, Streptococcus pyogenes, also known as Group A Streptococcus (GAS). The condition arises not directly from the bacteria themselves, but from an abnormal immune response that occurs after the body attempts to fight the infection. This immune misfire leads to inflammation and tissue damage in various organs, most notably the heart, joints, skin, and brain. The disease typically appears two to four weeks after a throat infection, and while not everyone with strep throat develops rheumatic fever, certain factors greatly increase susceptibility, including repeated infections, genetic predisposition, and limited access to early medical treatment.
Group A Streptococcus Infection
The primary cause of rheumatic fever is infection with Streptococcus pyogenes, a bacterium responsible for strep throat and scarlet fever. This microorganism spreads easily through respiratory droplets when an infected person coughs or sneezes. Globally, it is estimated that over 600 million cases of strep throat occur annually, and while most are mild, untreated or inadequately treated infections can progress to rheumatic fever in 0.3% to 3% of cases.
When S. pyogenes infects the throat, it stimulates the body’s immune system to produce antibodies, proteins that target bacterial components known as antigens. Some of these bacterial antigens, especially the M protein on the surface of S. pyogenes, closely resemble proteins found in human tissues, including those in the heart valves, joints, and nervous system. Because of this similarity, known as molecular mimicry, the antibodies generated to fight the infection can mistakenly attack the body’s own tissues.
Importantly, the bacteria themselves do not directly damage heart or joint tissue. Instead, the immune response, involving both antibodies and white blood cells, causes inflammation that leads to the symptoms and complications characteristic of rheumatic fever. Once this immune response is triggered, it may persist even after the bacterial infection has been cleared, which explains why treatment of strep throat after the onset of rheumatic fever does not reverse the damage already done.
Pathophysiology
The underlying mechanism of rheumatic fever is an autoimmune process driven by molecular mimicry. When the immune system mistakes the body’s own tissues for foreign invaders, it triggers inflammatory reactions that affect multiple organ systems.
- Heart (Rheumatic Carditis): The most serious manifestation is inflammation of the heart, known as carditis. This may involve the inner lining (endocardium), the heart muscle (myocardium), or the outer covering (pericardium). Inflammation can lead to swelling and scarring of the heart valves, particularly the mitral and aortic valves, resulting in long-term complications such as valve stenosis (narrowing) or regurgitation (leakage). Over time, this can progress to rheumatic heart disease (RHD), a chronic condition that weakens the heart and may eventually cause heart failure. Studies suggest that up to 60% of individuals with rheumatic fever develop some degree of heart involvement.
- Joints (Migratory Arthritis): Joint inflammation, known as migratory polyarthritis, is one of the earliest and most common symptoms. It typically affects large joints such as the knees, ankles, elbows, and wrists, moving from one joint to another over several days. Unlike septic arthritis (infection inside the joint), this inflammation is sterile, caused by immune complexes rather than live bacteria.
- Skin and Subcutaneous Tissue: Rheumatic fever may cause erythema marginatum, a pink or ring-shaped rash with clear centers, and subcutaneous nodules, which are small, firm lumps under the skin. These nodules usually appear near joints or over tendons and indicate severe or prolonged disease.
- Brain (Sydenham’s Chorea): Neurological involvement, known as Sydenham’s chorea, arises when immune cells cross-react with brain tissue, particularly the basal ganglia, a region controlling movement. This results in involuntary, jerky movements of the hands, feet, and face, along with emotional instability and muscle weakness. Chorea may appear months after the initial infection and can persist for weeks to months.
At the microscopic level, tissue samples from affected organs show Aschoff bodies, distinctive areas of inflammation containing immune cells such as macrophages, T lymphocytes, and plasma cells. These are considered a hallmark of rheumatic fever and confirm the immune-mediated nature of the disease.
Risk Factors
The likelihood of developing rheumatic fever after a Group A Streptococcus infection depends on environmental, genetic, and socioeconomic factors.
- Frequent or untreated throat infections significantly increase risk. Children exposed to repeated infections over time are more likely to experience immune sensitization, making subsequent infections more likely to trigger rheumatic fever.
