The femme fatale Photuris. Photo by Bruce Marlin; click image for Creative Commons license and image source.

If I read my notes correctly, Thomas Eisner once had a pet thrush named Sybil who rejected only five insects out of the hundreds the entomologist offered her. They were all beetles. And one of them was a firefly.

For any other bird owner, this observation would have simply limited their pet’s meal options. But this was Thomas Eisner — one of the great entomologists and chemical ecologists of the 20th century. To him, it was a tantalizing clue, and he decided to find out what made the fireflies have all the thrush plate-appeal of haggis. What he stumbled onto was one of the great new natural history stories of the 20th century — and the latest in a string of Eisner’s greatest hits.

I know this because in fall of 1998 I was a student in BioNB 221 — Introduction to Animal Behavior — at Cornell University. Eisner, a professor at Cornell, taught the last six or so lectures, which I still have preserved in my notes. What I did not know at the time, and did not learn until afterward, was that Eisner was one of the great biologists of the 20th century. I found this out in later years, when his discoveries were featured in many an article at the New York Times, where I had a mysterious feeling of deja vu.

What I did know at the time was that I could not take my eyes off the screen while he was lecturing. I’m a fan of a good natural history story, which you may perhaps have gathered. Eisner — who was once E. O. Wilson‘s college roommate — was overflowing with them — and in many cases, because he’d figured them out himself. Sadly, Eisner died March 25. You can read more about his life in this fine remembrance by NYT reporter Natalie Angier*, whose daughter was lucky enough to inherit the contents of Eisner’s old burlap field bag and was, frighteningly to me, born around the time I sat listening to Eisner’s lectures. Angier wrote about his life. I want to share with you a few of the natural wonders I learned from him, sitting rapt in the darkened Uris Hall auditorium.

This Means War

Eisner’s specialty was the world of chemical warfare among plants and insects. Insects produce, steal, and reuse chemicals from plants and each other constantly. Millipedes can deploy hydrogen cyanide, whip scorpions acetic acid, and ants formic acid, but for Eisner, the poster child for entomological chemical defense was the bombardier beetle. “If you live on the ground,” he said, “you must either take flight quickly or defend yourself instantly.” The bombardier beetle went with option B.

The beetle takes chemicals called hydroquinones, mixes them with hydrogen peroxide and catalytic enzymes (peroxidase and catalase) in a reaction chamber in its hinder, and uses the resulting explosive formation of benzoquinones and heat to persuade frogs, ants, and spiders that their best meal options lie elsewhere.

Using grainy films he had shot himself, he showed us how beetles touched with probes could deploy a vicious defense with pinpoint accuracy in nearly any direction. He suspended the beetles over pH paper, so the 100°C benzoquinones they released would reveal their precision firepower.

This British film (which seems to have been created by intelligent design advocates who tried to abuse Eisner’s research for their ends**, so ignore the bit at the end. I couldn’t find another version, unfortunately.) incorporates some of the movies I saw that day, as well as explains how the beetle uses physical barriers to control its chemical defense system. I think you can even see Eisner in one of them for a few seconds at the end — he’s in the foreground.

And here’s David Attenborough describing the beetle in HD:

Don’t Feed on Me

Plants, too, load up on poison in hopes of warding off the hungry crowd. Nettle spines are filled with irritating chemicals, as are the latex canals or resin canals of flowering plants and conifers, respectively. Some plants store poisonous chemicals in their tissues like caffeine or nicotine, which in spite of their uplifting effects on humans, are actually insecticides.

But some insects have picked up on this gig, and begun using it to their advantage. Sawflies slice into the resin canals of pines and steal the sticky sap, storing it in special sacs for defense against ants. Monarch butterflies sequester milkweed toxins from their food, rendering themselves distasteful to predators. Assassin bugs coat their eggs with the noxious excretions from camphor weeds. Their young then reuse the chemicals for defense and to catch prey. We do this too, Eisner pointed out, by stealing the defense chemicals from fungi and other bacteria. We call them antibiotics.

