Evolutionary Pathways and Trajectories in Antibiotic Resistance

Abstract

Evolution is the hallmark of life. Descriptions of the evolution of microorganisms have provided a wealth of information, but knowledge regarding “what happened” has precluded a deeper understanding of “how” evolution has proceeded, as in the case of antimicrobial resistance.

A 21-Year Survey of Escherichia coli from Bloodstream Infections (BSI) in a Tertiary Hospital Reveals How Community-Hospital Dynamics of B2 Phylogroup Clones Influence Local BSI Rates

“…B2-I (STc131) was the only lineage that significantly increased during the period analyzed, and this transient increase was due to the expansion of both C1 and C2 subclades (mostly ESBL negative) and, probably, to CTX-M-27 in the last years, according to the emergence of this subclade in the community after the end of this study ( 22 ). Although the epidemiology of STc131 has extensively been documented ( 11 ), this work and that by Kallonen et al ( 17 ) are the only ones that reveal the coexistence of all STc131 subclades which, after a transient amplification, are incorporated into the E. coli population structure. The other predominant B2 subgroups varied greatly through the period studied, with some peaks of B2-II (STc73), B2-IX (STc95), and B2-VI (STc12) clones and also others (e.g., B2-VII, B2-X, and non-I/II) which are poorly documented in the literature.…”

“…However, the detection of B2 isolates of other non-ST131 clade C groups in people of all ages but predominantly in the range of 15 to 45 years and also in other nonhuman hosts ( 27 – 31 ), with the isolates eventually being able to circulate between them ( 26 , 28 ), would reinforce that they are part of the normal microbiota. Note than the notion of “pandemic” implies the extended spread of the clones in the community, and the increase in number and exposure to different hosts and environments necessarily tends toward an increase in genetic diversity ( 11 ). In fact, there is a notion that the “high-risk clones” emerge from the epidemicity of commensals which precedes the spread of multiresistant bacterial clones ( 28 , 32 ).…”

“…Among the 7 major phylogenetic groups of the species (A, B1, B2, C, D, E, and F), B2 is nowadays predominant in clinical and fecal isolates from adults and children of Western areas ( 7 – 9 ). Despite the apparent persistent structure of E. coli in the gut of these individuals, clonal expansions of emerging sequence type complexes (STcs) have periodically occurred ( 10 , 11 ). Currently, several E. coli phylogenetic groups and some of the 10 B2 E. coli subgroups known (B2-I to B2-X) are overrepresented by certain sequence type complexes (STcs) (e.g., B2-I [STc131], B2-II [STc73], B2-IX [STc95], D [STc69].…”

Mathematical Models of Plasmid Population Dynamics

“…Finally, as discussed previously, the introduction of mobile elements encoding for drug resistance genes into clinical environments can produce plasmid-related outbreaks of antimicrobial-resistant pathogens ( Mayer, 1988 ). In this scenario, it could be argued that the responsibility for the outbreak lies not on a particular bacterial strain but on a plasmid that is shared between different hosts and, therefore, the drug resistant problem could be viewed from a plasmid-centric perspective ( Wang and You, 2020 ; Baquero et al, 2021 ). We believe that mathematical modeling and computer simulations provide powerful tools to control the spread and evolution of plasmid-encoded drug resistance genes and, in the future, maybe even to propose new therapeutic avenues that control plasmid-driven antibiotic resistance.…”

Allogenous Selection of Mutational Collateral Resistance: Old Drugs Select for New Resistance Within Antibiotic Families

“…Of course, that will not prevent the evolution of resistance to the members of these novel families, except if they are used very prudently or in combination therapy. In any case, the consideration of complex networks of collateral susceptibility (Imamovic and Sommer, 2013), and collateral resistance (allogenous selection) merits further exploration to reduce the dynamics of evolutionary paths and trajectories in antibiotic resistance (Baquero et al, 2021).…”