
Hookworms are longer-lived than viruses and bacteria;
they could have had a more significant effect on human evolution.
Humans live in all sorts of places—high deserts, tropical lowlands, frigid tundra. Over the millennia, you’d expect each population’s assortment of genes to evolve to reflect the demands and dangers of its home environment: those who live in the deserts would possess genes for extra skin pigments to help keep their tender integument from burning (like African peoples), and those who live in sub-zero climes much of the year would have genes that keep them well-insulated in fat (like the Inuit). But what if factors other than climate, like the food available nearby or the viruses, bacteria, and parasites native to the area, also had an effect on various human populations’ genetic toolkits?
It’s a fascinating question, but, given that we have to reconstruct all this supposed evolution from the current state of modern genomes, finding an answer isn’t easy. A recent paper takes an important first step by looking for correlations between 500,000 different genetic markers and certain environmental characteristics, like humidity, temperature, the local diet, and the prevalence of parasites and other pathogens.
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Parasitic wasps have a terrifying but weirdly impressive knack for taking over the bodies and brains of other many-legged creatures, making spiders weave them bespoke silk cocoons, obedient cockroaches incubate their eggs, and paralyzed, partially devoured ladybugs guard their young. But for the European paper wasp, as a new study describes, the tables are turned: It’s the host rather than the parasite—and the things the Xenos vesparum fly larvae inside it lead it to do are at least as odd as any of the above.
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What’s the News: Infections that change an organism’s personality are a strange little corner of biology, with toxoplasmosis, which brainwashes mice and rats to have no fear of cats, topping the list. But scientists think that more pedestrian infections could play a role in shaping personality, especially when they happen early in life. Ducklings provide the latest data that this theory may have something to it.
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Don’t you forget about bumblebees. While DISCOVER and others have extensively covered the mysterious colony collapse disorder that’s been crashing honeybee populations around the world, bumblebees have not escaped the tide of doom.
Sydney Cameron leads a team that just published a new study of bumblebees in this week’s Proceedings of the National Academy of Sciences, and tallied up some scary numbers.
The relative abundance of four species of bumble bees over the past few decades has dropped by more than 90%—and those disappearing species are also suffering from low genetic diversity, which makes them that much more susceptible to disease or any other environmental pressures. [TIME]
In addition, the geographic ranges of those species shrunk precipitously—between 23 and 87 percent, depending upon the case. That reduction in range could have catastrophic impacts on agriculture:
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The wild pink salmon of western Canada are in trouble: In the early 2000s, their numbers in some locations swiftly dropped by 90 percent or more. One explanation put forth for this steep population decline is that sea lice, parasites ubiquitous on farmed salmon, jumped to the wild variety of the fish. But this week in the Proceedings of the National Academy of Sciences, a new study casts doubt on that idea and says the sea lice are not to blame.
When Gary Marty of the University of California, Davis, and his colleagues looked at that aspect for the Broughton Archipelago of western Canada, they found that salmon survival was not lower in years when the juveniles passed by louse-infested farms. This, they say, suggests that something other than sea lice must be reducing survival rates. [New Scientist]
Marty’s team checked up on a decade worth of data dating back to before the 2002 crash, and found a few interesting things. First, they say, the predominance of the lice in wild populations appears to predict the number found in farms a little later, suggesting the parasites travel from wild salmon to farmed ones and not the other way around. Second, they argue, it does appear that a high number of lice in the farmed fish predicts higher than normal exposure for the juveniles of the wild variety, but that increased exposure can’t account for the huge population drop in the wild salmon.
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Here’s one that I didn’t touch on in DISCOVER’s creepy gallery of zombie animals controlled by mind-altering parasites: A parasitic fungus called Ophiocordyceps unilateralis that infects a plain old carpenter ant and takes over its brain, leading the ant to bite into the vein that runs down the center of a leaf on the underside. The ant dies shortly thereafter, but the fungus gains the nutrients it needs to grow this crazy stalk out of the ant’s body and release spores to create the next generation of ant-controlling fungi.
This cryptic cycle has been going on for at least 48 million years.
In a study forthcoming in Biology Letters, Harvard’s David Hughes argues that a fossilized leaf found in a fossil-rich part of Germany’s Rhine Rift Valley bears the scars of the ant’s trademark death bite. The ant bites down hard so the fungus will have a stable position when it grows a stalk out of the ant’s head. But even so, Hughes says, he doubted the mark would turn up in the fossil record—that is, until serendipity reared its random head:
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Biologists are a step closer to figuring out the bizarre animals known as bdelloid rotifers, thanks to a new study in Science.
