Pseudomonas aeruginosa, the primary human pathogen in the genus Pseudomonas, is widely distributed in nature. It is found in soil, water, plants, and animals. Although it may colonize healthy humans without causing disease, it is also a significant opportunistic pathogen and a major cause of nosocomial (hospital-acquired) infections. P. aeruginosa is regularly a cause of nosocomial pneumonia, nosocomial urinary tract infections, surgical site infections, infections of severe burns, and infections of patients undergoing either chemotherapy for neoplastic disease or antibiotic therapy. P. aeruginosa is motile (it has polar flagella) and aerobic or facultative. P. aeruginosa does not ferment carbohydrates but can utilize alternate electron acceptors, such as nitrate, in anaerobic respiration. Nutritional requirements are minimal, and the organism can grow on a wide variety of organic substrates. In fact, P. aeruginosa can even grow in laboratory water baths, hot tubs, intravenous (IV) tubing, and other water-containing vessels. This explains why the organism is responsible for so many nosocomial infections.

A. Pathogenesis

 P. aeruginosa disease begins with attachment to and colonization of host tissue. Pili on the bacteria mediate adherence, and mucoid strains predominate in patients with cystic fibrosis (CF). The mucoid capsule is composed of a repeating polymer of mannuronic and glucuronic acids called alginate. The alginate capsule is only expressed after a so-called “patho-adaptive mutation” occurs. Alginate expression confers resistance to phagocytosis and clearing in the CF lung. Host tissue damage facilitates adherence and colonization. P. aeruginosa produces numerous toxins and extracellular products that promote local invasion and dissemination of the organism.

B. Clinical significance

P. aeruginosa causes both localized and systemic illness. Virtually any tissue or organ system may be affected. Individuals most at risk include those with impaired immune defenses.

1. Localized infections: These may occur in the eye (causing keratitis and endophthalmitis following trauma), ear (causing external otitis, or swimmer's ear, and invasive and necrotizing otitis externa, particularly in older adult diabetic patients or trauma patients), skin (causing wound infection, as shown in Figure 1, and pustular rashes occurring in epidemics associated with use of contaminated whirlpools, hot tubs, and swimming pools), urinary tract (particularly in hospitalized patients who have been subjected to catheterization, instrumentation, surgery, or renal transplantation), respiratory tract (causing pneumonia in individuals with chronic lung disease, congestive heart failure, or cystic fibrosis, particularly in patients who have been intubated or are on ventilators for longer than than a few days), gastrointestinal tract (causing infections ranging from relatively mild diarrheal illness in children to severe, necrotizing enterocolitis in infants and neutropenic cancer patients), and the CNS (causing meningitis and brain abscesses, particularly in association with trauma, surgery, or tumors of the head or neck). Localized infections have the potential to lead to disseminated infection. [Note: The organism has a propensity to invade blood vessel walls.]

Fig1. Pseudomonas infection of the pinna of the ear.

2. Systemic infections: Infections reflecting systemic spread of the organism include bacteremia (most common in patients whose immune systems have been compromised), secondary pneumonia, bone and joint infections (in IV drug users and patients with urinary tract or pelvic infections), endocarditis (in IV drug users and patients with prosthetic heart valves), CNS (mainly when the meninges are breached), and skin/soft tissue infections. P. aeruginosa is feared because it can cause severe hospital-acquired infections, especially in immunocompromised hosts. It is often antibiotic resistant due to expression of a number of efflux pumps, complicating the choice of therapy .

C. Laboratory identification

P. aeruginosa can be isolated by plating on a variety of media, both nonselective (for example, blood agar) and moderately selective (for example, MacConkey agar as shown in Figure 2). Identification is based on the results of a battery of biochemical and other diagnostic tests. Serologic typing is used in the investigation of clusters of cases, which may stem from exposure to a common source. [Note: A clue to its presence is a characteristic fruity odor, both in the laboratory and at the bedside.] P. aeruginosa typically produces a blue-green pigment called pyocyanin and is oxidase positive.

Fig2. Summary of Pseudomonas disease. 1 Indicates first-line drugs.

 D. Treatment and Prevention

Specific therapy varies with the clinical presentation and the antibiotic sensitivity pattern of the isolate. It is difficult to find antibiotics effective against P. aeruginosa because of its rapid development of resistance mutations and its own innate mechanisms of antibiotic resistance. Pseudomonas infections typically occur in patients with impaired defenses. Therefore, aggressive antimicrobial therapy (often a combination of two bactericidal antibiotics, such as an aminoglycoside, an antipseudomonal β-lactam, or a quinolone) is generally required (see Figure 2).