Entomologists believe that European honey bees (Apis mellifera) and Asian honey bees (Apis cerana) branched from the same genetic forebear a few million years ago. Like European bees, Asian bees live in colonies, produce honey, and can be easily domesticated. Asian bees are smaller and less hairy, with more distinct stripes on the abdomen, and they tend to fly faster and more erratically. They are also more defensive. They swarm and spread more quickly, and their smaller colonies produce less honey. Thus it is the European bee that has accompanied humans, spreading from Europe to every temperate place where humans have settled. Scientists speculate that some one hundred years ago, the European bee completed its circumnavigation of the globe. They believe it moved from west to east via the Trans-Siberian Railroad and was reunited in Asia with its Eastern siblings, as well as the mites with which they coexisted.
Sometime in the early 1950s, the mite made its own fateful move. Some—perhaps only one—of those Asian mites jumped successfully from Apis cerana onto the Western honey bee. Scientists believe it happened somewhere in eastern Russia. In the 1960s, the mite spread through Russia and North Africa. By the 1970s, it had moved across Europe; mites were found in Paraguay in the 1970s, too. Someone also found a lone mite in Maryland in 1979. But until Gary Oreskovic spotted his bloodred tick on a September Wisconsin morning in 1987, the United States considered itself uninfested. No more: the mites blanketed the North American continent in the late 1980s and early 1990s, then jumped to South Africa. They reached New Zealand in 2000, where beekeepers lost more than thirty thousand hives; more than two thousand beekeepers “retired” soon after. In 2008, mites landed in Hawaii. To date, Australia is the only major beekeeping nation that has not hosted a mite. The varroa mite had once lived in the inconspicuous shadows where most creepy-crawly species reside, garnering little attention. But once it pitched the entire global bee supply into precipitous decline, this previously harmless parasite was, abruptly, the bee world’s public enemy number one.
So the bee world embarked on a crash course in varroa mite physiology. For four decades now, entomologists have studied it intensely, learning about its life cycle, its sex life, its behavioral propensities, its chemical sensitivities. The more they’ve learned, the more complex they’ve found the mite’s relationship with the honey bee to be. For instance, the mite’s effects appeared to vary as it traveled the globe: bees in South America and eastern Russia were relatively resistant; those in Western Europe and North America suffered near-universal mortality. In addition, the varroa mites on European bees were noticeably larger than those on their Asian siblings; scientists first attributed this variation to the fact that European bees and colonies are larger, offering the mites more nutrients and hosts on which to thrive. But in 2000, an Australian bee pathologist named Denis Anderson reached another conclusion.
I first heard Denis Anderson speak about the varroa mite at a beekeeping conference I attended with John Miller. Anderson wore jeans and a collared shirt opened a couple of buttons farther than most insect geeks would dare; he looked more Steve Irwin swashbuckler than entomology nerd, and he made varroa mites sound as interesting—and menacing—as saltwater crocodiles or box jellyfish. Anderson smiles easily, almost compulsively. He’s got quizzical arched eyebrows, a sharp nose, and a boyish face ringed by thick, shaggy brown hair and a beard. Although he is pushing sixty, his hair betrays barely a hint of gray. He travels the world studying bees and their diseases, spending six months a year at the entomology department of the Commonwealth Scientific and Industrial Research Organisation in Canberra, and the other six months in the field studying bee diseases and pests across Asia. He is the principal scientist working on bee populations and the varroa mite in Australia, which, as the last varroa-free bastion, has the luxury of devoting funds to more esoteric investigations than do afflicted nations, whose research dollars go mainly toward finding chemicals to kill it.
Anderson first began working with the varroa mite while doing field research in Papua New Guinea, Australia’s closest neighbor to the north. It was a fascinating place for a bee pathologist. Thanks to the political and migratory forces that swept the island of New Guinea in the twentieth century, Asian and European bees intermingled there, providing an excellent laboratory for observing the behaviors of the pathogens they shared. Australian missionaries had brought European bees to New Guinea before World War I, while Asian honey bees arrived in the 1970s, after the Indonesian government relocated thousands of Javanese farmers to Irian Jaya, on the western side of the island. Those peasants brought their own domestic animals, such as chickens, pigs, and Asian bees. And they also brought the Asian bees’ theretofore harmless co-rider, Varroa jacobsoni.