Eisner told us of plant chemicals stolen and presented as nuptial gifts among moths, where female choose males whose flirting, aromatic antennae tell them they have stored the most alkaloid derivatives. That implies the male is both fittest and has the most to give to the pair’s offspring. For if the female mates, the male will transfer not only his sperm, but his alkaloid collection, which the female will carefully store with her eggs for the use of her young. Other moths do the same with salts they siphon from puddles.

And he told us of the evesdropping of kairomones — chemicals that, unlike pheromoes, used for intraspecies communication (like the moths), or allomones, which benefit the emitter of an interspecies pair (like the benzoquinones of the bombardiers or the stinking of skunks), benefit the receiver and betray the emitter. Think, for example, of the carbon dioxide that gives you away to mosquitoes; any scent, really, that betrays prey to predators can qualify. Eisner called it a “chemical gestalt”, the effect of “inevitable chemical leakage”. But the tables can also be turned. Predatory rotifers called Asplanchna unwittingly emit chemicals that alert prey rotifers called Brachionus to grow defensive spikes (read more about rotifers from this blog here and here).

One of my favorite Eisner stories, one that has especially stuck with me all these years, was about true bugs entomologists were attempting to rear in petri dishes on damp paper towels. The bugs’ development was, however, stalling; they could not be coaxed to adulthood. The scientists were baffled. Until, that is, someone noticed the paper towels were made from balsam fir, a tree that emits allomones to stunt insect development. This chemical was, apparently, surviving the paper-making process and continuing to thwart the trees’ insect enemies — even in death.

Bolas spiders use imitation pheromones — another allomone — to lure male moths in search of a date (the females, apparently, are immune to the spider’s charms). This video depicts the unfortunate result:

You may have heard of parasitoid wasps — the Alien-style predators of spiders, caterpillars and other insects that lay their eggs in their prey, where the young maggots proceed to devour their hosts’ organs while still alive before finally using their hosts’ spent husks as pupae from which young wasps emerge. But perhaps you did not know that some plants injured by caterpillars or aphids call out chemically to parasitoids to defend them. But the story gets better; the immune system of the host in some cases is destroyed by viruses injected by the parasoitoid wasps along with their eggs. “And(I underlined this in my notes) the viruses have also been incorporated into the wasp genome.” To which I further wrote, “1 organism now? Whoa.”

He told us how mammals, too, use pheromones. Babies can distinguish their mother’s milk from others, he said, and the scent of male armpits can regularize erratic female ovulation. In mice, the scent of strange male urine blocks implantation of fertilized eggs in female mice; the effect and reason may be similar to an article I just saw last week about mares aborting fetuses to save themselves investing energy in foals likely to be killed by rival stallions anyway. This could explain the spectacularly high miscarriage rate in mares (around 30%) who are trucked out to mate with top stallions but housed while pregnant with other males. That this is likely to have not one whit of effect on the way breeders practice horse husbandry is testament to the often hidebound thinking of humans.

The Bee-Letters of Flowers

But on top of all this research into chemical crossfire, Eisner also dabbled in the world of light and visual communication. Those who have studied physics know the electromagnetic spectrum of which light is a part is a vast array of energy. Earth’s atmosphere filters much that arrives, and most of what makes it through falls in the 320 to 2300 nm range. What we perceive as visible light falls in the 380 to 750 nm range. But that leaves a large part of the spectrum invisible to us. What if other animals could see different colors or different parts of the electromagnetic spectrum? As it turns out, they do.

We cannot see ultraviolet. But, through experiments worked out by a whole host of Germans, we know bees do. Conversely, bees cannot see red. Their vision lies in the 340 – 650 nm range. Blue, red, and green are the human primary colors. But the bee primary colors are yellow, blue, and ultraviolet. That implies there are a spectrum of colors that they see that we cannot. My mind bent a bit as I heard this — there’s a whole world of color out there that we can’t see!

And those colors needed names. Yellow + blue we can see along with bees — we call that blue green. But what about blue + ultraviolet? That was dubbed “bee blue”. Yellow + ultraviolet? “bee purple”. And, as it turns out, flowers are adorned in these shades, invisible to us but brilliantly displayed for bees. Flowers probably first used UV-absorbing pigments as sunscreen, Eisner said, and only later turned to them to decorate their petals. Now, bee blue and bee purple form pollen guides for bees, often flecking the tips of flowers and leaving a yellow disc in the center as a bullseye. You can see the effect in this photo collage of black-eyed susans with ultraviolet tips and a yellow center, though the bee would see both yellow and ultraviolet simultaneously as bee purple.

