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Pseudomonas aeruginosa bacteremia and endocarditis

Pseudomonas aeruginosa bacteremia and endocarditis
Literature review current through: Jan 2024.
This topic last updated: Oct 12, 2022.

INTRODUCTION — Pseudomonas aeruginosa is among the top considerations in the differential diagnosis when treating patients who are suspected of having severe hospital-acquired infections.

The epidemiology, clinical manifestations, diagnosis, and treatment of P. aeruginosa bacteremia and endocarditis will be reviewed here.

The general principles of antimicrobial treatment of infections caused by P. aeruginosa, including antibiotic options and decisions on combination therapy, are discussed in detail elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections".)

The clinical manifestations and management of other P. aeruginosa infections and the epidemiology and pathogenesis of infection with this organism are also discussed separately.

(See "Epidemiology, microbiology, and pathogenesis of Pseudomonas aeruginosa infection".)

(See "Pseudomonas aeruginosa pneumonia".)

(See "Pseudomonas aeruginosa skin and soft tissue infections".)

(See "Pseudomonas aeruginosa infections of the eye, ear, urinary tract, gastrointestinal tract, and central nervous system".)

(See "Cystic fibrosis: Antibiotic therapy for chronic pulmonary infection", section on 'Pseudomonas aeruginosa' and "Cystic fibrosis: Antibiotic therapy for pulmonary exacerbations".)

BACTEREMIA

Epidemiology — Bloodstream infection (BSI) with P. aeruginosa is most commonly hospital-acquired and is a problem worldwide [1-6]. In a prospective analysis from the SCOPE (Surveillance and Control of Pathogens of Epidemiologic Importance) database of 24,179 hospital-acquired bloodstream infections occurring in 49 hospitals in the United States between 1995 to 2002, Pseudomonas species accounted for 4 percent of cases and were the third leading cause of gram-negative infections [5]. In certain settings, such as intensive care units, the proportion of gram-negative bloodstream infections due to P. aeruginosa is even higher. As an example, in one review of liver transplant recipients, approximately 35 percent of bloodstream infections were with P. aeruginosa, which had an attributable mortality of 30 percent [7]. In a retrospective study, Pseudomonas spp was the second most common cause of gram-negative BSIs after E. coli (31 percent) in BSIs among patients with hematologic or solid organ malignancies [8]. (See "Gram-negative bacillary bacteremia in adults", section on 'Microbiology' and "Intravascular catheter-related infection: Epidemiology, pathogenesis, and microbiology".)

Risk factors for P. aeruginosa bacteremia include [3,6,9-15]:

Neutropenia or other immunodeficiency (eg, hematologic malignancy, solid organ or bone marrow transplantation, or HIV infection)

Advanced age

Pancreatobiliary tract disease

Severe burns

Indwelling central venous or urinary catheter

Antimicrobial use within the prior three months (eg, piperacillin-tazobactam, antipseudomonal carbapenem, fluoroquinolone, aminoglycoside, ceftriaxone use) [15,16]

Traumatic wounds that have been contaminated with fresh water

Recent hospitalization

P. aeruginosa bacteremia in immunocompetent patients is primarily associated with the use of indwelling urinary, central venous catheters, or traumatic or surgical wound infections [17]. A case-control study of Korean patients with P. aeruginosa bacteremia in the emergency department setting found that respiratory tract infection was an independent risk factor, whereas diabetes mellitus and urinary tract infection were negative clinical predictors [18].

Pancreatobiliary tract disease is an additional important risk factor for bacteremia, independent of underlying malignancy or immunosuppression [19]. Pancreatobiliary sources and complications from endoscopic retrograde cholangiopancreatography (ERCP) appear to be increasing in frequency as the cause of P. aeruginosa bacteremia in many regions. Clusters of P. aeruginosa bacteremias after ERCP have been traced to inadequate cleaning or disinfection of endoscopes [20].

Hospital-acquired P. aeruginosa bacteremia may result from primary infection in the lungs, biliary and gastrointestinal tract, urinary tract, skin and soft tissues, or from infected intravascular catheters [4,19,21]. The source of the bacteremia is unknown in up to 40 percent of cases.

Clinical features — Although it is usually impossible to distinguish patients with P. aeruginosa bacteremia from patients with bacteremia due to other gram-negative rods based on clinical features alone, patients with P. aeruginosa infection are more likely to have a fatal outcome. (See 'Prognosis' below.)

