Bed bug cases are on the rise after a 50 year absence from much of the Western world. But why now? We explore the genetics and bizarre biology of these parasitic pests. In the news, we examine the fungal disease killing Ash trees across Europe that may decimate up to 40% of British woodland...
In this episode
01:10 - The Rise of the Bed Bug
The Rise of the Bed Bug
with Toby Fountain, University of Sheffield
Chris - Bed bug infestations are on the rise. Although UK has been relatively clear of them for the last 50 years, we are now seeing a rapid rise in the number of cases, but it's not entirely clear why. Now, scientists are turning to genetic techniques to help them uncover the cause of this bed bug comeback and Toby Fountain is a PhD researcher at Sheffield University where he's looking at this very question. Hello, Toby.
Toby - Hello.
Chris - Ever been bitten by one?
Toby - Unfortunately, I have, yes.
Chris - What was it like? What happened?
Toby - It's not very pleasant. The thing with bed bugs is they don't like to just bite you once. They tend to bite you several times because they're trying to find a juicy capillary, so what you normally find is you get a row of bites. So, even one individual might bite you 5 or 6 times, so quite grim really.
Chris - Tell us about the organism responsible. What are these bugs? What do they look like? How would I recognise one?
Toby - Bed bugs are small, flightless parasites that suck on our blood. They're visible to the naked eye and adults are about the size of an apple pip. They're a dark, reddy-brown colour. So, they're quite cryptic. They do hide away in lots of places, but if you saw one on your arm, you'd definitely be able to see it. They're bigger than a flea for example.
Chris - Where do they hang out? We call it bed bugs, but it's that a reasonable name for them?
Toby - They don't actually like being in the bed because they might get squashed, so where they actually tend to live is cracks and crevices around the bed, and what they'll do is when you're sleeping, they'll stealthily march out, they'll bite you, they'll feed on you, and then as quickly as they can, they'll scuttle away to their safe hidey hole. So they don't actually sleep in the bed with you in a majority of cases.
Chris - Reassuring, although not much. How do they find you?
Toby - There's actually a number of mechanisms they use depending on the scale. So, what they can do is they use CO2 for example. So, the carbon dioxide that you breathe out, they can pick up very quickly and when they get a bit closer to you, they use a combination of infrared and also they smell you. The chemicals coming off your body, they smell you and that's kind of how they locate you.
Chris - And then the rest is history, I suppose you could say. Speaking of which, looking back in time, these organisms, these insects were much more common as a pest in people's homes than they are today thankfully. Why were they more common then and why did they disappear?
Toby - Yes, that's the thing a lot of people don't know is they were very common in the UK until about the 1940s and it was a part of everyday life for people to live with bugs. But when it got sort of about the 1940s, the government here introduced more stringent public health legislation and we also saw the development of powerful insecticides like DDT, and they've been presumed to be what's been responsible for bringing the numbers right down. Now, the mystery is that in the last 10 or 15 years, they've started coming back. We're starting to get increased reports of them and what we're trying to do is kind of work out why that is.
Chris - Is that a comprehensive thing if you look at pretty much any western country, you're going to find this similar sort of trend or is it just in Britain?
Toby - No, no. It's seen across the western world, the United States and Australia for example. They haven't really had very many reports of bugs until a similar time, so that's the interesting bit; that this pattern has happened globally at the same time.
Chris - And in countries that didn't use insecticides and things, have they always stayed high or was there just a massive global reduction in their incidents?
Toby - No, I think they're still maintained. For example, in Africa, they have always had a high number of bugs and that's still been a common feature of life out there.
Chris - So, how are you using the power of genetics in your research to try to understand a bit about what these insects are doing?
Toby - First and foremost, I'm an Evolutionary Biologist, so one of the things I'm interested in is how genetic diversity is maintained within populations. So we know genetic diversity is very important as it will allow organisms to adapt to external pressure. Now bed bugs are very interesting because it looks like humans are responsible for moving them around. What my research is finding is that it's usually just a very small number of related individuals that eventually start new infestations. And because this number is so small, you get quite a lot of inbreeding and mating with relatives causes a reduction in your genetic diversity which can be detrimental for many species, but not the bug.
So, what we're using is basically DNA fingerprinting. This allows us to look at different variable regions in bed bug DNA between individuals and then we can compare how related individuals are. Now, this is very interesting from an evolutionary standpoint, but it also has a number of very useful practical applications. For example, we're starting to identify the exact numbers of bugs which do start infestation. And also, what we'll be able to do is identify what infestations are linked which is going to have some important practical applications for pest controllers.
Chris - So, do you have to go sites of outbreaks and physically find bed bugs or do people kindly send them to you?
Toby - It's actually a combination of the two. I remember early in my PhD, it was a bit strange because I was advertising for people to send me their bugs which I hadn't expected when I started. I've also been to a number of infestations myself and it's really that side of my work that's really opened up to me how much of a problem they are. When I started, I read the literature. They sounded like they're pretty bad, but I think it's not until you've actually stepped inside a home with a substantial bug problem, and you see how horrible it actually is, and what real pressure there is to try and to come up with adequate control strategies to get rid of them.
