Tag Archives: populations
Fly turns honeybees into little zombies
Latest woe is horrific, but is not what’s crashing bee populations
zombie bee
A researcher at Oregon State University has reported Oregon’s first documented case of a “zombie” fly infecting a honeybee, but he doubts that the parasite at the moment poses a threat to the bee, which is a vital pollinator of some of the state’s key crops.
Ramesh Sagili, a honeybee specialist with the OSU Extension Service, stumbled upon a belly-up bee on a sidewalk under a street light on campus in Corvallis one morning in late July, according to a press release Tuesday from OSU. He placed it in a vial in his lab, and four days later seven maggots crawled out of the bee’s neck. Almost three weeks after that, one matured into an Apocephalus borealis fly, commonly called a zombie fly because of the disoriented behavior it is suspected of causing the bees to exhibit at night.
The finding comes amid rising concern about the health of honeybees, which have been hit by a mysterious phenomenon called colony collapse disorder in which adult honeybees disappear from a hive, either entirely or in large numbers. It came to light in late 2006 when beekeepers on the East Coast began to see their honeybee colonies dwindle. The disorder has since spread to other states. A cause has not been determined, but suspects include mites, viruses, malnutrition, pesticides, a lack of genetic diversity, and stress that results from commercial hives being trucked around the country to pollinate crops.
Sagili doubts that the fly is playing a role in the widespread die-off of honeybees, which are crucial pollinators for various Oregon crops, including blueberries, pears, cherries, apples, clover, cranberries and vegetable seeds.
“It’s a stretch to say the fly is correlated to colony collapse disorder,” he said. “At this point, I don’t think it’s a threat. I don’t think it’s at the level where it can depopulate hives in large numbers.”
Earlier this year in a journal article, researchers in California became the first to document that the fly attacks honeybees. They discovered the parasite in honeybees in California and South Dakota, the only states besides Oregon where fly-infected honeybees, or ZomBees, have been reported.
The fly is known to parasitize bumblebees but little is known about its impact on them in Oregon, said Sujaya Rao, an entomologist at OSU.
Sagili hypothesizes that the fly is just now being found in honeybees because it may be trying to branch out from its other hosts when they’re not available. He added that although honeybees are widely studied, it’s possible that scientists just never saw the parasite because they usually preserve their collected bees in alcohol, which would kill the larvae and keep them from popping out.
The brownish-red fly lays its eggs inside the bees and is smaller than a fruit fly, is native to North America and has been found in Canada and states including Alaska, Georgia, Maine, Minnesota, New Mexico and New York, said Brian Brown, the curator of entomology at the Natural History Museum of Los Angeles County and an expert on the parasitic fly.
Brown said the fly has been in Oregon for thousands of years, but it just never has been found in a honeybee in the state until no
ZOMBIE OUTBREAK? – Are Zombie Bees Infiltrating Your Neighborhood?
Parasite zombie flies and a honeybee; courtesy of John Hafernik/SF State University
Zombie bees are not science fiction. They are real—and real threat to already-threatened U.S. honeybee populations.
Honeybees (Apis mellifera) in California and South Dakota have been observed acting zombielike, wandering away from their hives at night and crawling around blindly in circles.
These insects have been rendered insensate by a parasitizing fly that lays eggs in the bees’ bodies. After the bee dies a lonesome death, pupae crawl out and grow to adult flies that seek new bodies to infect.
Such a sight startled John Hafernik, a professor of biology at San Francisco State University, when he looked at dead honey bees he had collected on campus. He soon started noticing clumps of dead bees under light fixtures in the area. He and his colleagues found that this bizarre bee behavior was the result of the fly Apocephalus borealis (they described their findings in January in the journal PLoS ONE). After sampling hives around the Bay Area, they found that, disturbingly, more than three quarters were infected with this parasite.
Honeybee colonies have been collapsing at an alarming rate in the U.S. for the past several years. And without these important pollinators, many of our favorite foods, from almonds to zucchini would be difficult to produce. Scientists have implicated viruses, fungi, mites and other invaders in colony collapse disorder, but Hafernik suspects this parasite is a new villain on the scene. “Honeybees are among the best-studied insects,” he said in a prepared statement in January. “We would expect that if this has been a long-term parasite of honeybees, we would have noticed.”
How do you catch a zombie bee? A “ZomBee” trap; courtesy of John Hafernik/SF State University
Now, to see how far the zombified bee problem has spread, he and his colleagues are enlisting the help of the whole continent. They have launched ZomBeeWatch.org, a citizen science project that allows people to help them track suspicious bee behavior and collect specimens. Through the project, which launches in full today, they are hoping to find “if this parasitism is distributed widely across North America,” Hafernik said in a new statement.
