At the JS West egg farm, south of Modesto, Calif., one chicken house has the new, spacious cages that egg producers and animal welfare advocates say keep chickens happier.
At the JS West egg farm, south of Modesto, Calif., one chicken house has the new, spacious cages that egg producers and animal welfare advocates say keep chickens happier.

for a PENNY an EGG : ‘ENRICHED CAGES’
http://www.npr.org/blogs/thesalt/2012/01/26/145900751/ex-foes-stage-coop-detat-for-egg-laying-chickens
Farmers, Humane Society Partner On Chicken-Cage Revolution
by Dan Charles / January 26, 2012

When I first saw the press release, I figured it had to be an April Fools’ joke. The Humane Society of the United States, a voice of outrage against all heartless exploitation of animals, joining hands with the United Egg Producers, which represents an industry that keeps 200 million chickens in cages? But it’s true. This unprecedented partnership is asking Congress to pass a law (just introduced this week) that’s supposed to improve the lives of egg-laying hens. If passed, it would be the first federal law that takes into account the emotional lives of farm animals. Specifically, it would force egg producers to build new, roomier housing for hundreds of millions of birds. Some background: Ninety percent of America’s eggs are laid by chickens that live in long rows of metal wire cages. Each cage holds about eight hens, and they’re packed in pretty tightly. At the henhouse that I visited recently, owned by a family-run enterprise called JS West and Cos. in Modesto, Calif., each hen has, on average, 67 square inches — less than the area of a standard sheet of paper. John Bedell, who’s in charge of egg production at this site, says the chickens are not being mistreated. “Hear that sound?” he says. “When they’re just sort of clucking away, making that sound, that’s the sound of happy chickens.”

To be sure, the air in this building is pretty clean (especially considering that 150,000 chickens live in it), the temperature is comfortable, and the hens don’t have to worry about foxes eating them. But ever since cages became standard in the egg industry some 50 years ago, many people have been horrified by them. “These birds can’t even spread their wings,” says Paul Shapiro, a senior director at the Humane Society of the United States. “These are living, feeling, sentient animals who are caught up in the food system, and at a bare minimum, they deserve not to be tortured for their entire lives; not to be immobilized to the point where they can’t even extend their limbs.”Despite their outrage, though, advocates of animal welfare weren’t able to do much against the cages. For egg producers, the cages made economic sense. They made egg production possible on an unprecedented scale, delivering cheap eggs to consumers. But over the past few years, the situation has changed dramatically. The shift started in Europe. In 1999, the European Commission approved a directive that orders egg producers to give their chickens almost twice as much room. The directive finally took effect this year, on New Year’s Day. Major food retailers, especially in northern Europe, have gone further, and now sell only eggs from cage-free operations, where hens run around loose in barns.

Here in the U.S., California took the lead. In 2008, voters there overwhelmingly approved a proposition that the Humane Society of the U.S. drafted. “What Prop. 2 says is that laying hens must be able to stand up, lie down, turn around and fully extend their limbs. That’s it,” says Shapiro. The law takes effect in 2015. This may sound simple, but egg producers say it has created paralysis, because they have no idea what it requires. Does it mean that chickens have to be cage-free? Does it just mean bigger cages? How big is big enough? Regulators in California have provided no answers. On top of that, similar voter initiatives passed in other states. Gene Gregory, president of United Egg Producers, which represents companies that produce about 95 percent of the country’s eggs, says it looked like the industry would have to satisfy dozens of different — as well as confusing — state requirements. “It was going to be a nightmare, trying to produce eggs and have a free flow of eggs across state lines. So we reached out to the Humane Society and said, ‘Let’s have a conversation about this,’ ” says Gregory.  To the astonishment of many, the Humane Society was willing to talk. Shapiro says it was a chance to have an impact on the welfare of chickens all across the country, including in states where animal-rights activists weren’t likely to get any new regulations passed. In early July, the two sides announced that they had reached an agreement to jointly lobby Congress for new federal rules that would phase out all traditional chicken cages within 15 years. The law was formally introduced this week.

As a minimum, the chickens would have to be held in so-called enriched cages — a style developed in Europe. These cages are a compromise between efficient, large-scale production and letting chickens do some things that they seem to really like. At the JS West farm, south of Modesto, one chicken house already has these cages. I notice right away that chickens in this building have almost twice as much space as the ones I saw next door. Jill Benson, one of the company’s owners, points out other features. There are metal bars for the birds to perch on, and enclosed spaces, called nest boxes. Those spaces seem really popular among the hens. The new cages at JS West feature enclosed spaces, shown in red, called nest boxes. The spaces seem really popular among the hens. “The birds, in fact, line up to go into the nest box,” says Benson. “They like to go out of the bright light and go into a nest box to lay their eggs.” As we watch, we catch a glimpse of one chicken doing exactly that. A wet, warm egg rolls slowly out of the nest box. Perches and nest boxes are specifically required in the new proposed law.

Benson says she wants this law to pass. Building new chicken houses would cost her company millions of dollars. But she says she can live with that. It probably works out to about an extra penny per egg. But most important: She’d know exactly what to build, and the rules would be the same across the country. So if United Egg Producers, representing 95 percent of all U.S. egg production, wants this law and some of the industry’s fiercest enemies do too, who could be against it? Well, as it happens, some influential farm organizations. Beef producers, hog farmers, dairy farmers and the American Farm Bureau have all lined up against it. Bill Donald, a rancher in Melville, Mont., and president of the National Cattlemen’s Beef Association, says it would be a terrible precedent to get the government involved in keeping farm animals happy. Who knows what regulations might come next? “It isn’t a very large leap from egg production to chicken production to beef production,” he says. It’s a situation that would have been unthinkable just a year ago: Egg farmers arm in arm with the Humane Society of the United States, in a political battle with ranchers and dairymen.

The new cages at JS West feature enclosed spaces, shown in red, called nest boxes. The spaces seem really popular among the hens.

CAGE FREE
http://stoptherotteneggbill.org/site/c.8qKNJWMwFbLUG/b.7867921/k.C798/About_Us.htm
Egg Industry Bill Would Keep Hens in Cages Forever

“Opposing ballot measures is very expensive. The only way we can avoid them is through federal preemption. That is the reason why we need federal legislation.” — Gene Gregory, President, United Egg Producers

The egg industry’s trade association – the United Egg Producers (UEP) – has hatched an insidious plan: It is now pushing for federal legislation that, if enacted, would forever keep hens locked in cages, despite the wishes of the vast majority of the American public. Under the guise of “enriching” cages, the egg industry’s legislation would: Nullify existing state laws that ban or restrict battery cages. Deprive voters of the right and ability to pass ballot measures banning cages. Deny state legislatures the ability to enact laws to outlaw battery cages or otherwise regulate egg factory conditions.

To accomplish this, UEP’s federal legislation would amend what is known as the “Egg Products Inspection Act.” Specifically, the amendment (H.R. 3798) seeks to federally establish that egg factory cages would be legally accepted as a national standard that could never be challenged or changed by state law or public vote. UEP claims that its legislation would eventually result in “progress” for laying hens. Just the opposite is true. In reality, the egg industry merely agreed to slowly (at the glacial pace of 18 years) continue the meager changes in battery cage conditions that are already occurring due to state laws and public pressure. Please help make clear to our elected leaders that the egg industry’s unprecedented attack on anti-cruelty laws, states’ rights, and animal protection must not stand. Click here to read a veterinary perspective on the Rotten Egg Bill.

Responding to the Rotten Egg Bill’s (H.R. 3798) Specific Points
For political cover, UEP inserted a few diversionary provisions. None of them holds up to scrutiny.

Ammonia Levels: The Rotten Egg Bill contains nothing that alters current standards for “ammonia levels.” The bill merely duplicates UEP’s existing standards (which allow unhealthful levels of ammonia) and seeks to put that into federal law.

Forced Molting and Euthanasia: As for ending the practice of forced molting of hens by “starvation” and water deprivation – egg companies do not advocate that to begin with. Far from changing any currently accepted molting practice, the bill merely adopts UEP’s own existing standards. The same goes for “euthanasia” standards and other empty provisions tossed in to distract from the central issue: keeping hens in cages.

UEP’s Game of Inches: Prior to the Rotten Egg Bill, the egg industry passed state legislation calling for 116 square inches of cage space per hen. With a mere 8 square inch adjustment, UEP’s federal bill calls for a still cruel and depriving 124 square inches per hen – “phased-in” over 18 years. This token modification does not “double” the cage space from what UEP has already advocated as a standard. The bill’s own proponents have stated that a hen needs at least 216 square inches just to spread her wings.

Decriminalizing Animal Abuse: The bill contains no criminal penalties whatsoever. While overriding state laws which do contain appropriate criminal penalties, the Rotten Egg Bill would shift all authority to the industry-controlled USDA.

Fraudulent Labeling: As far as labeling egg cartons, UEP’s Rotten Egg Bill certainly would do that. For the very first time, the fraudulent term “enriched” cages would begin appearing on egg cartons nationwide – in order to deflect public concern – and to increase egg sales from caged hens.

The position of the Humane Farming Association and other responsible activists and organizations remains clear: Cruelty is cruelty. There is no such thing as an “enriched” battery cage. No humane organization should ever endorse these abusive confinement systems. Our state laws and voting rights must not be given away.

“If the legislation does not advance, [industry] would be headed toward cage-free production as the dominant, if not the only, form of egg production.” — Feedstuffs, agribusiness news journal, explaining why the egg industry is seeking to advance its federal legislation 


A lone hen escapes from her battery cage (photo: Farm Sanctuary)

‘ENHANCED COLONY HOUSING’
http://inthesetimes.com/ittlist/entry/12625/new_legislation_would_improve_living_conditions_of_egg-laying_hens/
New Legislation Would Improve Living Conditions of Egg-Laying Hens
by Patrick Glennon / Jan 26, 2012

Earlier this week, a group of lawmakers introduced a bill in the House that would seek to ameliorate the living conditions of egg-laying hens. H.R. 3798, the Egg Products Inspection Act Amendments of 2012, is the result of a joint effort of the Humane Society of the United States (HSUS) and the United Egg Producers (UEP). Wayne Pacelle, president and CEO of HSUS, said in a press release that the resolution is “historic and unprecedented,” reflecting a degree of cooperation between animal rights activists and industry representatives hitherto unseen.

Chad Gregory, Senior Vice President of UEP, noted that the changes will require $4 billion in sacrifices, but that the move is necessary and that the industry is a willing partner: “This has been an incredibly grueling process, but we’re here today excited to recognize and celebrate this monumental achievement.” For years, HSUS has lobbied for state-level regulation of industrial egg production. A complex web of varying state regulations—reflecting radically different conceptions of animal treatment and welfare—was very costly for the UEP, which represents 88 percent of U.S. egg production. Looking to standardize regulation and to appease its critics, UEP began working with HSUS in July 2011.

The primary purpose of the legislation is to phase out the use of battery cages—tiny confines that currently house over 280 million hens in the U.S. These cages can be as small as a piece of printer paper, leaving no room for a hen to extend her wings, stand up or stretch. Stacked in tiers, battery cages prohibit hens from engaging in their natural behavior. As a result, hens can become crazed, pecking violently at neighboring birds and themselves. Curing the symptom rather than addressing the cause, many egg producers cut off hens’ beaks to prevent them from mauling others, instead of allowing them greater space to roam.

The legislation would affect a number of changes on the industry, should it pass Congress:
• It would replace battery cages with “enhanced colony housing.” These new environs would give birds double the space of average battery cages.
• After a phase-in period of larger housing facilities, the legislation would mandate environmental enhancements—such as perches and scratch pads—that would provide outlets for hens’ instinctive behavior.
• The resolution would also require clearly detailed labeling on all eggs nationwide that describe the living conditions of the animals. These labels would include: “eggs from caged hens,” “eggs from hens in enhanced cages,” “eggs from cage-free hens” and “eggs from free range hens.”

In addition, the resolution would rectify several other cruel industry practices, including forced molting—the technique of depriving hens water and feed in order to stimulate quicker egg-laying cycles. The legislation would provide great relief to many birds currently held in inhumane conditions across the United States. Many other deplorable practices, however, would remain intact. Egg-laying hens are genetically manipulated to produce eggs at a higher rate. While this accelerates egg production, it also causes hens’ bodies to degenerate faster. Hens usually remain in egg production for only a year, after which they are killed at a young age for use in animal feed or low-quality chicken meat products. Even if their life were to become slightly more comfortable with double the (very small) space they currently have, they would still likely continue to die very prematurely.

Additionally, the industry treats male chicks born to egg-laying hens with shocking disregard. Chickens have been genetically altered in order to enhance their economic output—this means that “broilers” (chickens reared for meat production) have been genetically altered to produce a greater amount of breast meat and that layers have been genetically altered to optimize egg production. As a consequence of the U.S. market’s preference for broiler-meat, the male chicks of layers have no economic benefit for agribusiness. Male chicks are thus “destroyed” shortly after birth. This is done through numerous ways. They are sometimes sucked through air tubes and thrown against an electric pad, electrocuting them. Others are sent on a conveyor belt through what is known as a macerator (think: wood chipper). Reforming the industrial food production system is an important way of improving animals’ lives, but basic reforms shouldn’t obscure other cruelties that are inherent to the system.

chickens on egg farm
A still image from a Humane Society of the United States undercover video shows caged chickens on an egg farm. A Florida effort that would outlaw the gathering of undercover photos and video was dropped, but five other states are still attempting to pass similar laws in 2012. (Humane Society of the United States)

MEANWHILE : VIDEOTAPING in FACTORY FARMS still LEGAL  [without the consent of the hens?]
http://www.latimes.com/news/local/environment/la-me-gs-florida-drops-animal-farm-antivideotaping-effort-20120126,0,5292310.story
Florida Legislature drops anti-videotaping language
by Dean Kuipers  /  January 26, 2012,

The Florida Legislature has dropped a controversial provision that would have made it a crime to photograph or videotape on agricultural facilities without consent. We have reported previously on this blog that several states have attempted to thwart whistle-blowers and animal rights activists by making it a crime to record images on a farm, lab or other animal enterprise. Of course, many other actions such as trespassing, removing animals and other acts are already illegal.

Florida was taking a lead in this push, but in the last few days its legislature has removed the image collection language – derisively called an “ag gag” provision by activists – from state House Bill 1021 and state Senate Bill 1184. “These bills threaten animal welfare,” says Suzanne McMillan, director of Farm Animal Welfare for the American Society for the Prevention of Cruelty to Animals, who has monitored these bills. “However, they also threaten constitutional rights, they have a chilling effect on speech. Which is a serious concern. Any time you limit speech, legally, a higher threshold needs to be met and it’s certainly not being met in this case.” The animal welfare organization points out that an undercover video made at a Florida dairy farm was used to pass humane slaughter and euthanasia laws. That video showed calves with gunshot wounds left in a watery pit to drown.

Video and photos gathered by undercover activists and even news reporters has been a mainstay of investigative journalism for decades. There has been some question as to whether the actual gathering of images also violates the broad federal 2006 Animal Enterprise Terrorism Act, which makes it illegal to negatively affect the profits of an animal enterprise. The Center for Constitutional Rights is currently challenging that financial harm provision in court. Four other states are now considering such video and photo bans, including Indiana, Iowa, Minnesota and Nebraska. “These bills are a direct threat to us controlling our food supply and to the American public understanding where it’s food comes from,” McMillan adds . “If large animal agribusiness has nothing to hide, why is it supporting these kinds of bills? Time and again, undercover investigations have revealed these exact problems: food safety concerns, animal welfare violations, environmental violations.”

from ESCAPED DOMESTIC HOUSEPETS
http://www.dailytelegraph.com.au/news/sydney-nsw/wild-pretty-boys-show-their-word-skills/story-e6freuzi-1226136276472

Entire flocks of wild galahs, sulphur-crested cockatoos and corellas are learning to talk. The wild birds are being taught by pet birds that have escaped or been released by their owners and joined the flocks. “We have had people call us thinking they are going mad or had something put into their drink because they’ve gone out to look at the flock of birds in their backyard and all the birds have been saying something like ‘Who’s a pretty boy then?’,” Martyn Robinson, the Australian Museum’s naturalist, said yesterday.

Mr Robinson said the city was now home to large numbers of galahs, sulphur-crested cockatoos and corellas that had fled the state’s far west during the decade-long drought. “They’ve decided to stay and even begun to breed in the city, and if a pet bird of their species escapes their cage or is released because their owner’s moving or whatever, they naturally join the wild flocks,” he said. “These birds are very smart birds and very social and communication and contact is important between them. “So the pet bird begins to say things it’s been taught by its owner and the rest of the flock learns and starts speaking too, to mimic the pet bird,” Mr Robinson said. “I just hope a pet that’s been taught dirty words doesn’t join a flock.”