- The disease is most common in areas with overcrowded housing, inadequate sanitation, and limited access to healthcare, conditions that facilitate the spread of streptococcal infections. Schools and dormitories are frequent hotspots for outbreaks.
- In many low-resource settings, antibiotics may not be available, or treatment courses may not be completed, allowing infections to persist. In such areas, up to 10 per 100,000 people may develop rheumatic fever each year, compared to fewer than 1 per 100,000 in high-income countries.
- Evidence suggests that certain individuals are genetically more susceptible to rheumatic fever. Studies have identified associations between specific human leukocyte antigen (HLA) types (such as HLA-DR and HLA-DQ alleles) and increased risk. Twin studies also support a hereditary component, estimating that genetics account for about 60% of individual susceptibility.
- Rheumatic fever primarily affects children aged 5–15 years, corresponding with the peak age for strep throat infections. It is slightly more common in females, particularly in cases leading to Sydenham’s chorea or chronic rheumatic heart disease.
- Poverty, lack of education, and inadequate healthcare infrastructure contribute to persistent high rates of rheumatic fever in many parts of Africa, South Asia, and the Pacific Islands. In contrast, improved living conditions and healthcare access have nearly eliminated the disease in most industrialized nations.
Signs and Symptoms
Rheumatic fever presents with a range of clinical features that reflect inflammation in various organ systems. These features are divided into major and minor manifestations, which guide diagnosis and clinical assessment.
Major Clinical Manifestations
The major signs of rheumatic fever include carditis, polyarthritis, chorea, erythema marginatum, and subcutaneous nodules.
- Carditis involves inflammation of the heart layers, often affecting the endocardium and valves, leading to murmurs, heart enlargement, and heart failure symptoms.
- Polyarthritis appears as migratory, painful swelling of large joints such as knees, ankles, elbows, and wrists.
- Chorea is a neurological symptom characterized by involuntary, rapid, jerky movements, mainly affecting the face and limbs.
- Erythema marginatum presents as pink, non-itchy, ring-shaped skin rashes on the trunk and limbs.
- Subcutaneous nodules are firm, painless lumps found over bony prominences like elbows and knees.
These major features indicate active systemic inflammation and are essential for diagnosing rheumatic fever.
Minor Clinical Manifestations
Minor manifestations are less specific but support the diagnosis when combined with major signs and evidence of recent streptococcal infection.
Common minor symptoms include:
- Fever typically ranging between 38°C and 39°C.
- Arthralgia, which means joint pain without swelling.
- Elevated inflammatory markers such as ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein).
- Prolonged PR interval on an electrocardiogram, indicating cardiac involvement.
Minor criteria alone are insufficient for diagnosis but provide important clinical clues when present with major manifestations.
Diagnostic Criteria
The diagnosis of rheumatic fever relies on the Jones criteria, which incorporate major and minor clinical findings along with evidence of a preceding streptococcal infection.
The requirements are:
- Presence of two major manifestations or
- One major and two minor manifestations,
- Plus evidence of recent Group A Streptococcal infection confirmed by positive throat culture, rapid antigen test, or elevated antistreptolysin O (ASO) titers.
This combination ensures an accurate diagnosis and distinguishes rheumatic fever from other febrile illnesses with similar symptoms.
Diagnosis of Rheumatic Fever
Diagnosing rheumatic fever involves a detailed clinical assessment combined with specific laboratory and imaging techniques. The evaluation relies on identifying signs of recent streptococcal infection alongside characteristic symptoms and test results.
Medical History and Physical Examination
A thorough medical history is critical, focusing on recent episodes of sore throat or confirmed streptococcal pharyngitis. The clinician looks for symptoms such as fever, joint pain, and involuntary movements.
Physical examination targets signs like carditis (murmurs, tachycardia), polyarthritis, subcutaneous nodules, erythema marginatum, and chorea. These manifestations form part of the Jones criteria, used to guide diagnosis.
