Bye, bye Helicobacter – or back with a vengeance?

Bye Jonas Waldenström

Of all inhospitable places, your stomach is one of the most hostile. Made to dissolve the food you eat, this interior body chamber is a veritable hell and any bug aiming to infect your intestines needs to survive a long hydrochloric acid bath. Thus, your stomach is a barren, acid wasteland. Or, at least that was what everyone believed until two Australian researchers – Barry Marshall and Robin Warren – entered the limelight. The duo repeatedly found curved rod-shaped bacilli in gut biopsies from humans with gastritis, and speculated that it may be the causative agent behind this and other gut diseases.

Say hello to Mr Helicobacter pylory! He is a curved rod with a bunch of flagellae. He likes to live in your stomach.

At first no one believed them; their findings were directly contradicting the existing paradigm. They were criticized, even ridiculed. ‘Something living in the stomach?! Bah, humph! Contamination, dear fellows, CONTAMINATION!’ However, quite soon it became clear that Marshall and Warren were right. Even more so, the bug – nowadays known as Helicobacter pylori – not only thrived in the stomach, it was also a pathogen associated with important human scourges as peptic ulcers and stomach cancers. Suddenly there was a biological target to hit in order to tackle these diseases – a major finding that has changed the lives of many, many people in the world. In recognition of their contribution to science, Marshall and Warren were awarded the Nobel Prize in Physiology or Medicine in 2005. Marshall also used himself as an experimental model to test the causality of Helicobacter pylori and gastritis. He simply swallowed a culture from a Petri dish and, yes, he developed the nasty symptoms! (As well as bad breath, mostly noted by his mother). Although not generally recommendable, it served a point and the Koch’s postulates were met.

The two laureates Marshall and Warren in their younger forms

Last week I attended the CHRO 2013 meeting in Aberdeen, Scotland. This biannual meeting brings together the biggest brains on Campylobacter, Helicobacter, and related organisms, and is a very nice melting pot. Here you can meet and discuss with friends and foes from the four corners of the world, and peek on the latest news from the research front. I really like these meetings, particularly because of the friendly attitude. This time the organizers wanted an historical perspective, as it is approximately 30 years since both Campylobacter and Helicobacter were recognized as pathogens (and also since the professors that was there at the start are soon to retire). I am generally a Campylobacter-guy (and flu-guy), and have only published one paper on Helicobacter. But I find the bug intriguing. Not only because of the link to diseases, but also their limited transmission (within families mostly, due to kissing, or perhaps fecal-oral transmission) that even make it possible to use them as a proxy of population origin. Make a map of Helicobacter relatedness and it will give a nice map of the world. It is also a bug that doesn’t cause disease quick, or at all. In fact, more than half of the world’s population is infected with Helicobacter, and the vast majority will never experience any symptoms. It is quite likely that you (or me) are carrying this bacterium right now, but that we only will have symptoms if our equilibrium is altered, by prolonged stress or other conditions.

Breaking a paradigm may at first be hard

The field has come a long way in the three decades of research. A success story really. Now we can fairly easily cure Helicobacter infections with different antibiotic therapies. Severe, bleeding peptic ulcers are nowadays rare. However, Helicobacter as a cause of gastric cancer is still a major issue. In fact, this bug is one of the top carcinogenic microorganisms we know of (together with human papilloma virus and Epstein-Barr virus) and stomach cancer is one of the most common cancers in the world responsible for roughly 9% of all cancers. So how can Helicobacter cause cancer? This isn’t all settled yet, and is likely multifaceted. A lot of the pathogenesis involved, including the different biomolecules and pathways, is so now targeted in research, and also how differences in lifestyle and genetics affect the likelihood of developing cancer.

The incidence of stomach cancer is highest in Asia, and there are now plans to perform large-scale eradication of Helicobacter in the human population in Japan. The tools are there, and now the question is if we can achieve the goal in practice? The infection can be detected with simple breath tests and only those persons that are positive need to get therapy. However, nuking away Helicobacter at large scale can come with a cost – and possibly a rebound. In essence, this is a biological manipulation of an ecosystem – bug and human in this case – through a mediator that is antibiotics. Let’s face it: our track record in fiddling with nature isn’t great. Consider the introduction of Aga toads in Australia, water lilies in Africa and many, many other examples of exogenous fauna manipulations. As regards diseases, despite a century of medical invention, drug discoveries and vaccine developments we have actually only terminated one single disease: smallpox. In many other cases we have just given ourselves respite while resistance is slowly developing.