WHO’s a PRETTY BOY?
http://www.australiangeographic.com.au/journal/Parrots-and-other-wild-birds-able-to-talk.htm
Pet parrots, such as cockatoos, that are let loose in the wild are teaching native birds to talk.
by Hannah Price / September 15 2011

If you hear mysterious voices from the trees – it’s likely just a curious cockatoo wanting a chat. Native parrots, especially cockatoos, seem to be learning the art of conversation from their previously domesticated friends. The Australian Museum’s Search and Discover desk, which offers a free service to identify species, has received numerous reports of encounters with talkative birds in the wild from mystified citizens who thought they were hearing voices. Martyn Robinson, a naturalist who works at the desk, explains that occasionally a pet cockatoo escapes or is let loose, and “if it manages to survive long enough to join a wild flock, [other birds] will learn from it.”

Birds mimic each other
As well as learning from humans directly, “the birds will mimic each other,” says Jaynia Sladek, from the Museum’s ornithology department. “There’s no reason why, if one comes into the flock with words, [then] another member of the flock wouldn’t pick it up as well.” ‘Hello cockie’ is the most common phrase, though there have been a few cases of foul-mouthed feathered friends using expletives which we can’t repeat here. The evolution of language could well be passed on through the generations, says Martyn. “If the parents are talkers and they produce chicks, their chicks are likely to pick up some of that,” he says. This phenomenon is not unique; some lyrebirds in southern Australia still reproduce the sounds of axes and old shutter-box cameras their ancestors once learnt.

Birds of a feather chat together
In rural areas talking parrots will probably begin to lose their language abilities, says Martyn, with some words “likely to just disintegrate a bit and become part of that particular flock’s repertoire.” However, in Australia’s big cities like Sydney, Melbourne and Brisbane, cockatoos will probably maintain and improve their vocabulary due to regular contact with humans. “That’s certainly the case in the Botanic Gardens [in Sydney],” says Martyn. “If you say ‘hello’ or ‘hello cockie’ to the cockatoos, and if they’re interested in you and not just picking around for food, you may well trigger a response.”


PARROT LITERATURE, PARROT ORAL HISTORIES…
http://www.bbc.co.uk/news/magazine-14930062
How can birds teach each other to talk?
by Megan Lane / 16 September 2011

Wild parrots in Australia are apparently picking up phrases from escapee pet cockatoos who join their flocks. Why – and how – can some birds talk? Those strolling in Sydney’s parks are being startled by squawks of “Hello darling!” and “What’s happening?” from the trees. Wild birds such as galahs, sulphur-crested cockatoos and corellas are repeating phrases passed on by domesticated counterparts that escaped or were released, says naturalist Martyn Robinson, of Sydney’s Australian Museum. The museum has received numerous reports of talkative wild birds from startled members of the public. Birds are social creatures, and chicks learn to communicate by imitating the sounds made by their parents and those at the top of the flock’s pecking order. Unlike humans, birds do not have vocal cords. Instead, they are thought to use the muscles and membranes in their throats – specifically the syrinx – to direct airflow to make tones and sounds.

Not all birds can learn to make entirely new sounds. To date, only three groups of distantly related birds have been found to have this ability: songbirds; parrots such as cockatoos and parakeets; and hummingbirds. “These birds are very smart birds and very social, and communication and contact is important between them,” Robinson told Australia’s Daily Telegraph. “So the pet bird begins to say things it’s been taught by its owner and the rest of the flock learns and starts speaking too, to mimic the pet bird.” Although parrots can make noises that sound like words, they’re just mimicking sounds they find appealing, says Les Runce of the UK’s Parrot Society. “It may be a nursery rhyme, a football chant, a microwave pinging or a phone ringing.”

Young birds, like human babies, learn to speak or sing through imitation, says behavioural biologist Johan J Bolhuis, of Utrecht University in the Netherlands. In research published in August inNeuroscience Research, he describes “a transitional period of early vocalisation, which is called ‘babbling’ in humans and ‘subsong’ in birds.” And, he tells the BBC News website, parrots and some songbird species can learn throughout their lives, such as the Sydney example. “I have studied budgerigars – small parrots – that can teach each other to speak Japanese words. “In this and other research we found that the brains of these birds are organised in a similar way to human brains with regard to vocal learning. Also, the same genes are involved in song and speech.” He adds that birdsong has a “primitive grammar” that is quite different from the complex grammar of human language. “Bird research can teach us a lot about the development of human speech and the problems that may occur – stuttering, for instance. So, parrots and songbirds may hold important clues as to how we humans can learn to speak and acquire languages.”

Parrot fanciers keen to teach their own pretty polly to talk may have to repeat their chosen phrase over and over. But the bird may pick it up after a single listen. “Parrots have good memories and only need to hear a sound once to reproduce it,” says Runce. “A friend’s daughter had an ingrown toenail, banged it and let out an almighty shriek. Their bird has still got that one, and that was 30 years ago.”

GROW YR OWN MICROBIAL SLAVE ARMY
http://news.discovery.com/tech/bacteria-salt-water-make-hydrogen-fuel-.html
Bacteria, Salt Water Make Hydrogen Fuel
by Jesse Emspak / Sep 21, 2011

The ‘hydrogen economy’ requires a lot of things, but first is an easy and cheap supply of hydrogen. There are lots of ways to make it, but most of them don’t produce large quantities quickly or inexpensively.  Professor Bruce Logan, director of the Hydrogen to Energy Center at Penn State University, has found a way to change that. He used a process called reverse electrodialysis, combined with some ordinary bacteria to get hydrogen out of water by breaking up its molecules. Water — which is made of two atoms of hydrogen and one of oxygen — can be broken down with electricity. (This is a pretty common high school science experiment). The problem is that you need to pump a lot of energy into the water to break the molecules apart.

Logan thought there had to be a better way. He combined two methods of making electricity — one from microbial fuel cell research and the other from reverse electrodialysis. In a microbial fuel cell, bacteria eat organic molecules and during digestion, release electrons. In a reverse electrodialysis setup, a chamber is separated by a stack of membranes that allow charged particles, or ions, to move in only one direction. Filling the chamber with salt water on one side and fresher water on the other causes ions to try and move to the fresher side. That movement creates a voltage. Adding more membranes increases the voltage, but at a certain point it becomes unwieldy. By putting the bacteria in the side of the reverse electrodialysis chamber with the fresh water, and using only 11 membranes, Logan was able to generate enough voltage to generate hydrogen. Ordinarily he would need to generate about 0.414 volts. With this system, he can get .8 volts, nearly double. (The microbial part of the cell generates 0.3 volts and the RED system creates about 0.5.)

Using seawater, some less salty wastewater with sewage or other organic matter in it and the bacteria, Logan’s apparatus can produce about 1.6 cubic meters of hydrogen for every cubic meter of liquid through the system of chambers and membranes. Another bonus is that less energy goes into pumping the water — if anything, flow rates and pressure have to be kept relatively low so as not to damage the membranes.  Making hydrogen cheaper is a necessity if hydrogen cars are to be a reality. Some car companies already make hydrogen-powered models. The state of Hawaii is already experimenting with hydrogen fuel systems. Producing cheaper, abundant hydrogen — especially from sewer water and seawater — is a big step in that direction.

LIMITLESS
http://www.bbc.co.uk/news/science-environment-14976893
Harvesting ‘limitless’ hydrogen from self-powered cells
by Mark Kinver / 20 September 2011

US researchers say they have demonstrated how cells fueled by bacteria can be “self-powered” and produce a limitless supply of hydrogen. Until now, they explained, an external source of electricity was required in order to power the process. However, the team added, the current cost of operating the new technology is too high to be used commercially. Details of the findings have been published in the Proceedings of the National Academy of Sciences.

“There are bacteria that occur naturally in the environment that are able to release electrons outside of the cell, so they can actually produce electricity as they are breaking down organic matter,” explained co-author Bruce Logan, from Pennsylvania State University, US. “We use those microbes, particularly inside something called a microbial fuel cell (MFC), to generate electrical power. “We can also use them in this device, where they need a little extra power to make hydrogen gas. “What that means is that they produce this electrical current, which are electrons, they release protons in the water and these combine with electrons.”

Prof Logan said that the technology to utilize this process to produce hydrogen was called microbial electrolysis cell (MEC). “The breakthrough here is that we do not need to use an electrical power source anymore to provide a little energy into the system. “All we need to do is add some fresh water and some salt water and some membranes, and the electrical potential that is there can provide that power.” The MECs use something called “reverse electrodialysis” (RED), which refers to the energy gathered from the difference in salinity, or salt content, between saltwater and freshwater.

In their paper, Prof Logan and colleague Younggy Kim explained how an envisioned RED system would use alternating stacks of membranes that harvest this energy; the movement of charged atoms move from the saltwater to freshwater creates a small voltage that can be put to work. “This is the crucial element of the latest research,” Prof Logan told BBC News, explaining the process of their system, known as a microbial reverse-electrodialysis electrolysis cell (MREC). “If you think about desalinating water, it takes energy. If you have a freshwater and saltwater interface, that can add energy. We realized that just a little bit of that energy could make this process go on its own.”

Artistic representation of hydrogen molecules (Image: Science Photo Library)

He said that the technology was still in its infancy, which was one of the reasons why it was not being exploited commercially. “Right now, it is such a new technology,” he explained. “In a way it is a little like solar power. We know we can convert solar energy into electricity but it has taken many years to lower the cost. “This is a similar thing: it is a new technology and it could be used, but right now it is probably a little expensive. So the question is, can we bring down the cost?” The next step, Prof Logan explained, was to develop larger-scale cells: “Then it will easier to evaluate the costs and investment needed to use the technology. The authors acknowledged that hydrogen had “significant potential as an efficient energy carrier”, but it had been dogged with high production costs and environmental concerns, because it is most often produced using fossil fuels.

Prof Logan observed: “We use hydrogen for many, many things. It is used in making [petrol], it is used in foods etc. Whether we use it in transportation… remains to be seen.” But, the authors wrote that their findings offered hope for the future: “This unique type of integrated system has significant potential to treat wastewater and simultaneously produce [hydrogen] gas without any consumption of electrical grid energy.” Prof Logan added that a working example of a microbial fuel cell was currently on display at London’s Science Museum, as part of the Water Wars exhibition.


Bacterial hydrolysis cell with reverse electrodialysis stack

a FEW GRAINS Of SALT
http://live.psu.edu/story/55172
‘Inexhaustible’ source of hydrogen may be unlocked by salt water / September 19, 2011

A grain of salt or two may be all that microbial electrolysis cells need to produce hydrogen from wastewater or organic byproducts, without adding carbon dioxide to the atmosphere or using grid electricity, according to Penn State engineers. “This system could produce hydrogen anyplace that there is wastewater near sea water,” said Bruce E. Logan, Kappe Professor of Environmental Engineering. “It uses no grid electricity and is completely carbon neutral. It is an inexhaustible source of energy.” Microbial electrolysis cells that produce hydrogen are the basis of this recent work, but previously, to produce hydrogen, the fuel cells required some electrical input. Now, Logan, working with postdoctoral fellow Younggy Kim, is using the difference between river water and seawater to add the extra energy needed to produce hydrogen. Their results, published in the Sept. 19 issue of the Proceedings of the National Academy of Sciences, “show that pure hydrogen gas can efficiently be produced from virtually limitless supplies of seawater and river water and biodegradable organic matter.”

Logan’s cells were between 58 and 64 percent efficient and produced between 0.8 to 1.6 cubic meters of hydrogen for every cubic meter of liquid through the cell each day. The researchers estimated that only about 1 percent of the energy produced in the cell was needed to pump water through the system. The key to these microbial electrolysis cells is reverse-electrodialysis or RED that extracts energy from the ionic differences between salt water and fresh water. A RED stack consists of alternating ion exchange membranes — positive and negative — with each RED contributing additively to the electrical output. “People have proposed making electricity out of RED stacks,” said Logan. “But you need so many membrane pairs and are trying to drive an unfavorable reaction.” For RED technology to hydrolyze water — split it into hydrogen and oxygen — requires 1.8 volts, which would in practice require about 25 pairs of membranes and increase pumping resistance. However, combining RED technology with exoelectrogenic bacteria — bacteria that consume organic material and produce an electric current — reduced the number of RED stacks to five membrane pairs.

Previous work with microbial electrolysis cells showed that they could, by themselves, produce about 0.3 volts of electricity, but not the 0.414 volts needed to generate hydrogen in these fuel cells. Adding less than 0.2 volts of outside electricity released the hydrogen. Now, by incorporating 11 membranes — five membrane pairs that produce about 0.5 volts — the cells produce hydrogen. “The added voltage that we need is a lot less than the 1.8 volts necessary to hydrolyze water,” said Logan. “Biodegradable liquids and cellulose waste are abundant and with no energy in and hydrogen out we can get rid of wastewater and by-products. This could be an inexhaustible source of energy.” Logan and Kim’s research used platinum as a catalyst on the cathode, but subsequent experimentation showed that a non-precious metal catalyst, molybdenum sulfide, had 51 percent energy efficiency.

CONTACT
Bruce Logan
http://www.engr.psu.edu/ce/enve/logan/
email : blogan [at] psu [dot] edu

WASTEWATER
http://www.fastcompany.com/1775321/coming-soon-wastewater-batteries-that-could-power-your-house
Batteries That Run On (And Clean) Used Toilet Water
by Ariel Schwartz / Aug 22, 2011

Humans should have a little more respect for dirty toilet water. In recent years, wastewater has become something of a commodity, with nuclear plants paying for treated wastewater to run their facilities, cities relying on so-called “toilet to tap” technology, and breweries turning wastewater into biogas that can be used to power their facilities. Soon enough, wastewater-powered batteries may even keep the lights on in your house or, at the very least, in the industrial plants that clean the wastewater.

Environmental engineer Bruce Logan is developing microbial fuel cells that rely on wastewater bacteria’s desire to munch on organic waste. When these bacteria eat the waste, electrons are released as a byproduct–and Logan’s fuel cell collects those electrons on carbon bristles, where they can move through a circuit and power everything from light bulbs to ceiling fans. Logan’s microbial fuel cells can produce both electrical power and hydrogen, meaning the cells could one day be used to juice up hydrogen-powered vehicles.

Logan’s fuel cells aren’t overly expensive. “In the early reactors, we used very expensive graphite rods and expensive polymers and precious metals like platinum. And we’ve now reached the point where we don’t have to use any precious metals,” he explained to the National Science Foundation. Microbial fuel cells still don’t produce enough power to be useful in our daily lives, but that may change soon–Logan estimates that the fuel cells will be ready to go in the next five to 10 years, at which point they could power entire wastewater treatment plants and still generate enough electricity to power neighboring towns. There may also be ones that use–and in the process-desalinate–salt water, using just the energy from the bacteria. And if the microbial fuel cells don’t work out, there’s another option: Chinese researchers have developed a photocatalytic fuel cell that uses light (as opposed to microbial cells) to clean wastewater and generate power. That technology is also far from commercialization, but in a few years, filthy water will power its own cleaning facilities one way or another.

FELINE AIDS RESEARCH
http://www.guardian.co.uk/science/2011/sep/11/genetically-modified-glowing-cats
Glow cat: fluorescent green felines could help study of HIV
Scientists hope cloning technique that produced genetically modified cats will aid human and feline medical research
by Alok Jha / 11 September 2011

It is a rite of passage for any sufficiently advanced genetically modified animal: at some point scientists will insert a gene that makes you glow green. The latest addition to this ever-growing list – which includes fruit flies, mice, rabbits and pigs – is the domestic cat. US researcher Eric Poeschla has produced three glowing GM cats by using a virus to carry a gene, called green fluorescent protein (GFP), into the eggs from which the animals eventually grew. This method of genetic modification is simpler and more efficient than traditional cloning techniques, and results in fewer animals being needed in the process. The GFP gene, which has its origins in jellyfish, expresses proteins that fluoresce when illuminated with certain frequencies of light. Poeschla, of the Mayo Clinic in Rochester, Minnesota, reported his results in the journal Nature Methods. This function is regularly used by scientists to monitor the activity of individual genes or cells in a wide variety of animals. The development and refinement of the GFP technique earned its scientific pioneers the Nobel prize for chemistry in 2008.

