Amphibian Chytrid Crisis: A Deep Dive into a Deadly Disease

Guest post by Tristan Williams, MEnvSc Candidate at the University of Toronto-Scarborough

We currently live in an era of mass extinction, where many species around the world are at high risk of being lost forever, and among these species, amphibians are at much higher risk of extinction than any other (Wake and Vrendenburg, 2008). This comes from a combination of many factors, including climate change, habitat destruction and human land use, the presence of invasive species, and as we’ll be looking at here: the fungal infection chytridiomycosis.

Chytridiomycosis is a skin disease caused by a chytrid fungus, either Batrachochytrium dendrobatidis (Bd), or Batrachochytrium salamandrivorans (Bsal). Though these fungi may be small, they are a big deal when it comes to the health and stability of amphibian populations. They have been implicated for the heavy decline or even outright extinction of a large number of amphibian species, making it potentially the most impactful wildlife disease known (Scheele et al., 2014). These fungi have a number of traits that make it easy for them to spread to amphibians. One such trait is the ability to reside within a host without causing infection, using it as a reservoir from which it can spread to more vulnerable species (Fisher, 2017). This can be seen in the example of the midwife toad and alpine newt, which are carriers for Bsal, and can lead to infection of fire salamander populations.

Figure 1: Potential pathways for the spread of Bsal in Europe, from Fisher 2017.

The zoospores of these fungi also have two forms which contribute to their spread among amphibian population. The first is the motile aquatic form, which allows them to establish infection during the tadpole stage (Fisher, 2017). The second is the non-motile form, called an encysted spore, which has a thick cell wall, and are highly resilient. These encysted spores are capable of persisting in the environment while retaining their infectiousness, without needing a host at all for a long period of time. And if that wasn’t enough, it could be the case that birds can act as carriers for these encysted spores, bringing the fungus to new locations and further contributing to the spread of disease over larger distances. As noted by Fisher et al. (2017), it really does seem like amphibians really are in peril from a perfect pathogen. But what exactly do these fungal infections do to amphibians that make it such a problem?

Amphibians are cutaneous respirators. They “breathe” through their skin, allowing them to maintain the correct osmotic balance of electrolytes and water within the body. This is what makes chytrid fungi such a unique threat to amphibians. To other organisms the development of a cutaneous chytrid infection is usually not a big deal, but to amphibians it can directly interfere with their ability to respire (Voyles et al., 2009). The ensuing loss of electrolytes impairs the ability of the heart to function, blood flow to the rest of the body is reduced, and cardiac arrest leads to death as a result of complete collapse of the circulatory system. However, even before that occurs, the now physically impaired and lethargic individual is likely to become a victim of predation or a combination of other stressors as well. As an example of the potential severity of this disease, fire salamanders in the Netherlands that were infected with Bsal experienced a mortality rate of over 96% (Fisher, 2017). A very morbid and unfortunate situation our amphibian friends find themselves in.

Normally, the mucus layer present on the skin of amphibians contains a number of antimicrobial peptides and lysozymes, as well as symbiotic bacteria which all contribute to innate defenses against invading pathogens (Rollins-Smith et al., 2011). Amphibians have also shown to be capable of developing an acquired immune response to chytrid fungi after exposure, with some even developing Bd specific antibodies. So then why is chytridiomycosis such a problem for amphibians? The answer appears to be because chytrid fungi are capable of suppressing immune responses in many species before these defenses are capable of protecting against infection (Ellison et al., 2014). Other environmental stressors can also interfere with the ability of amphibians to mount an appropriate immune defense. Lack of food resources, temperature stress, or exposure to chemicals like pesticides can all increase the likelihood of fungal infection (Rollins-Smith et al., 2011). Furthermore, the amphibian life cycle itself can impair the ability of an individual to resist infection. When a tadpole undergoes metamorphosis into an adult, the immune system also goes through a drastic transition to maturity. This period of time provides an opening for infection to develop while the defenses of the amphibian aren’t at full capacity. Ultimately, this means that the ability for a species of amphibian to defend against chytrid fungi varies heavily based on the level of innate and acquired defenses mounted, the health of the habitat, the climate, and what part of the life cycle the species in question is in.

