Ecogenetics of antibiotic resistance in Listeria monocytogenes.
Fernando BaqueroVal F LanzaMélodie DuvalTeresa M CoquePublished in: Molecular microbiology (2020)
The acquisition process of antibiotic resistance in an otherwise susceptible organism is shaped by the ecology of the species. Unlike other relevant human pathogens, Listeria monocytogenes has maintained a high rate of susceptibility to the antibiotics used for decades to treat human and animal infections. However, L. monocytogenes can acquire antibiotic resistance genes from other organisms' plasmids and conjugative transposons. Ecological factors could account for its susceptibility. L. monocytogenes is ubiquitous in nature, most frequently including reservoirs unexposed to antibiotics, including intracellular sanctuaries. L. monocytogenes has a remarkably closed genome, reflecting limited community interactions, small population sizes and high niche specialization. The L. monocytogenes species is divided into variants that are specialized in small specific niches, which reduces the possibility of coexistence with potential donors of antibiotic resistance. Interactions with potential donors are also hampered by interspecies antagonism. However, occasional increases in population sizes (and thus the possibility of acquiring antibiotic resistance) can derive from selection of the species based on intrinsic or acquired resistance to antibiotics, biocides, heavy metals or by a natural tolerance to extreme conditions. High-quality surveillance of the emergence of resistance to the key drugs used in primary therapy is mandatory.
Keyphrases
- listeria monocytogenes
- antibiotic resistance genes
- endothelial cells
- heavy metals
- human health
- microbial community
- induced pluripotent stem cells
- wastewater treatment
- risk assessment
- climate change
- mental health
- pluripotent stem cells
- healthcare
- public health
- escherichia coli
- gram negative
- genetic diversity
- dna methylation
- mesenchymal stem cells
- klebsiella pneumoniae
- copy number
- antimicrobial resistance
- drug induced