Sibylla Bostoniensis

Canonical link: https://siderea.dreamwidth.org/1787739.html

[Special content warning: discussion of existential threats to humanity. Highly depressogenic content. This might not be the best thing to read if you're given to despair or if despair is unsafe for you. Maybe give this post a pass if you are not in a place, emotionally, to handle it.]


Previous: Part 3: Climate Change



17.

So not only is the human species hitting the population level and density that makes us exceptionally vulnerable to contagious illness, and not only has Covid lowered our physiological, psychological, social, and legal defenses against infectious disease, climate change has already been directly leading to expansion of the ranges of animals that carry zoonotic diseases that can infect humans.

But wait. There's more.

Mora et al.'s work was not just about how climate change will affect (largely increase) the proliferation of illnesses through the changing of ranges of zoonosis-bearing animals. It's title was "Over half of known human pathogenic diseases can be aggravated by climate change". It's not limited to zoonoses, and it's not limited to how diseases spread: it looked at many other ways that climate change acts on diseases.

Climate change doesn't just impact the behavior of animals that carry contagious diseases. It can work changes directly on the pathogens themselves.

2022, HuffPost:

But the problem [described in Mora et al.'s paper] is far more complex than how any single climate stressor might interact with and exacerbate each infectious disease. It’s not a 1-to-1 connection; many pathogens can be transmitted to humans in multiple different ways. The paper identified more than 1,000 unique pathways between climate hazards and disease outbreaks.

Additionally, so far I've mostly been talking about infectious diseases that are contagious between humans. When we speak of "spillover events", we're talking about a zoonotic disease circulating in a non-human species that infects a human who then passes it on to other humans. These are in many ways the most alarming diseases because these are the ones that could possibly go pandemic.

But let us not fail to appreciate that there are infectious diseases that could start to afflict our species – or increase their lethality and prevalence – which do not jump from human to human. They are not what we think of as contagious, because they do not spread directly between humans the way Covid does.

Some of these diseases directly rely on environmental conditions to propagate and infect organisms, including us. Environmental conditions that will be directly altered by climate change.

Consider coccidiodomycosis, aka Valley fever, a dust-borne disease caused by a soil-dwelling fungus. It provides an edifying example.

2017 Jul 13: American Lung Association (lung.org, institutional blog post): "How Climate Change Has Led to an Increase in Valley Fever" by editorial staff:

Valley fever, or coccidiodomycosis, is a lung disease that is on the rise in the U.S., especially in the Southwest. Cases of valley fever have gone up 400 percent from 1998-2015, according to the Centers for Disease Control and Prevention.

2022 April 22: Inside Climate News: "Climate Change is Spreading a Debilitating Fungal Disease Throughout the West":

Inhaling just one microscopic spore of the coccidioides fungus—cocci for short—can lead to a disease that kills around 200 people every year and leaves thousands of others struggling with fatigue, pneumonia, night sweats and headaches that can drag on for years. The spores can drift, invisible in the air, up to 75 miles from where the wind picks them up.

One way that climate change can change the prevalence of Valley fever is by changing local environmental conditions to make make a larger area congenial for its growth, thus expanding its geographical range:

2019 Aug 30: GeoHealth (journal): "Expansion of Coccidioidomycosis Endemic Regions in the United States in Response to Climate Change" by Morgan E. Gorris et al.:

We estimated the area potentially endemic to Valley fever using a climate niche model derived from contemporary climate and disease incidence data. We then used our model with projections of climate from Earth system models to assess how endemic areas will change during the 21st century. By 2100 in a high warming scenario, our model predicts that the area of climate-limited endemicity will more than double, the number of affected states will increase from 12 to 17, and the number of Valley fever cases will increase by 50%. The Valley fever endemic region will expand north into dry western states, including Idaho, Wyoming, Montana, Nebraska, South Dakota, and North Dakota.

