Four years ago, my father became a beekeeper. A year into his hobby, one of his three hives died. It was sudden and, at first, mysterious. The thing that struck me then — and that has stayed with me since — was just how little I knew about these animals my father was keeping, and that he keeps still. The cause of the hive’s collapse wasn’t a virus or invasive parasite; nothing so exotic. Just a case of bad-luck biology: One of the hives split, and the new colony came with a dud queen. Maybe she didn’t mate with any drones, maybe the drones were infertile, or maybe it was all the queen’s fault. Whatever it was, she wasn’t laying eggs. Dad’s friend Paul, a fellow beekeeper and a man who knows bees better than most, said that a childless hive is called alaying worker. And so everything fell apart.

Much can go wrong in a hive. A worker bee’s existence is carefully measured: It’s an egg for about three days, a larva for six, a pupa for two or three, and then, for three weeks, an active bee — a she, always, and the bee we see outside of the hive. Older bees care for eggs and larvae and pupae and train younger bees, even as they leave the hive. The cycle is so precise, predetermined, and vital that to lose a few days from a bee’s life throws a wrench in the whole system. Even a minor ailment that takes days off a bee’s life can lead to a colony collapsing. To remain healthy, a hive must constantly stave off invasion from other insects as well as from bacteria and viruses and bigger beasts—bears, for example, or (far worse than bears) us.

Bees are dying. In the U.S., ten million hives have died in the last six years. In 2006, the thing that was and still is killing the bees was given a name: colony collapse disorder (CCD). A break from the normal, a confused state, a systemic disruption: disorder. It’s a very specific word, specific enough so that when you’re talking to scientists who study CCD and you misspeak, they correct you. “Don’t call it a disease,” Michelle Flenniken, a microbiologist at Montana State University, tells me when I call her. “It’s a disorder.”

At about the same time my father started keeping bees, Flenniken began researching and cataloging bee pathogens. She is working to identify all of the viruses that afflict bees, because “before you know what causes the disorder, you need to know what’s out there, and we don’t. Not yet.”

Flenniken plucks bees from healthy hives to find out what molecules and bits of genetic material they carry. Before she got into honeybees, Flenniken studied the human microbiome, all the tiny life forms living on and inside us. We know astonishingly little about these organisms. For every ten bacteria that live in and on us, there’s just one human cell (though our cells are much bigger — the collected bacteria wouldn’t be bigger or heavier than a soup can). The belly button contains about 1,400 different strains of bacteria, nearly half of which were unknown until a few years ago. The skin is an ecosystem; our bodies are full of ecosystems. If we knew how all the ecosystems worked, and what they looked like under healthy circumstances, then we could begin to better diagnose, and perhaps cure, persistent conditions. For example, severe eczema is beginning to be better understood, and treated, by studying the microbiomes on our skin.

We’re bigger than bees and more complicated, which is good news because, as early as it is in the study of the human microbiome, it’s even earlier in the research of that of bees. Just this year, a team at Yale published a paper on the “specific gut microbiota of the honey bee,” in which they suggest that the stomachs of social bees would be “an ideal model for studying functional, structural, and evolutionary aspects of host-associated microbial communities: many characteristics resemble the gut microbiota of humans…” The bee stomach isn’t as complex as ours. It can be sequenced and studied and, soon, known. By better knowing bees, we might better know ourselves.


Flenniken uses a microarray to look at bees’ microbiomes. The array is essentially a chip that contains thousands of very tiny receptacles for capturing genetic material. In this case, Flenniken’s samples undergo “ultra deep sequencing,” which leaves her with RNA to stare at. She can now search for “exogenous infectious agents” — viruses that came from outside the hive. Her microarray is unique. It was developed specifically for bees by Joseph DeRisi, who runs a lab at the University of California, San Francisco, where he hunts for the genetic causes of persistent human illnesses. He’s studied avian flu and SARS, but his most important work is in malaria. By studying the malaria parasite’s genes, DeRisi identified a weak spot, which drugs or vaccines might exploit.

Two years ago, Flenniken and a team of scientists discovered the RNA of four previously unknown exogenous infectious agents. One, the Lake Sinai virus strain 2 (so called because it was found near Lake Sinai, South Dakota), is linked to chronic bee paralysis. Might it be linked to CCD? “We don’t know,” Flenniken says.

Do honeybees have a flu season? Do they get colds? We don’t know these things, either. We don’t even know, really, what it looks like in a healthy hive to have something bad come in that doesn’t destroy the hive. To understand colony collapse it is crucial that we first know more about healthy bees, then look again at unhealthy bees. “The problem,” Flenniken says, “is catching a colony before it collapses.” It’s a catch-22: To run a good study, she’d need half healthy hives (the control) and half hives doomed to fail. But of course it’s impossible to know a hive will fail, because she doesn’t yet know what’s causing the failure. So all she can do is gather and test samples, which takes time and requires money.

Today Flenniken is “examining the sublethal effects of pesticides” on bees. She’s looking to see “if viruses are a biomarker,” she explains, then translates: “If you are stressed because it’s finals week, a virus might give you a cold. We’re doing something like that in the lab, giving doses of virus that shouldn’t kill the bee outright, and studying the immune response to see if that’s a quantitative measure of the stress of the bee.”

Bee stress is a big deal right now, because so much of a bee’s stress today is our fault. We keep bees, work them, and truck them all the way across the country to pollinate our crops, which carry chemicals. The chemicals ride back into the hive on the backs of the bees and imbalance the order of the hive in a large variety of ways, leading to the possibility of a collapse. Then we feed them on corn syrup.

The corn syrup was what, in a roundabout way, had led me to Flenniken. On April 29, a team of entomologists at the University of Illinois published a paper that suggested a link between honeybees’ corn-syrup intake and their hives’ colony collapse. It isn’t that corn syrup is toxic to bees. In fact, it was more about what wasn’t in the corn syrup — an acid that is essential to immunity and detoxification and found mostly in pollen grains. You know what’s steeped in pollen grain? Honey. Give the bees more honey.

Flenniken’s work is similar to that of the researchers at the University of Illinois behind the corn-syrup paper. By knowing a healthy bee from a stressed bee, a dying bee, or a bee in recovery, she might learn the markers that predict CCD. A disorder isn’t cured by finding a smoking gun. This is slow work. But there is hope.

Beekeepers have the most to lose in this fight to save bees and are going to great lengths to better care for their charge. I was introduced to DeRisi and Flenniken through a beekeeper named Dan Cummings. Cummings is an almond farmer, mainly, but you can’t have almonds without honeybees, so he got into keeping. For six years Cummings was the chairman of Project Apis M., a consortium of concerned keepers that raises money to fund honeybee research. He’s a fierce advocate for providing bees with natural-forage opportunity, which means planting more native plants, rotating crops — giving bees a balanced diet, basically.

Four years ago I knew very little about these animals. Today I’m struck still by how great a mystery they remain and how, the more we find out about what ails them, the more it seems to be what ails us.