The Beekeeper's Lament (17 page)

Their efforts posed some thorny problems. First and foremost, the disappearing bees had, well, disappeared and were thus difficult to examine. Researchers were left with a few immature adults and brood and the smattering of foragers that still remained in affected hives. And the problem was so widespread—more than a third of cultivated bees had died across at least thirty-six states—that it was difficult to ascertain which deaths were truly the result of the new disorder and which were due to the litany of other pathogens and environmental insults bombarding bee colonies. Entomologists needed access to control groups that had not been exposed to the same environment. But bees are uncontrollable; it was nearly impossible to find any that scientists could be certain had not been exposed to the same influences as the diseased ones. So vanEngelsdorp and entomologists across the country began to sift through the clues, applying a Sherlock Holmes–style process of elimination. They surveyed scores of beekeepers whose stocks had suffered from CCD, and scores whose bees hadn’t. They talked to beekeepers who moved their bees and those who didn’t, to small-scale organic beekeepers and large-scale industrial operations. No obvious pattern emerged; the disorder had been found across all groups.

They looked for specific ailments. They found high mite loads in some CCD bees, not others. They found fungi in the guts of many, but not all. They found contamination from past varroacide use, legal and unauthorized, in many CCD hives, but also in many non-CCD hives. They found contamination from crop-applied pesticides, but no clear pattern. They combed through climate and satellite data to look for weather-related problems, but found nothing to explain the nationwide distribution of the problem. They considered bad corn syrup, fructose, and pollen substitutes that beekeepers might have fed their bees, but nothing immediately stood out. They contemplated the issue of beekeeper neglect. Some of the worst cases showed telltale signs of bad beekeeping, but some of the nation’s most diligent beekeepers also had the disorder.

The scientists looked and looked. They found no easy answer. For all the advanced science available to them, it was almost as if they were back in the era before Langstroth invented his hive, blind to the mysteries that went on inside a colony’s walls. They admitted that they were as bewildered as the beekeeper next door, and certainly more so than the armchair apiarists on the Internet who had already decided the problem was neonicotinoids or genetically modified corn or cell phone transmissions: “Lots of guesses, and I have my own, but I’ve also changed opinion since I’ve seen so many cases in so many areas,” Montana State University entomologist Jerry Bromenshenk, one of the scientists in the CCD working group, wrote in an Internet beekeeping chat room. “Funny, the CSI teams on TV do this in an hour.” It would take much longer than an hour, a month, or even a year to tease out an answer to this mystery.

T
HE FACT IS, YOU DON’T ALWAYS KNOW WHY BEES DIE.
S
OMETIMES
, they just do. On a perfect January day with just a hint of winter’s chill and the first yellow blooms of spring mustard beginning to unfurl, John Miller and I visited a bee yard that he kept for two friends from North Dakota—beekeeping brothers, one a retired crop extension specialist and the other a plant pathologist who got to know Miller when they both served as officers in the North Dakota Beekeepers Association in the early 1980s. They ran their bees in North Dakota in the summer and Miller took the brothers’ hives south with his own bees for the winter pollination circuit. I couldn’t say the brothers’ yard was quite as pleasant as those Miller reserved for his own bees—he’s only human—but there was nothing wrong with it. The hives lay in a sunny flat spot along a bleached clay road surrounded by cut-off buttes that had been carved away to provide terra-cotta for a nearby quarry. The spot wasn’t idyllic, but there was ample forage, water, and sunshine, and a bee doesn’t ask for more than that.

Still, the brothers’ colonies weren’t doing well. There were mites. Some of the hives were infested with mouse-turd-sized small hive beetles—the relatively new honey bee hitchhiker that eats, poops, oozes, and wreaks general havoc in an apiary. I had visited lots of bee yards with Miller by then, but these were the first hive beetles I had seen, and the hives in which they were found were underweight and understrength. There were also real mouse turds, from real mice that had eaten their way into one of the hives. When a colony is weakened, mice are able to nest in a hive without meeting the usual deadly reception. Miller doesn’t like to see bees die, but his compassion doesn’t extend to all creatures. He has no remorse about smashing a mouse with his hive tool, which he did with one efficient stroke that left a little beast with its diminutive paws splayed upward and a tiny trickle of blood pooling below its smashed head. Most of Miller’s hives had come into spring with six to eight frames each, teeming with bees and stocked with honey, pollen, or brood, but the hives in this yard were only three to four frames strong, even without mice and beetles. “They got fed and medicated; they don’t have many ticks,” Miller said. “I can’t tell why they’re crappy bees.”