Patients with gram-negative bacteremia due to P aeruginosa typically present with fever, tachycardia, and tachypnea. Disorientation, hypotension, and respiratory failure (due to either pneumonia or acute respiratory distress syndrome [ARDS]) are other common complications, especially in immunocompromised or debilitated patients. Additional clinical manifestations will vary by the site of the primary infection. (See "Gram-negative bacillary bacteremia in adults", section on 'Clinical manifestations' and "Pathophysiology of sepsis".)

Rarely, patients with P. aeruginosa bacteremia develop ecthyma gangrenosum (picture 1), a skin lesion that results from perivascular bacterial invasion of the media and adventitia of arteries and veins with secondary ischemic necrosis. Although ecthyma gangrenosum is not pathognomonic of P. aeruginosa infection, the presence of these lesions should immediately raise the high probability that P. aeruginosa is the causative organism. This is discussed in detail elsewhere. (See "Pseudomonas aeruginosa skin and soft tissue infections", section on 'Ecthyma Gangrenosum'.)

Other skin lesions that may occasionally accompany pseudomonal bacteremia include: diffuse maculopapular lesions, painful clusters of small vesicles or pustules, flat sharply-demarcated areas of cellulitis that may initially mimic erysipelas and become necrotic with time, and metastatic soft tissue abscesses that may appear on the extremities and fingertips [22,23].

Treatment

Empiric antibiotic therapy — Prompt administration of effective antimicrobial therapy is a critical initial step in the management of P. aeruginosa bacteremia (table 1) as delayed therapy correlates with increased mortality (see 'Prognosis' below). We favor the use of combination antimicrobial therapy for empiric therapy of known or suspected P. aeruginosa bacteremia prior to determination of drug susceptibility. In high-risk patients (such as those with neutropenia or severe burns and others with sepsis/shock), the rationale for the use of combination therapy in select situations is discussed elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Role of combination antimicrobial therapy'.)

Selection of empiric agents should also be informed by the local P. aeruginosa susceptibility patterns. Discussion of empiric therapy for gram-negative rod bacteremia and when P. aeruginosa should be covered is also found elsewhere. (See "Gram-negative bacillary bacteremia in adults", section on 'Empiric antimicrobial therapy' and "Gram-negative bacillary bacteremia in adults", section on 'Indications and rationale for coverage of P. aeruginosa'.)

Directed antibiotic therapy and duration — When the isolate and results of susceptibility testing are known, antimicrobial therapy should be adjusted accordingly. In general, there is no convincing clinical evidence that using two active antipseudomonal agents offers a mortality benefit over a single active agent. This is discussed in detail elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Rationale'.)

Thus, for most patients with P. aeruginosa bacteremia, we suggest directed therapy with a single intravenous antipseudomonal antibiotic to which the isolate is susceptible (table 1); however, aminoglycosides should not be used as a single agent.

Treatment duration is largely dictated by the primary site of infection.

For immunocompetent patients, we administer antibiotic therapy for 7 to 10 days as long as source control has been achieved (eg, via removal of infected catheters or drainage of abscesses ); if patients responded promptly to these interventions and antimicrobial therapy; and there is no bony, endovascular, pulmonary, or central nervous system (CNS) involvement. If the isolate is susceptible to fluoroquinolones and there are no concerns about gastrointestinal tract absorption of oral medications, patients can be transitioned to oral ciprofloxacin or levofloxacin to complete their course of therapy. Longer courses of therapy may be warranted if source control is uncertain or if there are known seeded sites of infection that are not amenable to drainage. Duration of treatment for P. aeruginosa osteomyelitis, endocarditis, pneumonia, and CNS infection are discussed elsewhere. (See "Nonvertebral osteomyelitis in adults: Treatment", section on 'Clinical approach' and 'Treatment' below and "Pseudomonas aeruginosa pneumonia", section on 'Duration of therapy' and "Health care-associated meningitis and ventriculitis in adults: Treatment and prognosis", section on 'Duration'.)

