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Prostate cancer is increasingly looking like an infectious disease, a new study shows, and may be sexually transmitted


 

The-Scientist.com, September 8, 2009, by Tabitha M. Powledge  —  Mounting evidence suggests that prostate cancer is an infectious disease caused by a recently identified virus. The latest report, published today (September 7) in the Proceedings of the National Academy of Sciences, found the virus was associated especially with aggressive prostate cancers and noted that “all individuals may be at risk” for infection.

The notion that prostate cancer is an infectious disease like cervical cancer would not surprise most cancer experts, said Ila Singh of the University of Utah, the study’s senior author. Almost 20% of visceral cancers are now proven infectious diseases, and there is a lot of indirect evidence from epidemiology and genetics that prostate cancer may be one of them.

The suspect is xenotropic murine leukemia-related virus (XMRV), a gammaretrovirus similar to viruses known to cause cancer in animals. Researchers at Columbia University and the University of Utah found the virus in more than a quarter of some 300 prostate cancer tissue samples, especially in malignant cells. That prostate cancer is a viral disease is not yet proven, but this is the third independent confirmation that XMRV infects prostate tissue.

Singh pointed out that clinicians badly need better tools for distinguishing between prostate cancers that are potentially deadly and those that develop so slowly that the affected men die of something else. “We have no idea if this virus is such a marker but it clearly needs to be investigated further,” she said.

Research has long hinted that prostate cancer, also like cervical cancer, is a sexually transmitted disease. Eric Klein and colleagues at the Cleveland Clinic in Ohio reported in July that both human semen and one of its major components, acid phosphatase, increase XMRV infectivity for prostate cells 100-fold. They also found the virus in prostatic secretions of men with prostate cancer. “That really strongly suggests that XMRV is sexually transmitted,” he said. Klein was part of a group in Cleveland and the University of California, San Francisco, that in 2006 first identified XMRV in prostate tumors. He was not involved in today’s paper.

Klein said the July findings suggested a biological mechanism for sexually transmitted XMRV infection. If a man with viral particles in his lower genital tract has intercourse and deposits semen in his partner, acid phosphatase in the semen could increase the virus’s ability to infect prostate tissue of the partner’s subsequent partners.

Singh cautioned, “We can’t really say that it’s an STD at this point.” Her lab is looking for XMRV in semen and also in women’s cervical samples.

Many steps lie ahead for demonstrating conclusively that an infectious agent, in particular XMRV, causes prostate cancer. One approach is to inject lab animals with the virus and follow the results. Researchers have been trying to develop an animal model, but XMRV, although derived from a mouse virus, has since acquired an envelope that prevents it from infecting most strains of lab rodents, according to Singh. Klein’s colleagues are working on a monkey model.

Klein and his colleagues showed last year that XMRV integrates into host DNA. So another proof would be to demonstrate that XMRV inserts near a gene that promotes cell growth. “That would be very convincing proof for most people that the retrovirus is involved in causing cancer,” said Singh. Her group is working on that possibility with Frederic Bushman, a microbiologist at the University of Pennsylvania.

Establishing an infectious cause for prostate cancer would offer men something they have never had before: potential ways of preventing this common deadly disease. The new paper emphasizes how establishing a viral cause for prostate cancer could affect biomedical research. It would trigger epidemiological studies, vaccine development, and studies on interference with viral replication and antiviral therapies.

Klein noted that the US National Cancer Institute is now encouraging collaboration on XMRV studies among far-flung research groups. Prostate cancer strikes 1 in 6 US men and is second only to skin cancer in causing their deaths from cancer.

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KevinMD.com  —  It started as a small perianal abscess. She didn’t seek medical attention, hoping it would just go away. The swelling increased, the pain worsened. She started getting dizzy and nauseous and lightheaded and one night passed out after going for dinner with her family. When I saw her in the ER she was frankly septic and in extremis. Antibiotics and fluids were commenced. I rushed her to the OR.

