A microsporidian like this is one-half of the perp identified as the cause of Honeybee Colony Collapse Disorder. This isn't the exact species, but is instead another microsporidian called Fibrillanosema that infects amphipods. Neat rows of polar filament cross sections line either side like cannon on a British Man o' War. In 3D, these coil around in a big spiral. Creative Commons Leon White

For the last several years, honeybee colonies have been emptying out like keggers at which the cops have arrived — and the bees show every sign of being just as out of it as drunk college kids. They abandon their hives to die alone and cold in the wild, striking a huge blow to North American apiculture and, until now, anyway, leaving everyone scratching their heads.

Well, no longer. Though early reports identified an Israeli virus as one possible cause, a serendipitous bioinformatics project taken on by, of all people, the military, along with Montana researchers, has identified a dual cause of colony collapse: a previously unidentified DNA-virus, and a fungus called Nosema ceranae.

For those who’ve been paying attention, a Nosema parasite of bees has been around quite a long time — Nosema apis. But the new species, Nosema ceranae, appears to have come from Asia. Is this yet another introduced species decimation story? ( See Elm, American; Chestnut, American; and White Pine, Western) Or did we just never notice it here before? (the species can only be separated by DNA or scanning electron microscope — not by light microscope) Too early to tell. And still, no one knows what the fungus and virus combo is doing to make the bees lose it:

Still unsolved is what makes the bees fly off into the wild yonder at the point of death. One theory, Dr. Bromenshenk said, is that the viral-fungal combination disrupts memory or navigating skills and the bees simply get lost. Another possibility, he said, is a kind of insect insanity.

Translation: Zombification, a well known problem for insects under the influence of parasites (see Parasitoid wasps, and Cordyceps fungi)

Here’s the critical bit from the NYT article announcing the discovery:

Dr. Bromenshenk’s team at the University of Montana and Montana State University in Bozeman, working with the Army’s Edgewood Chemical Biological Center northeast of Baltimore, said in their jointly written paper that the virus-fungus one-two punch was found in every killed colony the group studied. Neither agent alone seems able to devastate; together, the research suggests, they are 100 percent fatal.

Since a 100 percent correlation seems pretty convincing, so let’s go with the assumption these guys are right for now. And since the virus is as yet unidentified and undescribed, let’s take a bit of a closer look at Nosema. Because Nosema is interesting. Really interesting. As recently as 10 years ago this group of organisms — colloquially known as microsporidia — was classified with next to Giardia, the most ancestral (aka primitive) nucleated (aka eukaryotic) organism known. Seriously. This would be like putting Homo sapiens at the base of the eukaryotic family tree*, because it turns out Nosema is a seriously evolved fungus.   And in this case, as you’ll see, that crucial bit of taxonomic information makes a big practical difference in attacking this problem.

Microsporidians are all single-celled parasites that can infect nearly any eukaryotic host, but most have specialized on insects. They have a bunch of crazy standard features. First off, Nosema has no mitochondria, which is usually a requirement for self-respecting nucleated cells. Such nucleated cells, called the eukaryotes — or all life that isn’t bacteria or the similar looking archaea — employ tiny intra-cellular organelles called mitochondria to make energy using food and oxygen in the air. For the purposes of this post, we will ignore mitochondria’s fascinating origin story and incredible biochemical gymnastics and simply focus on the utter necessity of these organelles to the business of being alive for air-breathing eukaryotes (cyanide is fatal because it stops up the energy-producing works inside mitochondria), and how utterly strange it is that the otherwise unrelated groups of microsporidia, the parasite Giardia, and the amoebic parasite Entamoeba histolytica all lack them.

Instead, they possess an organelle called a mitosome, which seems to be a vestigial mitochondrion — that is, what’s left after the mitochondria are no longer necessary for cell upkeep and they start to degenerate to save the organism energy. Another example of vestigial and remnant structures might be the tiny leg bones still produced inside some snakes and whales — though these creatures’ ancestors stopped using their legs millennia ago, there is still a part a part of their genome that makes a much reduced and apparently energetically inconsequential vestige of them.