Chris - And returning to your question of studying diversity of bed bugs. You do the genetic fingerprinting. You are able to study how these things originate and how they spread. What actually are you able to tell about the pattern of spread? Are we able to blame low cost airlines for sending people off on package holidays, they then stay in low cost accommodation which is riddled with bed bugs, bring them back here, and then they spawn an outbreak at home, and then that propagates around the country?
Toby - Okay, well the first thing we can say is actually that cleanliness of a property has very little to do with the chance of having a bug. You're as likely to get them from a very cheap hotel or hostel as you are to from one unlucky high class hotel, which could have them equally as much. While it's probably a bit early to say if they're coming from a certain place or not, what we're definitely finding is a pattern of humans moving them around. So, if you remember I said at the start that bed bugs can't fly. They can only walk. So, what you might expect in that situation is, the further you go away from an infestation, the less related individuals are going to be...
Chris - Well, they can fly if you put them in an airplane of course.
Toby - Exactly, so what you can do with that is you can see that naturally, if we weren't contributing to that spread, if humans weren't contributing, we'd see this isolation by distance pattern, we'd see that it's the further you move away, the less related a bug would get. But you rightly said, couple that with us now flying a lot more, we're not seeing that expected pattern. So, that is giving support that humans are actually facilitating their long range spread.
09:23 - The Bed Bug's Bizarre Sex Life
The Bed Bug's Bizarre Sex Life
with Dr Richard Naylor, Bed Bug Foundation
Ben - Bed bugs are one of a very small handful of species who demonstrate an unusual type of mating behaviour known as "traumatic insemination". This is where the male, rather than delivering sperm into a specially evolved organ actually pierces the abdomen of the female and delivers the sperm directly into her abdominal cavity. To explain more about the biological adaptions that allow a female to survive this, we are joined by Dr. Richard Naylor who works with the Bed Bug Foundation. Richard, thank you for joining us. This doesn't sound like a very efficient or effective way of inseminating...
Richard - It's not at all efficient or effective for the female. Well, it's effective. They do have offspring as a result of it, but it's not the female that drive it.
Ben - What actually happens? Once the male has punched his way through and delivered his sperm, presumably there are specialised organs then within the cavity that take the sperm to the right place. He can't just make a hole wherever he wants it and the sperm just finds its way to an egg or can it?
Ben - So, from the male's perspective, he can just deliver his sperm as and where. If there are sperm storage organs then that like in many other insects would imply that you can get multiple matings. Does this mean the female actually gets stabbed many times and then selects out the sperm that she wants to use?
Richard - There's no evidence to show that the female can select which sperm she wants to use, but you're absolutely right. There are multiple matings upon multiple matings. The males, we know, mate tens and tens of times more frequently than females need to be mated in order to stay fully fertile. So, we know that this is bad for females because the males are just mating far more than they need. A female bed bug needs to mate about once every 5 weeks and it's likely to be 5 or 10 times a day that the males will mate with the females if they get the chance.
Ben - How do the females actually survive this? Well, the clue is in the name, isn't it? It sounds traumatic.
Richard - It is traumatic. We know that they don't survive as well as they would if they were only receiving mating every 5 weeks. We've done these experiments and we've shown that females pay a cost in terms of their longevity, their lifespan of about 25% as a result of natural mating rates. So we know that this mating system is bad for females, but they don't have any control over it. It's a male-driven mating system, so the males impose the mating rate on the females.
Ben - I mentioned at the beginning that there are not very many species that actually undergo this and I can see why. What is the sort of selective pressure that caused this to evolve? You would think as it is so costly for the females that it would very quickly adapt out.
Richard - Yeah, that's right. If you imagine a biological system where males and females are working together to produce the most offspring between them, you would expect it to adapt out as you say. But that's not what we think is happening. We think there's a conflict between males and females and what's in it for the males is that it's always the last male that sires the most offspring. And so, males are competing to be the last one and that's what's driving this elevated mating rate.
Ben - Now we also mentioned earlier that there is, of course, as with any injury there is a risk of infection. What adaptations do the females have in order to be able to heal, to repair the wound, and to stop themselves just being taken over immediately by a bacterial or fungal infection?
Richard - Well, in the bed bug, there's a very similar system in the whole family, the Cimicidae and they all showed different levels of adaptation. But in the bed bug, the females have a little pocket which receives the sperm, this little pocket is called the spermalege, and it's packed full of immune cells, something like our white blood cells has a very high concentration of them in this little area. It looks like a little patch of cotton wool and it's probably about the size of a large grain of brown sugar. This little area of immune cells does a very good job at mopping all those bacteria and also, stopping hemolymph from leaking back out through the wound that the males make.
Ben - Now, species like bed bugs have just what we call an innate immune system. So, unlike our immune system which can learn to recognise a threat and then adapt, and then the next time you get infected with the same bug, you are even better at fighting it off. With just the innate system that they have, presumably, it must be really quite aggressive to just fight and kill off everything.
