Rheumatic Fever


Rheumatic fever (RF) is a systemic illness that may occur following group A beta hemolytic streptococcal (GABHS) pharyngitis in children. RF and its most serious complication, rheumatic heart disease (RHD), are believed to result from an autoimmune response; however, the exact pathogenesis remains unclear. Studies in the 1950s during an epidemic on a military base demonstrated 3 per cent incidence of RF in adults with streptococcal pharyngitis not treated with antibiotics. Studies in children during the same period demonstrated an incidence of only 0.3 per cent. Cardiac involvement is reported to occur in 30-70 per cent of patients with their first attack of RF and in 73-90 per cent of patients when all attacks are counted.


RF develops in children and adolescents following pharyngitis with GABHS (ie, Streptococcus pyogenes). The organisms attach to the epithelial cells of the upper respiratory tract and produce a battery of enzymes, which allows them to damage and invade human tissues. After an incubation period of 2-4 days, the invading organisms elicit an acute inflammatory response, with 3-5 days of sore throat, fever, malaise, headache, and elevated leukocyte count. In a small percent of patients, infection leads to RF several weeks after the sore throat has resolved. Only infections of the pharynx initiate or reactivate RF.

Direct contact with oral or respiratory secretions transmits the organism, and crowding enhances transmission. Patients remain infected for weeks after symptomatic resolution of pharyngitis and may serve as a reservoir for infecting others. Penicillin treatment shortens the clinical course of streptococcal pharyngitis and more importantly prevents the major sequelae.

GABHS organisms are gram-positive cocci, which frequently colonize the skin and oropharynx. These organisms may cause suppurative diseases (eg, pharyngitis, impetigo, cellulitis, myositis, pneumonia, puerperal sepsis). GABHS organisms also may be associated with nonsuppurative diseases (eg, RF, acute poststreptococcal glomerulonephritis). Group A streptococci (GAS) elaborate the cytolytic toxins, streptolysins S and O. Of these 2 toxins, streptolysin O induces persistently high antibody titers that provide a useful marker of GAS infection and its nonsuppurative complications.

GAS, as identified using the Lancefield classification, has a group A carbohydrate antigen in the cell wall that is composed of a branched polymer of L-rhamnose and N-acetyl-D-glucosamine in a 2:1 ratio. GAS may be subserotyped by surface proteins on the cell wall of the organism. The presence of the M protein is the most important virulence factor for GAS infection in humans. More than 90 M serotypes have been identified, some of which have a long terminal antigenic domain (ie, epitopes) similar to antigens in various components of the human heart. Rheumatogenic strains often are encapsulated mucoid strains, rich in M proteins, and resistant to phagocytosis. These strains are strongly immunogenic, and anti-M antibodies against the streptococcal infection may cross-react with components of heart tissue (ie, sarcolemmal membranes, valve glycoproteins).

Acute RHD often produces a pancarditis, characterized by endocarditis, myocarditis, and pericarditis. Endocarditis is manifested as mitral and aortic valve insufficiency. Severe scarring of the valves develops during a period of months to years after an episode of acute RF, and recurrent episodes may cause progressive damage to the valves. The mitral valve is affected most commonly and severely (65-70 per cent of patients); the aortic valve is affected second most commonly (25 per cent). The tricuspid valve is deformed in only 10 per cent of patients, almost always in association with mitral and aortic lesions, and the pulmonary valve rarely is affected. Severe valve insufficiency during the acute phase may result in congestive heart failure (CHF) and even death (1 per cent of patients). Whether myocardial dysfunction during acute RF is related primarily to myocarditis or is secondary to CHF from severe valve insufficiency is not known. When pericarditis is present, it rarely affects cardiac function or results in constrictive pericarditis.

Chronic manifestations occur in adults with previous RHD from residual and progressive valve deformity. RHD is responsible for 99 per cent of mitral valve stenosis in adults, and it may be associated with atrial fibrillation from chronic mitral valve disease and atrial enlargement.


In the US:

RF is now uncommon among children in the US. Incidence of RF and RHD has decreased in the US and other industrialized countries during the past 80 years. Prevalence of RHD in the US is now less than 0.05 per 1000 population, with rare regional outbreaks reported in Tennessee in the 1960s and in Utah, Ohio, and Pennsylvania in the 1980s. In the early 1900s, incidence was reportedly 5-10 cases per 1000 population. Decreased incidence of RF has been attributed to the introduction of penicillin or a change in the virulence of the streptococci.