It was 1989, just a couple of years after the mite had arrived in the United States, and Anderson was well aware of the damage inflicted on European bees in the Northern Hemisphere. In New Guinea, the mite was everywhere, on both European and Asian bees. But Anderson quickly noticed that it seemed to behave differently on the European bees of New Guinea than on European bees elsewhere. The mites weren’t able to reproduce inside the brood cells, and thus were unable to spawn populations large enough to endanger hives. “When I first saw this I was new to the varroa mite and I thought, ‘What I’m looking at here is just an aberration,’ ” Anderson says. But it wasn’t an aberration; it was the norm there. Varroa mites were not able to replicate in European hives. “I looked at it for four years and said, ‘Look, this mite is not reproducing.’ ”
The question was why: were the European bees resistant to varroa mites in New Guinea, or were the mites themselves different? Anderson devised an experiment. He raised European queen bees in Perth, Australia, and he artificially inseminated them with semen from a single drone, so their offspring would come from a narrow genetic base. Then he moved twenty of those offspring to New Guinea and twenty to Germany, to see how they responded to the mites found in each location. In New Guinea, the hives did fine. In Germany, they collapsed. The mites found in Germany could readily reproduce in the Perth bee colonies. Those in New Guinea could not.
He then conducted the same experiment in Java, the densely populated island that is home to Indonesia’s capital city, Jakarta, and found that the mites there could not reproduce in European colonies. But in 1994, soon after Anderson’s experiment concluded, he began hearing reports that varroa mites in Java had suddenly begun to reproduce on European bees, killing colonies across the island. He examined samples of mites from collapsing hives and noticed that they were much larger than the ones he had studied in New Guinea and Java in previous years. And while the larger mites had overrun the hives, he could also find the smaller mites—which were still not reproducing. It was then, he says, that he had his own eureka moment: “I realized that there were two mites here,” he says.
The new mites in Java were not only larger; they were also more oblong. By the mid-1990s, DNA technology had evolved to the point where it was possible to sequence segments of the genetic code from the mites. So Anderson studied the variation in sequence of a particular mitochondrial gene on both mites and found them to be different. He then traveled across Asia collecting additional samples, sequencing their genes as well. He discovered that there was not just one mite riding around on the world’s Asian honey bees, but a complex of mites, comprising four entirely different species and eighteen separate regional genotypes. Of those eighteen, only two were found in European bee colonies globally—and neither belonged to the species that had long been blamed for causing the damage to global bee populations. Varroa jacobsoni, the mite Anderson found in New Guinea, was native to Indonesia and could not reproduce in the brood of the European bee. It was, University of Georgia entomologist Keith Delaplane wrote in a 2001 editorial in a bee science journal, a “benign homebody, still restricted essentially to its original host . . . and not the culprit to worldwide calamity that we had thought.” The mites didn’t behave differently in different regions because the host bees were different. No, the mites behav
ed differently because they were, in fact, different mites. For three decades, Anderson realized, entomologists had been studying the wrong mite.
The culprit was not Varroa jacobsoni, but the larger mite, one of the two genotypes that could reproduce in European bees. One of the offending genotypes had originated somewhere on the Korean peninsula; the other in Japan. The Japanese mite was the one that had found its way to South America in the 1970s via a shipment of varroa-infested bees from Japan to Paraguay. It had remained restricted in both the damage it caused and the scope of its spread. The far more pathogenic variant had evolved on the Korean peninsula. At some point it made the transspecies jump from Apis cerana onto Russian bees and spread to Europe and the United States. Those Korean mites showed little genetic variation in Anderson’s studies, suggesting that there may have been only one single female mite that made the reproductive jump between hosts—a founding foundress, so to speak, that cloned herself around the world. Delaplane compared Anderson’s discovery to a “scientific revolution,” if not on par with the discovery of gravity and relativity, one that was nonetheless earth-shattering “for that fraction of the world’s scientists who work on the parasitology of Apis mellifera.” As discoverer of a new species, Anderson was entitled to naming rights. Rather than christening it Varroa andersonii—“I don’t think I would like to be remembered as a parasitic mite”—or by reference to its homeland, he opted for a devastatingly apt, melodramatic, even comic-bookish moniker: Varroa destructor.
