The Boma

Everything is everywhere: How microbes move through a city

• International Livestock Research Institute • Season 2 • Episode 4

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Little is known about how bacteria spread through different sections of a city. Now the most extensive study of its kind uncovers some critical answers of how bacteria move through Nairobi, lessons that could have implications for the wider world. After all, what is being seen in Nairobi today could easily be in New York or Paris by tomorrow morning.

Presenters Elliot Carleton and Brenda Coromina hear from ILRI scientists Dishon Muloi and Eric Fèvre as they find out how urbanisation could produce the next disease outbreak.

Read more:
A new model of pathogen transmission in developing urban landscapes

Music: Flute Song by Moby courtesy of mobygratis.com

 Elliot: Welcome back to The Boma. A podcast from the International Livestock Research Institute where we discuss how sustainable livestock is building better lives in the Global South. 

My name is Elliot Carleton.

Brenda: And I’m Brenda Coromina.

Elliot: Today, we’re taking a close look at life in the city, through the eyes of a pathogen. Over half of all people in the world live in urban areas, and this number is increasing. 

Brenda: There are many benefits to urban life… and there are downsides. Like, urbanisation is one of the main causes of infectious disease outbreaks.

Elliot: If we want to stop pathogens from causing outbreaks, here’s what we need to know:

Dishon: If a pathogen was to emerge in urban population, how would it behave? How would it flow? What are the bottlenecks for the flow of this particular pathogens? How would it affect populations, both humans and animals?

Brenda: That’s Dishon Muloi, an ILRI epidemiologist and the lead author of a recent major study looking at how diseases interact between humans, livestock, and environments. The study began way back in 2013, when a group of scientists from ILRI, the University of Liverpool and the University of Edinburgh in the UK, and several other places, decided to take a closer look at how pathogens actually move around a city. 

Elliot: Because pathogens aren’t just spread by people. They can also hitch a ride on animals.

Eric Fevre is a principal scientist at ILRI and a professor of veterinary infectious diseases at the University of Liverpool.

Eric: Urban environments everywhere are impacted by wildlife species that live within them and exploit particular kinds of habitat. And on the other, urban environments are places where livestock are either raised or consumed. And so there's this whole mishmash of things going on that mean that people relate to animals or parts of animals in different ways in those urban settings.

Elliot: In this case, the ‘urban setting’ the scientists investigated was Nairobi, the capital of Kenya. Nairobi is a bustling metropolitan city, and it’s very diverse, but it’s also a typical representative of a tropical city in a developing country. 

Eric: If you look at a city like Nairobi from the air or just driving through it, it's clearly subdivided into many, many ecological niches. There's rich and poor. There's high and low. There's the parts of Nairobi where the soil is different in one place to another. There's the massively densely populated versus the lightly populated. There's the parts that are served by certain types of food system and others, which are much more chaotic.

Brenda: Over 5 million people live in Nairobi. And about 60 percent of them live on just 6 percent of the city land, in close-packed housing. 

Elliot: What’s more, the city also houses animals, whether intentionally or not. There are wild birds, rats, monkeys, and domestic livestock. In fact, Nairobi alone is home to over 1.3 million livestock.

Eric: So we tossed and turned a lot in at the beginning of this project on what pathogen we wanted to really spend our time looking at.

Dishon: So for us, we chose, which was a very common bacterium called E.coli. So this pathogen is it's found pretty much in every form of life. Well, mostly vertebrates. So if I was to sample your your hands now or your gut or your food or animals you keep, you would find this bacterium.

So we could use this pathogen as an exemplar pathogen for all other all other other particular bacteria.

Brenda: Now, E.coli isn’t always a pathogen. It’s only some strains which are harmful. But we’ll get to why and how a bit later. 

Elliot: The scientists decided to take samples from humans, animals and the environment in 99 households across Nairobi. Then they would sequence the genomes of the E. coli bacteria they found in the samples and compare them. 

Brenda: Kind of like building a map of all the different E.coli strains across Nairobi.

Eric: And I guess we expected to find that people who had contact with livestock in urban spaces had a particular kind of risk profile when it came to emerging pathogens and that people who didn't have contact with livestock or didn't have contact with animals had a much lower risk of exposure to potential emerging pathogens. That I guess would have been our hypothesis before we started to get there.

Brenda: That makes sense. Most of our known infectious diseases are zoonoses – they can be spread between humans and animals – and 3 out of 4 new infectious diseases come from animals. Like COVID-19.

Elliot: Not to mention other issues which could help spread disease, like poor sanitation, or the handling of animal products, over-using antibiotics, unsafe food...