Limited observational data support this relatively abbreviated course of antibiotics for uncomplicated P. aeruginosa bacteremia [24,25]. In a retrospective study of 249 patients with P. aeruginosa bacteremia, a shorter duration of antibiotics (7 to 11 days, median 9) was associated with a similar odds of death and recurrent infection as a longer duration (11 to 21 days, median 16) after adjustment for risk factors for severe disease [24]. Almost all patients had appropriate source control, and patients treated for more than 21 days, presumably because of complicated infections, were not included. The antibiotic courses included a step down to an oral fluoroquinolone in about a third of patients in both groups. Despite the limitations of this study, including unmeasured confounders, these data support a conclusion that an abbreviated course can be an appropriate strategy for select patients.

However, the optimal duration of therapy remains uncertain when dealing with bacteremia due to MDR P. aeruginosa, as most studies have not critically examined outcomes by the duration of therapy. Moreover, studies focusing on novel antibiotics with activity against MDR gram-negative bacilli compared outcomes with existing standards of care or to the best available therapy. Total durations of treatment in such studies varied from 5 to 21 days depending on the specific clinical trial protocols, the sites of infection, and assessments of clinical response. Thus at present we can make no firm recommendations as to the optimal duration of therapy for patients with MDR P. aeruginosa bacteremia [25,26].

For neutropenic patients, we use a single active agent and continue it for at least 14 days and until the neutrophil count has recovered. Some experts continue to use two intravenous antipseudomonal antibiotics from different classes to which the isolate is susceptible for the first three to five days of treatment to ensure clinical improvement because of the high mortality risk, despite the absence of data to support the practice.

See other topic reviews for duration of treatment for other types of infection (eg, pneumonia, soft tissue infection, biliary infection) that may be complicated by bacteremia.

Antipseudomonal agents and their dosing are discussed elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotics with antipseudomonal activity'.)

Other interventions — In addition to antimicrobial therapy, the primary site of infection should also be addressed. All infected catheters should be removed, and abscesses or obstructions should be drained or removed whenever possible.

Prognosis

Mortality — Bacteremia due to P. aeruginosa is associated with a high mortality rate compared with bacteremia due to other gram-negative bacilli or gram-positive organisms [27-30].

One study, which prospectively compared 314 patients with bacteremia due to P. aeruginosa or S. aureus, found that mortality was significantly higher with P. aeruginosa than with either methicillin-susceptible S. aureus (MSSA) or methicillin-resistant S. aureus (MRSA) (30.6 percent, 16.2 percent, and 13.5 percent, respectively) [27]. In a retrospective analysis of 136 patients with P. aeruginosa bacteremia, the 30-day mortality rate was 39 percent [28]. Similar mortality rates have been reported among children and adolescents with P. aeruginosa bacteremia in the setting of neutropenia [29].

The reported 30-day mortality attributable to carbapenem-resistant P. aeruginosa bacteremia is also high, ranging between 8 and 18.4 percent [30].

Risk factors for poor prognosis — Mortality is especially high in neutropenic patients and in patients who present with or develop septic shock.

In a study of 133 episodes of P. aeruginosa bacteremia, a stepwise logistic regression analysis identified four variables as independently influencing outcome [31]:

Development of septic shock

Granulocyte count <500/mm3

Inappropriate initial antibiotic therapy

Development of septic metastasis

Other studies have shown that the prognosis of P. aeruginosa bacteremia is closely related to the underlying condition of the host and the primary site of infection. In a study of 100 episodes of P. aeruginosa bacteremia, survival directly correlated with underlying disease [32]. Twenty-six of 47 patients (55 percent) with nonfatal underlying conditions survived, compared with 2 of 13 (15 percent) and 16 of 64 (25 percent) with rapidly fatal and ultimately fatal underlying conditions, respectively. Mortality is also usually higher when the bacteremia accompanies a pulmonary infection [33]. In one study, patients with underlying malignancy (hematologic or solid organ) were shown to have a 30-day mortality of 22 percent following Pseudomonas-associated BSI [8].

Drug resistance may also negatively impact prognosis. Two studies found that strains of P. aeruginosa that produce metallo-beta-lactamases or specific (PER-1) extended spectrum beta-lactamases cause unusually high mortality rates when present in the bloodstream [34,35]. In a prospective multicenter study of 632 cases of P. aeruginosa bacteremia, carbapenem resistance (n = 145) was not associated with higher mortality overall (35 versus 27 percent with susceptible strains); however, in a subgroup analysis, higher 30-day mortality rates were noted among patients with few comorbidities when carbapenem resistance was present (adjusted odds ratio [OR] 6 to 10) [36]. Variables that have been associated with mortality in patients with BSI due to MDR P. aeruginosa include presentation with septic shock and inadequate initial antimicrobial therapy [37].

