The Theory and Practice of Statistical Ecology

Evidential statistics

with mark taper, brian Dennis and Subhash lele

For many years, there has been a growing understanding of the importance of theory in Ecology and Evolution, with theory being an organized complex of models. Functionally, science works by comparing models. Science progresses when old (possibly good) models are replaced with better models. Evidential statistics is an honest approach whose primordial premise is to avoid the true model assumption. The core inferential entity is the evidence function, which is a data based estimate of the relative distance of two models to truth or reality. In classical error statistics, the strength of evidence is conceived of as synonymous with the error probability. In evidential statistics, the evidence and the error probabilities are distinct statistical entities, both of inferential interest.

As different as this all seems from classical and Bayesian statistics, most inference tools can be viewed evidentially in a single coherent framework, including model identification, model uncertainty estimation, parameter estimation, parameter uncertainty estimation, pre-data error control, post-data strength of evidence and the design of experiments. Despite all these advantages, the evidential statistics approach is largely unknown to working scientists.

The aim of this research topic is to rectify this widespread ignorance by informing working scientist of the utility and flexibility of evidential statistics. We put together a special issue with both papers that convey basic concepts and papers that convey technical subtleties sufficient to conduct real scientific research, as well as practical advice that can be easily incorporated into the teaching of undergraduate and graduate courses. The topic consists of a mix of new original research, reviews, commentaries and perspectives on topics related to evidential statistics (see article types).

stochastic community dynamics applied to studies of the vaginal microbial flora

with larry j forney and jacques ravel

In this NIH funded study we use ecological theory and stochastic processes to define changes in the composition, structure and function of vaginal bacterial communities as well as host responses that elicit vaginal signs and symptoms. By doing so we aim at increasing our understanding of factors that contribute to homeostasis of healthy vaginal microbiomes. To do this we leverage a unique set of samples and metadata that were prospectively collected daily by 135 women for 10 weeks as part of the Human Microbiome Project (HMP) between 2009-2010. In this study, women completed daily diaries in which they reported vaginal symptoms including vaginal odor, discharge, irritation, burning, and itching as well as behavioral data. Once per day women self-collected vaginal samples to determine vaginal pH and Nugent scores (for diagnosing bacterial vaginosis) and archived samples for use in determining the composition of vaginal bacterial communities, their metagenomes, host and microbe gene expression patterns, metabolomes and profiles of cytokines and chemokines reflecting the status of the immune system.

evolution of antibiotic resistance

with eva m top, ben kerr and houra merrikh

Newly acquired multi-drug resistance (MDR) plasmids are often not stably maintained in the absence of antibiotics. However, we and others have shown that single mutations in the bacterial host, the plasmid, or both can rapidly improve the persistence of these plasmids.

These genetic changes either ameliorate the plasmid fitness cost to the host or decrease the plasmid loss rate during cell division. We and others recently showed that the reduction in cost of a newly acquired plasmid can be (directly or indirectly) linked to chromosomally encoded helicases. Specifically, our results suggest that mutations in accessory helicase genes (uvrD and xpd/rad3) improved the persistence of a self-transmissible MDR plasmid by amelioration of the plasmid fitness cost. This is consistent with a study showing that in Pseudomonas aeruginosa, mutations in a gene encoding a putative accessory helicase reduced plasmid cost. Importantly, we also showed for the first time that these chromosomal mutations can pre-adapt the bacteria to other MDR plasmids, leading to their enhanced persistence (which we refer to as increase in plasmid permissiveness). This suggests that bacteria with increased permissiveness can serve as stable repositories for multiple MDR plasmids, eventually generating strains with an expanded arsenal of resistance genes. This possibility has never been tested. Furthermore, our findings suggest that plasmid-helicase interactions may be critical for the retention of newly acquired MDR plasmids, and may serve as new drug targets. Unfortunately, the molecular mechanisms underlying the effects of helicase and other mutations on plasmid cost and persistence are still not known.

In this multidisciplinary NIH-funded project we propose to test the following hypotheses: (i) chromosomal plasmid-adaptive mutations can pre-adapt bacteria to other MDR plasmids; (ii) this plasmid permissiveness can expand the spectrum of antibiotic resistance traits within a bacterial species; and (iii) accessory helicases are linked to the persistence of newly acquired MDR plasmids across a wide spectrum of bacterial pathogens. These hypotheses are tested using a combination of molecular techniques and bacteria-plasmids population dynamics models fitted to experimental time series data.

the evolution of diversity in anthrax

with jason k blackburn, sadie ryan, Bob holt and wayne getz

In this NIH funded study we use a multi-pronged approach to study the genetic and the ecological aspects of pathogens whose transmission is environmentally-mediated. This type of transmission is the primary mode of infection for a number of important multi-host diseases in wildlife and livestock, including several zoonoses (diseases that spillover into humans) and is explicitly linked to host movements and foraging in areas where the pathogen is maintained in environmental reservoirs. Calculating the basic reproduction number R0 in such systems requires that we estimate the contribution of each reservoir to new cases. In contrast to traditional basic reproduction number estimates, this requires modeling interactions between naïve (susceptible) hosts and stationary environmental reservoirs. To do this we must unpack the transmission process into its pathogen shedding, environmental persistence, and host contact (pathogen ingestion or inhalation) components. Such contact rates can be characterized from a combination of local host movement and foraging patterns driven by larger-scale seasonal resource selection. Persistent environmental pathogen reservoirs can be modelled as individual, local infectious zones (LIZs) with their own demography and spatial distribution; the life history of these LIZs influence host foraging locally. In this 4-year EEID project, we provide a novel combined geospatial and mathematical approach for estimating R0 for environmentally-mediated transmission. We will then assess the efficacies of control strategies impacting different components of the transmission process.