Richard - We've always thought about insects as having very basic, simple, and not very advanced immune systems and to some extent, that's right. But it is a very effective immune system. It has several different components to it and one of the most important components is lysozyme. It releases lysozyme and this chops up bacteria. It can detect bacteria being introduced and then elevate these various components of its immune system and just fire all these toxic chemicals at the bacteria and hopefully wipe them out. In the bed bug, it does a pretty good job in that immune organ.
Ben - So, does that mean that there's something that we can learn from the bed bugs about potentially how to fight off infections or to make new antibiotics?
Richard - Antimicrobial peptides are one of the things that insects have that we've been exploring as a medication. What's interesting about insect immune systems is that bacteria don't seem to evolve resistance to them. So we've all heard of antibiotic resistance, which is rendering all of our antibiotics that we use in the medical profession useless because the bacteria are evolving to cope with them. And we don't see nearly as much resistance to antimicrobial peptides which is one of these tools that the insects use. So yes, there are lots of people working on that very question - can we learn from insects to help ourselves?
15:46 - Earliest evidence for bows, arrows and human language
Earliest evidence for bows, arrows and human language
Delicate stone arrowheads dating from 71,000 years ago have been unearthed in South Africa, providing the earliest indirect evidence for high-level human language and technological capacity.
The discovery, announced in the journal Nature, was made by University of Cape Town archaeologist Kyle Brown and his colleagues at a site called Pinnacle Point on South Africa's southern coast.
Digging through a 14m thick sediment layer dating back to over 70,000 years, the team uncovered a series of microliths - small, worked stone bladelets measuring between 2.5 and 3.5 centimetres in length - spanning an 11,000 year period.
The blades, which bear a strong resemblance to similar microliths made in more recent times and used as arrowheads, show consistent craftmanship and refinement over time suggesting that the technology needed to make them was being passed on over many human generations.
Making these tools would have been very complicated, involving selecting and transporting the right stones, heat-treating them to make them workable, turning them into bladelets and microliths, working bone or wood sections to fashion mounts for them, and then using other materials to fix them in place to form arrows or darts.
Such are the challenges in doing all of this, and over such a sustained period, these earth arrow-makers must have had language to enable them to transmit these complex ideas among themselves, the team surmise.
Previously, anthropologists and archaeologists have suggested that language didn't appear until 40-50,000 years ago, speculating that a genetic change that endowed individuals with enhanced cognitive abilities occurred around this time. This argument is rendered much less tractible in the face of these new findings.
And, more pugnaciously, as Kyle Brown and his colleagues point out in their paper, the discovery also probably explains why Neanderthals, the other hominin species around at the same time, didn't fare too well in the aftermath either.
"Microlith-tipped projectile weapons extended the effective range of lethal interpersonal violence, and would have conferred substantive advantage on modern humans as they left Africa and encountered Neanderthals equipped with only hand-cast spears."
19:36 - Modelling Human Disease with a Lung-on-a-Chip
Modelling Human Disease with a Lung-on-a-Chip
Mimicking human organs and diseases in the lab could help to investigate diseases and rapidly screen compounds to find new drugs, and now, researchers at the Wyss Institute for Biologically Inspired Engineering at Harvard University have made a lung-on-a-chip capable of modelling a human condition called pulmonary oedema.
The lung-on-a-chip device itself was first demonstrated two years ago by the same team, led by Donald Ingber, founding director of the Wyss Institute. It consists of a polymer structure about the size of a USB memory stick, containing a number of hollow channels. Two of these channels are separated by a porous membrane, which is coated on one side with human lung cells, and the other with cells from very small blood vessels known as capillaries. By passing air over the upper surface and blood-like medium over the underside, this chip can model interactions that occur at the surface of the lung. Two other channels on the sides of the chip can expand and contract to deform the interface to mimic human breathing.
This new research, published in Science Translational Medicine, demonstrates abnormal function of a human lung. A drug used in cancer chemotherapy, interleukin-2 (IL-2) is known to have a serious side effect of causing pulmonary oedema, where fluid can leak into the air spaces in the lungs. If the lung-on-a-chip is truly modelling a human lung, we should see leakiness across the lung tissue as a result of administering IL-2.
This was exactly what they saw. At similar doses and over similar time frames, the lung-on-a-chip experienced the leakiness, reduction in oxygen transport and clotting of an oedema patient. The experiment went one step further and identified something completely novel about oedema - the very act of breathing increases fluid leakage over three-fold.
Organs-on-a-chip can be used for very high-throughput, replicable and controllable drug screening - potentially doing away with the need for some animal studies and increasing the rate at which we can identify new drugs. To find out is their model could work in this way, the team then tested potential therapeutic agents, including a new class of drug called a Transient Receptor Potential Vanilloid 4 (TRPV4) channel blocker being developed by GlaxoSmithKline. The team found that the symptoms in the lung-on-a-chip were prevented by this drug, a result that fits well with GSK results from mouse models.
