Forest conservation and restoration to reduce human diarrheal disease

In the NCEAS SNAPP Ecological Levers for Health working group, we’re collecting examples of local or regional interventions that can have direct, measurable benefits for human health (via reduced infectious disease) AND the environment – win–win solutions. The case studies that we’ve collected thus far are so cool that we just can’t wait to share them! In September, I shared a story about vulture conservation and rabies. This week, I’ll tell you about plants and diarrheal disease.

Two years ago, I adopted a tiny blue Aussie puppy: a wild, brilliant beast with a thirst for adventure… and water. I mean he really likes water – jumping in it, biting it, blowing bubbles in it, fishing sticks out of it, etc. And the dirtier that water is, the better. So I set my puppy loose at the duck pond at our local gem of a dog park, where I had seen my previous dog and dozens of other dogs safely drink the water. Days later, my precious puppy developed severe diarrhea, and just hours after the onset of his symptoms, he became terrifyingly lethargic. The enteric pathogens that he had guzzled in the pond water might have killed him if we had not immediately sought out veterinary care. But fortunately, antibiotics and rehydration allowed Carrot to make a full recovery, and he grew up to be the healthy mud monster pictured below. From that experience, I re-learned an important lesson from disease ecology: pathogens often have minimal effects on adult animals, which have developed resistance/immunity during prior exposure, but the same pathogens can be deadly for juveniles during their first exposure.

This principle doesn’t just apply to puppies: diarrheal disease is the second leading cause of global childhood mortality for children under five years old. That’s hundreds of thousands of children dying every year because they did normal childhood things – like eating, drinking, and playing outside – and became infected by waterborne or foodborne pathogens like rotaviruses, Vibrio cholerae, and Salmonella. Many more children become infected by these pathogens and survive their illnesses, only to experience lasting physiological impacts. For instance, diarrhea leads to malnourishment, and malnourishment increases a child’s risk of future infection and diarrhea, creating a vicious cycle of ill health that can retard physical and mental development.

How can we remedy this huge global burden of childhood morbidity and mortality? The good news is that we already have substantially reduced the global impacts of childhood diarrheal disease by (1) improving hygiene and sanitation to reduce peoples’ exposure to the pathogens and (2) using oral rehydration therapy to treat children who are suffering from diarrhea, so that they do not die from dehydration. However, millions of people still lack access to clean water resources and quality healthcare, and an unthinkable number of children are still dying each year, and thus there is still much to do. Today, I want to broaden the scope of potential solutions: are there ecological solutions that can help reduce human exposure to enteric pathogens as a complement to current public health efforts?

But before we discuss specific ecological solutions, it’s worth discussing how these pathogens enter and persist in water sources in the first place. In some cases, the pathogens are pumped into public water sources directly from sewage pipes or human bodies (e.g., people swimming and defecating at water access points). In other cases, the pathogens reach public water sources via runoff from the environment after they’ve been excreted by humans and/or animals. When these pathogens reach a waterbody, they do not necessarily find and infect a human. For instance, if the pathogen is buried under the sediment in a stream, degraded by sunlight, consumed by microorganisms, or destroyed by plant biocides, it will never reach a human host. So ideally, ecological solutions will reduce the number of pathogens reaching waterbodies and/or increase pathogen death rates in those waterbodies. With this in mind, let’s talk about one class of ecological solutions for waterborne enteric pathogens: can plants be a win–win solution for conservation and human health?

In my freshmen year as an undergrad, my favorite professor made us “draw and describe, in excruciating detail, the difference between an urban and rural hydrograph.” I received full marks, so let’s assume I’m an expert: in urbanized areas with lots of buildings and paved, impervious surfaces, stormwater reaches streams and rivers quickly, whereas in rural areas with lots of trees and permeable soil, stormwater reaches streams and rivers relatively slowly (see below). And of course, it isn’t just water that reaches those streams and rivers. In urban environments, pollutants and pathogens within the stormwater also make it to downstream waterbodies faster, meaning that fewer pathogens die before reaching water sources where they can encounter and infect people. Therefore, human-caused hydrological changes should affect human disease burdens.