The reason parasites like these can get away with dispensing with their mitochondria is that  precisely because they are parasites, they bathe in nutrients inside their host. They don’t need to breathe; their host does it for them. This seems to have happened several times in unrelated parasite groups. But because single-celled organisms possess few morphological characters, these groups were originally all placed together because they shared what few traits we could see: degenerate mitochondria (mitosomes), a double nucleus (microsporidia often have this, and Giardia always does — why is this adaptive for a parasite? No clue.), and a parasitic lifestyle. So a bunch of these funky parasites were thrown together into a classification called “archezoa“.

But someone must have studied these organisms’ DNA and found a very different story: microsporidia aren’t primitive protists, and aren’t related to Giardia and Entamoeba at all. They’re highly evolved fungi called zygomycetes — the same group that produces the bread mold Mucor and most snow molds that live at the foot of melting snowbanks that I wrote about in an August issue of High Country News. As recently as just 10 years ago, as printed in my copy of “The Variety of Life”, by Colin Tudge, they were still placed firmly at the base of the eukaryotic family tree — not near the tips of the branches, embedded in the fungi. It seems that the “archezoa” was really more of a niche than a true taxonomic grouping based on relatedness — these things evolved to occupy the same parasitic niches, and in the process, evolved similar adaptations, much as whales and fish look alike but come from very different sides of the tracks.

Zygomycetes are so called from the greek for “yoke” because they make a special sexual reproductive structure called a zygosporangium that yokes together two fungi of different mating types (=gender). As fungi, they follow the typical fungal body plan of being a bunch of thin filaments (aka mold). To look at a zygomycete, you would definitely think “fungus”. Not so with microsporidia! They tend to be single celled spores. But they also have cell walls made in part of chitin — another trait that unites the fungi.

But here’s the *really* weird thing about microsporidia. They are parasitic fungi that have evolved to look like protists and *act* like nematocytes (the stinging cells of jellyfish and anemones): Inside the spore is a coiled harpoon-like injection apparatus (go here to see it in 3D, rather than the 2D view at the top of this post) they use to get themselves into host cells. Just like nematocytes (covered in this post), the coiled “rope” of the harpoon turns inside out when the cell is triggered — and does so in less than 2 seconds. Once deployed, this long narrow filament (common size: .1-.2 micrometers in diameter by 50-500 micrometers long — click here to see one whose spring has sprung) inserts itself in a host cell and pumps the contents of the microsporidian inside. Pretty soon, the now zombified cell gets busy making little microsporidia.

Here’s the final important point, from the NYT:

They said that combination attacks in nature, like the virus and fungus involved in bee deaths, are quite common, and that one answer in protecting bee colonies might be to focus on the fungus — controllable with antifungal agents — especially when the virus is detected.

So without the taxonomic work to know these little jobbies are actually fungi and not protists, we wouldn’t know that we might have a chance of tackling the major threat to bees today with existing fungicides. Who says taxonomy is pointless?

____________________________________________________________________

* OK, maybe not quite. Since Nosema is a severely reduced parasite, it’s more like putting mistletoes — severely reduced parasitic plants — down there.

Dengue virions (virus particles). They are the stack of what look like gumballs getting ready to avalanche at upper right.

Climate change scientists predicted this day would come: Dengue (den-GEE) Fever has re-entered the Florida Keys after an absence of 66 years. The tropical illness, once banished — like malaria– from the deep south, has re-established itself in the Florida Keys, where the CDC estimates that 5% of the population have already been infected.

It is possible the reintroduction has nothing to do with climate change. Certainly increased international travel likely brought us West Nile virus from Eurasia independent of temperature. But warming climates make it easier for the mosquitoes who carry the virus to make a living in more and more northerly climes.

I meant to write about this earlier when I first noticed it in the June 2 issue of New Scientist. But it was a recent article in the New York Times about how locals are shrugging it off that made me take notice.

Though an initial bout with Dengue may seem relatively innocuous, that is deptive. There are four strains of the virus that cause disease, but contracting one doesn’t confer long-term immunity to the others. In fact, it seems to make things worse through a phenomenon delightfully and unusually straight-forwardly named original antigenic sin. If your immune system mounts a response to one form of the virus, it makes antibodies whose blueprints are remembered by special cells called memory B cells. If a slightly different version of the same thing comes along, your body will try to mount a response to it using the cells it’s already manufactured. But because they don’t match well, your immune response ends up being less effective than if it had gotten a chance to tackle the virus with a clean slate.