This gives us confidence in the lung-on-a-chip, suggesting it really is acting as a genuine organ might, at least when it comes to pulmonary oedema. Other organs, organ systems and other conditions, should follow and will likely change the future of drug discovery and testing.
21:52 - What is Ash Dieback?
What is Ash Dieback?
with Professor Michael Shaw, Reading University and Professor Chris Gilligan, Cambridge University
Chris - A major news story in the UK this month has been the discovery of ash dieback disease, a fungal infection that destroys ash trees unfortunately. To find out more about this threat and whether or not we can control it before it spreads further, we're joined by Reading University Plant Pathologist Professor Michael Shaw and Cambridge University's Professor of Mathematical Biology, Chris Gilligan who's also chairing the government's task force looking at this. We'll begin with Michael first. Hello, Michael.
Michael - Hello.
Chris - First of all, what is this disease that were calling colloquially 'ash dieback'?
Michael - It's a fungus which spreads by spores which form on fallen leaves and can infect leaves of a healthy tree and then spread from there into the bark, and the conductive tissues of the tree, and cause wilting of shoots. Eventually in small trees it will girdle the trunk and kill it. In older trees, it kills shoots and maybe branches, and weakens the tree so that it becomes vulnerable to succumb to things which wouldn't normally be a lethal disease.
Chris - Is it just ash trees that are vulnerable to this particular infection or can it hop on to other trees and species too?
Michael - As far as we're aware, it affects a group of ash trees. Particularly the common European Ash which is the one we have, a couple of other species. It seems to be less effective, less of a serious problem on far eastern ashes and in fact, the evidence at the moment is that it comes from the far east. It seems to exist in a benign form, co-existing fairly happily with certain types of ash tree in Japan and presumably the wider far east.
Chris - How do we think that something from the far east took up residence in Britain?
Michael - It's taken up residency in Britain because some time in the early 1990s, it took up residence somewhere in eastern Europe, let's say in Poland and it's been spreading from there as a spreading infection since that time. It was in Scandinavia in the mid 2000s, by 2009, I think, 90% of Danish ash trees had some signs of infection. It's now in France as far as the Massif Central. So, this is a big spreading wave of infection. How it got to Poland, we don't know.
Chris - We're hearing this number of 90% of ash trees are vulnerable. Is this a reflection on the fact that not all ash trees are made equally? Are there different subtypes of ash tree?
Michael - Well, no. it's more that ash trees are sexually reproducing so they're quite variable. And in studying trees which appear to have been less badly affected in Denmark and in Norway as well, it's been found that some trees appear to have survived because they're genuinely more resistant to the infection. In looking at the progeny of those, looking at the seeds that arise from those trees, there are estimates of maybe 1% of the population will be able to survive.
Chris - So, is the long term prospect that will end up selecting out the trees that are vulnerable to this, but will breed a new strain of trees just naturally which are naturally resistant to it. So we just have to wait for one generation of ash trees and then we'll have trees that are not vulnerable so the problem will go away.
Michael - Probably more than one generation because you'd have a sort of sputtering epidemic. You'd have some trees which survive the first waves anyway. I think that is probably correct. The only catch there is to think what the generation time of an ash tree is, particularly to get some of the more attractive landscape trees that may be over a century old. So we're talking for the next maybe decade or two, we would see perhaps a third of the landscape and forest trees around us disappearing; ash is extremely common species. Then gradually, there would be a repopulation from resistant individuals. Of course, the disease may evolve at the same time, so we can't be absolutely sure what is going to happen.
Chris - And can it be treated if you've got a tree which has got it? Is there any way to save that tree or is these curtains, you've got to chop it down?
Michael - Trees don't have an adaptive immune system. So there's no way in which you can immunise a tree against this infection. The kinds of disease management we might use on crop plants which involve chemical fungicides are not feasible or would have side effects worse than the disease itself if you use them in the open environment, because you would have to keep repeating them. So, a parallel kind of disease would be apple scab which is often treated with 5 fungicide treatments in a year. And that would have to go on indefinitely. So, there isn't really any way in which we can cure a tree. For an urban tree, a much loved specimen tree, it may be possible. I'm sure people will be trying injecting fungicide directly into the tree, but it will be expensive and unfeasible in the wider environment.
Chris - Intravenous treatment for a tree. Let's bring Chris Gilligan who is chairing the government's task force and he's also a plant scientist at Cambridge University. So Chris, you've been down to advice the government. What did you tell them?
Chris G. - I've come into this really as an epidemiologist and a mathematical modeller with some experience of developing models for a range of pathogens that might come in and attack a range of species including guard trees, but also, we've worked on bubonic plague in the past for example and used some similar methodology. Essentially, one wants to think what are the 3 or 4 key questions that we might want to address in thinking about an invading pathogen? The first is, you want to predict the spread. Secondly, you want to identify regions that are most at risk. Then you want to think about the effectiveness of management strategies as Michael has been referring to, and also telling us where to look in order to determine how the pathogen is spreading, and that's where we use mathematics.