 It is abundantly clear that amphibian populations are in great danger as a result of this disease outbreak, so the obvious follow-up question is what can we do about this ongoing threat? While there is no silver bullet for stopping chytridiomycosis outright, there are a number of potentially promising forms of intervention that could help to bring mortality rates down to less extreme levels. In short-term or small scales, the direct treatment of individuals with antifungals is shown to be an effective method of temporarily controlling an outbreak, but more long-term measures are needed to ensure success in restoring populations (Garner et al., 2016). Scheele et al. (2014) provide a framework of three potential classes of action to protect amphibians from fungal infection. The first class is Environmental Manipulation. As mentioned previously, there are a number of environmental factors that influence the chance of successful infection. Reducing the presence chemical pollutants can reduce stress on amphibian populations are lower infection rates. The creation of warm regions in the habitat, such as warm pools of water, areas of high sun exposure to bask in, or the introduction of artificial heat sources can also allow species to initiate behavioural fever, raising their body temperature to levels that are no longer ideal for chytrid fungi to survive. Finally, methods such as bio-augmentation, which involves introducing microbes with the ability to inhibit chytrid fungi to the environment, can potentially provide an ecosystem-wide treatment, so long as proper testing is done to ensure that this will not negatively impact the environment in any way. 

Artificial ponds for the captive breeding of the endangered Pseudophryne corroboree.

(Figure 2 from Scheele et al., 2014)

When manipulation is not a reasonable solution, the Amphibian Introduction class is next in line. This involves the translocation of amphibian populations to refugia: environments that are ideal for the species, but poor for chytrid fungus. This method does require that it is ensured that this translocation will not cause any impacts in the new environment. Alternatively, captive bred amphibians can be added to wild populations in order to increase the buffering capacity of the ecosystem, allowing higher likelihood of survival for a population even after an chytrid epidemic. Finally, failing the previous two classes, the last class is Ex-Situ Conservation, which involves keeping colonies in captivity. Infected individuals are treated with chemicals or heat to kill the fungus, and individuals are bred in order to improve resistance among the population while maintaining genetic diversity (Scheele et al. 2014).

While these treatments are still in development and have not been used in proper field tests yet, they definitely have the potential to rescue amphibian populations. However, the fact remains that many amphibians around the world are critically imperilled, so there is clear need for feasibility research as soon as possible if we want to prevent any more extinctions. The loss of mass amounts of amphibians could lead to huge impacts on many ecosystems around the world, and it is all but guaranteed to happen unless we take action.

Literature Cited:

Ellison AR et al. 2014. Fighting a Losing Battle: Vigorous Immune Response Countered by Pathogen Suppression of Host Defenses in the Chytridiomycosis-Susceptible Frog Atelopus zeteki. G3-Genes Genom Genet 4(7): 1275-1289.

Fisher MC. 2017. Ecology: In peril from a perfect pathogen. Nature 544(7650): 300-301.

Garner TWJ et al. 2016. Mitigating amphibian chytridiomycoses in nature. Philos T Roy Soc B 371(1709).

Rollins-Smith LA et al. 2011. Amphibian Immune Defenses against Chytridiomycosis: Impacts of Changing Environments. Integr Comp Biol 51(4): 552-562.

Scheele BC et al. 2014. Interventions for Reducing Extinction Risk in Chytridiomycosis-Threatened Amphibians. Conserv Biol 28(5): 1195-1205.

Voyles J, et al. 2009. Pathogenesis of Chytridiomycosis, a Cause of Catastrophic Amphibian Declines. Science 326(5952): 582-585.

Wake DB and Vredenburg VT. 2008. Are we in the midst of the sixth mass extinction? A view from the world of amphibians. P Natl Acad Sci USA 105(1): 1466-1473.

