Burkholderia cepacia

Updated: Mar 15, 2023
Author: Sara Ahmed, MBBS, MRCP(UK), FCPS; Chief Editor: Michael Stuart Bronze, MD 



Burkholderia cepacia is an aerobic gram-negative bacillus found in various aquatic environments. B cepacia is an organism of low virulence and is a frequent colonizer of fluids used in the hospital (eg, irrigation solutions, intravenous fluids). B cepacia rarely causes infection in healthy hosts. Based on phenotypic and genotypic analyses, B cepacia is divided into 9 genomovars that constitute the B cepacia complex (BCC).


B cepacia almost always is a colonizing organism rather than an infecting organism, but it may be important when isolated from body fluids that are ordinarily sterile. The pathophysiology of B cepacia infection mirrors that of other nonfermentative aerobic gram-negative bacilli.



United States

B cepacia ordinarily is not a pathogen in the ambulatory setting, but it may colonize and/or infect the respiratory tract of patients with cystic fibrosis or bronchiectasis. B cepacia also may cause central venous catheter–related infections in patients with cancer and in those on hemodialysis. B cepacianosocomial pneumonia has rarely been reported, usually in patients treated with fluoroquinolones and ceftazidime. Skin and soft-tissue infections, surgical-wound infections, and genitourinary tract infections with B cepacia have been reported.

According to the US Cystic Fibrosis Foundation’s 2021 National Patient Registry, 1.4% percent of all persons with cystic fibrosis were infected with B cepacia complex compared to 2.6% in 2012. 


B cepacia generally is not a pathogen in the ambulatory setting, but it may colonize and/or infect the respiratory tract of patients with cystic fibrosis or bronchiectasis.


If an intravenous infusate contains high numbers of B cepacia, direct injection into the bloodstream may result in gram-negative bacteremia.

Mortality and morbidity are highest in those with impaired pulmonary function (eg, cystic fibrosis, bronchiectasis, chronic granulomatosis disease).

Disease severity (defined by the Simplified Acute Physiology Score II) and age are independent predictors of mortality.[1]

Malignancy and a higher SOFA score at the onset of bacteremia are associated with high mortality rates.[2]


Burkholderia has no racial predisposition.


Burkholderia has no age predisposition.


Signs and symptoms of B cepacia infections are related to the organ system involved and are indistinguishable from infections with other pathogens.




A history of the use of irrigant solutions that may have contained B cepacia is epidemiologically important.


Physical examination is referable to the organ system involved.


B cepacia is a nonfermentative, aerobic, gram-negative bacillus formerly classified as Pseudomonas. Unlike Pseudomonas aeruginosa, B cepacia is an organism of low virulence with a limited ability to cause infection in humans.

B cepacia survives and multiplies in aqueous hospital environments, where it may persist for long periods.[3]

Sources of B cepacia colonization include the following:

  • Personnel - Hands, antiseptic soaps, hand lotion[4]

  • Respiratory equipment and/or fluids - Respirator tubing condensate, ultrasonic nebulizers, inhalation medications

  • Intravenous lines and/or fluids - Intravenous solutions, central venous catheters

  • Pressure-monitoring devices - Pressure transducer fluids

  • Urine and/or fluids - Indwelling urinary catheters, urometers, irrigation solutions


Because B cepacia is normally a colonizer, no complications are expected.



Diagnostic Considerations

B cepacia recovered from blood cultures may represent infection, pseudo infection, or actual infection from contaminated intravenous fluids (infusate-related).

Regard the recovery of B cepacia from the respiratory secretions or urine of catheterized patients as colonization until proven otherwise.

B cepacia is a common cause of catheter-associated bacteriuria in hospitalized patients. B cepacia commonly colonizes the urine and is potentially pathogenic only in individuals with impaired host defenses (eg, patients on steroids or those with diabetes, systemic lupus erythematosus [SLE], multiple myeloma, cirrhosis, or chronic granulomatous disease).

B cepacia is an extremely rare cause of nosocomial pneumonia. In ventilated patients with presumed nosocomial pneumonia who have fever, pulmonary infiltrates, and leukocytosis, B cepacia cultured from respiratory secretions generally represents colonization rather than infection.

Nosocomial infections caused by B cepacia include the following:

  • Catheter-associated bacteriuria - Indwelling urinary catheters
  • Central line-associated bloodstream infection - Central venous catheters (CVCs)
  • Urinary tract infection - following urinary tract instrumentation
  • Secondary bacteremia - Arterial monitoring devices
  • Pseudobacteremia - Contamination of blood during collection and/or processing of blood cultures

There also have been reports of B cepacia as a cause of endocarditis in individuals with drug addiction or prosthetic heart valves, endophthalmitis and subdural empyema, brain abscesses, and meningitis.[5, 6, 7, 8, 9, 10, 11]



Laboratory Studies

Culture B cepacia from body fluids.

Although B cepacia–positive cultures from nonsterile sites (eg, respiratory secretions, urine in the setting of foley catheters) nearly always represent colonization, presence in sterile body fluids such as blood or CSF mandates consultation with an infectious disease specialist.



Medical Care

Patient-to-patient spread of B cepacia may be minimized and/or prevented with effective infection-control measures.