Fournier’s gangrene is a devastating condition. The only hope for cure is rapid, definitive surgical debridement. The CT above suggests the degree of gas gangrene extension in the gluteal and peri-rectal soft tissue spaces. There’s nothing fancy about this surgery. You cut and debride until all the necrotic fat and skin and muscle is gone. It leaves a horrible wound. Sometimes you have to divert stool with a colostomy to facilitate clean wound care post-operatively.

Here’s the thing. When I was called, I was told I had a patient “to see in the morning” regarding a perianal abscess. I thought, OK. But then I checked the computer at home and saw her WBC count was over 35K. Routine perianal abscesses don’t give you white counts that high. So I had them run her through the scanner as I was driving in. The key thing with any necrotizing soft tissue infection (NSTI) is getting the patient to the OR ASAP. And you have to be able to identify those patients who are at high risk for NSTI. Here’s some key indicators to assess:

1) Extreme leukocytosis (anything over 20K ought to make you nervous)
2) Hyponatremia (Sodium levels less than 135 strangely enough are almost universally seen with NSTI’s. My patient presented with a sodium of 123)
3) Hypotension (well duh, sepsis)
4) Appearance of skin (look for bullae, purplish discoloration, desquamation of skin, etc)
5) Crepitus on exam (anaerobic bacterial production of gas in the subcutaneous tissues)
6) Extreme pain, seemingly out of proportion

When Patient Handoffs Go Terribly Wrong

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The New York Times, September 4, 2009, by Pauline W. Chen MD  —  I have always felt uneasy about patient handoffs, transferring my responsibility as a doctor to another physician. We cannot be on duty all the time, but I worry that I am playing some real-life medical version of the children’s game “Telephone” where the complexity of my patient’s care will be watered down, misinterpreted and possibly mangled with each re-telling. I wonder, too, if it is only a matter of time before the kind of mistake that happened to Joey (not his real name) might happen to one of my patients.

Two-year-old Joey had been healthy since birth. But a few weeks before I met him, his mother noticed that the left side of his face had started to swell. By the time he appeared in clinic, it looked as if a ping pong ball had been permanently lodged in his cheek.

Despite the senior surgeon’s years of experience, removing the mass from Joey’s cheek proved to be a challenge. It had insinuated itself into every possible crevice; and the nerve that innervated the muscles of his mouth and cheek – the nerve of facial expression – was embedded deep within.

The senior surgeon spent hours daintily picking away at the mass, sorting through strands of fibrous connective tissue, many of them neuronal doppelgangers, in order not to injure the buried nerve. After being nibbled at with surgical instruments for hours, the toddler’s flayed cheek looked more like a puppy’s well-worn chew toy than any recognizable set of anatomical structures. When the surgeon had at last cleaned the strand he believed was the nerve, he looped a slender yellow rubber tie around it. Then, without warning, the surgeon put down his instruments and looked up at the clock. He barked at the nurse to call for one of his colleagues, then stepped away from the table and ripped off his surgical mask and gown. “You take over,” he said when his colleague came into the room. “It’s mostly out, but I need to leave.” None of us knew if he had to attend to another urgent patient matter in the hospital or how long he might be gone.

The covering surgeon stepped up to the table, poked his finger around the remnants of the mass, then pulled on the rubber tie and the presumptive nerve. “What’s this?” he asked, reaching for a pair of scissors.

Without waiting for a response, he snipped the strand in two.

That night, I hovered outside of Joey’s room, waiting for him to wake up, laugh, cry or simply move his mouth. But it wasn’t until two days later, after we had removed all the gauze covering his incision, that I saw what I had feared I would. Joey grinned, but his left cheek remained frozen. His once symmetrical smile had been transformed into a contorted grimace.

