Scientists Discover What’s Killing The Bees And It’s Worse Than You Thought

The mysterious mass die-off of honey bees that pollinate $30 billion worth of crops in the US has so decimated America’s apis mellifera population that one bad winter could leave fields fallow.

Now, a new study has pinpointed some of the probable causes of bee deaths and the rather scary results show that averting beemageddon will be much more difficult than previously thought.

Scientists had struggled to find the trigger for so-called Colony Collapse Disorder (CCD) that has wiped out an estimated 10 million beehives, worth $2 billion, over the past six years.

Suspects have included pesticides, disease-bearing parasites and poor nutrition. But in a first-of-its-kind study published today in the journal PLOS ONE, scientists at the University of Maryland and the US Department of Agriculture have indentified a witch’s brew of pesticides and fungicides contaminating pollen that bees collect to feed their hives.

The findings break new ground on why large numbers of bees are dying though they do not identify the specific cause of CCD, where an entire beehive dies at once.

When researchers collected pollen from hives on the east coast pollinating cranberry, watermelon and other crops and fed it to healthy bees, those bees showed a significant decline in their ability to resist infection by a parasite called Nosema ceranae.

The parasite has been implicated in Colony Collapse Disorder though scientists took pains to point out that their findings do not directly link the pesticides to CCD. The pollen was contaminated on average with nine different pesticides and fungicides though scientists discovered 21 agricultural chemicals in one sample.

Scientists identified eight ag chemicals associated with increased risk of infection by the parasite.

Most disturbing, bees that ate pollen contaminated with fungicides were three times as likely to be infected by the parasite. Widely used, fungicides had been thought to be harmless for bees as they’re designed to kill fungus, not insects, on crops like apples.

“There’s growing evidence that fungicides may be affecting the bees on their own and I think what it highlights is a need to reassess how we label these agricultural chemicals,” Dennis vanEngelsdorp, the study’s lead author, told Quartz.

Labels on pesticides warn farmers not to spray when pollinating bees are in the vicinity but such precautions have not applied to fungicides.

Bee populations are so low in the US that it now takes 60% of the country’s surviving colonies just to pollinate one California crop, almonds. And that’s not just a west coast problem—California supplies 80% of the world’s almonds, a market worth $4 billion.

In recent years, a class of chemicals called neonicotinoids has been linked to bee deaths and in April regulators banned the use of the pesticide for two years in Europe where bee populations have also plummeted. But vanEngelsdorp, an assistant research scientist at the University of Maryland, says the new study shows that the interaction of multiple pesticides is affecting bee health.

“The pesticide issue in itself is much more complex than we have led to be believe,” he says.

“It’s a lot more complicated than just one product, which means of course the solution does not lie in just banning one class of product.”

The study found another complication in efforts to save the bees: US honey bees, which are descendants of European bees, do not bring home pollen from native North American crops but collect bee chow from nearby weeds and wildflowers.

That pollen, however, was also contaminated with pesticides even though those plants were not the target of spraying.

“It’s not clear whether the pesticides are drifting over to those plants but we need take a new look at agricultural spraying practices,” says vanEngelsdorp.

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Further Reading:

http://www.thepost.on.ca/2013/06/19/bees-dying-by-the-millions

Evolution on the inside track: Study shows how viruses in gut bacteria change over time

Humans are far more than merely the sum total of all the cells that form the organs and tissues. The digestive tract is also home to a vast colony of bacteria of all varieties, as well as the myriad viruses that prey upon them. Because the types of bacteria carried inside the body vary from person to person, so does this viral population, known as the virome.

By closely following and analyzing the virome of one individual over two-and-a-half years, researchers from the Perelman School of Medicine at the University of Pennsylvania, led by professor of Microbiology Frederic D. Bushman, Ph.D., have uncovered some important new insights on how a viral population can change and evolve – and why the virome of one person can vary so greatly from that of another. The evolution and variety of the virome can affect susceptibility and resistance to disease among individuals, along with variable effectiveness of drugs.

Their work was published in the Proceedings of the National Academy of Sciences.

Most of the virome consists of bacteriophages, viruses that infect  rather than directly attacking their human hosts. However, the changes that bacteriophages wreak upon bacteria can also ultimately affect humans.

“Bacterial viruses are predators on bacteria, so they mold their populations,” says Bushman. “Bacterial viruses also transport genes for toxins,  that modify the phenotype of their bacterial host.” In this way, an innocent, benign bacterium living inside the body can be transformed by an invading virus into a dangerous threat.

At 16 time points over 884 days, Bushman and his team collected stool samples from a healthy male subject and extracted  using several methods. They then isolated and analyzed DNA contigs (contiguous sequences) using ultra-deep  .

“We assembled raw sequence data to yield complete and partial genomes and analyzed how they changed over two and a half years,” Bushman explains. The result was the longest, most extensive picture of the workings of the human virome yet obtained.

The researchers found that while approximately 80 percent of the viral types identified remained mostly unchanged over the course of the study, certain viral species changed so substantially over time that, as Bushman notes, “You could say we observed speciation events.”

This was particularly true in the Microviridae group, which are bacteriophages with single-stranded circular DNA genomes. Several genetic mechanisms drove the changes, including substitution of base chemicals; diversity-generating retroelements, in which reverse transcriptase enzymes introduce mutations into the genome; and CRISPRs (Clustered Regularly Interspaced Short Palindromic Repeats), in which pieces of the DNA sequences of bacteriophages are incorporated as spacers in the genomes of bacteria.

Such rapid evolution of the virome was perhaps the most surprising finding for the research team. Bushman notes that “different people have quite different bacteria in their guts, so the viral predators on those bacteria are also different. However, another reason people are so different from each other in terms of their virome, emphasized in this paper, is that some of the viruses, once inside a person, are changing really fast. So some of the viral community diversifies and becomes unique within each individual.”

Since humans acquire the bacterial population—and its accompanying virome—after birth from food and other environmental factors, it’s logical that the microbial population living within each of us would differ from person to person. But this work, say the researchers, demonstrates that another major explanatory factor is the constant evolution of the virome within the body. That fact has important implications for the ways in which susceptibility and resistance to disease can differ among individuals, as well as the effectiveness of various drugs and other treatments.