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Infective Endocarditis Treatment & Management

  • Author: John L Brusch, MD, FACP; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 15, 2015
 

Approach Considerations

The major goals of therapy for infective endocarditis (IE) are to eradicate the infectious agent from the thrombus and to address the complications of valvular infection. The latter includes both the intracardiac and extracardiac consequences of IE. Some of the effects of IE require surgical intervention. Emergent care should focus on making the correct diagnosis and stabilizing the patient with acute disease and cardiovascular instability. General measures include the following:

  • Treatment of congestive heart failure
  • Oxygen
  • Hemodialysis (may be required in patients with renal failure)

In most cases, the etiologic microbial agent is not known while the patient is in the ED. Three sets of blood cultures should be drawn over a few hours, and then empiric antibiotic therapy tailored to the patient’s history and circumstances may be administered (see Antibiotic Therapy, below).

No special diets are recommended for patients with endocarditis; however, if the patient has congestive heart failure, administer a sodium-restricted diet. Activity limitations are determined by the severity of the illness, complications (eg, stroke), and the presence of significant congestive heart failure.

Mild congestive heart failure resulting from valvular insufficiency or myocarditis may be managed with standard medical therapy. Often, this is progressive, and despite achieving a microbiological cure, it requires valvular surgery.

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Antibiotic Therapy

Antibiotics remain the mainstay of treatment for IE.

In the setting of acute IE, institute antibiotic therapy as soon as possible to minimize valvular damage. Three to 5 sets of blood cultures are obtained within 60-90 minutes, followed by the infusion of the appropriate antibiotic regimen. By necessity, the initial antibiotic choice is empiric in nature, determined by clinical history and physical examination findings.

Empiric antibiotic therapy is chosen based on the most likely infecting organisms. Native valve endocarditis (NVE) has often been treated with penicillin G and gentamicin for synergistic coverage of streptococci. Patients with a history of intravenous (IV) drug use have been treated with nafcillin and gentamicin to cover for methicillin-sensitive staphylococci. The emergence of methicillin-resistant S aureus (MRSA) and penicillin-resistant streptococci has led to a change in empiric treatment with liberal substitution of vancomycin in lieu of a penicillin antibiotic.

Prosthetic valve endocarditis (PVE) may be caused by MRSA or coagulase-negative staphylococci (CoNS)[16] ; thus, vancomycin and gentamicin may be used for treatment, despite the risk of renal insufficiency. Rifampin is necessary in treating individuals with infection of prosthetic valves or other foreign bodies because it can penetrate the biofilm of most of the pathogens that infect these devices. However, it should be administered with vancomycin or gentamicin. These latter 2 agents serve to prevent the development of resistance to the rifampin.

Substitution of linezolid for vancomycin should be considered in patients with unstable renal function because of the difficulty of achieving therapeutic trough levels in this situation.

Linezolid or daptomycin are options for patients with intolerance to vancomycin or resistant organisms.[70] Organisms with a minimum inhibitory concentration (MIC) to vancomycin of equal to or greater than 2 mcg/mL should be treated with alternative agents. Appropriate regimens should be devised in consultation with a specialist in infectious disease.

In the case of subacute IE, treatment may be safely delayed until culture and sensitivity results are available. Waiting does not increase the risk of complications in this form of the disease.

Eradicating bacteria from the fibrin-platelet thrombus is extremely difficult because (1) the high concentration of organisms present within the vegetation (ie, 10-100 billion bacteria per gram of tissue), (2) their position deep within the thrombus, (3) their location in both a reduced metabolic and reproductive state, and (4) the interference of fibrin and white cells with antibiotic action. For all of these reasons, bactericidal antibiotics are considered necessary for cure of valvular infection.

IV administration is preferred because more reliable therapeutic levels are achieved with this route. Orally administered antibiotics have been used as suppressive therapy for incurable valvular infections (ie, inoperable PVE).

Treat all patients in a hospital or skilled nursing facility to allow adequate monitoring of the development of complications and the response to antibiotic therapy.

American Heart Association guidelines for treatment

The American Heart Association (AHA) has developed guidelines for treating IE caused by the most frequently encountered microorganisms. (Go to updated guidelines [October 2007].) Antibiotic doses are predicated on normal renal function.

Adult NVE caused by penicillin-susceptible S viridans, S bovis, and other streptococci (MIC of penicillin of ≤0.1 mcg/mL) should be treated with one of the following regimens:

  • Administer penicillin G at 12-18 million U/d IV by continuous pump or in 6 equally divided doses for 4 weeks
  • Administer ceftriaxone at 2 g/d IV for 4 weeks. It may be given intramuscularly (IM) for short periods if venous access problems develop; ceftriaxone allows once-a-day outpatient IV therapy for clinically stable patients.
  • Administer penicillin G and gentamicin at 1 mg/kg (based on ideal body weight) every 8 hours for 2 weeks; short-course therapy with ceftriaxone and gentamicin for 2 weeks is a cost-effective regimen and is effective in selected patients; short-course therapy is recommended for those with uncomplicated NVE caused by sensitive S viridans and of less than 3 months’ duration
  • In patients who are allergic to penicillin, use vancomycin at 30 mg/kg/d IV in 2 equally divided doses for 4 weeks; the vancomycin dose should not exceed 2 g/d unless serum levels are monitored and can be adjusted to attain a peak vancomycin level of 30-45 mcg/mL 1 hour after completion of the intravenous infusion of vancomycin

For NVE caused by relatively resistant streptococci (MICs of penicillin of 0.1-0.5 mcg/mL), the following regimens are recommended:

  • Administer penicillin G at 18 million U/d IV, either by continuous pump or in 6 equally divided doses, for 4 weeks
  • Administer cefazolin at 6 g/d IV in 3 equally divided doses for 4 weeks
  • Both of the above regimens are combined with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for the first 2 weeks of therapy
  • For patients who are allergic to penicillin, administer vancomycin at 30 mg/kg/d IV in 2 equally divided doses (usually, do not exceed 2 g/d unless serum levels are monitored) for 4 weeks; peak vancomycin levels of 30-45 mcg/mL should be attained 1 hour after completion of the intravenous infusion

IE caused by nonresistant enterococci, resistant S viridans (MICs of penicillin G of >0.5 mcg/mL), or nutritionally variant S viridans and PVE caused by penicillin-G–susceptible S viridans or S bovis should be treated as follows:

  • Administer penicillin G at 18-30 million U/d IV, either by continuous pump or in 6 equally divided doses daily, combined with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for 4-6 weeks
  • Alternatively, administer ampicillin at 12 g/d by continuous infusion or in 6 equally divided doses daily, combined with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for 4-6 weeks
  • In patients who are allergic to penicillin, administer vancomycin at 30 mg/kg/d in 2 equally divided doses (usually, do not exceed 2 g/24 h unless serum levels are monitored). This may be combined with gentamicin for 4-6 weeks of treatment. A peak vancomycin level of 30-45 mcg/mL should be attained 1 hour after completion of the intravenous infusion.

Enterococcal PVE generally responds as well as disease involving native valves. Six weeks of treatment is recommended for patients with symptoms of enterococcal IE of more than 3 months’ duration, with relapsed infection, or with PVE.

A combination of an inhibitor of cell wall synthesis (ie, penicillin, vancomycin) with an aminoglycoside (ie, gentamicin, streptomycin) is necessary to achieve bactericidal activity against the enterococci. Tobramycin or amikacin does not act synergistically with antibiotics active against the bacterial cell wall.

Increasing numbers of enterococci have aminoglycoside-inactivating enzymes that make them relatively resistant to the usual synergistic combinations. These aminoglycoside-resistant strains have an MIC of 2000 mcg/mL or more for streptomycin and 500 mcg/mL or more for gentamicin. Of gentamicin-resistant enterococcal strains, 25% are susceptible to streptomycin.