Culling Koalas for Conservation

Guest post by Stefanie Thibert, who is currently enrolled in the Professional Masters of Environmental Science program at the University of Toronto-Scarborough

Euthanizing diseased koalas may be the most effective management strategy to save koalas from extinction in Queensland. A recent study published in the Journal of Wildlife Disease suggests that if 10% of terminally diseased and sterile koalas were culled while other infected koalas were treated with antibiotics, chlamydial infections could be completely eliminated and population sizes could increase within four years. 

The beloved koala relaxing in a eucalyptus tree
(Source:http://www.onekind.org/be_inspired/animals_a_z/koala/) 

Although koalas are under pressure from habitat degradation, dog attacks and road accidents, disease burden is the largest threat to its population sizes. It is estimated that 50% of the current koala population in South-East Queensland is infected with the Chlamydia spp. The sexually transmitted disease causes lesions in the genitals and eyes, leading to blindness, infertility, and ultimately death. Rhodes et al. (2011) suggest that reversing the observed population decline in Queensland koalas would require either entirely eliminating deaths from cars and dogs, complete reforestation, or reducing deaths caused by Chlamydia by 60%. It is clear that the best conservation tool is to reduce the prevalence of chlamydial infection.

In the study, Wilson et al. (2015) examined the potential impact of euthanizing koalas infected with Chlamydia. As shown in Figure 1, computer simulation models were used to project koala population sizes based on four separate intervention programs: “no intervention”, “cull only”, “treat only”, and “cull or treat”. In the “cull or treat” program, sterile and terminal koalas were euthanized, while infected kolas that were not sterile or terminal were treated with antibiotics. It was concluded that the “cull or treat” is the most successful intervention program for increasing long-term population growth and eliminating chlamydial infections. 

The projected numbers of koalas in the Queensland population under different intervention programs.(From Wilson et al. 2015)

Without intervention, it is estimated that merely 185 koalas will persist in 2030. Under both the “cull only” and “treat only” intervention, it would take seven years before there would be greater koalas numbers than there would be without intervention. Under the “cull or treat” program, the population size was projected to overtake the no-intervention population after four short years. The population size in 2030 is also greatest under the “cull or treat” intervention. The increase in koala numbers in the “cull or treat” strategy is due to the considerable decrease in the prevalence of Chlamydia.

As expected, the proposal received considerable attention and was scrutinized by the public. Some argue that it is inhumane, while others suggest alternative management strategies. However, when it comes down to it, the science is clear. Euthanizing can be done in a humane way, and it is the most effective method for conservation of the species. The only real alternative to culling is treatment with antibiotics, which is costly, requires an immense amount of monitoring, and has been shown to take much longer to eliminate the disease and increase population sizes.

The question we must ask ourselves is: we cull other species, so why not koalas? For instance, in the United States, the culling of four million cattle successfully prevented bovine tuberculosis from spreading to humans. Even when based on sound scientific research, culling has always been dismissed as a management option for the iconic Australian marsupial. In 1997, culling was suggested as a method to protect the overabundant koala population on Kangaroo Island, but sterilization and relocation was used instead. It is amazing that a program that was significantly more expensive and less effective was chosen because the public could never think of killing the adorable and innocent koala.

Managing koala populations is clearly a case in which science intersects with emotion. However, it is essential that we put our emotions aside, and make a decision that is based on scientific evidence. Let us remember that the study only suggests culling or treating 10% of the population each year, which is equivalent to approximately 140 koalas. It is also important to improve the communication of science to the public. It needs to be made abundantly clear that without culling, the koala populations will continue to decrease.

To read the full article visit: http://www.bioone.org/doi/full/10.7589/2014-12-278 

References:

Oliver, M. (2015, October, 20). Proposal to euthanise koalas with chlamydia divides experts. The Guardian. Retrieved from: http://www.theguardian.com/world/2015/oct/20/proposal-to-euthanise-koalas-with-chlamydia-divides-experts.