In the case of the glowing cats, the scientists hope to use the GM animals in the study of HIV/Aids. “Cats are susceptible to feline immunodeficiency virus [FIV], a close relative of HIV, the cause of Aids,” said professors Helen Sang and Bruce Whitelaw of the Roslin Institute at the University of Edinburgh, where scientists cloned Dolly the sheep in 1996. “The application of the new technology suggested in this paper is to develop the use of genetically-modified cats for the study of FIV, providing valuable information for the study of Aids. “This is potentially valuable but the uses of genetically modified cats as models for human diseases are likely to be limited and only justified if other models – for example in more commonly used laboratory animals, like mice and rats – are not suitable.” Dr Robin Lovell-Badge, head of developmental genetics at the Medical Research Council’s national institute for medical research, said: “Cats are one of the few animal species that are normally susceptible to such viruses, and indeed they are subject to a pandemic, with symptoms as devastating to cats as they are to humans. “Understanding how to confer resistance is … of equal importance to cat health and human health.”

THAT GLOW GREEN
http://www.newscientist.com/article/dn20896-glowing-transgenic-cats-could-boost-aids-research.html?DCMP=OTC-rss&nsref=online-news
Glowing transgenic cats could boost AIDS research
by Andy Coghlan / 11 September 2011

Three cats genetically modified to resist feline immunodeficiency virus (FIV) have opened up new avenues for AIDS research. The research could also help veterinarians combat the virus, which kills millions of feral cats each year and also infects big cats, including lions. Prosaically named TgCat1, TgCat2 and TgCat3, the GM cats – now a year old – glow ghostly green under ultraviolet light because they have been given the green fluorescent protein (GFP) geneMovie Camera originating from jellyfish. The GM cats also carry an extra monkey gene, called TRIMCyp, which protects rhesus macaques from infection by feline immunodeficiency virus or FIV – responsible for cat AIDS. By giving the gene to the cats, the team hopes to offer the animals protection from FIV. Their study could help researchers develop and test similar approaches to protecting humans from infection with HIV.

Cat immunity
Already, the researchers have demonstrated that lab cultures of white blood cells from the cats are protected from FIV, and they hope to give the virus to the cats to check whether they are immune to it. “The animals clearly have the protective gene expressed in all their tissues including the lymph nodes, thymus and spleen,” says Eric Poeschla of the Mayo Clinic College of Medicine in Rochester, Minnesota, who led the research. “That’s crucial because that’s where the disease really happens, and where you see destruction of T-cells targeted by HIV in humans.” The animals are not the first GM cats, but the new method is far more efficient and versatile than previous techniques. The first cloned cat, born in 2001, was the only one to survive from 200 embryos, each created by taking an ear cell from cats, removing the nucleus and fusing it with a cat egg cell emptied of its own nucleus. Poeschla’s technique is far more direct, far more efficient and far simpler, and has already been used successfully to make GM mice, pigs, cows and monkeys. He loads genes of interest into a lentivirus, which he then introduces directly into a cat oocyte, or egg cell. The oocyte loaded with the new genes is then fertilised and placed in the womb of a foster mother. From 22 implantations, Poeschla achieved 12 fetuses in five pregnancies, and three live births. And out of the 12 fetuses, 11 successfully incorporated the new genes, demonstrating how efficient the method is. One surviving male kitten, TgCat1, has already mated with three normal females, siring eight healthy kittens that all carry the implanted genes as well, showing that they are inheritable. But there are doubts about whether cats will replace monkeys as the staples of HIV research. “It’s fantastic they’ve created GM cats,” says Theodora Hatziioannou of the Aaron Diamond AIDS Research Center in New York City. “But what makes research in monkeys so much better is that SIV in monkeys is much more closely related to HIV, so it’s more straightforward to draw conclusions than it would be with FIV.

 

THAT GLOW RED
http://news.nationalgeographic.com/news/2009/05/photogalleries/glowing-animal-pictures#/cats-cloned-glowing-animals_11832_600x450.jpg
May 14, 2009 / Photo by Choi Byung-kil/Yonhap via AP

How does it glow?
Red fluorescent protein, introduced via a virus into cloned DNA, which was implanted in cat eggs, then implanted in mother (2007)

What can we learn?
Scientists at Gyoengsang National University in South Korea both cloned a Turkish Angora house cat and made it fluorescent—as shown in the glowing cat (left) photographed in a dark room under ultraviolet light. (The nonfluorescent cat, at right, appears green in these conditions.) The scientists weren’t the first to clone a cat–they weren’t even the first to clone a fluorescent cat. But they were the first to clone a cat that fluoresces red. It’s hoped that the red glow, which appears in every organ of the cats, will improve the study of genetic diseases.


CONTACT
Eric Poeschla
http://mayoresearch.mayo.edu/mayo/research/poeschla/
http://mayoresearch.mayo.edu/staff/poeschla_em.cfm
email : Poeschla.Eric [at] mayo [dot] edu

PRESS RELEASE
http://www.nature.com/nmeth/journal/vaop/ncurrent/full/nmeth.1703.html
http://www.mayoclinic.org/news2011-rst/6434.html
Mayo Clinic Teams with Glowing Cats Against AIDS, Other Diseases
New Technique Gives Cats Protection Genes / September 11, 2011

Mayo Clinic researchers have developed a genome-based immunization strategy to fight feline AIDS and illuminate ways to combat human HIV/AIDS and other diseases. The goal is to create cats with intrinsic immunity to the feline AIDS virus. The findings — called fascinating and landmark by one reviewer — appear in the current online issue of Nature Methods. Feline immunodeficiency virus (FIV) causes AIDS in cats as the human immunodeficiency virus (HIV) does in people: by depleting the body’s infection-fighting T-cells. The feline and human versions of key proteins that potently defend mammals against virus invasion — termed restriction factors — are ineffective against FIV and HIV respectively. The Mayo team of physicians, virologists, veterinarians and gene therapy researchers, along with collaborators in Japan, sought to mimic the way evolution normally gives rise over vast time spans to protective protein versions. They devised a way to insert effective monkey versions of them into the cat genome. “One of the best things about this biomedical research is that it is aimed at benefiting both human and feline health,” says Eric Poeschla, M.D., Mayo molecular biologist and leader of the international study. “It can help cats as much as people.”

Dr. Poeschla treats patients with HIV and researches how the virus replicates. HIV/AIDS has killed over 30 million people and left countless children orphaned, with no effective vaccine on the horizon. Less well known is that millions of cats also suffer and die from FIV/AIDS each year. Since the project concerns ways introduced genes can protect species against viruses, the knowledge and technology it produces might eventually assist conservation of wild feline species, all 36 of which are endangered. The technique is called gamete-targeted lentiviral transgenesis — essentially, inserting genes into feline oocytes (eggs) before sperm fertilization. Succeeding with it for the first time in a carnivore, the team inserted a gene for a rhesus macaque restriction factor known to block cell infection by FIV, as well as a jellyfish gene for tracking purposes. The latter makes the offspring cats glow green.

The macaque restriction factor, TRIMCyp, blocks FIV by attacking and disabling the virus’s outer shield as it tries to invade a cell. The researchers know that works well in a culture dish and want to determine how it will work in vivo. This specific transgenesis (genome modification) approach will not be used directly for treating people with HIV or cats with FIV, but it will help medical and veterinary researchers understand how restriction factors can be used to advance gene therapy for AIDS caused by either virus. The method for inserting genes into the feline genome is highly efficient, so that virtually all offspring have the genes. And the defense proteins are made throughout the cat’s body. The cats with the protective genes are thriving and have produced kittens whose cells make the proteins, thus proving that the inserted genes remain active in successive generations.

The other researchers are Pimprapar Wongsrikeao, D.V.M., Ph.D.; Dyana Saenz, Ph.D.; and Tommy Rinkoski, all of Mayo Clinic; and Takeshige Otoi, Ph.D., of Yamaguchi University, Japan. The research was supported by Mayo Clinic and the Helen C. Levitt Foundation. Grants from the National Institutes of Health supported key prior technology developments in the laboratory.


A ‘glow in the dark’ kitten viewed under a special blue light, next to a non-modified cat. Both cats’ fur looks the same under regular light. {Photograph: Mayo Clinic}

TARGETING SECTOR THREE
http://www.pnas.org/content/early/2011/06/15/1105315108.abstract
http://online.wsj.com/article/SB10001424052702303936704576397491582757396.html#project%3DTARGETING_HIV3
http://online.wsj.com/video/news-hub-wall-st-tool-has-success-in-aids-fight/C4322662-F312-4BF8-9160-737DFE01BF02.html
http://online.wsj.com/article/SB10001424052702303936704576397491582757396.html
New Math in HIV Fight
by Mark Schoofs / June 21, 2011

Scientists using a powerful mathematical tool previously applied to the stock market have identified an Achilles heel in HIV that could be a prime target for AIDS vaccines or drugs. The research adds weight to a provocative hypothesis—that an HIV vaccine should avoid a broadside attack and instead home in on a few targets. Indeed, there is a rare group of patients who naturally control HIV without medication, and these “elite controllers” most often assail the virus at precisely this vulnerable area. “This is a wonderful piece of science, and it helps us understand why the elite controllers keep HIV under control,” said Nobel laureate David Baltimore. Bette Korber, an expert on HIV mutation at the Los Alamos National Laboratory, said the study added “an elegant analytical strategy” to HIV vaccine research. “What would be very cool is if they could apply it to hepatitis C or other viruses that are huge pathogens—Ebola virus, Marburg virus,” said Mark Yeager, chair of the physiology department at the University of Virginia School of Medicine. “The hope would be there would be predictive power in this approach.” Drs. Baltimore, Korber and Yeager weren’t involved in the new research.

One of the most vexing problems in HIV research is the virus’s extreme mutability. But the researchers found that there are some HIV sectors, or groups of amino acids, that rarely make multiple mutations. Scientists generally believe that the virus needs to keep such regions intact. Targeting such sectors could trap HIV: If it mutated, it would disrupt its own internal machinery and sputter out. If it didn’t mutate, it would lie defenseless against a drug or vaccine attack. The study was conducted at the Ragon Institute, a joint enterprise of Massachusetts General Hospital, the Massachusetts Institute of Technology and Harvard University. The institute was founded in 2009 to convene diverse groups of scientists to work on HIV/AIDS and other diseases.

Two of the study’s lead authors aren’t biologists. Arup Chakraborty is a professor of chemistry and chemical engineering at MIT, though he has worked on immunology, and Vincent Dahirel is an assistant professor of chemistry at the Université Pierre et Marie Curie in Paris. They collaborated with Bruce Walker, a longtime HIV researcher who directs the Ragon Institute. Their work was published Monday in the Proceedings of the National Academy of Sciences. To find the vulnerable sectors in HIV, Drs. Chakraborty and Dahirel reached back to a statistical method called random matrix theory, which has also been used to analyze the behavior of stocks. While stock market sectors are already well defined, the Ragon researchers didn’t necessarily know what viral sectors they were looking for. Moreover, they wanted to take a fresh look at the virus. So they defined the sectors purely mathematically, using random matrix theory to sift through most of HIV’s genetic code for correlated mutations, without reference to previously known functions or structures of HIV. The segment that could tolerate the fewest multiple mutations was dubbed sector 3 on an HIV protein known as Gag. Previous research by Dr. Yeager and others had shown that the capsid, or internal shell, of the virus has a honeycomb structure. Part of sector 3, it turns out, helps form the edges of the honeycomb. If the honeycomb suffered too many mutations, it wouldn’t interlock, and the capsid would collapse.

For years, Dr. Walker had studied rare patients, about one in 300, who control HIV without taking drugs. He went back to see what part of the virus these “elite controllers” were attacking with their main immune-system assault. The most common target was sector 3. Dr. Walker’s team found that even immune systems that fail to control HIV often attack sector 3, but they tend to devote only a fraction of their resources against it, while wasting their main assault on parts of the virus that easily mutate to evade the attack. That suggested what the study’s authors consider the paper’s most important hypothesis: A vaccine shouldn’t elicit a scattershot attack, but surgical strikes against sector 3 and similarly low-mutating regions of HIV. “The hypothesis remains to be tested,” said Dan Barouch, a Harvard professor of medicine and a colleague at the Ragon institute. He is planning to do just that, with monkeys. Others, such as Oxford professor Sir Andrew McMichael, are also testing it. The Ragon team’s research focused on one arm of the immune system—the so-called killer T-cells that attack other cells HIV has already infected. Many scientists believe a successful HIV vaccine will also require antibodies that attack a free-floating virus. Dr. Chakraborty is teaming up with Dennis Burton, an HIV antibody expert at the Scripps Research Institute in La Jolla, Calif., to apply random matrix theory to central problems in antibody-based vaccines.


Originally developed more than 50 years ago to describe the energy levels of atomic nuclei, the theory is turning up in everything from inflation rates to the behaviour of solids. So much so that many researchers believe that it points to some kind of deep pattern in nature that we don’t yet understand. “It really does feel like the ideas of random matrix theory are somehow buried deep in the heart of nature,” says electrical engineer Raj Nadakuditi of the University of Michigan, Ann Arbor.

RANDOM MATRIX THEORY
http://online.wsj.com/article/SB10001424052702303936704576398143823831876.html
How Random-Matrix Theory Found Its Way Into a Promising AIDS Study
by Mark Schoofs / June 21, 2011

Random-matrix theory is a mathematical method for finding hidden correlations within masses of data. It doesn’t just find pairs, a relatively easy task, but can detect groups of many correlated units and even groups that change over time, adding and losing members. The theory was developed in the middle of the 20th century by Nobel laureate Eugene Wigner and others to address problems in nuclear physics. In the 1990s and early 2000s, physicists applied it to the stock market. A major event such as a severe recession will act on almost all stocks together, a correlation so broad it has little use. At the other extreme are millions of random correlations – stocks rising or falling together purely by chance. But some stocks, such as those of car companies and parts makers, act in true correlation.

Sure enough, random-matrix theory filtered out the “noise” of random correlations and overwhelming events to reveal such genuine correlations. One of the authors of that finding, physicist Parameswaran Gopikrishnan, working with Boston University physics professor H. Eugene Stanley, is now a managing director at Goldman Sachs Group Inc. “Of course,” Dr. Stanley said, “we know those sectors are correlated anyway.” But his team found the sectors purely by using random-matrix theory “without looking at the innards of the companies,” he explained. That proved the power of the theory, which Dr. Stanley believes could act as an early-warning system for stock-market analysts. If one company in a sector “wanders away and stops being correlated, that would tell you something is going on” in that firm. Arup Chakraborty, a chemistry and chemical engineering professor at MIT, knew of random-matrix theory from the stock market work and from a scientific colleague who had used it to analyze enzymes, though not in HIV. Dr. Chakraborty thought it could help find sectors of HIV that rarely undergo multiple mutations – and it did.

ENTER the MATRIX
http://www.newscientist.com/article/mg20627550.200-enter-the-matrix-the-deep-law-that-shapes-our-reality.html
The deep law that shapes our reality
by Mark Buchanan / 07 April 2010

Suppose we had a theory that could explain everything. Not just atoms and quarks but aspects of our everyday lives too. Sound impossible? Perhaps not. It’s all part of the recent explosion of work in an area of physics known as random matrix theory. Originally developed more than 50 years ago to describe the energy levels of atomic nuclei, the theory is turning up in everything from inflation rates to the behaviour of solids. So much so that many researchers believe that it points to some kind of deep pattern in nature that we don’t yet understand. “It really does feel like the ideas of random matrix theory are somehow buried deep in the heart of nature,” says electrical engineer Raj Nadakuditi of the University of Michigan, Ann Arbor.

All of this, oddly enough, emerged from an effort to turn physicists’ ignorance into an advantage. In 1956, when we knew very little about the internal workings of large, complex atomic nuclei, such as uranium, the German physicist Eugene Wigner suggested simply guessing. Quantum theory tells us that atomic nuclei have many discrete energy levels, like unevenly spaced rungs on a ladder. To calculate the spacing between each of the rungs, you would need to know the myriad possible ways the nucleus can hop from one to another, and the probabilities for those events to happen. Wigner didn’t know, so instead he picked numbers at random for the probabilities and arranged them in a square array called a matrix.

The matrix was a neat way to express the many connections between the different rungs. It also allowed Wigner to exploit the powerful mathematics of matrices in order to make predictions about the energy levels. Bizarrely, he found this simple approach enabled him to work out the likelihood that any one level would have others nearby, in the absence of any real knowledge. Wigner’s results, worked out in a few lines of algebra, were far more useful than anyone could have expected, and experiments over the next few years showed a remarkably close fit to his predictions. Why they work, though, remains a mystery even today. What is most remarkable, though, is how Wigner’s idea has been used since then. It can be applied to a host of problems involving many interlinked variables whose connections can be represented as a random matrix.