Continuously infused ampicillin (serum level of 16 mcg/mL) is probably the best therapy for aminoglycoside-resistant enterococci. Alternative choices are imipenem, ciprofloxacin, or ampicillin with sulbactam. Vancomycin does not appear to be as useful as the aforementioned antibiotics.

Enterococcus faecalis may become resistant to the penicillins because of their production of beta-lactamases. These strains can be treated with ampicillin combined with sulbactam or with vancomycin combined with gentamicin.

High peak levels of gentamicin are not necessary to establish synergistic bactericidal activity against enterococci. Peak gentamicin levels of 3-5 mcg/mL, with a trough of less than 2 mcg/mL, frequently can be obtained with a dose of gentamicin of 1 mg/kg IV every 8 hours. Once-a-day gentamicin dosing should not be used because a prolonged postantibiotic effect against gram-positive organisms does not occur, and synergistic killing requires the simultaneous presence of an agent active in the cell wall and an aminoglycoside.

A study indicates that gentamicin usage, even for synergy, is associated with decreasing renal function. However, overall mortality does not appear to be increased. Certainly, gentamicin therapy should be continued to achieve synergy against enterococci, but the practice of administering gentamicin for 5 days in the treatment of S aureus IV drug abuse (IVDA) IE should be questioned.

Vancomycin-resistant isolates of Enterococcus faecium and Enterococcus faecalis (ie, vancomycin-resistant enterococci [VRE]) produce some of the most challenging nosocomial infections. Presently, no therapy has been proven highly effective for IE caused by strains of VRE.

Quinupristin/dalfopristin (ie, Synercid) may suppress E faecium bacteremia but frequently is not bactericidal. Other options for therapy include linezolid, a combination of ampicillin and imipenem, and chloramphenicol. In one small series, the combination of ampicillin and ceftriaxone was found to be useful against VRE. Often, the valve must be replaced to achieve a cure.

NVE caused by methicillin-sensitive S aureus (MSSA) should be treated as follows:

  • Administer nafcillin or oxacillin at 2 g IV every 4 hours for 4-6 weeks
  • Administer cefazolin at 2 g IV every 8 hours for 4-6 weeks
  • For patients who are allergic to penicillin, administer vancomycin at 30 mg/kg (usually, do not to exceed 2 g/24 h unless serum levels are monitored) for 4-6 weeks; a peak vancomycin level of 30-45 mcg/mL should be attained 1 hour after completion of the intravenous infusion.

Vancomycin therapy is associated with a significant failure rate (up to 35%) in the treatment of MSSA and MRSA bloodstream infection (BSI)/IE. It appears that vancomycin should not be used to treat infections with staphylococci with an MIC of greater than 1.5-2 mcg/mL. In these cases, alternative agents such as linezolid or daptomycin should be used.

PVE caused by MSSA should be treated as follows:

  • Administer nafcillin or oxacillin at 2 g IV every 4 hours for 6 weeks or longer
  • Alternatively, administer cefazolin at 2 g IV every 8 hours for 6 weeks or longer
  • Each of these options should be combined with rifampin at 300 mg orally every 8 hours for 6 weeks or longer and with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for the first 2 weeks
  • PVE caused by MRSA should be treated with vancomycin at 30 mg/kg (not to exceed 2 g/d unless serum levels are monitored) for 6 weeks or longer combined with rifampin and gentamicin as outlined above; a peak vancomycin level of 30-45 mcg/mL should be attained 1 hour after completion of the IV infusion; a significant concern is that MRSA may become resistant to vancomycin.

Treatment with linezolid appears to result in outcomes superior to those with vancomycin against many types of infections caused by MRSA and MSSA. The use of linezolid should be strongly considered instead of vancomycin in patients who are seriously ill. Another advantage of linezolid is that its dose does not need to be adjusted in patients with renal failure.

White blood cell counts, red blood cell counts, and platelet counts need to be monitored frequently while the patient is on linezolid. The risk of developing serotonin syndrome is low. After the fourth week of therapy, the risk of hematological and neuropathic complications rapidly increases.

Daptomycin (6 mg/kg/24 h) has been approved for the treatment of S aureus BSI and right-sided IE. Higher doses of daptomycin (12 mg/kg/24 h) are more effective, with little increase in adverse effects. Patients who have received vancomycin have a higher rate of resistance to daptomycin.

HACEK microorganisms should be treated as follows:

  • Administer ceftriaxone at 2 g/d IV for 4 weeks
  • Alternatively, administer ampicillin at 12 g/d by continuous pump or in 6 equally divided doses daily; this may be combined with gentamicin at 1 mg/kg (based on ideal body weight) IM or IV every 8 hours for 4 weeks

Culture-negative NVE is usually treated with vancomycin and gentamicin. In patients who have previously received antibiotics, initial therapy should consist of either ampicillin-sulbactam plus gentamicin (3 mg/kg/d) or vancomycin plus gentamicin and ciprofloxacin. Because of the increased risk of renal failure with gentamicin, the latter regimen is preferred.

Patients with culture-negative PVE are usually given vancomycin and gentamicin, targeting possible enterococcal or CoNS infections. In patients with suspected PVE who have previously received antibiotics, enteric therapy should consist of vancomycin, gentamicin, cefepime, and rifampin. Because of the risk of developing resistance to rifampin, many clinicians would start this antibiotic only after the blood cultures results become negative.

Treatment of other microorganisms is as follows:

  • For P aeruginosa, administer ceftazidime, cefepime, or imipenem, combined with high-dose tobramycin at 8 mg/kg/d in 3 divided doses, to attain peak blood levels of 15-20 mcg/mL, for 6 weeks
  • For enteric gram-negative rods (eg, E coli, Proteus mirabilis), administer ampicillin, ticarcillin-clavulanic acid, piperacillin, piperacillin-tazobactam, ceftriaxone, or cefepime combined with gentamicin or amikacin for 4-6 weeks
  • For Streptococcus pneumoniae, administer ceftriaxone at 2 g/d IV or vancomycin (if penicillin allergy or high-level penicillin G resistance [MIC of 2 mcg/mL or more]) for 4 weeks
  • For diphtheroids, administer penicillin G at 18-24 million U/d in 6 divided doses or vancomycin combined with gentamicin for 4 weeks
  • For Q fever ( C burnetii infection), administer doxycycline combined with rifampin, trimethoprim-sulfamethoxazole, or a fluoroquinolone for 3-4 years

PVE is especially difficult to treat because the microorganisms adhere to the foreign body and may make them impervious to the bactericidal action of agents active in the cell wall. All patients with PVE require at least 6 weeks of antimicrobial therapy. Rifampin is the key drug in the treatment of PVE, as it is one of the only antimicrobial agents that penetrate the biofilm laid down by S aureus and CoNS. Because of the risk of these organisms developing resistance to rifampin, many clinicians withhold the addition of rifampin until blood cultures have cleared.

Penicillin-sensitive S viridans PVE should be treated with 2 weeks of penicillin G or ceftriaxone combined with gentamicin, followed by 4 weeks of penicillin G or ceftriaxone.

If the S viridans PVE is caused by an organism with a penicillin MIC of 0.2 mcg/mL or more, penicillin G or ceftriaxone combined with gentamicin combination therapy should be administered for 4-6 weeks. If the combination therapy is administered for only 4 weeks, penicillin G or ceftriaxone should be continued for an additional 2 weeks. Vancomycin is substituted for penicillin or ceftriaxone if the patient has a history of severe, immediate penicillin hypersensitivity, such as urticaria, anaphylaxis, or angioedema.