The problem is two-fold. First, antibiotic therapy imposes an enormous selection pressure. Any bug out there with any type of resistance to the drug will be at an advantage and can increase in frequency in the population. Given the generation time of bacteria vs. men, the bugs are usually those running the shots. (For an excellent view of evolutionary medicine please view Professor Andrew F. Read’s TED-talk.) The harder we hit, the higher the gain is for the mutants. And if therapy coverage isn’t good enough foci in the population of humans may still carry the bacterium and transmit it back. Helicobacter is a bit special, I admit as much, and perhaps easier to eradicate than other diseases. Still, the question is whether the limited distribution of the bacterium, the efficacy of therapy, and stringent follow-up is enough to get rid of Helicobacter, or, whether one is creating super-resistant bacteria that will increase in frequency? We don’t want to have any Darwinian-demon helicobacters.

The second problem is the ‘what if’-dilemma. Okay, Helicobacter pylori is for certain a pathogen. But it isn’t causing disease in all humans, rather in specific persons under certain environmental conditions. Stress, coffee and diet will influence your gut, and the ability for Helicobacter to cause harm. But what if Helicobacter is also providing some benefits to us? Something we are not even aware of. Maybe they outcompete other potential stomach colonizing bacteria? A particular worry could be the >20 other Helicobacter species described in other animal species (of which some have also been detected in humans). What if they find a niche in humans in the post-Helicobacter pylori world? Are they big velicoraptors waiting in the shadows?

Time will tell. And risks and benefits need to be weighed. Undoubtedly, an effective strike at a bug is really tempting if it will reduce the incidence of gastric cancer in the years to come.

Waldenström, J., On, S.LW., Ottvall, R., Hasselquist, D., Harrington, C.S. & Olsen, B. 2003. Avian reservoirs and zoonotic potential of the emerging human pathogen Helicobacter canadensis. Applied and Environmental Microbiology 69: 7523-7526.

Ebola, Chikungunya and Newcastle – of places, names and Mallard viruses

By Jonas Waldenström

Home of the Ebola

Unlike most organisms, viruses are often named after the site they were first found. Sometimes these names give a flare of dark jungles, full of mosquitoes, and the eyes of unknown animals that stare at you in the dark. Surely, the name Ebola is enough to spark fears in any man. This virus, named after a river in Congo, is one of the ugliest viruses we know of: a hemorrhagic fever virus where you literally bleed to death. I think of the Heart of Darkness, that dark Joseph Conrad novel. It makes me shiver, every time. A related virus is Marburg virus, named after a city in Germany where a laboratory worker accidently infected himself and caused the first human case. Although from Germany and not a deep African jungle, a Marburg virus still sounds like a vicious killer, especially if said with a thick German accent.

Chikungunya to the right. To the left is the cat Shigella.

Another favorite is the chikungunya virus. I can’t decide whether it is the name of a fluffy rabbit, or something very deadly. Mixed feelings for that name. The virus is pretty bad though. A mosquito borne illness first discovered in Tanzania, but which name does not denote the place of origin, but the local name for “that which bends up“. That prosaic word stems from the contorted posture of patients suffering joint pain and arthritic symptoms. However, although interesting (read: horrific) diseases, neither Ebola, nor Chikungunya virus are to be found in Mallards – my pet model species. But there is a city virus that does infect Mallards: Newcastle disease virus!

This week in the Virology Journal we published an article on the occurrence of Newcastle disease virus in Mallards sampled at Ottenby. Newcastle disease virus, or NDV for short, should not be mistaken for Newcastle Brown Ale. The latter is a pretty nice beer, the former an infectious disease of birds. In fact, NDV – or avian paramyxovirus type 1 which it is also called – can be a devastating disease in poultry. It is fairly rare in Northern Europe, but occasionally there are outbreaks in poultry. To complicate matters even more, there are three different classes, or pathotypes, of NDV depending on their severity of infection. Lentogenic viruses are fairly benign, and are not associated with severe disease, while mesogenic and velogenic strains are real killers. The difference between the pathotypes is related to genetic differences in the F protein of the virus, a key player in the fusion of the virus with the host cell. In order to infect the cell, the F protein must be cleaved by host proteases at the F0 cleavage site, and velogenic strains can be cleaved by many more types of proteases than lentogenic strains thereby causing a more systemic, less local, disease.