The first discovery of a link between Wigner’s idea and something completely unrelated to nuclear physics came about after a chance meeting in the early 1970s between British physicist Freeman Dyson and American mathematician Hugh Montgomery. Montgomery had been exploring one of the most famous functions in mathematics, the Riemann zeta function, which holds the key to finding prime numbers. These are numbers, like 2, 3, 5 and 7, that are only divisible by themselves and 1. They hold a special place in mathematics because every integer greater than 1 can be built from them. In 1859, a German mathematician called Bernhard Riemann had conjectured a simple rule about where the zeros of the zeta function should lie. The zeros are closely linked to the distribution of prime numbers.

Mathematicians have never been able to prove Riemann’s hypothesis. Montgomery couldn’t either, but he had worked out a formula for the likelihood of finding a zero, if you already knew the location of another one nearby. When Montgomery told Dyson of this formula, the physicist immediately recognised it as the very same one that Wigner had devised for nuclear energy levels. To this day, no one knows why prime numbers should have anything to do with Wigner’s random matrices, let alone the nuclear energy levels. But the link is unmistakable. Mathematician Andrew Odlyzko of the University of Minnesota in Minneapolis has computed the locations of as many as 1023 zeros of the Riemann zeta function and found a near-perfect agreement with random matrix theory. The strange descriptive power of random matrix theory doesn’t stop there. In the last decade, it has proved itself particularly good at describing a wide range of messy physical systems.

Universal law?
Recently, for example, physicist Ferdinand Kuemmeth and colleagues at Harvard University used it to predict the energy levels of electrons in the gold nanoparticles they had constructed. Traditional theories suggest that such energy levels should be influenced by a bewildering range of factors, including the precise shape and size of the nanoparticle and the relative position of the atoms, which is considered to be more or less random. Nevertheless, Kuemmeth’s team found that random matrix theory described the measured levels very accurately (arxiv.org/abs/0809.0670). A team of physicists led by Jack Kuipers of the University of Regensburg in Germany found equally strong agreement in the peculiar behaviour of electrons bouncing around chaotically inside a quantum dot – essentially a tiny box able to trap and hold single quantum particles (Physical Review Letters, vol 104, p 027001). The list has grown to incredible proportions, ranging from quantum gravity and quantum chromodynamics to the elastic properties of crystals. “The laws emerging from random matrix theory lay claim to universal validity for almost all quantum systems. This is an amazing fact,” says physicist Thomas Guhr of the Lund Institute of Technology in Sweden.

Random matrix theory has got mathematicians like Percy Deift of New York University imagining that there might be more general patterns there too. “This kind of thinking isn’t common in mathematics,” he notes. “Mathematicians tend to think that each of their problems has its own special, distinguishing features. But in recent years we have begun to see that problems from diverse areas, often with no discernible connections, all behave in a very similar way.” In a paper from 2006, for example, he showed how random matrix theory applies very naturally to the mathematics of certain games of solitaire, to the way buses clump together in cities, and the path traced by molecules bouncing around in a gas, among others. The most important question, perhaps, is whether there is some deep theory behind both physics and mathematics that explains why random matrices seem to capture essential truths about reality. “There must be some reason, but we don’t yet know what it is,” admits Nadakuditi. In the meantime, random matrix theory is already changing how we look at random systems and try to understand their behaviour. It may possibly offer a new tool, for example, in detecting small changes in global climate.

Back in 1991, an international scientific collaboration conducted what came to be known as the Heard Island Feasibility Test. Spurred by the idea that the transmission of sound through the world’s oceans might provide a sensitive test of rising temperatures, they transmitted a loud humming sound near Heard Island in the Indian Ocean and used an array of sensors around the world to pick it up. Repeating the experiment 20 years later could yield valuable information on climate change. But concerns over the detrimental effects of loud sounds on local marine life mean that experiments today have to be carried out with signals that are too weak to be detected by ordinary means. That’s where random matrix theory comes in.

Over the past few years, Nadakuditi, working with Alan Edelman and others at the Massachusetts Institute of Technology, has developed a theory of signal detection based on random matrices. It is specifically attuned to the operation of a large array of sensors deployed globally. “We have found that you can in principle use extremely weak sounds and still hope to detect the signal,” says Nadakuditi. Others are using random matrix theory to do surprising things, such as enabling light to pass through apparently impenetrable, opaque materials. Last year, physicist Allard Mosk of the University of Twente in the Netherlands and colleagues used it to describe the statistical connections between light that falls on an object and light that is scattered away. For an opaque object that scatters light very well, he notes, these connections can be described by a totally random matrix.

What comes up are some strange possibilities not suggested by other analyses. The matrices revealed that there should be what Mosk calls “open channels” – specific kinds of waves that, instead of being reflected, would somehow pass right through the material. Indeed, when Mosk’s team shone light with a carefully constructed wavefront through a thick, opaque layer of zinc oxide paint, they saw a sharp increase in the transmission of light.
Random matrix theory comes up with strange possibilities not suggested by other analyses, which are then borne out by experiments

Still, the most dramatic applications of random matrix theory may be yet to come. “Some of the main results have been around for decades,” says physicist Jean-Philippe Bouchaud of the École Polytechnique in Paris, France,” but they have suddenly become a lot more important with the handling of humungous data sets in so many areas of science.” In everything from particle physics and astronomy to ecology and economics, collecting and processing enormous volumes of data has become commonplace. An economist may sift through hundreds of data sets looking for something to explain changes in inflation – perhaps oil futures, interest rates or industrial inventories. Businesses such as Amazon.com rely on similar techniques to spot patterns in buyer behaviour and help direct their advertising. While random matrix theory suggests that this is a promising approach, it also points to hidden dangers. As more and more complex data is collected, the number of variables being studied grows, and the number of apparent correlations between them grows even faster. With enough variables to test, it becomes almost certain that you will detect correlations that look significant, even if they aren’t.

Curse of dimensionality
Suppose you have many years’ worth of figures on a large number of economic indices, including inflation, employment and stock market prices. You look for cause-and-effect relationships between them. Bouchaud and his colleagues have shown that even if these variables are all fluctuating randomly, the largest observed correlation will be large enough to seem significant. This is known as the “curse of dimensionality”. It means that while a large amount of information makes it easy to study everything, it also makes it easy to find meaningless patterns. That’s where the random-matrix approach comes in, to separate what is meaningful from what is nonsense.

In the late 1960s, Ukrainian mathematicians Vladimir Marcenko and Leonid Pastur derived a fundamental mathematical result describing the key properties of very large, random matrices. Their result allows you to calculate how much correlation between data sets you should expect to find simply by chance. This makes it possible to distinguish truly special cases from chance accidents. The strengths of these correlations are the equivalent of the nuclear energy levels in Wigner’s original work. Bouchaud’s team has now shown how this idea throws doubt on the trustworthiness of many economic predictions, especially those claiming to look many months ahead. Such predictions are, of course, the bread and butter of economic institutions. But can we believe them?

To find out, Bouchaud and his colleagues looked at how well US inflation rates could be explained by a wide range of economic indicators, such as industrial production, retail sales, consumer and producer confidence, interest rates and oil prices. Using figures from 1983 to 2005, they first calculated all the possible correlations among the data. They found what seem to be significant results – apparent patterns showing how changes in economic indicators at one moment lead to changes in inflation the next. To the unwary observer, this makes it look as if inflation can be predicted with confidence. But when Bouchaud’s team applied Marcenko’s and Pastur’s mathematics, they got a surprise. They found that only a few of these apparent correlations can be considered real, in the sense that they really stood out from what would be expected by chance alone. Their results show that inflation is predictable only one month in advance. Look ahead two months and the mathematics shows no predictability at all. “Adding more data just doesn’t lead to more predictability as some economists would hope,” says Bouchaud.

In recent years, some economists have begun to express doubts over predictions made from huge volumes of data, but they are in the minority. Most embrace the idea that more measurements mean better predictive abilities. That might be an illusion, and random matrix theory could be the tool to separate what is real and what is not. Wigner might be surprised by how far his idea about nuclear energy levels has come, and the strange directions in which it is going, from universal patterns in physics and mathematics to practical tools in social science. It’s clearly not as simplistic as he initially thought.

AUDIO TRANSCRIPT
http://carlzimmer.com/books/aplanetofviruses/index.html
http://blogs.discovermagazine.com/loom/category/a-planet-of-viruses/
http://www.npr.org/2011/05/06/136057352/carl-zimmer-explores-the-weird-lives-of-viruses

IRA FLATOW: They’ve learned to live pretty much anywhere in the world and to use nearly any living thing for a host. And here is the astounding statistic: Viruses kill half the bacteria in the ocean every day. Every day, viruses kill half the bacteria in the ocean. And they invade a microbe host 10 trillion times a second around the world. But are the viruses alive themselves? How do you – how did they get there? How did they get here? And now that so many bacteria are developing resistances to antibiotics, is it time to unleash viruses on them? Are these just astounding to me or did you – when you did your research for this book – these are just amazing.
Mr. ZIMMER: Yeah. Yeah. I just had to keep going over and over it again, because I would look up, for example, how many viruses there on earth. And the number I get is, I keep finding, is 10 to the 31st power. That’s one with 31 zeroes after it, which is 10 billion trillion, trillion. That’s more stars than are in the universe. If you had a lot of spare time and you want to stack all those viruses end to end, they would go about 100 million light years.

FLATOW: Tell me about the oceans. They eat half the bacteria in the oceans every day?
Mr. ZIMMER: Yeah. It’s funny. There used to be a time when people thought the oceans are pretty much virus-free. But now we realize that there might be, say, maybe a billion viruses in every teaspoon of water. And they’re attacking the bacteria. There’s lots of bacteria in the ocean. And so they will just do a slaughter of these bacteria every day. Of course, the bacteria grow back pretty fast, but still it’s a tremendous thing because all those bacteria contain carbon and lots of nutrients. And so they’re constantly cycling all this to the ocean and into the atmosphere.

FLATOW: You know, when you said that there are 10 to the 31 viruses…
Mr. ZIMMER: Mm-hmm.
FLATOW: …then it seems almost incredible that our body is fighting off so many viruses every day. It must be being attacked all the time by viruses. And we’re fighting them off if they’re everywhere, right?
Mr. ZIMMER: Well, they’re also inside of us.
FLATOW: Yeah.
Mr. ZIMMER: So you look pretty healthy today. There are probably about -from the latest estimates I saw – about four trillion viruses inside of you right now. And they’re not making you sick, because they’re infecting all the bacteria that live inside of you.
FLATOW: So they’re holding off the bacteria from attacking me, also, possibly.
Mr. ZIMMER: Right. Or they might actually be helping the bacteria. They might be balancing the ecosystem in there so that some species do well and others don’t.

FLATOW: Now these bacteria that are all over the ocean and killing half – the viruses that are killing half the bacteria, how does that affect the ecosystem if you’ve got all these dead bacteria raining down in the ocean all the time?
Mr. ZIMMER: That’s right. So you got a lot more carbon that’s freed up and moving around. And there’s actually a big question about where exactly that carbon goes. Do the bacteria there just suck it back up again, or does it rain back down? What would the world be like without all these viruses? One pretty dramatic idea is that, actually, you know, all that carbon that’s coming out and then getting sucked back up could be affecting the Earth’s climate because any of that carbon that gets back up in the atmosphere is going to be trapping heat. So, you know, the temperature we’re at is partly set by viruses.

FLATOW: Mm-hmm. Let’s talk about one of my favorite topics I’ve been talking about over the years. And you have a chapter in your book about bacteriophages, viruses that eat, attack bacteria. And this was first discovered when?

Mr. ZIMMER: This was first discovered in World War I. So people knew a bit about viruses before then for about 30 years, but they had found them in people, in animals and in plants. But then a doctor, a Canadian doctor named Felix d’Herelle discovered that there were viruses that could wipe out bacteria. He would treat a dish of bacteria with fluid that he had filtered out from – actually from patients who are sick with dysentery. And he found that he could just kill these bacteria. And, eventually, what he concluded was that these were viruses that were attacking them. And it was a pretty radical idea at the time. People didn’t believe him. Nobel Prize winners were going after him. But he held to it. He actually became the hero – fictionalized hero in a novel called “Arrowsmith,” made a movie out of it. And he actually did quite well. He actually started a whole business of using these viruses to treat bacterial infections. In France, you could go out and buy these things.

FLATOW: And so there were viruses that could – that are – that exist in nature that could kill the worst bacterial infections, the bacteria that cause these infections we know. MRSA, all these things, there are natural occurring viruses that could kill them.
Mr. ZIMMER: Yeah. Every species of bacteria has a bunch of different species of phages that can kill it. That’s just evolution. It’s been going on for billions of years. And you can just go out, I mean, every time scientists go out, they’ll find a new phage for attacking a particular species of bacteria.

FLATOW: So why aren’t they sitting in our medicine cabinet? Or are the doctors giving us injections of these things?
Mr. ZIMMER: It’s a strange, wonderful, historical fluke. Basically, what happened was in the 1930s, scientists started to discover antibiotics. And here were chemicals, they were reliable, they knew how to make them, and everyone said, oh, these are the silver bullet. And so phage therapy disappeared, except for the Soviet Union. Everywhere else, everyone switched over to antibiotics. And that was -we’ve had a pretty good run with antibiotics, but now it’s not looking so good, because we’re getting bacteria that are resistant to them, as you said.

FLATOW: And so why don’t we have FDA approval of some of these things?
Mr. ZIMMER: You know, the FDA has a lot of – the FDA’s kind of sluggish.
FLATOW: That’s diplomatic.
Mr. ZIMMER: And if you go to them and say, hi, I’ve got a virus, and I want to go infect patients with it because it’ll kill bacteria, it’s kind of hard to get them to sign off on. In fact, they’re not even sure how to approve it, ironically. And so, there’s a lot of research going on right now, here in the United States, to develop them. They’re just starting to crack that barrier. So now there are actually food sprays where you – companies can spray phages on their food to stop food poisoning.

FLATOW: So, there might be some hope, because I’ve been talking about this for decades with other scientists that say this is just silly, basically.
Mr. ZIMMER: Yeah. It gets sillier all the time, because we’re getting better at selecting the right phage for the job, you know? You can create, what they call, libraries of these viruses, and you could imagine them being in a hospital. So you come in with an infection, and they take a sample, and then they go check out their library of phages and see which one will do the best job. And then they send them after your bacteria.

FLATOW: And the almost magical thing to me is even as the bacteria mutates to become resistant to that virus, you’ll get another virus that mutated with it, or knows how to attack that bacteria.
Mr. ZIMMER: That’s right. Antibiotics can’t evolve. Viruses can. And not only that, but we know how to engineer them now, so you can actually insert genes to make them more effective.

FLATOW: I’m just – you know, some things are just so illogical.
Mr. ZIMMER: Yeah. Maybe in 10 years.
FLATOW: The kinds of – 10 years from now. At least it’s not 30.

FLATOW: Let’s go to John in Bethesda. Hi, John.

JOHN (Caller): Hello. Good afternoon.
FLATOW: Hi, there.
JOHN: So my question is – I use United Streaming in my classes, and they have a video on viruses. And in this particular – or this video, it says that viruses are the oldest form of – and I think they use life loosely. But if viruses require a living host, how could they be the oldest living thing on Earth?
Mr. ZIMMER: Well, you know, it could be what they’re saying there is that their hosts are long since gone and they’re still around. There are actually some viruses that are weirdly primitive. So, for example, plants can get infected with things that are called viroids. They don’t even have a protein shell. They’re just naked genes that can infect plants, and they’re tiny, tiny little things.

JOHN: Are these like prions in humans?
Mr. ZIMMER: Well, no, because they’re actually made out of a single strand of DNA – RNA. So prions are proteins. These are viruses. They’re made of RNA.
JOHN: OK.
Mr. ZIMMER: But these or something like them could be just relics of the earliest stages of life, back when maybe there weren’t even any cells. You have to just think of kind of a soup of genes, and maybe some genes were good at parasitizing others and getting them to make copies of themselves.