Years later I am still haunted by the memory of Joey and that handoff which went terribly wrong. I don’t know what caused the first surgeon to suddenly leave. And because the operation was so difficult and the field of view so small, I’m not sure if the nerve might have been damaged or transected even before the second surgeon stepped in. But I do know that the surgeons never communicated clearly about what had been done when they traded places at the table. And I also know that transitions between physicians are now, more than ever, a routine and frequent part of health care.

Like many others among my professional peers, I find myself signing out and my patients being handed off more than I ever thought would happen. While older patients with multiple chronic conditions will see up to 16 doctors a year, some of the healthiest younger patients I see count not only a primary care physician among their doctors but also a handful of specialists. Hospitalized patients, no longer cared for by their primary care doctors but by teams of fully trained doctors, or hospitalists, in addition to groups of doctors-in-training, are passed between doctors an average of 15 times during a single five-day hospitalization. And young doctors, with increasing time pressures from work hours reforms, will sign over as many as 300 patients in a single month during their first year of training.

While these changes have led to improvements in certain aspects of quality of care and better rested physicians, it has also resulted in frank fragmentation. It’s hardly surprising, then, that according to two recent studies, the vast majority of hospitalized patients are unable to name their doctor, and an equally large percentage of their discharge summaries have no mention of tests and studies that are pending.

Over the last decade, medical researchers and educators turned their attention increasingly to this issue. I spoke recently to Dr. Vineet M. Arora, an assistant professor of medicine at the University of Chicago, who studies patient handoffs and the ways in which they might be improved.

Handoffs are supposed to mitigate any issues that arise when doctors pass the responsibility for patient care to a colleague. “But that requires investing time and effort,” Dr. Arora said, “and using handoffs as an opportunity to come together to see how patient care can be made safer.”

Most of the time, however, handoffs are fraught with misunderstanding and miscommunication. Physicians who are signing out may inadvertently omit information, such as the rationale for a certain antibiotic or a key piece of the patient’s surgical history. And doctors who are receiving the information may not assume the same level of responsibility for the care of that patient. “Handoffs are a two-way process,” Dr. Arora observed. “It’s a complex interplay.” Missed opportunities to impart important patient information result in more uncertainty for the incoming doctor. That uncertainty leads to indecision which can ultimately result in significant delays during critical medical decisions.

More recently, Dr. Arora pointed out, researchers have begun looking for new ways to approach patient handoffs, studying other high-stakes shift-oriented industries like aviation, transportation and nuclear power, as well as other groups of clinicians.

“We can borrow from the models of other health care practitioners,” Dr. Arora said. Nurses, for example, have long placed great importance on the process of handing off patients. “It’s pretty difficult to find and interrupt a nurse during shift change because they have made it a high priority,” Dr. Arora remarked. “There’s a dedicated time, a dedicated room, a culture that has developed around it. In contrast, physicians have historically emphasized continuity much more than handoffs. As a result, doctors’ signouts happen quickly, last-minute and on the fly.”

By incorporating more efficient methods of communication, the hope is that patient care transitions will eventually become seamless and less subject to errors. But even more important than teaching and learning those methods, Dr. Arora says, will be transforming physician attitudes.

“It’s critical that we invest the time and that our payment system eventually reflects how important that time is,” Dr. Arora said. “But we also need to change our profession’s thinking so that handoffs are a priority and not an afterthought. We need to be able to say that the ability to transition care well is an important metric by which you will be judged to be a good doctor.

“Good handoffs are about best practices, about being a good doctor. Investing time in them is the right thing to do.”

Saving Bees: What We Know Now

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Phil Hawkins/Bloomberg News Newly hatched honeybees in an almond orchard in Wasco, Calif.

| Rowen Jacobsen, author of “Fruitless Fall: The Collapse of the Honey Bee and the Coming Agricultural Crisis,” discusses how honeybee health is linked to the health of the entire environment.