The Newcastle Disease Virus has a distinct circular capsid with small spikes.

So what did we do? Given that outbreaks are rare in Sweden, and occur mainly in late autumn, we wanted to know how prevalent NDV was in our Mallard population and whether this species could be involved in transmission. We screened roughly 2300 samples collected from migratory Mallards for the presence of NDV RNA. A molecular typing method is like a fishing expedition: you need to have the right equipment and the right bait to get the fish. Or, in our case, positive amplification of NDV RNA of the F gene in real-time-PCR assays. It took a lot of time and effort to optimize the protocols.

And what did we find? Twenty of the samples, some from the same individuals sampled more than once, were positive for NDV. This makes NDV pretty rare in Mallards, at least compared to influenza A virus that can be found in a prevalence of 10-30% at Ottenby in autumn. I had expected to see more infections, and the NDV was one of the viruses I had thought to include in coming viral pathogen assemblage studies. At the moment it feels a bit to rare to work efficiently with, but we will see. Paramyxoviruses are interesting and besides the NDV there is nearly two handfuls of other avian paramyxoviruses to screen for. The phylogenetic analysis, and the sequencing of the F cleavage site placed the Mallard viruses in the lentogenic group. And the risk for poultry from the Mallard viruses should be negligible.

NDV phylogeny from the study. Original picturee from http://www.virologyj.com/content/10/1/285

It is always nice to get a paper out. In the old days you could actually feel the glossy paper between your fingers – those days are more or less gone, with online-only and printed pdf. But it still feels good. And it feels even better today, after a few pints of microbrewery beer in Aberdeen – this is the closest I have been to Newcastle in years!

The full paper: Tolf, C., Wille, M., Haidar, A-K., Avril, A., Zohari, S. & Waldenström, J. 2013. Prevalence of avian paramyxovirus type 1 in Mallards during autumn migration in the western Baltic Sea region. Virology Journal 10:285.

Rollin’ rollin’ rollin’ – Aberdeen here we come

I feel like a cow on pasture, happy as a lark. Am on my way westward bound; first train to Copenhagen and then a flight to Aberdeen in Scotland! Why am I so happy? Well, first of all I have been home with the kids for roughly a month, on paternal leave, and it feel good to do some grown-up things for a change – like going to a conference. (And, yes, I love my kids, etc., etc., but it will be good to do something else for a few days). Secondly, I will meet a lot of colleagues from around the world, chitchat about bacteria and life, swing a jug of ale (or two) and enjoy the scenic interior of a conference venue.

The last part is true – if you go visit an exotic place for a conference, chances are that you mainly will spend your time in the hotel and in the conference venue. Long hallways with carpets, English breakfast and a touch of bland dullness. This particular conference series – Campylobacter, Helicobacter and Related Organisms, CHRO – is a biannual thing. Usually, the hosting countries are chosen so that it is Europe every second time, and US/rest of the world the other times. My first CHRO conference was in Freiburg, southern Germany in 2001, and then I went to Aarhus in Denmark in 2003, and Rotterdam in 2009. This means I skipped Australia in 2005, Japan in 2007 and Vancouver in 2011. Am I stupid or what?

This time I will be chairman in a session, which bespoke of a transition of states since that first conference in Germany. I can still remember it. It was my first conference what so ever, I had no clue what to expect. Sure as hell I did not expect to give a talk in front of 500+ people in the biggest session. Rock star stage and bright lights. I was the only one that used old-fashioned OH-slides… But it was good, I got a kick-start in Campylobacter research and many of the contacts I got there and then are with me still. And that is what makes conferences a great place to be: you learn the latest advancements in your field, and you make friends. And friends are good to have in science. And in life.

Admittedly, conferences are also places where people get too drunk, end up in the wrong bed and doing other bad deeds. But let’s not worry about that now. Aberdeen here we come!

This flu, that flu, and Tamiflu®

By Jonas Waldenström

Lovely start of the day. Not.

It is early morning, just before the alarm clock is about the give the wake-up call. You lie in bed. It is an ordinary day, just as all others; a day at work, kids at shool and all other steps on the treadmills that make up our lifes. But hey, what’s this? Your throath is dry, and your nose is warm. On top of that: headache, nausea and fever. Shit – you are sick! Is it the flu? Fuck!