JOHN: And then would there be a possibility if these bacteria phages mutating to become pathogenic to humans if you use them on the bacteria?
Mr. ZIMMER: No, because, you know, bacterial biology and human biology are profoundly different. And, so, you know, it, you know, these phages are specific just for one species of bacteria. But, you know, we share a common a ancestry with bacteria that lived, I don’t know, maybe three-and-a-half, four billion years ago. So you – and, you know, you have phages with you right now in your body when you’re perfectly healthy. Every time you have yogurt or eat pickles, you’re eating phages. So you don’t have anything to worry about with them.

FLATOW: Going to have some (unintelligible) yogurt and pickles today. We’re talking with Carl Zimmer, author of “A Planet of Viruses,” a really interesting book. And it’s a quick read. It’s chockfull of all kinds of interesting facts. For example, there’s a chapter in your book that deals with retrovirus DNA in our own genome. How do we get viruses in our genome?
Mr. ZIMMER: Well, they’re everywhere. Well, retroviruses – we’re most familiar with HIV. That’s a retrovirus. And what – the way the retroviruses reproduce is they actually take their genetic material and insert it into our own chromosomes. And then our chromosomes then make new viruses. Every now and then, on very rare occasions, a retrovirus will end up in, say, a sperm cell or an egg and insert its genes there. And then suddenly, if that sperm or egg become – gives rise to a new organism, a new animal, a new person, every cell in that body has got that virus. And it turns out that over tens, hundreds and millions years, our ancestors have been picking up viruses like this, and they’ve been clogging our genomes. So now they are probably about 100,000 elements in the human genome that you can trace to a virus ancestor. It makes up about 8 percent, all told, of our genome. Just bear in mind that all of the genes that encode proteins only make up 1.2 percent of our genome. So we’re much more virus than human, really.

FLATOW: Nathan in Denver. Hi, Nathan.

NATHAN (Caller): Hello. Thanks for taking my call.
FLATOW: Hi, there.
NATHAN: Hey. I have a biochemist friend that recently told me that he’s under the impression that climate change could potentially have a big effect on releasing viruses – maybe in frozen soils, I don’t know all the details – that we’ve never been exposed to or never encountered. Can you talk a little bit about how climate change is going to affect the world of viruses?
Mr. ZIMMER: Well, I doubt that it’s going to be unleashing viruses from the soil to make us sick. I mean, viruses are pretty delicate things. However, it could mean that insects that carry viruses could move into new territories and start making people sick with things like dengue fever, for example. And so those kind of shifts are things that we need to worry about. I mean, we also need to be concerned just about viruses hopping from one species to another. So SARS, you may recall, came from bats, actually. And through animal markets in China and things like that, they were able to get into our species. And fortunately, in the case of SARS, we seemed to have beaten that thing down. But in the case of HIV, that was a chimpanzee virus that got into humans several times, and with horrible consequences.

FLATOW: Hmm. So we should be saying that just like we – there’s a phrase, oh, there’s an app for that, if you have a bacteria, oh, there’s a virus for that.
Mr. ZIMMER: There’s a virus for everything.
FLATOW: To conquer MRSA, you could – there’s a virus that could conquer MRSA or these other…
Mr. ZIMMER: Potentially. Potentially, yeah.
FLATOW: And we could genetically engineer one.
Mr. ZIMMER: That’s right. I mean…
FLATOW: If we had to.
Mr. ZIMMER: Yeah. You can add in new genes. So, for example, there are viruses that have been engineered with extra enzymes to actually break up biofilms. So bacteria protect themselves by forming these gooey carpets. And so scientists at MIT have engineered viruses that can just blast that biofilm away.

FLATOW: In the minute or two we have left, let’s talk about papillomavirus. You have a story in your book on how scientists were studying rabbits with horn-like warts on their heads, a sort of jackalope kind.
Mr. ZIMMER: Yeah…
FLATOW: I think we have on our website, a picture of that. It’s just amazing.
Mr. ZIMMER: Yeah. Well, if you ever go out West, you see pictures, postcards of jackalopes, which are just rabbits with little prong or antlers stuck on them. But, in fact, rabbits do sometimes form these horn-like things on their heads, and it’s caused by papillomaviruses which get into their skin and actually sort of speed up the growth of the skin cells. And it was through – partly through the discovery of these, quote, unquote, “jackalopes” that scientists discovered that viruses can be an important cause of cancer. Fifteen percent of all human cancers are caused by viruses, and the papillomavirus causes cervical cancer.

FLATOW: Is there anything about viruses you don’t know… that you want to more of, or you think we should know more about? Are there questions that still remain about viruses?
Mr. ZIMMER: Yes. Because I’m sure that the more that scientists explore extreme places, the weirder the viruses are that they’re going to discover. I mean, they’ve even discovered now viruses that infect other viruses. So there’s no telling what they’re going to be finding out next.

FLATOW: And they could – and they would be living in even the hostile areas, deep in those thermal vents, things all over the oceans.
Mr. ZIMMER: Yeah. Oh, well, like, I write on the book about a cave, about a mile underground with these gigantic, 60-foot long gypsum crystals. It’s a bizarre place. And there’s a little bit of water in there, and – which has some bacteria in it, and those have viruses in them. So anywhere that there is life, you’re going to find viruses -maybe even on other planets.

RETROVIRUSES and YOU
http://www.guardian.co.uk/science/audio/2011/may/09/science-weekly-podcast-virus-supercooperators
http://pressblog.uchicago.edu/2011/05/03/traffic_carl_zimmer_and_w_ian.html

The New York Times calls Carl Zimmer “as fine a science essayist as we have.” In his widely admired books, essays, and blogs, Zimmer charts the frontiers of biology. Booklist acclaimed his most recent title A Planet of Viruses as “absolutely top-drawer popular science writing.” Zimmer is a lecturer at Yale University, where he teaches writing about science and the environment. He is also the first Visiting Scholar at the Science, Health, and Environment Reporting Program at New York University’s Arthur L. Carter Journalism InstituteW. Ian Lipkin, MD, is the director of the Center for Infection and Immunity, John Snow Professor of Epidemiology, and professor of neurology and pathology in the Mailman School of Public Health and the College of Physicians and Surgeons at Columbia University. His specialty is detecting new viruses and testing links between viruses and diseases. In A Planet of Viruses, Zimmer describes Lipkin’s discovery of West Nile Virus in the United States, as well as his work uncovering hidden strains of the common cold. Zimmer also profiled Lipkin in November 2010 for the New York Times.

Dear Carl,

I just finished A Planet of Viruses. It’s a compelling read that explores new frontiers in microbe hunting and the complex path from disease association to disease causation, a path we have not fully traveled. As with any book there are holes to be filled; nonetheless, this is an excellent roadmap!

We typically think of viruses as pathogens, but there is abundant and increasing evidence that they had an important and positive role in our evolution as mammals and the planet we live in. Retroviruses, a special kind of RNA virus of which HIV is the most famous, intercalate their genetic code into their host’s. When host cells replicate their DNA, the virus replicates with it. If the virus makes its way to a sperm or egg cell, the virus wins the (rare) opportunity to get passed on from parent to child, over and over again. These genetic infiltrators, known as endogenous retroviruses, have integrated themselves into mammalian genomes over millions of years. They activate genes during pregnancy to produce proteins that prevent rejection of a fetus as a foreign body, likely facilitating the evolution of the placenta and live birth. Marine viruses, known as bacteriophages, which are the most abundant viruses on earth, shape our ecosystem by infecting and lysing bacteria in deep-sea sediment, thus affecting how nutrients are recycled.

Initiatives like the Human Microbiome Project, which surveys the human body’s resident microorganisms and how they interact with our genes to influence health and disease, have mostly focused on bacteria. However, scientists cannot continue to ignore viruses, fungi, and other bugs! Traditionally, we have focused on bacteria because they are easy to clone, allowing us to replicate parts of their genome that may shed light on our own evolution. With the advent of newer and “sexier” technologies like virus detection microchips and high throughput sequencing, we can turn our attention to studying our interactions with viruses in more detail. As we learn more about the viruses in our gastrointestinal and respiratory tracts, I will be very much surprised if there are no helpful inhabitants among them.

Carl, you also discuss zoonotic diseases like AIDS, influenza, SARS, and Ebola, but let’s not forget that how investigators decide where and when to sample for potential pathogens is also important. Hotspot modeling allows us to target surveillance efforts to ‘hot spots’ for human disease—the areas where human pathogens are most likely to emerge. The EcoHealth Alliance is a pioneer in this field and an advocate for the idea of One Health, which promotes collaboration among environmental scientists, vets, and clinicians.

And what about those curious about how microbe hunters do what we do? What are the platforms we use to find known and novel agents? How do we prove relationship to disease (or equally important, disprove a causative relationship)? Carl, let’s give them directions! The work we do the Center for Infection and Immunity helps to answer some of those queries. We provide links to papers and interviews that address these challenges as well as video demonstrations of some relevant technologies

Last (but not least), as this is not a peer reviewed publication, and I have been encouraged to let my imagination run free, I wonder whether you might consider a chapter in a potential sequel focused on how microbes may alter host behavior to enhance their growth and dissemination. For example, rabies is associated with the inability to swallow, leading to the accumulation of saliva that contains rabies virus, and with aggressive (rabid) behavior that facilitates its spread. It is possible, though I have no experimental proof, that when herpes simplex virus infects the sacral ganglia, it may (in)advertently stimulate nerve endings in the pelvic area , promoting sexual activity and increasing the likelihood it will move into another host.

Carl, thanks again for sending me a preview copy of your book. I look forward to many spirited discussions!

Best,
W. Ian Lipkin

Dear Ian:

Thanks for your reflections. There’s a lot to ponder in them, but I’m most intrigued by your most speculative ideas—namely, whether viruses manipulate their hosts for their own benefit. As we discover more and more viruses, I suspect that scientists will indeed find good evidence that at least some viruses act like puppet masters.

I first became familiar with this sort of strategy while writing my previous book, Parasite Rex. Some of the most spectacular examples of parasite manipulation come from animal parasites. The lancet fluke—a parasitic flatworm—has a life cycle that takes it from snails to ants to grazing mammals like cows or sheep. Getting from one species to another is no simple feat. The lancet fluke has ways of manipulating one host after another to make its way through life. Mammals release the fluke eggs in their droppings, which are then eaten by snails. The snails defend themselves by coating the eggs in slime and then “coughing” them up. Ants passing by find the slime delicious, and devour it, along with the eggs inside.

Once inside the ant, the fluke eggs hatch, and the parasites develop. When they’re ready for their next host, they begin to alter the ant’s behavior. At twilight, the ant crawls up a blade of grass and clamps onto the tip. That’s when grazing mammals are likely to pass by and devour the grass, and the ant, and the parasites inside. If the ant does not get eaten by dawn, the parasite causes it to release its grip and crawl down to the ground, where it can enjoy the shade until the end of the next day—when it feels the urge to climb again.

There are many such examples, and for some reason most of them come from parasitic animals—tapeworms, parasitoid wasps, thorny-headed worms, and the like. I don’t think that this bias reflects the superior sophistication of parasitic animals over non-animal parasites like viruses. I think it’s just another case of the drunk looking for his keys under a lamp post—not because the keys are there, but because that’s where it’s easier to look.

Consider, for example, the fungus Cordyceps. This little mushroom has no animal nervous system. It’s just a mass of fungal cells. Yet Cordyceps manages to manipulate ants as well as lancet flukes. Ants pick up its spores on the ground, whereupon the fungus penetrates its host exoskeleton and starts to grow inside. It doesn’t kill its host, however. Instead, it feeds on the ant’s internal fluids until it’s ready for its next stage of life. The ant then starts to climb—not to the tip of a blade of grass, but to the underside of a leaf a few feet off the ground. The ant clamps onto a vein in the leaf, whereupon the fungus sprouts a flower-like stalk out of its head, which showers spores on the ants below.

While Cordyceps may not have the complexity of the animal nervous system, however, it’s not simple. Fungi have big genomes. Yeast, for example, has about 6,500 genes. There’s a lot of storage capacity in such a genome to encode lots of sophisticated strategies. A parasitic fungus might be able to use some of its many genes to make proteins that interacted with its host’s nervous system to direct it to just the right spot on a leaf. Viruses, on the other hand, typically only have a handful of genes.

Are ten genes enough for a virus to manipulate a host? I suspect they may well be. After all, scientists have already shown how viruses can manipulate us in other ways, such as the way that human papillomaviruses can speed up the growth and division of their host cells. There’s nothing particularly special about behavior that would make it beyond the reach of viruses. They’d just need to make proteins that could shut down certain genes in neurons or switch other ones on to produce big changes. And as I mention in A Planet of Viruses, scientists are now finding giant viruses that contain over a thousand genes. Perhaps they have unappreciated powers of manipulation, too.

Parasitologists have one big piece of advice for anyone who wants to investigate whether viruses manipulate their hosts: don’t be fooled by mirages. It is very tempting to see any change in a host as the product of a fine-tuned adaptation in its parasite. But it’s also possible that a strange host behavior is merely a byproduct of being infected. It’s not easy to distinguish between these alternatives. One way is to measure just how big of a difference these “manipulations” make to parasites. Robert Poulin of the University of Otago has studied a parasitic fluke that infects cockles on the beaches of New Zealand. It then needs to get into the shore birds that eat the cockles to move to the next stage of its life cycle. And it just so happens that the infected cockles lose the ability to burrow. So if you walk around on the beach in New Zealand, a lot of the cockles you see may be infected and unable to dig back down into the sand.

Seems like a great way for the parasite to boost its odds of getting into a bird, right? Well, Poulin worked through a detailed model of the parasite life cycle and discovered that it actually makes little difference. For one thing, the cockles also get eaten by other predators in which the parasite can’t survive. So Poulin concludes that this case of “manipulation” could not have evolved because it benefited the parasites. Instead, it’s just a side-effect. If someone wants to see if the aggression caused by rabies is a manipulation, they could try to carry out a similar test. It wouldn’t be easy, but it would be interesting.

Still, it would be a mistake to look only for the most fine-tuned adaptations in viruses. Just consider a single-celled protozoan called Toxoplasma, which normally has a life cycle that takes it from cats to rats and other mammal prey and back to cats again.Toxoplasma does not make rats sick. Instead, it forms harmless cysts in rat brains. And there it seems to manipulate rats in a very precise way: it causes them to lose their fear of cat odor. This change may make them easier prey for cats, boosting the reproductive success of the parasite.

Toxoplasma is a serious health problem for humans. Pregnant women need to avoid contact with cat litter or garden soil, because they may pick up the parasite and accidentally ingest it. While healthy adults can keep Toxoplasma in check, fetuses with immature immune systems cannot. Toxoplasmosis can thus cause serious brain damage, as the parasite grows unchecked. Toxoplasmosis is also a serious concern for adults with compromised immune systems—due to AIDS or immune-suppressing drugs taken after organ transplants.

In human adults, the parasite may be benign, but it does appear to cause some shifts in personality. Some studies suggest that people with Toxoplasma are more likely to get into car accidents, for example. It would be a mistake to see these personality shifts as the parasite’s strategy for getting us eaten by cats. For one thing, Toxoplasmawas probably not a common disease in humans until the domestication of house cats—when we came into close contact with their parasite-laden droppings. For another, I doubt my pet cats would ever consider me a potential breakfast.

Still, the fact that these personality shifts are not fine-tuned adaptations does not make them unimportant. Could some psychological disorders, like depression, be the result of viruses that alter the behavior of their regular animal hosts? And as virologists like you discover new viruses moving into our species from other animal hosts, I wonder if they’ll bring their puppetmaster tricks with them.

Best,
Carl

DESTROY THEM ALL? or LEARN SOMETHING?
http://pressblog.uchicago.edu/2011/05/12/traffic_carl_zimmer_and_richar.html
Should Smallpox Be Put To Death?

Richard Preston is the author of seven books, includingThe Hot ZoneThe Cobra Event, and The Demon in the Freezer. He is a regular contributor to the New Yorker, and his awards include the American Institute of Physics Award and the National Magazine Award. Preston also the only person who isn’t a medical doctor ever to receive the Centers for Disease Control’s Champion of Prevention Award for public health.

Dear Carl:

There’s a debate in the scientific community about what to do with the remaining stocks of smallpox virus on the planet. Should the virus be preserved so that it can be studied? Or should the virus be destroyed, so that—in theory at least—it would become extinct and would not threaten the human species again?

