Pediatric Bacterial Endocarditis 

Updated: Mar 31, 2016
Author: Michael H Gewitz, MD; Chief Editor: Syamasundar Rao Patnana, MD 

Overview

Background

Bacterial endocarditis is a microbial infection of the endothelial surface of the heart. Signs and symptoms of bacterial endocarditis are diverse; therefore, the practitioner must have a high degree of suspicion to make an early diagnosis. In addition, classification that implicates the disease’s temporal aspect, etiology, anatomic site of infection, and relevant pathogenic risk factors is essential in therapeutic and prognostic considerations.[1] (See History and Physical Examination.)

Go to Infective Endocarditis for more complete information on this topic. 

Pathophysiology

Features of bacterial endocarditis are due to bacteremia, local cardiac invasion by organisms, peripheral embolization, and the formation of immune complexes.

High-velocity flow through a stenotic or incompetent valve or an abnormal communication between systemic and pulmonary circulations causes turbulence at the valve, within the communication, or downstream where the flow eddies. This turbulence damages or denudes the endothelium, to which platelets and fibrin can adhere, and a small, sterile nonbacterial thrombotic endocardial lesion forms.

In addition, indwelling intravascular catheters may directly traumatize the endocardium or valvular endothelium. Circulating bacteria and inflammatory cells adhere to and grow in these thrombi, forming an infected vegetation. Once vegetation forms, the constant blood flow may result in embolization to virtually any organ in the body. A brisk immunologic response is produced.

Acute heart failure may be due to valve destruction or distortion and/or rupture of the chordae tendineae. Chronic heart failure may be due to progressive valvular insufficiency with worsening ventricular function. (See Epidemiology.)

Vasculitis may result from circulating immune complexes that may deposit on various endothelial surfaces. Local complement activation appears to generate an immune response that causes vascular injury. (See Epidemiology.)

Renal insufficiency resulting from immune complex–mediated glomerulonephritis occurs in less than 15% of patients with endocarditis and may cause hematuria and, rarely, azotemia, which is independent of circulatory dynamics.

Not uncommonly, and especially in neonates, infective endocarditis produces septic embolic phenomena, such as osteomyelitis, meningitis, and pneumonia. (See Etiology and Epidemiology.)

Etiology

Microbiology

A select group of organisms causes most cases of endocarditis. Gram-positive organisms, particularly alpha-hemolytic streptococci (Streptococcus viridans), Staphylococcus aureus, and coagulase-negative staphylococci, are the most common offenders. S aureus is the most common cause of acute bacterial endocarditis.

Enterococci are rare, but dangerous, causative organisms, because they often are highly resistant to antibiotic treatment.

Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella species (HACEK organisms) are particularly common in neonates and immunocompromised children.

Fungal endocarditis is a severe disease with a poor prognosis. Complications are common.

Culture-negative endocarditis

Culture-negative endocarditis occurs when a patient has typical clinical or echocardiographic findings of endocarditis, with persistently negative blood cultures. Common causes include recent antibiotic therapy, or infection caused by a fastidious organism that grows poorly in vitro.

Risk factors

High-risk conditions include the following:

  • Cyanotic congenital heart disease

  • Valvulopathy in a cardiac transplantation patient

  • Prosthetic valve

  • Intravenous drug use

  • Previous episode of bacterial endocarditis

  • Surgical systemic to pulmonary shunts and conduits

  • Central venous catheters (especially neonates)

  • Residual cardiac defect post surgical or catheter intervention for that defect

Epidemiology

In the United States, the incidence of endocarditis is approximately 1 case per 1000 pediatric hospital admissions.[2] This incidence has remained essentially unchanged over the past 40 years; however, the distribution of etiologies has shifted.

Rheumatic heart disease, which was once common, is now rare as a condition associated with endocarditis. In contrast, the advent of sophisticated cardiac procedures and early intervention with improved survivor rates has led to an increase in congenital heart disease as the underlying condition in children with endocarditis. Preexisting cardiac abnormalities are found in approximately 75-90% of children with bacterial endocarditis.[3] In premature neonates, the prevalent use of chronic indwelling catheters and prolonged hospitalization with frequent interventional therapies has led to an increased incidence of endocarditis even when the heart is structurally normal.

Race-, sex-, and age-related demographics

No racial or sex predilection is observed.

Bacterial endocarditis is most frequently observed in adults, but the incidence in children and infants with congenital heart disease or central indwelling venous catheters continues to rise.

