Edinburgh Diseases Transmission workshop - about the presenters

I’m interested in epidemic models and the underlying assumptions made in models, especially those run as black boxes. 

I'm also interested in determining the "best wrong model" - i.e. the simplest model which can usually explain the data but when it fails, can provide an indication of what important effects are missing.  

The most interesting models are oversimplified, because if they're exactly right it implies you already understood the system, so didn't learn anything new.

Graeme's university profile

Rowland uses combinations of mathematical and statistical models, simulations and networks (increasingly combining all four) to study the transmission, spread and persistence of infectious diseases through populations of livestock, wildlife and humans. He has mainly worked on diseases of livestock, with foot-and-mouth disease and bovine Tuberculosis featuring prominently, though recently has had an (unsurprising) emphasis on COVID-19.

Much of this work focuses on understanding how complexity of contact results in complexity of disease behaviour, in turn influencing our approaches to disease control. Simple population models are at the core of developing insights into the fundamental processes underpinning transmission dynamics, with complex datasets ranging from pathogen sequence data to detailed knowledge of daily contact patterns used to translate those principles into impactful insights about real diseases.

Rowland's university profile

Dr Samantha Lycett is a Senior Lecturer / Group Leader in Pathogen Phylodynamics, at Roslin Institute, University of Edinburgh. 

Research interests in evolution and epidemiology of viruses and bacteria in animal and zoonotic disease systems using advanced computational, bioinformatic and phylogenetic / phylodynamic modelling techniques. 

Current active research projects in several pathogens, host adaptations, epistatic interactions, effect of escape mutations, and evolution of virulence.  Since 2020 Dr Lycett is additionally working on SARS-CoV-2 spread and evolution in the human population.

Sam's university profile

For several years we have explored  how trypanosome parasites prepare for their transmission by tsetse flies. This has uncovered the molecular machinery underlying the process, which operates as a community response via density-dependent quorum sensing.

The identified molecules have provided tools and markers to dissect factors that contribute to the parasites’ infection dynamics and transmission potential. In particular we have focused on how quorum sensing can be modulated in parasites experiencing competing trypanosome genotypes and those that have escaped vector transmission.

This approach highlights how a reductionist understanding of molecular mechanisms can help the understanding of the dynamics of disease spread in the field and, potentially, the adverse consequences of drug treatment.

Keith's lab website

Áine O'Toole is a member of the Rambaut Group at Edinburgh University. Áine graduated with BA in Genetics from Trinity College Dublin and went on to learn computer programming in the McLysaght lab where she competed a two-year MRes in Molecular Evolution. After completing the MSc section of the Wellcome Trust Hosts, Pathogens & Global Health PhD Programme at Edinburgh University, she joined the Rambaut Group as part of the ARTIC Network to complete her PhD in molecular epidemiology.

She has travelled to Ghana and Pakistan to provide hands-on training and give bioinformatic and phylogenetic workshops for viral genomics.  Until the COVID-19 pandemic, Áine was in the final year of her PhD research and had been developing software for poliovirus surveillance in Pakistan and viral outbreak investigations in a clinical setting.

This year, Áine has developed tools such as pangolin and civet, and defined SARS-CoV-2 lineages to help researchers around the world track the spread of SARS-CoV-2.

Áine's website

Amy’s research focuses on understanding how parasites impact the fitness and dynamics of their wild hosts, specifically by recognising the complexities that are inherent in natural systems. Her research approach integrates an array of methodologies to maximise the potential of ecological and evolutionary studies to address key questions about host-parasite interactions, including how to improve host health and develop effective disease control strategies. 

For most of her research, Amy uses a small mammal – parasite community system which can be investigated both in the wild under natural conditions, and in controlled experiments in the laboratory.  This system is focused on wood mice and their very diverse parasite and pathogen community (including >30 species) where she can follow individuals throughout their life and measure how host characteristics impact infection/coinfection and transmission.

Amy's lab website

Transition of the malaria parasite from the host to the vector represents a significant bottleneck in the parasite life-cycle. Blocking this step would break the cycle of infection, prevent spread of the parasite and consequently result in an effective approach to combat malaria.