Scientists hypothesize this may be the reason why people who’ve been infected twice are more likely to develop the more severe form of dengue, dengue hemorrhagic fever. Any time you see the word “hemorrhagic” in a virus’s name, that is not a good sign. It means bleeding — in this case, from leaky capillaries in such places as your gums, mouth, eyes, vagina, gut, skin pores, etc. Doesn’t that sound fun?

And this is not a virus that only attacks the weak. Though mortality rates are low, severe outbreaks have gripped South America in the last few years, including 55,000 reported cases, over 500 cases of Dengue Hemorrhagic Fever and over 60 deaths in Rio de Janeiro in 2008. Did I mention there is no vaccine or cure? Buckle your seatbelts, Southerners.

Aedes aegypti is the mosquito carrier of the Dengue virus. As you can see, the mosquitoes are ready and willing throughout the south. According to the CDC, 2.5 billion people, or 40% of the world’s population, live in areas where there is a risk of dengue transmission. Add the United States to the list.

Dengue viruses are in the Flavivirus family, named for the Yellow Fever Virus (Flavus is Latin for yellow)*. In this family you will also find West Nile virus, Tick-borne Encephalitis virus, and Hepatitis C virus. They’re all rather non-descript little round membrane-bound jobbies about 40-60 nanometers wide. Inside is a polyhedral (a 3-D polygon) protein structure called a nucleocapsid that is 25-30 nm across. Inside that is single-stranded positive-sense RNA (a kind of molecule that contains the information necessary to make proteins) that encodes the virus’s genes. You can get a better sense for how the capsid nestles into the lipid (fatty) membrane in the upper left image here. As with all viruses, the relationship between the Flaviviruses and everyone else is very uncertain, so no tree for you.

One final, adorable note. Apparently, in rural Australia they have trained schoolchildren to depost a “water bug” (in reality a freshwater copepod awesomely called Mesocyclops) that eats mosquito larvae into containers of standing water to help fight transmission of Dengue. Advantages: cost-effective, environmentally friendly. Disadvantage: the copepod is a host for the Guinea worm (remember them?). Good thing Australia doesn’t have Guinea worms.

_________________________________________________________

*Is it just me or do they need a Flava’Flavivirus family as well?

Apparently, in addition to all things jelly, I’m fascinated by all things blobby. You’ll note the restraint I used in not posting anything about that blob they found floating off the coast of Alaska last summer. It seemed obvious right from the start that that was simply your run-of-the mill algal bloom. These blobs, on the other hand, would quite mystify me without  the help of a reassuring National Geographic narrator.

I’m pretty sure this is the same stuff that builds up in the water you leave the dishes in the sink too long. Is it just me or did you also half-expect to see an eyeball or two floating around in one of those things?

It seems like this may be some sort of biofilm, which is a very sexy subject in the world of biology right now. Biofilms are essentially thin coats of bacteria and bacterial slime (technically known as extracellular polymeric substance, or EPS) on teeth, stream cobbles, catheters, lawyers, etc. (just kidding lawyers! Don’t sue!)  These things are apparently everywhere — even on the thin skin of water at the surface of the ocean — and this way of life represents an up-till-now severely underappreciated bacterial lifestyle. 99 percent of bacteria may live in biofilms.

And yet  these don’t seem like classic biofilms as they aren’t tightly packed or adhered to a surface. They seem to be somewhere in the no-man’s-land between a biofilm and marine snow, the slow rain of decaying microbial matter that eventually coats the ocean floor. Both marine snow and mucilages incorporate much more than just bacteria — like crustaceans, plankton and viruses. For whatever reason the marine snow in the northeastern Mediterranean is piling up faster than the life in the water column or on the sea floor can take it out. Which seems odd, because in the deep sea, the locals will quickly consume anything that isn’t ballistic-grade plastic, and I’m pretty sure they have their R&D departments working on that too.

Whatever they are, they are unusual, and probably prospering by climate change. I love weird manifestations of life, but there is good-weird and there is bad-weird. The kind of weird that smothers fish and spreads E. coli is definitely bad-weird.

For the PLoS paper that inspired this video, click here.