Other factors that have been associated with poor prognosis include the presence of polymicrobial (versus monomicrobial bacteremia) and advanced age [28,38,39]. In a study of patients with hematologic malignancies who had Pseudomonas infections, hypophosphatemia, hypoproteinemia, and high serum lactate were associated with an increased risk of septic shock on multivariate analysis [40].

Effect of antimicrobial therapy on prognosis — The choice and timing of antibiotic therapy is particularly crucial. As an example, in one study of 410 episodes of P. aeruginosa bacteremia, cure was substantially higher in patients receiving appropriate antibiotics than in those who did not (67 versus 14 percent), and a one- to two-day delay in administering appropriate antibiotics reduced the cure rate from 74 to 46 percent [41]. In one prospective ICU study, inadequate antimicrobial therapy was statistically associated with a higher mortality rate (62 versus 28 percent, RR 2.18, 95 percent CI 5.09-9.24, p<0.001) [42]. Approximately 10 percent of patients in this study had P. aeruginosa bacteremia.

The prognosis of P. aeruginosa bacteremia in neutropenic patients with hematologic malignancies has improved over time [43]. One retrospective study showed an improved prognosis of P. aeruginosa bacteremia in the years 1992 to 1996 compared with 1976 to 1982 [44]. This improvement was due mainly to changes in the management of the infection:

More frequent use of new anti-pseudomonal beta-lactams and ciprofloxacin instead of aminoglycosides as monotherapy.

Prompt removal of catheters.

ENDOCARDITIS

Epidemiology — Infective endocarditis (IE) due to P. aeruginosa is uncommon, but when it occurs, it is strongly associated with injection drug use (IDU) and/or prosthetic heart valves [45] and pacemakers. More than 90 percent of cases of IE due to P. aeruginosa have been reported in people who inject drugs (PWID), and most patients had no previous structural heart disease. P. aeruginosa IE tends to occur in specific geographic locations; epidemics of this infection have been described in PWID, mainly users of pentazocine and tripelennamine, presumably associated with mixing of drugs in contaminated water [46,47].

P. aeruginosa is also an occasional cause of hospital-acquired endocarditis, accounting for 10 percent of cases in one small ICU series [48].

Clinical features — In general, the clinical manifestations of IE are similar whether due to P. aeruginosa or other organisms. However, given the close association with IDU, the most frequently involved valve is the tricuspid. Additionally, multiple valve involvement can occur. In a study of 34 cases from one center, 13 had isolated involvement of the tricuspid valve and an additional case had tricuspid and pulmonic valve infection [49].

Since tricuspid infection is common, many patients present with pulmonary manifestations, including cough, chest pain, and hemoptysis. Such patients often have multiple discrete lung lesions that may progress to cavitation. Patients with left-sided valvular infections often develop fulminant or rapidly progressive symptoms that are due to either congestive heart failure or embolism of large or medium-sized arteries. Ring and annular abscesses are also frequent complications [49]. (See "Right-sided native valve infective endocarditis".)

Patients with tricuspid valve infection typically have a less fulminant course and better prognosis than patients with left-sided valvular involvement. In one study, 20 of 25 patients with right-sided infection recovered with medical or combined medical/surgical therapy compared with only three of nine patients with left-sided infection [50].

The clinical manifestations of endocarditis are discussed in detail elsewhere. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

Diagnosis — In the setting of P. aeruginosa bacteremia, the diagnosis of endocarditis can be made with echocardiography and application of the Duke Criteria for endocarditis. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

The vast majority of patients with P. aeruginosa bacteremia do not have IE, and even those patients who have underlying risk factors for IE, such as patients with prosthetic heart valves, can have P. aeruginosa bacteremia in association with a urinary tract or wound infection. Thus, it would be impractical and of low yield to perform echocardiography in all patients with P. aeruginosa bacteremia. We evaluate for IE among patients with P. aeruginosa bacteremia in the following settings:

Failure to clear bloodstream infection on appropriate therapy

Presence of other stigmata of IE, including new regurgitant murmurs or evidence of embolic disease to the periphery, lungs, or central nervous system

Presence of underlying conditions increasing the risk of IE, including injection drug use, prosthetic valve, cardiac devices, and a previous history of endocarditis [51]. In an observational study of bacteremia in patients with cardiac devices, pseudomonal bacteremia was highly associated with cardiac device-related infection (odds ratio 50.28, 95% CI 4.16-606.93) compared with bacteremia from other gram-negative organisms [52].