The clinician also assesses for evidence of previous rheumatic fever or underlying heart disease. A detailed neurological exam may identify Sydenham chorea, a key clinical feature.
Laboratory Tests
Laboratory confirmation includes evidence of recent group A streptococcal infection. Elevated or rising antistreptolysin O (ASO) titers and anti-DNase B antibodies support this.
Inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are usually elevated, indicating systemic inflammation.
Complete blood count (CBC) may show leukocytosis. Throat culture or rapid antigen detection test (RADT) identifies streptococcal presence but may be negative if infection has resolved.
Imaging Techniques
Echocardiography is essential to detect carditis and valve involvement even when clinical signs are subtle. It reveals valve thickening, regurgitation, or pericardial effusion.
Chest X-rays can assist in evaluating cardiac enlargement or pulmonary congestion secondary to heart failure.
Electrocardiogram (ECG) abnormalities such as prolonged PR interval can support the diagnosis by indicating cardiac involvement.
| Test | Purpose | Key Findings |
| ASO and anti-DNase B | Evidence of recent strep infection | Elevated antibody titers |
| ESR, CRP | Assess inflammation | Raised levels |
| Echocardiogram | Cardiac evaluation | Valve lesions, regurgitation |
| ECG | Electrical heart activity | Prolonged PR interval |
Complications of Rheumatic Fever
Rheumatic fever can cause lasting damage to several body systems. These complications primarily affect the heart, joints, nervous system, and other organs, requiring careful management to reduce long-term risks.
Rheumatic Heart Disease
Rheumatic heart disease represents the most serious and life-threatening consequence of rheumatic fever. It develops as a result of chronic inflammation and scarring of the heart valves following repeated or severe episodes of rheumatic fever. The immune-mediated attack on cardiac tissues leads to valvulitis, in which the leaflets of the valves, most commonly the mitral and aortic valves, become thickened, deformed, and eventually calcified.
Over time, this damage may cause valve stenosis (narrowing that obstructs blood flow) or regurgitation (leakage of blood backward through the valve). The resulting hemodynamic burden can lead to heart failure, atrial fibrillation, pulmonary hypertension, and an increased risk of thromboembolism or stroke.
Patients with rheumatic heart disease often present years after the initial infection, sometimes during early adulthood, with symptoms such as shortness of breath, fatigue, chest discomfort, or palpitations. Echocardiography is critical for diagnosis and monitoring progression. In severe cases, surgical intervention, including valve repair or replacement, becomes necessary to restore normal cardiac function.
Joint Involvement
Arthritis is one of the earliest and most recognizable manifestations of rheumatic fever. It typically presents as a migratory polyarthritis, meaning the inflammation moves from one joint to another, most commonly affecting the large joints such as the knees, ankles, elbows, and wrists.
Patients experience severe joint pain, redness, and swelling that may last for several days before subsiding and appearing in another joint. Despite the intensity of pain and inflammation, this form of arthritis does not cause permanent joint damage or deformity.
The joint inflammation usually resolves completely with appropriate anti-inflammatory treatment, such as high-dose aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs). However, untreated arthritis can significantly impair mobility and quality of life during the acute phase. While rare, chronic arthralgia or recurrent joint pain may persist for weeks
Neurological Effects
Among the most distinctive neurological manifestations of rheumatic fever is Sydenham chorea, also known as “St. Vitus’ dance.” It is a delayed autoimmune reaction that affects the basal ganglia, a brain region responsible for coordinating voluntary movements.
Patients with chorea exhibit involuntary, rapid, irregular, and jerky movements of the face, hands, and feet, often accompanied by muscle weakness, slurred speech, and emotional instability. These symptoms may appear weeks to months after the initial streptococcal infection and tend to worsen with stress or fatigue.
Though chorea is usually self-limiting, lasting from several weeks to months, it can cause significant psychological distress and functional impairment. Supportive management includes sedatives, anticonvulsants (such as valproic acid or carbamazepine), and emotional support. In severe or persistent cases, corticosteroids may be considered to reduce inflammation in the central nervous system.
