Faculty Opinions recommendation of Evolutionary dynamics on any population structure.

Abstract Background IPD caused by Sp2 (non-PCV13 serotype) is relatively rare. However, Sp2 has a high potential for causing IPD including meningitis. Large-scale outbreaks of Sp2 IPD are rare and were not reported post-PCV implementation. We describe Sp2 IPD outbreak in Israel, in the PCV13 era, caused by a novel clone. Additionally, we analyzed the population structure and evolutionary dynamics of Sp2 during 2006–2018. Methods An ongoing, population-based, nationwide active surveillance, conducted since July 2009. PCV7/PCV13 were implemented in Israel in July 2009 and November 2010, respectively. All isolates were tested for antimicrobial susceptibility, PFGE, MLST and whole-genome sequencing (WGS). Results. Overall, 173 Sp2 IPD cases were identified; all isolates were analyzed by MLST (Figure 1). During 2016–2017, Sp2 caused 7.6% of all-IPD, a 7-fold increase compared with 2006–2015, and ranked second (after serotype 12F causing 12%) among IPD isolates. During 2006–2015, 98% (40/41) Sp2 IPD were caused by the previously reported global ST-1504 clone. The outbreak was caused by a novel clone ST-13578, not previously reported (Figure 2). WGS analysis confirmed that ST-13578 was related, but genetically distinct from ST-1504, observed exclusively before the outbreak. A single strain of clone ST-74 previously globally reported was identified in 2017–2018. An additional case was identified in an adult in the UK, following a family visit from Israel. The ST-13578 clone was identified only in the Jewish population and was mainly distributed in 3 of the 7 Israeli districts. All tested strains were penicillin-susceptible (MIC < 0.06 μg/mL). Conclusion To the best of our knowledge, this is the first widespread Sp2 outbreak since PCV13 introduction worldwide, caused by a novel clone ST-13578. The outbreak is still ongoing, although a declining trend was noted since 2017. Disclosures All Authors: No reported Disclosures.

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Population Structure and Evolutionary Dynamics of Wild-Weedy-Domesticated Complexes of Common Bean in a Mesoamerican Region

Crop Science ◽

10.2135/cropsci2004.0340 ◽

2005 ◽

Vol 45 (3) ◽

pp. 1073-1083 ◽

Cited By ~ 62

Author(s):

Daniel Zizumbo-Villarreal ◽

Patricia Colunga-GarcíaMarín ◽

Emeterio Payró de la Cruz ◽

Patricia Delgado-Valerio ◽

Paul Gepts

Keyword(s):

Population Structure ◽

Common Bean ◽

Evolutionary Dynamics

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Population structure and evolutionary dynamics of pathogenic bacteria

BioEssays ◽

10.1002/1521-1878(200012)22:12<1115::aid-bies9>3.0.co;2-r ◽

2000 ◽

Vol 22 (12) ◽

pp. 1115-1122 ◽

Cited By ~ 149

Author(s):

John Maynard Smith ◽

Edward J. Feil ◽

Noel H. Smith

Keyword(s):

Population Structure ◽

Pathogenic Bacteria ◽

Evolutionary Dynamics

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Population structure across scales facilitates coexistence and spatial heterogeneity of antibiotic-resistant infections

10.1101/469171 ◽

2018 ◽

Author(s):

Madison S. Krieger ◽

Carson E. Denison ◽

Thayer L. Anderson ◽

Martin A. Nowak ◽

Alison L. Hill

Keyword(s):

