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.
Perhaps the accumulation of weeks or months of pesticide exposure from pollen collected from fields sprayed with neonicotinoids had finally tipped the balance in the nation’s beehives. Perhaps, Hackenberg concluded, because residues remain in the plants at low levels for weeks after application, the poisons could accumulate in honey and pollen all summer. As bees turned to their stockpiles to survive the fall and winter, the neonicotinoids might degrade their nervous systems, causing disorientation, reduced immunity to disease—and perhaps mass die-offs like those seen in the cases of CCD.
There was plenty of circumstantial evidence to support these theories, and like Hackenberg, a number of respected beekeepers believed their losses correlated with exposures to the pesticides. Gene Brandi, Miller’s television replacement on the NBC story about CCD, lost half his hives in the winter of 2007–2008 after he rented them to a watermelon farmer in the San Joaquin Valley. Only later did he learn that the farmer had treated his watermelon crop with neonicotinoids; the hives that Brandi sent elsewhere survived. Initial studies seemed to indicate that pesticides could certainly be a factor: researchers found extraordinarily high levels of various pesticides in the wax, pollen, and bees that they extracted from CCD-affected hives. In studies led by Maryann Frazier, another Penn State entomologist, forty-six different pesticides were found in 108 pollen samples analyzed, and seventeen different chemicals were discovered in one single colony. Some were approved for use in hives to kill varroa mites. Some were garden-variety pesticides; some were systemic chemicals such as neonicotinoids. They even found insecticides that were no longer in use, like DDT, which was banned more than twenty-five years ago.
Farm chemicals clearly stick around in hives in greater numbers and for longer times than had previously been believed. This was true for neonicotinoids as well. There was also new evidence that neonicotinoids were more potent than previously believed: in December 2007, Bayer CropScience released a study that found that test trees given the same neonicotinoid doses regularly used on citrus and almond groves contained residual amounts high enough to kill bees, and that it persisted in the leaves of the trees for more than a year. With prodding from industry leaders like Brandi and Hackenberg, the National Honey Bee Advisory Board asked the EPA to ban the product. Instead the EPA called for further testing, allowing the products to remain on the market until the studies’ conclusion in 2014.
Despite mounting evidence that neonicotinoids can harm bees in smaller doses than previously understood, there are major problems with the hypothesis that pesticides alone cause CCD. There is, first of all, the fact that while the latest round of bee disappearances began in the fall of 2006, neonicotinoids have been on the market in the United States since 1994. That said, their use has increased dramatically in the last decade. Says Hackenberg, the products are now used on “everything—I mean literally everythi
ng, from your dog and cat to corn, soybeans, cotton, vegetables, lawns, and golf courses.” Still, bees have settled in fields of sunflowers, canola, corn, and melons treated with the chemicals for years, to little obvious ill effect. Spokesmen for Bayer are quick to point out that there have been zero reports of CCD losses in Australia, which has also used neonicotinoids for many years. In addition, the prohibition of the chemicals in France has done little to restore healthy bee populations. French bee colonies never quite rebounded from the die-offs of the late 1990s, suggesting that there may be some other factor responsible for their continued malaise.
Most researchers now agree that pesticides don’t appear to be the sole cause of CCD losses. A 2009 study at the French National Institute for Agricultural Research found pesticides in troubling numbers in all the hives tested, CCD or no, but found no evidence that any individual pesticide occurred more frequently in CCD apiaries than in control ones. (In fact, healthier hives often had higher levels of some pesticides, especially the varroa-killing chemical coumaphos.) Perhaps, though, chronic exposure to low doses of poisons weakened bees sufficiently so that another pathogen—one that would under normal circumstances cause only limited mortality—was able to finish them off. The French study showed that bees that did not succumb to pesticides or nosema alone often did succumb when exposed to both nosema and nonlethal doses of pesticides.