Resources

The first alarms about the sudden widespread disappearance of honeybees came in late 2006, and the phenomenon soon had a name: colony collapse disorder. In the two years that followed, about one-third of bee colonies vanished, while researchers toiled to figure out what was causing the collapse. A study published last week in the Proceedings of the National Academy of Sciences surmises that there may not be a single pathogen involved but a collection of culprits. What have entomologists and beekeepers learned in the last few years of dealing with the crisis? We asked May R. Berenbaum, an author of the study, and other experts for an update.


Getting Off the Crisis Treadmill

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Rowan Jacobsen is author of “Fruitless Fall: The Collapse of the Honey Bee and the Coming Agricultural Crisis.”

Thanks to the terrific gene sleuthing of May Berenbaum and others, it looks like the pieces of the colony collapse disorder puzzle are starting to fit together. And we can stop arguing about who was right: The virus camp, the fungus camp, the pesticide camp, the varroa mite camp, or the nutrition camp. It turns out everybody was right. (Well, everybody except the cell-phone and microwave-tower camps.)

Colony collapse disorder and swine flu are manifestations of the same underlying issue: the global diaspora of organisms.

The viruses compromise bees’ ability to manufacture proteins, and proteins are the tools bees use to fight off pathogens, to detoxify pesticides, to repair their cells, and to meet all the world’s other challenges. If bees lived in an utterly non-stressful world, they could go on despite the viruses. But of course they don’t live in a world anything like that.

Even if we have at last identified the root cause of colony collapse disorder, it shouldn’t give us any comfort. Just as knowing the source of “swine” flu doesn’t help us cure it, identifying CCD will not make it go away.

In fact, both diseases can be seen as manifestations of the same underlying issue: The global diaspora of organisms. Honeybees are just one of the many species we depend on that are struggling mightily to withstand a steady stream of novel parasites and pathogens they have never encountered before, and have no tools to defend against. As the honeybee geneticist Tom Rinderer put it, “What has happened to our bees? Jet planes have happened.” Even if we miraculously come up with solutions for varroa mites, IAPV and the latest threats to honeybees, there will simply be another “black swan” that nobody could have predicted.

Read more…

If anything, this latest news about CCD makes the problem more relevant to the future, because it confirms what every holistic systems thinker has been telling us. Honeybee health is inextricably linked to the health of the entire environment, including our own. If we can create systems of domestic food production that take their cues from the cycles of nature, and let honeybees play the roles they evolved to play, then the system will take care of itself. But if we continue to push the system farther and farther out of equilibrium by relying on chemical shortcuts and fossil fuel intervention to fix the inevitable breakdowns, then we will never get off the crisis treadmill.


Profound Changes

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Kim Flottum is the editor of Bee Culture magazine and the author of “The Backyard Beekeeper” and “The Backyard Beekeeper’s Honey Handbook.”

Pesticides, bacterial diseases and varroa mites have been implicated in the search for the causes of colony collapse disorder. Plus, viruses in conjunction with environmental stresses are suspects, and University of Illinois scientists have discovered what occurs at the genetic level of CCD. I suspect it is only a matter of time before the pathogens are known.

Meanwhile, individual beekeeping operations have been damaged, some beyond repair because of this malady. Others have been able to recover. The overall picture is, however, not quite as bleak as the press and the blogosphere might lead you to imagine. Colony numbers in the U.S. show the resiliency of American beekeepers.

But beekeepers know that changes are necessary. The changes involve effective and efficient management of varroa mite populations. A beekeeper’s obvious first choice is to manage honeybee lines that are resistant to or tolerant of these mites. But there is a very limited quantity of these bees, and they are expensive. Or beekeepers can choose a line of bees that tolerates mites to a great degree, but differ in behavior from the bees they are familiar with. Russian bees are resistant to the mites, but their seasonal timetable is much different from that of the bees most U.S. beekeepers are used to.

