In 1882, Gessard first isolated Pseudomonas, a strictly aerobic, gram-negative bacterium. The organism is ubiquitous, with a predilection to moist environments. Pseudomonal species have been found in soil, water, plants, and animals; Pseudomonas aeruginosa colonization reportedly occurs in more than 50% of humans.
Pseudomonas is a clinically significant and opportunistic pathogen, often causing nosocomial infections. In addition to causing serious and often life-threatening diseases, these organisms exhibit innate resistance to many antibiotics and can develop new resistance after exposure to antimicrobial agents. Some pseudomonal species that previously were considered the causative agents of old diseases now are being reexamined for their potential use as biological warfare agents.
The current classification of the genus Pseudomonas is divided into 5 groups based on ribosomal RNA (rRNA)/DNA homology. Of the more than 20 pseudomonal species that have been isolated from human clinical specimens, the following 4 representative organisms are discussed in this article:
P aeruginosa (homology group I)
Pseudomonas cepacia (group II)
Pseudomonas pseudomallei (group II)
Pseudomonas mallei (group II)
Although P aeruginosa is a common human saprophyte, it rarely causes disease in healthy persons. Most infections with this organism occur in compromised hosts. Examples of compromising conditions include disrupted physical barriers to bacterial invasion (eg, burn injuries, IV lines, urinary catheters, dialysis catheters, endotracheal tubes) and dysfunctional immune mechanisms, such as those occurring in neonates, cystic fibrosis (CF), AIDS, neutropenia, complement deficiency, hypogammaglobulinemia, and iatrogenic immunosuppression. The pathogenesis of this organism is multifaceted and involves a variety of toxins and proteases (eg, exotoxin A, lecithinase) and the glycocalyx "slime."
Pseudomonal infection, as described by Pollack, occurs in 3 stages: (1) bacterial attachment and colonization, followed by (2) local invasion, and (3) dissemination and systemic disease. In healthy children, disease is limited primarily to the first 2 stages (as in diseases such as otitis externa, urinary tract infections (UTIs), dermatitis, cellulitis, and osteomyelitis), although recent case reports describe bacteremia, sepsis, and GI infections in previously healthy children. In immunocompromised hosts, including neonates, infection can progress rapidly through the 3 stages and cause pneumonia, endocarditis, peritonitis, meningitis, ecthyma gangrenosum (EG), and overwhelming septicemia.
In 1949, Walter Burkholder of Cornell University first described P cepacia (now known as Burkholderia cepacia) as the phytopathogen responsible for the bacterial rot of onions. In the 1950s, B cepacia was first reported as a human pathogen that causes endocarditis. Subsequently, the organism has been isolated in numerous catheter-associated UTIs, wound infections, and IV catheter‘«Űassociated bacteremias.
In 1971, this species was reported as the causative organism of foot rot in US troops on swamp training exercises in northern Florida; it also was isolated from troops serving in Vietnam's Mekong Delta. In 1972, B cepacia was discovered as an opportunistic human pathogen in a patient with CF. Since then, B cepacia has emerged with increasing frequency as the cause of pneumonia and septicemia in children with CF.