Prognosis

The prognosis of bacterial endocarditis varies with the etiologic agent.[4] Infection by a penicillin-sensitive Streptococcus, if diagnosed early, has a cure rate of nearly 100%.

Because many infections are diagnosed late or are due to resistant organisms, the average mortality rate is approximately 16-25%.

Mortality rate

The overall mortality rate for endocarditis in pediatric patients is approximately 16-25%. Improved general health care, improved dental care, early treatment, and antibiotic prophylaxis have decreased the mortality rate.[3]  Mortality is mostly due to secondary congestive heart failure (CHF) or to the complications of systemic emboli. Russell et al reported an overall mortality of 15% in children who underwent surgery.[5]

Heart failure with acute, severe aortic insufficiency is associated with high mortality rates.

Morbidity

Cardiac complications include heart failure, new valvular disease, valve ring abscess, myocardial disease or abscess, conduction abnormalities (including arrhythmia or heart block), and pericardial disease. In rare cases, coronary artery embolic events can occur.

Vasculitis may result from circulating immune complexes that may deposit on various endothelial surfaces. Local complement activation appears to generate an immune response that causes vascular injury.

Endocarditis commonly produces septic embolic phenomena, such as osteomyelitis, meningitis, and pneumonia, with neonates most prone to these complications.

Embolic complications are most common in patients with large or highly mobile lesions. Peripheral vascular complications include splenic emboli with infarction or abscess, embolization to the pulmonary artery, and emboli to the femoral artery, resulting in extremity pain and decreased pulses.

Mycotic aneurysms occur in 10-20% of patients with endocarditis. They are often multiple and may involve any vessel.

Cutaneous manifestations include petechiae, Osler nodes, Janeway lesions, and splinter hemorrhages.

Neurologic syndromes include cerebral embolism, infarction, and intracerebral hemorrhage and stroke. Seizures, meningitis, and mental status changes have also been reported. Neurologic abnormalities occur in approximately 30-40% of patients and are most frequent in endocarditis caused by S aureus. Symptoms include stroke, intracerebral hemorrhage, and subarachnoid hemorrhage.

Renal embolism and infarction occur in patients with bacterial endocarditis. This complication may result in pain in the flank or abdomen but may be asymptomatic in as many as 50% of cases. Glomerular disease is a common finding, and is usually not of serious clinical significance because renal failure rarely occurs. However, renal insufficiency resulting from immune complex–mediated glomerulonephritis occurs in less than 15% of patients with endocarditis and may cause hematuria and, rarely, azotemia.

Hepatosplenomegaly is noted in approximately 15-20% of patients.

Neonates with endocarditis may also have feeding problems, respiratory distress, or tachycardia.

Factors that increase the risk of complications include prosthetic valve endocarditis, left-sided endocarditis, infection with S aureus or fungi, previous endocarditis, cyanotic congenital heart disease, systemic-to-pulmonary shunts, and a poor response to antibiotic therapy.

Go to Neurological Sequelae of Infective Endocarditis for more complete information on this topic.

Patient Education

American Heart Association (AHA) guidelines for the prevention of bacterial endocarditis should be emphasized to the family of each patient identified as being at high risk. These recommendations underwent significant changes in 2007.[6]

All children at risk and their families should also be instructed about the importance of maintaining the best possible oral health.

Patient and parent education is critical to ensuring appropriate antimicrobial prophylaxis before high-risk dental procedures are performed in children with cardiac conditions having a highest risk for complications from endocarditis.

 

Presentation

History

Patients with acute bacterial endocarditis (ABE) present with an acute, toxic, febrile illness and symptoms that have lasted less than 2 weeks. (Between 85% and 99% of patients are febrile.) Often, the heart is structurally normal before ABE onset.

Features in the patient’s history can include fatigue, chills, sweats, anorexia, malaise, cough, headache, myalgia and/or arthralgia, and confusion.

A history of intravenous (IV) drug use may be elicited, as it was in the patient whose chest x-ray is below.

A young adult with a history of intravenous drug u A young adult with a history of intravenous drug use diagnosed with right-sided staphylococcal endocarditis and multiple embolic pyogenic abscesses on chest radiograph.

 

Patients with congenital heart disease and fever require special consideration.