Enterococcal PVE therapy is complicated by the multiple types of enterococcal antimicrobial resistance, including beta-lactamase production (rare), different types of aminoglycoside-inactivating enzymes (more common), and VRE (increasingly common). If the enterococci are highly resistant to both gentamicin and streptomycin, ampicillin should be administered for 8-12 weeks by continuous infusion.

No effective therapy is known for VRE PVE.

Patients with PVE must be monitored carefully for signs of valve dysfunction, congestive heart failure, and heart block. They should also be monitored for clinical response to therapy, conversion of positive blood culture results, renal function status, and serum blood levels of vancomycin and aminoglycosides.

Valve replacement surgery should be performed promptly if any of the following occurs: moderate-to-severe congestive heart failure, valve dysfunction, perivalvular or myocardial abscess formation, the presence of an unstable valve that is becoming detached from the valve ring, more than one embolic episode with persistent vegetations observed on transtracheal echocardiogram, or the presence of vegetations larger than 1 cm in diameter.

If PVE does not respond to antimicrobial therapy and blood cultures results remain positive or if a relapse of bacteremia occurs after infection, the prosthetic valve should be replaced. In the presence of microorganisms that have no microbicidal agent (eg, VRE, fungi) or in the presence of other recalcitrant organisms (eg, P aeruginosa, S aureus, enteric gram-negative rods, Brucella species, C burnetii), past clinical experience shows that early replacement of the prosthetic valve improves the chances for cure.

Fungal endocarditis is rare and primarily occurs after prosthetic valve surgery and in individuals who abuse intravenous drugs. Candida species and Aspergillus species are the organisms most frequently encountered. Currently available antifungal agents have not been successful in eliminating fungal IE. The only cures for proven fungal IE have resulted when surgical excision of the infected valves was combined with amphotericin B therapy.

Empiric therapy of IVDA IE should be aimed at S aureus. Whether to use vancomycin or oxacillin/nafcillin depends on the incidence of MRSA in the community. Generally, gram-negative organisms occur infrequently, and delay in covering them initially is acceptable.

Some clinicians obtain peak and trough blood samples during the course of antimicrobial therapy of IE in order to run serum bactericidal tests. These tests are performed by incubating serial 2-fold dilutions of serum that contains antimicrobials with an inoculum of 100,000 colony-forming units per milliliter of the target microorganism that has been previously isolated from the patient’s blood for 24-48 hours.

Peak antimicrobial concentrations that inhibit and kill the bacteria at a 1:32 or greater dilution in serum are a consistent predictor of a favorable clinical response. Antimicrobial dosages are adjusted to try to attain this goal. However, many clinicians feel that the serum bactericidal test does not have a reproducible result, and these clinicians rely on standardized tests of antimicrobial susceptibility (ie, MICs) and serum antimicrobial assays of peak and trough levels to determine whether sufficient amounts of antimicrobial agents are being administered.[71, 72, 73, 74, 75, 76]

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Management of S aureus Bacteremia

Management of S aureus bacteremia in the presence of an intravascular catheter includes promptly removing the catheter, initiating appropriate antibiotic therapy, monitoring of blood culture results in 24-48 hours, and performing transesophageal echocardiography (TEE).

If the follow-up blood culture and TEE findings are negative and no evidence of metastatic infection is found, then 2 weeks of antistaphylococcal therapy is appropriate.

If the follow-up blood culture findings are positive and the TEE results indicate the presence of IE, then the patient is treated for 4-6 weeks with antistaphylococcal antibiotics.

If the follow-up blood culture results are positive and the TEE findings show no evidence of IE, then metastatic infection, such as a splenic abscess or osteomyelitis, must be considered while appropriate antibiotic therapy is continued and while the extracardiac source of infection is sought.

It is important to recognize that, in up to one third of cases, a cause of persistent BSI is not identified. A good deal of these may be explained by endotheliosis. For the time being, the duration of antibiotic therapy for each case of S aureus catheter-related BSI must be individualized. The author and others would treat cases that meet the criteria of continuous bacteremia for a total of 4 weeks despite a negative TEE result.[77, 78, 79]

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Anticoagulation Therapy

Although thrombosis is a key element of IE, anticoagulation with warfarin (Coumadin, Jantoven) is controversial. Indeed, evidence indicates patients who are anticoagulated have worse outcomes than those who are not anticoagulated. Patients who are treated with anticoagulation appear to have a higher rate of intracerebral bleeding. If an established reason for anticoagulation (eg, deep venous thrombosis, presence of a mechanical prosthetic valve) exists, a standard regimen of anticoagulation should be followed.

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Indications for Surgery

Approximately 15-25% of patients with IE eventually require surgery.

Indications for surgical intervention in patients with NVE are as follows:

  • Congestive heart failure refractory to standard medical therapy
  • Fungal IE (except that caused by Histoplasma capsulatum)
  • Persistent sepsis after 72 hours of appropriate antibiotic treatment
  • Recurrent septic emboli, especially after 2 weeks of antibiotic treatment
  • Rupture of an aneurysm of the sinus of Valsalva
  • Conduction disturbances caused by a septal abscess
  • Kissing infection of the anterior mitral leaflet in patients with IE of the aortic valve

Congestive heart failure in a patient with NVE is the primary indication for surgery. A second relapse, during or after completion of treatment, requires replacement of the valve.

Paravalvular abscess and intracardiac fistula almost always require surgical intervention. Patients with culture-negative NVE who remained febrile for more than 10 days should be considered surgical candidates. Persistent hypermobile vegetations, especially those with a history of embolization beyond 7 days of antibiotic therapy, should be treated with surgery. Cardiac surgery should be considered in patients with multiresistant organisms (eg, enterococci).

The indications for surgery in patients with PVE are the same as those for patients with NVE, with the addition of the conditions of valvular dehiscence and early PVE. Orally administered antibiotics have been used as suppressive therapy for incurable valvular infections (ie, inoperable PVE).

Surgery is often required for treatment of metastatic infections (eg, cerebral and other types of aneurysms and macroabscesses of the brain and spleen). Many cerebral abscesses may not be accessible. If this is the case, they can be monitored because 30% may heal when treated medically.

Occasionally, local debridement and the administration of appropriate antibiotics may be sufficient to cure an uncomplicated pacemaker pocket infection. However, most studies indicate that complete removal of the system is necessary for cure in most cases. Many patients in whom this is not possible eventually die of complications from relapsing infection. This aggressive approach is especially necessary when dealing with pacemaker IE.

The AHA 2010 guideline update on CIED infections and their management recommends complete removal of infected CIED and leads for the following patients:[35]

  • All patients with definite CIED infection, as shown by valvular and/or lead endocarditis or sepsis
  • All patients with CIED pocket infection, as shown by abscess formation, device erosion, skin adherence, or chronic draining sinus without involvement of the transvenous section of the lead system
  • All patients with valvular endocarditis without definite involvement of the lead(s),device, or both

Patients with occult staphylococcal bacteremia

The guideline update states that complete removal is reasonable in patients with persistent occult gram-negative bacteremia despite appropriate antibiotic therapy.[35]

Removal of the device and leads is not indicated in the following cases:[35]

  • A superficial or incisional infection that does not involve the device, leads, or both
  • Relapsing bloodstream infection due to a non-CIED source and for which long-term suppressive antimicrobials are required

After removal of the infected device, placing a temporary transvenous pacer is best. Immediate insertion of a permanent pacemaker at a new site can be safely accomplished.