This group of near-microscopic aquatic organisms has lived for tens of millions of years without sex, can withstand blasts of gamma radiation, and if their habitat dries up they can survive for years in a dessicated state. Two years ago, DISCOVER covered the findings that determined how these all-female invertebrates manage to diversify their genes without sex: Their genome breaks apart when they dry up, and as they reassemble when water returns, they pull in new DNA from a host of other beings. Now, the new study says, drying up is also the key to how rotifers avoid parasites that would normally take advantage of their asexual ways.
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Could the Chicago Field Museum’s mighty Tyrannosaurus Rex, a dino named Sue, have been toppled by a lowly parasite? According to a recent study in the journal PLoS ONE, a microbe commonly found in pigeons may be responsible for holes in the dinosaur‘s mandible, holes that were previously thought to be bite marks. Paleontologists compared a similar infection in a modern predatory bird to the T-Rex holes and found surprising similarities.
The researchers think the parasite, a protozoan named Trichomonas gallinae, settled in the back of Sue’s throat, and in nine other Tyrannosaurs … studied with similar holes. The parasite caused inflammation that eventually damaged the jawbone [Los Angeles Times], first forming lesions and then eroding the bone away. The inflammation would have choked off the dino’s esophagus, they say, eventually starving the T. Rex to death.
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In an ironic twist, the weaponry of the fire ants that have invaded the American South is also their potential downfall. Entomologists have found that the fire ants’ venom contains chemical compounds that attract their natural foes, the parasitic phorid flies that turn ants into zombies before decapitating them.
The invasive red fire ants first came from South America by boat, and from their original disembarkation point in Mobile, Alabama, they have spread across the South, from Texas to Maryland. Their painful stings and their habit of shorting out electrical equipment make them a serious pest to humans, and biologists have been attempting to control their numbers by importing and distributing the parasitic phorid flies. But until now, researchers didn’t know how the flies homed in on the ants. So researcher Henry Fadamiro hooked electrodes up to the antennae of flies to investigate which of several stimuli prompted nerves to fire. By exposing the antennae to extracts from different ant glands and body parts, the researchers determined that juice from the venom glands got antennae buzzing [Science News].
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Scientists may finally be on their way to controlling the pesky fire ants that have invaded the American South: They’re releasing swarms of parasitic flies that first turn the ants into zombies and then decapitate them. The non-native ants are at the top of scientists’ hit lists because they cause an estimated $1 billion in damage in Texas each year. The insects swarm on circuit breakers and other electrical equipment, damaging them severely. Swarms of the stinging insects can also severely injure humans and can kill smaller animals, such as calves and pets, that stumble across nests [Los Angeles Times].
Over the past ten years, Texas agricultural researchers have begun releasing several species of phorid flies, imported for this task from the South America. The flies “dive-bomb” the fire ants and lay eggs. The maggot that hatches inside the ant eats away at the brain, and the ant starts exhibiting what some might say is zombie-like behavior…. “There is no brain left in the ant, and the ant just starts wandering aimlessly. This wandering stage goes on for about two weeks” [Fort Worth Star-Telegram], says researcher Rob Plowes. Eventually the ant’s head falls off and the mature fly emerges, ready to lay its own eggs in a new round of ants.
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In a classic tale of symbiosis, researchers have determined that a parasitic wasp got its most potent weapon from an ancient virus that may have attacked it around 100 million years ago.
When a parasitic wasp wants to lay its eggs in a caterpillar, it takes steps to ensure that everything goes according to plan: Along with the eggs, it injects a powerful dose of virus-like particles. Not only do these disable the caterpillars’ immune system to stop it attacking the eggs, they also cause paralysis and keep the host from pupating – turning the caterpillar into an eternally youthful larder and nursery for the wasp grubs [New Scientist]. But the nature of the wasp’s poison has been a subject of debate.
The virulent particles, were named polydnaviruses because they resemble viruses; they consist of protein-encased, double-stranded DNA pieces. But their DNA doesn’t match that of any other known virus, and a closer analysis showed that the particles contained mostly wasp DNA. That had entomologists wondering if the wasps had come up with the virus-imitating particles themselves. “The spectre arose that the wasps were doing really clever genetic engineering that looks just like a virus but is really a wasp invention” [New Scientist], explains lead researcher James Whitfield.