Rarely, patients may experience residual neuropsychiatric symptoms, such as obsessive-compulsive behaviors or mood disturbances, indicating a longer-term impact on neural pathways.
Other Long-Term Effects
While heart, joint, and neurological complications are the most common, rheumatic fever can affect other tissues as well. Skin manifestations, though less frequent, are valuable diagnostic clues during the acute phase.
Two classic dermatologic signs are:
- Erythema marginatum – a non-itchy, pink, ring-shaped rash that typically appears on the trunk and proximal limbs but spares the face.
- Subcutaneous nodules – small, firm, painless lumps over bony prominences such as the elbows, knees, or spine, which indicate ongoing inflammation.
Additionally, prolonged inflammation can lead to systemic symptoms such as chronic fatigue, malaise, and weight loss, which may persist for months after the acute illness. Recurrent rheumatic fever episodes increase the likelihood of cumulative cardiac and systemic damage, reinforcing the need for continuous antibiotic prophylaxis to prevent relapse.
Treatment Options
The management of rheumatic fever is multifaceted, targeting the underlying infection, the inflammatory response, and any resulting organ damage. A comprehensive treatment plan aims to eradicate the streptococcal bacteria, reduce inflammation, prevent recurrence, and minimize long-term complications.
Antibiotic Therapy
Antibiotic therapy is essential to eliminate the Group A Streptococcus bacteria responsible for rheumatic fever. The standard treatment involves benzathine penicillin G, administered either as a single intramuscular injection or as oral penicillin V for 10 days.
For patients allergic to penicillin, macrolide antibiotics such as erythromycin or azithromycin serve as effective alternatives.
Once the acute infection is cleared, secondary prophylaxis becomes essential to prevent reinfection and recurrence. This typically involves monthly intramuscular penicillin injections (or daily oral penicillin) for several years, and in high-risk patients, potentially lifelong.
The World Health Organization (WHO) recommends that patients with carditis and residual heart disease continue prophylaxis for at least 10 years after the last episode or until age 40, whichever is longer.
Anti-Inflammatory Medications
To manage the acute inflammatory phase, high-dose aspirin remains the drug of choice. It effectively reduces fever, arthritis, and joint pain over a course lasting 2–6 weeks.
In patients with severe carditis or poor response to salicylates, corticosteroids (such as prednisone) are used to suppress the immune response and reduce cardiac inflammation. The dose is gradually tapered to avoid rebound inflammation.
In cases of Sydenham chorea, neuroleptic medications or anticonvulsants may be added to control involuntary movements and behavioral symptoms.
Supportive Care
Supportive care plays an equally important role in recovery. Bed rest is recommended during the acute phase to minimize cardiac workload and joint stress. Physical activity should be reintroduced gradually once inflammation subsides and clinical stability is achieved.
Patients should undergo regular cardiac evaluations, including echocardiograms, to detect progressive valve dysfunction early.
In cases of established rheumatic heart disease, heart valve surgery (repair or replacement) may become necessary. Anticoagulants and heart failure medications (like diuretics and beta-blockers) are often prescribed to manage complications such as atrial fibrillation or left ventricular dysfunction.
Preventing Rheumatic Fever
The prevention of rheumatic fever is a cornerstone of public health in reducing the global burden of rheumatic heart disease. Because rheumatic fever arises as a delayed autoimmune reaction to infection with Group A Streptococcus (GAS), prevention requires both early treatment of the primary infection and long-term protection against recurrence.
In essence, the strategy is twofold, primary prevention, which stops the first attack from developing, and secondary prevention, which prevents repeated episodes that lead to chronic complications.
Primary Prevention
Primary prevention aims to interrupt the disease process before rheumatic fever develops, by identifying and treating Group A Streptococcus infections promptly and completely. The vast majority of rheumatic fever cases begin with acute streptococcal pharyngitis, commonly known as strep throat, or occasionally scarlet fever.
Children aged 5 to 15 years represent the most vulnerable group, as GAS infections are especially prevalent in school-aged populations and can easily spread in crowded environments such as classrooms and dormitories.