Population Structure ◽

Evolutionary Dynamics ◽

Resistance Management ◽

Antibiotic Use ◽

Antibiotic Consumption ◽

Host Population ◽

Antibiotic Resistant ◽

Resistance Risk ◽

Geographical Regions ◽

Wide Range

ABSTRACTAntibiotic-resistant infections are a growing threat to human health, but basic features of the eco-evolutionary dynamics remain unexplained. Most prominently, there is no clear mechanism for the long-term coexistence of both drug-sensitive and resistant strains at intermediate levels, a ubiquitous pattern seen in surveillance data. Here we show that accounting for structured or spatially-heterogeneous host populations and variability in antibiotic consumption can lead to persistent coexistence over a wide range of treatment coverages, drug efficacies, costs of resistance, and mixing patterns. Moreover, this mechanism can explain other puzzling spatiotemporal features of drug-resistance epidemiology that have received less attention, such as large differences in the prevalence of resistance between geographical regions with similar antibiotic consumption or that neighbor one another. We find that the same amount of antibiotic use can lead to very different levels of resistance depending on how treatment is distributed in a transmission network. We also identify parameter regimes in which population structure alone cannot support coexistence, suggesting the need for other mechanisms to explain the epidemiology of antibiotic resistance. Our analysis identifies key features of host population structure that can be used to assess resistance risk and highlights the need to include spatial or demographic heterogeneity in models to guide resistance management.

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Evolutionary dynamics on any population structure

Nature ◽

10.1038/nature21723 ◽

2017 ◽

Vol 544 (7649) ◽

pp. 227-230 ◽

Cited By ~ 139

Author(s):

Benjamin Allen ◽

Gabor Lippner ◽

Yu-Ting Chen ◽

Babak Fotouhi ◽

Naghmeh Momeni ◽

...

Keyword(s):

Population Structure ◽

Evolutionary Dynamics

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Evolution of an asymptomatic first stage of infection in a heterogeneous population

Journal of The Royal Society Interface ◽

10.1098/rsif.2021.0175 ◽

2021 ◽

Vol 18 (179) ◽

pp. 20210175

Author(s):

Chadi M. Saad-Roy ◽

Bryan T. Grenfell ◽

Simon A. Levin ◽

P. van den Driessche ◽

Ned S. Wingreen

Keyword(s):

Population Structure ◽

Life History ◽

Evolutionary Dynamics ◽

Population Heterogeneity ◽

Life History Strategies ◽

Specific Power ◽

Central Feature ◽

Evolutionarily Stable Strategies ◽

Infectious Stage

Pathogens evolve different life-history strategies, which depend in part on differences in their host populations. A central feature of hosts is their population structure (e.g. spatial). Additionally, hosts themselves can exhibit different degrees of symptoms when newly infected; this latency is a key life-history property of pathogens. With an evolutionary-epidemiological model, we examine the role of population structure on the evolutionary dynamics of latency. We focus on specific power-law-like formulations for transmission and progression from the first infectious stage as a function of latency, assuming that the across-group to within-group transmission ratio increases if hosts are less symptomatic. We find that simple population heterogeneity can lead to local evolutionarily stable strategies (ESSs) at zero and infinite latency in situations where a unique ESS exists in the corresponding homogeneous case. Furthermore, there can exist more than one interior evolutionarily singular strategy. We find that this diversity of outcomes is due to the (possibly slight) advantage of across-group transmission for pathogens that produce fewer symptoms in a first infectious stage. Thus, our work reveals that allowing individuals without symptoms to travel can have important unintended evolutionary effects and is thus fundamentally problematic in view of the evolutionary dynamics of latency.

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Eco-evolutionary dynamics of nested Darwinian populations and the emergence of community-level heredity

10.1101/827592 ◽

2019 ◽

Cited By ~ 3

Author(s):

Guilhem Doulcier ◽

Amaury Lambert ◽

Silvia De Monte ◽

Paul B. Rainey

Keyword(s):

Population Structure ◽

Evolutionary Dynamics ◽

Developmental Process ◽

Ecological Factors ◽

Community Level ◽

Top Down ◽

Cell Level ◽

Factors Affecting ◽

Parental Phenotype ◽

Evolution By Natural Selection

AbstractInteractions among microbial cells can generate new chemistries and functions, but exploitation requires establishment of communities that reliably recapitulate community-level phenotypes. Using mechanistic mathematical models, we show how simple manipulations to population structure can exogenously impose Darwinian-like properties on communities. Such scaffolding causes communities to participate directly in the process of evolution by natural selection and drives the evolution of cell-level interactions to the point where, despite underlying stochasticity, derived communities give rise to offspring communities that faithfully re-establish parental phenotype. The mechanism is akin to a developmental process (developmental correction) that arises from density dependent interactions among cells. Knowledge of ecological factors affecting evolution of developmental correction has implications for understanding the evolutionary origin of major egalitarian transitions, symbioses, and for top-down engineering of microbial communities.