Cucumber flowers in natural light(left), and in ultraviolet falsely colored yellow(right). To bees, the flowers would appear bee purple with a yellow target -- the pollen guide. Creative Commons kevincollins123. Click for license and link.

The inability of bees to see red means that pink are red flowers are almost never pollinated by bees. On the contrary, only butterflies and hummingbirds — which are not red-blind — are attracted to red flowers. Eisner wrote papers about his experiments in this world as well, examples of which you can see here and here.

Which brings us back to what is likely his most famous experiments in light communication — the Tale of Photinus and Photuris. Following up on the expectorated clues provided by Sybil, Eisner extracted chemicals from the fireflies with various solvents. He discovered that the firefly she spat out — Photinus — contained a steroid called lucibufagin. When fireflies are caught, they “bleed” hemolymph full of this chemical. Spiders who catch and taste them let them go. They even release fruit flies merely painted with the chemical, the scientists discovered. Eisner found Photinus was chock-full of the chemical right from the start of the season. A larger firefly, Photuris, also contained this chemical. But only the females. And only later in the season. He began to glimpse the truth of a dark story.

Male fireflies searching for females make a species-specific pattern of flashes. Females respond with a single blink, but with a species-specific time delay from the male call. Photuris, coveting the chemicals of Photinus, imitates that response. When the male lands thinking he is about to get lucky, he gets eaten instead, and the female accumulates the chemical that allows her to escape predation by spiders and yes, thrushes.

How could one man do and learn so much? Perhaps because he never let the Lab get in the way of Life. This passage from Angier’s piece, in particular, explains why I love Eisner — and to a large degree why being a modern biologist was not for me.

Ian Baldwin, a professor of molecular ecology at the Max Planck Institute for Chemical Ecology in Germany, who studied with Dr. Eisner  in the 1980s, said of his mentor: “He articulated the value of natural history discovery in a time of natural history myopia. We train biologists today who can’t identify more than four species, who only know how to do digital biology, but the world of analog biology is the world we live in. Tom was a visionary for nonmodel systems. He created narratives around everything he did.”

In today’s “shiny polished science world, he was proof that there is no experience that can substitute for being out in nature,” said Dr. Berenbaum. “It’s classy, not low-rent, to stay grounded in biological reality.”

Thank you for the stories, Dr. Eisner, wherever you are.

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*My answer to the question of “Who are your favorite science writers?” with “Natalie Angier” probably terminated my interview for a science journalism internship at a major daily newspaper about seven years ago. The editor seemed to lose interest in me at that point. I wasn’t going to lie, and I’m still offended on her behalf.

** Indeed, they have also done so to my graptolites post. They linked to my blog post as part of a post using graptolites as proof of “stasis”.

Creative Commons Jeans_photos, photo by Fred Hort. Click for link to license.

In 1928, a farmer in Western Australia named Jack Trott was plowing a field newly carved from the Outback by fire. An unusual crack in the soil caught his attention. In it was something extraordinary — a sweet-smelling pallid little flower of the first known completely subterranean plant: the Western Underground Orchid, Rhizanthella gardneri*.

Strange things are known to lurk under Australia’s soils (these come once again to mind), and these flowers must surely be counted among their ranks (although not perhaps for much longer — fewer than 50 individuals are known to exist). Obviously, living your entire life underground is weird for a group of organisms (i.e., plants) known for its sun worship. True to their underground creds, these orchids never break the surface. Or rather, they do break it (crack it, usually), but they never break on through, in the Doors-ensian sense. The flowers form within a few inches of the surface, but get no further. The sweet smell is clearly a lure for pollinators — identity still TBD — to their underground digs.

As orchids go, they are odd in in that their “flower” is actually a cluster of flowers in a cup called a “capitulum”, or “little head”. If you look at the picture, you’ll see a bunch of upside-down teardrop shapes; those are the flowers, in which orchid afficianados can no doubt see a faint resemblance to more conventional orchids that this “flower” as a whole quite lacks.