In contrast to trends in the US, RF and RHD have not decreased in developing countries. Retrospective studies in developing countries demonstrate the highest figures for cardiac involvement and the highest recurrence rates of RF. Worldwide, an estimated 5-30 million children and young adults have chronic RHD, and 90,000 patients die from this disease each year.


RHD is the major cause of morbidity from RF, and it is the major cause of mitral insufficiency and stenosis in the US and the world. Variables that correlate with severity of valve disease are the number of previous attacks of RF, the length of time between the onset of disease and start of therapy, and sex (the prognosis for females is worse than for males). Insufficiency from acute rheumatic valve disease resolves in 70-80 per cent of patients if they adhere to antibiotic prophylaxis.


Native Hawaiians and Maori (both of Polynesian descent) have a higher incidence of RF. Incidence of RF in these patients is 13.4 per 100,000 hospitalized children per year, even with antibiotic prophylaxis of streptococcal pharyngitis. Otherwise, race (when controlled for socioeconomic variables) has not been documented to influence the disease incidence.


RF occurs in equal numbers in males and females. Females with RF fare worse than males and have a slightly higher incidence of chorea.


RF is principally a disease of childhood, with a median age of 10 years; however, RF also occurs in adults (20 per cent of cases).


Acute RF is a systemic disease. Thus, patients may present with a large variety of symptoms and complaints.

History of an antecedent sore throat 1-5 weeks prior to onset is present in 70 per cent of older children and young adults. Only 20 per cent of younger children can recall an antecedent sore throat.

Other symptoms on presentation may include fever, rash, headache, weight loss, epistaxis, fatigue, malaise, diaphoresis, and pallor.

Patients also may have chest pain with orthopnea or abdominal pain and vomiting.

Finally, history may reveal complaints more specific to RF.

Migratory joint pain

Nodules under the skin

Increased irritability and shortened attention span with personality changes, such as pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS)

Motor dysfunction

History of previous RF

Patients with previous RF are at a high risk of recurrence.

Highest risk of recurrence within 5 years of the initial episode

Greater risk of recurrence with younger age at the time of the initial episode

Generally, recurrent attacks similar to the initial attack (however, risk of carditis and severity of valve damage increase with each attack)


Revised in 1992, the modified Jones criteria provide guidelines for making the diagnosis of RF. The Jones criteria require the presence of 2 major or 1 major and 2 minor criteria for the diagnosis of RF. Having evidence of previous GAS pharyngitis is also necessary. These criteria are not absolute, and the diagnosis of RF can be made in patients with only confirmed streptococcal pharyngitis and chorea.


It may occur late and be the only manifestation of RF.

Indolent Carditis:

Patients presenting late to medical attention months after the onset of RF may have insufficient support to fulfill the criteria.

Newly ill patients with a history of RF, especially RHD, who have supporting evidence of a recent GAS infection and who manifest either a single major or several minor criteria: Distinguishing recurrent carditis from preexisting significant RHD may be impossible.

Evidence of previous GAS pharyngitis (One of the following must be present):


Polyarthritis is the most common symptom and frequently is the earliest manifestation of acute RF (70-75 per cent). Characteristically, the arthritis begins in the large joints of the lower extremities (ie, knees, ankles) and migrates to other large joints in the lower or upper extremities (ie, elbows, wrists). Affected joints are painful, swollen, warm, erythematous, and limited in their range of motion. The pain is out of proportion to clinical findings. The arthritis reaches maximum severity in 12-24 hours and persists for 2-6 days (rarely more than 4 wk, but has been reported to persist 44 d) at each site and is migratory but not additive. The arthritis responds rapidly to aspirin, which decreases symptoms in affected joints and prevents further migration of the arthritis. Polyarthritis is more common and more severe in teenagers and young adults than in younger children. Patients suffering multiple attacks may exhibit destructive arthritis (Jaccoud arthritis).


