Burkholderia cepacia is an aerobic, gram-negative, nonfermentative bacillus widely distributed in the environment, including in water, soil, fruits, and vegetables. B cepacia often is found in liquid reservoirs or moist environments, reflecting the organism's innate ability to survive and grow in water sources with minimal nutritional sources. Since discovered as a phytopathogen, its microbiologic characterization has taken a circuitous path. First characterized microbiologically in the 1950s and 1960s, the organism was placed in the genus Pseudomonas in 1984.1 However, subsequent characterization of the genus Pseudomonas, including rRNA-DNA hybridization, led to the proposal to establish a new genus Burkholderia with the type strain being B cepacia. The epidemiology of B cepacia as a nosocomial pathogen has taken an equally interesting course. The first nosocomial outbreak reported was in 1966, when an outbreak of urinary tract infections in children was traced to contaminated water that was used as a bladder irrigant during cystoscopy.2 Since that time, B cepacia has been associated with many real and pseudo-outbreaks of bloodstream, urinary tract, respiratory tract, and other nosocomial infections.3 These outbreaks have been traced to a wide variety of sources including tap, distilled, or deionized water and intrinsically or extrinsically contaminated chlorhexidine, topical cocaine, benzalkonium chloride, povidone-iodine, savlon, quaternary ammonium solutions, or respiratory therapy equipment. Much of the epidemiology of B cepacia has been elucidated because of the propensity of this pathogen to cause colonization and infection in cystic fibrosis patients. In the mid-1980s, several authors showed that B cepacia was increasing in prevalence in cystic fibrosis patients and that colonization and infection was associated with increased hospitalization, rapid pulmonary function decline, and death.4-6 In this population, the organism causes chronic respiratory colonization and intermittent exacerbations of bronchitis or pneumonia. Active surveillance in approximately 100 cystic fibrosis centers since 1986 has documented an annual incidence and prevalence of 1% and 3.5%, respectively. Studies have documented nosocomial transmission of B cepacia in cystic fibrosis patients, associated with contaminated respiratory therapy equipment and via person-to-person transmission.In addition, B cepacia has been documented to be transmitted in cystic fibrosis summer camps and in other social settings involving these patients.10", A strong association also has been found between B cepacia colonization and prior aminoglycoside therapy, thus reemphasizing the need to review guidelines for antimicrobial usage and prophylaxis in patients with cystic fibrosis. These and other findings have led to the recommendation for cohorting of B cepacia-colonized or B cepacia-infected cystic fibrosis patients and for placement of these patients in contact isolation." Implementation of these measures has led to decreased nosocomial transmission.12