But also weird for orchids, these flowers subvert the usual fungus-orchid BFF relationship. Many, if not most orchids, have what is usually euphemistically termed an “intimate” relationship with fungi. That starts on day one: germination. Orchids are notoriously difficult to start from seed because they store no food of their own and must be in the presence of their preferred fungal partner — under Goldilocks conditions — to sprout. For most wild orchids, your best source of information on what that fungus and those conditions might be would be your nearest Magic 8-Ball.

Not actually natural size (anymore).

Most photosynthetic, self-sufficient orchids seem to associate with saprophytic or parasitic fungi. But R. gardneri has found a different niche: myco-heterotrophy, or exploiting the mycorrhizal fungi of other plants. In this case, it gets all up in the business of the fungal partners of Melaleuca uncinata, the broom bush. Mycorrhizae are fungi that encase or invade the roots of nearly every land plant. This is good; without them, plants would have a considerably rougher go of it. The usual exchange is sun-made plant glucose in exchange for a vastly improved water and mineral uptake thanks to the exponential surface area increase made possible by a network of fungal filaments extending well beyond the roots. Mycoheterotrophic plants break into the mycorrhizal associaton of a fungus and another plant and steal some of the goodies for themselves.

R. gardneri is not the first plant to have figured this sweet deal out. Here in Colorado there are at least two pale pink spiky plants terrorize our fungi: the Heath-family pinedrops, and the Orchid-family spotted coralroot. I often see pinedrops and spotted coralroot on hikes in the mountains, where the former associates with (probably parasitizes) mycorrhizal truffle fungi in the genus Rhizopogon (related to the bolete genus Suillus for those who care) and the latter goes after mycorrhizal Russula, which make the majority of the red-capped, white-stalked (and usually poisonous and/or disgusting) mushrooms found in the temperate forest.  I wrote about another Heath-family floral parasite that I used to encounter often here. In spite of exceptions like pinedrops, almost all mycoheterotrophs are orchids.

In all these cases, these plants have lost their chlorophyll. But none have taken the admittedly drastic step (for a plant) of entirely forsaking wind and rain, sun and cloud.

Chloroplasts: Not Just for Photosynthesis Anymore

The Western Underground Orchid has, and in the process, has gone farther toward forsaking its planthood (if its planthood can be tied to the vir(d)ility of its chloroplasts — the cell bits responsible for photosynthesis) than any other plant.

Chloroplasts — as first understood with genius by Lynn Margulis — are what remains of a fateful meal billions of years ago. A bigger cell engulfed a smaller photosynthetic one, probably a cyanobacterium, or blue-green alga. But the alga didn’t go quietly. It managed to survive and thrive in its would-be predator. It became its partner instead. Already in that cell were the remains of bacterial cells who had long ago struck a similar bargain: mitochondria, the power-packs of the cell. You have these ancient bacteria still in nearly every cell of your body. Plants have both mitochondria (which is how we know that endosymbiotic event happened first) and chloroplasts, the descendants of the world’s luckiest alga. And both still have DNA, the remains of their bacterial chromosomes.

Chloroplasts inside a true moss -- each one a descendant of an alga that gave a predatory cell indigestion billions of years ago. Its offspring (and that of a few other lucky photosynthetic microbes cum organelles) blanket the planet. Creative Commons Krisitian Peters, click image for license link.

But in R. gardneri, 70% of its expected chloroplast genes are gone, according to a new paper in Molecular Biology and Evolution. And the total length of the R. gardneri’s chloroplast chromosome (which is still circular like all most good bacteria) is just 59,190 base pairs, also the smallest for a land plant on record.

Chloroplasts are where the proteins and other cogs of photosynthesis are manufactured. They’re where photosynthesis takes place too. But it seems that even chloroplasts must have some functions in the cell aside from harnessing light. Because Rhizanthella has gone as far as any plant in ditching their chloroplasts since they spend their entire lives underground, ensuring zero photosynthesis takes place. So maybe the news isn’t that they’ve shed 70 % of their chloroplasts genes. It’s that they still have 30% of them. What are those genes still doing there? And what can they tell us about how other parasites operate?