A membrane, some proteins, and 8 segments of RNA: all there is to influenza. A false color transmission electrion micrograph of the influenza virus. Image courtesy CDC/ Erskine. L. Palmer, Ph.D.; M. L. Martin

Until 1933, it was impossible to see a virus. Oh, we knew they were out there. But no one had the faintest clue what they looked like. 1933 marked the year transmission electron microscopy finally achieved resolutions finer than light microscopes were capable of and made it possible to finally glimpse the agents that had mottled tobacco leaves, streaked tulip petals, scarred the faces and bodies of millions, or paralyzed, maimed, and killed millions more.

So what’s with the doofy colors? Yes, in spite of the awesomely awesome resolution that transmission and scanning electron microscopes provide us with, scientists and alarmist pandemic book cover designers can’t seem to resist painting them with gaudy colors (see above). OK, I admit the colors do seem to spice up the images. But this isn’t even a case of colorizing something that was colorful to start with — viruses are quite clear. So what a revelation to see a glass artist team with scientists to produce anatomically correct transparent glass sculptures of viruses and other wee animalcules. That’s exactly what British artist Luke Jerram has done, and his creations are truly illuminating.

It's hard to believe, but cashews actually *do* grow on trees. A glass model of Anacardium occidentale, the cashew tree, on display in the Harvard Glass Flower Collection. Model by Leopold and Rudolf Blaschka.

I must say that his models remind me very much of the intricate glass 19th century models of fungi, invertebrates, and plants I discovered in my college days in dusty corners of Cornell and Harvard, many of which were created by the father and son team of Leopold and Rudolf Blaschka in Dresden, Germany from the 1880s to 1930s. They definitely get my vote for having the C00Lest Jobs EVAR. Intended as teaching aids, they date from a time when color photographs were unheard of and microscopes were a bit primitive. The colored glass models were able to show fine detail far better than either an engraved image or tiny eyepiece could, they did so in 3D, and as the Harvard people like to point out, glass flowers bloom year round. It’s nice to see that everything old is new again.

Viral family trees

The filaments of the Marburg virus, which can be straight or contain a "shepherd's crook", and which gave the filovirus family its name.This photo of the Marburg virus brought to you by the number 11, the letter d, a backwards Egyptian s, and an important (and suggestive) year in US history with a bubble wand on top. Also, by the CDC and Drs. Erskine Palmer, Russell Regnery, and Hermann Rorschach, who in no way support or endorse my interpretation. Magnification 100,000 x.

As if the bats of the world didn’t already have enough to contend with, what with their bad (albeit sometimes deserved) rap for rabies and drinking human blood, numerical decline thanks to habitat loss, and the White Nose Syndrome that is anihilating the bats of eastern North America (and maybe eventually all of North America), last month came news that a reservoir for the deadly Marburg virus had been confirmed: African cave-dwelling fruit bats.

This is big news because scientists have been looking for the natural reservoir species for Marburg and its cousin Ebola for some time. Marburg and Ebola are hemorrhagic fever viruses that are among the deadliest on the planet*. They are sole members of the Filovirus family, and are single-stranded negative-sense RNA viruses. Mortality rates range between a quarter and nine-tenths of those infected. And Marburg is not a pleasant way to go. Here’s how the CDC describes it:

After an incubation period of 5-10 days, the onset of the disease is sudden and is marked by fever, chills, headache, and myalgia. Around the fifth day after the onset of symptoms, a maculopapular rash, most prominent on the trunk (chest, back, stomach), may occur. Nausea, vomiting, chest pain, a sore throat, abdominal pain, and diarrhea then may appear. Symptoms become increasingly severe and may include jaundice, inflammation of the pancreas, severe weight loss, delirium, shock, liver failure, and multi-organ dysfunction.

Sounds fun! Hemorrhagic fevers are so called because they somehow punch holes in capillary walls that allow blood to seep into the body and out of certain external openings you would not wish blood to ever pass through. As recounted in Richard Preston’s gruesome early 90’s bestseller  The Hot Zone , this can cause people to spill or spatter infectious blood all over any unfortunate passersby or airline seatmates (sometimes the little “summon stewardess” button can’t fully convey the depth of your need). It must be said, however, that the bleeding isn’t usually what kills you, and that unlike its cousin Ebola, Marburg is not nearly so inclined to make you bleed from bodily orifices. Whew!