And we’re seeing that. For instance, in a massive study of 300,000 children in 35 nations, deforestation upstream from a child’s house was found to be strong predictor of whether the child had high risk of diarrheal disease, presumably because many pathogens were entering the waterbodies upstream (Herrera et al. 2017). (But this was only true for the poor children – the wealthier children living in cities probably had better access to sanitation infrastructure.) Similarly, in Brazil, children living near protected forests were less likely to experience diarrheal disease (Bauch et al. 2015). These large-scale correlational studies suggest that protecting forests might be a win–win solution for conserving biodiversity and reducing childhood diarrhea!

Of course, many forests have already been cut down, so it’s too late to preserve them for human health. In those cases, reforestation/restoration might be a win–win solution. For instance, Herrera et al. (2017) predicted that increasing upstream forest cover by 30% would reduce childhood diarrheal risk as much as improved sanitation and hygiene!

But re-forestation is a big undertaking, and as far as I know, no one has experimentally evaluated the effects of re-forestation on human disease yet. An easier/faster intervention to slow the rate that pathogens and other pollutants reach streams and rivers might be replanting vegetation just within riparian buffers. It’s still unclear whether replanting riparian vegetation can reduce human infection, but in some studies, the number of enteric pathogens and/or fecal indicator bacteria within streams has decreased after riparian buffers were restored, which suggests that human infectious risk would be reduced by stream-side vegetation. This remains an important avenue for future research.

So, preserving or restoring forests and/or riparian buffers can reduce the number of pathogens reaching waterbodies and potentially reduce human infection, but can plants also reduce the number of pathogens that reach human hosts after reaching waterbodies? Potentially! For instance, at Indonesian islands without wastewater treatment systems, there are fewer human bacterial pathogens in seagrass meadows than in nearshore waters that lack seagrass meadows (Lamb et al. 2017). Furthermore, disease burdens in corals are lower near seagrass meadows, too, suggesting that preserving or restoring seagrass meadows could be a win–win for human health and conservation. This is a great correlational study, but is there any experimental evidence that aquatic/marine plants reduce environmental pathogen loads or human disease burdens?

Yep! You may have seen something similar to the photograph below in a town near you. It’s a constructed wetland. Specifically, it’s the Dominguez Gap Wetland, which was created to treat stormwater before it reached the LA River and then the Pacific Ocean. Constructed wetlands like this one are typically designed to filter heavy metals, excess nitrogen and phosphorous, and other chemical pollutants from stormwater. But they can also remove viruses, bacteria, protozoans, and other pathogens from runoff waters. For instance, by forcing viruses to hang out in the slow-flowing water for a while, the wetlands ensure that many viruses die from UV exposure long before they reach downstream waterbodies. Several studies have shown that constructed wetlands successfully reduce environmental pathogen loads, and now we need studies that link constructed wetlands and human disease risk.

However, there are many varieties of constructed wetlands – they vary in retention time, turbidity, whether they contain plants or not, whether there is subsurface or surface water flow, etc. And some designs are better at removing pathogens from stormwater than others. Furthermore, even really efficient constructed wetlands might fail to reduce pathogen loads to levels that are safe for human use, depending on how many pathogens are entering the environment. Therefore, if we want to use constructed wetlands to reduce human exposure to enteric pathogens, we need to design them carefully.

So there you have it! “Plants” – or environmental characteristics associated with plants – can reduce the number of human pathogens that reach waterbodies and pathogen survival time within waterbodies. And lower pathogen loads in waterbodies presumably reduce human disease, especially childhood diarrheal risk. As far as I can tell, no one is currently using forest protection/restoration or constructed wetlands on a large scale to try to prevent childhood diarrhea, but “plants” could be “ecological levers for health” that advance both conservation and human health goals.

If you know of any existing, planned, or in-progress forest protection, reforestation, or constructed wetland interventions aimed at reducing human diarrheal diseases, please let me know! And if you can think of any other win–win solutions for conservation and human health, we’d love to hear about them.

References:

Bauch, Simone C., Anna M. Birkenbach, Subhrendu K. Pattanayak, and Erin O. Sills. “Public Health Impacts of Ecosystem Change in the Brazilian Amazon.” Proceedings of the National Academy of Sciences 112, no. 24 (June 16, 2015): 7414–19. https://doi.org/10.1073/pnas.1406495111.