Chris - What are you finding so far?
Chris G. - We're finding that this is a challenging pathogen. It has spread as Michael has said rapidly, well over a period of 10 years right across from Poland, now into the UK. We're working very closely with a range of government scientists to identify where the signs of infection are, whether they're in mature trees or whether they're in sites in which young saplings have been introduced. And that distinction is very important, particularly in thinking about the mechanisms for spread and also the potential for control.
Chris - A lot in the newspapers have had things like, they've said, "Now, it's in mature trees. The horse is bolted. There's not a lot we can do." Is that because if it's in mature trees, that's an indicator that it's out there in the wild and spreading, and that all the control strategies of nurseries, you can do all that you like, but you're not going to stop something once it's out there in the wild tree community?
Chris G. - Well, these are early days yet and we're simply developing models and testing them. My group is working almost 24 hours a day at present to develop models as fast and importantly, to test the models as rigorously as we can.
Chris - What about the distribution of ash trees around the country though? Do you make assumptions about where all the ash trees are and are they fairly homogeneously scattered across the country or are there hotspots, pockets if you like of where there are lots of ash trees, and then not very many?
Chris G. - This is one of the big challenges in dealing with an invading pathogen particularly of plants because although people might immediately think we know where all the ash trees are, in fact, we don't. We know where a lot of them are and a lot of effort has been taken up over the last week, in links with the Forestry Commission to determine what are the best data that we possibly can get in order to obtain a map of where the ash trees are, and particularly the connectivity and breaks in the distribution of the ash trees. We now have, I think the best possible map that could be got in time.
Chris - When foot and mouth came to Britain about 11 years ago, that was controlled by removing all of the animals in infected areas, just literally blitzing them. It's almost creating a sort of fire break and then sterilising an area. Will that strategy not work here? Could we not home in on areas where there are active infections in trees and remove all of the trees, and therefore, remove the source of infection?
Chris G. - This is exactly why, as a mathematical modeller, I would say we need to have the mathematical models in order to be able to do the 'what if' scenarios to compare different types of control. We have very recently over the last few years in fact, been looking at the spread of another disease of trees called 'sudden oak death' in the United States where it's devastating larger areas of California and the equivalent pathogen is ramorum disease of Larch in this country. And we have used the model to identify a culling strategy that is likely to have some effect in reducing the spread of disease. To reduce all of the disease, to eradicate it in fact, would be extremely difficult and extremely expensive.
Chris - So, let's just ask Michael to wrap this up for us. Michael, what do you think the sort of long term prospects are? Are we going to face a Britain with no ash trees because they make up what 40% of our natural woodland stock, don't they?
Michael - I don't think it's quite 40%. No, but it's a very large proportion. It will make a very big hole in the landscape and I am pessimistic. I hope Chris's group will do the sums, but a windblown disease is a very difficult thing to control. And so, I am pessimistic that over the next decade or two, we'll see a lot of tree deaths. As I say, in our children's lifetimes hopefully, we will see some recovery to a more stable position, but it's not looking good.
32:23 - Password Passed Down Before Hatching
Password Passed Down Before Hatching
In Fairy-wrens (Malurus cyaneus), hungry chicks need to give a password to get food from their mother, and research published in Current Biology shows that they learn this password while still in the egg.
t's important for a Fairy-wren to recognise its own young because they are subject to parasitism by cuckoos - in particular the Horsfield's bronze-cuckoo. Adult cuckoos lay their eggs in fairy-wren nests, and leave the young to be brought up by the wren. A developing cuckoo chick will eventually throw all of the other chicks from the nest, meaning that all of the wren's resources go into bringing up someone else's offspring. This is hugely costly, so the wrens have evolved a range of behavioural and acoustic ways to cope.
Sonia Kleindorfer at Flinders University and colleagues in America and Austria monitored 15 nests for the entire nesting period, recording all of the wren songs. They discovered a previously unknown vocalisation, now called the incubation call, which females only used when they were alone and incubating their eggs - stopping as soon as the eggs hatched.
They also recorded the young after they hatched, and were particularly interested in the calls made whilst begging for food. Noticing significant differences between different nests, they then compared the begging calls with the incubation calls from the same nest, and found a shared audio "signature" in both types of call.
This could indicate that the call is learned while still in the egg, or may be genetically hard-coded into the chicks. To find out, they did a series of foster-parent experiments by swapping complete clutches of eggs into unrelated nests and looking for similarities in vocalisations. They found that the similarities were significantly greater for parents and their foster chicks than for genetically related animals incubated by a different mother, reinforcing the idea that these signatures are learned, rather than inherited. Further evidence comes in the fact that similarity between mother and parent was related to how frequently the mother called during incubation - a dose-dependent response, to use medical terminology.
The research didn't entirely rule out a genetic component, as certain elements in the song showed similarities with biologically similar but fostered animals, hinting that genes still play an important role.