Pancarditis is the most serious complication and the second most common complication of RF (50 per cent). In advanced cases, patients may complain of dyspnea, mild-to-moderate chest discomfort, pleuritic chest pain, edema, cough, or orthopnea. On physical examination, carditis most commonly is detected by a new murmur and tachycardia that is out of proportion to the fever. New or changing murmurs traditionally have been considered necessary for a diagnosis of rheumatic valvulitis. The murmurs of acute RF are from valve regurgitation, and the murmurs of chronic RF are from valve stenosis. Frequently examine patients in whom the diagnosis of acute RF is made due to the progressive nature of the disease. Some cardiologists have proposed that evidence of new mitral regurgitation from Doppler echocardiography, even in the absence of accompanying auscultatory findings, may be sufficient for making the diagnosis of carditis, particularly if the echo findings resolve along with other manifestations of RF. This criterion for carditis is not accepted uniformly and remains specifically excluded in the 1992 revised Jones criteria because of insufficient data at the time of publication.

CHF may develop secondary to severe valve insufficiency or myocarditis. Physical findings associated with heart failure include tachypnea, orthopnea, jugular venous distention, rales, hepatomegaly, a gallop rhythm, and peripheral swelling and edema. A pericardial friction rub indicates that pericarditis is present. Increased cardiac dullness to percussion, muffled heart sounds, and a paradoxical pulse are consistent with pericardial effusion and impending pericardial tamponade. Confirm this clinical emergency with ECG, and evacuate the effusion by pericardiocentesis if it is producing hemodynamic compromise.


This finding occurs in 10-30 per cent of patients with RF. Patients present with difficulty writing, involuntary grimacing, purposeless (ie, choreiform) movements of the arms and legs, speech impairment, generalized weakness, and emotional lability. Physical findings include hyperextended joints, hypotonia, diminished deep tendon reflexes, tongue fasciculations ("bag of worms"), and a "milk sign" or "relapsing grip" (ie, alternate increases and decreases in tension when the patient grips the examiner's hand). Occasionally, chorea is predominantly unilateral. Choreiform movements cease with sleep.

In the absence of a family history of Huntington chorea or findings consistent with systemic lupus erythematosus, the diagnosis of acute RF is almost certain. A long latency period exists between streptococcal pharyngitis (1-6 mo) and the onset of chorea, and a history of an antecedent sore throat frequently is not obtained. Patients with chorea often do not demonstrate other Jones criteria. Chorea is slightly more common in females than males. Chorea also is known as rheumatic chorea, Sydenham chorea, chorea minor, and St Vitus dance. Daily handwriting samples can be used as an indicator of progression or resolution of disease. Complete resolution of the symptoms typically occurs, with improvement in 1-2 weeks and full recovery in 2-3 months; however, incidents have been reported in which symptoms wax and wane for several years.

The PANDAS disorder may be associated with chorea. Children have been identified in whom GAS infection appears to have triggered a relapsing-remitting symptom complex characterized by obsessive-compulsive personality disorder, and/or a tic disorder, and neurologic abnormalities (eg, cognitive defects, motoric hyperactivity). The symptoms may include emotional lability, separation anxiety, and oppositional behaviors, and they are prepubertal in onset. Some have proposed that the streptococcal infection triggers the formation of antibodies that cross-react with the basal ganglia of genetically susceptible hosts in a manner similar to the proposed mechanism for Sydenham chorea and causes the symptom complex.

Erythema Marginatum:

This characteristic rash, also known as erythema annulare, occurs in 5-13 per cent of patients with acute RF. Erythema marginatum begins as 1- to 3-cm diameter, pink-to-red nonpruritic macules or papules located on the trunk and proximal limbs but never on the face. The lesions spread outward to form a serpiginous ring with erythematous raised margins and central clearing. The rash may fade and reappear within hours and is exacerbated by heat. Thus, if the lesions are not observed easily, they can be accentuated by the application of warm towels, a hot bath, or the use of tangential lighting. The rash occurs early in the course of the disease and remains long past the resolution of other symptoms. Erythema marginatum also has been reported in association with sepsis, drug reactions, and glomerulonephritis.

Subcutaneous nodules: Subcutaneous nodules are now an infrequent manifestation of RF. The frequency has declined during the past several years to 0-8 per cent of patients with RF. When present, the nodules appear over the extensor surfaces of the elbows, knees, ankles, knuckles, scalp, and spinous processes of the lumbar and thoracic vertebrae (attached to the tendon sheath). The nodules are firm, nontender, and free from attachments to the overlying skin, and they range from a few millimeters to 1-2 cm. The nodules number from 1 to dozens, with a mean of 3-4. Histologically, the nodules contain areas resembling the Aschoff bodies observed in the heart. Subcutaneous nodules generally occur several weeks into the disease and resolve within a month. They are strongly associated with severe rheumatic carditis, and in the absence of carditis, question the diagnosis of subcutaneous nodules.

