The pseudomonads are a heterogeneous group of gram-negative bacteria that have in common an inability to ferment lactose. Formerly classified in the genus Pseudomonas, the members of this group have been assigned to three medically important genera—Pseudomonas, Burkholderia, and Stenotrophomonas—whose biologic behaviors encompass both similarities and marked differences and whose genetic repertoires differ in many respects. The pathogenicity of most pseudomonads is based on opportunism; the exceptions are Burkholderia pseudomallei and Burkholderia mallei, which are primary pathogens.
Pseudomonas aeruginosa, the major pathogen of the group, is a significant cause of infections in hospitalized patients and in patients with cystic fibrosis (CF; Chap. 285). Cytotoxic chemotherapy, mechanical ventilation, and broad-spectrum antibiotic therapy set up conditions that predispose to colonization and infection of increasing numbers of hospitalized patients by this pathogen. The other members of the genus Pseudomonas—Pseudomonas putida, Pseudomonas fluorescens, and Pseudomonas stutzeri—infect humans infrequently.
The genus Burkholderia comprises >40 species, of which Burkholderia cepacia is most frequently encountered in Western countries. Like P. aeruginosa, B. cepacia is both a nosocomial pathogen and a cause of infection in CF. The other medically important members of this genus are B. pseudomallei and B. mallei, the etiologic agents of melioidosis and glanders, respectively.
The genus Stenotrophomonas contains one species of medical significance, Stenotrophomonas maltophilia (previously classified in the genera Pseudomonas and Xanthomonas). This organism is strictly an opportunist that “overgrows” in the setting of potent broad-spectrum antibiotic use.
P. aeruginosa is found in most moist environments. Soil, plants, vegetables, tap water, and countertops are all potential reservoirs for this microbe, as it has simple nutritional needs. Given the ubiquity of P. aeruginosa, it is clear that simple contact with the organism is not sufficient for colonization or infection. Clinical and experimental observations suggest that infection by P. aeruginosa occurs concomitantly with compromised host defenses, mucosal trauma, physiologic derangement, and antibiotic-mediated suppression of normal flora. Thus, it comes as no surprise that the majority of P. aeruginosa infections occur in intensive care units (ICUs), where these factors frequently converge. The organism is initially acquired from environmental sources, but patient-to-patient spread also occurs in clinics and families.
In the past, burned patients appeared to be unusually susceptible to P. aeruginosa. For example, in 1959–1963, Pseudomonas burn-wound sepsis was the principal cause of death in 60% of burned patients dying at the U.S. Army Institute of Surgical Research. For reasons that are unclear, P. aeruginosa infection in burns is no longer the major problem that it was during the 1950s and 1960s. Similarly, in the 1960s, P. aeruginosa appeared as a common pathogen in patients receiving cytotoxic chemotherapy at many institutions in the United States, but it has subsequently diminished in importance. Despite this subsidence, P. aeruginosa remains ...