Smallpox virus, or Variola major, is the cause of probably the worst infectious disease in human history. During the nineteenth and twentieth centuries, experts believe that smallpox killed half a billion people, accounting for far more deaths than all the wars of the time. Smallpox is a grisly and supremely painful disease. The disease has around a 33 percent case-fatality rate in unvaccinated patients. That is, a third of the disease’s victims who haven’t been vaccinated die. The victims suffer from an incredibly painful rash—blisters known as pustules stud the body. The survivors are typically left with scars for life. About ten percent of fatal smallpox cases consist of hemorrhagic smallpox, a manifestation of the disease in which the victim dies with hemorrhagic symptoms, including bleeding from the orifices. Smallpox virus spreads in the air from person to person, traveling in tiny droplets spewed when an infected person speaks or coughs. The vast majority of the world’s population today has little or no immunity to smallpox, because vaccination ceased during the 1970s.

Smallpox was declared eradicated globally in 1980 by the World Health Organization (WHO), after a remarkable and heroic WHO-led effort to eradicate the virus worldwide. Today, the only remaining samples of live smallpox virus are stored in just two locations: a high-security lab at the Centers for Disease Control in Atlanta, Georgia, USA, and in the Vector State Research Center in Siberia, Russia. For a number of years, now, various member nations of the WHO have been pressing the WHO to order those stocks destroyed.

The smallpox virus stock at the CDC occupies a volume about the size of a basketball; the virus samples are frozen in small plastic tubes the size of pencil stubs. The Russian stock is probably similar. It would be very easy to destroy the virus: just heat it up. But should it be destroyed? A series of defectors from the old Soviet Union have revealed that the Soviet Union weaponized smallpox; that the virus was a mainstay of the clandestine Soviet biowarfare program. Illicit stocks of smallpox may have been taken out of Russia; nobody knows where the virus might exist on earth today in the form of undisclosed, secret stocks of the virus.

Researchers using live smallpox virus at the CDC have been studying the virus in an effort to develop antiviral drugs that would be effective against a smallpox infection. The drugs might also be effective against genetically engineered smallpox. The genome sequence of smallpox virus is publicly available and can be downloaded from the Internet. Some day it will probably be technically feasible to recreate live smallpox from its genome sequence. Even if all the living smallpox were destroyed, it might be brought back to life in a lab somewhere, some day.

D. A. Henderson, who led the WHO eradication of smallpox, argues that the virus should be destroyed, regardless of whether it can be recreated. He argues that if the WHO makes smallpox extinct, then anyone who later had the live virus would be committing a crime against humanity and could be prosecuted in international courts. On the other hand, researchers who are developing defenses against smallpox argue that the disease is simply too dangerous to destroy; they argue that we must continue to study it under the principle of Sun Tzu, “Know thy enemy.”

What do you think?

Richard

smallpox-virus1.jpgSARS virus

Dear Richard:

Your question is a timely one. On May 16, the World Health Organization will be having their annual meeting, and one of the items on their agenda is a global consensus about what to do with the world’s remaining smallpox stocks. If WHO does decide on eradication, it will be an historical moment. We humans have only eliminated two viruses from the wild. Smallpox was the first. The second, as of last October, is rinderpest, a devastating scourge of cattle. For now, both smallpox and rinderpest remain in laboratory stocks. But if WHO decides to get rid of the smallpox lab stocks, too, the virus may be eliminated from the planet.

The prospect of such a milestone raises the question of why we haven’t been able to wipe out any of the other viruses that plague us. In some cases, it’s because viruses have escape routes. In 2004, for example, SARS burst on the scene, killing 774 people in total before quarantines and other public health measures beat it back. There have been no reported cases of SARS since then in humans, but SARS is probably thriving. It spread from animal hosts—bats and civets—to humans, and it doubtless retreated back to them.

Some viruses are hard to eradicate because they’re lurkers. HIV takes years to produce symptoms, making it hard to recognize and treat infected people. By the time it makes itself known, people may have spread it to many other victims. And doctors still lack vaccines for HIV and many other viruses. In all these respects, smallpox is a peculiar virus. Unlike SARS, smallpox only infects humans. Unlike HIV, smallpox makes itself known in a matter of days. It’s also unusual in that there’s a cheap, effective smallpox vaccine. Combined, these three factors made it possible to effectively break the transmission cycle of smallpox and thereby drive it towards extinction.

Whenever a species goes extinct, we lose the opportunity to get to know it better. I’m sure no one would shed a tear at the extinction of smallpox, but, as you note, there’s a lot we still don’t understand about the virus. I don’t think getting the opportunity to try people for crimes against humanity is worth giving up the chance to learn more about smallpox. Even if smallpox never rears its ugly head again, that knowledge could still be valuable. Studies on smallpox DNA suggest that it evolved just a few thousand years ago from a pox that infected African rodents. Many closely related pox strains infect animals today, and they have plenty of chances to evolve into a new human pox. In 2003, for example, people in the Midwest came down with monkeypox, an African virus that is closely related to smallpox. It was baffling at first that an African pox could infect American victims. Eventually public health workers determined that the victims got the virus from prairie dogs they all bought at the same Missouri pet store. If smallpox can help us prepare for the next pox, we should resist the urge to annihilate it.

Carl


Bacteriophages on Bacterial Cell

PHAGE THERAPY
http://pressblog.uchicago.edu/2011/05/20/traffic_carl_zimmer_and_timoth.html

Timothy Lu is assistant professor of electrical engineering at MIT, where he heads the Synthetic Biology Group. Carl wrote a profile of Lu last year inTechnology Review.

Dear Carl:

Bacteriophages are the most abundant biological particles on earth, but due to their size, and perhaps ubiquity, most of us don’t think of them very often. Phages are essentially just bacterial viruses. When it comes to viruses, the popular notion is that they are bad entities that are responsible for disease and suffering. The truth is, however, that phages are very different from human viruses. Phages do not infect human cells and are not responsible for the viral diseases that plague mankind, such as AIDS, herpes, cervical cancer, and the common cold. Furthermore, phages have had a tremendous impact on modern biology and biotechnology.

Much of our early scientific efforts to understand genetic regulation were carried out in the humble phage. Phage proteins called recombinases are an integral component for the construction of “knockout animals,” which cannot express particular genes—an indispensable tool in modern biological research. Phage display, a technique for sticking a library of peptides on phage surfaces and panning for targets to which these peptides will bind, has been used to make nanowires for batteries, identify new antibodies to treat human diseases, and understand the basic science which underlie protein-protein interactions.

Despite their importance as major research tools in the biomedical community, however, research into the use of phages as human therapeutics has garnered a mixed reputation in the Western world. Soon after their discovery in the early twentieth century, phages were tried as novel antimicrobial agents. Indeed, one can imagine the excitement that the early phage researchers must have experienced when observing the lysis—or clearing of bacterial cultures—by the addition of a newly discovered biological agent! However, early reports claiming impressive successes at treating bacterial infections with phages were later tempered by failures in other settings and repeated trials.

Looking back, it is likely that a lack of detailed understanding of phage biology was responsible for much of these failures. Unlike antibiotics, which act like broad-spectrum bombs that blast all bacteria, good or bad, in their paths, phages are targeted warriors, the biological equivalent of a sniper or laser-guided missile. This targeted behavior is beneficial because it avoids killing bacteria which are good for us, as opposed to antibiotics which cause collateral damage. However, this targeted behavior also has its flaws because to effectively treat a specific bacterial contamination with phages, one must understand the bacterial compositions in detail and know what mixture of phages to use against them. Such capabilities were not available or known during the early days of phage therapy.

Thus, the subsequent discovery of antibiotics, along with their simplicity and miracle successes, largely displaced phages from antimicrobial research in Western medicine in the latter half of the twentieth century. As a result, the notion of phage therapy often elicits justifiable skepticism when discussed as an alternative to antibiotics today, even though the antibiotics pipeline has dried up and we are in desperate need of new strategies to combat the rising tide of antibiotic-resistant superbugs.

Fortunately, in the past few decades, there has been a renaissance brewing in the phage world. Commercial, government, and academic labs have begun to tackle the fundamental issues that have held back phage therapy using rigorous molecular tools. To use phages to effectively treat bacterial contaminations, these labs have been developing technologies for classifying bacterial populations, identifying the right combination of phages to use, and optimizing phage properties using evolutionary or engineering approaches.

Instead of tackling the high hurdles that need to be crossed for direct human use, many labs and companies have chosen to apply phages to other applications in industrial, environmental, and diagnostic settings. For example, Intralytix makes phages to treat listeria contaminations of food, Omnilytix makes phages that control bacterial infections on tomatoes and peppers, and Microphage makes phages that can detect and report on the presence of harmful antibiotic-resistant superbugs, such as MRSA. A company called Novophage is advancing the use of phages for industrial applications, where they have the potential to enhance energy inefficiency and decrease biofouling (for full disclosure, I am a founder of this startup). Major advantages of phages compared with chemical biocides and pesticides include greater biocompatibility and decreased environmental toxicity. Using natural biological particles to combat biological problems is consistent with our society’s continuous drive to reduce the use of harmful chemicals and is, I believe, a great application for phages in the modern era of biotechnology.

The hurdle that has yet to be overcome is the use of phages for human therapeutics, the original application area for phage therapy. Nonetheless, given the great need for new antimicrobial therapies and the inroads that these laboratories have been making into optimizing phages for practical applications, the prospect of effective phage therapy being applied to human infectious diseases in Western medicine seems to be growing!

Tim

05Ion.jpg
a bacteriophage

Dear Tim:

In all my work as a science writer, I can’t think of a story as strange as the history of phage therapy. It’s been nearly a century since the Canadian physician Felix d’Herelle discovered viruses that infect bacteria. And yet, despite great promise, phage therapy has yet to become a mainstay of medicine.

What makes the story even stranger is that Herelle could see the promise of phage therapy as soon as he discovered the viruses. He was soon using them to treat dysentery and cholera. When four passengers on a French ship in the Suez Canal came down with bubonic plague, Herelle gave them phages. All four victims recovered. He went on to conduct large-scale public health campaigns for the British government in colonial India. Phage therapy became so well-known that Herelle inspired the central character in Sinclair Lewis’s 1925 best-selling novel Arrowsmith. Phage therapy became big business: Herelle developed commercial drugs that were sold by the company that’s now known as L’Oreal, which were used to treat skin wounds and to cure intestinal infections.

Felix_dHerelle.jpg
Felix d’Herelle

But by the time he died in 1949, Herelle had sunk into obscurity. Doctors had abandoned phage therapy for antibiotics. His dream did not vanish entirely, however. On his travels, Herelle met Soviet scientists who wanted to set up an entire institute for research on phage therapy. In 1923 Herelle helped establish the Eliava Institute of Bacteriophage, Microbiology, and Virology in Tbilisi, which is now the capital of the Republic of Georgia. At its peak, the institute employed 1200 people to produce tons of phages. In World War II, the Soviet Union shipped phage powders and pills to the front lines, where they were dispensed to infected soldiers.

Soviet scientists continued to investigate phage therapy after World War II. They conducted the best trial of the viruses in 1963. They enrolled 30,769 children in Tbilisi. Once a week, about half the children swallowed a pill that contained phages against dysentery. The other half of the children got a pill made of sugar. To minimize the influence of the environment as much as possible, the Eliava scientists gave the phage pill only to children who lived on one side of each street, and the sugar pill to the children who lived on the other side. The Eliava scientists followed the children for 109 days. Among the children who took the sugar pill, 6.7 out of every 1,000 got dysentery. Among the children who took the phage pill, that figure dropped to 1.8 per 1,000. In other words, taking phages caused a 3.8-fold decrease in a child’s chance of getting dysentery.

Phage therapy only began to attract interest in the West after the fall of the Soviet Union, when Soviet scientists could communicate more freely with the rest of the world. And yet, as you point out, the U.S. government has been leery of approving viruses for medical treatments. Gone are the days when a physician like Herelle could pretty much do as he pleased. As a result, many companies and investors are reluctant to embrace his phages.

If phage therapy can leap over these hurdles, I think that there are a vast number of potential applications. Treating a skin infection is just the start. Phages, after all, are part and parcel of every person’s inner ecology. Our bodies are home to 100 trillion bacteria and other microbes. Recent surveys estimate that these microbes play host to about four trillion phages, which come in about 1,500 different species. In some cases, our phages kill their hosts, and thus maintain an ecological balance in our mouths, noses, guts, and other nooks and crannies. In other cases, phages insert genes into their microbial hosts, giving them new powers.

The human microbiome is not merely an infestation we tolerate. It plays many different roles in our bodies. Microbes synthesize vitamins for us, regulate how much energy we get from our food, fight off invading pathogens, nurture our immune system, and potentially even influence our behavior. It may be possible to manipulate the microbiome through the phages that have coevolved with it for millions of years.

Carl

phytoplankton_070305.jpg
phytoplankton

OCEANS FULL
http://pressblog.uchicago.edu/2011/05/27/traffic_carl_zimmer_and_penny.html
A Billion Viruses in the Sea

Sallie W. “Penny” Chisholm is the Lee and Geraldine Martin Professor of Environmental Studies and professor of biology at MIT. Her research lab seeks to advance our understanding of the ecology and evolution of microbes in the oceans, and how they influence global biochemical cycles. In January 2010, she was awarded the Alexander Agassiz Medal, for “pioneering studies of the dominant photosynthetic organisms in the sea and for integrating her results into a new understanding of the global ocean.”

Dear Carl,
Thank you for giving viruses the recognition they deserve. As you point out, the discovery of viruses in the oceans is relatively recent. It seems that about once every decade there are similar major discoveries in oceanography that change the way we think about ocean ecosystems. One of these—a discovery by the late John Martin—was that iron availability limits the growth of phytoplankton (your ‘geoengineers’) over large regions of the oceans. This changed the major ‘drivers’ of carbon dioxide absorption by the oceans, and climate models had to be changed accordingly.

Evidence that iron—carried from land to ocean via atmospheric dust—limits the ocean’s capacity to draw carbon dioxide out of the atmosphere has fueled the idea that large scale ocean iron fertilization could be used for engineering Earth’s climate. What does this have to do with viruses (you are wondering)? Well, it turns out that iron has been used to flocculate viruses for wastewater treatment, and to concentrate them from ocean water for scientific study. What if iron dust deposition does the same in the oceans? What if it not only stimulates phytoplankton growth, but also reduces phytoplankton death rates by ‘precipitating viruses’ and settling them out of the system? Might this phenomenon help explain the observed relationships between iron dust deposition and atmospheric carbon dioxide in ice cores? This has been proposed by MIT’s Hyman Hartman, who has also suggested that we might enhance phytoplankton’s capacity to draw carbon dioxide from the atmosphere by (somehow) killing off viruses in the oceans. I doubt he is truly serious. But I also doubted the seriousness, twenty years ago, of people proposing ocean iron fertilization (OIF) as a means of carbon sequestration. Today, research on OIF for geoengineering is endorsed by leading scientists.

Whether or not one takes seriously the idea of global geoengineering with anti-virals, a thought experiment along these lines quickly exposes the complexity of marine microbial systems (give it a try!). In fact, recent field experiments have revealed one of the many possible unexpected consequences; it turns out that when you reduce all the viruses in a sample of seawater you actually decrease the carbon fixation of cyanobacteria, because reduced lysis of heteotrophic bacteria deprives cyanobacteria of essential nutrients they need to grow optimally. In a nutshell, even these simple microbial systems are so complex that it is impossible to predict the consequences of removal of one component.

Just some food for thought.
Penny


CroV, the ocean’s largest microbe

Dear Penny:
It is funny how what at first seems absurd when it comes to virus can eventually become conventional wisdom. The very idea that the ocean harbored many viruses was absurd as late as the 1980s. Seawater just seemed like a terrible place for viruses to survive. But when scientists began to give a close look at the ocean, they discovered otherwise. A single spoonful of seawater might harbor a billion viruses. Most of those viruses proved to be bacteriophages—in other words, they infect bacteria. That’s not surprising, because the most abundant hosts in the oceans are microbes. But what is surprising is the effect that those marine phages have on life in the sea. Viruses kill half of all the bacteria in the oceans every day. As you note, the rupturing of all those cells (known as lysis) dumps vast supplies of nutrients into the ocean, possibly fertilizing other microbes to grow faster. Since the microbes of the ocean pull down huge amounts of heat-trapping carbon dioxide from the atmosphere (and also return a lot of it back there), the overall effect that viruses have on the climate could potentially be huge. I can’t help but find the idea of viruses influencing the climate a bit absurd—but the more I learn about viruses in the ocean, the more accustomed I get to it.

Your speculations about viral geoengineering bring a fitting close to the discussions we’ve been having on this blog over the past month. Once scientists discovered viruses, they began to acquire the power to control them. They were able to develop vaccines and public health measures that could sometimes slow their spread. In many cases, we’ve only had moderate success in controlling viruses, but in a few case—such as those of smallpox and rinderpest—we are now at the point where we could soon eradicate entire species of virus from the face of the Earth.