Other Clinical Manifestations

Abdominal Pain:

Abdominal pain usually occurs at the onset of acute RF, resembles other conditions with acute microvascular mesenteric inflammation, and may mimic acute appendicitis.


Patients may complain of arthralgias on presentation. In the history, determining if the patient has taken aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) is important because these may suppress the full manifestations of the disease. Arthralgia cannot be considered a minor manifestation if arthritis is present.


Epistaxis may be associated with severe protracted rheumatic carditis.


Fevers greater than 39°C with no characteristic pattern are present initially in almost every patient with acute RF. The fever may be low grade (38.0-38.5°C) in children with mild carditis or absent in patients with pure chorea. The fever decreases without antipyretic therapy in approximately 1 week, but low-grade fevers persist for 2-3 weeks.

Rheumatic pneumonia: Patients present with the same signs as an infectious pneumonia. Differentiate rheumatic pneumonia from respiratory distress related to CHF.


Other Problems to be Considered:

Controversy exists as to whether the entity of poststreptococcal reactive arthritis (PSRA) is along the clinical continuum of RF or is a separate clinical entity. PSRA is characterized by objective arthritis in the setting of a vigorous immune response to streptococcal antigens; however, the arthritis is nonmigratory and poorly responsive to aspirin. Children with PSRA do not fulfill modified Jones criteria. Most pediatric rheumatologists treat PSRA with the same antibiotic prophylaxis provided to individuals with RF.


Lab Studies:

Throat culture

Throat cultures for GABHS infections usually are negative by the time symptoms of RF or RHD appear.

Make attempts to isolate the organism prior to the initiation of antibiotic therapy to help confirm a diagnosis of streptococcal pharyngitis and to allow typing of the organism if it is isolated successfully.

Rapid Antigen Detection Test

This test allows rapid detection of GAS antigen, allowing the diagnosis of streptococcal pharyngitis to be made and antibiotic therapy to be initiated while the patient is still in the physician's office.

This test reportedly has a specificity of greater than 95 per cent but a sensitivity of only 60-90 per cent. Thus, obtain a throat culture in conjunction with the rapid antigen detection test.

Antistreptococcal Antibodies

Clinical features of RF begin when antistreptococcal antibody levels are at their peak. Thus, these tests are useful for confirming previous GAS infection. Antistreptococcal antibodies are particularly useful in patients who present with chorea as the only diagnostic criterion.

Sensitivity for recent infections can be improved by testing for several antibodies. Check antibody titers 2 weeks apart to detect a rising titer. The most common extracellular antistreptococcal antibodies tested include antistreptolysin O (ASO) and anti-DNase B, antihyaluronidase, antistreptokinase, antistreptococcal esterase, and anti-nicotinamide adenine dinucleotide (anti-NAD). Antibody tests for cellular components of GAS antigens include antistreptococcal polysaccharide, antiteichoic acid antibody, and anti-M protein antibody.

In general, the antibodies to extracellular streptococcal antigens rise during the first month after infection and then plateau for 3-6 months before returning to normal levels after 6-12 months. When the ASO titer peaks (2-3 wk after onset of RF), the sensitivity of this test is 80-85 per cent.

The anti-DNase B has a slightly higher sensitivity (90 per cent) for detecting RF or acute glomerulonephritis. Antihyaluronidase frequently is abnormal in patients with RF with a normal ASO titer, may rise earlier, and persists longer than elevated ASO titers during incidents of RF.

Acute-phase Reactants:

C-reactive protein and erythrocyte sedimentation rate are elevated in individuals with RF due to the inflammatory nature of the disease. Both tests have high sensitivity but low specificity for RF.

Heart Reactive Antibodies:

Tropomyosin is elevated in persons with acute RF.

Rapid detection test for D8/17: This immunofluorescence technique for identifying the B-cell marker D8/17 is positive in 90 per cent of patients with RF, and it may be useful for identifying patients who are at risk of developing RF.

Imaging Studies:

Chest radiography

Cardiomegaly, pulmonary congestion, and other findings consistent with heart failure may be observed on chest radiograph in individuals with RF.

When the patient has fever and respiratory distress, the chest radiograph helps differentiate between CHF and rheumatic pneumonia.