Another way that climate change can change the proliferation of Valley fever is by increasing the frequency of the dust storms by which it infects humans:

2017 May 6: Geophysical Research Letters (journal): "Intensified dust storm activity and Valley fever infection in the southwestern United States" by Daniel Q. Tong et al.:

Abstract

Climate models have consistently projected a drying trend in the southwestern United States, aiding speculation of increasing dust storms in this region. Long-term climatology is essential to documenting the dust trend and its response to climate variability. We have reconstructed long-term dust climatology in the western United States, based on a comprehensive dust identification method and continuous aerosol observations from the Interagency Monitoring of Protected Visual Environments(IMPROVE) network. We report here direct evidence of rapid intensification of dust storm activity over American deserts in the past decades (1988–2011), in contrast to reported decreasing trends in Asia and Africa. The frequency of windblown dust storms has increased 240% from 1990s to 2000s. This dust trend is associated with large-scale variations of sea surface temperature in the Pacific Ocean, with the strongest correlation with the Pacific Decadal Oscillation. We further investigate the relationship between dust and Valley fever, a fast-rising infectious disease caused by inhaling soil-dwelling fungus (Coccidioides immitis and C. posadasii) in the southwestern United States. The frequency of dust storms is found to be correlated with Valley fever incidences, with a coefficient (r) comparable to or stronger than that with other factors believed to control the disease in two endemic centers (Maricopa and Pima County, Arizona).

Plain Language Summary

Computer models predict that as the Earth warms, the Southwest United States will become drier. In the already arid Southwest, this means more dust storms and even potential environmental catastrophes such as desertification and another “Dust Bowl.” Using a newly reconstructed data record, we found that indeed this region is seeing more dust storms in the past decades. There was a 240% increase in the number of large dust storms between 1990s and 2000s. The sharp increase of dust storms is likely driven by tiny changes of sea surface temperature in the northern Pacific Ocean. In the Southwest frequented by dust storms, the infection rate of Valley fever has mysteriously gone up more than 800% from 2000 to 2011. Little is known about what drives the fast rise, although a number of factors are found moderately correlated to the outbreaks. In two endemic centers, dust storms are found to better correlated with the disease than any other known controlling factor. This work implied a potential teleconnection between large-scale climate variations and infectious disease in sensitive regions, although future work is needed to confirm the linkages.

Valley fever provides us one example of how the human infectious disease burden will likely increase due to climate change directly affecting the vigor, dispersion, and infectiousness of infectious agents, entirely independently of host species, possibly in multiple ways.

There are others.




18.

If zoonosis is a word destined for heavy use in our future, so is thermotolerance.

Again, the HuffPost article about Mora's research:

In their paper, UH researchers break down the ways one crisis has helped fuel another. Climate change has brought people and pathogens in closer proximity. [...] Additionally, climate impacts have allowed for pathogens to more successfully reproduce and become more virulent, while simultaneously blunting our own ability to avoid and fight off disease.

Climate change can drive changes directly in pathogens, themselves. And one of the things it appears it can drive is evolution of the ability to tolerate higher temperatures. And that can have much worse and more far-reaching consequences than it first appears.

Consider the infectious yeast (i.e. a fungus) Candida auris, about which there was a 2020 Radiolab episode I recently linked to, "Fungus Amungus". To summarize, C. auris initially emerged as a known infection of humans only in 2009, and then as a comparatively mild ear infection (hence it's name, "auris" meaning "ear") that could only attack the immunocompromised. But then, abruptly, in 2016, it turned lethal, and emerged separately on three different continents. It turned out not to be one strain which got around, but four distinct genetic variants, that somehow all emerged simultaneously.

There's a theory about how and why this previously mild-mannered microbe rather suddenly got its teeth into us, resting on these facts:

2019 July 6: Fungi (journal): "On the Origins of a Species: What Might Explain the Rise of Candida auris?" by Brendan Jackson et al.:

C. auris possesses distinctive properties compared with many other Candida species, including its close relatives. It can grow at temperatures as high as 42 °C (108 °F) [24,29,30]. Although many people associate fungal growth with warm conditions, few fungi can grow at temperatures at or above 37 °C. In one study, the number of surviving fungal isolates declined by 6% for every 1 °C increase in the 30–40 °C range [31].

Thirty-seven degrees celsius is, of course, regular human body temperature (98.6ºF). C. auris is able to infect humans now because it's developed the rather unusual-among-fungi trait of being able to survive at typical human body temperature, so it can colonize human skin.

And it can survive at more than 37º C, it can – very unusually amoung fungi – survive up to 42º C (107.6º F). That's survival well in excess of human fevers, which is exceptionally terrible, because...