Use foley catheters only as long as necessary. If possible, avoid their use in compromised hosts predisposed to urinary tract infections (eg, patients with diabetes, SLE, multiple myeloma).

Preventing B cepacia colonization of respiratory secretions in intubated patients who are in ICUs and on broad-spectrum antibiotics is difficult.


Consultation with an infectious disease specialist helps to differentiate B cepacia colonization from infection.


Effective infection-control measures can minimize or limit the spread of B cepacia and other organisms in the ICU.

Recovered B cepacia should be considered a nonpathogen unless proven otherwise.

If B cepacia is recovered from several patients in the same area, sections of an ICU or ward can become the focus for further B cepacia colonizations within the hospital setting.

Appropriate isolation procedures rather than antimicrobial therapy should be used to control the spread of B cepacia colonization among patients.



Medication Summary

B cepacia almost always is a colonizer; therefore, antimicrobial treatment is unnecessary and may be harmful unless infection is proven.

B cepacia, as a non-aeruginosa pseudomonad, usually is resistant to aminoglycosides, antipseudomonal penicillins, and polymyxin B.[12]

Antimicrobial therapy should be selected based on in vitro susceptibility testing. Treatment duration is guided by the resolution of clinical symptoms and decline in inflammatory markers like C- reactive protein and white blood cell count.

B cepacia often is susceptible to trimethoprim-sulfamethoxazole (TMP-SMX), cefepime, meropenem, minocycline, and tigecycline and has varying susceptibility to ceftazidime and fluoroquinolones.

Isolates of B cepacia complex from individuals with cystic fibrosis are typically more resistant compared to isolates from those without cystic fibrosis, most likely due to previous exposure to antibiotics and variations in the species of B cepacia complex found in these patient groups.[13]

Cefiderocol may be a reasonable option for multidrug-resistant strains as it has shown activity against B cepacia in vitro (although CLSI breakpoints are not established), but clinical data are lacking.[14, 15]

Ceftazidime-avibactam has shown activity against multidrug-resistant B cepacia complex strains and was found to be useful in persistent bacteremia.[16]  

Temocillin may offer potential benefits for patients with cystic fibrosis (CF) who are infected with Burkholderia cepacia complex (Bcc).[17]  








Class Summary

Empiric antimicrobial therapy should cover the most likely pathogens in the context of the clinical setting.

Trimethoprim/sulfamethoxazole (Bactrim DS, Septra DS)

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity includes common urinary tract pathogens, except P aeruginosa.

Cefepime (Maxipime)

Fourth-generation cephalosporin with good gram-negative coverage; similar to ceftazidime, but with better gram-positive coverage.

Tigecycline (Tygacil)

A glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. Inhibits bacterial protein translation by binding to 30S ribosomal subunit and blocks entry of amino-acyl tRNA molecules in ribosome A site. Indicated for complicated skin and skin-structure infections caused by E coli, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible and -resistant isolates), S agalactiae, S anginosus group (includes S anginosus, S intermedius, S constellatus), S pyogenes, and B fragilis.

Meropenem (Merrem IV)

Semisynthetic carbapenem antibiotic that inhibits bacterial cell wall synthesis. Effective against most gram-positive and gram-negative bacteria.

Has slightly increased activity against gram-negative bacteria and slightly decreased activity against staphylococci and streptococci compared to imipenem.

Minocycline (Dynacin, Minocin)

Treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma. Was found to be effective in some non-tuberculotic mycobacterial infections.


Class Summary

Cefiderocol belongs to the class of cephalosporin antibiotics, which are commonly used to treat bacterial infections. However, unlike other cephalosporins, cefiderocol has a unique side chain that allows it to bind to ferric iron, a key nutrient for bacterial growth, and use the bacterial iron transport system to cross the outer membrane of gram-negative bacteria.Once inside the bacterial cell, cefiderocol's cephalosporin moiety binds to penicillin-binding proteins (PBPs), which are enzymes involved in the final step of peptidoglycan synthesis in bacterial cell walls. This binding inhibits the transpeptidation reaction, preventing the formation of cross-links between peptidoglycan chains and leading to cell wall damage and bacterial death.


Class Summary

Ceftazidime functions by binding to the penicillin-binding proteins (PBPs) in bacterial cell walls, which inhibits the final step of peptidoglycan synthesis and consequently prevents cell wall biosynthesis. As a result, the bacteria eventually lyse because of the continuous activity of cell wall autolytic enzymes, while the assembly of the cell wall is halted. However, certain bacteria can produce beta-lactamase enzymes that break down beta-lactam antibiotics such as ceftazidime, rendering them ineffective. Avibactam is a beta-lactamase inhibitor that can inactivate some beta-lactamases, preserving the effectiveness of ceftazidime against resistant bacteria. However, some bacteria have developed beta-lactamase enzymes that can break down beta-lactam antibiotics, including ceftazidime, making them ineffective. Avibactam is a beta-lactamase inhibitor that can inactivate certain beta-lactamases, protecting ceftazidime from degradation and improving its effectiveness against these resistant bacteria. The combination of ceftazidime and avibactam is known as ceftazidime-avibactam and is used to treat certain types of bacterial infections.