Is selection relevant in the evolutionary emergence of drug resistance?

Day, Troy; Huijben, Silvie; Read, Andrew F.

doi:10.1016/j.tim.2015.01.005

Cited by 93 publications

(119 citation statements)

References 38 publications

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“…We were also able to detect Tn5801 in predominant antibiotic-resistant clonal lineages associated with human infections, such as S. aureus (CC8, CC5, and ST239) and E. faecium (ST17 and ST18) from the 1990s, or early lineages of E. faecalis (CC8). However, our data and available knowledge necessitate a carefully interpretation of the relationship between the emergence and persistence of antibiotic resistance and selective processes of particular clones due to antimicrobial treatments (42). In this respect, we should take into account therapeutic strategies and relevant bacterial features that could have facilitated the selective acquisition of certain elements by particular clones.…”

Section: Discussionmentioning

confidence: 99%

Diversity and Evolution of the Tn 5801-tet (M)-Like Integrative and Conjugative Elements among Enterococcus, Streptococcus, and Staphylococcus

León‐Sampedro

Novais

Peixe

et al. 2016

Antimicrob Agents Chemother

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Section: Discussionmentioning

confidence: 99%

Diversity and Evolution of the Tn 5801-tet (M)-Like Integrative and Conjugative Elements among Enterococcus, Streptococcus, and Staphylococcus

León‐Sampedro

Novais

Peixe

et al. 2016

Antimicrob Agents Chemother

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“…These include determining the extent to which resource competition plays a role in such a complex environment as the patient’s body 98 and obtaining accurate parameters of traits that determine resource competition in the human body, 98 including nutrient availability in various sites of infection. 101 …”

Section: Use Of Suppressive Drug Combinations In the Clinicmentioning

confidence: 99%

Suppressive drug combinations and their potential to combat antibiotic resistance

Singh

Yeh

2017

J Antibiot

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Antibiotic effectiveness often changes when two or more such drugs are administered simultaneously, and unearthing antibiotic combinations with enhanced efficacy (synergy) has been a longstanding clinical goal. However, antibiotic resistance, which undermines individual drugs, threatens such combined treatments. Remarkably, it has emerged that antibiotic combinations whose combined effect is lower than that of at least one of the individual drugs can slow or even reverse the evolution of resistance. We synthesize and review studies of such so-called “suppressive interactions” in the literature. We examine why these interactions have been largely disregarded in the past, the strategies used to identify them, their mechanistic basis, demonstrations of their potential to reverse the evolution of resistance, and arguments for and against using them in clinical treatment. We suggest future directions for research on these interactions, aiming to expand the basic body of knowledge on suppression and to determine their applicability in the clinic.

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“…However, the less aggressive approach may also provide benefits by directly improving our ability to control evolving pathogen populations [34,59]. More specifically, because drug-sensitive and drug-resistant cells compete for resources, aggressive treatments that eliminate sensitive cells may remove competitive barriers that slow the growth of resistant cells (Figure 1) [60].…”

Section: Introductionmentioning

confidence: 99%

Antibiotics can be used to contain drug-resistant bacteria by maintaining sufficiently large sensitive populations

Hansen

Karslake

Woods

et al. 2019

Preprint

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Treatment strategies for infectious disease often aim to rapidly clear the pathogen population in hopes of minimizing the potential for antibiotic resistance. However, a number of recent studies highlight the potential of alternative strategies that attempt to inhibit the growth of resistant pathogens by maintaining a competing population of drug-sensitive cells. Unfortunately, to date there is little direct experimental evidence that drug sensitive cells can be leveraged to enhance antibiotic containment strategies. In this work, we combine in vitro experiments in computer-controlled bioreactors with simple mathematical models to show that drug-sensitive cells can enhance our ability to control bacterial populations with antibiotics. To do so, we measured the "escape time" required for drug-resistant E. coli populations to eclipse a threshold density maintained by adaptive antibiotic dosing. While populations containing only resistant cells rapidly escape containment, we found that matched populations with sensitive cells added could be contained for significantly longer. The increase in escape time occurs only when the threshold density-the acceptable bacterial burden-is sufficiently high, an effect that mathematical models attribute to increased competition. The results provide direct experimental evidence linking the presence of sensitive cells to improved control of microbial populations.

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Is selection relevant in the evolutionary emergence of drug resistance?

Cited by 93 publications

References 38 publications

Diversity and Evolution of the Tn 5801-tet (M)-Like Integrative and Conjugative Elements among Enterococcus, Streptococcus, and Staphylococcus

Diversity and Evolution of the Tn 5801-tet (M)-Like Integrative and Conjugative Elements among Enterococcus, Streptococcus, and Staphylococcus

Suppressive drug combinations and their potential to combat antibiotic resistance

Antibiotics can be used to contain drug-resistant bacteria by maintaining sufficiently large sensitive populations

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