The thermotolerance of C. auris allows it to cause invasive human infections, including tolerating the fever response, and has led to speculation that it may be able to infect birds [24], whose body temperatures usually range 40–42 °C, raising the possibility of an avian reservoir.

The theory promugated by Casadevall and his co-authors is that climate change has given Candida auris an opportunity to evolve the thermotolerance that allows it to attack warm-blooded animals like us.

2019 July 23: mBio: "On the Emergence of Candida auris: Climate Change, Azoles, Swamps, and Birds" by Arturo Casadevall et al. Abstract:

The most enigmatic aspect of the rise of Candida auris as a human pathogen is that it emerged simultaneously on three continents, with each clade being genetically distinct. Although new pathogenic fungal species are described regularly, these are mostly species associated with single cases in individuals who are immunosuppressed. In this study, we used phylogenetic analysis to compare the temperature susceptibility of C. auris with those of its close relatives and to use these results to argue that it may be the first example of a new fungal disease emerging from climate change, with the caveat that many other factors may have contributed.

One of the fascinating bits of evidence they cited to substantiate this possibility is this other research:

2005 July: Journal of Thermal Biology: "If you can’t stand the heat, stay out of the city: Thermal reaction norms of chitinolytic fungi in an urban heat island" by M.A. McLean et al.:

Elevated soil and air temperatures in urban heat islands have been exerting evolutionary pressure on organisms for decades in some cities. We measured thermal reaction norms (18–26 °C) for growth rate of four species of common chitinolytic fungi from an oak forest in an urban heat island and a corresponding rural area. Urban isolates of Chrysosporium pannorum and Trichoderma koningii grew faster than rural isolates at 26 °C, but grew slower than rural isolates at 18 °C. Urban isolates of Torulomyces lagena and Penicillium bilaii grew as fast or faster than rural isolates at all temperatures. These differences in thermal reaction norms between urban and rural isolates suggest that urbanization has caused both thermal specialization and counter-gradient variation in the fungal community.

In other words, they are finding that species of fungus in cities are evolving to thrive in urban heat islands.

Why would climate change – global warming – change the evolutionary pressures on a microbe like this, when there's perfectly good very warm spots on earth already? There's a number of possible answers, including that gradualness is providing them the evolutionary on-ramp they needed, or that, as Casadevall suggests, climate change may be changing the behaviors of other organisms around it, changing evolutionary pressure.

For another example, consider the bacterium Vibrio vulnificus – "vulnificus", Latin, "wound-making" – that lives in saltwater ecosystems and infects a variety of organisms, including us. It turns out to already have an interesting relationship to temperature:

2020 Mar 27: Frontiers in Microbiology (journal): "The Effect of the Environmental Temperature on the Adaptation to Host in the Zoonotic Pathogen Vibrio vulnificus" by Carla Hernández-Cabanyero et al:

Interestingly, the severity of the vibriosis in the eel and the human depends largely on the water temperature (highly virulent at 28°C, avirulent at 20°C or below) and on the iron content in the blood, respectively. The objective of this work was to unravel the role of temperature in the adaptation to the host through a transcriptomic and phenotypic approach. [...] Our results suggest that warm temperatures activate adaptive traits that would prepare the bacteria for host colonization (metabolism, motility, chemotaxis, and the protease activity) and fish septicemia (iron-uptake from transferrin and production of O-antigen of high molecular weight) in a generalized manner, while environmental iron controls the expression of a host-adapted virulent phenotype (toxins and the production of a protective envelope). Finally, our results confirm that beyond the effect of temperature on the V. vulnificus distribution in the environment, it also has an effect on the infectious capability of this pathogen that must be taken into account to predict the real risk of V. vulnificus infection caused by global warming.

In other words, warmth doesn't just make V. vulnificus proliferate, it makes it behave differently: it makes it more infectious.

