Tag Archives: disease
Quantifying 25 years of disease‐caused declines in Tasmanian devil populations: host density drives spatial pathogen spread (2021) Cunningham et al., Ecology Letters, https://doi.org/10.1111/ele.13703
While the Tasmanian Tiger has made news this last month for all the wrong reasons, there’s still another famous species of Tasmanian mammal which deserves just as much attention (probably more given that we can still save this one from extinction). The Tasmanian devil has seen its populations declined considerably over the last three decades, largely due to the emergence of a transmissible facial tumour, the devil facial tumour disease (DFTD).
The way the devils interact mean that even at low densities, the disease can still be transmitted through a population. The aggressive nature of Tasmanian devil mating (which occurs even when there are few devils around) is a big transmission vector. This unfortunately means that extinction due to DFTD was recently thought to be a likely endpoint.
Today’s authors wanted to test to how strongly the devil density influenced the spread of DFTD, and whether the drop in population that the disease causes means that we’re likely to see the disease’s effects wear off at some point, and Tasmanian devil populations stabilise.
What They Did
Long-term data is an absolute must for a study like this. Luckily, the Tasmanian government has run ‘spotlight surveys’ along 172 road transects for the last 25 years. These involve driving slowly along a 10 kilometre stretch of road and recording mammal presence using a handheld spotlight. This was combined with further surveys designed to obtain density at smaller scales to come up with a predictive estimate of devil density in Tasmania from 1985 to 2035.
The team also used occurrence data for DFTD to figure out how quickly it initially spread through Tasmania, and modelled the spread into a new region against the density of the devils in that region.
Did You Know: Devil Reintroduction
The Tasmanian devils are an Australian icon, and a lot of money has been put into figuring out how to save their species. Suggestions have been made to reintroduce DFTD-free population back onto mainland Australia, where their presence may even help reduce the effect of cats and foxes. However it is also possible that the introduction of a new predator could instead put added pressure on mainland species already threatened by invasive predators. Studies into this are ongoing, and you can check out more on them at the articles linked below.
Read More: Releasing the Devil
What They Found
Tasmanian devil density may have played a large role in the initial spread of the disease, explaining why it spread so quickly through certain parts of Tasmania. This isn’t hugely surprising, though the precision with which the authors modelled its spread will be absolutely crucial for effective conservation.
What is really interesting is that the Tasmanian devil population back before the disease struck were probably much lower than initially thought. If this sounds depressing, the other big takeaway is that based on the predictions here, the decline in devil numbers should ease off soon, meaning the disease is unlikely to result in the extinction of Tasmania’s most iconic endemic species.
Normally authors will mention interesting future research which could build on the research they’ve carried out. Standard practice. Here, my ‘problem’ is that the authors mention some research so incredibly tantalising I’m angry at them for bringing it up. What will be important in the future is looking at devil genotypes. The genetic makeup of some devils will make them more resistant to the disease, and identifying and moving these individuals to areas where the disease is rampant could help fight DFTD. Having said that, it could also help produce more aggressive strains of the disease. GIVE ME ANSWERS.
This is a good news story, which often feel quite scant in the world of ecology. But it doesn’t mean the devil is out of the woods yet. Actually the woods themselves are a massive problem, seeing as Australia’s rates of deforestation are among the worst in the world. We need to constantly monitor the population to figure out where local extinctions are likely.
This study is also a fantastic example of how important long-term monitoring is for ecologists. Studies like the one used here are hard to fund (more on that here), but their value to ecologists in allowing us to figure out what drives population fluctuations is enormous.
Sam Perrin is a freshwater ecologist currently completing his PhD at the Norwegian University of Science and Technology who has spent way too much time looking at photos of Tasmanian mammals over the last 2 weeks. You can read more about his research and the rest of the Ecology for the Masses writers here, see more of his work at Ecology for the Masses here, or follow him on Twitter here.
This is a guest post by Professor Emma Despland
Zoonotic diseases, or diseases that jump from animals to people, are not a new phenomenon. Many well-known human diseases first originated in animal populations. In some cases, animals are the main sources of human infection and human-to-human transmission is rare or null (e.g. rabies); other diseases persist in animal populations and occasionally jump to humans, seeding a human outbreak (e.g. plague), and yet others jumped from animals to people long ago and have been circulating in human populations ever since (e.g. measles). However, novel zoonotics have been appearing with disturbingly increasing frequency.Read more
Exposure to potentially cannibalistic conspecifics induces an increased immune response (2020) Murray et al., Ecological Entomology, https://doi.org/10.1111/een.12806
Plasticity is a powerful force in nature that allows organisms to change the way they look, the way they act, and even their own physiological processes. Prey species commonly exhibit plastic responses when they are exposed to predators, and recent studies have shown that these predator-induced effects can affect the immune function of the prey species. Because of this, predators have the potential to modify disease dynamics, either increasing disease/parasite infection by reducing the prey’s immune function, or decreasing disease by increasing immune function.
Interestingly, predators are not the only organisms that consume prey species. Some prey species eat both members of their own trophic level (an intraguild predator, see Did You Know) and members of their own species (a cannibal). Because they act like a predator (by eating a prey organism), there’s a possibility that these cannibalistic individuals may have the same effect on their potential victims. Today’s authors used larval dragonflies to investigate that exact question.
Image Credit: Pharexia, Ratherous, AKS471883, Source Data from Johns Hopkins University CSSE, The Centers for Disease Control and Prevention, New York Times, CNBC.
