File:Viruses-13-01331-g002-550.jpg

English: Figure 2. Antibiotic resistance mechanisms of the Burkholderia cepacia complex. Bcc members are resistant to a wide range of antibiotic compounds as a result of their large repertoire of both innate and acquired resistance mechanisms. Resistance to 𝛽

-lactam antibiotics is achieved through a combination of reduced membrane permeability (A), mutated penicillin-binding proteins (B), and chromosomally encoded 𝛽

-lactamases (C). Extrusion via porins (D) and efflux pumps (E) are responsible for resistance to a large number of compounds, including trimethoprim, chloramphenicol, tetracyclines and certain quinolones, while mutation of dihydrofolate reductase provides additional resistance to trimethoprim (F). At the outer membrane, LPS modifications prevent aminoglycoside binding and therefore block the trafficking of these compounds into the cell (G), while the reduced negative charge of the outer membrane reduces the binding of polymyxins and cationic antimicrobial peptides (H), thereby rendering Bcc species less vulnerable to these compounds.