Olmstead, A.L., & Rhode, P.W. (2004). An impossible undertaking: The eradication of bovine tuberculosis in the United States. Journal of Economic History, 64, 734-772.

Rhodes, J.R., Ng, C.F., de Villiers, D.L., Preece, H.J., McAlpine, C.A., & Possingham, H.P. (2011). Using integrated population modeling to quantify the implications of multiple threatening processes for a rapidly declining population. Biological Conservation, 144, 1081–1088.

Wilson, D., Craig, A., Hanger, J., & Timms, P. (2015). The paradox of euthanizing koalas to save populations from elimination. Journal of Wildlife Diseases, 51, 833-842.


Does context alter the dilution effect?

Understanding disease and parasites from a community context is an increasingly popular approach and one that has benefited both disease and ecological research. In communities, disease outbreaks can reduce host populations, which will in turn alter species' interactions and change community composition, for example. Community interactions can also alter disease outcomes - decreases in diversity can incr-

Frogs in California killed by the chytrid fungus
(source: National Geographic News)

ease disease risk for vulnerable hosts, a phenomenon known as the dilution effect. For example, in a high diversity system, a mosquito may bite individuals from multiple resistant species as well as those from a focal host, potentially reducing the frequency of focal host-parasite contact. Hence the dilution effect may be a potential benefit of biodiversity, and multiple recent studies provide evidence for its existence.

Not all recent studies support this diversity-disease risk relationship, however, and it is not clear whether the dilution effect might depend on spatial scale, the definition of disease risk used, or perhaps the system of study. A recent paper in Ecology Letters from Alexander Strauss et al. does an excellent job of deconstructing the assumptions and implicit models behind the dilution effect and exploring whether context dependence might explain some of the variation in published results. The authors develop theoretical models capturing hypothesized mechanisms, and then use these to predict the outcomes of mesocosm experiments.

Suggested mechanisms behind the dilution effect include 1) that diluter species (i.e. not the focal host) reduce parasite encounters for focal hosts, with little or no risk to themselves (resistant); and 2) diluters may compete for resources or space against the focal host and so reduce the host population, which should in turn reduce density dependent disease risk. But, if these are the mechanisms, there are a number of corollaries that should not be ignored. For example, what if the diluter species is the poorer competitor and so competition reduces diluter populations? What if diluter species aren't completely resistant to disease and at large populations are susceptible? The cost/benefit analysis of having additional species present may differ depending on any number of factors in a system.

The authors focus on a relatively simple system - a host species Daphnia dentifera, a virulent fungus Metschnikowia bicuspidata, and a competitor species Ceriodaphnia sp.. Observations suggest that epidemics in the Daphnia species may smaller where the second species occurs - Ceriodaphnia removes spores when filter feeding and also competes for food. By measuring a variety of traits, they could estimate the R* and R0 values - roughly, low R* values indicated strong competitors and high  R0 values indicated groups that have high disease transmission rates. Context dependence is introduced by considering three different genotypes of the Daphnia: these genotypes varied in R* and R0 values, allowing them to test whether changing competitive ability and disease transmission in the Daphnia might alter the strength or even presence of a dilution effect. Model predictions were then tested directly against matching mesocosm experiments.

The results show clear evidence of context dependence in the dilution effect (and rather nice matches between model expectations and mesocosm data). Three possible scenarios are compared, which differ in the Daphnia host genotype and its competitive and transmission characteristics. 

1. Dilution failure: the result of a host genotype that is a strong competitor, and a large epidemic (low R*, high R0). 
2. Dilution success: the result of a host that is a weak competitor and a moderate epidemic (host has high R*, moderate R0). 
3. Dilution irrelevance: the outcome of a host that is a weak competitor, and a small epidemic (high R*, low R0). 

From Strauss et al. 2015. The y-axis shows percent host population infected, solid lines show the disease prevalence without the diluter; dashed show host infection when diluter is present.

