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Testing the Role of Multicopy Plasmids in the Evolution of Antibiotic Resistance
Published on: May 2, 2018
Host adaptation and convergent evolution increases antibiotic resistance without loss of virulence in a major human
Alicia Fajardo-Lubián1, Nouri L Ben Zakour1, Alex Agyekum1
1Centre for Infectious Diseases and Microbiology, The Westmead Institute for Medical Research, The University of Sydney and Westmead Hospital, Sydney, New South Wales, Australia.
Abstract:
As human population density and antibiotic exposure increase, specialised bacterial subtypes have begun to emerge. Arising among species that are common commensals and infrequent pathogens, antibiotic-resistant 'high-risk clones' have evolved to better survive in the modern human. Here, we show that the major matrix porin (OmpK35) of Klebsiella pneumoniae is not required in the mammalian host for colonisation, pathogenesis, nor for antibiotic resistance, and that it is commonly absent in pathogenic isolates. This is found in association with, but apparently independent of, a highly specific change in the co-regulated partner porin, the osmoporin (OmpK36), which provides enhanced antibiotic resistance without significant loss of fitness in the mammalian host. These features are common in well-described 'high-risk clones' of K. pneumoniae, as well as in unrelated members of this species and similar adaptations are found in other members of the Enterobacteriaceae that share this lifestyle. Available sequence data indicate evolutionary convergence, with implications for the spread of lethal antibiotic-resistant pathogens in humans.
Insights
Antibiotic resistance is rising in bacteria like Klebsiella pneumoniae. A key outer membrane protein (OmpK35) is often lost, while another (OmpK36) adapts, enhancing survival and antibiotic resistance in humans.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Evolutionary Biology
Background:
- Increasing human population density and antibiotic use drive the emergence of specialized bacterial strains.
- Antibiotic-resistant 'high-risk clones' have evolved enhanced survival mechanisms within the human host.
Purpose of the Study:
- To investigate the role of the major matrix porin (OmpK35) in Klebsiella pneumoniae colonization, pathogenesis, and antibiotic resistance.
- To understand the relationship between OmpK35 absence and changes in the osmoporin (OmpK36).
Main Methods:
- Analysis of Klebsiella pneumoniae isolates.
- Comparative genomics and functional assays (implied).
Main Results:
- The major matrix porin (OmpK35) is frequently absent in pathogenic Klebsiella pneumoniae isolates and is not essential for host colonization, pathogenesis, or antibiotic resistance.
- Absence of OmpK35 is associated with specific adaptations in the osmoporin (OmpK36), conferring enhanced antibiotic resistance without compromising host fitness.
- These adaptations are prevalent in 'high-risk clones' and other Klebsiella pneumoniae strains, as well as in related Enterobacteriaceae.
Conclusions:
- Loss of OmpK35 and adaptation of OmpK36 represent a convergent evolutionary strategy in Klebsiella pneumoniae.
- These bacterial adaptations contribute to the increased prevalence and lethality of antibiotic-resistant pathogens in humans.
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