The AHA 2010 guideline update on CIED infection recommends careful evaluation of each patient to determine if a CIED is still needed. Replacement device implantation should not be ipsilateral to the extraction site. The guideline suggests the contralateral side, the iliac vein, and epicardial implantation as preferred alternative locations.[35]

The AHA 2010 guideline recommends that if blood cultures were positive before the device extraction, blood cultures should be taken after the device removal, and new device placement should be delayed until blood cultures have been negative for at least 72 hours. If valvular infection is present, placement of new transvenous lead should be delayed for at least 14 days after CIED system removal.[35]

In the past, removal of the intracardiac leads that had been in place for several months often necessitated open heart surgery. The use of laser technology to dissolve the pacemaker lead adhesions has proven successful, with a 94% success rate. The risk of dislodging vegetations during removal of infected leads is negligible. Patients whose leads cannot be removed are started on permanent antibiotic suppression.[80, 81]

The AHA 2010 CIED guideline update states that long-term suppressive antimicrobial therapy should be considered for patients with CIED infection who are not candidates for CIED removal. Such therapy should not be administered to patients who are candidates for CIED removal.[35]

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Prevention of Infective Endocarditis

Approximately 15-25% of cases of IE are a consequence of invasive procedures that produce a significant bacteremia. Because only 50% of those who developed valvular infection following a procedure were identified as being candidates for antibiotic prophylaxis, only approximately 10% of cases of IE can be prevented by the administration of preprocedure antibiotics. Maintaining good oral hygiene is probably more effective in the overall prevention of valvular infection because gingivitis is the most common source of spontaneous bacteremias.

Consider prophylaxis against IE in patients at higher risk. Patients at higher risk include those with the following conditions:

  • Presence of prosthetic heart valve
  • History of endocarditis
  • Cardiac transplant recipients who develop cardiac valvulopathy
  • Congenital heart disease with a high-pressure gradient lesion

The presence of a coronary artery stent is not considered to place the patient at high risk for endocarditis.

Also consider prophylaxis in patients before they undergo procedures[82] that may cause transient bacteremia, such as the following[83] :

  • Any procedure involving manipulation of gingival tissue or the periapical region of teeth, or perforation of the oral mucosa
  • Any procedure involving incision in the respiratory mucosa
  • Procedures on infected skin or musculoskeletal tissue including incision and drainage of an abscess
  • Prophylaxis is no longer routinely recommended for gastrointestinal or genitourinary procedures.

Prevention of vascular catheter infections is an important prophylactic approach in preventing nosocomial infective endocarditis (NIE). Protective factors include the insertion and maintenance of catheters by an infusion therapy team, the use of topical disinfectants and antibiotics, and the practice of coating catheters with antimicrobial agents.

No double-blind studies have been performed to support the use of systemically administered antibiotics for the prevention of pacemaker or intracardiac defibrillator infections. However, awaiting definitive studies, the authors recommend prophylactic antibiotics, as with any implantable device. Of course, strict sterile technique must be followed. Antibiotic prophylaxis is not recommended for prevention of CIED infection in patients with pacemakers or intracardiac defibrillators during invasive procedures not directly related to device manipulation.[35] Pacemaker infection due to transient bacteremias is uncommon.[84]

There appeared to be no dramatic increase in rates of hospitalization following the changes to the recommendations for antibiotic prophylaxis in 2007.[24]

For more information, see Antibiotic Prophylactic Regimens for Endocarditis.

American Heart Association guidelines for prophylaxis

The AHA periodically compiles recommendations for IE prophylaxis (Go to updated guidelines, October 2007).[85] It is important to remember that these are not standards but guidelines and thus may be modified in particular circumstances. The guidelines remain unproven by randomized controlled clinical trials. Indeed, many examples of failure of these recommendations have been noted, even when they are applied appropriately.[86]

The 3 major steps in the pathogenesis of IE that are vulnerable to antibiotic prophylaxis are the following:

  1. Killing of the pathogen in the bloodstream before it can adhere to the valve
  2. Preventing adherence to the valve/fibrin-platelet thrombus
  3. Eradicating any organisms that have attached to the thrombus

Successful antibiotic prophylaxis requires identifying those patients who are at risk, prioritizing the procedures that require prophylaxis, and selecting an appropriate antibiotic regimen. In general, bactericidal antibiotics are used. However, bacteristatic agents are probably effective in most circumstances.

Although the 2007 guidelines are a marked improvement because they prioritize the cardiac conditions and procedures that require antibiotic prophylaxis and emphasize the importance of promoting good oral hygiene, they offer little direction in dealing with the ever-growing problem of antibiotic-resistance patterns of S viridans and enterococci.

The importance of antibiotic prophylaxis of calcific valvular disease in elderly patients also needs to be more fully discussed. Calcific valvular disease is the most common underlying cardiac risk factor for the development of IE in this age group.

The author’s preference is to administer parenteral prophylactic antibiotics to patients with prosthetic valves because of the severe consequences of PVE.

The United Kingdom’s NICE 2008 guidelines on prophylaxis against IE differ from the AHA recommendations. The NICE guidelines do not recommend antibiotic prophylaxis for IE in patients undergoing dental procedures; however, they agree with the AHA guidelines in not recommending prophylaxis for those undergoing procedures in the upper and lower gastrointestinal tracts, the genitourinary tract, or the upper and lower respiratory tracts.[34]

Subsequent to the 2008 NICE guidelines recommending abolition of all IE antibiotic prophylaxis, prescriptions for such prophylaxis dropped almost 80% without any apparent cases of IE.[87] However, the authors of this article recommend continuing to follow the current AHA guidelines, especially in the presence of an intracardiac prosthetic device.

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Special Considerations

Failure to consider the diagnosis, especially in patients with a history of IV drug use and a low-grade fever, is a medicolegal pitfall. Many malpractice suits are caused by a failure to diagnose and a delay in diagnosis accompanied by a poor outcome for the patient.

As a rule for primary care clinics, do not administer antimicrobial agents to febrile patients with heart murmurs without first obtaining at least 2 sets of blood cultures.

The perception that most IE is preventable is wrong. Frequent episodes of transient bacteremia occur with chewing and other activities of daily life. Proving that a failure to give prophylaxis before dental and surgical procedures resulted in IE is difficult. However, this does not prevent legal action alleging IE as a consequence of failing to give the antimicrobial prophylaxis recommended by the AHA.

When a central venous line is needed, not inserting the line when a patient is known to be bacteremic is advisable. If no alternative to placing the line is available, bactericidal antimicrobial agents should be administered to try to prevent the development of IE.

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Consultations

In general, both a cardiologist and an infectious diseases specialist should be involved in the care of patients with IE. Consulting a cardiothoracic surgeon may be necessary. Personnel in the clinical microbiology laboratory must have the skill to isolate the organism, properly identify it, and perform susceptibility testing appropriate for the growth characteristics and requirements of the organism (with determination of the MIC of clinically relevant antimicrobial agents). To obtain the best possible information, the attending physician should work closely with the microbiology laboratory personnel.

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Long-Term Monitoring

Monitoring for posttreatment bacteremia

Patients should have blood cultures taken after 3-4 days of treatment to document eradication of the bacteremia. Blood cultures during treatment are essential if persistent fever or other signs develop that suggest failing treatment.

Failure to sterilize the bloodstream, despite adequate serum levels of appropriate antibiotics, should prompt a search for metastatic infection (eg, abscesses, especially splenic, or mycotic aneurysm).

Fever lasting longer than 10 days into therapy with an indicated antibiotic regimen should be of concern and should prompt a search for suppurative complications. Approximately 30% of patients have a return of fever after the initial response. This is usually caused by an intracardiac abscess or metastatic infection. Causes of unresponsive fever include myocardial or septal abscesses, large vegetations that resist sterilization, and metastatic infection. Occasionally, fever in patients with uncomplicated IE may take as long as 3 weeks to abate.