Of course, all models are simplifications of the real world, and it is possible that in more diverse systems the dilution effect might be more difficult to predict. However, as competition is a component of most natural systems, its inclusion may better inform models of disease risk. Other models for other systems might suggest different outcomes, but this one provides a robust jumping off point for future research into the dilution effect.

Alexander T. Strauss, David J. Civitello, Carla E. Caceres and Spencer R. Hall. 2015. Success, failure and ambiguity of the dilution effect among competitors. Ecology Letters. 18: 916–926. 

Why greater diversity – even of parasites – might decrease infections

Pieter T. J. Johnson, Daniel L. Preston, Jason T. Hoverman, and Bryan E. LaFonte. 2013. Host and parasite diversity jointly control disease risk in complex communities. PNAS. Early view.

(Host competence - the tendency of host species to become infected and maintain infection.)

There is often a disconnect between the reality that communities and ecosystems are diverse assemblages with numerous, often complicated and variable interactions, and ecological research, which (perhaps necessarily) focuses on interactions between at most two or three species at a time. Disease ecology similarly has often considered interactions between particular host/parasite species pairs. Some researchers have considered the diversity of host species as an important factor in explaining disease transmission and mortality, but the reality is that parasites also interact, and most hosts harbour multiple parasites. Studying disease dynamics in the context of multi-parasite, multi-host interactions is increasingly recognized as key to understanding disease transmission and severity in communities.

With this in mind, a new paper from Pieter Johnson and colleagues attempts to combine research into the effects of both parasite and host diversity on disease. Two possible hypotheses predict the effect of diversity on disease transmission: the ‘dilution effect’ suggests that the presence of multiple hosts should decrease transmission risk, if the result of additional species is a decline in community competence. It is also hypothesized, somewhat contradictorily, that increased host diversity should support a greater variety of parasites, and parasite life cycles. Both these hypotheses take a host-centric view: understanding how changes in host diversity alter disease risk also requires that we understand how changes in parasite diversity affect disease transmission.

Mutations caused by Ribeiroia infection.
From:http://www.nature.com/scitable/knowledge/library/ecological-consequences-of-parasitism-13255694

The authors looked at the contribution of host and parasite diversity to parasite transmission success using field data and laboratory experiments. First, they looked at existing data on infections of the pathogenic trematode Ribeiroia ondatrae, in amphibian species. Observations showed a positive correlation between larval trematode diversity (parasites) and the richness of free-living species (hosts). Of course the two diversities might be correlated for many unrelated reasons, like site isolation, evolutionary history, or habitat productivity. But a closer analysis showed what appeared to be an interaction between Ribeiroia infection in Pseudacris regilla (Pacific tree frog, the most common amphibian in the survey) and the total number of amphibian species at a site (figure below). Infection by Ribeiroia was highest when there was low amphibian richness and low parasite richness. It dropped significantly lower when amphibian richness was high and/or parasite richness was high.

From Johnson et al. 2013 PNAS. Results of field observations.

In addition to these observations, the authors manipulated both parasite and host species richness, first in small laboratory microcosms and then in larger and more realistic outdoor mesocosms. Results from the laboratory microcosms showed that increases in both amphibian richness (one vs. three species) and parasite richness (one vs. five species) reduced the average number of Ribeiroia in Pseudacris regilla as well as the total infection rate in the amphibian community. The mesocosms had similar results, with both host and parasite diversity negatively influencing Ribeiroia infection. In support of the generality of these results, effect sizes were comparable between the two experiments. These effects were also quite large: for example, in the mesocosm high-host, high-parasite richness treatment there were 52.4% fewer Ribeiroia per P. regilla and 38.2% fewer Ribeiroia overall compared to the low-host, low-parasite richness. Clearly multi-species interactions are crucial for understanding infection by Ribeiroia.

From Johnson et al. 2013 PNAS. Results of the microcosm and mesocosm experiments,
 showing the effects of host and parasite diversity on transmission.