But the discovery of viruses has also revealed to us that they are not merely things that make us sick and must be eradicated. Phages can kill life-threatening bacteria, for example. For now, however, phage therapy is not standard medical procedure, in part because governments are a bit queasy about approving viruses as living drugs. As your MIT colleague Tim Lu explained last week, he’s taking his research in a different direction, using phages to destroy the biofilms that grow in heating and cooling systems in buildings. In effect, he’s trying to heal architecture. It’s a natural progression from bodies to buildings to the entire planet. At least it’s natural to speculate about using anti-virals to change the global climate. Still, I can’t help but think—what kind of drug store could fill that prescription?

Carl

CONTACT
Carl Zimmer
http://carlzimmer.com/
http://blogs.discovermagazine.com/loom/
email : Mail [at] CarlZimmer [dot] com

EVOLUTION in DAYS
http://carlzimmer.com/articles/2006.php?subaction=showfull&id=1177181182&archive=&start_from=&ucat=9&
Evolution in a Petri Dish
by Carl Zimmer / 2006

Charles Darwin never thought he could witness evolutionary change. He relied instead on indirect clues. He looked at its effects after millions of years — in the fossil record and in the similarities and differences among living species. He got clues to the workings of evolution from the work of pigeon breeders, who consciously chose which birds could reproduce and thus created birds with extravagant plumage. But that was artificial selection — not natural selection that had been operating long before humans came on the scene. Darwin was pretty sure that natural selection worked too slowly for him or anyone else to witness. Darwin got a great many things right, but on this score, he was most definitely wrong. Just ask Paul Turner. In his lab at the department of ecology and evolutionary biology, Turner and his colleagues watch evolution play out in a matter of days. They observe organisms acquire new traits, adapt to new habitats, and become new species in the making.

Turner can hold one of these experiments in his hand. It’s a sealed petri dish. “So here we have a lawn of bacteria,” he says, gesturing to a cloudy smear in the dish. Then he points out a large clear spot in the middle of the lawn, where millions of the bacteria have died. “That’s a beautiful example of a plaque,” he says. There’s a tinge of admiration in his voice. The plaque was made by an organism Turner is particularly fond of: a virus known as phi-6. The virus invades bacteria and uses their cellular machinery to make hundreds of copies of itself. The bacteria rupture, and the new viruses escape. As the bacteria die, they leave behind a clear spot. The plaques are evidence of the virus’s staggering powers of reproduction. In a day, a single virus can produce a billion offspring. From generation to generation their genes mutate, creating opportunities for the viruses to evolve. They evolve so quickly, in fact, that scientists can set up experiments to test ideas about how evolution works. And because viruses carry just a handful of genes, scientists can identify exactly which mutations provide an evolutionary edge. “They’re really one of the few organisms we can study in the lab from nuts to bolts,” says Turner. “We can see the molecular changes.”

Turner has become a leader in a relatively young field: experimental evolution. He is using bacteria and viruses — especially phi-6 — to investigate some of the most profound questions about life on Earth. How do new species emerge? Why do so many species reproduce sexually, when they could just clone themselves? Why do organisms evolve into peaceful cooperators in some cases and ruthless competitors in others? In many of these experiments, Turner and his colleagues are searching for rules that may govern the evolution of all living things. But the research also has a practical side. While phi-6 infects bacteria, viruses similar to phi-6 like to infect humans — including HIV and influenza. New viruses such as SARS are also now emerging. Their emergence is a case of evolution in action: the viruses acquire mutations that allow them to shift from an animal host to humans. Turner’s research may help scientists better understand how that transition happens. “Within our lifetime we’re going to see more and more viruses shift onto humans,” he says. “What are the next likely pathogens to emerge? That’s something we’d like to predict.”

Turner, now 39, started out with an interest in larger fauna and flora. He grew up in upstate New York, where he loved to wander through the forests. “I was the kid who always liked to go to the zoo,” he says. As an undergraduate at the University of Rochester he thought he might like to be a biologist, and in 1989 he started graduate work at the University of California-Irvine. It was when he got to know Richard Lenski that he made the jump from macroscopic to microscopic. Lenski had started his career studying beetles in North Carolina forests, but he had been frustrated by how long it took to run experiments to tease out the forces controlling their populations. Many of the same basic forces also govern the existence of microbes, which breed far faster. And microbes are an ideal lab organism — so small and fast-breeding that scientists can run many trials of the same experiment simultaneously to make sure their results are valid.

So Lenski began running experiments on harmless strains of the gut bacteria Escherichia coli. In one series of experiments, he founded 12 colonies from the genetically identical offspring of a single microbe. Each colony was allotted only a meager supply of glucose. Lenski expected that, with food so scarce, natural selection would favor individuals that grew faster than others. He froze samples of bacteria from many generations; he would thaw them out later to compare them with their descendants. The experiment is still running today, some 40,000 generations later. The bacteria in all 12 colonies have evolved to the point where they can reproduce nearly twice as fast as the microbe Lenski started out with. Lenski (who now teaches at Michigan State University) interviewed Turner at Irvine when he was a prospective student. “Paul had some ideas about investigating carrion — rotting meat — and some of the interesting ecological interactions that might take place there,” he remembers. “Anyone who was attracted to that system, I figured, must be more interested in the questions themselves than in nature and all its beauty.” Lenski suggested that hauling rotting meat into a laboratory might make for difficult experiments, and described his own work. Turner was immediately interested. “I knew then that Paul was my kind of scientist,” Lenski says. At first, admits Turner, “the faith you put into working with things you cannot see was a very foreign concept for me.” But he started running experiments on E. coli to track how genes were gained and lost over the generations. It was only when he had almost finished graduate school that he shifted his research down to the even smaller scale of viruses. A scientist named Lin Chao, then at the University of Maryland, gave a talk at Irvine about his research on phi-6. Chao was using the virus to answer a particularly deep and difficult question in biology: why does sex exist?

Although sex is the only way humans naturally reproduce, some other species do well enough without it. Whiptail lizards in the southwestern United States, for example, are all female. Their eggs require no sperm to begin developing into healthy baby lizards; in essence, they just clone themselves. The late great biologist John Maynard Smith once pointed out that sex should put organisms at an evolutionary disadvantage. It takes two individuals to reproduce sexually, but just one to clone. Over a few generations, that difference should allow a population of cloners to become far bigger than one of sexual reproducers. “Our problem is to explain why sex arose, and why it is today so widespread,” Maynard Smith wrote in 1999. “If it is not necessary, why do it?”

Viruses, Chao recognized, would allow scientists to explore this question like never before. Billions of them can reside on a dish, they reproduce quickly, and some, including phi-6, sometimes engage in their own sort of sexual reproduction. When a single phi-6 invades a host cell, it makes clones of itself. Its genetic material is inserted into the host, and the host begins producing copies of the virus’s genes and pieces of the virus’s protective protein shell. These chunks of genes and shell float around inside the microbe before assembling themselves into new viruses. All the new viruses are clones of the original invader, differing only by whatever mutations emerged as their genes were produced. If two or more phi-6 viruses invade the same cell at the same time, their host produces new copies of both sets of genes — which can then mix together. The new viruses carry combinations of genes from the original invaders. In other words, the new viruses have two (or more) parents. They are the product of viral sex.

Turner was fascinated by the way Chao was using viruses to study a big evolutionary question. And he was struck by the fact that phi-6 could serve as a model for similar viruses that have sex and infect humans — viruses such as influenza and HIV. “I’m living in southern California, and the AIDS crisis is starting to become a big deal,” he recalls. “It was becoming clear that HIV was doing major damage. It all dovetailed.” Turner joined Chao’s lab as a postdoctoral student. They proceeded to design a series of experiments to explore the interplay of sex and evolution in phi-6. They created lines of promiscuous viruses and celibate ones. To make celibate viruses, they kept the ratio of viruses to hosts low, so that each microbe was invaded by just one virus. For the promiscuous line, they made sure the viruses outnumbered their hosts, so that each microbe was infected on average by five different viruses. They allowed the viruses to invade new hosts and replicate for many generations. They then measured how quickly the evolved lines of viruses could replicate compared with their ancestors.

Turner and Chao discovered that the promiscuous viruses sped up their replication. Turner suspects that one important factor behind their success was their ability to trade genes. Imagine that two viruses invade a single microbe. One of them carries an inferior gene that slows down its replication, and the other virus is slowed down by a different inferior gene. When they invade their host, they can produce a superior virus by combining their good genes and leaving the bad ones behind. Viruses may not be alone in benefiting from stripping out bad genes with sex. Other researchers have been examining sexual reproduction in other organisms, and they’ve found similar patterns. Susanne Paland and Michael Lynch at Indiana University recently published a study on water fleas. Some species of water fleas reproduce sexually, while some do not. Paland and Lynch discovered that the asexual water fleas accumulated harmful mutations four times faster than the sexual ones. This sort of genomic hygiene may have played a role in the evolution of our own distant ancestors as well, as they shifted permanently to sexual reproduction.

But the mystery of sex is far from solved. Turner and Chao’s work is proof of that. Viruses that have lots of sex, their experiments revealed, evolve into cheaters. Natural selection favored viruses that could use the proteins made by other viruses in the same cell. By exploiting their neighbors, these cheaters could put more resources into reproducing quickly. “Why do something for yourself, if you can get someone else to do it for you?” says Turner. Cheating is a classic puzzle of science. In 1968, the ecologist Garrett Hardin wrote an influential essay known as “The Tragedy of the Commons.” Hardin asked his readers to picture a pasture open to all the herders in the region. The rational choice for each herder would be to add more animals to his herd. But since all the herders are increasing their herds, they’re making a collective demand on the commons larger than it can support. The herders might try to stave off destruction of the commons by limiting their herds. But this solution can easily come undone, since individuals may still be tempted to cheat. “Ruin is the destination toward which all men rush, each pursuing his own best interest,” Hardin wrote.

The evolutionary parallel might be a species of birds that live on a remote island, eating seeds from a single species of plant. For their long-term survival, it would make sense for the birds not to gorge themselves on the seeds and drive the plant extinct. But natural selection cannot shape instincts to reach some long-term goal. It can only shape the behavior of individuals based on their reproductive success. Turner and Chao demonstrated this in their virus work when they showed that too much sex may be a bad thing (at least from an evolutionary point of view). Viruses that had evolved with lots of sex, they found, became too good at cheating. When viruses that had adapted to a promiscuous life were forced to reproduce on their own, they reproduced far more slowly. “It’s a beautiful study,” comments Lenski. “It’s like the tragedy of the commons on a microscopic scale.”

Unlike other life forms, viruses lack the means to reproduce themselves. Viruses typically get into their hosts by latching onto proteins on the surface of cells and managing to gain passage inside. Different species have different proteins on the surface of their cells. If a virus’s key doesn’t fit a species’ lock, it cannot make that species a host. Turner is intrigued by how that key sometimes changes. A virus may mutate in such a way that allows it to slip into cells of another species. It often takes many of these mutations for a virus to complete such a transition. But it’s clear that viruses do manage to make the transition fairly frequently. Influenza viruses reside in birds and other animals; when a strain evolves the ability to spread quickly from human to human, it can become a pandemic — like the 1918 Spanish flu pandemic, which killed 20 million people before it was over. Scientists are now watching a new strain of bird flu spread across the world, acquiring mutations that allow it to infect humans. It still can’t spread from human to human, but it may be just a few mutations away.

Meanwhile, we are also encountering entirely new diseases thanks to host-shifting viruses. HIV-1 began as a chimpanzee virus. Hunters likely contracted the virus through cuts, and while most of the viruses died off, a few survived. In the 1930s strains of the virus began establishing themselves in humans, and eventually became specialized on our own species. SARS Coronavirus appears to have emerged from civet cats sold in Chinese markets. It’s just going to get worse, Turner predicts. “As the human population continues to grow, we’re a target. We’re also creating agricultural landscapes where there were wild landscapes. We’re driving native species out into the open, and those native species can be reservoirs for viruses.” As serious as the threat of emerging viruses is, scientists still know relatively little about how viruses shift hosts. They cannot, for example, confidently predict which viruses in animals are most likely to colonize human hosts in the future. They still need to understand some of the basic rules of this particularly dangerous sort of evolution.

Turner believes that phi-6 can shed light on some of those rules. Like HIV, it has its own host of choice. The strain that Turner studies lives on plant bacteria called Pseudomonas syringae. Turner is carrying out experiments to see which conditions favor its shift to other bacteria. “Right now we’re at the early stages of looking at those questions,” he says. Turner’s graduate student Siobain Duffy has been studying phi-6 to track the earliest stages of host-jumping. Previous research suggested that viruses face some serious challenges in jumping from one host to another. Instead of a clean leap, viruses apparently had to make a gradual shift. Early in a transition, the virus needed to live in both its new host and its old one. Yet being a jack-of-all-trades may not make much evolutionary sense for a virus. A mutation that made a virus able to invade a new species might interfere with its ability to invade its traditional host. Many studies on evolution hinted at such trade-offs.

Duffy began to search for signs of a trade-off. She prepared lawns of bacteria from 14 different types of Pseudomonas. She then added phi-6 to their dishes and allowed the viruses to infect their new hosts for one day. The vast majority of viruses failed miserably at the task. But Duffy identified 30 mutant viruses that succeeded in creating plaques. Duffy then looked at the genes of the mutants. She focused on a gene that encodes a protein called P3. The virus uses its P3 protein to attach to its host. Since each type of host has different proteins on its surface, it seemed likely that P3 would likely undergo mutations in viruses that could attach to new hosts. She discovered that each of the host-shifters did indeed carry a mutant P3 gene. Remarkably, the mutant genes differed only by a single “letter” from the normal code. That’s all it takes for phi-6 to invade a new host: one random mutation in a single gene could do it. And while the host species Duffy studied were all in the genus Pseudomonas, many are separated by millions of years of evolution.

All told, Duffy identified nine mutations that allowed host-shifting. In some cases only one virus carried a particular mutation; in others, nine shared the same one. To measure the cost of these mutations, Duffy then infected the original Pseudomonas host with viruses carrying each of the nine mutations. When she checked how quickly they reproduced, she found that seven out of the nine mutations caused the viruses to grow more slowly on their original host. The discovery, which she and Turner and their colleagues reported in the journal Genetics earlier this year, marks the first time that scientists have precisely measured the cost of being a jack-of-all-trades. But the other two mutations go against conventional wisdom: phi-6 strains with these mutations can still grow quickly on their old host. In other words, sometimes a virus can be a jack-of-all-trades for free. Duffy also discovered another unexpected result: some mutations discovered in a virus infecting one new host could also let it infect another new host that it had not yet seen.

Does this mean that we’re vulnerable to any virus with a host-shifting mutation? Not quite, says Turner. On their own, these sorts of mutations are not enough to allow a virus to spread into a new species: “It has to mutate and sustain itself long enough to take off.” Turner and his students have been closely observing one host-shifting strain of phi-6, and they find that it grows ten times slower in the new host than the old one. Slow growth can put a new strain of virus at risk. If the viruses aren’t producing enough offspring, they might not find new hosts to infect, and the new strain could become extinct. But Turner and his students have now shown that we shouldn’t take too much comfort in that fact. Turner and postdoctoral researcher John Dennehy are exploring what it takes for a new strain of virus to survive this dangerous passage. Dennehy put a host-shifting strain to the test by forcing it to shift back and forth, between its old and new hosts, four times.

The virus proved remarkably resilient. Dennehy and Turner had expected that, in the trials with small founding populations, the virus strain would become extinct in its new host. Instead, it survived and managed to expand its numbers. Somehow, reproducing in the old host gives viruses an extra boost when they infect the new host. Based on what scientists know about viruses, that shouldn’t make a difference. But it does. “And that’s mysterious,” says Turner. “There’s no good reason for that. It’s like an ecological hangover.” It’s possible, he thinks, that the virus grabbed one or more key proteins from the previous host.

These experiments are just the first steps in Turner’s study of host-shifting. Dennehy is now trying to create experiments that mimic natural conditions more accurately. He hopes to create dishes in which different species of bacteria live side by side. He’s curious to see how the viruses “decide” which species to infect. Duffy meanwhile has been allowing host-shifting mutants to evolve. She wants to see whether they can shift completely to a new host — becoming, in other words, a new species.

