Scientists reveal ‘epidemics aren’t random’ in ‘world-first’ UK research

Donald Trump refers to Covid-19 as the ‘plague from China’

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Revolutionary research at the University of Stirling has shed new light on disease evolution, revealing “epidemics aren’t random”. Scientists led by Biological and Environmental Sciences expert Dr Stuart Auld used crustacean clones to examine whether epidemics could be repeated, and how different environments can affect their scale.

The Daphnia magna, a crustacean capable of cloning itself, was used to repeatedly run epidemics.

We were able to show that epidemics aren’t random processes

Dr Stuart Auld

All simulations began using identical population of hosts and pathogens in different environments.

This allowed experts to explore numerous factors calculating epidemic size and disease evolution.

Tightly-controlled lab conditions created complex natural environments using ponds containing Daphnia and its sterilising bacterial pathogen Pasteuria ramosa.

Taken in tandem, these precisely pin-pointed how such ecological conditions interacted and impacted epidemics’ size.

These also revealed how epidemics altered the creatures’ ability to resist the bacterium, and infection in general.

Dr Auld said: “We know that epidemics vary: the Black Death was worse than the Great Plague of London despite being caused by the same bacterium, but it’s hard to know why.

“In our study, we were essentially able to put the same animal into different environments and see how susceptible it was to infection.

“Each pond differed in its temperature profile and all manner of other ecological conditions, but the starting set of hosts and pathogens was the same.

“This study is almost unheard of – it was like examining the Black Death 16 times over, but each time under different environmental conditions.

“We were able to show that epidemics aren’t random processes; they are repeatable and predictable when you know a bit about the wider environment.”

Variables such as temperature, acidity, access to algal food and predator densities allowed the researchers to forecast the severity of epidemics.

In addition, the overall disease coevolution – the amount by which hosts evolved to be resistant and pathogens evolved to become more infectious – is now far better understood.

The research is part of the longer-term Stirling Outdoor Disease Experiment project.

This mission’s overall aim is to map how ecological and environmental variation affects disease evolution.

Dr Auld added: “Following the outbreak of COVID-19 and the way it has dramatically impacted our lives, disease evolution is now very much of interest to the general public.

“We must better understand the general underlying processes that govern the size and severity of disease outbreaks.

“Any underlying knowledge that helps us better predict disease dynamics – for human, animal and crop diseases – will ultimately be of benefit to society.”

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