Collins, Rob, Malcolm Mcleod, Mike Hedley, Andrea Donnison, Murray Close, James Hanly, Dave Horne, et al. “Best Management Practices to Mitigate Faecal Contamination by Livestock of New Zealand Waters.” New Zealand Journal of Agricultural Research 50, no. 2 (June 1, 2007): 267–78. https://doi.org/10.1080/00288230709510294.

Daigneault, Adam J., Florian V. Eppink, and William G. Lee. “A National Riparian Restoration Programme in New Zealand: Is It Value for Money?” Journal of Environmental Management 187 (February 1, 2017): 166–77. https://doi.org/10.1016/j.jenvman.2016.11.013.

Falabi, J. A., C. P. Gerba, and M. M. Karpiscak. “Giardia and Cryptosporidium Removal from Waste-Water by a Duckweed (Lemna Gibba L.) Covered Pond.” Letters in Applied Microbiology 34, no. 5 (2002): 384–87.

Graczyk, Thaddeus K., Frances E. Lucy, Leena Tamang, Yessika Mashinski, Michael A. Broaders, Michelle Connolly, and Hui-Wen A. Cheng. “Propagation of Human Enteropathogens in Constructed Horizontal Wetlands Used for Tertiary Wastewater Treatment.” Applied and Environmental Microbiology 75, no. 13 (July 1, 2009): 4531–38. https://doi.org/10.1128/AEM.02873-08.

Hench, Keith R., Gary K. Bissonnette, Alan J. Sexstone, Jerry G. Coleman, Keith Garbutt, and Jeffrey G. Skousen. “Fate of Physical, Chemical, and Microbial Contaminants in Domestic Wastewater Following Treatment by Small Constructed Wetlands.” Water Research 37, no. 4 (February 1, 2003): 921–27. https://doi.org/10.1016/S0043-1354(02)00377-9.

Herrera, Diego, Alicia Ellis, Brendan Fisher, Christopher D. Golden, Kiersten Johnson, Mark Mulligan, Alexander Pfaff, Timothy Treuer, and Taylor H. Ricketts. “Upstream Watershed Condition Predicts Rural Children’s Health across 35 Developing Countries.” Nature Communications 8, no. 1 (October 9, 2017): 811. https://doi.org/10.1038/s41467-017-00775-2.

Johnson, Kiersten B., Anila Jacob, and Molly E. Brown. “Forest Cover Associated with Improved Child Health and Nutrition: Evidence from the Malawi Demographic and Health Survey and Satellite Data.” Global Health, Science and Practice 1, no. 2 (August 2013): 237–48. https://doi.org/10.9745/GHSP-D-13-00055.

Lamb, Joleah B., Jeroen A. J. M. van de Water, David G. Bourne, Craig Altier, Margaux Y. Hein, Evan A. Fiorenza, Nur Abu, Jamaluddin Jompa, and C. Drew Harvell. “Seagrass Ecosystems Reduce Exposure to Bacterial Pathogens of Humans, Fishes, and Invertebrates.” Science 355, no. 6326 (February 17, 2017): 731–33. https://doi.org/10.1126/science.aal1956.

Maseyk, Fleur J. F., Estelle J. Dominati, Toni White, and Alec D. Mackay. “Farmer Perspectives of the On-Farm and off-Farm Pros and Cons of Planted Multifunctional Riparian Margins.” Land Use Policy 61 (February 1, 2017): 160–70. https://doi.org/10.1016/j.landusepol.2016.10.053.

Pattanayak, Subhrendu K., and Kelly J. Wendland. “Nature’s Care: Diarrhea, Watershed Protection, and Biodiversity Conservation in Flores, Indonesia.” Biodiversity and Conservation 16, no. 10 (September 1, 2007): 2801–19. https://doi.org/10.1007/s10531-007-9215-1.

Quiñónez-Díaz, M. J., M. M. Karpiscak, E. D. Ellman, and C. P. Gerba. “Removal of Pathogenic and Indicator Microorganisms by a Constructed Wetland Receiving Untreated Domestic Wastewater.” Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering 36, no. 7 (2001): 1311–20.

Russell, Richard C. “Constructed Wetlands and Mosquitoes: Health Hazards and Management Options—An Australian Perspective.” Ecological Engineering 12, no. 1 (January 1, 1999): 107–24. https://doi.org/10.1016/S0925-8574(98)00057-3.