The results make it clear that if you want to understand disease transmission in communities, both host and parasite diversity should be considered. To some extent, both of the initial hypotheses were supported – host and parasite diversity were correlated in the wild, but (in agreement with the dilution effect) infection rates declined as host diversity increased. One factor missing from these hypotheses is the dynamics of the parasite community: in the paper, the authors found models of transmission that included both host and parasite richness were superior. Further, past and future studies that consider only host richness may be inadvertently accounting for the effects of parasite richness on transmission as well, if those two host and parasite diversities are correlated.

There are a number of possibilities for why both host and parasite communities alter parasite transmission success. If host diversity changes the susceptibility of the community to infection (i.e. as diversity increases, the number of low competence/susceptible species increases) then low-competence hosts could act as sinks for parasite infections. Increases in parasite diversity could result in inter-parasite competition and interactions via host immunity.

One future step will be to move beyond simple measurements of species richness to understanding how species identity or characteristics are tied to the putative mechanisms. For example, how do communities of host species vary from low to high diversity sites? Do sites in fact tend to assemble with increasing numbers of low competence host species? The implications are also of interest to other types of studies of community ecology – after all, host-parasite interactions are not very different from predator-prey interactions, and similarly, despite knowing that interactions are complex and involve multiple species, we tend to focus on two or three species examples.

New Tool Reveals Where Ticks Eat Breakfast

You have a much greater chance of getting sick from a tick bite today than you did 30 years ago. But a new tool might allow researchers to better understand why more ticks are making people sick.

“If you’re a health inspector and a bunch of people get food poisoning, the first thing you’d want to know is where they ate last. If you’re a disease ecologist and a bunch of ticks have a pathogen, the first thing you’d want to know is where the ticks ate last,” said Brian Allan, a post-doctoral researcher at the Tyson Research Station in St. Louis.

Allan led a team of researchers in developing a novel technology that probes the genetic contents of ticks’ gut. The tool can determine which wildlife species provided the tick’s last meal and which pathogens came along with that meal.

In the first study to use the new technology, Allan and his colleagues focused on several rapidly emerging diseases transmitted by the lone star tick. These include two pathogens responsible for a potentially fatal bacterial infection known as ehrlichiosis [ur-lick-ee-oh-sis]. In Missouri, over 200 cases of ehrlichiosis were documented last year.

Allan et al.'s study showed that about 80 percent of pathogen-positive ticks had fed on white-tailed deer. They also found that squirrels and rabbits were capable of infecting ticks at a higher rate than deer. However, since the lone star tick feeds on squirrels and rabbits less frequently, they account for a smaller percentage of infection.

Allan and his colleagues hope that the technique will shed light on theoretical questions in the field of ecology. They are especially interested in testing whether biodiversity is good for your health, a hypothesis known as “the dilution effect.”

Allan, B. F., L. S. Goessling, G. A. Storch, and R. E. Thach. 2010. Blood meal analysis to identify reservoir hosts for Amblyomma americanum ticks. Emerging Infectious Diseases 16: 433-440. DOI: 10.3201/eid1603.090911

Parasite competition enhances host survival

Contracting a parasite is bad. But is getting colonized by multiple parasitic species worse? This is an interesting and important question. The host is a resource, which can support a limited number of parasitic individuals, and so how does competition affect parasitic species and host mortality?
This was the premise of a recent paper by Oliver Balmer and colleagues, studying trypanosome infection of mice hosts. They engineered two transgeneic strains of the protozoan parasite, Trypanosoma brucei (African sleeping sickness), to fluoresce different colors in order to assess infections. They infected mice with each strain separately and together and measured host survival and parasite density.

They found that when both strains were present, they competitively suppressed each other and that the level of suppression depended on the initial density of each strain. One of the strains was more virulent than the other, and infection by both strains reduced mortality by 15% compared to infection by the virulent strain only. This is due to the suppression of the virulent strain by the low virulent strain.

The authors argue that strain source and intraspecific genetic diversity can have an important effect on host mortality. I would also argue that understanding interspecific interactions and within-host niche differences, would also be critical.