Read more…

In particular, Russian bees require extra work in late fall and early winter to accommodate the mid-winter almond crop in California. Almonds bloom in February and March, much earlier than any other major pollination crop. More than half of the bees in the U.S. are used to pollinate almond orchards, and many, if not most, migratory beekeepers depend on the crop for pollination income. The migratory beekeeping industry goes as the almond crop goes, and the crop is suffering from water shortages, price fluctuations – and beekeeper availability due to CCD and other forces.

The only alternatives to the use of resistant honeybees are chemical miticides that effectively and efficiently control varroa mites while they are in the hive. Newer products using essential oils are safe, effective but labor-intensive, while traditional choices require less labor but are less effective.

Reducing the insidious use of pesticides on everything honeybees eat has been a priority.

But for the longer term commercial beekeepers have concluded that if they are going to succeed in the migratory pollination business, they need to change and attend to the discoveries made in the search for clues to colony collapse disorder.

High on beekeepers’ lists, besides controlling Nosema ceranae, is reducing the insidious pesticide barrage applied to everything honeybees eat, and insuring that bees’ nutritional needs are met by feeding them better food more often. These management changes have been rapidly accepted and have lead to profound improvements in honeybee health.

The benefits? The pesticide abuse debacle in this country may have finally come to a head, and discussions among beekeepers, the Environmental Protection Agency and agricultural pesticide companies have begun (but is the new E.P.A. better than the last, and are chemical companies on the level?). Plus, honeybee health has gained more attention and made more progress in the last two years than the last three decades. Better resistant bees are next in line.

But most important? Awareness of the value of the beekeeping industry in the production of the food we need is better understood now than perhaps ever before.


Bias Against a Non-Native Species

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Joe Traynor is a bee broker for apiarists and almond growers. His company, Scientific Ag, is based in Bakersfield, Calif.

The current consensus is that bee problems are caused by multiple stressors. Bees, like us, carry viruses and harmful microbes all the time. When we (and they) get run down, these nasties can take over, making us sick. Colony collapse disorder peaked during 2007, which was also a year, due to drought conditions in many areas of the U.S., that good bee forage was in short supply; as a result, honeybees suffered nutritionally, making them more susceptible to viruses (carried and transmitted by varroa mites) and to a new (to the U.S.) fungus, nosema ceranae, believed to have been introduced here in 2007.

Possible culprits: developers, second-home buyers, corn producers – and conservation purists.

Bee forage was more plentiful during 2008 and as a result there were less incidences of CCD (we won’t know for a while how 2009 will turn out). Beekeepers that have kept their bees in top shape nutritionally have had lower than normal problems with colony collapse disorder.

There is no question that annual bee losses are far greater today than they were 20 years ago. Twenty years ago, before virus transmitting varroa mites were found in the U.S., 10 percent winter losses were normal; now 20 percent losses are normal and losses hit 36 percent in 2007 (around 30 percent in 2008). Beekeepers have to work much harder to keep their bees in good health than they did 20 years ago. This means paying close attention to nutrition, via supplemental feeding of both proteins and carbohydrates, and controlling both varroa mites and nosema (easier said than done as there are limited means of controlling these two pests).

Read more…

Natural bee forage, including some agricultural crops, is better for bees than artificial supplements. Bees, like us, require a varied diet to remain in top health. The ethanol boom has caused corn, a poor pollen source for bees, to replace clover and alfalfa, relatively good bee plants, in some parts of the U.S.

Increased urbanization, especially here in California, has resulted in the loss of excellent bee pasture. When baby boomers build a second home in the foothills of California (or in Montana) they don’t want any bees near their homes, so the first thing they do is evict beekeepers from long-held locations.

Nature Conservancy removes honeybees from its land because they originally came from Europe.

Counterintuitively, the Nature Conservancy has also contributed to bee problems. The group purchases large tracts of undeveloped land for the laudable purpose of preserving these tracts in their native state for future generations. Unfortunately it has a policy of evicting all non-native species from the property it acquires. This includes honeybees since they are an introduced species, brought over from Europe by early settlers.