To help out, you can sign up to collect sick-looking or dead bee specimens and observe them to see if parasite fly pupae emerge. Industrious citizen scientists can build light traps to attract any parasitized bees in their area (full instructions are on their site). And the researchers promise that even bees that do not turn out to be true “ZomBees” are important to report in an effort to better understand contributors to colony collapse.
“If we can enlist a dedicated group of citizen scientists to help us, together we can answer important questions and help honeybees at the same time,” Hafernik said.
Not sure what a zombie bee looks like? Here’s a video clip of a sick bee: http://www.youtube.com/watch?v=xs32DCaxU1U&feature=youtu.be (Read more about parasites that make their hosts act like zombies in the article “Zombie Creatures.”)
In case you’re wondering what we’ve been wondering—ahem, what else can these zombie flies infect?—ZomBee Watch has an answer: “The zombie fly only parasitizes insects and does not lay eggs on or in humans,” according to its website. “As far as we know, it does not transmit any diseases that are contractible by humans.” As far as we know…
ZOMBIE HISTORY – The Plague That Is Zombies
‘I hereby resolve to kill every vampire in America” writes the young Abraham Lincoln in the best-selling 2010 novel “Abraham Lincoln: Vampire Hunter.” Honest Abe doesn’t quite make good on his promise, and the grim results are all around us. Today, vampires spring from the shadows of our popular culture with deadening regularity, from the Anne Rice novels to the Twilight juggernaut to this year’s film adaptation about the ghoul-slaying Great Emancipator. Lately we’ve also endured a decadelong bout with the vampire’s undead cousin, the zombie, who has stalked films from “28 Days Later” to “Resident Evil” (the next sequel of which is due out this fall) and the popular TV show “The Walking Dead.”
Purists will hold forth on the differences between vampire and zombie, but the family resemblance is unmistakable. Both are human forms seized by an animal aggression, which manifests itself in an insatiable desire to feed on the flesh of innocents. (Blood, brains, whatever; it’s a matter of taste.) Moreover, that very act of biting, in most contemporary versions of both myths, transforms the victims into undead ghouls themselves.
Our vampires and zombies (as well as such poor relations as werewolves) all serve as carriers for vaguely similar saliva-borne infections. These mythical contagions are especially odd because they have so few analogues in the natural world. Indeed, there is really only one: the rabies virus.
A fatal infection of the brain, rabies is particularly devastating to the limbic system, one of the most primitive parts of the brain. Fear, anger and desire are hijacked by the virus, which meanwhile replicates prolifically in the salivary glands. The infected host, deprived of any sense of caution, is driven to furious attack and sometimes also racked with intense sexual urges. Today we know that most new diseases come from our contact with animal populations, but with rabies this transition is visible, visceral, horrible. A maddened creature bites a human, and some time later, the human is seized with the same animal madness.
Known and feared for all of human history—references to it survive from Sumerian times—rabies has served for nearly as long as a literary metaphor. For the Greeks, the medical term for rabies (lyssa) also described an extreme sort of murderous hate, an insensate, animal rage that seizes Hector in “The Iliad” and, in Euripides’ tragedy of Heracles, goads the hero to slay his own family. The Oxford English Dictionary documents how the word “rabid” found similar purchase in English during the 17th century, as a term of illness but also as a wrenching state of agitation: “rabid with anguish” (1621), “rabid Griefe” (1646).
The roots of the vampire myth stretch back nearly as far. Tales of vampire-like creatures, formerly dead humans who return to suck the blood of the living, date to at least the Greeks, before rumors of their profusion in Eastern Europe drifted westward to capture the popular imagination during the 1700s.
In its original imagining, though, the premodern vampire differed from today’s in one crucial respect: His condition wasn’t contagious. Vampires were the dead, returned to life; they could kill and did so with abandon. But their nocturnal depredations seldom served to create more of themselves.
All that changed in mid-19th century England—at the very moment when contagion was first becoming understood and when public alarm about rabies was at its historical apex. Despite the fact that Britons were far more likely to die from murder (let alone cholera) than from rabies, tales of fatal cases filled the newspapers during the 1830s. This, too, was when the lurid sexual dimension of rabies infection came to the fore, as medical reports began to stress the hypersexual behavior of some end-stage rabies patients. Dubious veterinary thinkers spread a theory that dogs could acquire rabies spontaneously as a result of forced celibacy.