This hypothetic and unfortunate morning scenario is not a rare occurrence. In fact, ever day, a fraction of the human population is down with a disease – caused by bacteria and viruses, and more rarely by fungi or protozoa. However, not all bugs are potent enough to keep you in bed. Many can be cleared by the immune system without you even knowing it. It has been estimated that each of us are at all times on average infected with 12 different viruses. On average! And in, and on, your body there are bacteria waiting for an opportunity to establish infection. We are, in truth, a walking goodie bag for pathogens!

But we are not helpless. The goodie bag is shielded by different lines of defenses in order to protect our cells from invading pathogens. It is just like a battlefield of old times. First line defenses are structural obstacles, such as skin, nails and other solid barriers that keep the bugs out. (There are also behavioral defenses, such as wash your hands, don’t eat poo, stay away from rabid dogs, etc). Then, different excretions of slimy substances, like snot in your nose, mucus in your airways and in your gut – all there to wash the bad guys away. There is also an army of specialized molecules and cells of the immune system patrolling around in our blood and lymphatic systems. Some of these guys are rather non-specific brutes, punching holes in bacterial membranes, others have the function of whistle blowers, recruiting the heavy machinery in forms of macrophages and neutrophils. This perpetual war is constantly waged in our system, each and every day. Even now when I sip my morning coffee and write this blog. Hail the immune system – it is your best friend (and sometimes your worst enemy, but that’s a topic for another day)!

On top of the natural defenses, we humans have invented a range of drugs to help fight diseases. We are best at fighting bacteria, mainly because their metabolism and their cell membranes are so different from ours. This means that we can attack them with substances that are harmful for them, but which actions have negligeble effect on ourselves. Antibiotics are, in other words, a nuke that only kills bacterial cells. For viruses the best defense is vaccination, triggering the memory part of the immune system to produce pathogen-specific defenses. Drugs are usually less effective against viral infections, as the virus particles spend most of the time inside cells, and thereby are harder to nail. Secondly, as viruses do not have a metabolism of their own there are fewer targets for us to aim at.

With that said, there are acutally a few substances that work on viruses. One famous drug is Tamiflu®, or oseltamivir as it also known as, which works against influenza virus infections. If you know Tamiflu by name it is likely due to the attention the bird flu (H5N1) and the swine flu (H1N1) viruses got during the last decade. You might even have taken it yourself during an influenza infection? Oseltamivir is what is called a neuraminidase inhibitor. Simply, it interferes with the catalytic action of the influenza virus’ surface protein neuraminidase (the N part of the name used in classification of subtypes). Neuraminidase proteins help releasing new virions from an infected cell, by scissoring of all the anchorage of the particle with the cell wall, and if this process is halted there will be less spread of viruses and a reduced number of infected cells.

It is not a wonder drug. My physician friends say it reduces symptoms with a day or two in already infected patients. The best effect is seen when the drug is used prophylactic, to reduce the chances of becoming sick. This property is what have made governments all over the world to stockpile it, in the case of a new flu pandemic and the shit hits the fan. A defense of sorts, albeit a rather weak one. But, a weak defense is better than none – as there will take time to generate, and to distribute, a new vaccine in case of a pandemic.

However, a weapon needs to stay sharp, otherwise it looses its use. Many antibiotics are nowadays countered by bacteria with acquired resistance. Trying to fight resistant bacteria with the wrong antibiotic is like fighting windmills with horses. Not very effective. The best way of keeping a weapon sharp is actually not to use it. Keep it on the shelf, and not prescribe it to patients. The same story as for antibiotic resistance goes for Tamiflu – resistant seasonal flu viruses started to appear not long after the drug was first prescribed in larger quantities. With time, the proportion of resistant phenotypes has increased, clearly indicating that there is a selective advantage for human-adapted flu viruses to be resistant to this drug. And that the benefits overweighs any costs associated with this trait. The question is whether the mutations that render the virus resistant occurs also in wild type viruses, those that have not yet crossed species barriers and jumped from birds to mammals and humans? And what mechanisms that induce resistance?