AS AUSTRALIA’S PREEMINENT BEE PATHOLOGIST, ANDERSON is keenly involved in his nation’s efforts to prevent that destruction from spreading to Australia’s shores, striving to keep any foreign bee that could harbor the mite well away from the island continent. This is no easy task in an era of slapdash mobility. Bees have crossed all the great oceans. They arrive on all variety of conveyances: in the pockets of bee collectors looking for the next great queen; in the holds and spars of ships; in airplane baggage compartments. The problem is compounded by the fact that the world is no longer dealing with only one dangerous species of mite. Since Anderson observed and named Varroa destructor, another variant has jumped from Asian to European bees. As luck would have it, it has done so in the very population Anderson first became familiar with, in the very location where he first studied the mite.
In 2008, reports emerged from New Guinea about beekeepers losing Apis mellifera colonies at an alarming rate. Anderson went to look at the situation. “The first colony I opened,” he says grimly, “there were reproducing mites in nearly every cell.” He couldn’t be certain, without access to sophisticated technology not available in New Guinea, which species of mite was causing the problems. So he improvised: he retrieved some Varroa jacobsoni from an Asian bee colony and compared them to the ones that had infested the European colonies, taking photos of both with his digital camera and uploading the images on a laptop. They were exactly the same size and shape. He shipped a sample to a lab in Australia for genetic testing. “Sure enough,” he says, “it was a population of Java mites.” The jacobsoni mites had, for the first time, begun reproducing in European colonies. The prospect is unsettling, because like Varroa destructor, these newly pathogenic jacobsoni mites could carry unfamiliar viruses that could cause even more problems for already-embattled bee populations across the world. In addition, Anderson doesn’t know yet whether the jacobsoni mites that can now reproduce on European bees can still reproduce on Asian ones. If they can, it only hastens the inevitable moment when the varroa mite will reach Australia: “The way that mite will get out of New Guinea,” Anderson says, “is on the Asian honey bee.”
The European honey bee doesn’t fare well in the tropical lowlands of New Guinea. It needs lots of care and tending to survive. The Asian honey bee has no such problems; it is considered an invasive species there. It swarms easily and travels long distances. Since its introduction in Irian Jaya, it has spread across the island to the former Australian territory of Papua New Guinea, and east to the island of New Britain, and 1,300 miles farther to the Solomon Islands. It has also made incursions onto Australian soil: in May 2007, a beekeeper from Cairns, in far northeastern Australia, was called to remove a swarm from the mast of a yacht in drydock. He realized that the bees were unusual and called officials from the local agriculture authority. The officials recognized the bees as Apis cerana and promptly declared an emergency. Queensland biosecurity officials restricted all movements of managed Australian bees and sent three surveillance teams racing through the continent’s lightly populated north country in search of swarms. They put out a call for citizens to report any unusual bee sightings, combed the area with sweep nets, and tested the pellets of bee-eating birds for Apis cerana DNA. They also used a process called “beelining”—capturing and marking foraging Asian bees that had been lured to strategically placed sugar feeding stations, then releasing and tracking them back to their nests.