Which isn't to say climate change isn't also just making it proliferate:

2016: PNAS (journal): "Climate influence on Vibrio and associated human diseases during the past half-century in the coastal North Atlantic" by Luigi Vezzulli et al.:

In this study, for the first time to our knowledge, experimental evidence is provided on the link between multidecadal climatic variability in the temperate North Atlantic and the presence and spread of an important group of marine prokaryotes, the vibrios, which are responsible for several infections in both humans and animals. Using archived formalin-preserved plankton samples collected by the Continuous Plankton Recorder survey over the past half-century (1958–2011), we assessed retrospectively the relative abundance of vibrios, including human pathogens, in nine areas of the North Atlantic and North Sea and showed correlation with climate and plankton changes. Generalized additive models revealed that long-term increase in Vibrio abundance is promoted by increasing sea surface temperatures (up to ∼1.5 °C over the past 54 y) and is positively correlated with the Northern Hemisphere Temperature (NHT) and Atlantic Multidecadal Oscillation (AMO) climatic indices (P < 0.001). Such increases are associated with an unprecedented occurrence of environmentally acquired Vibrio infections in the human population of Northern Europe and the Atlantic coast of the United States in recent years.

The effect of climate change on V. vulnificus in the wild is not just due to increased ambient planetary temperatures in a general way, but apparently also specifically to sea level rise and to storms inundating coastal land and bodies of fresh water with sea water:

2020 Mar 1: Environmental Microbiology (journal): "In hot water: effects of climate change on Vibrio–human interactions" by Brett A. Froelich and Dayle A. Daines:

Due to their preference for warm, slightly salty water, the brackish water found in estuaries as well as coastal floodwaters provide significant opportunities for Vibrio spp. growth. In the U.S., the Gulf coast region states of Texas, Alabama, Florida, Mississippi and Louisiana have had the most reported cases of vibriosis (CDC, 2005). For example, when the floodwaters of Hurricane Rita and Katrina receded in October 2005, the number of pathogenic vibrios (V. cholerae, V. vulnificus and V. parahaemolyticus) in samples taken from both Lake Pontchartrain near-shore sites as well as from canals in New Orleans were highly enriched. Twenty-two cases of Vibrio-related illnesses were reported in the 2 weeks following Hurricane Katrina, with five of these resulting in death (Morantz, 2005).

The warming of coastal waters has increased both the temporal range of Vibrio spp. as well as heightened the potential for Vibrio–human interactions, as when waters are warmer, people spend more time recreating at the beach. However, when there is increased flooding, non-recreational contact with Vibrio-containing waters occurs as well.

The increase in strength and number of named storms, such as hurricanes, nor'easters and tropical storms and cyclones due to elevated climatic energy can also affect Vibrio infection risk in a variety of ways. The freshening of coastal systems that result from increased rainfall can extend the boundaries of these pathogens that are normally restricted by fully marine waters (Esteves et al., 2015). Strong winds or storm surge can push the salinity front further upstream than normal, exposing new areas to the non-cholera vibrios, which have a minimal salinity requirement (Fries et al., 2008; Hsieh et al., 2008). Finally, the wind-driven mixing can bring sediments or deeper waters to the surface, potentially exposing those fishing, recreating, or performing rescue operations (Wetz et al., 2008).

2022 Oct 19: NY Post: "Flesh-eating bacteria infects Florida communities ravaged by Hurricane Ian" by Katherine Donlevy:

Florida communities devastated by Hurricane Ian are facing a new threat of flesh-eating bacteria — weeks after the massive storm swept across the state.

As of last Friday, the Sunshine State reported 65 infections of Vibrio vulnificus this year, while there were only 37 cases reported prior to the storm that made landfall on Sept. 28, according to Florida Department of Health data.

Lee County, home to the Ian-ravaged communities of Fort Myers and Sanibel Island, accounts for most new cases of Vibrio vulnificus, which eats away at the flesh in open wounds.

“DOH-Lee is observing an abnormal increase in cases of Vibrio vulnificus infections as a result of exposure to the floodwaters and standing waters following Hurricane Ian,” Lee County Department of Health spokesperson Tammy Soliz told CNN.

“Since September 29, 2022, 26 cases of Vibrio vulnificus associated with Hurricane Ian have been reported to DOH-Lee. All 26 cases had wound infections with exposure to Hurricane Ian floodwaters that occurred from the storm surge entering their homes or during post-storm clean-up. There have been six deaths among Lee County residents.”

At least 11 people in the Sunshine State have died from Vibrio vulnificus infection this year, according to Florida Department of Health data.

A third example are the enteroviruses, the class of virus that includes polio, spread by the oral-fecal route, typically through contaminated water. A recent study found that enteroviruses that evolve more thermotolerance are surprisingly also more resistant to chlorine, one of humanity's primary disinfectants.