Bees have experienced mysterious die-offs from time immemorial. Long before CCD came along, they even disappeared without a trace. Langstroth, for instance, described hives that were “found, on being examined one morning, to be utterly deserted. The comb was empty, and the only symptom of life was the poor queen herself, ‘unfriended, melancholy, slow,’ crawling over the honeyless cells.” In the case of CCD, though, honey is left behind. But Langstroth described that condition, too. “Occasionally,” he wrote, “after the death of the bees, large stores of honey are found in their hives.” Since Langstroth’s time, such happenings have been documented regularly. An 1869 issue of
Bee Culture
magazine described mysterious departures in which hives were left with ample honey stores. In Colorado in 1891 and 1896, in a case known as “May Disease,” large clusters of bees vanished—queens still there. There were the epidemics between 1905 and 1919 that killed 90 percent of the bee colonies on Britain’s Isle of Wight; for many years, the term “Isle of Wight disease” was the common name for losses for which beekeepers could find no obvious explanation. There were nebulous tales of large-scale dead-outs, as dead hives are sometimes called, across the United States, from Florida to California to Oregon, in 1915; more were reported in 1917 in New Jersey, New York, Ohio, and Canada. In the 1960s bees disappeared mysteriously in Texas, Louisiana, and California—no bacteria, mite, fungus, virus, or parasite appeared to explain it; those bees that remained in the abandoned colonies appeared healthy and had plenty of honey. In 1975 Australia suffered a bout of “disappearing syndrome”; that same year a similar epidemic of “disappearing disease” cropped up in Mexico and then spread to twenty-seven U.S. states. Neither bore obvious explanation. There were also heavy losses in France from 1998 to 2000. And now there was CCD.

So the symptoms of CCD were distinct—disappearing foragers, a healthy queen left behind, ample honey stores, no signs of excessive mite or fungal infection—but not unprecedented. Bees often die away from the hive. When confronted with high virus levels, they seem to know they are sick and leave on purpose, so as not to infect others, sacrificing themselves the same way our ancestors must have done. Miller likes that idea. It makes the ruthlessly indiscriminate way that bees die seem somehow almost meaningful.

Think about that . . .

Grandpa walked out of the igloo, and fed himself to the polar bear when he knew his time had come. . . .

Is it so, that the 900,000 neuron bee-brain has,

in a secret chamber,

the altruistic knowing to go? . . .

Bees die. Bees disappear, and sometimes in droves. They have done the same in the past, and not infrequently. “What’s unique about this situation,” says vanEngelsdorp, “is that we’ve never had it to this extent.” Such massive, inexplicable losses have never been reported so widely.

In September 2007, a few months after the disorder was first identified, the CCD team led by Penn State’s Cox-Foster, who did the first genetic analysis on Hackenberg’s bees, conducted a cutting-edge “metagenomic” analysis and found that a little-known pathogen called Israeli acute paralysis virus (IAPV) was present in 96 percent of the hives stricken with CCD. Furthermore, all the infected samples had come from operations that had imported bees from Australia after the varroa die-off in 2005. This suggested that the virus was imported from Australia along with the bees. The disease, which was first identified in Israel in 2004 and has since been found in many locations across the world, causes bees to suffer paralytic seizures. They are typically found trembling, twitching, and flailing dramatically just outside the hive. (“They’re suffering,” Miller whispered to me as we watched a video of a bee dying from IAPV at a beekeeping conference.) Though the symptoms of CCD were nothing like those of IAPV, the report concluded that IAPV was “strongly correlated with CCD.”

