Pseudomonas aeruginosa and other members of this group of gram-negative bacilli are opportunistic pathogens that frequently cause hospital-acquired infections, particularly in ventilator patients, burn patients, and patients with chronic debility. Many sites can be infected, and infection is usually severe. Diagnosis is by culture. Antibiotic choice varies with the pathogen and must be guided by susceptibility testing because resistance is common.
Pseudomonas is ubiquitous and favors moist environments. In humans, P. aeruginosa is the most common pathogen, but infection may result from P. paucimobilis, P. putida, P. fluorescens, or P. acidovorans. Other important hospital-acquired pathogens formerly classified as Pseudomonas include Burkholderia cepacia and Stenotrophomonas maltophilia. B. pseudomallei causes a distinct disease known as melioidosis that is limited mostly to the Asian tropics (see Melioidosis).
P. aeruginosa is present occasionally in the axilla and anogenital areas of normal skin but rarely in stool unless antibiotics are being given. In hospitals, the organism is frequently present in sinks, antiseptic solutions, and urine receptacles. Transmission to patients by health care practitioners may occur, especially in burn and neonatal ICUs, unless infection control practices are meticulously followed.
Diseases Caused by Pseudomonas
Most P. aeruginosa infections occur in hospitalized patients, particularly those who are debilitated or immunocompromised. P. aeruginosa is a common cause of infections in ICUs. HIV-infected patients, particularly those in advanced stages, are at risk of community-acquired P. aeruginosa infections.
Pseudomonas infections can develop in many anatomic sites, including skin, subcutaneous tissue, bone, ears, eyes, urinary tract, and heart valves. The site varies with the portal of entry and the patient's vulnerability. In hospitalized patients, the first sign may be overwhelming gram-negative sepsis.
Skin and soft-tissue infections:
In burns, the region below the eschar can become heavily infiltrated with organisms, serving as a focus for subsequent bacteremia—an often lethal complication.
Deep puncture wounds of the foot are often infected by P. aeruginosa. Draining sinuses, cellulitis, and osteomyelitis may result. Drainage from puncture wounds often has a sweet, fruity smell.
Folliculitis acquired in hot tubs is often caused by P. aeruginosa.
External otitis, common in tropical climates, is the most common form of Pseudomonas infection involving the ear. A more severe form, referred to as malignant external otitis (see Malignant External Otitis), can develop in diabetic patients. It is manifested by severe ear pain, often with unilateral cranial nerve palsies, and requires parenteral therapy.
Ecthyma gangrenosum is a skin lesion that occurs in neutropenic patients and is usually caused by P. aeruginosa. It is characterized by erythematous, centrally ulcerated, purple-black areas about 1 cm in diameter occurring most often in the axillary, inguinal, or anogenital areas.
Respiratory tract infections:
P. aeruginosa is a frequent cause of ventilator-associated pneumonia. In HIV-infected patients, Pseudomonas most commonly causes pneumonia or sinusitis. Pseudomonas bronchitis is common late in the course of cystic fibrosis. Isolates from patients with cystic fibrosis have a characteristic mucoid colonial morphology.
Pseudomonas is a common cause of nosocomial UTI, especially in patients who have had urologic manipulation or obstructive uropathy. Pseudomonas commonly colonizes the urinary tract in catheterized patients, especially those who have received broad-spectrum antibiotics.
Ocular involvement generally manifests as corneal ulceration, most often after trauma, but contamination of contact lenses or lens fluid has been implicated in some cases.
Rarely, Pseudomonas causes acute bacterial endocarditis, usually on prosthetic valves in patients who have had open-heart surgery or on natural valves in IV drug abusers.
Many Pseudomonas infections can cause bacteremia. In nonintubated patients without a detectable urinary focus, especially if infection is due to a species other than P. aeruginosa, bacteremia suggests contaminated IV fluids, drugs, or antiseptics used in placing the IV catheter.
Diagnosis depends on culturing the organism from the site of infection: blood, skin lesions, drainage fluid, urine, CSF, or eye. Localized infection may produce a fruity smell, and pus may be greenish.
Hot-tub folliculitis resolves spontaneously and does not require antibiotic therapy.
External otitis is treated with 1% acetic acid irrigations or topical drugs such as polymyxin B or colistin. More severe infection is treated with fluoroquinolones.
Focal soft-tissue infection may require early surgical debridement of necrotic tissue and drainage of abscesses in addition to antibiotics.
Small corneal ulcers are treated with ciprofloxacin 0.3% or levofloxacin 0.5%. Fortified (higher than stock concentration) antibiotic drops, such as tobramycin 15 mg/mL, are used for more significant ulcers. Frequent dosing (eg, q 1 h around the clock) is necessary initially. Eye patching is contraindicated because it produces a dark warm environment that favors bacterial growth and prevents administration of topical drugs.
Asymptomatic bacteriuria is not treated with antibiotics, except during pregnancy and before urologic manipulation. Patients with symptomatic UTIs can often be treated with levofloxacin 500 mg po once/day or ciprofloxacin 400 mg po bid.
Parenteral therapy is required, typically with an aminoglycoside plus an antipseudomonal β-lactam, an antipseudomonal cephalosporin (eg, cefepime, cefoperazone), or the carbapenems meropenem or imipenem.
Right-sided endocarditis can be treated with antibiotics, but usually the infected valve must be removed to cure an infection involving the mitral, aortic, or prosthetic valve.
In neutropenic patients with marginal renal function, nonaminoglycoside combinations, such as double β-lactams or a β-lactam plus a fluoroquinolone, are also satisfactory.
P. aeruginosa resistance may occur among patients treated with ceftazidime, ciprofloxacin, gentamicin, meropenem, or imipenem.
Last full review/revision August 2009 by Burke A. Cunha, MD
Content last modified February 2012