The conservancy recently took over a large tract of land in San Diego County that provided sustenance for many commercial bee colonies. The bee colonies were evicted and are now competing for ever diminishing bee pasture in the San Diego area (there are probably 100,000 commercial bee colonies competing with each other in San Diego County alone).

Evicting commercial (European) bees from Nature Conservancy holdings is shortsighted as it creates a vacuum that allows Africanized honeybees, which are prevalent in Southern California and are becoming more prevalent in other parts of the U.S., to establish themselves on the group’s property. The recent finding of fossilized honeybees in the U.S. (thousands of years old but now extinct) may cause the conservancy to change its policy, but beekeepers aren’t holding their breath on this.

The costs of keeping bees in good condition to ward off colony collapse disorder have increased dramatically over the past two years. A main reason CCD has decreased this past year is that beekeepers are spending much more time and money keeping their bees healthy.

Increased pollination fees for agricultural crops requiring honeybees are paying for these increased bee maintenance costs.


A Viral Overload

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May R. Berenbaum is a professor of entomology at the University of Illinois at Urbana-Champaign.

A few things have changed with respect to colony collapse disorder in the past year. First, whereas surveys conducted by the Apiary Inspectors of America estimated CCD losses in America’s managed honeybee colonies during the winters of 2006-2007 and 2007-2008 at 36 percent and 32 percent, over the winter of 2008-2009 losses dipped to 29 percent, possibly indicating a decline in severity.

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Secondly, an extensive survey conducted by researchers from two land grant colleges, the U.S. Department of Agriculture and two Belgian universities examined adult and larval bees and hive products from almost 100 colonies for parasites, pathogens, pesticides and nutritional factors. Although no single diagnostic difference was identified, one consistent finding was that colony collapse disorder bees were infected with multiple pathogens; over 50 percent of CCD colonies, e.g., were infected with three or more viruses, almost twice the percentage of healthy colonies.

Most recently, a whole-genome honeybee microarray analysis allowed investigators from the University of Illinois at Urbana-Champaign and the U.S.D.A. to examine differences in patterns of expression of all 10,000+ genes in the honeybee genome, the sequencing of which was completed in 2006. Multiple comparisons of hives varying geographically, temporally, and in CCD severity winnowed the list of genes whose expression was most closely associated with the disorder down to a handful representing fragments of ribosomes, the “protein factories” of the cells, thus implicating ribosome breakdown as a “root cause” of CCD.

Read more…

Genetic material from common bee pathogens also on this microarray revealed, as before, that CCD bees were infected with a greater number of viruses, specifically picornalike viruses, all of which cause infection by hijacking the ribosome, reprogramming the “factory” to make viral proteins instead of honeybee proteins. Thus, viral overload may lead to ribosome breakdown, which is manifested as CCD. Together these studies may explain why so many explanations of colony collapse disorder seem plausible; in the absence of functional ribosomes, bees would be hard-pressed to respond to any of the multiple stresses to which they are subjected in 21st century apiculture – pathogens, pesticides or nutritional deficiencies.

Detecting the ailment early might give beekeepers a chance to provide supportive care.

As for practical applications of these findings, the most immediately useful product of the microarray study is an objective genetic diagnostic indicator of colony collapse disorder – the ribosome fragments. Such a diagnostic indicator would be useful in determining whether other CCD-like disappearances in England, Spain and elsewhere are in fact colony collapse disorder or entirely different in origin.

Early diagnosis of the ailment might not be directly useful – there are no vaccines to combat bee viruses and no known ways to patch up broken ribosomes – but beekeepers who detect this breakdown early on may be able to provide supportive care to help their bees recover.


Living With a Crisis

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Marla Spivak is a professor of entomology and social insects at the University of Minnesota.