In individuals with acute RDH, echocardiography identifies and quantitates valve insufficiency and ventricular dysfunction.

In persons with mild carditis, Doppler evidence of mitral regurgitation may be present during the acute phase of disease but resolves in weeks to months.

In contrast, patients with moderate-to-severe carditis have persistent mitral and/or aortic regurgitation. The most important echocardiographic features of mitral regurgitation from acute rheumatic valvulitis are annular dilatation, elongation of the chordae to the anterior leaflet, and a posterolaterally directed mitral regurgitation jet.

During acute RF, the left ventricle frequently is dilated in association with a normal or increased fractional shortening. Thus, some cardiologists believe that valve insufficiency (eg, from endocarditis), rather than myocardial dysfunction (eg, from myocarditis), is the dominant cause of heart failure in individuals with acute RF.

In individuals with chronic RHD, echocardiography tracks the progression of valve stenosis and may help determine the time for surgical intervention. The leaflets of affected valves become thickened diffusely, with fusion of the commissures and chordae tendineae. Increased echodensity of the mitral valve may signify calcification.

Other Tests:


Sinus tachycardia most frequently accompanies acute RHD. Alternatively, some children develop sinus bradycardia from increased vagal tone. No correlation exists between bradycardia and severity of carditis.

First-degree atrioventricular (AV) block (prolongation of PR interval) is observed in some patients with RHD. This abnormality may be related to localized myocardial inflammation involving the AV node or to vasculitis involving the AV nodal artery. First-degree AV block is a nonspecific finding and should not be used as a criterion for the diagnosis of RHD. Its presence does not correlate with the development of chronic RHD.

Second-degree (ie, intermittent) and third-degree (ie, complete) AV block with progression to ventricular standstill have been described. However, heart block in the setting of RF typically resolves with the rest of the disease process.

In individuals with acute pericarditis, ST segment elevation may be present, most marked in leads II, III, aVF, and V4 through V6.

Finally, patients with RHD may develop atrial flutter, multifocal atrial tachycardia, or atrial fibrillation from chronic mitral valve disease and atrial dilation.


Cardiac catheterization: This study is not indicated in acute RF.

Histologic Findings: Pathologic examination of the insufficient valves may demonstrate verrucous lesions at the line of closure. Aschoff bodies (ie, perivascular foci of eosinophilic collagen surrounded by lymphocytes, plasma cells, and macrophages) are found in the pericardium, perivascular regions of the myocardium, and endocardium. The Aschoff bodies assume a granulomatous appearance with a central fibrinoid focus and eventually are replaced by nodules of scar tissue. Anitschkow cells are plump macrophages within Aschoff bodies. In the pericardium, fibrinous and serofibrinous exudates may produce an appearance of "bread and butter" pericarditis.

Medical Care: Direct medical therapy toward eliminating the GAS pharyngitis (if still present), suppressing inflammation from the autoimmune response, and providing supportive treatment of CHF. Oral penicillin V remains the drug of choice for treatment of GAS pharyngitis. When oral penicillin is not feasible or dependable, a single dose of intramuscular benzathine penicillin G is therapeutic. For patients who are allergic to penicillin, administer erythromycin or a first-generation cephalosporin. Other options include clarithromycin for 10 days, azithromycin for 5 days, or a narrow-spectrum (first-generation) cephalosporin for 10 days. As many as 15 per cent of penicillin-allergic patients also are allergic to cephalosporins. Do not use tetracyclines and sulfonamides to treat GAS pharyngitis.

For recurrent GAS pharyngitis, a second 10-day course of the same antibiotic may be repeated. Alternate drugs include narrow-spectrum cephalosporins, amoxicillin-clavulanate, dicloxacillin, erythromycin, or other macrolides.

GAS carriage is difficult to eradicate with conventional penicillin therapy. Thus, oral clindamycin (20 mg/kg/d PO in 3 divided doses for 10 d) is recommended.

In general, antimicrobial therapy is not indicated for pharyngeal carriers of GAS. Exceptions include the following:

Outbreaks of RF or poststreptococcal glomerulonephritis

Family History of RF

During outbreaks of GAS pharyngitis in a closed community

When tonsillectomy is considered for chronic GAS carriage

When multiple episodes of documented GAS pharyngitis occur within a family despite appropriate therapy

Following GAS toxic shock syndrome or necrotizing fasciitis in a household contact

Treatment of the acute inflammatory manifestations of acute RF consists of salicylates and steroids. Aspirin in anti-inflammatory doses effectively reduces all manifestations of the disease except chorea, and the response typically is dramatic.