Monitoring for complications

Patients should be monitored for the development of the following complications:

  • Valvular dysfunction, usually insufficiency of the mitral or aortic valves
  • Myocardial or septal abscesses
  • Congestive heart failure
  • Metastatic infection
  • Embolic phenomenon
  • Organ dysfunction resulting from immunological processes

Complications, such as congestive heart failure resulting from valvular insufficiency and embolization, may occur after bacteriologic cure has been achieved. (Note that the diagnosis of developing congestive heart failure or valvular insufficiency is based on clinical findings, not solely on echocardiographic measurements.) The onset of valve dysfunction or moderate-to-severe congestive heart failure should lead to an evaluation for immediate valve replacement.

Monitoring for relapse

Relapse of IE usually occurs within 2 months of finishing clinically effective therapy. Infection with S aureus, enterococci, and gram-negative organisms (especially P aeruginosa) is associated with a high rate of relapse. Enterococcal infection of the mitral valve has the greatest potential for relapse.

Recurrent IE occurs most often in individuals who abuse IV drugs. Valvular infections in these patients recur at a rate of 40%. Those with pretreatment symptoms of IE of more than 3 months’ duration are at greater risk for relapse. Other significant risk factors for recurrence include a previous episode of IE, the presence of a prosthetic valve, and congenital heart disease.

In general, infected vascular catheters should be removed and should not be replaced over a guidewire. Surgically implanted devices, such as Broviac or Hickman catheters, do not necessarily need to be removed unless evidence of IE, a tunnel infection, or suppurative thrombophlebitis is present or if the infecting organism is a Corynebacterium species, a Pseudomonas species, a fungus, S aureus, or a Mycobacterium species. If bacteremia persists longer than a few days, the catheter must be removed.[88, 89]

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Contributor Information and Disclosures
Author

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven A Conrad, MD, PhD Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Jon Mark Hirshon, MD, MPH Associate Professor, Department of Emergency Medicine, University of Maryland School of Medicine

Jon Mark Hirshon, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Public Health Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Keith A Marill, MD Faculty, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor, Harvard Medical School

Keith A Marill, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Medtronic Ownership interest None; Cambridge Heart, Inc. Ownership interest None; General Electric Ownership interest None

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Epaulard O, Roch N, Potton L, Pavese P, Brion JP, Stahl JP. Infective endocarditis-related stroke: diagnostic delay and prognostic factors. Scand J Infect Dis. 2009. 41(8):558-62. [Medline].

  2. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med. 1994 Mar. 96(3):200-9. [Medline].

  3. Brusch JL. Infective endocarditis and its mimics in the critical care unit. Cunha BA, ed. Infectious Diseases in Critical Care. 2nd ed. New York, NY: Informa Healthcare; 2007. 261-2.

  4. Karchmer AW. Infective endocarditis. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 7th ed. WB Saunders Co; 2005. 1633-1658.

  5. Karchmer AW. Infective endocarditis. Harrison’s Principles of Internal Medicine. 16th ed. McGraw-Hill; 2005. 731-40.

  6. Lerner PI, Weinstein L. Infective endocarditis in the antibiotic era. N Engl J Med. 1966 Feb 17. 274(7):388-93 concl. [Medline].

  7. Lerner PI, Weinstein L. Infective endocarditis in the antibiotic era. N Engl J Med. 1966 Feb 3. 274(5):259-66 contd. [Medline].

  8. Lerner PI, Weinstein L. Infective endocarditis in the antibiotic era. N Engl J Med. 1966 Jan 27. 274(4):199-206 contd. [Medline].

  9. Brusch J. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007.

  10. Baddour LM, Wilson LM. Infections of prosthetic valves and other cardiovascular devices: intravascular devices. Mandell GL, Bennett JE, Dolin R, eds. Mandel, Douglas and Bennett’s Principles and Practice and Infectious Diseases. 5th ed. Philadelphia, Pa: Elsevier; 2005. 1022-44.

  11. Weinstein LW, Brusch JL. Infective Endocarditis. New York, NY: Oxford University Press; 1996.

  12. Wang A, Athan E, Pappas PA, Fowler VG Jr, Olaison L, Paré C, et al. Contemporary clinical profile and outcome of prosthetic valve endocarditis. JAMA. 2007 Mar 28. 297(12):1354-61. [Medline].

  13. Miró JM, del Río A, Mestres CA. Infective endocarditis in intravenous drug abusers and HIV-1 infected patients. Infect Dis Clin North Am. 2002 Jun. 16(2):273-95, vii-viii. [Medline].

  14. Soong G, Chun J, Parker D, Prince A. Staphylococcus aureus activation of caspase 1/calpain signaling mediates invasion through human keratinocytes. J Infect Dis. 2012 May 15. 205(10):1571-9. [Medline]. [Full Text].

  15. Xiong YQ, Fowler VG, Yeaman MR, Perdreau-Remington F, Kreiswirth BN, Bayer AS. Phenotypic and genotypic characteristics of persistent methicillin-resistant Staphylococcus aureus bacteremia in vitro and in an experimental endocarditis model. J Infect Dis. 2009 Jan 15. 199(2):201-8. [Medline]. [Full Text].

  16. Chu VH, Miro JM, Hoen B, Cabell CH, Pappas PA, Jones P, et al. Coagulase-negative staphylococcal prosthetic valve endocarditis--a contemporary update based on the International Collaboration on Endocarditis: prospective cohort study. Heart. 2009 Apr. 95(7):570-6. [Medline].

  17. Reyes MP, Ali A, Mendes RE, Biedenbach DJ. Resurgence of Pseudomonas endocarditis in Detroit, 2006-2008. Medicine (Baltimore). 2009 Sep. 88(5):294-301. [Medline].

  18. Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG Jr, Bayer AS, et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. 2009 Mar 9. 169(5):463-73. [Medline].

  19. Baddour LM, Cha YM, Wilson WR. Clinical practice. Infections of cardiovascular implantable electronic devices. N Engl J Med. 2012 Aug 30. 367(9):842-9. [Medline].

  20. Baddley JW, Benjamin DK Jr, Patel M, Miró J, Athan E, Barsic B, et al. Candida infective endocarditis. Eur J Clin Microbiol Infect Dis. 2008 Jul. 27(7):519-29. [Medline]. [Full Text].

  21. Chu VH, Woods CW, Miro JM, Hoen B, Cabell CH, Pappas PA, et al. Emergence of coagulase-negative staphylococci as a cause of native valve endocarditis. Clin Infect Dis. 2008 Jan 15. 46(2):232-42. [Medline].

  22. Hill EE, Herijgers P, Claus P, Vanderschueren S, Herregods MC, Peetermans WE. Infective endocarditis: changing epidemiology and predictors of 6-month mortality: a prospective cohort study. Eur Heart J. 2007 Jan. 28(2):196-203. [Medline].

  23. Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med. 2001 Nov 1. 345(18):1318-30. [Medline].

  24. Bor DH, Woolhandler S, Nardin R, Brusch J, Himmelstein DU. Infective endocarditis in the u.s., 1998-2009: a nationwide study. PLoS One. 2013. 8(3):e60033. [Medline]. [Full Text].

  25. Tleyjeh IM, Steckelberg JM, Murad HS, Anavekar NS, Ghomrawi HM, Mirzoyev Z, et al. Temporal trends in infective endocarditis: a population-based study in Olmsted County, Minnesota. JAMA. 2005 Jun 22. 293(24):3022-8. [Medline].

  26. Mendiratta P, Tilford JM, Prodhan P, Cleves MA, Wei JY. Trends in hospital discharge disposition for elderly patients with infective endocarditis: 1993 to 2003. J Am Geriatr Soc. 2009 May. 57(5):877-81. [Medline].

  27. Kiefer T, Park L, Tribouilloy C, Cortes C, Casillo R, Chu V, et al. Association between valvular surgery and mortality among patients with infective endocarditis complicated by heart failure. JAMA. 2011 Nov 23. 306(20):2239-47. [Medline].