As it quickly became clear in late February and early March that COVID-19 was not going away anytime soon, attention turned to trying to figure out when and where the virus would spread. Epidemiologists and virologists have had their work cut out for them, trying to simultaneously reassure and warn people the world over about the dangers, the nature and the potential timeline of the virus.
So it came as somewhat of a surprise to see ecologists try and tip their hat into the ring. Early on in the pandemic, teams of ecologists sprang up, trying to use Species Distribution Models to predict the spread of the virus. And whilst this might sound helpful, many of these studies lacked collaboration with epidemiologists, and their predictions very quickly fell flat. Some studies suggested that areas like Brazil and Central Africa would be largely spared by the virus, which quickly turned out not to be the case. Flaws in the studies were spotted quite quickly by concerned members of both the ecological and epidemiological communities alike, and a few teams got started on responses.
If you’re unlucky, you already know that humans possess a skin microbiome. It sounds gross, but it’s simply an entire ecosystem of microbes like bacteria living on our skin (maybe it is gross). Some of them help us, others might make us sick, for example when they enter open wounds. Plants have a similar set-up, hosting different ecosystems of bacteria on their leaves.
Hopefully, at this point I’ve made your skin crawl (because as you now know, it is literally crawling). But that microbiome can actually tell us some fascinating things about the animal or plant we’re looking at. So today, I’ll go through exactly what metagenomics is, and some of the information we can glean from a plant’s surface (I am a botanist after all).
Of poisons and parasites—the defensive role of tetrodotoxin against infections in newts (2018) Johnson et al., Journal of Animal Ecology, https://doi.org/10.1111/1365-2656.12816
Many organisms in nature produce powerful (and sometimes deadly) toxic substances, often taken as evidence that prey evolved chemical defenses against predators. Interestingly, these chemical defenses are deadly not only to predators, but also to parasites. This complementary defense, in addition to the ubiquity of parasites themselves, indicate that parasites may have had a hand in the evolution of host toxicity.
One particularly potent toxin found in the animal kingdom is tetrodotoxin (TTX). It can cause paralysis, difficulty with breathing, and even death in some cases. Newts in the genus Taricha are notorious for having high concentrations of TTX in their skin and eggs, and this has long been thought to have evolved as a defense against predators. In particular, Taricha newts and garter snakes (Thamnopholis spp.) are a classic example of arms-race dynamics (see Did You Know). Despite this relationship, newt toxicity and snake resistance to the toxin don’t always match up perfectly in nature, suggesting that other factors may influence newt toxicitiy. The goal of today’s study was to study parasitic infection and compare it to variation in toxicity among two newt species, the rough-skinned newt (T. granulosa) and the California newt (T. torosa).
Image Credit: The Witcher, 2020
Science and movies often don’t go well together*. It’s no-one’s fault. Science can often be boring and riddled with uncertainties, and movies and TV require plot advancement and definitive results.
But you know what’s a scientific fact? That Henry Cavill’s chin can cut diamond, and if you thrust him into a cosplay outift he probably already had at home and send him out to slaughter a bunch of CGI monsters you’ll get something that is at the very least mildly enjoyable. And if you’re an invasion ecologist who runs a podcast looking at the ecology of movie monsters, mildly enjoyable monsters are enough to dedicate a blog post to.
Many organisms are vulnerable to a wide array of diseases and parasites throughout the course of their lives, but could scavengers help reduce that vulnerability? (Image Credit: The High Fin Sperm Whale, CC BY-SA 4.0, Image Cropped)
Do scavengers prevent or promote disease transmission? The
effect of invertebrate scavenging on Ranavirus transmission (2019) Le Sage et al., Functional Ecology, https://doi.org/10.1111/1365-2435.13335
As intimate as the host-parasite relationship is, it is important to keep in mind that it is embedded within a complex web of other interactions within the local ecological community. To add to this complexity, all of these interactions can feed back on and effect the host-parasite relationship. One ubiquitous part of all communities is the scavenger, an organism that feeds on dead and decomposing organisms. The authors of this paper wanted to investigate how scavengers affect disease transmission in local communities.
This question in interesting because it can easily go either way, depending on the community in question. Scavengers could lower disease transmission by eating infected organisms, thus removing contagious elements from the environment. However, scavengers could also increase transmission by promoting the spread of contagious elements in the community via their own waste after they consume infected tissues.
Fields full of herbaceous plants such as these can be incredibly diverse and complicated ecosystems, and the multitudes of species that inhabit them can influence the magnitude of disease that the organisms that inhabit it may encounter (Image Credit: LudwigSebastianMicheler, CC BY-SA 4.0, Image Cropped)
Past is prologue: host community assembly and the risk of infectious disease over time (2018) Halliday, F.W. et al., Ecology Letters, 22, https://dx.doi/10.1111/ele.13176
Everything in ecology is based around the environment that a focal organism inhabits, including the interactions it has with other organisms and the non-living aspects of the habitat itself (temperature, water pH, etc.). That being said, it’s no surprise that disease dynamics are likely to depend on the environment that a host inhabits, and that the environment itself is a product of what came before. That is to say, the group of organisms that originally populate a given ecosystem can have an effect on how that ecosystem will look in the future (lakes with freshwater mussels will have clearer water than those without).
The scientific literature is full of experiments, observations, and hypotheses about which environmental conditions lead to fluctuations in disease dynamics. As such, it is difficult to come to a consensus with a “one-size-fits-all” rule for disease dynamics and community structure. The authors of today’s study used a long-term experiment to determine what exactly moderates disease over time. Read more