Patients with subacute bacterial endocarditis (SBE) present with a more nonspecific, flulike illness and symptoms that may have lasted more than 2 weeks. Subacute bacterial endocarditis is more common in patients with an underlying congenital heart defect. Clinical findings are related to four underlying phenomena, namely, bacteremia (or fungemia), valvulitis, immunologic responses, and/or emboli.

Physical Examination

Physical findings are nonspecific and vary. Factors such as the duration of illness, microbiologic etiology, and patient's age may vary. Thus, the frequency with which different signs and symptoms are manifested is variable. One study that analyzed 76 consecutive cases revealed the following prevalences: fever,  99%; petechiae, 21%; changing murmur, 21%; hepatosplenomegaly, 14%; congestive heart failure, 9%; splenomegaly, 7%; splinter hemorrhages, 5%; retinal hemorrhages (Roth spots), 5%; Osler nodes, 4%; and arthritis, 3%.[7]

As previously mentioned, fever is present in 85-99% of patients with endocarditis. The fever is usually low grade, with a temperature rarely exceeding 39°C that is remittent and is typically not associated with rigors.

A new or changing heart murmur is noted in many patients. These murmurs may be difficult to identify in patients with subacute endocarditis or in infants and young children who may already have a clinically significant murmur secondary to congenital heart disease.

Peripheral signs may be observed, although extracardiac manifestations of endocarditis are less common overall in children than in adults. Petechiae are the most common of these signs (20-40%). They are found on the palpebral conjunctiva, the buccal or palatal mucosa, and the extremities. However, petechiae are not specific for endocarditis.

Splenomegaly is a common finding on abdominal examinations.

Splinter and subungual hemorrhages are dark red, linear streaks in the nail beds of the fingers and toes. Osler nodes are small, tender, subcutaneous nodules that develop in the pulp of the digits.

 

DDx

Diagnostic Considerations

Using the modified Duke Criteria (see Workup), the diagnosis of endocarditis is based on pathologic or clinical findings.[8] Pathologic criteria for definite infectious endocarditis include microorganisms on cultures or histology in a vegetation or histologic confirmation of active disease in a vegetation or intracardiac abscess.

Differential Diagnoses

 

Workup

Approach Considerations

Under the modified Duke criteria, the clinical criteria for definite infectious endocarditis includes 2 major, 1 major and 3 minor, or 5 minor criteria, as follows (see Diagnostic Considerations.)[8] :

Major criteria

Major criteria include positive blood cultures, in this case 2 separate cultures for a typical endocarditis microorganism, such as Streptococcus viridans or a HACEK organism (Haemophilus parainfluenzae, H aphrophilus, H paraphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, or Kingella species); persistently positive blood cultures; or evidence of infection with a Coxiella organism and/or Q fever.

Another criterion is the presence of positive echocardiographic findings (eg, oscillating mass and/or vegetation, paravalvular abscess, or dehiscence of a prosthetic valve).

A third criterion is new valvular regurgitation.

Minor criteria

Minor criteria include the following:

  • Predisposing condition (history of IV drug use or congenital heart disease)

  • Fever with a temperature of more than 38°C

  • Vascular phenomena (arterial emboli, septic pulmonary infarcts, intracranial hemorrhage, conjunctival hemorrhage, Janeway lesions [painless, hemorrhagic lesions on the palms and soles])

  • Immunologic phenomena (glomerulonephritis, Osler nodes, Roth spots, a positive result for rheumatoid factor)

  • Positive blood culture findings without meeting the criteria above or serologic evidence of active infection consistent with endocarditis

  • Definite infective endocarditis may be diagnosed if there is pathologic evidence of intracardiac or embolized vegetation or intracardiac abscess, or 2 major, or 1 major and 3 minor, or 5 minor clinical criteria are present

  • Infective endocarditis is considered possible if 1 major and 1 minor or 3 minor criteria are present

  • The diagnosis of infective endocarditis may be rejected if a firm alternate diagnosis is confirmed, if “infective endocarditis syndrome" resolves within 4 days of antibiotic therapy, if no pathologic evidence of infective endocarditis is found at surgery or autopsy within 4 days of antibiotic therapy, or if the case does not meet "possible infective endocarditis" criteria

Go to Infective Endocarditis for more complete information on this topic.

Blood Culture

The most definitive laboratory tests for bacterial endocarditis are multiple blood cultures that grow an organism known to cause endocarditis.

Blood cultures should be obtained from all patients with fever of unclear etiology who have a pathologic heart murmur, a history of heart disease, or previous endocarditis.