  28. Kang DH, Kim YJ, Kim SH, et al. Early surgery versus conventional treatment for infective endocarditis. N Engl J Med. 2012 Jun 28. 366(26):2466-73. [Medline].

  29. Thuny F, Grisoli D, Collart F, Habib G, Raoult D. Management of infective endocarditis: challenges and perspectives. Lancet. 2012 Mar 10. 379(9819):965-75. [Medline].

  30. Wallace SM, Walton BI, Kharbanda RK, Hardy R, Wilson AP, Swanton RH. Mortality from infective endocarditis: clinical predictors of outcome. Heart. 2002 Jul. 88(1):53-60. [Medline]. [Full Text].

  31. Durante-Mangoni E, Bradley S, Selton-Suty C, Tripodi MF, Barsic B, Bouza E, et al. Current features of infective endocarditis in elderly patients: results of the International Collaboration on Endocarditis Prospective Cohort Study. Arch Intern Med. 2008 Oct 27. 168(19):2095-103. [Medline].

  32. Sonneville R, Mirabel M, Hajage D, et al. Neurologic complications and outcomes of infective endocarditis in critically ill patients: The ENDOcardite en REAnimation prospective multicenter study. Crit Care Med. 2011 Jun. 39(6):1474-1481. [Medline].

  33. Chu VH, Cabell CH, Benjamin DK Jr, Kuniholm EF, Fowler VG Jr, Engemann J, et al. Early predictors of in-hospital death in infective endocarditis. Circulation. 2004 Apr 13. 109(14):1745-9. [Medline].

  34. [Guideline] National Institute for Health and Clinical Excellence. Prophylaxis against infective endocarditis. Antimicrobial prophylaxis against infective endocarditis in adults and children undergoing interventional procedures. 2008. (NICE clinical guideline No. 64).

  35. [Guideline] Baddour LM, Epstein AE, Erickson CC, et al. Update on cardiovascular implantable electronic device infections and their management: a scientific statement from the American Heart Association. Circulation. 2010 Jan 26. 121(3):458-77. [Medline].

  36. Crawford MH, Durack DT. Clinical presentation of infective endocarditis. Cardiol Clin. 2003 May. 21(2):159-66, v. [Medline].

  37. Di Salvo G, Habib G, Pergola V, Avierinos JF, Philip E, Casalta JP, et al. Echocardiography predicts embolic events in infective endocarditis. J Am Coll Cardiol. 2001 Mar 15. 37(4):1069-76. [Medline].

  38. Eknoyan G, Lister BJ, Kim HS, Greenberg SD. Renal complications of bacterial endocarditis. Am J Nephrol. 1985. 5(6):457-69. [Medline].

  39. Pruitt AA, Rubin RH, Karchmer AW, Duncan GW. Neurologic complications of bacterial endocarditis. Medicine (Baltimore). 1978 Jul. 57(4):329-43. [Medline].

  40. [Guideline] Sexton DJ, Spelman D. Current best practices and guidelines. Assessment and management of complications in infective endocarditis. Cardiol Clin. 2003 May. 21(2):273-82, vii-viii. [Medline].

  41. Snygg-Martin U, Gustafsson L, Rosengren L, Alsiö A, Ackerholm P, Andersson R, et al. Cerebrovascular complications in patients with left-sided infective endocarditis are common: a prospective study using magnetic resonance imaging and neurochemical brain damage markers. Clin Infect Dis. 2008 Jul 1. 47(1):23-30. [Medline].

  42. Terpenning MS, Buggy BP, Kauffman CA. Infective endocarditis: clinical features in young and elderly patients. Am J Med. 1987 Oct. 83(4):626-34. [Medline].

  43. Bansal RC. Infective endocarditis. Med Clin North Am. 1995 Sep. 79(5):1205-40. [Medline].

  44. Conlon PJ, Jefferies F, Krigman HR, Corey GR, Sexton DJ, Abramson MA. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis. Clin Nephrol. 1998 Feb. 49(2):96-101. [Medline].

  45. Cosmi JE, Tunick PA, Kronzon I. Mortality in patients with paravalvular abscess diagnosed by transesophageal echocardiography. J Am Soc Echocardiogr. 2004 Jul. 17(7):766-8. [Medline].

  46. Cunha BA, Gill MV, Lazar JM. Acute infective endocarditis. Diagnostic and therapeutic approach. Infect Dis Clin North Am. 1996 Dec. 10(4):811-34. [Medline].

  47. Fowler VG Jr, Scheld WM, Bayer AS. Endocarditis and intravascular infections. Mandell GL, Bennett JA, Dolin R, eds. Principles and Practice of Infectious Diseases. 6th ed. Philadelphia, Penn: Elseiver; 2005. 975-1021.

  48. Roberts NK, Somerville J. Pathological significance of electrocardiographic changes in aortic valve endocarditis. Br Heart J. 1969 May. 31(3):395-6. [Medline].

  49. Robinson SL, Saxe JM, Lucas CE, Arbulu A, Ledgerwood AM, Lucas WF. Splenic abscess associated with endocarditis. Surgery. 1992 Oct. 112(4):781-6; discussion 786-7. [Medline].

  50. Weinstein L. Life-threatening complications of infective endocarditis and their management. Arch Intern Med. 1986 May. 146(5):953-7. [Medline].

  51. Weinstein L, Schlesinger JJ. Pathoanatomic, pathophysiologic and clinical correlations in endocarditis (first of two parts). N Engl J Med. 1974 Oct 17. 291(16):832-7. [Medline].

  52. Wang CC, Lee CH, Chan CY, Chen HW. Splenic infarction and abscess complicating infective endocarditis. Am J Emerg Med. 2009 Oct. 27(8):1021.e3-5. [Medline].

  53. Kradin RL. Pathology of infective endocarditis. Brusch JL, ed. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007. 101-18.

  54. Brusch JL. Pathoanatomical, pathophysiological and clinical correlations. Brusch JL, ed. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007. 119-41.

  55. [Guideline] Towns ML, Reller LB. Diagnostic methods current best practices and guidelines for isolation of bacteria and fungi in infective endocarditis. Infect Dis Clin North Am. 2002 Jun. 16(2):363-76, ix-x. [Medline].

  56. Thuny F, Grisoli D, Collart F, Habib G, Raoult D. Management of infective endocarditis: challenges and perspectives. Lancet. 2012 Mar 10. 379(9819):965-75. [Medline].

  57. Archibald LK, Pallangyo K, Kazembe P, Reller LB. Blood culture contamination in Tanzania, Malawi, and the United States: a microbiological tale of three cities. J Clin Microbiol. 2006 Dec. 44(12):4425-9. [Medline]. [Full Text].

  58. Bates DW, Goldman L, Lee TH. Contaminant blood cultures and resource utilization. The true consequences of false-positive results. JAMA. 1991 Jan 16. 265(3):365-9. [Medline].

  59. Khatib R, Riederer K, Saeed S, Johnson LB, Fakih MG, Sharma M, et al. Time to positivity in Staphylococcus aureus bacteremia: possible correlation with the source and outcome of infection. Clin Infect Dis. 2005 Sep 1. 41(5):594-8. [Medline].

  60. Lee A, Mirrett S, Reller LB, Weinstein MP. Detection of bloodstream infections in adults: how many blood cultures are needed?. J Clin Microbiol. 2007 Nov. 45(11):3546-8. [Medline]. [Full Text].

  61. [Guideline] Mermel LA, Allon M, Bouza E, Craven DE, Flynn P, O'Grady NP, et al. Clinical practice guidelines for the diagnosis and management of intravascular catheter-related infection: 2009 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2009 Jul 1. 49(1):1-45. [Medline].