In The Hot Zone, Preston described (at least in my memory) how some cases of Marburg or Ebola were found in people who recently visited mines or caves or who had spent times in rooms or factories where bats roosted. Although some people seemed to acquire the virus from sick apes or bushmeat, scientists already suspected the virus reservoir, or full-time host, was not apes or monkeys, because they die just as we do from the virus. Suspiciously, however, apes and monkeys that transmitted the virus had often fed at fruit trees that bats frequented. But repeated tests of bats and the sticking of unfortunate “sentinel species” in caves to see if they got sick could never produce leads. For decades, scientists were baffled and frustrated. How could such a deadly virus remain so mysteriously hidden?

Then four years ago a survey of more than a thousand small vertebrates Gabon and Democratic Republic of Congo during an Ebola outbreak turned up evidence of asymptomatic Ebola infection in bats, hinting they might be the long-sought reservoir. Inspired, scientists in 2007 finally isolated antibodies and Marburg virus genetic fragments from fruit bats. Then last month an article in PLoS Pathogens contained the damning evidence: the isolation of live infectious viruses from the Egyptian fruit bat (Rousettus aegyptiacus) in Kitaka Cave, Uganda. There can be little doubt now that bats are carriers.

Could you resist this face? No! Bad bat! Don't give me deadly Marburg Hemorrhagic Fever! The Egyptian Fruit Bat, Rousettus aegpitiacus. Courtesy Dawson, Creative Commons Attribution 2.5 License.

The infected bats appeared healthy, and the genetic diversity of the viruses found in Kitaka Cave seems to indicate Marburg has been living with and adapting to the bats for a long time. If the virus had only recently penetrated the bat population from another species, you’d expect there to be only one or a few virus types.

Moreover, a significant share of the bats in the surveyed cave are infected. About 5.1% of their sample hosted the virus, which, if extrapolated, would mean over 5,000 bats out of an estimated 100,000 in the cave are infected. And indeed, two miners infected in Kitaka were sickened by different strains of the virus, implying they picked up their diseases independently and that human transmission is not a rare event. The strains, though different, closely matched the sorts of strains found in the scientists’ fruit bat samples.

Although the viral lineages were highly variable within Kitaka Cave, some strains found in one part of Africa were much more closely related to strains found in caves hundreds of miles away than they were to strains in their bat neighbors. As the bats migrate hundreds of miles and mingle over most of the continent annually, it’s not hard to see why Africa may be one giant Marburg virus melting pot.

I just hope this news doesn’t prompt a bat holocaust in Africa on the part of people, corporations, or authorities. Bats have enough troubles already and [cliche alert] provide valuable ecosystem services[/cliche alert] by hoovering up pesky insects and/or dispersing seeds. The solution, I think, is bat avoidance, though how practical that is in a mine I do not know.

Note to self: scratch caving in Africa off to-do list**.

————————————————————

*In other news, the first-ever case of Marburg in the United States was recorded in February in Colorado . . . wait, what? A deadly Ebola relative made its way to Colorado this year and I didn’t even know it? How they managed to keep the fact that a virus with a 90% mortality rate was in Colorado on the DL I’ll never know, although I did find an article in the Rocky (RIP) about it ex post facto. I need to start keeping closer tabs on our local newsgathering establishment.

**Several of the people who got sick (including the Colorado victim) did so after visiting some sort of “python cave” in Uganda that also is home to thousands of bats (do the snakes just sit on the ground with their mouths open waiting for manna from heaven?). Second note to self: question sanity if *ever* consider visiting something called a “python cave”.

“Snakes. . . . why’d it have to be snakes?”

“Pythons. Very dangerous. You go first.”

Kind of eerie and ghostly, isn’t it?

It’s a virus that infects bacteria, looks like the lunar lander, and was among the first viruses ever discovered. These guys may also be the most ubiquitous biological entities on the planet; you may be swallowing untold millions in every accidental mouthful of fresh or seawater. Did I mention the water’s teeming with the bacteria and archaea they prey on too?

Most viruses are either simple rods, spheres, or polyhedrons (often icosahedrons — 20-sided polyhedra, of course). This baby is both and then some. In the world of virus architecture, this is the fully loaded Corvette with T-tops, all-leather seats, and pre-installed hot chick. It is a natural work of art.

So why didn’t someone think of this sooner?

I have no idea who this guy is but I like how he thinks. There’s a certain delicious irony in using old computers to build models of . . . viruses. My capsid’s off to you, sir. Who needs a lawn gnome when you can have a lawn phage?