Brenda: Yep. And we should give the scientists credit - this was a really, really complex study that took years of planning!

Eric: Work like this that's across multiple scales and that is that takes on such a human dimension, has to involve multiple backgrounds, multiple disciplines, and be very interdisciplinary. 

Eric: We do our biology informed by what a social scientist or an anthropologist tells us about the way the city is organized 

And those people study the planning or the human settlement patterns in the light of what we've told them about the biology. And that's interdisciplinary. And that was really very evident in this work. 

Dishon: We came into logistical challenges the sort of experiment we designed here. Is this mind blowing. You can imagine sampling humans their livestock, domestic wildlife, which includes rodents, bugs, birds and other and other and other animals, it's a logistical nightmare. And then all of that is just overlaid within a very complex city, which is Nairobi. Whether this is this insane levels of traffic and and other and other challenges 

Elliot: So this was a very unique study. And now I think we all want to know—what exactly did they find out?

Dishon: Everything is everywhere.

Dishon: What we found was that the E. coli of our population was extremely diverse. And at the same time, we found that some the bacteria genotypes found in one location of the city were also found another location in the same city. So, for instance, e. coli A could be found in location A, and E. coli B could be found in location B of a different part of the city.

And at the same time, we also found similar bacterial types in Nairobi, match other similar bacteria in other global locations.

Brenda: That means… everyone in a city can be reached by a pathogen? 

Elliot: Yeah. It looks like the microbes in a city aren’t really restricted to certain locations. 

Eric: Nairobi. I think this applies to most tropical cities is really a soup where everything is mixed up, and the ecological subdivisions of the city - Yes, they are different from each other, but from the from the point of view of a pathogen that's looking how how to move from one place to another, there are very few boundaries between those ecological systems. So if we just take some examples of from people for example, there are people who live in super high density, low income settlements, slum housing, and there are people who live in very rich parts of the city with five acre gardens. But the people who work in those houses live in the slums.

And so there's a daily commute between the super rich and the super needy, I guess we could call them. 

From a more ecological perspective, there are multiple rivers that flow through the city, and most importantly, as we found in in our work, there is an abundance of synanthropic wildlife or ‘wildlife that like to live around humans’ that mix it up.

And so if Nairobi is a soup, the wildlife in the form of rats, birds or bats, are really the spoons that are stirring that soup and then moving between different environments all the time and having contact with each other and exploiting all of these different ecologies and connecting them together. And so there isn't really microbial isolation in Nairobi in the way that we had originally imagined.

Brenda: But importantly, there are some barriers in that living ‘soup’. Not enough to stop bacteria being shared… but enough to slow sharing down.

Dishon: What we found is that sharing, wildlife to wildlife. With occasional sharing between humans, livestock and wildlife. And we also found that if sharing was to occur or was to occur, it it mostly occurred within household confines.

We posit that the household acts as a barrier to ensures that bacteria do not cross freely across the city.

And again, going back to what we said initially, which was if a pathogen was too was to imagine a population, how would it flow? It basically says that if a pathogen was to to emerge within a city confines like Nairobi, there are bottlenecks. The first bottleneck is the host, that is transmission is mostly likely to occur within the particular host group.

And then secondly, the second the second bottleneck would be households, that is transmission will most likely occur within geographical confines. 

Elliot: So basically, Eric and Dishon are saying that it can be harder for pathogens to spillover from one species to another. And it can also be harder for them to flow from one household to another. 

But now I’m wondering—what is the broader significance of these findings? And how might they be useful?

Eric: We might imagine that a new a new pathogen or a pathogen would spread in communities almost as a wave. Most pathogens are modeled that way. 

Eric: But actually, what we find here is that the process by which this soup gets mixed is is a much more stepwise process. 

Eric: And that's really important because it means that if we can predict where and how these kinds of things start to happen, that we can reinforce those boxes to stop things from spreading from them into the next one. And so it gives us a lot more insight into how we can prevent the much more rapid spread of infectious diseases than we might otherwise have thought before.

Brenda: There’s something else. Because they were looking at E.coli bacteria, they could also track patterns of antibiotic resistance across the city. And that was revealing too.

Elliot: How so?

Brenda: Well, first off, antibiotic resistant E. coli – like non-resistant E. coli – were also everywhere across the city. And the resistance profile – the genes they had - were very similar in samples from animals and from humans.

Elliot: Could that be because humans and livestock are treated with the same kinds of antibiotics?

Brenda: Partly, but the pattern Eric and Dishon and their colleagues uncovered suggests something else. You see, one of the ways bacteria become resistant – aside from mutating to become resistant, which is pretty rare -- is by sharing copies of a little circle of DNA that carries the resistance genes. It’s called a plasmid. And the transfer of plasmids is quite common. 