  62. Weinbaum FI, Lavie S, Danek M, Sixsmith D, Heinrich GF, Mills SS. Doing it right the first time: quality improvement and the contaminant blood culture. J Clin Microbiol. 1997 Mar. 35(3):563-5. [Medline]. [Full Text].

  63. Weinstein MP. Blood culture contamination: persisting problems and partial progress. J Clin Microbiol. 2003 Jun. 41(6):2275-8. [Medline]. [Full Text].

  64. Casella F, Rana B, Casazza G, Bhan A, Kapetanakis S, Omigie J, et al. The potential impact of contemporary transthoracic echocardiography on the management of patients with native valve endocarditis: a comparison with transesophageal echocardiography. Echocardiography. 2009 Sep. 26(8):900-6. [Medline].

  65. Choussat R, Thomas D, Isnard R, Michel PL, Iung B, Hanania G, et al. Perivalvular abscesses associated with endocarditis; clinical features and prognostic factors of overall survival in a series of 233 cases. Perivalvular Abscesses French Multicentre Study. Eur Heart J. 1999 Feb. 20(3):232-41. [Medline].

  66. [Guideline] Cheitlin MD, Armstrong WF, Aurigemma GP, Beller GA, Bierman FZ, Davis JL, et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines for the Clinical Application of Echocardiography). Circulation. 2003 Sep 2. 108(9):1146-62. [Medline].

  67. Jassal DS, Picard MH. Echocardiography. Brusch JL, ed. Infective Endocarditis: Management in the Era of Intravascular Devices. New York, NY: Informa Healthcare; 2007. 255-72.

  68. Roe MT, Abramson MA, Li J, Heinle SK, Kisslo J, Corey GR, et al. Clinical information determines the impact of transesophageal echocardiography on the diagnosis of infective endocarditis by the duke criteria. Am Heart J. 2000 Jun. 139(6):945-51. [Medline].

  69. Feuchtner GM, Stolzmann P, Dichtl W, Schertler T, Bonatti J, Scheffel H, et al. Multislice computed tomography in infective endocarditis: comparison with transesophageal echocardiography and intraoperative findings. J Am Coll Cardiol. 2009 Feb 3. 53(5):436-44. [Medline].

  70. Fowler VG Jr, Boucher HW, Corey GR, Abrutyn E, Karchmer AW, Rupp ME, et al. Daptomycin versus standard therapy for bacteremia and endocarditis caused by Staphylococcus aureus. N Engl J Med. 2006 Aug 17. 355(7):653-65. [Medline].

  71. Baddour LM, Wilson WR, Bayer AS, Fowler VG Jr, Bolger AF, Levison ME, et al. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America. Circulation. 2005 Jun 14. 111(23):e394-434. [Medline].

  72. Buckholz K, Larsen CT. Severity of gentamicin is nephrotoxic effect on patients with infective endocarditis: a prospective observation of cohort study of 373 patients. Clinical Infect Dis. 2009. 48:65-71.

  73. Cunha BA. Persistent S. aureus acute bacteremia: clinical pathway for diagnosis and treatment. Antibiot for Clin. 2006. 10:39-46.

  74. Falagas ME, Manta KG, Ntziora F, Vardakas KZ. Linezolid for the treatment of patients with endocarditis: a systematic review of the published evidence. J Antimicrob Chemother. 2006 Aug. 58(2):273-80. [Medline].

  75. Jones T, Yeaman MR, Sakoulas G, Yang SJ, Proctor RA, Sahl HG, et al. Failures in clinical treatment of Staphylococcus aureus Infection with daptomycin are associated with alterations in surface charge, membrane phospholipid asymmetry, and drug binding. Antimicrob Agents Chemother. 2008 Jan. 52(1):269-78. [Medline]. [Full Text].

  76. Sakoulas G, Moise-Broder PA, Schentag J, Forrest A, Moellering RC Jr, Eliopoulos GM. Relationship of MIC and bactericidal activity to efficacy of vancomycin for treatment of methicillin-resistant Staphylococcus aureus bacteremia. J Clin Microbiol. 2004 Jun. 42(6):2398-402. [Medline]. [Full Text].

  77. Fowler VG Jr, Li J, Corey GR, Boley J, Marr KA, Gopal AK, et al. Role of echocardiography in evaluation of patients with Staphylococcus aureus bacteremia: experience in 103 patients. J Am Coll Cardiol. 1997 Oct. 30(4):1072-8. [Medline].

  78. Fowler VG Jr, Miro JM, Hoen B, Cabell CH, Abrutyn E, Rubinstein E, et al. Staphylococcus aureus endocarditis: a consequence of medical progress. JAMA. 2005 Jun 22. 293(24):3012-21. [Medline].

  79. Khatib R, Johnson LB, Fakih MG, Riederer K, Khosrovaneh A, Shamse Tabriz M, et al. Persistence in Staphylococcus aureus bacteremia: incidence, characteristics of patients and outcome. Scand J Infect Dis. 2006. 38(1):7-14. [Medline].

  80. Duval X, Selton-Suty C, Alla F, Salvador-Mazenq M, Bernard Y, Weber M, et al. Endocarditis in patients with a permanent pacemaker: a 1-year epidemiological survey on infective endocarditis due to valvular and/or pacemaker infection. Clin Infect Dis. 2004 Jul 1. 39(1):68-74. [Medline].

  81. [Guideline] Olaison L, Pettersson G. Current best practices and guidelines indications for surgical intervention in infective endocarditis. Infect Dis Clin North Am. 2002 Jun. 16(2):453-75, xi. [Medline].

  82. Mekontso Dessap A, Zahar JR, Voiriot G, Ali F, Aissa N, Kirsch M, et al. Influence of preoperative antibiotherapy on valve culture results and outcome of endocarditis requiring surgery. J Infect. 2009 Jul. 59(1):42-8. [Medline].

  83. [Guideline] Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007 Oct 9. 116(15):1736-54. [Medline].

  84. Pronovost P, Needham D, Berenholtz S, Sinopoli D, Chu H, Cosgrove S, et al. An intervention to decrease catheter-related bloodstream infections in the ICU. N Engl J Med. 2006 Dec 28. 355(26):2725-32. [Medline].

  85. Dajani AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAMA. 1997 Jun 11. 277(22):1794-801. [Medline].

  86. Bach DS. Perspectives on the American College of Cardiology/American Heart Association guidelines for the prevention of infective endocarditis. J Am Coll Cardiol. 2009 May 19. 53(20):1852-4. [Medline].

  87. Thornhill MH, Dayer MJ, Forde JM, et al. Impact of the NICE guideline recommending cessation of antibiotic prophylaxis for prevention of infective endocarditis: before and after study. BMJ. 2011 May 3. 342:d2392. [Medline]. [Full Text].

  88. Nishimura RA, Carabello BA, Faxon DP, Freed MD, Lytle BW, O’Gara PT, et al. ACC/AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. Aug 2008. 118(8):887-96.

  89. Netzer RO, Altwegg SC, Zollinger E, Täuber M, Carrel T, Seiler C. Infective endocarditis: determinants of long term outcome. Heart. 2002 Jul. 88(1):61-6. [Medline]. [Full Text].

  90. US Food and Drug Administration. FDA Drug Safety Communication: Serious CNS reactions possible when linezolid (Zyvox®) is given to patients taking certain psychiatric medications. Available at http://www.fda.gov/Drugs/DrugSafety/ucm265305.htm. Accessed: July 27, 2011.

  91. Boggs W. Ampicillin-Ceftriaxone Effective for E. faecalis Endocarditis. Medscape. Feb 12 2013. Available at http://www.medscape.com/viewarticle/779187.

  92. Fernández-Hidalgo N, Almirante B, Gavaldà J, Gurgui M, Peña C, de Alarcón A, et al. Ampicillin Plus Ceftriaxone Is as Effective as Ampicillin Plus Gentamicin for Treating Enterococcus faecalis Infective Endocarditis. Clin Infect Dis. 2013 Feb 25. [Medline].