Other theories rose and fell. In the fall of 2009, a spate of newspaper articles trumpeted a British team’s conjecture that the problem was a lack of variety among queen-bee mates—queens were not promiscuous enough, in effect. They were mating with fewer drones, creating a less genetically diverse population that was more vulnerable to disease and other biological insults. This may be one factor in the honey bee’s difficulties in recent years, but the British study had not even gotten under way before press releases issued forth. Every scientist, it seemed, looked at the disorder through the prism of his or her own particular specialty and circumstances; every advocate favored his own particular cause or worldview. The disorder was so poorly defined that it was easy to shape to fit one’s own conclusions. “A lot of people are jumping on everything dead and saying it’s CCD,” vanEngelsdorp told me. “It’s like saying anyone who dies is dying of cancer.”
Plenty of bees have died since CCD was identified, but not all perished from CCD. Mortality studies conducted by vanEngelsdorp found that beekeepers had been experiencing losses of about a third of the nation’s bee herd each year since 2007, much higher than the 15 percent loss they considered “acceptable.” But CCD was not always the main factor. In 2008, beekeepers reported symptoms of CCD in 60 percent of colonies that died; in 2010, however, they reported the same symptoms in only about a third of the dead colonies, and only 5 percent of beekeepers believed CCD was the main cause of their losses. The leading cause that year was starvation. “If anything, it’s shown us that bees are dying in a lot of different ways,” vanEngelsdorp said.
Many unaffected beekeepers, meanwhile, still placed the blame on the old standby, PPB (piss-poor beekeeping). Because the case definition of CCD was rather loose and open to interpretation, it is indeed likely that losses from any number of less glamorous causes were dumped into the large bucket of CCD, and that many beekeepers weren’t able to check their hives often enough, especially in winter, to know whether their lost bees vanished quickly and en masse, as they do in CCD, or simply died from some other cause. Still, many of the same beekeepers who blamed the first year’s losses on bad beekeeping ate their words in the second year, when they too lost huge proportions of their colonies. Richard Adee, the nation’s largest beekeeper, was an outspoken proponent of the PPB theory in 2007. In 2008 he lost 40 percent of his outfit to the disorder. Even Miller will admit, under duress, that though he didn’t have the unique experience of finding an entirely deserted bee yard, he did sometimes open a hive to find lots of honey and just a handful of bees. Though he continued to blame such problems on varroa mites or Nosema ceranae, he admitted, “I’m sure half of what we were seeing was probably related to symptoms described as CCD.”
It is hard for a prideful beekeeper to cede control of his narrative. But tarring beekeepers who have suffered from the disorder with the broad brush of incompetence, says vanEngelsdorp, is like accusing someone who catches the flu of not washing her hands enough—perhaps she didn’t, but plenty of conscientious people get the flu, too. Sometimes bad things happen to good beekeepers. “I don’t think there are any beekeepers who survived the last twenty years, who survived the varroa mite, who aren’t good beekeepers,” vanEngelsdorp says. “We’ve lost them already.”
SCIENTISTS HAVE BEGUN TO COME TO A VAGUE CONSENSUS about the CCD deaths, though it’s not a particularly satisfying one. A 2009 study from the CCD working group concluded that the distribution of CCD apiaries suggested either a contagious condition or exposure to a common risk factor—neighboring colonies tended to die together—and that CCD colonies generally had higher viral loads and were coinfected with a greater number of pathogens than were the control colonies. A later study confirmed that CCD bees carried increased viral loads, particularly from a suite of picorna-like retroviruses that hijack cellular production of important proteins and work much like another retrovirus, HIV, which leaves humans vulnerable to opportunistic diseases that someone with a healthy immune system would easily ward off. A 2010 study found that in colonies with Nosema ceranae infection, the retroviruses were at levels two to three times higher than in healthy colonies—the presence of both nosema and the viruses together appeared to be a strong predictor of a colony’s collapse. Later that year, a Montana team, using military technology developed to test for bioterrorism attacks, discovered that a pathogen called insect iridescent virus, which had not previously been found in honey bees, was strongly correlated with CCD losses in conjunction with nosema infection. The study received a lot of attention, with headlines again declaring the case closed, but in fact it only reinforced the notion that there is more than one pathogen affecting the nation’s bees—and that we don’t know why that is the case.
