Beware of the snail

Have you recently flown into the US from abroad? On the landing card it asks if you’ve been in contact with things should not be brought into the US.

Have you encountered agriculture or been on a farm?

Have you been exposed to people coughing ebola?

And then one slightly odd question that gets overlooked:

Are you carrying snails? (paraphrasing here)

This is because snails are actuallly really deadly. Or more specifically they are a vector for some really deadly parasites. Read about it, and how to control the snail/parasite spread over at Science FridayLymnea-snail.

Notes from the Field: The Maelstrom of Bee Viruses

I recently completed my PhD (yay!) and started my postdoc (eep!). I’m working at Martin-Luther University in Halle-Wittenburg. It’s no secret that I’m obsessed with the genetics of coevolution, I studied it in snails and trematodes in New Zealand for the last 6 years. So this postdoc is a change of pace in a very similar subject.



I’m studying the genetics of host-parasite coevolution in bees and their viruses. Specifically, I’m looking at host shifts, the genetics of increased virulence and the effect of recombination and migration on local adaptation. WHO’S EXCITED JUST BY READING THAT LAST SENTENCE? Me.

Honey bees with their varroa mites (the red dots near their wings)

Honey bees with their varroa mites (the red dots near their wings)

Let’s start with a little background. Bees have been declining across Europe and the US for the last few decades and the reason why isn’t quite clear. One hypothesis is that it is due to infestation with varroa mites, tiny mites that feed on the hemolymph of honey bees and increased in prevalence across Europe over the past few decades (similar pattern around the world except for Australia). However, the extent to which the varroa kills/harms/reduces the fitness of honey bees is unclear.


Enter the virus (and me, really). There are a series of viruses that are found in bees everywhere, including in honey bees, bumble bees and wild bees, Deformed Wing Virus (DWV). But it’s been at relatively low levels, and doesn’t seem to cause serious mortality within hives. Unless, that is, DWV occurs with varroa mites. Then the virus sweeps through the population, annihilating the hive. So, is this increase in virulence of DWV associated with an ecological shift, such that the varroa mites are injecting the virus when they feed, rather than the bees simply eating the virus when it’s found on flowers? Or is it a genetic change that has caused the virus to sweep through populations where it previously was fairly benign. And does this effect honey bees, or is it spilling over into the bumble bee and wild bee populations?

Honey bees with DWV.

Honey bees with DWV.

Which brings me to the field. The first step of my postdoctoral position has been to collect honey bees and bumble bees from islands off the coast of Scotland. Why islands? Because everything on the mainland is saturated with varroa mites. To compare the effect of the virus on bumble bee populations with and without varroa we’re looking at three types of islands: islands without honey bees (varroa can only infect honey bees), islands with honey bees and that don’t have varroa, and islands with honey bees and varroa. The list of things I want to do with this data is long, and will involve another post (stay tuned), but for starters we’re looking for transcriptional difference between the virus in these three types of islands.

And maybe looking at local adaptation. Or trying to understand how long it takes negative frequency dependent selection to act within an haplodiploid population. Or using spatial covariance to find the genomic regions involved in coevolution. Stay tuned kids, this is going to get exciting.

In the meantime, I’ve got to go collect some more bees.

Where the bees are. In this case, Colonsay Scotland.

Where the bees are. In this case, Colonsay Scotland.


Save the tapeworm! And the Kakapo…

One of New Zealand big five species to see (think African safari checklist, but for flightless birds in New Zealand) is the kakapo. These parrots can live up to 95 years (maybe longer) and is very close to extinction.

So tape worms were found within a pair of captive kakapos, conservation biologist dewormed them.

Which may have been a mistake. Hamish G. Spenc

“Some of these parasites may turn out to be quite good for their hosts” – Hamish G. Spencer

Want to find out why? Check out the article over at the New York times!


The enemy of my parasite is my… Frenemy?

Parasites are all around and often problematic.