When the teams found and destroyed three colonies within a one-kilometer radius of the yacht harbor, it became clear that the bees had been living there long enough to swarm and spread. Authorities reckoned that they could have been onshore for as long as three months. The search widened, and by July 2010 they had found more than one hundred Asian beehives. It seemed unlikely that they could stop its spread: the Asian honey bee had probably become endemic to northern Queensland. Tests on the bees and comb from the nests showed that all the nests were related and had descended from a single colony—probably a swarm that hitched a ride on a boat from New Guinea, eluding quarantine inspection. The tests also confirmed that there were no mites on the bees. Although the risk remained that the Asian bees would rob and attack European bees or outcompete them for food, Australia had dodged the varroa bullet for the time being. Still, Anderson knows that it is only a matter of time before varroa mites arrive on Australian shores. It might be the newly destructive New Guinea variety, the Korean variant, or another damaging genotype newly cooked up in the global bee melting pot. “It’s not a matter of if it will arrive,” he says, “but when.” Anderson’s knowledge of varroa mite genetics will do little in the short term to stanch its spread or control the devastation. For in addition to being a remarkably destructive creature, the varroa mite is also a tremendously adaptive one.
THIS IS A LESSON JOHN MILLER LEARNED THE HARD WAY IN the winter of 2005. In the initial period after American beekeepers first encountered the varroa mite, treatment was easy. A beekeeper simply placed an Apistan strip in each hive in the fall and forgot about it. The Apistan killed the mites, which never grew numerous enough to overwhelm the hives. But after about ten years the medicine stopped working. Apistan, it turned out, killed most of the mites, but small numbers survived, and over the years the surviving mites reproduced, replicating the genetic capacity that resisted the miticide and growing in population until, finally, the resistant survivors’ offspring made up the majority of mite populations. The medication had selected for stronger, more resistant mites. Fortunately, a second compound, called coumaphos, was in the process of EPA approval and was rushed to market. Coumaphos was also effective against mites, but it was much harder on bees. Soon after Miller began applying it, he noticed that his queens were less fertile, and that they failed, and died, sooner. Miller’s friend Kevin Ward—who produces some of the best star thistle honey on the planet—likes to joke that coumaphos “killed everything but the mite.”
Beekeepers had resorted to protecting their frail charges with the very thing they had been fighting against since the dawn of industrial agriculture: pesticides. Starting in the 1950s and ’60s, lethal chemicals like methyl parathion and Furadan had been sprayed on crops nationwide and nearly indiscriminately, killing birds, wild insects, and managed bees. The effects were dramatic: when foragers were inadvertently caught in a spray of pesticides, they would fall out of the air as they were flying. If bees survived the initial dusting or visited a flower that had recently been sprayed, they might bring back contaminated nectar that would doom the whole h
ive. For weeks after chemicals were applied, fields remained lethal, their fences pasted with placards warning “Peligro”—danger.
For beekeepers, the danger was more than hypothetical: their livelihood could be destroyed with one poorly timed spray or wrongly placed pass of a crop duster. Miller remembers being “popped” by a stray plume of Furadan that drifted over his hives from alfalfa fields near Tracy, California. Dead bees piled up not only in the “customary puddle o’ death” outside the hives, but also, more disturbingly, inside the hives. “I was fighting tears,” he says, “bagging up bees.” When he sent them to a state lab for analysis, the techs told him they had never measured Furadan levels that high in bees. In California and some other states, farmers are required to inform beekeepers when they treat crops with insecticides; in others, the onus falls on the beekeeper to keep abreast of farmers’ pesticide plans. That was next to impossible. Treatments applied miles away could kill entire bee yards when a drift traveled unexpectedly on the prevailing breeze.
Beekeepers hated everything about insecticides. Before the onslaught of the varroa mite, the strongest thing any self-respecting beekeeper would put in his hive was an antibiotic called Terramycin to treat American foulbrood. Now they were forced to dose their own hives with chemicals. “It ran counter to everything we believed about good husbandry,” Miller says. But the only other choice was not to treat for varroa mites—and guarantee the loss of 80 to 90 percent of their operation. Few beekeepers were willing to do that. So Miller swallowed his pride and continued to use the coumaphos. For three or four years, it did the trick.
The Beekeeper's Lament: How One Man and Half a Billion Honey Bees Help Feed America Page 7