If rapid improvement is not observed after 24-36 hours of therapy, question the diagnosis of RF.

Attempt to obtain aspirin blood levels from 20-25 mg/dL, but stable levels may be difficult to achieve during the inflammatory phase because of variable GI absorption of the drug. Maintain aspirin at anti-inflammatory doses until the signs and symptoms of acute RF are resolved or residing (6-8 wk) and the APRs have returned to normal.

Anti-inflammatory doses of aspirin may be associated with abnormal liver function tests and GI toxicity, and adjusting the aspirin dosage may be necessary.

When discontinuing therapy, withdraw aspirin gradually over weeks while monitoring the APRs for evidence of rebound. Chorea most frequently is self-limited but may be alleviated or partially controlled with phenobarbital or diazepam.

If moderate-to-severe carditis is present as indicated by cardiomegaly, CHF, or third-degree heart block, add oral prednisone to salicylate therapy.

Continue prednisone for 2-6 weeks depending on the severity of the carditis, and taper prednisone during the last week of therapy.

Discontinuing prednisone therapy after 2-4 weeks, while maintaining salicylates for an additional 2-4 weeks, can minimize adverse effects.

Include digoxin and diuretics, afterload reduction, supplemental oxygen, bed rest, and sodium and fluid restriction as additional treatment for patients with acute RF and CHF. The diuretics most commonly used in conjunction with digoxin for children with CHF include furosemide and spironolactone.

Initiate digoxin only after checking electrolytes and correcting abnormalities in serum potassium.

The total loading dose is 20-30 mcg/kg PO qd, with 50 per cent of the dose administered initially, followed by 25 per cent of the dose 8 and 16 hours after the initial dose. Maintenance doses typically are 8-10 mcg/kg/d PO in 2 divided doses. For older children and adults, the total loading dose is 1.25-1.5 mg PO, and the maintenance dose is 0.25-0.5 mg PO qd. Therapeutic digoxin levels are present at trough levels of 1.5-2 ng/mL.

Afterload reduction (ie, using ACE inhibitor captopril) may be effective in improving cardiac output, particularly in the presence of mitral and aortic insufficiency. Judiciously start these agents in the absence of hypovolemia.

When heart failure persists or worsens during the acute phase after aggressive medical therapy, surgery is indicated to decrease valve insufficiency.

Preventive and prophylactic therapy is indicated after RF and RHD to prevent further damage to valves. Primary prophylaxis (initial course of antibiotics administered to eradicate the streptococcal infection) also serves as the first course of secondary prophylaxis (prevention of recurrent RF and RHD).

An injection of 0.6-1.2 million units of benzathine penicillin G intramuscularly every 4 weeks is the recommended regimen for secondary prophylaxis for most US patients. Administer the same dosage every 3 weeks in areas where RF is endemic, in patients with residual carditis, and in high-risk patients.

While oral penicillin prophylaxis also is effective, data from the World Health Organization indicate that the recurrence risk of GAS pharyngitis is lower when penicillin is administered parentally.

The duration of antibiotic prophylaxis is controversial. Continue antibiotic prophylaxis indefinitely for patients at high risk (eg, health care workers, teachers, daycare workers) for recurrent GAS infection. Ideally, continue prophylaxis indefinitely, because recurrent GAS infection and RF can occur at any age; however, the American Heart Association currently recommends that patients with RF without carditis receive prophylactic antibiotics for 5 years or until aged 21 years, whichever is longer. Patients with RF with carditis but no valve disease should receive prophylactic antibiotics for 10 years or well into adulthood, whichever is longer. Finally, patients with RF with carditis and valve disease should receive antibiotics at least 10 years or until aged 40 years.

Patients with RHD and valve damage require a single dose of antibiotics 1 hour before surgical and dental procedures to help prevent bacterial endocarditis. Patients who had RF without valve damage do not need endocarditis prophylaxis. Do not use penicillin, ampicillin, or amoxicillin for endocarditis prophylaxis in patients already receiving penicillin for secondary RF prophylaxis (relative resistance of oral streptococci to penicillin and aminopenicillins). Alternate drugs recommended by the American Heart Association for these patients

Submitted By

Thomas K Chin, Md, & Clyde Worley, Md

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