Playback experiments then confirmed that hearing this password did cause adults to behave differently towards the offspring, and were far more likely to abandon a brood that didn't use this signature in their calls. Females were also recorded calling to males to solicit food, and including the same signature as in their incubation calls. The males also seemed to learn the password, and would adapt their behaviour accordingly by, for example, reducing feeding rate when exposed to calls that didn't match.
The researchers argue that, as cuckoo eggs are added to the nest at a later stage than the wren's own eggs, they are therefore exposed to fewer incubation calls, and have less opportunity to learn to mimic the mother. Kleindorfer and colleagues argue that this gives the wrens an advantage against the cuckoos in an acoustical arms race, and help to avoid wasting resources bringing up an unrelated chick.
35:20 - Human Hormones Feminising Fish - Planet Earth Online
Human Hormones Feminising Fish - Planet Earth Online
with Charles Tyler, University of Exeter
What happens to the hormone disrupting chemicals found in contraceptive pills or hormone replacement therapies once they've passed through the body?
Well, they end up in the sewage system and eventually as effluent into the rivers. But it seems many of these chemicals are still active and they've having an effect on fish.
Planet Earth Podcast presenter Richard Hollingham has been talking to Charles Tyler from the University of Exeter, a world expert on the problem...
Charles - One particular group of chemicals that we've been focused on are chemicals called oestrogens, or environmental oestrogens and these are chemicals that can mimic and copy the body's hormone oestrogen, which is a female sex hormone. And these oestrogens include natural steroid oestrogens derived from women, derived from the human population; they include contraceptive oestrogens, from the contraceptive pill. Also, actually, things like horse oestrogens, equine oestrogens, which are used in hormone replacement therapy, and then in addition to that they also include chemicals that copy and mimic the structure of those natural steroid oestrogens, so various industrial products.
Richard - Now, we're in one of your aquarium labs at the University of Exeter and surrounded - well floor to ceiling - by transparent tanks full of, well, beautifully colour zebra fish zipping backwards and forwards, and they're called zebra fish because they have these stripes running horizontally along them and each one, I suppose, I can't really measure them because they are going so fast are about 2 cm long.
Charles - These are one of the key model species we now use to try and help us understand how some of these chemical I mentioned, how they work in the body. Because we know now from studies on wild fish that they're being affected by these chemicals that are being discharged, they're being feminised, males are being feminised essentially. And so one of the big questions that we're trying to address in relation to the use of the zebra fish is how and where these chemicals work in the body.
Richard - And you say they're being feminised, what do you mean by that?
Charles - That males are showing traits or characteristics which are normally found in females. So defining feminisation in fish includes they're producing proteins which are normally only found in females, the yoke proteins, for example, which normally go into the eggs. They include alterations in structures within the testes so the male gonad. They include, in particular, the presence of developing eggs within the testes so quite unusual phenotypes and quite unusual effects are being seen in the fish as a consequence of exposure to these oestrogens.
Richard - Now these zebra fish in here are not ordinary zebra fish. These are engineered to help you with the work?
Charles - Absolutely. These aren't native to English rivers and we're using these very much of a model to try, as I say, to understand how chemicals work in the body. And this is some work that Tetsuhiro Kudoh, a colleague, and myself have been developing over time to help us understand where these chemicals work in the body. So, these are what we call transgenic fish and essentially there's some clever little genetic constructs have been placed into these fish in turn which then produce a green florescence, they glow green essentially, in target tissues which are receiving and responding to these environmental oestrogens.
Richard - Now if you're a male fish feminisation sounds like a bad thing, but not necessarily and this is what you're investigating now.
Charles - Absolutely. So our concern really has been that we find this widespread feminisation of fish in English rivers but we don't know whether it's causing effects at a level of the population. Now it matters if you're an individual fish and you are feminised because you have a reduced capability to breed but does that really matter from the point of view of population? When we think about protecting the environment, we don't protect at the level of the individual for wildlife like we do for human health, we protect at the level of population. So some of our parallel work now is trying to address whether there are changes in the populations of wild fish living in English rivers.
Richard - And how do you go about doing that at a population level? You can see these zebra fish in the tank and you can see if they've got this florescence so they're being feminised but how do you take that next step?
Charles - Addressing the population level consequences of something like this is an extremely difficult and challenging question to address. In fact there are very few examples for any chemicals discharged into the environment where you can assure population level effect and link it to a specific chemical. The way we're going about it is we're trying to address whether there has been changes in the genetic structure, changes in the genetics of wild populations and we're doing this by comparing those genetics of fish in the more polluted rivers compared to those in cleaner environments. So, we're using specific genetic tools to help us identify if the populations have changed.
40:31 - Finding and Fighting Bed Bugs
Finding and Fighting Bed Bugs
with Clive Boase, the Pest Management Consultancy
Chris - Cases of bed bug infestations we've heard are on the rise, but how do you know you've actually got them and what can you do if you have got them? Clive Boase is from the Pest Management Consultancy. Hello, Clive.