But recent work from Kayla King has demonstrated that some microbial parasites can evolve to be mutualistic and defend against more virulent parasites.  And what’s more this shift from foe to friend can happen rapidly.

Read the paper here, or the synopsis over at National Geographic.


Another Bacteria that Causes Lyme Disease

Sure, finding new and interesting species and describing them is exciting.

But finding new bacteria that cause a well understood disease? Equally if not more exciting (my little parasitic loving heart is all aflutter!).

While it has long been thought that lyme disease is caused by one bacterium (Borrelia burgdorferi), researchers at Mayo Clinic found something floating around in blood samples of people suspected of having Lyme disease that is totally different.

It has been named Borrelia mayoniiand it is remarkably similar to it’s lyme disease causing brethren. But it also has some important differences.

Read all about it over at NPR


Save the Bananas!

Interesting facts: All commercial bananas in the US/Europe/Canada (really all imported bananas) are all decended from one banana grown on the estate of the Duke and Duchess of Devonshire (Chatsworth House).

They are all clonal, which makes them particularly susceptible to a coevolving disease.

Such as Panama Disease, which is now killing off bananas in the thousands.

What’s more, this has happened before… and may result in there being no bananas left on our grocery shelves.

Read more about it over at the BBC.


When infection is unavoidable, fruit flies ramp up recombination

So, you wanna head back to my place after this and make some recombinant offspring?

Imagine you find yourself in the midst of a large-scale epidemic, similar to the scenarios portrayed in movies like Contagion or Outbreak (or both!). The disease is extremely contagious, and the probability of becoming infected is high. Now imagine that scientists fail to discover a cure. There is no Dustin Hoffman-led team of military virologists available to develop a vaccine and save humanity, and the disease persists, with the potential to infect subsequent generations. In this harsh, disease-ridden environment, how could you ensure that your future offspring would survive?

It turns out, if you were a fruit fly, you might rely on recombination.

Disease is thought to have played a major role in shaping the reproductive strategies of animals. The Red Queen hypothesis predicts that species experiencing parasite-related selection pressures are more likely to evolve sexual reproduction, along with increased rates of outcrossing and recombination. This is because, in the ongoing evolutionary arms race between hosts and parasites, a little bit of genetic variation can make it a lot harder for the parasite to “win.”

But while strategies for increasing genetic variation may improve disease resistance, they often come at a cost. Increased recombination, in particular, can reduce fitness by breaking up locally adaptive combinations of alleles. One potential way to get around this issue is to increase recombination rates only when the risk of infection is high. However, we have yet to observe direct evidence of parasite-induced recombination in animals.

In a study recently published in Science, Singh et al. sought to investigate the capacity of fruit flies to plastically increase recombination in response to infection. To do this, the researchers infected Drosophila melanogaster females with a variety of parasites, and observed the proportion of recombinant offspring the females produced.

In order to track recombination events, researchers took advantage of the known genetic basis of two visible phenotypic traits. The ebony locus and the rough locus occupy nearby positions on the same chromosome in D. melanogaster, and recessive mutations at each of these loci have easily identifiable effects on the phenotype. For this study, the researchers generated females heterozygous at both ebony and rough.

Next, the researchers infected females with one of several different types of parasites. Two distinct (but similarly disturbing-sounding) methods were used to infect flies, depending on the type of parasite involved. In some trials, the researchers stabbed adult flies in the thorax with a needle covered in disease-causing bacteria. In other trials, the researchers housed larval flies with female parasitic wasps, allowing the wasps to inject their eggs directly into the larvae. Seriously, these flies must have been terrified.

A parasitic wasp (Leptopilina heterotoma) probes for fruit fly larvae with her ovipositor.

A parasitic wasp (Leptopilina heterotoma) probes for fruit fly larvae with her ovipositor. (Photo courtesy of Dr. Michael Martin)

Finally, the researchers backcrossed infected females to double-mutant males, and examined the resulting offspring. Sorting through thousands of individual flies, researchers identified recombinant offspring as those that exhibited one mutant trait but not the other.