All bees – honeybees and native bees – are still in decline, and it is a serious issue. It is true there is less news coverage of bee health issues, but bees are not faring better. Over 30 percent of our honeybee colonies die every year, from colony collapse disorder or other causes. Some native bumblebee species have become nearly impossible to find, and we don’t know how many other native bees are threatened.

Beekeepers are treading water, replacing as many colonies as economically feasible for their operations. Researchers are hard at work using cutting-edge methods to determine why honeybee colonies are collapsing and how we can mitigate the decline of all bees.

While bees may have faded from the news, they have not faded from the public eye. In fact, the opposite has occurred. People are more aware than ever about bees. The crisis has helped us understand the importance of pollinators to our diet and environment and many people want to know how they can help.

What can we do to help bees? Plant lots of flowers that provide nectar and pollen for bees, and reduce pesticide use. These two tangible and relatively easy actions, when implemented by many people, can save our bees and restore health and diversity to our agricultural and urban landscapes.


Needed: More Disease-Resistant Bees

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Diana Cox-Foster is a professor of entomology at Pennsylvania State University.

In the almost three years since the plight of honeybees caught the public’s attention, we have learned that bees are faced with many different obstacles, some naturally occurring (such as diseases) and others that are byproducts of human activity.

The honeybees in the U.S. have been in trouble since the introduction of parasitic mites (Varroa and tracheal mites) in the late 1980’s. Varroa has continued to be the major problem, in part because the mites have become resistant to the acaricides used for control.

Our study of hundreds of pollen samples showed on average six different pesticides. Do chemicals impair bees’ immune systems?

Colony collapse disorder has severely affected many beekeepers in the United States and caused some to go bankrupt. We have learned much about CCD, but we are still a long way from determining its exact causes and how to mitigate this disease. Of major worry is that these same causes may be affecting native insect pollinators. This translates into concerns not only for security of our food crop production but also for the overall health of the ecosystems that we depend upon for survival.

Data indicate that colony collapse disorder here in the U.S. has a common set of symptoms that differ from colony losses associated with late-summer or over-winter death. CCD colonies have elevated levels of at least one of three closely related viruses: Israeli Acute Paralysis Virus, Kashmir Bee Virus or Acute Bee Paralysis Virus. The microsporidian parasite Nosema ceranae by itself does not appear to be a major cause of hive mortality in the U.S.

Studies at Penn State indicate that Israeli Acute Paralysis Virus can cause some of the symptoms of CCD. However, we think that stress is an added major component and that other microbes and parasites present in the bees play a role. Stresses such as sub-lethal pesticide exposure and lack of adequate nutritional sources (pollen and nectar) may be affecting the bees. In hundreds of samples of incoming pollen, a team at Penn State and the U.S.D.A. has found that over 99 percent have at least one pesticide contaminant, on average six different pesticides, and up to 35 different pesticides in a single sample. Over 100 different pesticides have been identified.

Bees need more flower or pollen sources nationwide.

What impact do these chemicals have on bee health via impairment of bee’s immune system to fight off diseases like viruses, through impact on bee behavior, or by decreasing colony build-up and reproduction? We have preliminary data to suggest that all of these aspects are part of the problem, but we do not know to what extent or exactly how, preventing mitigation of this stress.

New approaches are needed to mitigate the problems in pollinator health. It is clear that our recent recommendations to the beekeepers are having a positive effect: sterilize the equipment from collapsed colonies using gamma irradiation, use soft chemicals to control Varroa mites and Nosema, and feed artificial pollen when needed. Prior to CCD, these measures would not have significantly affected overall colony survival. However, these are temporary Band-Aids; these methods are costly and do not eliminate the underlying causes.

Beekeeping operations need sustainable solutions to stay in business and provide essential pollination services. Needed are new strains of bees with more resistance to diseases and parasites. The impact of pesticides needs to be lessened. Lastly, bees need more flower or pollen/nectar sources nationwide. In summary, we are a long way from “solving” the pollinator crisis.