Vymazal, Jan. “Removal of Enteric Bacteria in Constructed Treatment Wetlands with Emergent Macrophytes: A Review.” Journal of Environmental Science and Health. Part A, Toxic/Hazardous Substances & Environmental Engineering 40, no. 6–7 (2005): 1355–67.

Wu, Shubiao, Pedro N. Carvalho, Jochen A. Müller, Valsa Remony Manoj, and Renjie Dong. “Sanitation in Constructed Wetlands: A Review on the Removal of Human Pathogens and Fecal Indicators.” The Science of the Total Environment 541 (January 15, 2016): 8–22. https://doi.org/10.1016/j.scitotenv.2015.09.047.

Other photo credits from our Tweets:

1. Universal Children’s Day
2. Water use art

Saving endangered vultures might save human lives

In the NCEAS SNAPP Ecological Levers for Health working group, we’re collecting examples of local or regional interventions that can have direct, measurable benefits for human health (via reduced infectious disease) and the environment – win-win solutions. The case studies that we’ve collected thus far are so cool that we just can’t wait to share them! So today I’m going to share a story about vulture conservation and human infectious disease. The bite-sized, Tweetstorm version of the story is available at @parasiteecology.

Let’s start with the obvious: vultures are crazy awesome birds. They have a gross/creepy reputation because they’re a bit funny looking, they eat dead stuff, and they have some odd habits, like defecating on their own legs to increase evaporative cooling. But they also have some animal superpowers: they can smell things that are kilometers away, they can fly despite being huge, and their stomach acids are so brutal that they can literally eat anthrax for breakfast.

But even superbirds have their Kryptonite. In the past few decades, millions of vultures have died after consuming human-sourced poisons. One such poison is Diclofenac, an NSAID that is used in veterinary medicine. Because a single carcass is typically visited by many vultures, contamination with the drug in discarded livestock carcasses can have huge impacts on vulture populations. And it did. For instance, in India, populations of three vulture species (Gyps indicus, G. tenuirostris, and G. bengalensis) plummeted by 97-99% in just one decade!! Globally, the majority of vulture species are facing extinction (critically endangered, endangered, or threatened), but the vulture extinction crisis in India is especially notable.

With local and global conservation efforts and funding already stretched thinly over thousands of endangered species, why should we care about vulture conservation, specifically? Well, for starters, vultures have been spiritual and cultural icons forever. Ever seen a Western movie? Watched the Jungle Book? Gone for a walk or a drive in the wilderness? Yeah, life without vultures would be weird. It’d also smell terrible. As obligate scavengers, vultures’ unique adaptations allow them to find carcasses much sooner than many facultative scavengers (e.g., dogs, raccoons, rodents). And vultures tend to pick carrion bones clean – and might even eat the bones! – whereas other scavengers often only eat specific tissues. That means that in a world without vultures, putrefying carrion would be more common. And not just “in the wild.” Many cities around the world have rudimentary waste management, at best, and vultures are a major player in waste removal/reduction.

But in a world overrun by carrion, the stench would be the least of our problems. Carcasses repulse us because they are hotspots of disease risk – sources of exposure to anthrax, botulism, and other infectious agents. And more subtly, abundant carrion might also increase populations of animal reservoirs for disease, like rodents and feral dogs. For instance, when vulture populations drastically declined in India in the 1990s – and carrion availability hypothetically increased – the feral dog population increased by millions, despite ongoing sterilization programs. We can’t be sure that vulture declines caused the increase in feral dog populations, because many other things changed in India during that same period (e.g., urbanization). But vulture declines are one possible driver of increased feral dog populations, and during the same period, the risk of feral dog bites increased, as did the number of human deaths due to rabies (Markandya et al. 2008).

Rabies kills 59,000 people per year – mostly in rural Asia and Africa, where access to treatment is limited – and almost all of these human rabies infections come from feral dog bites. Asia and Africa are also the hotspots of global vulture declines, and this spatial correlation suggests that adding an ecological intervention – in the form of vulture conservation – to ongoing dog sterilization and public health interventions might be a successful way to reduce rabies transmission. But interventions won’t be supported by the public and policy makers unless they are demonstrably cost-effective. So Markandya et al. (2008) figured out the economic cost of rabies in India and the cost of vulture conservation in India, and concluded that the benefits of reduced rabies outweighed the costs of vulture conservation. This could be a practical win-win!