Even in your garden-variety plant, the chloroplast genome is sharply reduced compared to its cyanobacterial ancestor. When a cell goes from going it solo to living in a co-op, there’s a lot of genes it doesn’t pay to make in-house. There may be genes already doing the same thing in the host cell’s nucleus, or just not usable from inside another cell anymore. Over time, natural selection will prune these genes away, since they are costly to make if not being used. Other genes, perhaps because it’s more efficient to regulate and transcribe them there, get shuttled to and permanently housed in the nucleus. What’s left is chiefly what’s essential for the business of turning light into sugar, Job #1 for the choroplast.

But in Rhizanthella, which has clearly boarded up the photosynthetic apparatus, there remain 37 genes coding for 20 proteins, 4 ribosomal RNAs (an important constituent of ribosomes), and 9 transfer RNAs (essential tools for turning RNA into proteins within the ribosome; they ferry the appropriate amino acid to the appropriate RNA codon). Scientists checked DNA made from the messenger RNA they found in the chloroplasts; they were all being spliced and edited correctly, implying they were, in fact, still being used, in spite of the strip mining of the rest of the genome.

Toxoplasma gondii motherships constructing new invasion craft. Creative Commons Ke Hu and John Murray. Click image for license link.

Compare those 37 genes to a standard photosynthetic orchid, in this case Phalaenopsis aphrodite, whose chloroplast genome has 110 genes. Even the parasite Toxoplasma gondii, notorious for its mind-control abilities (which chiefly involve making hosts — including accidental hosts like humans — do risky things to increase their odds of predation, or from the parasite’s point of view, getting to the next host), actually seems to have been photosynthetic in a previous life, and even it still contains 53 genes on its presumed remnant chloroplast genome, according to the authors.

Thus ex-photosynthetic plants of all sorts seem to share a minimum set of chloroplast genes, and they must be doing so because the chloroplast performs some sort of important non-photosynthetic function that can’t be transferred to the nucleus.

In fact, the scientists compared the reduced gene sets found in parasite ex-chloroplasts from a variety of groups. As mentioned above, they found strong similarities, suggesting that when photosynthetic parasites of any ancestry — related or not — give up free-living, they tend to lose and retain the same sorts of chloroplast genes. This knowledge could provide us with lines of attack in ex-photosythetic parasites that go after us or our crops or livestock. The bare-bones Rhizanthella genes could tell us which genes are most essential — and thus the best targets.

Thanks to convergent evolution, loss of similar genes in parasitic chloroplasts makes it look like Toxoplasma gondii (cause of Toxoplasmosis in humans and cats) is closely related to the plant parasites beechdrops and Western Underground Orchid. Ummm, no.

But wait. Does that mean the chloroplast — the sugar-making machine of plants — does things other than just photosynthesize? Yes. And parasitic plants like R. gardneri are how we know what those things are.

Of the genes that are left on the R. gardneri chloroplast genome, almost all of them encode proteins needed for translation (getting from RNA to protein). Five of the remaining transfer RNAs seem to have remained because either they must interact with many other chloroplast proteins and versions from the main cell would not necessarily recognize the appropriate proteins, or because they have quirky physical modifications that make the chloroplast translation machinery unable to recognize their cellular equivalents. In other words, for these genes, evolution’s backed itself into a corner it’s not easy to get out of with simple chance mutation and natural selection, so instead, it preserves the status quo.

But all these translation-related genes are probably still there for a larger reason: they are necessary to translate the four remaining non-translation related genes on the genome: one making a protein essential for membrane synthesis and two others likely involved in making it, and a fourth gene that makes a protein that seems to have a hand in a variety of important plant processes, at least one of which must be essential. Mutations in the chloroplast’s translation genes are probably fatal because the chloroplast can then no longer make this handful of genes.

Why must these four genes be expressed in the chloroplast and not in the nucleus? The authors hypothesize it has to something to do with a wonderfully vague term called “control by epistasy of synthesis”. As far as I can tell, that means the compartmentalization of these proteins in the chloroplast is essential to their proper synthesis and integration into large protein complexes. So there you have it: the chloroplast may stick around in parasitic plants because it’s handy as a clean manufacturing facility for making parts of a few complicated proteins.