For microbiologic documentation, obtaining 5-7 mL of blood from children (1-3 mL in infants) in 3 separate samplings within 1-24 hours is recommended, according to the clinical presentation.

The above recommendation is valid if the child is not ill. However, if child is ill, three cultures may be obtained with 1 hour separating the first and last culture, before administering antibiotics.

Venous blood samples should be obtained from different peripheral sites.

It is not necessary to time blood sampling with fever because bacteremia in infective endocarditis is usually continuous.

The microbiology laboratory should be notified of the clinical suspicion for endocarditis. Cultures should be grown aerobically and anaerobically for at least 1 week.

If no growth is observed by the second day of incubation, 2 more blood cultures should be obtained.

Blood cultures should be repeated during therapy to demonstrate the clearance of bacteremia.

Complete Blood Count

Anemia is present in 70-90% of patients and is usually normocytic and normochromic. Leukocytosis is noted in less than 50% of patients.

Erythrocyte Sedimentation Rate and C-Reactive Protein

The erythrocyte sedimentation rate (ESR) is elevated in almost all patients except those with CHF, renal failure, and disseminated intravascular coagulation (DIC). The mean ESR is 55 mm/h.

The C-reactive protein, although nonspecific, is elevated in most patients but decreases with successful treatment. Levels of C-reactive protein may be used to monitor response to antibiotic therapy.

Rheumatoid Factor

A positive rheumatoid factor is observed in 40-50% of patients with endocarditis of more than 6 weeks' duration. Immune complexes are also observed in patients with prolonged disease.

Urinalysis

Urinalysis may reveal proteinuria (50-60%) and/or microscopic hematuria (30-50%).

Echocardiography

Echocardiography is the primary modality for detecting endocarditis in patients in whom the diagnosis is suspected. In fact, echocardiographic features suggestive of infectious endocarditis are considered major criteria for confirming the diagnosis. Typical findings include vegetations, abscesses, and new valvular insufficiency.

Transthoracic echocardiography (TTE) has a greater sensitivity in infants and children than in adults. Its reported sensitivity is as high as 81%. It is the most common form of imaging used in children and is usually sufficient in most clinical circumstances. It should be remembered that very small vegetations are hard to detect because of the sensitivity of the echo signals.  

Transesophageal echocardiography (TEE) is occasionally required when transthoracic acoustic windows are inadequate. This is most likely to occur in patients who are obese or very muscular, who have had cardiac surgery, or have pulmonary hyperinflation. TEE is especially useful in detecting aortic root abscess, involvement of the sinuses of Valsalva, and prosthetic valve dehiscence.

MRI

Magnetic resonance imaging (MRI) has identified paravalvular extension of infection, aortic root aneurysms, and fistulas. Its utility relative to echocardiography has not been widely established.

 

Treatment

Approach Considerations

Bacterial endocarditis is a disease in which complete eradication of the organism is required. Bacteria involved in endocarditis are relatively protected from phagocytic activity by the vegetation, which contains high concentrations of bacteria with relatively low metabolic rates. Prolonged parenteral therapy is the only way to achieve bactericidal serum levels for the time needed to kill all the bacteria present in a vegetation of endocarditis. Treatment generally ranges from 4-8 weeks.[1, 9]

The following principles of management of infective endocarditis are worth considering:

  • Selection of the antibiotic agents is based on the sensitivity of the offending organism to antibiotics
  • Bactericidal rather than bacteriostatic antibiotics are preferable
  • Intermittent intravenous antibiotic administration to achieve high concentration of the antibiotic is recommended; a bactericidal level of 1:8 or greater should be achieved
  • Prolonged (4-8 weeks) treatment to ensure eradication of the organism is generally required
  • Documentation of cessation of bacteremia prior to discontinuation of antibiotics is suggested
  • Surgery may be necessary in some cases as detailed below.

Go to Infective Endocarditis for more complete information on this topic.

Medical Care in Pediatric Bacterial Endocarditis

Therapy is tailored according to the etiologic agent.[10] Because of the high risk for morbidity and mortality associated with bacterial endocarditis, individual therapy should be discussed between all consultants with the available antibiotic sensitivity testing carefully reviewed.

Penicillin-susceptible streptococcal endocarditis (PSSE) on native cardiac valves is treated with penicillin G for 4 weeks or penicillin or ceftriaxone combined with gentamicin for 2 weeks. Penicillin-resistant streptococcal endocarditis (PRSE) on native cardiac valves is treated with penicillin, ampicillin, or ceftriaxone for 4 weeks, combined with gentamicin for the first 2 weeks.