But how do we conserve vultures? In addition to captive rearing programs to immediately buffer vulture populations, the most important conservation action was to switch from the lethal vet med Diclofenac to a vulture-friendly vet med, like Meloxicam. India, Nepal, and Pakistan all banned Dicofenac in 2006, and since then, vulture population declines seem to have slowed or even reversed (see below – Prakash et al. 2012)! But because the vulture populations are so small, the most recent populations estimates are admittedly rather uncertain, so these trends should be viewed cautiously.

If Diclofenac is banned, why aren’t vulture populations growing like crazy? For starters, vultures are K-selected species, so their populations grow slowly even under the best conditions. And despite the ban, Diclofenac is still readily acquired, so some contaminated carcasses are still finding their way into the food chain. It’s also possible that the sheer number of feral dogs in India is hampering vulture recovery, if the vultures are being outcompeted by dogs for available carrion.

Since Indian vulture populations haven’t rebounded yet – they’ve only (hopefully) stopped declining – we wouldn’t actually expect that available carrion, dog populations, and the incidence of human rabies have decreased. So it’s too soon to say whether this ecological intervention successfully reduced human infectious disease, as predicted. To further complicate measuring the public health success of this intervention, rabies isn’t a notifiable disease in India, so human rabies cases and deaths often go unreported. Therefore, if the human health impacts of vulture conservation in India are ever going to be decisively evaluated, some intensive surveying of vulture populations, dog populations, and human rabies cases will be required in the near future.

In conclusion, education/policy initiatives for vulture conservation are predicted to be #Levers4Health – mutually beneficial solutions for human infectious disease and conservation. But enacting these interventions can be tricky, and measuring their long term success might be prohibitively difficult. We’ll be eagerly awaiting more news and data on vulture conservation, feral dog populations, and human infectious diseases from Asia and Africa.

Do you know of other examples of potential win-win solutions for reducing human infectious diseases and advancing conservation goals? If so, we’d love to hear about them! You can let us know in the comments, on Twitter, or by email!

If you’d like to learn more about the vulture conservation crisis and it’s impacts on human health, check out these references:

Balmford, A. 2013. Pollution, politics, and vultures. Science 339: 653-654.

Buechley, E.R, and Ç.H. Şekercioğlu. 2016. The avian scavenger crisis: Looming extinctions, trophic cascades, and loss of critical ecosystem functions. Biological Conservation 198: 220-228.

Gangosa, L., R. Agudo, J.D. Anadón, M. de la Riva, A.S. Suleyman, R. Porter, and J.A. Donázar. 2012. Reinventing mutualism between humans and wild fauna: insights from vultures as ecosystem services providers. Conservation Letters 6(3): 172-179.

Green, R.E., J.A. Donazar, J.A. Sanchez-Zapata, and A. Margalida. 2016. Potential threat to Eurasian griffon vultures in Spain from veterinary use of the drug diclofenac. Journal of Applied Ecology 53: 993-1003.

Ogada, D.L.,  et al. 2016. Another continental vulture crisis: Africa’s vultures collapsing toward extinction. Conservation Letters 9(2): 89-97.

Markandya, A., T. Taylor, A. Longo, M.N. Murty, S. Murty, and K. Dhavala K. 2008. Counting the cost of vulture decline – an appraisal of the human health and other benefits of vultures in India. Ecological Economics 67:194-204.

Prakash, V, et al. 2012. The population decline of Gyps vultures in India and Nepal has slowed since veterinary use of Diclofenac was banned.  PLoS ONE 7(11): e49118. doi:10.1371/journal.pone.0049118

Photo/figure credits from the Tweetstorm can be found on the figures, or at these locations:

(4, 6, 8, and 15) BirdLife South Africa has a bunch of great fact cards that are worth sharing. You can check out the rest here.

(7) Thanks, Disney, for our childhoods.

(10) Photo credit to Corrinne

(12) Figure credit to Steven Vanek

(13) Find this and other excellent illustrations here

(16) From here

(18) The LA times has a great series of condor release photos here

(19) Thanks to Ginger at NCEAS for being our photographer!

Predicting zoonotic spillover

[We’re taking a break from the “how to become a successful parasite ecologist” post series. More on that in a few weeks!]