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A species of European butterfly has an excellent trick for protecting itself during a vulnerable stage of life. As the caterpillars prepare to enter their inactive pupal stage they emit ant-like chemicals that cause red ants to scoop them up and bring them inside the ant colony. Then, to get star treatment, the caterpillars make a rhythmic noise that resembles the call of the ant queen. That’s enough to get the worker ants’ undivided attention, a new study shows. “They appeared to be treating the caterpillars as if they were the holiest of holiest, the pinnacle of power, the queen ant” [New Scientist], says lead researcher Jeremy Thomas.
If the colony is attacked, the worker ants save the caterpillar before they save ant larvae, and when food is scarce the ants have been known to kill their own larvae and feed them to the deceitful interlopers. But there’s one ant who is not fooled. Researchers set up an experiment in which a butterfly pupa pretending to be an ant queen was placed in a chamber with worker ants and four real ant queens. The ant queens began to attack and bite the caterpillar, but the workers intervened, biting and stinging their own queens, which they then pulled to a far corner of the chamber while other workers attended the pupa [AP]. Researchers note that this situation would not arise in the wild, where queens and larvae inhabit different chambers, but say it shows where the workers’ loyalty lies.
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The nasty parasite known as Guinea worm that has plagued humans since the days of the ancient Egyptians is on the verge of being completely eradicated, former president Jimmy Carter declared on Friday. The Carter Foundation has led the effort against Guinea worm, which could soon be remembered as the second disease to ever be wiped out by human efforts, smallpox being the first. There have been fewer than 5,000 cases of the disease in six African countries this year, and on Friday Carter announced two new grants dedicated to wiping out the final hotspots: The British government has pledged $15 million, while the Bill and Melinda Gates Foundation will contribute $40 million.
Guinea Worm is one of the worst parasites you can get. The worms burrow inside of you, grow to almost three feet long, are incredibly painful, and finally pop out of the skin and have to be reeled out, inch by inch, over many days [The New York Times blog]. The parasites have been found in Egyptian mummies, and the official name for the infection, dracunculiasis, references an archaic-sounding pain: it’s Latin for “affliction with little dragons.” Doctors have no vaccines or medicine with which to combat the parasite; instead they rely on prevention to keep people from getting infected. However, humans are the only host for the parasite, so ending outbreaks in human populations would destroy the worm forever.
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Pity the poor frogs: they’re one of the most endangered group of vertebrates on the planet, and new research shows that two of the factors in their plight are common, everyday farm chemicals. The study shows that atrazine, a weedkiller that’s widely used in agricultural areas, not only boosts the levels of parasitic flatworms in frog ponds, it also decreases tadpoles’ ability to fight off infections. If that wasn’t bad enough, previous research has found that runoff from phosphate fertilizers also boosts parasite levels. Taken together, researchers say, the weedkiller and the fertilizers are hitting frogs with a double whammy.
Amphibian populations around the world have been declining in recent decades, with many species on the brink of extinction. Infection with any of several species of tiny flatworms, known as trematodes, can trigger debilitating limb deformities in frogs. Severe infections can kill the amphibians. The question was why high rates of those deformities — and, presumably, trematode infections — began showing up across the nation in the mid-1990s [Science News]. The new findings suggest that the growing prevalence of the weedkiller atrazine in corn-growing regions since that time may be partly to blame for the woeful state of American amphibians.
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Tiny parasitic worms that cause chronic illness in millions of sub-Saharan Africans may increase their chances of contracting HIV, according to a new report. This study comes just a week after another set of researchers announced a different theory regarding a factor that could increase Africans’ susceptibility to the HIV virus, hypothesizing that a genetic variant found in people of African descent raises the risk of HIV infection.
In the latest study, researchers infected monkeys with the worms that cause schistosomiasis, and then injected them with a form of the HIV virus. They found that much lower amounts of the virus were necessary to give AIDS to the monkeys that had the parasitic worms, as compared to parasite-free monkeys. The phenomenon… needs to be verified in humans. But with primates a generally reliable model of AIDS pathology, it could help explain why sub-Saharan Africa, where 160 million people are infected with schistosomiasis, has 10% of the world’s population and 62% of its AIDS cases [Wired News].
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