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Eco-evolutionary dynamics of nested Darwinian populations and the emergence of community-level heredity

eLife ◽

10.7554/elife.53433 ◽

2020 ◽

Vol 9 ◽

Cited By ~ 4

Author(s):

Guilhem Doulcier ◽

Amaury Lambert ◽

Silvia De Monte ◽

Paul B Rainey

Keyword(s):

Population Structure ◽

Evolutionary Dynamics ◽

Developmental Process ◽

Ecological Factors ◽

Community Level ◽

Top Down ◽

Cell Level ◽

Factors Affecting ◽

Parental Phenotype ◽

Evolution By Natural Selection

Interactions among microbial cells can generate new chemistries and functions, but exploitation requires establishment of communities that reliably recapitulate community-level phenotypes. Using mechanistic mathematical models, we show how simple manipulations to population structure can exogenously impose Darwinian-like properties on communities. Such scaffolding causes communities to participate directly in the process of evolution by natural selection and drives the evolution of cell-level interactions to the point where, despite underlying stochasticity, derived communities give rise to offspring communities that faithfully re-establish parental phenotype. The mechanism is akin to a developmental process (developmental correction) that arises from density-dependent interactions among cells. Knowledge of ecological factors affecting evolution of developmental correction has implications for understanding the evolutionary origin of major egalitarian transitions, symbioses, and for top-down engineering of microbial communities.

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A general theoretical framework for trait-based eco-evolutionary dynamics: population structure, intraspecific variation, and community assembly

10.1101/2021.10.01.462789 ◽

2021 ◽

Author(s):

Jonas Wickman ◽

Thomas Koffel ◽

Christopher A Klausmeier

Keyword(s):

Population Structure ◽

Intraspecific Variation ◽

Functional Traits ◽

Community Assembly ◽

Evolutionary Dynamics ◽

Resource Competition ◽

Adaptive Dynamics ◽

Theoretical Framework ◽

Community Change ◽

Structured Populations

To understand how functional traits shape ecological communities it is necessary to understand both how traits across the community affect its functioning and how eco-evolutionary dynamics within the community change the traits over time. Of particular interest are so-called evolutionarily stable communities (ESCs), since these are the end points of eco-evolutionary dynamics and can persist over long time scales. One theoretical framework that has successfully been used for assembling ESCs is adaptive dynamics. However, this framework cannot account for intraspecific variation---neither locally nor across structured populations. On the other hand, in moment-based approaches, intraspecific variation is accommodated, but community assembly has been neglected. This is unfortunate as some questions regarding for example local adaptation vis-a-vis diversification into multiple species requires both facets. In this paper we develop a general theoretical framework that bridges the gap between these two approaches. We showcase how ESCs can be assembled using the framework, and illustrate various aspects of the framework using two simple models of resource competition. We believe this unifying framework could be of great use to address questions regarding the role of functional traits in communities where population structure, intraspecific variation, and eco-evolutionary dynamics are all important.

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Understanding the evolution of multiple drug resistance in structured populations

eLife ◽

10.7554/elife.65645 ◽

2021 ◽

Vol 10 ◽

Author(s):

David V McLeod ◽

Sylvain Gandon

Keyword(s):

Population Structure ◽

Evolutionary Dynamics ◽

Multiple Drug Resistance ◽

Drug Prescription ◽

Structured Populations ◽

Health Concern ◽

Multiple Drug ◽

Unified Framework ◽

Dynamical Equations

The evolution of multidrug resistance (MDR) is a pressing public health concern. Yet many aspects, such as the role played by population structure, remain poorly understood. Here we argue that studying MDR evolution by focusing upon the dynamical equations for linkage disequilibrium (LD) can greatly simplify the calculations, generate more insight, and provide a unified framework for understanding the role of population structure. We demonstrate how a general epidemiological model of MDR evolution can be recast in terms of the LD equations. These equations reveal how the different forces generating and propagating LD operate in a dynamical setting at both the population and metapopulation levels. We then apply these insights to show how the LD perspective: (i) explains equilibrium patterns of MDR, (ii) provides a simple interpretative framework for transient evolutionary dynamics, and (iii) can be used to assess the consequences of different drug prescription strategies for MDR evolution.

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