As predicted by the Red Queen hypothesis, infected females produced significantly more recombinant offspring than non-infected females. The researchers saw this pattern across all types of infection studied, including infection by species that parasitize D. melanogaster in the wild. Furthermore, the effect persisted across host life stages, with females producing more recombinant offspring even when infection occurred during the larval stage of development.

The study also provided some insight on the underlying mechanism for making more recombinant offspring, which – surprisingly – appears not to involve an actual increase in recombination rate. Instead, the culprit looks to be some form of transmission distortion, whereby recombinant gametes are promoted at the expense of non-recombinants.

This study highlights the remarkable ability of individual organisms to rapidly respond to changes in the environment, as well as the central role disease has played in shaping the evolutionary trajectory of animals.

But the reason I’m REALLY excited about these findings is because of their potential to reinvigorate the post-apocalyptic science fiction genre.

Picture this: 50 years after the emergence of an unprecedentedly deadly cross-species pathogen, the majority of the planet’s human population has been wiped out. The only people remaining are the highly recombinant offspring of those infected with (and ultimately killed by) the disease. In a world where survival of the fittest reigns supreme, these exceptionally disease-resistant individuals must attempt to rebuild society as they contend with resource shortages, lawless bands of savages, and the unknown genetic ramifications of the extreme levels of heterozygosity within their population.

It sounds like the beginnings of a pretty solid screenplay to me.

While you’re waiting for my movie to hit theaters, you can read the full text of the Science article here. And check out the video below (courtesy of Dr. Michael Martin), which shows a parasitic wasp female attempting to deposit her eggs in some (probably pretty freaked out) fruit fly larvae.

The Lady Gaga of ferns, and the Spartacus of ants

Friend of the blog (and former contributor) Devin Drown is wrapping up his first year on the faculty of the University of Alaska Fairbanks, where he’s been teaching the Principles of Evolution course. As a final assignment, Devin’s students are contributing posts to a class blog, Evolution, Naturally — and the first couple are great!

Margaret Oliver digs into the phylogenetic data used to support the renaming of a genus of desert-adapted, clonally reproducing ferns — after Lady Gaga. It turns out that the singer’s stage name is literally encoded in the DNA sequence that helps differentiate the new genus from its closest relatives, as Oliver illustrates in the best. Phylogeny. Figure. Ever.

(Evolution, Naturally)

Oliver’s Figure 3. (Evolution, Naturally)

Meanwhile, Alexandria Wenninger explains how some species of ants steal larvae from other ant colonies and raise them as workers — and how entomologists are discovering that those kidnapped workers can resist this unasked-for reassignment.

However, there is a growing body of evidence suggesting that the [captured workers] are not always so oblivious to their origins, as researchers observe more and more situations of what they are calling “slave (host) rebellion”. Czechowski and Godzinska, in their recent review article, “Enslaved ants: not as helpless as they were thought to be”, identify four types of rebelling behaviors, which range from aggressive acts by individual ants to a collective uprising against the parasites.

Feeling a little ill? Blame the trees (not just their pollen either)

A fungus called Cryptococcus gattii, has long known to be infective to humans… even though it’s found on trees.

This has particularly been a problem in Southern California, where people have been getting sick from C. gattii for yeas, and no one knew which tree was harboring the fungus. Find out who the culprit is and how they figured it out! 




Ed Yong on mind-controlling parasites

Here at Nothing in Biology Makes Sense, we’re fascinated by all the weird, baroque ways that living things influence and coevolve with each other—so Ed Yong’s new TED talk about mind-controlling parasites is right up our alley. Just like his writing—currently on display at National Geographic‘s Phenomena, among many other venues—it’s a compendium of nifty natural history punctuated with highly educational gross-outs and the occasional black-belt level pun.