2020 Sep 2: Environmental Science & Technology (journal): "Adaptation of Human Enterovirus to Warm Environments Leads to Resistance against Chlorine Disinfection" by Anna Carratalà et al.:

To understand how virus populations evolve under changing environmental conditions, we experimentally adapted echovirus 11 (E11) to four climate regimes. Specifically, we incubated E11 in lake water at 10 and 30 °C and in the presence and absence of sunlight. Temperature was the main driver of adaptation, resulting in an increased thermotolerance of the 30 °C adapted populations, whereas the 10 °C adapted strains were rapidly inactivated at higher temperatures. This finding is consistent with a source–sink model in which strains emerging in warm climates can persist in temperate regions, but not vice versa. A microbial risk assessment revealed that the enhanced thermotolerance increases the length of time in which there is an elevated probability of illness associated with swimming in contaminated water. Notably, 30 °C-adapted viruses also exhibited an increased tolerance toward disinfection by free chlorine. Viruses adapting to warm environments may thus become harder to eliminate by common disinfection strategies.

19.

Another way climate change might increase contact between humans and infectious agents is by an unfortunate bit of time travel: we don't know what infectious agents – possibly from before humans even evolved as a species – might be trapped in artic or antarctic ice or permafrost, still viable once thawed. And the poles are heating faster than the rest of the planet; more and more thawing is happening already.

2021 Jun: Frontiers in Veterinary Science (journal): "Reindeer Anthrax in the Russian Arctic, 2016: Climatic Determinants of the Outbreak and Vaccination Effectiveness" by Elena A. Liskova et al.:

The Yamal Peninsula in the Russian Federation experienced a massive outbreak of anthrax in reindeer (Rangifer tarandus) in July–August 2016, with 2,650 (6.46% of the total susceptible population) animals infected, of which 2,350 died (case fatality rate of 88.67%). In our study, we analyzed climatic and epidemiological factors that could have triggered the outbreak. [...] Abnormally high ambient temperature in the summer of 2016 contributed to the thawing of permafrost and viable Bacillus anthracis spores could have become exposed to the surface; the monthly average air temperatures in June, July, and August 2016 were 20–100% higher than those of the previous 30-year period, while the maximum air temperatures were 16–75% higher. Using the projected climate data for 2081–2100 according to the “worst case” RCP8.5 scenario, we demonstrated that the yearly air temperature may average above 0°C across the entire Yamal Peninsula, while the yearly number of days with a mean temperature above 0°C may rise by 49 ± 6 days, which would provide conditions for reactivation of soil anthrax reservoirs.

2016 Aug 1: The Guardian: "Anthrax outbreak triggered by climate change kills boy in Arctic Circle" by Alec Luhn: "Seventy-two nomadic herders, including 41 children, were hospitalised in far north Russia after the region began experiencing abnormally high temperatures":

A 12-year-old boy in the far north of Russia has died in an outbreak of anthrax that experts believe was triggered when unusually warm weather caused the release of the bacteria.

The boy was one of 72 nomadic herders, including 41 children, hospitalised in the town of Salekhard in the Arctic Circle, after reindeer began dying en masse from anthrax.

Five adults and two other children have been diagnosed with the disease, which is known as “Siberian plague” in Russian and was last seen in the region in 1941.

More than 2,300 reindeer have died, and at least 63 people have been evacuated from a quarantine area around the site of the outbreak.

“We literally fought for the life of each person, but the infection showed its cunning,”the Yamal governor, Dmitry Kobylkin, told the Interfax news agency. “It returned after 75 years and took the life of a child.”

The tabloid LifeNews reported that the boy’s grandmother died of anthrax at a nomad camp last week.

Authorities said the outbreak was linked to climate change. For the past month, the region has been experiencing abnormally high temperatures that have reached 95F.

Anthrax spores can survive in frozen human and animal remains for hundreds of years, waiting to be released by a thaw, according to Alexei Kokorin, head of WWF Russia’s climate and energy programme.

“Such anomalous heat is rare for Yamal, and that’s probably a manifestation of climate change,” he said.

Average temperatures in Russia have increased by 0.43C in the past 10 years, but the rise has been more pronounced in areas of the far north. The warmer climate has begun thawing the permafrost soil that covers much of Russia, including cemeteries and animal burial grounds. Thawing permafrost has also led to greater erosion of river banks where nomads often buried their dead, Kokorin said.