Thus did rabies embody the two dark themes—fatal disease and carnal abandon—that underlay the burgeoning tradition of English horror tales. Britain’s first popular vampire story was published in 1819 by John Polidori, formerly Lord Byron’s personal physician. The sensation it caused was due largely to the fact that its vampire, a self-involved, aristocratic Lothario, distinctly resembled the author’s erstwhile employer.
But Polidori’s Byronic ghoul only seduced and killed. It took until 1845, with the appearance of James Malcolm Rymer’s serialized horror story “Varney the Vampire,” for the vampire’s bite to become a properly rabid act of infection. For the first time readers were invited to linger on the vampire’s teeth, which protrude “like those of some wild animal, hideously, glaringly white, and fang-like.” And at the long tale’s end, Varney’s final victim (a girl named Clara) is herself transformed into a vampire and has to be destroyed in her grave with a stake.
Both these innovations carried over into the most important vampire tale of all, Bram Stoker’s “Dracula.” In Stoker’s hands, the vampire becomes a contagious, animalistic creature, and his condition is properly rabid. It is a lunge too far to claim (as one Spanish doctor has done in a published medical paper) that the vampire myth derived literally from rabies patients, misunderstood to be the walking dead. But it is clear that this central act of undead fiction—the bite, the infection, the transferred urge to bite again—has rabies knit into its DNA.
Over time, the vampire’s contagion infected his undead cousin, too. The original zombie myth, as it derived from Haitian lore, also involved the dead brought back to kill, but again without contagion—an absence that carried over to Hollywood’s earliest zombie flicks. In this and many other regards, the most influential zombie tale of the 20th century was nominally a vampire tale: Richard Matheson’s 1954 novel “I Am Legend,” whose marauding hordes of contagious “vampires,” victims of an apocalyptic infection, set the whole template for what we now think of as the standard zombie onslaught.
Since then, as Hollywood has felt the need to conjure ever more frightening cinematic menaces, the zombie has if anything grown increasingly rabid. The antagonists in Matheson’s novel can, at times, carry on an intelligent conversation with a normal human. By the 2007 film adaptation, starring Will Smith, the infected are howling, lunging, senselessly hateful animals inside a human form. Danny Boyle, the director of “28 Days Later,” has said outright that he modeled his zombie virus on rabies. But even if he hadn’t consciously done so, the name he gave that virus—”Rage”—already draws its power from the same centuries-old supply.
Westerners don’t have much cause to fear death from rabies these days. Thanks to the availability of vaccine, human fatalities in the U.S. have dropped to a handful per year; Britain got rid of the virus entirely in 1902, succeeding in just the sort of national eradication project that apparently stymied the vampire-slaying Abraham Lincoln. Yet the infected bite, the human turned animal aggressor, menaces us as often as ever on our flat screens and nightstands.
Rabies itself may be a distant concern, but the rabid idea, like Varney the vampire, still has teeth—and it still succeeds in spreading itself.
Top 5 places to watch it all go down End of the World 2012
End of the World 2012: Top 5 places to watch it all go down
Whatever you believe will happen on Dec. 21, 2012, it is an auspicious year to travel to the Mayan heartland.
No matter what you believe will or will not happen on Dec. 21, 2012, the day Mesoamerican astronomers pegged as the end of their 5,125-year long count calendar, one thing is certain: 2012 is an auspicious year to travel to the Mayan heartland.
Though there is no evidence that the Maya foretold any specific earthly event or cataclysm, it is an important cycle-ending nevertheless, and an excuse to celebrate and cleanse.
It’s also a reason to explore the Maya region. The most popular dates to travel to Mundo Maya — the common term for the region that includes southern Mexico, Guatemala, Belize, Honduras and El Salvador — are the summer solstice (June 20), the autumnal equinox (Sept. 21), and, of course, the winter solstice, which the Mayans call “13 b’aktun,” or Dec. 21.
There will be raucous celebrations, solemn fire ceremonies and a curious excitement at all minor and major Maya archaeological sites throughout the year. The biggest challenge is deciding where to begin. Here are the top 5 Mayan hotspots to mark whatever it is that might happen on Dec. 21, 2012.
Uxmal, Mexico
The best gateway to this stunning archaeological site is the city of Merida, a colonial jewel and wonderful destination in its own right. One of Merida’s main attractions is access to the Puuc Route, a distinctive chain of Maya archaeological sites that includes Uxmal, Kabah, Sayil and Labna.