PSSE on a prosthetic valve or other prosthetic material should be treated with penicillin, ampicillin, or ceftriaxone for 6 weeks, combined with gentamicin for the first 2 weeks. PRSE on a prosthetic valve or other prosthetic material is treated with penicillin, ampicillin, or ceftriaxone for 6 weeks, combined with gentamicin. Vancomycin can be used in patients who cannot tolerate penicillin or ceftriaxone. The duration of penicillin-resistant therapy for streptococcal endocarditis on a prosthetic valve is 6 weeks.

Susceptible enterococcal infection on native valves is treated with penicillin or ampicillin, combined with gentamicin, for 4-6 weeks. Infection on prosthetic material should be treated for at least 6 weeks.

Methicillin-susceptible S aureus (MSSA) infection on native valves is treated with nafcillin or oxacillin for at least 6 weeks. The addition of gentamicin for 3-5 days is optional. Methicillin-resistant S aureus (MRSA) infection on native valves is treated with vancomycin for at least 6 weeks, with or without 3-5 days of gentamicin.

MSSA infection on prosthetic tissue is treated with nafcillin or oxacillin plus rifampin for at least 6 weeks, in combination with gentamicin for 2 weeks. MRSA infection on prosthetic tissue is treated with vancomycin plus rifampin for at least 6 weeks, in combination with gentamicin for 2 weeks.

Gram-negative endocarditis caused by HACEK organisms is treated with ceftriaxone or ampicillin plus gentamicin for 4 weeks.

The 2015 American Heart Association (AHA) update on infective endocarditis includes dosing and monitoring recommendations for vancomycin, aminoglycosides, and β-lactams.[11] These appear to be based primarily on expert opinion and did not consider currently available evidence on pharmacokinetic and pharmacodynamic principles, particularly in pediatric patients.[12]  These authors[12] are concerned that the practitioners may hesitate to deviate from AHA guidelines; therefore, they suggest improvement in the recommended doses in the AHA statement, review of evidence in support of optimization of antibiotic doses, and recommend the addition of a pediatric clinical pharmacist to the therapeutic team.

Surgical Care in Pediatric Bacterial Endocarditis

Absolute indications for surgery include progressive cardiac failure, worsening valve obstruction or regurgitation, definitive perivalvular abscess, noncandidal fungal infection, and pseudomonal infection. Relative indications include persistent bacteremia despite appropriate antibiotic therapy, candidal endocarditis, and vegetations larger than 10 mm.

Surgery should be performed without delay in patients with severe CHF secondary to valvular regurgitation. Surgery for patients who have had a recent neurologic injury should be evaluated and possibly delayed to make modifications to avoid intracranial hemorrhage.

Russell et al studied 34 patients with infective endocarditis who underwent surgical intervention over a 21-year period. They found the Ross operation to be effective in patients with aortic valve endocarditis. However, the incidence of reoperation for valve and conduit replacement because of somatic growth was significant. Children younger than one year had a greater risk for death, but patients surviving to hospital discharge had good results with no recurrence.[5]

Dietary Considerations

No specific dietary restrictions are recommended in the literature for the patient with bacterial endocarditis.

Activity

Patients may be as active as they can tolerate. Patients may be ill and should remain hospitalized until they are hemodynamically stable, afebrile, with negative blood cultures, and not at high risk for complications.

Additional Inpatient Care in Pediatric Bacterial Endocarditis

Further inpatient care in patients with bacterial endocarditis is mostly supportive.

Hemodynamic and ventilatory support may be required for critically ill children.

Physical and occupational therapy is given to patients who are hospitalized for a long period.

Important aspects of care include the treatment of complications, such as CHF, neurologic injury, and splenic abscess.

Outpatient Care in Pediatric Bacterial Endocarditis

With the advent of home health facilities, more patients can complete parenteral antimicrobial therapy as outpatients after the initial acute infection is controlled.

After initial diagnosis and therapy in the hospital, patients in whom outpatient therapy is being considered must be hemodynamically stable and afebrile, must have negative blood cultures, and must be at low risk for complications.

Follow-up for monitoring of adherence to drug therapy and possible complications is essential.

