The Beekeeper's Lament: How One Man and Half a Billion Honey Bees Help Feed America

by Hannah Nordhaus

  Hackenberg dresses like a ranch hand, with a leather vest and jeans that extend somewhere close to his armpits. Like John Miller, Hackenberg is a talker. The first time I spoke with him, he had two or three phone conversations going on at the same time, and even so, his call-waiting was clicking in every few minutes. He talks loudly, with the wound-up patter of a horse-race announcer; a constant crescendo. So when his bees disappeared, he did what comes naturally to him: he started making phone calls. He called Jerry Hayes, Florida’s assistant chief of apiary inspection, and described the bee yard scene. Hayes told him that a Georgia beekeeper had just lost six hundred of his nine hundred hives in a similarly disconcerting manner. Hackenberg kept calling around and kept hearing about hives collapsing in the same way across the country—in Florida, Georgia, Texas, New York, California, Pennsylvania, and the Dakotas; thirty-six states eventually. All had remarkably similar symptoms: adult bees abruptly vanishing from the hive, leaving few bodies inside or nearby; a queen, a healthy store of brood, a few young adults left behind; and little to none of the typical pillaging that would be expected of a collapsed hive’s honey and pollen stockpiles.

  Hackenberg also shared his weird findings with scientists, including Dennis vanEngelsdorp, who was acting state apiarist in Pennsylvania. He and vanEngelsdorp had seen each other only a month before, in early November, at the annual Pennsylvania State Beekeepers Association meeting. Hackenberg spends summers in central Pennsylvania when he’s not on the road pollinating blueberries, apples, cantaloupes, pumpkins, cranberries, and almonds. He had just transported his hives down to his winter base in Florida, and he announced at the meeting that he was pleased with his bees—they were, he told vanEngelsdorp, “fantastic.” Perhaps that should have been the first sign—John Miller can attest that it’s the rare season that ends as it begins. Because sure enough, only a month later, Hackenberg called vanEngelsdorp to describe the woeful scene in his apiaries. VanEngelsdorp immediately assumed the problem was varroa mites—“we blame everything on varroa mite,” he says—but nonetheless asked Hackenberg to send him some dead colonies. When he examined the scattering of corpses that remained, says vanEngelsdorp, “we found the bees didn’t have varroa mite—but they did have every other condition going.”

  VanEngelsdorp, who was in his late thirties at the time, was a senior extension associate and Ph.D. candidate in Penn State University’s entomology department. A stocky, vaguely Norse-looking Canadian with a prow-like forehead and a thin covering of blond hair, vanEngelsdorp holds a master’s degree in entomology from Cornell and intends to finish his Ph.D., if ever he escapes the maw of permanent apiarian crisis. His work originally included a combination of research on bee epidemiology and outreach to local beekeepers to help them minimize the spread of disease. But after he autopsied Hackenberg’s bees, his job description changed. Typically, when a bee is sliced open, its viscera appear a creamy white. These bees were different. Their internal organs were blackened, their sting glands and intestinal tracts swollen, discolored, and full of melanized scar tissue, as if their insides had been incendiary-bombed.

  Hackenberg had also contacted vanEngelsdorp’s colleague Diana Cox-Foster, another Penn State entomologist who specializes in bee viruses and other pathogens. Cox-Foster conducted a molecular analysis on the afflicted bees. The results were mystifying: they had multiple viral, bacterial, parasitic, and fungal infections, but none seemed to suffer from the exact same infection. Some had deformed wing virus; some had sac-brood virus; some had black queen cell virus; some had chalkbrood; some had nosema; some had other viruses that hadn’t yet been identified. None had the same exact combination of pathogens. Nor did they have large loads of mites, as nearly everyone had expected. Had mites been responsible, the scientists would have found large numbers in surviving colonies or sealed up with the brood yet to hatch. They didn’t.

  What all this confounding evidence suggested wasn’t entirely clear. The affected bees’ immune systems—fragile under any circumstances—simply weren’t functioning as intended. Much as an AIDS patient suffers from a variety of exotic and typically rare infections, so did Hackenberg’s bee populations. The Penn State entomologists gave it an appropriately apocalyptic yet vague name, Colony Collapse Disorder, and set out to determine what it was.