Once a streptococcal infection is confirmed (or highly suspected), antibiotic treatment must be initiated immediately.
A 10-day course of penicillin or amoxicillin remains the treatment of choice and is proven to eradicate the organism effectively. For patients allergic to penicillin, erythromycin or other macrolides can be used.
Importantly, incomplete antibiotic courses are a major reason for the persistence of bacteria and the eventual development of rheumatic fever. Therefore, patients and caregivers must be educated about completing the full regimen, even after symptoms subside.
Prompt and complete treatment during this window, typically within 9 days of symptom onset, can almost entirely prevent rheumatic fever.
Secondary Prevention
While primary prevention targets initial infection, secondary prevention is directed at individuals who have already experienced rheumatic fever. Its purpose is to prevent recurrent episodes, which significantly increase the risk of developing chronic rheumatic heart disease.
Each subsequent attack of rheumatic fever can cause additional inflammation and scarring of heart valves, leading to cumulative, often irreversible damage. Therefore, strict and sustained prophylaxis is vital for long-term protection.
The standard regimen for secondary prevention is long-term antibiotic prophylaxis, most effectively achieved with benzathine penicillin G administered intramuscularly every 3 to 4 weeks.
This depot injection maintains bactericidal levels of penicillin in the bloodstream, providing continuous protection against new streptococcal infections.
Alternatively, for patients unable to tolerate injections, oral penicillin V twice daily may be used, though compliance tends to be lower with oral regimens.
The duration of prophylaxis depends on the severity of the disease and the extent of cardiac involvement:
- Without carditis: At least 5 years or until age 21 (whichever is longer).
- With carditis but no residual heart disease: 10 years or until age 25.
- With persistent valvular disease: At least 10 years after the last episode or until age 40 and in some cases, lifelong prophylaxis.
Adherence to these schedules is critical, as missed doses or early discontinuation can lead to reinfection and relapse.
Prognosis and Outcomes
Rheumatic fever prognosis varies depending on the severity of heart involvement and the timeliness of treatment. Patients may experience full recovery or develop complications that require ongoing medical care.
Recovery and Recurrence Rates
Most individuals with rheumatic fever recover fully within several weeks to months if treated promptly with antibiotics and anti-inflammatory medications. However, the risk of recurrence remains significant, especially if antibiotic prophylaxis is not maintained.
Recurrences occur primarily due to repeated streptococcal infections. They increase the chances of progressive valve damage, often leading to chronic rheumatic heart disease. Recurrence rates can be reduced by adhering to long-term antibiotic regimens.
Long-Term Management
Long-term management focuses on preventing repeat episodes and monitoring for chronic heart complications. Regular administration of intramuscular benzathine penicillin every 3–4 weeks for 5-10 years is standard, or longer if valve damage is severe.
Patients require routine cardiac evaluations, including echocardiograms, to detect worsening valve function. Management may include surgical intervention for severe valve disease.
Living With Rheumatic Fever
Managing rheumatic fever requires understanding the condition, adjusting daily habits, and accessing appropriate support. Careful attention to treatment and lifestyle helps reduce complications and improve quality of life.
Patient Education
Patients need a clear understanding of rheumatic fever’s cause, symptoms, and treatment. It is crucial to recognize early signs of recurrence, such as joint pain, fever, or involuntary movements.
Adherence to prescribed antibiotics, often penicillin, is essential to prevent recurrent attacks and heart damage. Patients should be informed about the importance of completing the full course, even if symptoms improve.
Awareness about the risk of rheumatic heart disease guides patients in scheduling regular follow-ups.
Lifestyle Modifications
Modifications focus on reducing physical strain and preventing infections. Patients are advised to avoid strenuous activities during active disease phases to minimize stress on the heart.
Maintaining good oral hygiene is important because dental infections can trigger streptococcal infections linked to rheumatic fever. Nutritional support emphasizing balanced diets aids recovery.
Avoiding crowded places during peak infection seasons reduces exposure to streptococcal bacteria. Patients should receive annual influenza vaccinations to prevent respiratory infections.