Transfer

Depending on their initial clinical presentation, patients may first be monitored in the intensive care unit (ICU) and then transferred to an inpatient ward when the clinical condition has stabilized and a response to treatment is evident.

Patients at high risk for developing complications from endocarditis may require transfer to a tertiary care center where pediatric cardiothoracic surgery is available.

Prevention of Pediatric Bacterial Endocarditis

Prevention of bacterial endocarditis with antimicrobial prophylaxis in high-risk children is key to their long-term survival and quality of life.[13]

Guidelines suggest that the following patients are at the highest risk and therefore should receive antibiotic prophylaxis prior to dental procedures involving manipulation of gingival tissue, the periapical region of the teeth, or the perforation of oral mucosa:

  • Patients with a prosthetic heart valve or with prosthetic material used for valve repair

  • Patients with previous endocarditis

  • Patients with significant valvular disease who have undergone cardiac transplantation

  • Patients with congenital heart disease

Patients in the fourth bullet point, above, include (1) persons with unrepaired or palliated cyanotic heart disease, (2) those with repaired heart disease with prosthetic material for the first 6 months postoperatively, and (3) those with repaired heart disease with residual significant lesion at the site of prosthetic material.

Antibiotic prophylaxis options for these highest-risk patients, when undergoing dental procedures, include the following:

  • Amoxicillin at 50 mg/kg orally 30-60 minutes before the procedure

  • In patients who are unable to take oral ampicillin, IV amoxicillin at 50 mg/kg or cefazolin or ceftriaxone 50 mg/kg intravenously or intramuscularly 30-60 minutes before the procedure

  • In patients with a penicillin allergy, cephalexin at 50 mg/kg orally; clindamycin at 20 mg/kg orally, intravenously, or intramuscularly; azithromycin at 15 mg/kg orally; or cefazolin or ceftriaxone at 50 mg/kg intravenously or intramuscularly

One recent study has evaluated the impact of the 2008 National Institute for Health and Clinical Excellence (NICE) guidelines that recommended the cessation of all antibiotic prophylaxis in the United Kingdom, even going farther than the 2007 American Heart Association guidelines in ommitting antibiotic prohylaxis for all patients under all circumstances. Although the results found no change in the trend of IE case development in the United Kingdom since the new guidelines and thus supported them, ongoing studies and clinical trials would still be useful to confirm whether antibiotic prophylaxis has any role in protecting some patients, particularly those at highest risk of complications from infective endocarditis.[14]

The AHA no longer recommends endocarditis prophylaxis for other nondental procedures, such as respiratory procedures (except for procedures in high-risk patients that involve incision of the mucosa, such as tonsillectomy and adenoidectomy), GI procedures, or genitourinary procedures.

Go to Antibiotic Prophylactic Regimens for Endocarditis for more complete information on this topic.

Consultations

Initial consultants for the patient suspected of having bacterial endocarditis should include an infectious disease specialist, a cardiologist, and often a cardiac surgeon.

 

Medication

Medication Summary

Antibiotics are used in the treatment of bacterial endocarditis and are also employed for prophylaxis.

Antimicrobial Agents

Class Summary

Treatment with antibiotics is specific to the etiologic agent and its characteristics. Therapy for penicillin-susceptible streptococcal endocarditis (PSSE), penicillin-resistant streptococcal endocarditis (PRSE), enterococcal endocarditis, methicillin-susceptible S aureus (MSSA), methicillin-resistant S aureus (MRSA), endocarditis caused by HACEK organisms (ie, Haemophilus parainfluenzae, H aphrophilus, H paraphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, or Kingella species), and fungal endocarditis are aimed at total eradication of the organism.

After antibiotic treatment, patients with endocarditis remain at high risk for recurrence and for complications of a recurrence. These patients are still recommended to receive prophylactic antibiotics for dental procedures involving manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa and for respiratory tract procedures that involve incision or biopsy of the respiratory mucosa.[6]

Penicillin G (Pfizerpen)

This is a first-line agent. It interferes with the synthesis of cell-wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Ampicillin (Omnipen, Principen)

Ampicillin has bactericidal activity against susceptible organisms. It is an alternative to amoxicillin when the patient cannot take oral medication. Bacterial endocarditis that is found to be a methicillin-susceptible S aureus (MSSA) infection on native valves is treated with nafcillin or oxacillin for at least 6 weeks.