In our zoonotic network, the Uppsala node headed by Dr Josef Järhult focuses on these kinds of questions. In his studies, Josef has shown that the concentration of oseltamivir that can occur in natural waters downstream cities during an outbreak of seasonal influenza is sufficient to cause wild type influenza viruses to evolve resistance. How can this be? Well, to start with not all of the drug is processed by the body, a rather large proportion is excreted in the urine. As the drug is fairly persistent, the treatment in the sewage plant will not affect it and it can thereby reach the natural water column. And in water there are ducks, and in ducks there are influenza viruses. Hence a potential way of making viruses resistant just by peeing out the drug in the toilet!

To study this in detail, Josef, his PhD student Anna Gillman, and colleagues from Uppsala, Umeå and Linnaeus Universities invented an infection model to study natural transmission of influenza viruses in ducks. I like to think of it as the ‘Järhult model’ – it is simple and elegant. What you do is to have a room in which you place two ducks. You infect the ducks in the bill with a suspension of virus. This artifical infection will cause the ducks to be infected with influenza viruses, and viruses will start to replicate in the gastrointestinal tract of the ducks. After a few days, virions are excreted with the feces and it is time to bring in some fresh ducks. In this case the new ducks will be infected by natural transmission via the fecal-oral route, and the backside of forced infections are avoided. By constantly, every two or three days, bring in new and take away old ducks one can passage viruses in a number of duck individuals and study what is happening with the viruses with time. As the main research question is induction of resistance mutations, Josef and coworkers can adjust exposure to Tamiflu in the drinking water, mimicking different environmental settings from the wild.

The ‘Järhult model’ from PLOS ONE 8(8):e71230

In a couple of publications, one which came out just a few weeks ago, the team (where our Kalmar ZEE laboratory is partaking) has shown exactly what happens when a wild type low-pathogenic virus is exposed to drug selection pressures. It seems that there is a certain drug concentration treshold that determines whether drug-resistant mutants will take over the virus population or not. Generally, the influenza virus is such a poor proof-reader during replication that loads of mutants are created in every infected cells. By pure numbers, any infected duck has the potential to carry a mutation that affects drug resistance. But, the selection pressure, in the case environmental load of the compound in the water, needs to be strong enough for it to increase in frequency. Actually, classic population biology, but on viruses and not beak length as in the Darwin finches of Galapagos.

Interestingly, resistance could be induced with the same relative ease in two very different types of neuraminidases, representing the two major classes of the proteins: the N1 group that contains the subtypes N1, N4, N5 and N8, and the N2 group that contains the subtypes N2, N3, N6, N7 and N9. The actual mutations are not the same, as these proteins functions slightly differently and have evolved separately for a long time. However, the phenotypic response is similar, and so is the growing take-over of resistant vs susceptible viruses in the virus populaton over time in the experiments. This also suggests that the initial mutation, which changes the neuraminidase function, is backed-up by later compensatory mutations that make sure that fitness is maintained in the mutant virus.

Dear reader, if you are still with me so far down on the page, you may ask what this is all good for. After all, a duck is duck, and a man is a man, and “I ain’t afraid of no virus”. Well, perhaps you should be worried. Sooner or later there will come a new flu pandemic, most likely caused by a virus with a genome partially derived from a duck influenza virus. When that happens we need every gun and man we can muster, and therefore we need to know if the Tamiflu bullet will be explosive or not. What weapons we have should be wielded wisely.

Links to the papers:

Gillman, A., Muradrasoli, S., Söderström, H., Nordh, J., Bröjer, C., Lindberg, R. H., Latorre-Margalef, N., Waldenström, J., Olsen, B. & Järhult, J. D. 2013. Resistance mutation R292K is induced in influenza A(H6N2) virus by exposure of infected Mallards to low levels of oseltamivir. PLOS ONE 8(8):e71230. doi:10.1371/journal.pone.0071230

Järhult, J.D., Muradrasoli, S., Wahlgren, J., Söderström, H., Orozovic, G., Gunnarsson, G., Bröjer, C., Latorre-Margalef, N., Fick, J., Grabic, R., Lennerstrand, J., Waldenström, J., Lundkvist, Å. & Olsen, B. 2011. Environmental levels of the antiviral oseltamivir induce development of resustance mutation H274Y in influenza A/H1N1 virus in Mallards. PLOS ONE 6(9): e24742. doi:10.1371/journal.pone.0024742

Perdeck revisited – or how well does a Mallard know its way?