Most scientists working on unraveling the CCD mystery have concluded that no single factor can be blamed for the malady. Instead, a combination of factors is probably responsible—some sort of interaction between pathogens and variables such as nutrition, weather, varroa mites, pesticides, and the modern insults of long-distance beekeeping. “I still go back to the death-by-a-thousand-paper-cuts theory,” says Miller. “That it’s some combination of stress, accumulated pathogens, chemical materials, overstimulation, near starvation—an accumulation of what we do.” Hives are stressed, and stressed hives appear to be susceptible to all variety of insults. This is not, of course, rocket science; Lorenzo Langstroth’s tenth axiom of beekeeping said as much back in the 1850s: “The essence of all profitable beekeeping is contained in [nineteenth-century beekeeping sage Johann Nepomuk] Oettl’s Golden Rule: KEEP YOUR STOCKS STRONG. If you cannot succeed in doing this, the more money you invest in bees, the heavier will be your losses.” But beekeepers aren’t sure anymore how to follow even the simplest rules of beekeeping. In the five years since CCD first was given a name, the only thing that is obvious, says vanEngelsdorp, is that “bees dying from CCD are just sicker than the ones that aren’t dying.”
SICK BEES DO PROVIDE SOME BENEFITS. SICK BEES ELEVATE pollination prices for healthy bees. Sick bees—especially those that die by baffling means and in large numbers—pique the interest of the media and thus recruit new converts to the cause of the honey bee: city people and environmental people and foodie people who never thought much about bees. Now they do; they read about bees and worry about them and plant flower gardens and buy local honeys and put hives on their roofs. Beekeepers, after years of losing bee-yard locations to sprawl, are now suddenly receiving phone calls from strangers offering prime locations to help the bees.
Sick bees get folks like John Miller lots of airtime: “Attention is easy; recognition is difficult,” Miller
once told me. “I gravitated towards attention.” The recent carnage has garnered Miller and his colleagues a lot of it. In February 2007, when the CCD story first broke, Dave Hackenberg woke up one morning to a phone call from his son, telling him he was on the front page of the Philadelphia Inquirer. “Over the next two days,” says Hackenberg, “a friend of mine tells me that I was in four hundred and eighty-something newspapers around the world.” He tore through more than five thousand airtime minutes on his cell phone in that first month. He wore out his phone in three months. After receiving an enormous bill, he called up his provider. “I told them what my story was, and the guy said, ‘Oh yeah, I read about you,’ ” and gave Hackenberg unlimited minutes. Sometimes it’s hard to be a media darling. Hackenberg estimates he spends 20 to 25 percent of his time in his role as the face of the CCD-stricken beekeeper, time that he’s not spending figuring out how to keep his beekeeping business—which has suffered crippling losses four years in a row—afloat. “I didn’t ask to be the guy that discovered anything,” he says.
But the attention to beekeepers has also wrought some long-overdue recognition—of the hard work required to keep bees alive these days; of the superhuman sacrifices required to make their living; of the quixotic delight beekeepers take in pursuing a difficult professional path. Perhaps that’s why I was drawn to Miller. Though I had long been exceedingly fond of honey, I had no particular affection for bees. Beekeepers, though, are a different story. They are heroic characters, tragic characters, anomalous characters. They do the hard thing. I could appreciate that. I had alit on a profession that’s even less commonsensical, even more economically obtuse, even lonelier than being a writer. Beekeepers deserve a little recognition for that.
The Beekeeper's Lament: How One Man and Half a Billion Honey Bees Help Feed America Page 15