Nafcillin (Unipen, Nafcil)

Ampicillin has bactericidal activity against susceptible organisms. It is an alternative to amoxicillin when the patient cannot take oral medication. Bacterial endocarditis that is found to be a methicillin-susceptible S aureus (MSSA) infection on native valves is treated with nafcillin or oxacillin for at least 6 weeks.

Oxacillin (Bactocill, Prostaphlin)

This is a bactericidal antibiotic that inhibits cell-wall synthesis. It is used to treat infections caused by penicillinase-producing staphylococci. Oxacillin may be used to start therapy when staphylococcal infection suspected.

Amoxicillin (Trimox, Moxatag)

Amoxicillin interferes with the synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria. It is used as prophylactic therapy in in specific, high-risk patients.

Ceftriaxone (Rocephin)

This agent is an alternative to penicillin. It is a third-generation cephalosporin with broad-spectrum gram-negative activity. It has decreased efficacy against gram-positive organisms and increased efficacy against resistant organisms. It arrests bacterial growth by binding 1 or more penicillin-binding proteins. Antibiotics for endocarditis prophylaxis may be required for patients before performing procedures that are high risk for bacteremia. Ceftriaxone may be used prophylactically for high-risk patients undergoing dental procedures.

Cephalexin (Keflex)

Cephalexin is a first-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell wall synthesis. It is bactericidal and effective against rapidly growing organisms forming cell walls. It is effective for treatment of infections caused by streptococci or staphylococci, including penicillinase-producing staphylococci. Cephalexin may be used prophylactically for high-risk patients undergoing dental procedures.

Gentamicin (Garamycin)

Gentamicin is an aminoglycoside antibiotic for gram-negative coverage. It is not the drug of choice, but consider using it if penicillins or other, less toxic drugs are contraindicated; if it is clinically indicated; or if mixed infections are caused by susceptible staphylococci and gram-negative organisms.

Dosing regimens for gentamicin are numerous; adjust the dose on the basis of creatinine clearance and changes in the volume of distribution. Follow up each regimen by measuring the trough level drawn 30 min before the third or fourth dose. Peak levels may be drawn 30 min after a 30-min infusion.

Vancomycin (Vancocin)

This is the drug of choice in patients who cannot receive or whose condition fails to respond to penicillins and cephalosporins or who have infections with resistant staphylococci. Vancomycin is a potent antibiotic that is directed against gram-positive organisms and is active against Enterococcus species. MRSA infection on native valves is treated with vancomycin for at least 6 weeks, with or without 3-5 days of gentamicin. To avoid toxicity, the current recommendation is to assay trough levels 0.5 hour before the fourth dose. In renal impairment, adjust the dose according to creatinine clearance.

Cefazolin

Cefazolin is a first-generation semisynthetic cephalosporin, which by binding to 1 or more penicillin-binding proteins, arrests bacterial cell wall synthesis and inhibits bacterial replication. In patients with penicillin allergies, cefazolin may be used for antibiotic prophylaxis for high-risk patients undergoing dental procedures.

Clindamycin (Cleocin, Cleocin Pediatric, ClindaMax Vaginal)

Clindamycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It distributes widely in the body, without penetration of the CNS. It is used in penicillin-allergic patients undergoing dental, oral, or respiratory tract procedures. It is useful for treatment against streptococcal and most staphylococcal infections. Clindamycin may be used prophylactically for high-risk patients undergoing dental procedures.

Azithromycin

Azithromycin is a macrolide antibiotic that acts by binding to the 50S ribosomal subunit of susceptible microorganisms and blocks the dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Azithromycin may be used prophylactically for high-risk patients undergoing dental procedures in patients who are penicillin allergic.

Rifampin

Rifampin inhibits RNA synthesis in bacteria by binding to the beta subunit of DNA-dependent RNA polymerase, which, in turn, blocks RNA transcription. Bacterial endocarditis with an MSSA infection on prosthetic tissue is treated with nafcillin or oxacillin plus rifampin for at least 6 weeks, in combination with gentamicin for 2 weeks. MRSA infection on prosthetic tissue is treated with vancomycin plus rifampin for at least 6 weeks, in combination with gentamicin for 2 weeks.

Amphotericin B (Amphocil, Fungizone)

Amphotericin B is produced by a strain of Streptomyces nodosus; it can be fungistatic or fungicidal. This agent binds to sterols (eg, ergosterol) in the fungal cell membrane, causing intracellular components to leak, with subsequent cell death. Amphotericin B may be effective in the treatment of fungal endocarditis.