“They didn’t bury deep because it’s hard to dig deep in permafrost,” he explained.

[...]

The disease from thawing human and animal remains can get into groundwater that people then drink. The boy in Salekhard died from the intestinal form of the disease, which typically results in fever, stomach pain, diarrhea and vomiting.

Of course, we don't know what nasty surprises are lurking in the polar regions, nor how virulent they might prove to be. But it turns out there are things we can do to get an estimate – a very vague one – of how likely they are to infect new species if they get out:

2022 Oct 19: Proceedings of the Royal Society B: Biological Sciences (journal): "Viral spillover risk increases with climate change in High Arctic lake sediments" by Audrée Lemieux et al.:

When confronted with a new host, a virus may even infect it and transmit sustainably in this new host, a process called ‘viral spillover’. However, the risk of such events is difficult to quantify. As climate change is rapidly transforming environments, it is becoming critical to quantify the potential for spillovers. [...] We then estimated the spillover risk by measuring the congruence between the viral and the eukaryotic host phylogenetic trees, and show that spillover risk increases with runoff from glacier melt, a proxy for climate change. Should climate change also shift species range of potential viral vectors and reservoirs northwards, the High Arctic could become fertile ground for emerging pandemics.

This research is discussed here:

2022 Oct 19: Phys.org: Climate change may boost Arctic 'virus spillover' risk by Sara Hussein:

A warming climate could bring viruses in the Arctic into contact with new environments and hosts, increasing the risk of "viral spillover", according to research published Wednesday. [...]

Scientists in Canada wanted to investigate how climate change might affect spillover risk by examining samples from the Arctic landscape of Lake Hazen. [...]

The team sampled soil that becomes a riverbed for melted glacier water in the summer, as well as the lakebed itself [...] "This enabled us to know what viruses are in a given environment, and what potential hosts are also present," said Stephane Aris-Brosou, an associate professor in the University of Ottawa's biology department, who led the work.

But to find out how likely they were to jump hosts, the team needed to examine the equivalent of each virus and host's family tree.

"Basically what we tried to do is measure how similar these trees are," said Audree Lemieux, first author of the research.

Similar genealogies suggest a virus has evolved along with its host, but differences suggest spillover.

And if a virus has jumped hosts once, it is more likely to do so again.

The analysis found pronounced differences between viruses and hosts in the lakebed, "which is directly correlated to the risk of spillover," said Aris-Brosou.

The difference was less stark in the riverbeds, which the researchers theorise is because water erodes the topsoil, removing organisms and limiting interactions between viruses and potential new hosts.

Those instead wash into the lake, which has seen "dramatic change" in recent years, the study says, as increased water from melting glaciers deposits more sediment.

"That's going to bring together hosts and viruses that would not normally encounter each other," Lemieux said.

That said,

The authors of the research [...] caution they are neither forecasting an actual spillover nor a pandemic.

"The likelihood of dramatic events remains very low," Lemieux said.

They also warn more work is needed to clarify how big the difference between viruses and hosts needs to be to create serious spillover risk.

But they argue that warming weather could increase risks further if new potential hosts move into previously inhospitable regions.

"It could be anything from ticks to mosquitoes to certain animals, to bacteria and viruses themselves," said Lemieux.

"It's really unpredictable... and the effect of spillover itself is very unpredictable, it can range from benign to an actual pandemic."

The team wants more research and surveillance work in the region to understand the risks.

"Obviously we've seen in the past two years what the effects of spillover can be," said Lemieux.

20.

Finally, while our species is, as I explained in Part 1 and Part 2, in an exceptionally bad position for a species to be in confronting elevated infectious threats, ours is not the only species vulnerable to the effects of climate change on infectious diseases.

Hitherto I have only discussed diseases that infect humans. But we humans, like all animals, are dependent on other living beings for nutrients.

Climate change does not only impact diseases that infect humans. Climate change impacts diseases that infect the living things we eat.

You're probably aware of the threat of infectious diseases to animals we eat – our livestock. Certainly you've heard of the risk of bird flu and swine flu.

You're probably haven't much thought about how there are also diseases that attack plants – including our crops.

