Burkholderia cepacia Medication

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

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.