The emergence and spread of antibiotic resistance poses a serious threat to public health, making infections harder to treat. But how does antibiotic resistance impact a pathogen’s ability to invade communities of other bacteria in the body (i.e. the microbiome)?
The microbiome can provide protection against colonisation by excluding pathogens from a metabolic niche, prompting a host immune response, or direct antagonistic interactions such as toxin production. However, many antibiotics were originally isolated from microbes or are adaptations of microbial products. As such, it’s possible that antibiotic resistance could provide cross-resistance in the microbiome.
In a new study, researchers linked specific antibiotic resistance mutations to changes in the ability of Pseudomonas aeruginosa to invade populations of different bacteria from the respiratory microbiome. They found that specific resistance mutations could impact the ability of the pathogen to invade, and the directionality of this depended on both the specific mutations and the type of bacteria from the respiratory microbiome. Lead author Selina Lindon said:
“The cost of these mutations can crucially depend on the community of the microbiome. The results help us better understand the potential for antibiotic-resistant pathogen strains to transmit between patients in a hospital, along with when and how the microbiome may shape this spread.”
Some ciprofloxacin-resistant strains showed both improved and diminished ability to invade depending on the type of bacteria it was invading, while others saw no impact on invasiveness from antibiotic resistance. Streptococcus species provided the strongest resistance to invasion, regardless of the antibiotic resistance strain. Senior author Dr Rachel Wheatley said:
“Understanding this interface between antibiotic resistance and species interactions has clear significance to our ability to predict the spread of antibiotic resistance in bacterial pathogens. Attempts to manipulate the respiratory microbiome should focus on promoting the growth of commensals that can provide robust inhibition of both wildtype and resistant mutant strains.”
To read more about this research, published in Evolution Letters, visit: https://doi.org/10.1093/evlett/qrae030