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* According to the poster of the flickr photograph I used to illustrate this post, Trott donated his specimen to an herbarium for identification and offered £100 to anyone who could find another. Although many looked, none was found until 1979, the year after Trott died. His widow, however, paid up.

Delannoy E, Fujii S, des Francs CC, Brundrett M, & Small I (2011). Rampant Gene Loss in the Underground Orchid Rhizanthella gardneri Highlights Evolutionary Constraints on Plastid Genomes. Molecular biology and evolution PMID: 21289370

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?

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

The one that blew me away was the parasite that has evidently converted itself (or rather, has been converted by evolution) from a snail into a worm-shaped set of gonads, much like adult tapeworms (or guinea worms!). The chief way scientists know it is a gastropod is its larvae — which still appear as “tiny, delicate snails.” Evolution: Totally Frickin’ Crazy/Awesome.

Still, just to prove that not all parasites are insects, worms, worm wannabes, or politicians, here is a plant parasite that I used to stumble upon all the time in the murky gloom while mucking around upstate New York forests hunting mushrooms and other oddities: Monotropa uniflora, also called Indian Pipe.

Monotropa uniflora (once-turned single flower, I think), also called Indian Pipe, Ghost Flower or (most luridly) Corpse Flower.

You see, parasitism can happen to anyone — even a nice flowering plant like Monotropa. Its flowers are the bulbs at the end of the curled-over stems, above. It is usually ghostly white or sometimes pink (though I’ve never personally seen a pink one) because it has no more need of chlorophyll, the chemical that allows most plants to convert sunlight into food. It has found a way to parasitize the fungi collectively called mycorrhizae (miko-rye’-zee) that are cooperative with nearly all trees (and, in fact, nearly all plants!).

Since the mycorrhizae get most of their food from the tree they are helping support, this little flower is in effect parasitizing the trees it grows under. Its proximal victims tend to be mychorrhizal fungi in the family Russulaceae (Roo’-syu-lay-see-ay or Russ’-you-lay-see-ay), which contains the prolific genera Lactarius and Russula. If you’ve ever been in the woods odds are you’ve seen the mushroom fruits of these fungi. Russula sp. tend to make very common but mostly inedible chalky white mushrooms with red caps and white spores that frustrate North American ‘shroomers looking for better, more edible fare. In Russia, they pickle and eat some. No accounting for taste (or cast-iron stomachs), I suppose.

Monotropa itself is in the blueberry or heath family, also called Ericaceae (Eric-ay’-see-ay, which you can see placed among its relatives here). This family contains many familiar berries, including blueberries, cranberries, lingonberries, and huckleberries (alert Val Kilmer). Members of this family usually prefer the acidic soils of peat and bogs often have  “urn-shaped” flowers in which the petals are all fused (botanists would say the  corolla, or whorl of petals, is united), which you can see in these blueberry flowers.

Vaccinum (blueberry) flowers. Photo by Thomas Kriese. Creative Commons Attribution 2.0 Generic License. Click image for link.

Though the petals of Monotropa aren’t united, they are clearly urn shaped, as you can see more clearly in this photo of the pink variant.

Note the bright orange pollen on the stamens around the dark-colored pistil, the tube that leads to the ovaries below. Photo by Magellan nh, Creative Commons Attribution 3.0 Unported License. Click image for link.

Since I moved out west I have not seen M. uniflora, though it allegedly does occur here. On the other hand, I see two other ghostly-pink parasitic plants all the time — pinedrops, also in the heath family, and spotted coralroot, an orchid (which also parasitizes mushrooms in the Russula family).

I seem to have written my way into an unplanned series on parasites. Let’s see if I can write my way out of it next time. Hmmm. I’m sensing slime molds in our future . . .

POTD discovered via The Loom.

So how does one go about acquiring a guinea worm? I’m glad you asked. It all starts with a copepod. During its life, an aspiring guinea worm must pass through both humans and a freshwater copepod. Remember the bioluminsecent bomb firing marine copepods I covered here?