Clive - Yeah, good evening.
Chris - So, tell us then, how do I know I've got bed bugs in my house? I mean, I haven't. I've done it before I'm done with my mortgage value of my property, but would I know?
Clive - Not surprisingly for blood-feeding insect, the first time you'll get of an infestation or the first time that most people get is the appearance of bites, and as we've heard earlier, these can be really quite unpleasant, red, itchy lesions. They could appear anywhere on your body, but most typically, they're on those parts of your body which are out of the covers when you're sleeping at night. So, it's going to be the neck and the shoulders and perhaps the sides of your face, maybe the arms; those parts of you that aren't covered up when you're in bed. Now of course, the trick is to recognise these as insect bites as opposed to some other kind of skin disorder. Many people we meet, their story running into a bed bug infestation is to say they had a skin condition. They put it down to maybe some kind of eczema or allergy, they treated it, and often, it's not until a few months later, 3, 5, 6, 7 months later that by some chance situation, the home owner actually spots insects in the bed and draws the connection between this hither-to eczema-type skin condition in the insects and realising it's not a skin condition at all. It's actually bites from the bed bugs. Bed bug awareness on the part of homeowners generally is perhaps one of the most important things that we've done to speed up the identification of individual infestations and as a result of that, the treatment and elimination of them.
Chris - So what advice can you give people about not bringing them home from their holidays?
Clive - If you're staying in a hotel or any other kind of accommodation away from home, then be aware of bed bugs. The chances of picking up bed bugs is actually very, very small. You know, I really wouldn't want to give the impression that the hotel industry in this country or any other country is awash with bed bugs. They're not. The figures we have show that the percentage of rooms affected by bed bugs are really very, very small, less than 1 in 1,000, sometimes down to 1 in 10,000.
Chris - How do you know that? Do you have to go and sleep in the bed and see if you get bitten?
Clive - No, we collect statistics from hotels and as I said, contrary to popular opinion, bed bugs are really not that common in hotels despite what you read in the newspapers. The most important things to protect yourself are; be very aware of buying second hand bedroom furniture. Think again about that second-hand mattress. Think about that second hand bed or that bedside table that you're thinking you might buy. Bed bugs are very commonly moved around on those sorts of items, so be aware of that. And again, don't move into premises where there are bed bugs. If you're thinking of renting a bed set or a flat or somewhere, have a look for signs of bed bug infestation. What we're looking for are the faecal spots of bed bugs. As we've said, bed bugs feed on blood, their faeces are very dark coloured, and typically, what we'll see is numbers of small dark spots, perhaps the size of a pinhead, maybe a millimetre across or so around bed bug harbourages and as Toby said, those harbourages maybe on or around the bed. So we might be looking for the beading around the mattress, around the buttons on the mattress, around joints in a wooden bedframe, where the skirting board joints along the wall, if you've got a white skirting against the wall, if we've got little bits of lose wallpaper, a back of the headboard will be the classic sign. So, if you're thinking of renting a furnished flat, a furnished bet set, have a look at those sorts of areas and if we're seeing little black spots around there, then be very, very careful.
Chris - So, if someone calls you in and you have a look at the bed and you see these black spots and that's the danger sign to you, what do you then do, tear the room apart to see if you can find them? What do you do?
Clive - In order to start a treatment programme, we really need to confirm that they really are there. We don't need to find every last one. We're just looking for enough of a sign to say, "Yup! The room is infested." And then a bed bug treatment programme might start.
Chris - Just in one room or does that mean, you got to blitz the whole flat or the whole house, or whatever?
Clive - Bed bugs as we've heard are really quite mobile and if we've got a typical 2, 3-bedroom house, if they're in one room, the chances are, they're in another. So, don't stop at the first room where the original sighting or the original concern is raised.
Chris - I mean, if you live in a block of flats or maisonette or something, if someone downstairs has got them, could they crawl up into your flat?
Clive - Yeah, absolutely they could. This last week, I've been working a number of premises doing research work there and there, in blocks of sheltered accommodation, we're finding individual flats that are if you like, a focus flat that is really quite heavily infested. Then around that, we have a number of adjoining flats, not just adjoining on one level, but above and even below as well as you say, where we're finding lighter bed bug infestations. The indication is that bed bugs are spread from that original focus flat. In some cases where we've got really heavily infested flats, if we step outside of that flat into the corridor, and we can see actually bed bugs in the corridor around the door frame, perhaps around the lights on the ceiling in the corridor, and then even when we turn around 180 degrees from that badly affected flat and into the flat opposite, lo and behold, we find a few bed bugs in there. So, they will - we talked earlier, I think Toby talked about passive dispersal of bed bugs, but active dispersal between blocks of flats is really very, very important. And it's something, I think going back a few years, perhaps we didn't realise it happened to the extent it really does. We didn't think bed bugs are particularly mobile. Now, we realise they are.
Chris - What about getting rid of them? Once you've found them, you've identified positively that they're there, how do you get rid of them?
