Host adaptation and convergent evolution increases antibiotic resistance without loss of virulence in a major human pathogen.
Alicia Fajardo-LubiánNouri L Ben ZakourAlex AgyekumQin QiJonathan R IredellPublished in: PLoS pathogens (2019)
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.
Keyphrases
- endothelial cells
- klebsiella pneumoniae
- escherichia coli
- multidrug resistant
- induced pluripotent stem cells
- pluripotent stem cells
- cardiovascular disease
- physical activity
- gram negative
- metabolic syndrome
- antimicrobial resistance
- type diabetes
- weight loss
- staphylococcus aureus
- cystic fibrosis
- electronic health record
- machine learning
- high intensity
- gene expression
- data analysis