Treatment — Treatment of P. aeruginosa IE usually necessitates the combination of antibiotics and surgery to achieve cure [2]. This is based on the fact that beta-lactam antibiotics have a slow onset of bactericidal activity against the organism, lack a postantibiotic effect, and can rapidly induce the development of resistance.

For antimicrobial therapy of P. aeruginosa IE, we suggest combination therapy with two intravenous antipseudomonal antibiotics from different classes to which the isolate is susceptible (table 1); one antibiotic should be an aminoglycoside unless the use is precluded by nephrotoxicity. The duration of therapy should be for at least six weeks. There are no published data comparing combination to monotherapy for P. aeruginosa IE, as it is a relatively uncommon infection; the vast majority of the published literature describes treatment with a combination antimicrobial regimen [47,53]. Specific antipseudomonal agents and their doses are discussed elsewhere. (See "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Antibiotics with antipseudomonal activity'.)

We routinely obtain early surgical consultation in all cases of P. aeruginosa endocarditis because of the association of improved prognosis with early valve replacement, particularly in the setting of left-sided disease (see 'Prognosis' below). When splenic abscesses complicate P. aeruginosa IE, splenectomy should be performed prior to valve replacement.

Additional surgical issues for native and prosthetic valve endocarditis are discussed elsewhere. (See "Surgery for left-sided native valve infective endocarditis" and "Surgery for prosthetic valve endocarditis".)

Phage therapy has been evaluated for P. aeruginosa endovascular infections in case reports and animal studies [54,55]. This strategy remains investigational; the frequency and significance of acquired resistance to phage treatment are uncertain issues.

Prognosis — P. aeruginosa endocarditis is associated with a poor outcome. In one study in patients with S. aureus and P. aeruginosa bacteremia, endocarditis was found to be an independent determinant of hospital mortality (OR 4.62; 95 percent CI 2.45-8.73) [27].In a review of 27 cases of P. aeruginosa IE in patients without injection drug use, mortality rates were 29 and 40 percent for community-acquired and hospital-acquired cases, respectively [56]. Age >60 years and a prosthetic device source were associated with even higher mortality rates.

In patients with left-sided IE due to P. aeruginosa, the prognosis for medical therapy is worse than for combined medical and surgical therapy in endocarditis due to most other organisms [46,47]. Early valve replacement has been shown to improve prognosis and is indicated in cases refractory to medical treatment and in complicated cases with hemodynamic instability. (See "Surgery for left-sided native valve infective endocarditis".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Treatment and prevention of infective endocarditis".)

SUMMARY AND RECOMMENDATIONS — Pseudomonas aeruginosa is one of the most commonly considered gram-negative aerobic bacilli in the differential diagnosis of a number of probable gram-negative infections. Consideration of this organism is important because it causes severe hospital-acquired infections, especially in immunocompromised hosts, is often antibiotic resistant, complicating the choice of therapy, and is associated with a high mortality rate. (See 'Introduction' above.)

Bacteremia

Bloodstream infection with P. aeruginosa is most commonly hospital-acquired. Risk factors for P. aeruginosa bacteremia include neutropenia or other immunodeficiency (eg, hematologic malignancy, solid organ or bone marrow transplantation, or HIV infection), advanced age, pancreatobiliary tract disease, severe burns, an indwelling central venous or urinary catheter, antimicrobial therapy within the last 30 days, and traumatic wounds that have been contaminated with fresh water. (See 'Epidemiology' above.)

Hospital-acquired P. aeruginosa bacteremia may result from primary infection in the lungs, biliary and gastrointestinal tract, urinary tract, skin and soft tissues or from infected intravascular catheters. (See 'Epidemiology' above.)