Stay at the wood-creaking Hacienda Uxmal, a stone’s throw from one of the Mayan world’s most detailed, stunning sites. Jacqueline Kennedy Onassis, Queen Elizabeth and the Shah of Iran have all stayed there. This December, Hacienda Uxmal will be the setting for Wilderness Travel’s “World of the Maya: Cycles of Time Symposium and Travel Event,” which will give 80 participants the chance to spend Dec. 21, 2012 with the world’s top Mayan studies scholars.
Riviera Maya, Mexico
Why should the end of the world be a hassle? Flying into Cancun is a breeze from most cities, and there are tens of thousands of beachside rooms from which to watch the calamity, or lack thereof, unfold. Stay in an over-the-top five-diamond, all-inclusive resort like Grand Velas or Hacienda Tres Rios, or choose a more budget-minded place in Playa del Carmen or Akumel. No matter what your thread-count is, you’ll have immediate access to many natural and Maya-related archaeological sites, theme parks and sacred water pits known as “cenotes.”
San Ignacio, Belize
The Cayo District in Western Belize has rivers, ruins and access to vast swaths of forest, including the Peten wilderness of northern Guatemala (and the Guatemalan archaeological sites of Tikal, Yaxha, and Uaxantun).
The whole area revolves around the tranquil town of San Ignacio, where a small, diverse population clings to the hillside and riverbanks. The Mopan and Macal Rivers meet here to form the Belize River, which runs out to the Caribbean. Cayo also boasts the best selection of jungle lodges anywhere in Central America, including many small, off-grid eco-resorts on the upper Macal. Some of these, notably The Lodge at Chaa Creek, are offering special tours and retreats in honor of 2012. There is a large event planned for Dec. 21, 2012 at Xunantunich archaeological site, and special solstice camping permits are being issued at Caracol.
Lago de Atitlan, Guatemala
This long-time escape for budget travelers and Spanish-language students is usually accessed via Antigua, Guatemala, a UNESCO World Heritage town of 35,000. Use Antigua as your base, then head west (and up) to one of the densest populations of living Maya in the world, where modern-day shamans still keep the calendars alive and are performing purification ceremonies throughout 2012. Here, in the volcanic hills surrounding Lago de Atitlan — the deepest, most scenic lake in all of Central America — scores of lakeside and upcountry communities offer tourism opportunities from primitive homestays to small, luxurious spas and resorts. All will have unique 2012 offerings.
Copan, Honduras
Honduras’ contribution to the Maya world consists of a single grand ancient city near its western border with Guatemala. The precision and detail of Copan’s artists and scribes earned it the nickname: “The Athens of the Maya world.”
More from GlobalPost: Video: New York’s Radio Doomsday
Copan does not tower vertically as Tikal does, to the north. But what it lacks in altitude, it makes up for in rich, important history, a gorgeous, tranquil valley, and an interesting selection of health-related retreat possibilities. Access Copan by flying into San Pedro Sula, Honduras, or drive there from Guatemala City or Antigua. You’ll stay in Copan Ruinas, a cozy little tourist town only a 20-minute walk from the main archaeological site. There are also Maya sweat lodges, spas, yoga retreats, and planned 2012 festivals
How a Zombie Outbreak Could Happen in Real Life
Could zombies actually exist? What would it take for human corpses to rise up and hunt the living? We often think zombies are scientifically impossible — but actually, they’re just very implausible. Here’s one wayThe Walking Dead could happen in real life.
To start our zombie thought experiment, we need to make some basic assumptions. First, we’re ignoring all supernatural zombie origins. We’re also going to set aside space radiation, mysterious comets, or Russian satellites. Our focus will be narrowed to biological origins –- a zombie contagion. Of course, there are many different zombie scenarios in books and film, and no one theory is going to cover all of them perfectly.
The first aspect of human zombification we need to tackle is basic zombie physiology. In virtually every zombie scenario, zombies are able to function despite increasing levels of physical deterioration due to injury or decomposition. There has to be some mechanism for transmitting neural impulses from the brain to various body parts, and for providing energy to muscles so they can keep operating.
The most common science fictional explanation for zombie outbreaks is a virus — but viruses and bacterial infections are not known for building large new physical structures within the body. So let’s count viruses out. Instead, the need for a mechanism to activate deteriorating body parts actually provides the cornerstone of what is, in my opinion, the strongest theory: fungal infection.