These plant diseases can't usually infect us, but they can poison us and they can kill our crops dead in the field such that we never get to eat them.

2013 Oct 30: New Phytologist (journal): "Rust fungi and global change" by Stephan Helfer:

Evidence obtained since the middle of last century suggests that reported threats to plant health as a result of new disease outbreaks have been increasing (Fletcher et al., 2010; Black, 2013). Google Scholar search hits for new reports on plant disease number 512 for the 30 yr from 1961 to 1990 and more than three times as many (1670) in the 22 yr from 1991 to 2012. Rust fungi feature in at least six and 39 of these reports, respectively, representing a ninefold annual increase. [...]

Many of these new occurrences are attributable to introductions through the movement of infected plants, rather than to natural extension of the range because of climate change. Occasionally they represent pathogen organisms new to science.

However, preliminary data suggest an additional role for climate change in the provision of new suitable climate space for disease incidence, leading to range extension (Desprez-Loustau et al., 2007a), as well as facilitated natural dispersal of plant pathogens, possibly through the occurrence of extreme weather events (Rosenzweig et al., 2001; Fletcher et al., 2010).

2013 Sept 1: Nature Climate Change (journal): "Crop pests and pathogens move polewards in a warming world" by Daniel P. Bebber, Mark A. T. Ramotowski & Sarah J. Gurr:

Global food security is threatened by the emergence and spread of crop pests and pathogens. Spread is facilitated primarily by human transportation, but there is increasing concern that climate change allows establishment in hitherto unsuitable regions. However, interactions between climate change, crops and pests are complex, and the extent to which crop pests and pathogens have altered their latitudinal ranges in response to global warming is largely unknown. Here, we demonstrate an average poleward shift of 2.7±0.8 km yr−1 since 1960, in observations of hundreds of pests and pathogens, but with significant variation in trends among taxonomic groups. Observational bias, where developed countries at high latitudes detect pests earlier than developing countries at low latitudes, would result in an apparent shift towards the Equator. The observed positive latitudinal trends in many taxa support the hypothesis of global warming-driven pest movement.

About this article, a news article (not a journal article) at Nature explains:

2013 Sept 1: Nature: "Crop pests advancing with global warming" by Eliot Barford:

Global movement of crop pests had never been comprehensively analysed. To fill this gap, Bebber and his colleagues made use of historical records held by CABI (formerly known as the Centre for Agricultural Bioscience International), which document crop pests and diseases around the world from 1822 to the present. “No one has looked at any of these datasets. This is the first such analysis,” says co-author Sarah Gurr, a plant pathologist also at Exeter.

Co-author Mark Ramotowski, who did his work as a student at the University of Oxford, UK, narrowed the CABI sample down from over 80,000 records to 26,776, focusing on the period since 1960, when they are ilkely most reliable. For 612 different pest species, the researchers identified the first year in which each was observed in a new country (or region for larger countries) and took that to be the date at which the pest reached that country or region’s average latitude.

The main vulnerability of their study was biases in the data. The group hypothesised that, in the absence of any real trend, pests would appear to be moving towards the equator rather than the poles. This is because wealthier countries have the scientific resources to detect pests earlier than others, and wealthier countries tend to be at higher latitudes. As countries develop and study their pests better, the pests’ range could appear to move into the tropics.

Instead, the team found that, on average, crop pests have been moving towards the poles at 2.7 kilometres per year, which is very close to the rate of climate change5. However, the rate of shift varied significantly for different groups and among individual species. [...]

“Many studies have shown that climate change is affecting the distribution of wild species populations. This is the first one to show that a similar process is happening in pest species,” says Gurr. She highlights the worrying finding that fungi and oomycetes are moving particularly quickly, at 7 and 6 km per year respectively.

---

The Great Age of Plagues
Table of Contents

• 0. Intro
• 1. Population
• 2. COVID-19
• 3. Climate Change
• 4. Climate Change, II – You are here
• 5. Conclusion

---

This post brought to you by the 166 readers who funded my writing it – thank you all so much! You can see who they are at my Patreon page. If you're not one of them, and would be willing to chip in so I can write more things like this, please do so there.

Please leave comments on the Comment Catcher comment, instead of the main body of the post – unless you are commenting to get a copy of the post sent to you in email through the notification system, then go ahead and comment on it directly. Thanks!