What a cool use of molecular technology to test basic hypotheses about disease ecology.

Balmer, O., Stearns, S., Schötzau, A., & Brun, R. (2009). Intraspecific competition between co-infecting parasite strains enhances host survival in African trypanosomes Ecology, 90 (12), 3367-3378 DOI: 10.1890/08-2291.1

Climate change increases West Nile Virus outbreaks in the U.S.

According to a study recently published in Environmental Health Perspectives, climate change has increased the prevalence of West Nile Virus infections in the United States. In one of the largest surveys of West Nile Virus cases to date, the authors find a correlation between increasing temperature and rainfall and outbreaks of the mosquito-borne disease between 2001 and 2005. Because warming weather patterns and increasing rainfall are both projected to accelerate with global warming, the authors predict that climate change will exacerbate West Nile Virus outbreaks in the future.

In the study, Dr. Jonathan Soverow and his collaborators matched more than 16,000 confirmed West Nile cases in 17 states to local meteorological data.

Warmer temperatures had the greatest effect on outbreaks. By extending the length of the mosquito breeding season and decreasing the amount of time it takes mosquitoes to reach their adult, biting stage, warmer weather means more biting mosquitoes longer. Moreover, increasing temperature speeds multiplication of the virus within insects, so mosquitoes in warmer climates have a greater viral load, making them more likely to infect humans.

Increased precipitation was also correlated with higher rates of West Nile Virus infection. A single, heavy rainstorm resulting in two or more inches of rain increased infection rates by 33%, while smaller storms had less of an effect on infection rates. Heavier rainfall events can increase disease prevalence by creating pools of water in which mosquitoes can breed and by increasing humidity, which stimulates mosquitoes to bite and breed. Total weekly rainfall had a smaller but significant effect on West Nile Virus infections, with an increase of 0.75 inch of rain/week increasing the number of infections by about 5%.

Warmer, wetter weather patterns might expand the niches of the mosquito species that carry West Nile Virus. In California, for instance, several mosquito species carrying the West Nile Virus have extended their ranges into higher elevations and coastal areas as temperatures have warmed. Changing weather patterns might also affect certain species of birds that are reservoirs for West Nile Virus. For example, droughts can push bird populations into urban areas, making West Nile Virus outbreaks in human populations more likely.

Soverow, J.E., G.A. Wellenius, D.N. Fisman, and M.A. Mittleman. 2009. Infectious disease in a warming world: How weather influenced West Nile Virus in the United States (2001-2005). Environmental Health Perspectives. Online 16 March 2009 DOI: 10.1289/ehp.0800487

Grazers chew, cereal gets sick

Managing plant disease is a major part modern agricultural practice, so it is important to understand the basic ecological dynamics of plant diseases. Some theoretical studies have found that the prevalence of plant diseases can be affected by the amount of herbivory in a system. Given that human land-use and the removal of top predators from many ecosystems has fundamentally changed the abundance and distribution of many herbivores, the repercussions of herbivory can have important cascading consequences throughout foodwebs –including disease dynamics. In the first experimental study of the interaction between herbivory and plant disease, the forthcoming paper in PNAS by Elizabeth Borer and colleagues, shows that increased exposure to large herbivores (e.g., mule deer) resulted in higher disease prevalence in the plant community. The disease they studied, barley and cereal yellow dwarf virus (shown in the photo), is transmitted by aphids, so herbivory does not cause increased transfer. Rather, herbivores changed community composition resulting in higher abundances of very susceptible species, creating a feedback where higher abundances resulted in higher infection rates due to a larger pool of potential hosts near by. These results are important for two reasons. First, this particular virus is an important agricultural disease. Secondly, we need to take a whole-community approach to understanding disease dynamics because these dynamics are not only a property of host-vector-pathogen interactions, but are subject to direct and indirect effects from interactions with other community members.

E. T. Borer, C. E. Mitchell, A. G. Power, E. W. Seabloom (2009). Consumers indirectly increase infection risk in grassland food webs Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0808778106