By Jonas Waldenström

At this time of the year the air is full of migrating birds. Some, as cranes or geese with their conspicuous formations are easily spotted with the naked eye, while other birds, including most smaller songbirds, fly at altitudes where you need a scope to see them. But you can often hear them; each species has its own tune, and an experienced ear can tell them apart on call alone.

The question “how do they find their way” is as old as the field of ornithology itself. Generally, migration wouldn’t be possible without some sort of compass; a way of telling the bird in which direction to move. It has been shown that birds may use the sun, the stars, and the earth’s magnetic field for assessing their heading. And in some species also visible cues, a sort of map sense from previous travels, or even olfactory cues (a posh word for smelling where home is). As the vast majority of birds migrate without the guidance of their parents (which seems reserved to some flock-living species), a juvenile bird must be born with not only the tools to assess where it is, but also a sense of where it should go.

One of the pioneering fathers of ornithology was the Dutch professor Albert Christiaan Perdeck. He made one of the first real tests on how birds can sense where they are going, and how they can adjust the course if they get out of track. In order to test this he wanted to do a displacement study, where birds should be experimentally transported to a novel site, far from the catching site. As this study was conducted in the 1950s, in the pre-gadget era of ornithology, he needed a species that he could catch in large quantities, and where ring recovery data could be collected. His choice of study animal was the European Starling Sturnus vulgaris, a common farmland bird in most of Northern Europe. Starlings in autumn can aggregate in huge flocks, sometimes consisting of several thousand individuals, and was thus a good target species for Perdeck.

With a remarkable enthusiasm, the team caught and ringed thousands of starlings. Some were released at the ringing site in the Hague, while the other half were transported with airplanes to Switzerland and released. After some time the ring recoveries started to come in, and the results were extremely interesting. It seemed as the young starlings had a vector compass, as the birds that were transported south stayed on the same heading as they had when they were caught. But instead of ending up in Holland, the young starlings ended up way south, sometimes even on the Iberian peninsula. I wrote ‘young’ deliberately, as there was a clear age effect. Where the juvenile birds continued on the same vector, the adult starlings compensated for the displacement, changed course and headed to the original winter quarters. Adult birds are more experienced, and in the starling case they were able to adjust to the circumstances and get back on the right track. A quite remarkable feat – some of my colleagues cant find their way to the university canteen without a helper…

Spurred by the old studies (classics, you could say) and the advancement of new tracking tools we conducted a similar experiment with Mallards. The study was a collaborative effort with scientists from Sweden, Germany, the UK and Denmark (with the lead from Professor Martin Wikelskii at the Max Plank Institute for Ornithology, in Constance, Germany). Today’s gadgets can do stuff Perdeck could only dream about. During two autumn seasons, we caught juvenile Mallard females at Ottenby – our beloved duck field site – and equipped a total of 76 birds with satellite GPS transmitters. Half of the ducks were released at Ottenby, and the other half were transported in a private airplane to Lake Constance in southern Germany and released there. The tags had solar panels and, in the best of circumstances, had the potential to send data for at least two years; providing highly accurate GPS fixes at several times a day.

However, the best of circumstances is not often met in nature. The tags on the birds in Ottenby had problems with the lack of sunshine during Swedish late autumn and winter, and many of them just went offline. But a fair number of tags delivered data on movements both in autumn/winter and in spring, when birds headed to their breeding grounds. Contrary to the Perdeck’s starlings, our displaced Mallards did not continue migration in autumn; they stayed in the Lake Constance region. Of the Mallards released at Ottenby, some continued migration to the general wintering area of our study population, that is Denmark and Germany, south to The Netherlands.

After the winter: “most of the translocated ducks headed straight north-north-east, as if heading towards Ottenby, with one duck going as far as northern Sweden. Three of the transported ducks, however, first headed in a more easterly direction and turned northwards when reaching the longitudes of the area the control birds migrated to. It is unclear how these birds decided when to turn north, but the movement trajectories could be interpreted as if individuals had noticed that they were in the wrong place and then corrected for the southward translocation. Based on the observation that this second group of transported ducks ended up in their potential natural breeding grounds, and the first group had a more northerly heading than the control group, we conclude that mallards, just like the starlings from Perdeck’s original experiment, can correct for translocation during the spring season following the experiment.”