Although the researchers were careful to say that IAPV was not necessarily the cause of CCD—and could in fact be merely a symptom, or its presence merely a coincidence, and that far more study was needed—the media was less fastidious in reporting what appeared to be the first big break in the case. A spate of articles trumpeted the solution to the CCD mystery and the link to Australian imports. A Pennsylvania senator urged the USDA to suspend all Australian bee imports, and the Australian beekeeping industry erupted in protest. A team led by Denis Anderson, the Australian scientist at the forefront of the varroa battles, quickly issued a rebuttal, calling links between CCD and IAPV “tenuous” at best. Anderson and a colleague noted that there had been no occurrences of CCD in Australia; that IAPV had been found in hives not suffering from CCD as well; and that other countries reporting CCD, such as Spain, Greece, and Poland, had not imported bees from Australia. Anderson also pointed out that IAPV had now been linked to bee deaths in the United States as far back as 2002—three years before Australian bees arrived on American shores. The “problem solved” headlines trailed off, a victim of uncertainty.

Other scientists had also begun researching the CCD mystery, and the next diagnosis was
Nosema ceranae
, a new strain of a long-known fungal infection that had recently jumped from Asian bees to European ones.
Nosema apis
—an infection found in European bees—had been present in both the United States and Europe for many years. The disease is often associated with extreme diarrhea in bees but is easily treated with an application of antibiotics just before the bees hunker down for the winter. (A disease of confinement,
Nosema apis
is usually only a problem during the cold months.) The new Asian strain, however, caused symptoms at strange times of year when beekeepers weren’t accustomed to treating it, symptoms that were in some cases suspiciously similar to those of CCD—bees died suddenly, often while away from the hive. Miller, blindsided by a summer epidemic of the new strain, lost 25 percent of his hives to it in 2008. After a particularly bad epidemic of deaths in Spain, a Spanish team declared nosema the main factor in the CCD epidemic: “We’ve no doubt at all it’s
Nosema ceranae
,” the lead scientist on the team told a Reuters journalist. There were some troubling incongruities, however: nosema had not been detected at levels considered high enough to cause collapse in many CCD colonies, and genetic tests revealed that the “new” nosema had been present in the United States since at least 1995 and was widespread across the country, both in locations affected by CCD and in those unaffected.

Probably the most common and persistent explanation for the disappearances placed the blame on pesticides—specifically the neonicotinoids that Hackenberg faulted for his own losses. France banned the products in 1999 after they were linked to major losses in sunflower fields and a disorder that local beekeepers took to calling “mad bee disease.” Sales had also been suspended in Germany, Italy, and Slovenia. The theory was a persuasive one. For as long as pesticides have existed, they have been responsible for massive bee losses. The chemicals are, after all, designed specifically to kill bugs, and honey bees are, despite their comic-book fuzzy reputations and close human connections, bugs—and thus tremendously vulnerable to chemicals designed to kill their exoskeletal brethren.

Hackenberg wasn’t a natural ally of the antipesticide crowd. His father was a farmer, and his livelihood in the pollination business depended on the agriculture industry. When he first started poking into what caused his bees to go missing, he emailed some friends in France, who sent him “all this propaganda about Gaucho and so on and so forth,” claiming that the problem was systemic pesticides. Systemics, he learned, work not by killing outright but by breaking down the immune system of the target insect.

He wasn’t persuaded at first, but, he says, “as time went on and I started digging, the pesticide thing kept coming back and kept coming back and kept coming back.” He recalled that some of his bees had disappeared after pollinating apples in New York and called the grower, and then the grower’s pesticide applicator, to find out what pesticides they had been spraying in 2005. He learned that it was Calypso, a popular neonicotinoid. He then set his wife to searching the Internet, and she found a University of Florida study that explained how systemic pesticides broke down termites’ immune systems—“they go out to feed, and they won’t come home,” Hackenberg says.

Studies have established that chemicals can often work in sublethal ways. Massive worldwide frog declines, for instance, have been linked to the commonly used weed killer atrazine. One theory is that the herbicide kills frogs in indirect and insidious ways by destroying floating mats of algae but allowing algae on pond bottoms to thrive on the increased sunlight. This in turn provides more food for underwater snails, which explode in population, as does a parasitic flatworm carried by the snails. The flatworm then parasitizes and kills the frogs. Scientists believe that atrazine may also damage the frogs’ immune systems, rendering them more vulnerable to various parasites that flourish in atrazine-affected environments. In complex ecosystems like freshwater ponds and beehives, balances can be tipped by unexpected factors, creating what amounts to ecological chain reactions.