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Updated: Jul 18, 2026
Antibiotic Efficacy Testing in an Ex vivo Model of Pseudomonas aeruginosa and Staphylococcus aureus Biofilms in the Cystic Fibrosis Lung
Published on: January 22, 2021
Microevolution of cytochrome bd oxidase in Staphylococci and its implication in resistance to respiratory toxins
Lalitha Voggu1, Steffen Schlag, Raja Biswas
1Microbial Genetics, University of Tübingen, 72076 Tübingen, Germany.
Abstract:
Pseudomonas aeruginosa and Staphylococcus aureus are opportunistic pathogens and frequently coinfect the lungs of cystic fibrosis patients. P. aeruginosa secretes an arsenal of small respiratory inhibitors, like pyocyanin, hydrogen cyanide, or quinoline N-oxides, that may act against the commensal flora as well as host cells. Here, we show that with respect to their susceptibility to these respiratory inhibitors, staphylococcal species can be divided into two groups: the sensitive group, comprised of pathogenic species such as S. aureus and S. epidermidis, and the resistant group, represented by nonpathogenic species such as S. carnosus, S. piscifermentans, and S. gallinarum. The resistance in the latter group of species was due to cydAB genes that encode a pyocyanin- and cyanide-insensitive cytochrome bd quinol oxidase. By exchanging cydB in S. aureus with the S. carnosus-specific cydB, we could demonstrate that CydB determines resistance. The resistant or sensitive phenotype was based on structural alterations in CydB, which is part of CydAB, the cytochrome bd quinol oxidase. CydB represents a prime example of both microevolution and the asymmetric pattern of evolutionary change.
Insights
Staphylococcus species exhibit varying resistance to Pseudomonas aeruginosa respiratory inhibitors. Resistance is linked to specific CydAB enzyme structures, demonstrating microevolution in bacterial defense mechanisms.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Evolutionary Biology
Background:
- Pseudomonas aeruginosa and Staphylococcus aureus are opportunistic pathogens often co-infecting cystic fibrosis lungs.
- P. aeruginosa produces respiratory inhibitors (e.g., pyocyanin, cyanide) affecting commensal flora and host cells.
Purpose of the Study:
- To investigate differential susceptibility of staphylococcal species to P. aeruginosa respiratory inhibitors.
- To identify the genetic basis for resistance and its evolutionary implications.
Main Methods:
- Comparative analysis of staphylococcal species' susceptibility to P. aeruginosa inhibitors.
- Genetic exchange experiments involving the cydB gene in S. aureus.
- Structural analysis of the CydAB enzyme.
Main Results:
- Staphylococcal species were categorized into sensitive (pathogenic) and resistant (nonpathogenic) groups.
- Resistance is conferred by the cydAB genes encoding a cyanide-insensitive cytochrome bd quinol oxidase.
- Specific structural alterations in CydB determine the resistant or sensitive phenotype.
Conclusions:
- The CydAB enzyme's structure dictates staphylococcal resistance to P. aeruginosa toxins.
- This study highlights microevolution and asymmetric evolutionary patterns in bacterial adaptation.
- Findings offer insights into bacterial interactions in polymicrobial infections.
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