  93. Yong MS, Saxena P, Killu AM, Coffey S, Burkhart HM, Wan SH, et al. The Preoperative Evaluation of Infective Endocarditis via 3-Dimensional Transesophageal Echocardiography. Tex Heart Inst J. 2015 Aug. 42 (4):372-6. [Medline].

 
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Acute bacterial endocarditis caused by Staphylococcus aureus with perforation of the aortic valve and aortic valve vegetations. Courtesy of Janet Jones, MD, Laboratory Service, Wichita Veterans Administration Medical Center.
Acute bacterial endocarditis caused by Staphylococcus aureus with aortic valve ring abscess extending into myocardium. Courtesy of Janet Jones, MD, Laboratory Service, Wichita Veterans Administration Medical Center.
A middle-aged man with a history of intravenous drug use who presented with severe myalgias and a petechial rash. He was diagnosed with right-sided staphylococcal endocarditis.
This is a magnified portion of a parasternal long axis view from a transthoracic echocardiogram. There is a small curvilinear vegetation on the mitral valve as indicated. The patient presented with a headache and fever, and CT scan of the brain revealed an occipital hemorrhage. The patient had a history of intravenous drug use and multiple blood cultures grew Staphylococcus aureus.
A young adult with a history of intravenous drug use, endocarditis involving the tricuspid valve with Staphylococcus aureus, and multiple septic pulmonary emboli. Pulmonary lesions on chest radiograph are most prominent in the right upper lobe with both solid and cavitary appearance.
Mitral valve: endocarditis with valve destruction and vegetation. Note the posterior leaflet of the mitral valve, with an irregular vegetation on the atrial surface, resulting in valve destruction at the commissure between the anterior leaflet and the posterior leaflet.
Aortic valve: healed endocarditis. Note the gaping hole with the fibrous rim, and a small strand at the free edge. The hole is at the line of closure. The affected valve is the left cusp. Note the right noncoronary cusp (immediate to the left in this image) demonstrates a small, multichanneled fenestration at the commissure, immediately adjacent to similar fenestrations in the left coronary cusp. These are physiologic lesions occurring with age and are unrelated to endocarditis.
Aortic valve: bicuspid, with infectious endocarditis. In this excised valve, note the bulky vegetations on the ventricular surfaces, with distortion of the valve surfaces.
Mitral valve: postrheumatic, with infectious endocarditis. A defect is seen in the scarred valve, with focal surface hemorrhage. The patient also underwent aortic valve replacement, as there was contiguous infection.
The surface of the valves, in most cases, demonstrates areas of acute neutrophilic inflammation with admixed fibrin and platelets. Degenerated bacterial colonies are seen at the left. Also, areas of microcalcification may mimic bacterial deposits.
Infectious endocarditis, subacute phase. Hemorrhage and prominent granulation tissue with neovascularity is apparent throughout. This aortic valve showed fibrin exudate on the ventricular surface (below), with more prominent organization and granulation on the aortic surface (above).
Infectious endocarditis, surface of valve leaflet with fibrin; higher magnification of previous image. A chronic infiltrate is seen, just under the denuded thrombosed surface, with primarily macrophages and focal macrophage giant cells.
Bioprosthetic valve with endocarditis. Note the large bacterial colony (staphylococci by culture) in the absence of significant inflammation; the xenograft tissue is not viable, and nuclear detail is not apparent.
Table 1. Clinical Features of Infective Endocarditis According to Causative Organism
Causative Organism(s) Clinical Features of IE
Staphylococcus aureus
  • Overall, S aureus infection is the most common cause of IE, including PVE, acute IE, and IVDA IE.
  • Approximately 35-60.5% of staphylococcal bacteremias are complicated by IE.
  • More than half the cases are not associated with underlying valvular disease.
  • The mortality rate of S aureus IE is 40-50%.
  • S aureus infection is the second most common cause of nosocomial BSIs, second only to CoNS infection.
  • The incidence of MRSA infections, both the hospital- and community-acquired varieties, has dramatically increased (50% of isolates). Sixty percent of individuals are intermittent carriers of MRSA or MSSA .
  • The primary risk factor for S aureus BSI is the presence of intravascular lines. Other risk factors include cancer, diabetes, corticosteroid use, IVDA, alcoholism, and renal failure.
  • The realization that approximately 50% of hospital- and community-acquired staphylococcal bacteremias arise from infected vascular catheters has led to the reclassification of staphylococcal BSIs. BSIs are acquired not only in the hospital but also in any type of health care facility (eg, nursing home, dialysis center).
  • Of S aureus bacteremia cases in the United States, 7.8% (200,000) per year are associated with intravascular catheters.
Streptococcus viridans
  • This organism accounts for approximately 50-60% of cases of subacute disease.
  • Most clinical signs and symptoms are mediated immunologically.
Streptococcus intermedius group
  • These infections may be acute or subacute.
  • S intermedius infection accounts for 15% of streptococcal IE cases.
  • Members of the S intermedius group, especially S anginosus, are unique among the streptococci in that they can actively invade tissue and form abscesses, often in the CNS.
Abiotrophia
  • Approximately 5% of subacute cases of IE are due to infection with Abiotrophia species.
  • They require metabolically active forms of vitamin B-6 for growth.
  • This type of IE is associated with large vegetations that lead to embolization and a high rate of posttreatment relapse.
Group D streptococci
  • Most cases are subacute.
  • The source is the gastrointestinal or genitourinary tract.
  • It is the third most common cause of IE.
  • They pose major resistance problems for antibiotics.
Nonenterococcal group D
  • The clinical course is subacute.
  • Infection often reflects underlying abnormalities of the large bowel (eg, ulcerative colitis, polyps, cancer).
  • The organisms are sensitive to penicillin.
Group B streptococci
  • Acute disease develops in pregnant patients and older patients with underlying diseases (eg, cancer, diabetes, alcoholism).
  • The mortality rate is 40%.
  • Complications include metastatic infection, arterial thrombi, and congestive heart failure.
  • It often requires valve replacement for cure.
Group A, C, and G streptococci
  • Acute disease resembles that of S aureus IE (30-70% mortality rate), with suppurative complications.
  • Group A organisms respond to penicillin alone.
  • Group C and G organisms require a combination of synergistic antibiotics (as with enterococci).
Coagulase-negative S aureus
  • This causes subacute disease.
  • It behaves similarly to S viridans infection.
  • It accounts for approximately 30% of PVE cases and less than 5% of NVE cases. [21]
Pseudomonas aeruginosa
  • This is usually acute, except when it involves the right side of the heart in IVDA IE.
  • Surgery is commonly required for cure.
HACEK (ie, Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)
  • These organisms usually cause subacute disease.
  • They account for approximately 5% of IE cases.
  • They are the most common gram-negative organisms isolated from patients with IE.
  • Complications may include massive arterial emboli and congestive heart failure.
  • Cure requires ampicillin, gentamicin, and surgery.
Fungal
  • These usually cause subacute disease.
  • The most common organism of both fungal NVE and fungal PVE is Candida albicans.
  • Fungal IVDA IE is usually caused by Candida parapsilosis or Candida tropicalis.
  • Aspergillus species are observed in fungal PVE and NIE.
Bartonella
  • The most commonly involved species is Bartonella quintana.
  • IE typically develops in homeless males who have extremely substandard hygiene. Bartonella must be considered in cases of culture-negative endocarditis among homeless individuals.
Multiple pathogens (polymicrobial)
  • Pseudomonas and enterococci are the most common combination of organisms.
  • It is observed in cases of IVDA IE
  • The cardiac surgery mortality rate is twice that associated with single-agent IE. [22]
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