Pseudomonas aeruginosa

Ps. aeruginosa is a motile aerobic Gram-negative bacillus that may appear singly, in pairs, or in short chains. It can be isolated from soil, water, plants, and animals, including humans. Since it thrives in a moist environment, human colonization often occurs in sites such as the perineum and external ear. Normal human colonization rates are as follows: skin, zero to 2 per cent; nasal mucosa, zero to 3 per cent; throat, zero to 7 per cent; stool, 3 to 24 per cent. Potential hospital reservoirs include respiratory equipment, disinfectant solutions, sinks, mops, and diagnostic instruments such as endoscopes.

Between 1985 and 1991, Ps. aeruginosa was the fourth most common nosocomial isolate in the United States, accounting for 10 per cent of nosocomial infections. Hospital-wide, it is the leading cause of nosocomial pneumonia (17 per cent), the third most common cause of urinary tract infections (12 per cent), and the fifth most common cause of surgical wound infection (8 per cent). It is the most common isolate in the ICU (13 per cent), where it is the leading cause of pneumonia (18 per cent), the fourth most common cause of urinary tract infections (12 per cent), and the third most common cause of wound infections (11 per cent).

Ps. aeruginosa rarely causes disease in healthy patients, but it preys upon the immunologically defenseless. It is both invasive and toxinogenic. There is a clear relationship between oropharyngeal and respiratory colonization and bacterial adherence to epithelium, but adherence requires loss of fibronectin, sputum proteases (particularly in patients with cystic fibrosis), and cellular injury (e.g. viral infection or mechanical injury from an endotracheal tube). Under certain conditions (particularly in cystic fibrosis), Ps. aeruginosa produces a polysaccharide glycocalyx biofilm that anchors it to surrounding cells and bacteria, and protects the bacteria from phagocytosis.

Invasiveness is regulated by proteases; elastase and alkaline protease are most closely associated with virulence. Tissue destruction of skin, lung, and cornea may occur, with cleavage of collagen, IgA, IgG, complement factors, and antiproteases. In addition to promoting dissemination, autolyzed tissue is a likely source of nutrients to perpetuate the process. A cytotoxin (leukocidin) is produced that is toxic to most eukaryotic cells by an action upon the cell membrane, mobilizing arachidonic acid to generate leukotrienes. Two hemolysins, phospholipase C and a heat-stable rhamnolipid, are produced and act synergistically to effect lipolysis and thereby promote tissue invasion. In pulmonary infections, phospholipase C is known to degrade phospholipids in surfactant, whereas the rhamnolipid inhibits mucociliary function in respiratory tract epithelium. In addition, exotoxin A is also produced by most clinical isolates. Exotoxin A is a potent inhibitor of protein synthesis, mediating systemic illness similar to the lipid A moiety of Pseudomonas endotoxin, in addition to having local effects on skin, cornea, and lung.

Ps. aeruginosa causes native tissue endocarditis in intravenous drug users, and can infect prosthetic valves. Depending upon the infected valve, consequences may include septic pulmonary or systemic emboli, conduction disturbances, intractable congestive heart failure, brain abscess, cerebritis, and metastatic skin lesions. Lower respiratory tract infections are common in patients with abnormal local respiratory or systemic host defenses. Pneumonia due to Ps. aeruginosa is fulminant and usually fatal (70 per cent). Radiographs reveal a diffuse bronchopneumonia that is typically bilateral and characterized by distinctive nodular infiltrates, sometimes with small areas of radiolucency. Such a pattern can be characteristic of pneumonia caused by Staph. aureus, but is unusual with other Gram-negative pneumonias. Bacteremic pneumonia is usually seen in the neutropenic cancer patient, but can occur in children or AIDS patients.

Bacteremia in the absence of pneumonia is common. Predisposition includes malignant disease, neutropenia, diabetes mellitus, organ transplantation, severe burns or trauma, AIDS, steroid or antibiotic therapy, intravascular catheters, and instrumentation of the urinary tract. Mortality is similar to that of Ps. aeruginosa pneumonia. Factors associated with death include persistent neutropenia, shock, inappropriate antibiotic therapy, lung or skin/soft tissue sources, inability to find the primary source, and renal failure.

Other ICU infections caused by Ps. aeruginosa include meningitis, brain abscess, eye infection, hematogenous bone and joint infection (osteomyelitis), urinary tract infection, and gastrointestinal infection. Central nervous infections can arise from direct extension (e.g. paranasal sinusitis, where Ps. aeruginosa is the most common nosocomial isolate), inoculation (surgery, head trauma), or hematogenous seeding. Ps. aeruginosa is a frequent and devastating ocular pathogen, causing rapidly progressive destructive infections that are difficult to treat because antibiotics penetrate poorly. It is a genuine medical emergency, as preservation of vision is rare after infection has progressed to endophthalmitis. Gastroenteritis due to Ps. aeruginosa usually affects infants or neutropenic cancer patients.

Antibiotic therapy of Ps. aeruginosa infections is often difficult. Pneumonia, bacteremia, and bone and soft tissue infections always require two-drug therapy such as an aminoglycoside and an anti-pseudomonal penicillin (e.g. piperacillin or ticarcillin with or without a b-lactamase inhibitor) or a cephalosporin (e.g. cefoperazone, ceftazidime, or cefepime). Imipenem-cilastatin or a fluoroquinolone (e.g. ciprofloxacin) also have excellent anti-pseudomonal activity and can be used with the aminoglycoside. The choice of agent, which often must be empirical because of the fulminant nature of these infections, must be based on knowledge of local susceptibility patterns. Oral ciprofloxacin alone may be sufficient to treat uncomplicated urinary tract infections. Ocular infections require topical aminoglycoside drops and sometimes intraocular injections combined with multidrug parenteral therapy. Ceftazidime is probably the best agent for central nervous system infections; it is not clear whether the addition of either intravenous or intrathecal aminoglycosides improves outcome in meningitis.

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