  Among their first moves was to put together a collaborative “working group” representing a variety of disciplines and including USDA Research Service scientists, university entomologists, agricultural extension educators, and geneticists. To understand the distribution of the disorder, they conducted winter loss surveys, contacting bee inspectors who in turn contacted beekeepers across all fifty states, to find out where and how bees had died that year. The team also took samples from both healthy and afflicted hives in Florida, Georgia, California, and Pennsylvania. They put them on dry ice and sent them to various labs for analysis. Wax samples and bee corpses went to the pesticides group at Penn State, whose scientists examined the chemicals found in CCD hives and unaffected hives. Honey and pollen samples went to entomologists at North Carolina State University, who conducted a nutritional analysis of the food in the abandoned hives. The team shipped frozen bees to the Greene Infectious Disease Laboratory at Columbia University. Scientists there typically work with human tissue, but they agreed to employ a recently developed technique for reading short DNA sequences to create quick genetic profiles of the viruses, fungi, and parasites found in the CCD survivors. They sent samples to entomologists at the University of Illinois, who would compare the genomes of the affected bees to those of healthy colonies sequenced a few years earlier. They sent Hackenberg’s empty bee boxes to be irradiated by a company that uses gamma rays to kill bacteria on fruit and medical equipment. Then they repopulated the boxes with new bees to see whether they fared better in the sanitized equipment.

  In doing so, the team aimed to answer three fundamental questions. First: Was there a pathogen involved in the disorder—a new or reemerging strain of virus, bacteria, fungus, parasite, or amoeba? Second: Was there some type of nutritional or genetic stress, such as poor forage or a new genetic defect, that was present in CCD-afflicted bees but absent in healthy ones? And finally: Had the bees been exposed to pesticides or other environmental chemicals that might have compromised their immunity or affected their behaviors? The working group believed that those three hypotheses offered the most likely culprits in the mystery.

  Out in the general public, however, plenty of other theories floated about. Among the most outlandish were suppositions that the disappearing bees prefigured the coming Judgment Day, and the oft-repeated hypothesis that signals from cell phones led foragers astray. (“You should never let the bees have them,” joked a visitor to a beekeeper chat room. “They get distracted talking and never get any work done.”) Given how frequently beekeepers complained about poor cell signals in their bee yards, however, the argument never gained much traction.

  Beekeepers had their own, generally more plausible, ideas. Every so often, I’d get an email from Miller describing the latest theory waggling through the migratory hive. “The suspected pathogen is a new strain of nosema,” he’d write.

  Nosema is common in insects; you can inoculate grasshoppers with nosema spores,

  and watch them die

  A few days later, I’d receive another:

  psst.

  it’s BT Corn that’s killing the bees.

  you got it here,

  first.

  Hackenberg, for his part, blamed the bloodbath (or rather, the hemolymph-bath) on a class of pesticides called neonicotinoids, which are chemical forms of nicotine used to treat a wide variety of crops. Neonicotinoids are among the world’s best-selling insecticides. They are used on more than 140 different crops and in home gardens and flea collars, and they generate billions of dollars of sales a year. Developed by Bayer CropScience, Inc., they were first approved for use in the United States in the 1990s; fifty other companies have since jumped into the market, selling them
under catchy names like Gaucho, Poncho, Flagship, Assail, and Calypso. Neonicotinoids are sprayed on leaves, but also soaked onto seeds before they are planted. Because they are “systemic” pesticides, which are absorbed into every part of the plant, passing from the coated seeds through the plant’s circulatory system to the flowers, they remain in the plant—and its pollen and nectar—longer than many other insecticides. The neonicotinoid theory had a compelling logic, and lots of people in the environmental community quickly leapt to the same conclusion as Hackenberg—but it was, at that point, simply a theory. The CCD working group had a lot of methodical scrutiny—a lot of autopsies and surveys and studies and assays—ahead of them before they could declare the matter resolved.

  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.

  THE FACT IS, YOU DON’T ALWAYS KNOW WHY BEES DIE. SOMETIMES, 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 i
gloo, 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.”