We know that fungi can infect humans. We also know that fungal networks exist in most of the world’s forests. These mycorrhizal networks have a symbiotic relationship with trees and other plants in the forest, exchanging nutrients for mutual benefit. These networks can be quite large, and there are studies that demonstrate the potential for chemical signals to be transmitted from one plant to another via the mycorrhizal network. That, in turn, means that fungal filaments could perform both vascular and neural functions within a corpse.
This leads us to the following scenario: microscopic spores are inhaled, ingested, or transmitted via zombie bite. The spores are eventually dispersed throughout the body via the bloodstream. Then they lie dormant. When the host dies, chemical signals (or, more accurately, the absence of chemical signals) within the body that occur upon death trigger the spores to activate, and begin growing. The ensuing fungal network carries nutrients to muscles in the absence of respiration or normal metabolism.
Part of the fungal network grows within the brain, where it interfaces with the medulla and cerebellum, as well as parts of the brain involving vision, hearing and possibly scent. Chemicals released by the fungi activate basic responses within these brain areas. The fungi/brain interface is able to convert the electrochemical signals of neurons into chemical signals that can be transmitted along the fungal network that extends through much of the body. This signal method is slow and imperfect, which results in the uncoordinated movements of zombies. And this reliance on the host’s brain accounts for the “headshot” phenomenon, in which grievous wounds to the brain or spine seem to render zombies fully inert.
This leaves the problem of zombie metabolism. Where do the zombies get the nutrients needed to perform physical activity, plus the necessary nutrients to fuel the life-cycle of the fungi? This is most easily explained by the zombies’ constant, endless drive to devour meat. The fungal network would still need some way to metabolize meat, and zombies seem to be able to function even in the absence of a human digestive system.
It is possible that this particular fungi has evolved a means to extract energy and nutrients from meat in a similar manner to carnivorous plants. The ingestion of meat may actually be vestigial, an unintended result of the drive to bite. In this case, the fungi may draw energy from the decomposition of the host’s own organic material, which effectively puts a shelf-life on zombies (in addition to the deterioration of body structures beyond the point where the fungal network can compensate).
Accounts of dismembered parts moving purposefully may be apocryphal.
Now we have established a working theory for fungal zombies. How could such a disease arise? The goal of any biological organism is to live long enough to reproduce, but many pathogens are self-limited by their own lethality. The host dies before it has a chance to spread the pathogen inadvertently. This gives us two pathways for development of the zombie fungus. First, a fungal species existed that used the digestive tracts of mammals to travel. In other words, animals ingested the fungus, including spores. The spores were later defecated out in a new location. Some mutations occurred that caused the spores to gestate while still within the host. However, in most cases, the host’s immune system would destroy the fungus. Further mutations could lead to spores that only trigger once the host has died, avoiding this problem.
Another possibility is a fungal infection that was highly aggressive and caused rapid death within the host. That strain was not able to successfully reproduce as often as a mutated strain that delayed activation until post-mortem.
Of course, it’s one thing for a fungus to activate after the host dies, and quite another for the dead host to stand up and start attacking things. There are many evolutionary steps in between, which is why a zoonotic origin seems likely.
The precursor fungus could have been ingested by pigs, which are omnivorous. Captive pig populations, subject to overcrowding, would have been perfect places for the fungus to spread and mutate. In some poorly managed pig farms, dead pigs may have gone unnoticed, allowing post-mortem development of the fungus. Dead pigs were likely partially eaten by their living counterparts, allowing the fungal strains with post-mortem mutations to spread back into the population. The method of transfer from the pig population to the human population seems fairly obvious.
The evolution of fully mobile dead pigs probably started with a simple bite reflex that could transmit spores to nearby pigs. A bite combined with a muscular spasm, a sort of lunge, would work even better. After many generations, this developed into full post-mortem mobility. Thus, a dead host went from a drawback to an advantage, becoming a mobile platform for spore distribution. In fact, the zombie hunger drive may have originated as a spore distribution method –- only later was the ability to metabolize meat acquired. We can extrapolate this development to assume the further refinement of the fungal neural system, allowing for zombies which are far more coordinated and can run at nearly full speed.
While this type of behavior modification may seem unlikely, there is precedent for it within the animal world. Several species of parasitic wasps are able to reprogram the behavioral patterns of their hosts (bees, ants and even caterpillars), creating complex new behaviors beneficial to the wasp and detrimental to the host. While the hosts in these cases aren’t dead, this does demonstrate that complex chemical overrides can evolve in nature.
Hopefully scientists can develop an effective zombie fungicide in time.