Burkholderia and Pseudomonas

Jane L. Burns

Pseudomonas and Burkholderia species are nonlactose fermenting gram-negative bacilli that were previously classified in the same genus. The name Burkholderia was proposed in 1992 for 7 species that were previously classified as Pseudomonas.¹ Both genuses consist of nutritionally diverse water- and soil-borne organisms.

The most clinically important Pseudomonas species is P aeruginosa. It is an opportunistic pathogen that rarely causes disease in normal hosts, but it may cause serious infections in patients with underlying conditions, including neutropenia, immunodeficiency, and cystic fibrosis, and in hospitalized patients with wounds, burns, or indwelling catheters.

The B cepacia-complex (composed of 9 named species, eTable 255.1 )² is the most important group of organisms in the Burkholderia species, causing infections in patients with cystic fibrosis and chronic granulomatous disease. Burkholderia pseudomallei is the etiologic agent of melioidosis, a common pediatric infection in Southeast Asia. Other Burkholderia species that occasionally cause human disease are B mallei, the etiologic agent of glanders, a rare zoonosis seen in the Far East, and B gladioli, an occasional cause of cystic fibrosis infection.⁶

EPIDEMIOLOGY

Pseudomonas aeruginosa is found widely in the natural environment, including in soil and water, and is also endemic in most hospital environments. The epidemiology of P aeruginosa transmission is not well understood. Acquisition of environmental strains has been documented, as has person-to-person transmission in the setting of cystic fibrosis.

Burkholderia species are primarily plant and animal pathogens and are generally avirulent in healthy humans. Their distribution in nature appears to be somewhat more limited than pseudomonads, and they are less easily isolated from sources in the hospital environment, although nosocomial outbreaks have been reported.¹² There is also strong evidence of person-to-person transmission in cystic fibrosis.¹⁵

CLINICAL MANIFESTATIONS

Bacteremia with P aeruginosa is commonly seen in neutropenic or burn patients who have acquired the organism nosocomially. Nonaeruginosa pseudomonads have also been recognized as rare etiologic agents of septicemia in both immunocompromised patients and in previously well children. Burkholderia cepacia complex bacteremia has been described in cystic fibrosis patients and in patients with chronic granulomatous disease.^2,16

Both P aeruginosa and B cepacia complex are important causes of pulmonary infection in patients with cystic fibrosis. Pseudomonas aeruginosa can be isolated from the sputum of the majority of patients with cystic fibrosis.¹⁹ In contrast, B cepacia complex is generally found in the sputum of only a small proportion of cystic fibrosis patients.¹⁹ The most commonly isolated species are B cenocepacia and B multivorans. Burkholderia dolosa has recently been recognized to have severe manifestations in patients with cystic fibrosis, as well.²⁴

Pneumonia is a common manifestation of both P aeruginosa and B cepacia complex infections in subpopulations of immunocompromised patients. Pneumonia is also the most common manifestation of B cepacia complex in chronic granulomatous disease.^16,28

Urinary tract infections caused by P aeruginosa are associated with an indwelling urinary catheter or other foreign body, or are ascribable to obstruction of urinary drainage. Pseudomonas folliculitis caused by immersion in contaminated hot tubs is a superficial self-limited infection in healthy hosts.²⁹ Otitis externa, or “swimmer’s ear,” is most commonly caused by P aeruginosa.³⁰Pseudomonas aeruginosa is also the etiology of osteochondritis associated with a puncture wound of the foot through the sole of a sneaker.³¹B cepacia complex lymphadenitis has been described in chronic granulomatous disease.^16,28

Melioidosis caused by B pseudomallei is a common pediatric infection in rural Southeast Asia and has been reported as well in northern Australia, India, and Central America. Localized skin and soft tissue infections are the most common pediatric presentation followed by septic shock³³ which is associated with high mortality. Relapse is common in severe disseminated disease.³⁴

DIAGNOSTIC EVALUATION

Diagnosis of an invasive infection caused by Pseudomonas or Burkholderia spp is based on the isolation of the organism from a normally sterile site. In hospitalized patients, isolation of the organism may simply represent colonization, especially for patients with endotracheal tubes or tracheostomies, or may be indicative of disease. However, in cystic fibrosis pulmonary infection, isolation of either P aeruginosa or B cepacia complex is presumptive evidence of infection. Nonaeruginosa pseudomonads and B gladioli have also been isolated from cystic fibrosis sputum cultures, but their clinical significance is unclear.⁶

Diagnosis of melioidosis can be made by isolation of the organism from the blood or other affected site. However, serologic assays and molecular diagnostic tests are necessary for rapid diagnosis, because of the high mortality in septicemic disease.³⁵ Indirect hemagglutination antibody testing is most frequently used and is better in young children compared with adults because of the high seroprevalence in endemic areas. Sensitive and specific rapid serologic tests include an IgM enzyme immunoassay and immunochromatographic IgM and IgG assays that can be reported out within 10 minutes.³⁶ Polymerase chain reaction (PCR) detection of the B pseudomallei type 3 secretion system is highly specific but lacks sensitivity.³⁷

TREATMENT AND PREVENTION

Both Pseudomonas and Burkholderia spp are resistant to many antibiotics; susceptibility testing is required to determine optimum therapy. In addition, organisms can readily develop resistance after exposure to antimicrobial agents. Pseudomonas aeruginosa is commonly susceptible to extended-spectrum β-lactam agents (including ticarcillin with or without clavulanate, piperacillin with or without tazobactam, ceftazidime, cefoperazone, and cefepime) and aminoglycosides. Resistance to the quinolone antibiotics (including ciprofloxacin) seems to develop readily, and the carbapenem antibiotics are generally reserved for resistant isolates or for use in immunocompromised patients as a single agent. For uncomplicated infection in a normal host, treatment with a single agent and removal of a foreign body, where appropriate, may be adequate therapy. However, in immunocompromised hosts or cystic fibrosis lung infection, potentially synergistic two-drug combinations are recommended.^38,39Burkholderia cepacia complex organisms are even more intrinsically resistant to antibiotics than P aeruginosa⁴⁰ and are uniformly resistant to the aminoglycosides and polymyxin.⁴¹ The only drugs recommended for testing by the Clinical Laboratory Standards Institute are ceftazidime, minocycline, meropenem, and trimethoprim-sulfamethoxazole.⁴²Burkholderia pseudomallei is also highly resistant to antibiotics. Traditional therapies include ceftazidime, piperacillin, doxycycline, chloramphenicol, and trimethoprim-sulfamethoxazole.⁴⁴ In severe infections, ceftazidime in combination with trimethoprim-sulfamethoxazole is recommended.⁴⁵

Both in vitro and in vivo resistance have been reported, and because of the high rate of relapse in melioidosis, prolonged therapy for up to 6 months is recommended.^34,45

Both active and passive immunization strategies have been attempted for the prevention of P aeruginosa infections in high-risk populations, including in patients with cystic fibrosis, immunocompromised patients, and following burns or major trauma. Conjugated protein-polysaccharide vaccines appear to be the most promising.⁴⁹

Antibiotic suppression of chronic P aeruginosa infections in cystic fibrosis patients is widely practiced, because of the licensing of inhaled tobramycin.⁵⁰ In addition, aggressive therapy of early, acute P aeruginosa infections in cystic has been found to delay the onset of chronic infection.^52-55

REFERENCES

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