Our group aims to understand molecular mechanisms employed by the malaria parasite to respond and adapt to changing environments imposed during transmission from the host to the vector. We are specifically interested in signalling pathways regulating host-to-vector transition with the goal of identifying new transmission blocking strategies.

Nisha's lab website

Research in the Reece lab sits at the interface of parasitology, chronobiology and evolutionary ecology, motivated by the questions of “what makes a successful parasite” and “what limits their success”?

We investigate the strategies that parasites have evolved to cope with the challenges of their lifestyle, and exploit the opportunities it brings. Our research focuses on malaria parasites, which are an excellent model system, and they have immense applied relevance because malaria parasites and their relatives cause some of the most serious infectious diseases of humans, livestock, and wildlife.

Our research discovers surprising sophistication in parasite strategies for survival and reproduction. These strategies underpin the severity and infectiousness of parasites and so, understanding the evolutionary limits of parasite strategies may offer new ways to control infections.

Sarah's lab website

Immunity to malaria is often thought to be slow to develop but that only applies to defence mechanisms that function to eliminate parasites (resistance). In contrast, immunity to severe disease can be acquired quickly and without the need for improved pathogen control (tolerance). 

We have developed human re-challenge models of malaria to track the development of clinical immunity in real-time, and identify host adaptations that can promote fitness and survival in the absence of pathogen control.

Phil's lab website

Dr. Stagg is a Reader in epidemiological methodologies for infectious diseases who initially trained in the life sciences.

Her work spans tuberculosis, herpesviruses and infectious hepatitis and Is highly collaborative, sitting at the interface between epidemiology, pharmacology, health systems, behavioural sciences, mathematical modelling, health economics, and the laboratory sciences.  She has worked with national and international policy making bodies (National Institute for Health and Care Excellence UK, European Centre for Disease Prevention and Control, and the World Health Organization).

She is currently an advisor to the Scottish Parliament’s COVID committee, co-chair of UK Academics and Professionals to End Tuberculosis, and a member of the World Health Organization's core grouping for the European Tuberculosis Research Initiative.

The overall aim of our research is to understand how individual-level host heterogeneity scales up to population level disease outcomes. Part of the difficulty in linking individual variation to population-scale outcomes is that hosts can vary on multiple axes (e.g., behavioural, physiological, immunological) that affect their transmission potential.  Moreover, we lack well-characterized empirical systems that account for multiple facets of individual variation. 

To address this gap, we leverage the strengths of Drosophila as genetically tractable model of infection, immunity, and behaviour to develop it as a model system for experimental epidemiology. Our approach is to isolate the individual host traits that drive pathogen transmission, identify genetic and environmental drivers of variation for trait, and put this all back together as a more useful predictive framework of pathogen spread. 

Using a combination of experimental and modelling approaches we investigate 1) host and pathogen drivers of social group behaviour; 2) the genetic basis of individual variation in pathogen shedding and 3) the innate immune regulation of pathogen acquisition and spread.

Pedro's lab website

Bryan is a postdoctoral researcher who uses DNA sequencing, comparative genomics and phylogenetics to study clinically-important bacterial species.

Bryan previously worked with the Laboratory for Bacterial Evolution and Pathogenesis (Prof Ross Fitzgerald) at the Roslin Institute to study outbreaks of Legionnaires’ disease around Scotland.

More recently, Bryan has been working with the Epidemiology Research Group (Prof Mark Woolhouse) using genomics to understand how bacteria and antimicrobial resistance transmit between humans, animals and the environment using a One Health approach.

Bryan's university profile

Mark is Professor of Infectious Disease Epidemiology at the Usher Institute.

Transmissibility is the defining attribute of infectious diseases, and it has profound consequences for their epidemiology.

A quantitative understanding of the transmission is therefore central to infectious disease epidemiology and to evidence-based decisions on prevention and control strategies. Rapid assessment of transmission potential is central to knowing how to respond effectively to emerging disease events.

Mark's lab website