Clive - There's a number of options. There's the do-it-yourself option. There's not an option I'm in favour of. Again, when I get involved with people with bed bugs, there'll be this typical narrative history where eventually found they've got them. They will have tried to get rid of them themselves and they will tell me about, "Yes, we bought some aerosols. We bought some powder. We threw away the mattress. We got a new bed. We threw away the carpet and so on". After having done all that, they still got bed bugs. So, I would say that anybody who believes they've got bed bugs, they need professional advice and that professional advice may be input from a local authority pest control team, and there's still numbers of local authorities that offer pest control service, or a private company. And I think the important thing is to talk with a number of potential providers of the service, check out the service they can provide, check out the costs. Very importantly, ensure that they will guarantee they work, so it doesn't get a result, they will come back and do it again.
Can bed bugs transfer human diseases?
Toby - That's a good question. Luckily, it seems like no, they can't. We don't know why but often, parasites are very complicated transmission routes, but one doesn't seem to have evolved in the bugs luckily for us. But the bites are kind of a problem on their own because you can get quite severe reactions.
Is traumatic mating evolutionarily old?
Richard - No, it didn't preceded it. It came secondarily. Bed bugs do have a normal reproductive tract through which they lay their eggs and this is a way of the males bypassing the normal route to try and get more of the offspring for themselves.
Do bed bugs prefer certain people?
Toby - I don't think some people attract them more. It may just be that some habit that those people have, they may have gone to the same place which had an infestation and they were bring it back from that same area, but I'm not aware of any evidence that they prefer certain people to others.
Chris - Clive.
Clive - Bed bugs do seem to be really quite choosy. Time and time again, we hear a situation typically where we've got a couple of people and they say, "My wife gets bitten and I don't" or "My husband gets bitten and I don't". we don't fully understand that, but the reality is that bed bugs do appear to be quite choosy.
Chris - Rather like mosquitoes then because there are certainly mosquito attractive people and mosquito repellent people like my wife is an absolute magnet for them, I never get touched.
Clive - There are also people who don't react to mosquito bites and those that do, and sometimes the differences are down to the sensitivity to the person, the reactivity of the person rather than to the choice of the bed bugs. So, there's more work to be done in this area.
Can an electric blanket kill bed bugs?
Toby - It depends if you've got a super-hot electric blanket, but no.
Chris - A serious electric blanket, wouldn't it?
Toby - Yes, exactly!
No, they're quite happy at the temperatures an electric blanket would have. In fact, one of the hypotheses is that central heating - keeping the house a certain temperature - has actually helped them. They don't die off in the winter, which they might have done back before we could maintain a constant temperature.
I don't think an electric blanket would have the best thing for you!
Do bed bugs hibernate?
Toby - They don't really hibernate and it's now more that in the winter, we have these constant room temperatures, so the temperature drop isn't that big an issue.
Chris - Clive, anything to add? Should you strip the room, get rid of the curtains as well, asks Cameron?
Clive - Where we have a deep seated infestation and if we have items that can't be treated by the means, then yes, disposal of infested items may be a route to go down. But in general, most items can be treated either with insecticide or with heat treatment. But as Toby said, higher temperatures you need to get with the domestic electric blanket. We're looking at typically 55 - 60 degrees will be enough to cause bed bug mortality.
51:33 - How long could one survive eating yourself?
How long could one survive eating yourself?
We put this to Louise Anthony, a medical student at Addenbrookes hospital, Cambridge...
Louise - To work out how long someone could survive by eating their own limbs, we need to make a number of assumptions.
Firstly, we assume that the surgery and subsequent possible infection itself didn't kill them, and we'll ignore the massive energy demands of healing from such an injury. Then we need to assume that you can store your freshly harvested limbs safely, and that you have some cunning way of feeding yourself once you've removed both your arms.
So, with that in mind, we need to know what our daily calorific demands are, and how much energy is available in our limbs.
Firstly, how much raw limb is there to harvest? According to figures collected by NASA for their average 82.5Kg crew member, the arms and legs make up approximately 40% of body mass - in this case, around 32Kg.
To work out how much energy is available from this, we need to use something as a proxy, because little is known about the calorific value of human meat. In this case, we'll use uncooked pork chops, which, according to a well known high-street supermarket, offer 213 calories per 100g. This means that our 32Kg of limbs could provide an impressive 68,000 calories.
But how long would this last?
The World Health Organisation has an equation that we can use to calculate daily energy requirements. For a male in his 30s, this is 11.6 x weight in kilograms +879. To take into account level of physical activity, this is then multiplied by an "activity factor" of 1.2 for sedentary people up to 1.4 for people with very active lifestyles.
Again, we need to make some big assumptions here, as a person with no limbs will have a very different balance of lean muscle vs other tissue, which will alter their metabolic rate.
Using this equation for the remaining 50Kg man, we get a daily requirement of approx 1750 calories per day.
At this rate, our 68,000 calories of human limb should keep our survivor going for around about 39 days, or hopefully long enough to be rescued.