Thus, there was quite large differences between individuals in the translocated group, from those that seemed to take the shortest route north to Ottenby in spring, to those that followed a eastern direction (and then going north), more in the direction of what they should have had if the stayed in the normal wintering grounds: a flexibility in continental navigation and migration.

The article is open access and can be found here.

Apocalypse don’t-know-how – or where did the science go in the popular doom and gloom literature?

By Jonas Waldenström

I have thing for sci-fi and fantasy books. For periods I read little else but books with at least one flaming sword on the cover. Toss in a magician and some women in light clothes and it is a sure read. And, no, it doesn’t need to be poor literature. There are a number of really skilled writers that can tell a compelling story in beautiful prose. The challenge is to weed these authors out from the tons of really crappy Tolkien-copycat writers that flood the market.

Occasionally I read a doom and gloom book, like The Road by Cormac McCarthy, or Metro 2033 by Dmitrij Gluchovskij. Last night I finished World War Z: An Oral History of the Zombie War by Max Brooks. Yes it is true, I read the book instead of watching the movie. Kind of old fashion guy, I’d say. But hey, I am a freaking professor, so I should be old fashioned. Anyway, WWZ is a page-turner. Loads of zombies devouring flesh, eating entrails, moaning and groaning, creating havoc and scaring children. The story is also on how mankind responded to the zombie threat, first with panic, then with sacrifice, and lastly with vengeance and purging of the undead. And on how today’s societal structures and geopolitics influenced the post-apocalyptic world. For instance, India and Pakistan nuked themselves out of the board. USA, of course, liberated large parts of the world from their refuge west of the Rockies. Surprisingly, Cuba’s closed communism system transformed into a new democratic world power by immigrants. The people of North Korea disappeared into caves never to be seen again. Russia became a new Soviet Union, now with religion as a base.

Sometimes it is very technical account, with this and that ammo doing this and that harm to a zombie. You see, to kill the undead zombie you need to aim for the brain. Apparently a zombie can do without most things – energy, oxygen, metabolism, gastrointestinal systems, limbs – but not the brain. Thus to put the end to the gaul you need to hit the brain, either with a bullet, or with a handy medieval sword. And it is somewhere here I as a scientist start to feel neglected. So, the cause of zombie plague is a virus. Yes, a virus. OK, but what are the fundamental properties of a virus? First, they do not have their own metabolism and need to infect living cells in order to propagate. This doesn’t really go well in hand with metabolically dead bodies without circulation. How should the virus particle go about forcing the dead body to perform its new functions (namely: moaning, searching for living humans, devour human flesh, repeat cycle)? Second, a virus will have a genome – be it RNA or DNA – that encodes for proteins, which in turn perform certain functions. These functions can be described and analyzed.

Nowhere in the book is there a single scientist mentioned. No attempts to study the nature of this new disease. There is one guy who invents a wonder drug, but this is more on the lines of fraud than of science. One doesn’t need to go far in today’s society to see that scientists make up the forefront in the battle against new infections. For instance, a collaborative effort of the global virology community managed to crack the SARS nut and describe the corona virus that caused it. Today, there is a global task force on influenza, and other scientists try to identify the sources of MERS infections in Saudi Arabia. Thus, I have a real hard time to see that scientist wouldn’t have tried to tackle a zombie virus. It would have been better not to list the cause, or, take the extraterrestrial approach, than to say it is a virus.

But it is still an entertaining book. And it must be an awesome feeling to whack the undead in the head and saving the world. I probably need to see the movie, too. Perhaps there are scientists in that one – would be refreshing to see.

Finally, for those interested, there are a number of true pathogens that affects the behavior of their hosts. The term ‘parasite-induced trophic transmission’ (or PITT for short) deals with instances when a parasite alters the behavior of an intermediate host in order to increase transmission to the final host. There are liver flukes that make ants crawl up to the top of grass in order to be swallowed down by grazing ungulates. There are worms that make the antennae of garden snails to pulse and flash to attract predatory birds. There is a fungus that makes ants snap their jaws shut on the underside of a leaf so that the fungus can grow inside the body and then release the spores through a fruiting body extending out from the head of the ant. There are parasites that make honeybees into ‘zombees’ that fly around at night. There are hairworms that make terrestrial grasshoppers to hop out in water so that the worms can finish their lifecycle (while the grasshopper drowns).

However, none of these pathogens reanimates the corpse and make it go around eating things. And isn’t that nice?