Poop is pretty gross, and some poop is more disgusting than other poop. I’m sure you’d agree with both of those statements, but why? Imagine, if you will, that you are participating in one of my favorite activities: crawling in a narrow cave passage, with just enough room above you to wear your pack while you’re crawling. You round a corner and discover a very interesting conundrum: the small passage forks momentarily, and one fork contains a large pile of fresh raccoon poop, while the other is sprinkled with bat guano (less fresh). You’ll obviously avoid crawling directly through either one, but which is most important to avoid?

When parasites and pathogens that infect wildlife or domesticated species spillover into humans, it can be pretty terrible – think Ebola, SARS, rabies, etc. And depending on how you define “zoonosis” – we’ll get back to that in an upcoming post – you might say that most emerging infectious diseases of humans are caused by zoonotic parasites and pathogens. So disease ecologists should and do spend a lot of time trying to understand what causes the spillover of wildlife parasites into human populations, and how to predict and even control such spillover events.

The EcoHealth Alliance group is well known for tackling this important and complicated issue, and they recently published some great synthesis science in Nature that works towards understanding and predicting the origins of zoonotic viruses (Olival et al. 2017). Olival et al. (2017) created a database that contained every known virus of mammals and the 754 mammal species infected by those viruses. They also had trait information for each virus and each mammal species. Then they explored their massive mammal-virus data mountain with the intention of  answering ~4 big questions:

Which mammal species host the most known viruses, and what makes some mammal species have more viruses than others? As we’ve seen in other studies, the most important determinant of viral richness in each mammal species was the total disease-related research effort that has focused on that mammal species in the past. (This was also true for the number of zoonotic viruses per host species – see next). In other words, the more we look, the more we find! But Olival et al. (2017) take this one step further, and use model predictions to tell us where we should look to find the most new viruses and the most new zoonotic viruses – see below.

Which mammals host the most known zoonotic viruses, and what makes some mammal species have more zoonotic viruses than others? For the purposes of this paper, zoonotic viruses were defined as viruses detected at least once in humans and at least once in another mammal species. Proportionally speaking, bats, primates, and rodents had more zoonotic viruses than other mammal taxa. And some host traits that correlated with the number of zoonotic viruses per species included phylogenetic distance to humans, ratio of urban to rural human population in the host’s range (a possible measure of human-wildlife contact), and whether the species was hunted (another measure of human-wildlife contact). Even after controlling for all of those covariates, bats hosted higher proportions of zoonotic viruses than other mammal taxa.

If you’re a long time follower of this blog or the disease ecology literature, then you know that this isn’t the first study to find that bats host more than their fair share of zoonotic viruses. For instance, previous work had shown that bat species have more zoonotic viruses than rodent species, on average. (But there are more rodent species than bat species, so rodents host more total zoonotic viruses). Olival et al. (2017) confirm this with a dataset including many more viruses and mammal taxa, so the “bats are special” pattern is quite robust! If you’re wondering why bats host more proportionally more zoonotic viruses than other mammal taxa, you might be interested in these previous posts: here, here, and here.

Where do we expect to find the most undescribed viruses, and in particular zoonotic viruses? It turns out that if you want to find new zoonotic viruses, the best place to look would be bats in Northern South America. Cool! You can check out the neat maps in the paper if you’re interested in other taxa or geographic areas.

Did particular virus traits correlate with whether a virus has been observed to be zoonotic or not? Yes! For instance, viruses that that infected a greater range of non-human host species (i.e., host breadth), replicated in the cytoplasm, or were transmitted by vectors were more likely to be zoonotic. Of course, these viral traits don’t 100% predict whether a newly discovered virus will be zoonotic or not, but these descriptive models help to identify hypotheses that can explain why some viruses easily jump into humans and others don’t.

So… what does all of this tell us about poop in caves? Well, not much, actually. The Olival et al. (2017) study was meant to describe broad patterns and make predictions to guide future survey/surveillance efforts, not to inform specific risk assessments. But to follow up on my admittedly tenuous hook, we DO know that some mammals are far more likely to pass on viruses to humans than others. So if you have to choose between hugging a bat or a rabbit (or crawling through their poop), pick the rabbit!

But of course, it isn’t just viruses that we need to worry about; I was worried that the raccoon poop might contain Baylisascurus eggs. I’ll keep my eye out for their next Nature paper that does this study with all parasites and pathogens!