Bacteremic patients typically present with fever, tachycardia, and tachypnea. Disorientation, hypotension, and respiratory failure due to either pneumonia or acute respiratory distress syndrome are other common complications, especially in immunocompromised or debilitated patients. Although it is usually impossible to distinguish patients with P. aeruginosa bacteremia from patients with bacteremia due to other gram-negative rods on clinical grounds alone, patients with P. aeruginosa infection are more likely to have a fatal outcome and to develop ecthyma gangrenosum. The lesions of ecthyma gangrenosum (picture 1) involve the skin or mucous membranes, beginning as a small area of edema and quickly evolving into painless nodular lesions with central hemorrhage, ulceration, and necrosis. (See 'Clinical features' above and "Pseudomonas aeruginosa skin and soft tissue infections", section on 'Ecthyma Gangrenosum'.)

Prompt empiric therapy with an active antimicrobial agent (table 1) is critical in the management of known or suspected P. aeruginosa bacteremia, as delayed therapy correlates with increased mortality. In certain high risk patients (eg, patients with neutropenia or severe burns) and those with severe infections (eg, patients with sepsis/shock), we favor the use of combination antimicrobial therapy for empiric therapy. Otherwise, a single antipseudomonal agent is likely appropriate. In addition, infected catheters should be removed, and abscesses or obstructions should be drained or removed, whenever possible. The rationale for combination therapy in select settings is discussed elsewhere. (See 'Treatment' above and "Gram-negative bacillary bacteremia in adults", section on 'Empiric antimicrobial therapy' and "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Role of combination antimicrobial therapy'.)

When the isolate and results of susceptibility testing are known, antimicrobial therapy should be adjusted accordingly. In general, there is no clinical evidence that using two active antipseudomonal agents offers a mortality benefit over a single active agent. (See 'Treatment' above and "Principles of antimicrobial therapy of Pseudomonas aeruginosa infections", section on 'Role of combination antimicrobial therapy'.)

Thus, for most patients with P. aeruginosa bacteremia, we suggest treatment with a single intravenous antipseudomonal antibiotic to which the isolate is susceptible instead of a combination antimicrobial regimen (table 1) (Grade 2B). Aminoglycosides should not be used as a single agent. However, because of the high associated mortality rate of P. aeruginosa bacteremia in the setting of neutropenia, it is reasonable to continue a second active antipseudomonal agent for the first three to five days of treatment of neutropenic patients pending clinical improvement.

For immunocompetent patients with uncomplicated bacteremia and appropriate source control, we suggest a 7- to 10-day course of antibiotics (Grade 2C). Longer courses are warranted when source control is not adequate; when there is bony, endovascular, pulmonary, or central nervous system involvement; and in immunocompromised patients, such as those with neutropenia. (See 'Directed antibiotic therapy and duration' above.)

Bacteremia due to P. aeruginosa is associated with a high mortality rate compared with bacteremia due to other gram-negative bacilli as well as gram-positive organisms. (See 'Prognosis' above.)

Endocarditis

Infective endocarditis (IE) due to P. aeruginosa is uncommon, but when it occurs, it is strongly associated with injection drug use (IDU) and/or prosthetic heart valves and pacemakers. (See 'Epidemiology' above.)

Given the close association with IDU, the most frequently involved valve is the tricuspid valve. Additionally, multiple valve involvement can occur. Since tricuspid infection is common, many patients present with pulmonary manifestations, including cough, chest pain, and hemoptysis. Patients with left-sided valvular infections often develop fulminant or rapidly progressive symptoms that are due to either congestive heart failure or embolism of large or medium-sized arteries. Ring and annular abscesses are also frequent complications. (See 'Clinical features' above.)

In the setting of P. aeruginosa bacteremia, the diagnosis of endocarditis can be made with echocardiography and application of the Duke Criteria for endocarditis. In the absence of specific risk factors and signs of endocarditis, patients with P. aeruginosa bacteremia do not require work-up for endocarditis. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

For patients with P. aeruginosa infective endocarditis, we suggest combination antimicrobial therapy for the duration of the treatment course (Grade 2C). This regimen should include two antipseudomonal antibiotics from different classes to which the isolate is susceptible (table 1). (See 'Treatment' above.)

We suggest early surgical consultation in all cases of P. aeruginosa endocarditis because of the association of improved prognosis with early valve replacement or repair (Grade 2C). Particularly in patients with left-sided disease, the prognosis for medical therapy is worse than for combined medical and surgical therapy. (See 'Treatment' above and 'Prognosis' above.)

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Topic 2136 Version 25.0

References

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