Elliot: And so that must also be how E. coli can share harmful disease-causing genes…

Brenda: Yes. And here’s the thing. Plasmids can survive in the environment independently, until they are taken up into a bacterium, where they can be copied and may be released again.

Elliot: So then we should be tracking plasmids too if we want to trace the spread of antimicrobial resistance.

Brenda: And we need to do that, because as we heard in previous episodes, AMR is a very serious problem.

Dishon: We have seen in the last few months that all of the impact of drug resistance in our populations. We are now seeing infections which can’t be cured or treated due to due to drug resistance. 

People actually are saying this is an impending apocalypse. We are heading towards the dark days of medicine where you have a very simple, treatable infection and you can’t be treated.

So rather than looking at looking at the bacteria itself, we just focus on the bus, which is the plasmid. Right. So we are thinking of setting up ecological experiments which would involve tracking, tracking these plasmids, both in the clinic that is in the hospitals in the community, both humans and animal populations. And one thing would be asking the question, is there a chance that the plasmids which are found in hospitals which are probably multi-drug resistant? Could they be finding their way into the community?

 And if they do so, what is the chance they could die off, or could they become adapted to transmit further within the community

Eric: And how efficiently could we put up these barriers to prevent further transmission from happening? And I think that's a very important next practical question.

Elliot: So essentially, the scientists have mapped out the presence of AMR and bacteria types in urban environments. But now, what could be the next steps?

Eric: We know, for example, that from the work we've done that these wildlife species pick up the infections that they're transmitting primarily from waste, that humans are disposing of livestock waste in particular.

But once they've done that, where, where do they move to? How are they connecting with other members of their species group and other species altogether? And and really now, instead of seeing the world through the eyes of the pathogen, it's about seeing the world through the eyes of those wildlife species. And, and to then understand how they're moving around with those pathogens so their behavioral ecology, if you like. That's one important next question. 

Brenda: But you know, there’s a really important point here for policymakers and urban planners. 

Elliot: That the cities we live in can actually help prevent the next epidemic?

Brenda: Yes. Because people create the built environments they live in – and policymakers must take studies like these into account to keep people healthy and save lives. 

Eric: I think what's essential about this is that everything we do about how we design and create our cities or our lived environment more generally matters. 

ERic: It's it's equally important to think about pathogens as it is to think about some other element of the urban space when you design and plan your city. One really important element that actually came out in another piece of work that we did that was part of the same study is that the ecological footprint of the city is quite important for determining factor on wildlife diversity. So we've said that the wildlife are the spoons that stir the soup, but different kinds of wildlife exploit different habitats. So if you have green parks and open spaces and diverse ecologies within your city, you have more wildlife species. 

Brenda: And so having these green spaces can actually lower the risks of spreading pathogens.

Eric: But in a city that's heavily urbanized, where only a restricted number of city of organisms can exploit those environments. And let's be honest we’re basically talking about rats that live in people's houses, those rats are very good hosts. And vectors of these different pathogens. And the more you pour concrete in, the more you turn your turn to the urban environment into a human space devoid of ecology. The more you're encouraging the kinds of species that are better mixes of the soup. So if you're a planner, you have to think about the not just how you move from A to B and the traffic lights in your city, but you must think about all aspects of your city's ecology and how it impacts on the health of the people who live there.

Elliot: Dishon is hopeful that the barriers between scientists and policymakers are starting to come down. And that is in no small part thanks to the past couple of years, tough as they have been.

Dishon: I think we we in the last one or two years, thanks to COVID, we've seen the value of science at the fore in in our economies. For the first time, we saw politicians sitting down with scientists to discuss public health issues. That wasn't the case in many countries, especially in our low in our low and middle income countries, where we see very clear separation between science and policy. For the first time, we saw the role of policy, the role of science in policy. And it's something which motivates me is is this to expand the role of science in helping human health or helping livestock health and ultimately helping our global health? So for me, that's something which motivates me. every morning I wake up, in the smallest way I can contribute. Cut out

Brenda: And I think that’s a great place to leave off for today. Thank you so much to Dishon Muloi and Eric Fevre for helping us see a city through the eyes of a pathogen.

Elliot: And thank you to our listeners for joining us. We would love to hear your feedback on today’s episode or the whole podcast series. So please reach out to us on Twitter at BomaPodcast to let us know your thoughts, and also, what topics you’d like us to cover moving forward. And if you enjoyed today’s episode, please don’t forget to share and subscribe. I’m Elliot Carleton. 

Brenda: And I’m Brenda Coromina.