I need a wall-mounted set of copepod antennae to impress my guests. Hook 'em, 'pods! Photo by Uwe Kils. Creative Commons Attribution ShareAlike 3.0 License.

Well, this isn’t one of them. It’s another marine copepod species, but the best I could do right now by way of illustration. Marine copepods, in turn, have freshwater cousins, and these cousins are hosts for the young aquatic guinea worm larvae. After a few weeks in the copepods, the larvae are ready. Drink this water without filtering out the copepods and congratulations! You’ve just acquired your own pet guinea worm, and will become host to one of the most gruesome human parasites on Earth.

For when the copepods hit the stomach, the acid dissolves the copepods but not the guinea worm larvae. Instead, the females migrate to the lining of the small intestine, burrow through, get knocked up by tiny males who then die and dissolve, and then grow into two-foot long spaghetti strands that spend a year sightseeing your body. I don’t know about you, but the only entities I want roving my body are blood, immune cells, and the occasional miniaturized submarine.

Strangely enough, you usually don’t notice all this until the worm is full term, about a year after you drank their larvae. When the blessed moment arrives, the worm migrates to a patch of skin most commonly located on feet or legs, but which can also include “the head, torso, upper extremities, buttocks, and genitalia” (eep!) and release chemicals that cause a searingly painful blister to form, which then pops. Mrs. Worm emerges — but just her tip. The pain is so intense victims are driven mad by desire to plunge the extremity into cool water. When they do, the worm immediately secretes a cloudy liquid containing scores of her copepod-seeking young, thus beginning the cycle anew.

The treatment, known since ancient times, is hardly better. You take a matchstick, twig, or pencil, wrap the end of the worm around it, and then slowly pull her out a few centimeters a day, like (brace yourself) this:

Pull any faster and she breaks, defeating your efforts. It can take weeks or months to pull the whole thing out. In the meantime, your open sore can become infected by bacteria, and the pain is so bad you find it hard to move, work, or care for others. This is not a living organism that it is easy to feel sorry for anihilating.

Like rinderpest, guinea worm is an ancient scourge whose prevention has been long understood but which thrived on ignorance and poverty. All one has to do to prevent guinea worm is drink clean water, but clean water is a luxury for millions. The nuclear option is dosing local water bodies with copepod-icide. They (and anything else that happens to depend on copepods for food) can’t be happy about that. The alternative is behavior change — persuading people to filter their water through cloth (carefully checked for stray holes!) to strain out the fairly large copepods. That’s fine for adults, but often the victims are small children who don’t know any better when they get thirsty.

Dracunculus medinensis, as this pest is most formally known, is, believe it or not, a nematode, or round worm. Roundworms are distinguished from flatworms because they have a round (duh) body and true digestive tract: a tube that opens at the mouth and exits at the you-know-where. Nematodes crawl invisibly throughout your environment every day, in soil and fresh- and saltwater. They are among the most diverse groups on Earth, and probably heaviest by biomass, on earth.  They’re everywhere. I’ll never forget teaching introductory microscopy lab during my first year of grad school and seeing a very surprised nematode crawling around a dish with a thinly sliced apple we were observing. So believe me, you have almost certainly consumed many of these little guys in your day. As with most nematodes, it looked like this.

Obviously, pregnant guinea worm females are the ultra-super-uber-heavyweights of the nematode world, and, at least in my experience, atypcial. Many nematodes are harmless free-living soil-dwellers, like the Caenorhabditis elegans that has contributed so much to our knowledge of basic development and gene function. But there are also scores of nasty parasites of both plants and animals: root-knot nematodes, hookworms, pinworms, whipworms, heartworms, and Trichinella spiralis, the reason you should not eat undercooked pork. To see where the nematodes fit into the rest of the animals, click here.

In December Nigeria announced it was the latest country to be free of Dracunculus medinensis, leaving only four in Africa that are still beset. Jimmy Carter’s on the case, so you know it won’t be long. To see a slide show from Time that vividly illustrates the worm’s toll, click here, and to read the latest news about the eradication, see here and here.

And of final note, dracunculuiasis, the disease’s formal name, means “afflicted with little dragons.” Quite so. I am glad I will never experience that firsthand, I hope that soon no one else will either.