The research going on in Turner’s lab hints that viruses are even more adept at shifting hosts than previously thought. They may not have to sacrifice their ability to breed in their old host to begin breeding in their new one. And some viruses may not even need to be “trained” on human hosts. Mutations that allow them to infect rodents or other mammals may give them the ability to invade our cells as well. “It may be easy for viruses to enter a new host type even if they haven’t seen that new host type before. If something is hanging out in a mouse and jumps into a human, maybe that shouldn’t be so surprising,” Turner says. Turner pauses for a moment, noticing that he has caused a visitor some distress at the thought of viruses easily gliding into our species. Witnessing evolution is not always a happy thrill. “Scary,” he says. “Stay healthy. Wash your hands.”

Given the urgency of these risks, Turner finds the continuing debate over creationism versus evolution a dangerous distraction. “I could take somebody into the lab, and over the course of a week, I could prove to them that evolution actually happens in microbes,” says Turner. “And it has been profoundly important in the rise of antibiotic resistance and our inability to make effective anti-HIV drugs. We’d better be aware of it.” the end

http://thecompleteidiotsguidetobeekeeping.com/

Honey and bee : Entombed Pollen
‘Entombed’ pollen is identified as having sunken, wax-covered cells amid ‘normal’, uncapped cells. photo: Journal of Invertebrate Pathology

BAD INDICATOR: ‘ENTOMBMENT’
http://www.guardian.co.uk/environment/2011/apr/04/honeybees-entomb-hives
Honeybees ‘entomb’ hives to protect against pesticides, say scientists
by Fiona Harvey / 4 April 2011

Honeybees are taking emergency measures to protect their hives from pesticides, in an extraordinary example of the natural world adapting swiftly to our depredations, according to a prominent bee expert. Scientists have found numerous examples of a new phenomenon – bees “entombing” or sealing up hive cells full of pollen to put them out of use, and protect the rest of the hive from their contents. The pollen stored in the sealed-up cells has been found to contain dramatically higher levels of pesticides and other potentially harmful chemicals than the pollen stored in neighbouring cells, which is used to feed growing young bees. “This is a novel finding, and very striking. The implication is that the bees are sensing [pesticides] and actually sealing it off. They are recognising that something is wrong with the pollen and encapsulating it,” said Jeff Pettis, an entomologist with the US Department of Agriculture. “Bees would not normally seal off pollen.”

But the bees’ last-ditch efforts to save themselves appear to be unsuccessful – the entombing behaviour is found in many hives that subsequently die off, according to Pettis. “The presence of entombing is the biggest single predictor of colony loss. It’s a defence mechanism that has failed.” These colonies were likely to already be in trouble, and their death could be attributed to a mix of factors in addition to pesticides, he added. Bees are also sealing off pollen that contains substances used by beekeepers to control pests such as the varroa mite, another factor in the widespread decline of bee populations. These substances may also be harmful to bees, Pettis said. “Beekeepers – and I am one – need to look at ourselves in the mirror and ask what we are doing,” he said. “Certainly [the products] have effects on bees. It’s a balancing act – if you do not control the parasite, bees die. If you control the parasite, bees will live but there are side-effects. This has to be managed.” The decline of bee populations has become an increasing concern in recent years.“Colony collapse disorder”, the name given to the unexplained death of bee colonies, is affecting hives around the world. Scientists say there are likely to be numerous reasons for the die-off, ranging from agricultural pesticides to bee pests and diseases, pollution, and intensive farming, which reduces bee habitat and replaces multiple food sources with single, less nutritious, sources. Globalisation may also be a factor, as it spreads bee diseases around the world, and some measures taken to halt the deaths – such as massing bees in huge super-hives – can actually contribute to the problem, according to a recent study by the United Nations.

The loss of pollinators could have severe effects on agriculture, scientists have warned. Pesticides were not likely to be the biggest single cause of bee deaths, Pettis said: “Pesticide is an issue but it is not the driving issue.” Some pesticides could be improving life for bees, he noted: for many years, bees were not to be found near cotton plantations because of the many chemicals used, but in the past five years bees have begun to return because the multiple pesticides of old have been replaced with newer so-called systemic pesticides. Studies he conducted found that bees in areas of intensive agriculture were suffering from poor nutrition compared with bees with a diverse diet, and this then compounded other problems, such as infection with the gut parasite nosema. “It is about the interaction of different factors, and we need to study these interactions more closely,” he said. The entombing phenomenon was first noted in an obscure scientific paper from 2009, but since then scientists have been finding the behaviour more frequently, with the same results.

Bees naturally collect from plants a substance known as propolis, a sort of sticky resin with natural anti-bacterial and anti-fungal qualities. It is used by bees to line the walls of their hives, and to seal off unwanted or dangerous substances – for instance, mice that find their way into hives and die are often found covered in propolis. This is the substance bees are using to entomb the cells. The bees that entomb cells of pollen are the hives’ housekeepers, different from the bees that go out to collect pollen from plants. Pettis said that it seemed pollen-collecting bees could not detect high levels of pesticides, but that the pollen underwent subtle changes when stored. These changes – a lack of microbial activity compared with pollen that has fewer pesticide residues – seemed to be involved in triggering the entombing effect, he explained. Pettis was speaking in London, where he was visiting British MPs to talk about the decline of bee populations, and meeting European bee scientists.


BROUGHT TO YOU BY
http://www.independent.co.uk/environment/nature/exclusive-bees-facing-a-poisoned-spring-2189267.html
http://www.grist.org/article/food-2010-12-10-leaked-documents-show-epa-allowed-bee-toxic-pesticide-
http://www.grist.org/article/2011-01-21-top-USDA-bee-researcher-also-found-Bayer-pesticide-harmful
by Tom Phiilpott / 21 Jan 2011

Remember the case of the leaked document showing that the EPA’s own scientists are concerned about a pesticide it approved that might harm fragile honeybee populations? Well, it turns that the EPA isn’t the only government agency whose researchers are worried about neonicotinoid pesticides. USDA researchers also have good evidence that these nicotine-derived chemicals, marketed by German agrichemical giant Bayer, could be playing a part in Colony Collapse Disorder—the mysterious massive honeybee die-offs that United States and Europe have been experiencing in recent years. So why on earth are they still in use on million of acres of American farmland?

According to a report by Mike McCarthy, environment editor of the U.K.-based Independent, the lead researcher at the USDA’s very own Bee Research Laboratory completed research two years ago suggesting that even extremely low levels of exposure to neonicotinoids makes bees more vulnerable to harm from common pathogens. For reasons not specified in the Independent article, the USDA’s Jeffrey Pettis has so far not published his research. “[It] was completed almost two years ago but it has been too long in getting out,” he told the newspaper. “I have submitted my manuscript to a new journal but cannot give a publication date or share more of this with you at this time.” (I was not able to speak to Pettis for this post as he is in meetings all day today; but he’s agreed to an interview Monday.)

Pettis’s study focused on imidacloprid, which like clothianidin is a neonicotinoid pesticide marketed by Bayer as a seed treatment. The findings are pretty damning for these nicotine-derived pesticides, according to McCarthy. He summarizes the study like this: “The American study … has demonstrated that the insects’ vulnerability to infection is increased by the presence of imidacloprid, even at the most microscopic doses. Dr. Pettis and his team found that increased disease infection happened even when the levels of the insecticide were so tiny that they could not subsequently be detected in the bees, although the researchers knew that they had been dosed with it.”

To my knowledge, Pettis hasn’t spoken to U.S. journalists about his unpublished neonicotinoid research. But he did appear in a 2010 documentary called The Strange Disappearance of the Honeybees by U.S. filmmaker Mike Daniels, which has been screened widely in Europe but not yet in the United States, McCarthy reports. Pettis’ remarks in the film are what alerted the European press to his findings on neonicotinoids. I have not been able to view the film, but I have obtained a copy of the transcript [PDF] of the portion in which Pettis appears. The filmmaker caught up with Pettis at an international conference of bee scientists known as Apimondia in Montpellier, France, in September 2009. Apparently attendees had been buzzing (sorry) about research by Pettis showing that low levels of neonicotinoid pesticide interacted with common pathogens in a damaging way for bees. Pettis and his research collaborator, Penn State University entomologist Dennis Van Engelsdorp, spoke frankly about their findings for the film.

In the transcript, Pettis says he and his research team exposed two sets of honey bees to Nosema, a fungal pathogen toxic to honey bees. One set was also exposed to a neonicotinoid pesticide; the other not. “And we saw an increase, even if we fed the pesticide at very low levels—an increase in Nosema levels—in direct response to the low level feeding of neonicotinoids, as compared with the ones which were fed normal protein,” Pettis says in the film, according to the transcript. Van Engelsdorp stressed that the changes occurred even at levels of neonicotinoid exposure “below the limit of detection.” He adds:“The only reason we knew the bees had exposure [to neonicotinoid pesticides] is because we exposed them.”

This is potentially game-changing research for understanding Colony Collapse Disorder. Scientistshave been focusing on the interaction between the Nosema fungus and a virus called Iridoviridae as the culprit. Pettis’ research seems to suggest that neonicotinoids play a role, too—and at levels so low that researchers may be overlooking them. The grassroots group Food Democracy Now has a petition asking the EPA to ban Bayer’s toxic pesticide clothianidin.

So, let’s get this straight. The chief scientist at the top U.S. government bee-science institute completed research two years ago implicating a widely used, EPA-approved pesticide in what can plausibly be called an ecological catastrophe—the possible extinction of honeybees, which pollinate a huge portion of U.S. crops. Why are we just now hearing about this—and why are we only hearing about it through an obscure documentary filtered through a British newspaper? I’ll be digging into these questions next week. In the meantime, consider this. As I wrote in my December piece on this topic, Bayer’s neonicotinoid pesticides are taken up by millions of acres of corn plants every year and expressed in pollen fed on by countless honeybees. It’s time for the EPA and USDA to be absolutely open about their scientists’ concerns about these poisons—open about it, and willing to act on it.

CONTACT
Jeffery S Pettis
http://www.ars.usda.gov/pandp/people/people.htm?personid=10138
http://www.ars.usda.gov/Research/Research.htm?modecode=12-75-05-00
email : Jeffery.Pettis [at] ars.usda [dot] gov

OLD NEWS
http://www.guardian.co.uk/environment/2008/may/23/wildlife.endangeredspecies
Germany Bans Chemicals Linked to Honeybee Devastation
by Alison Benjamin / 23 May 2008

Germany has banned a family of pesticides that are blamed for the deaths of millions of honeybees. The German Federal Office of Consumer Protection and Food Safety (BVL) has suspended the registration for eight pesticide seed treatment products used in rapeseed oil and sweetcorn. The move follows reports from German beekeepers in the Baden-Württemberg region that two thirds of their bees died earlier this month following the application of a pesticide called clothianidin. “It’s a real bee emergency,” said Manfred Hederer, president of the German Professional Beekeepers’ Association. “50-60% of the bees have died on average and some beekeepers have lost all their hives.”

Tests on dead bees showed that 99% of those examined had a build-up of clothianidin. The chemical, produced by Bayer CropScience, a subsidiary of the German chemical giant Bayer, is sold in Europe under the trade name Poncho. It was applied to the seeds of sweetcorn planted along the Rhine this spring. The seeds are treated in advance of being planted or are sprayed while in the field. The company says an application error by the seed company which failed to use the glue-like substance that sticks the pesticide to the seed, led to the chemical getting into the air. Bayer spokesman Dr Julian Little told the BBC’s Farming Today that misapplication is highly unusual. “It is an extremely rare event and has not been seen anywhere else in Europe,” he said.

Clothianidin, like the other neonicotinoid pesticides that have been temporarily suspended in Germany, is a systemic chemical that works its way through a plant and attacks the nervous system of any insect it comes into contact with. According to the US Environmental Protection Agency it is “highly toxic” to honeybees. This is not the first time that Bayer, one of the world’s leading pesticide manufacturers with sales of €5.8bn (£4.6bn) in 2007, has been blamed for killing honeybees.

In the United States, a group of beekeepers from North Dakota is taking the company to court after losing thousands of honeybee colonies in 1995, during a period when oilseed rape in the area was treated with imidacloprid. A third of honeybees were killed by what has since been dubbed colony collapse disorder. Bayer’s best selling pesticide, imidacloprid, sold under the name Gaucho in France, has been banned as a seed dressing for sunflowers in that country since 1999, after a third of French honeybees died following its widespread use. Five years later it was also banned as a sweetcorn treatment in France. A few months ago, the company’s application for clothianidin was rejected by French authorities.

Bayer has always maintained that imidacloprid is safe for bees if correctly applied. “Extensive internal and international scientific studies have confirmed that Gaucho does not present a hazard to bees,” said Utz Klages, a spokesman for Bayer CropScience. Last year, Germany’s Green MEP, Hiltrud Breyer, tabled an emergency motion calling for this family of pesticides to be banned across Europe while their role in killing honeybees were thoroughly investigated. Her action follows calls for a ban from beekeeping associations and environmental organisations across Europe. Philipp Mimkes, spokesman for the German-based Coalition Against Bayer Dangers, said: “We have been pointing out the risks of neonicotinoids for almost 10 years now. This proves without a doubt that the chemicals can come into contact with bees and kill them. These pesticides shouldn’t be on the market.”

PREVIOUSLY on SPECTRE : COCAINE as METAPHOR
https://spectregroup.wordpress.com/2009/01/24/cocaine-as-metaphor/
A HIVE IS NOT JUST BEES
https://spectregroup.wordpress.com/2008/07/21/a-hive-is-not-just-bees/

TREATMENT-FREE BEEKEEPING
http://www.beeuntoothers.com/index.php/resources/microbe-refs
http://www.kirkwebster.com/index.php/collapse-and-recovery-the-gateway-to-treatment-free-beekeeping
http://www.kirkwebster.com/index.php/a-practical-plan-for-removing-all-treatment-from-commercial-apiaries
A Practical Plan For Removing All Treatment From Commercial Apiaries

Hobby beekeeping in America is obviously going to survive and thrive in the future. A small, but certain percentage of the population will always be fascinated by honeybees and want to be around them as much as possible—even if they don’t make a living from them. During these times when honeybees are always facing possible destruction by parasites, weather, pesticides or some combination of factors, and the basics of successful beekeeping have become unclear, these “amateurs” are the people who can and do experiment with every conceivable management practice until some of their methods succeed on a regular basis and then spread throughout the community. This pool of energy and enthusiasm, along with a strong and growing dedication among hobbyists to keeping bees without treatments, will ensure that a new, healthy beekeeping will eventually emerge, and also create a new generation of professional beekeepers who started with one colony, and eventually gave up other work in order to pursue bees full-time.

But it’s the commercial part of our industry that’s really having trouble now. There are a much smaller number of commercial beekeepers today than there were ten years ago, and no matter how much economic success someone may have had in the last few years, most of the community considers everything to be at risk, and watches with great concern the continuous decline of honeybee health and resilience. In an attempt to maintain a certain cash flow or standard of living, the focus remains fixed on killing mites and other parasites instead of using them as allies and assets, and on artificially propping up the bees in unhealthy situations (like almond pollination). In a large apiary with many investments spread out in different parts of the country and relatively few skilled people riding herd on all the bees, it can be very difficult to make basic changes, even when the desire is there.

I don’t think any of us who have managed to live from treatment-free beekeeping for the last several years would claim to be immune from the problems and concerns of the industry in general. But in the end the focus in health and the work of making the transition to non-treatment has made beekeeping much less stressful and more enjoyable, and has given us much hope for an interest in a positive future for beekeeping. It’s arguable now that treatment-free beekeeping can be just as profitable as any other beekeeping scheme. But these things were not easily won. In a certain sense it’s not all that complicated. My friend Chris Baldwin likes to say: “The people who are succeeding with untreated bees now are the ones who quit treating their bees.” But these were not people who were giving up or looking for an easier way. They were people who had made a commitment to a healthier future for beekeeping and had already done considerable thinking and working in that direction before they backed off their treatments. When I went through the process of gradually eliminating the treatments from my apiary, I didn’t know what I was doing and made many costly mistakes. There were no good models to follow at that time—at least for bees in the kind of environment where I live.

But things are different now. The number of beekeepers who are functioning without treatments is larger every year, and their collective experience and knowledge is growing and becoming more solid. As usual, there’s lots of speculation about what is really happening, biology-wise, in these cases. Don’t waste too much energy worrying about this. Scientists get paid to study these kinds of problems, and they will certainly share their results with you after they have impressed their peers by publishing an elegant paper in the right journal at the right time. Meanwhile, it’s much more fun and profitable to focus on the basics of healthy beekeeping, pay attention as you work, learn from your mistakes, and build on your successes. In North Carolina last fall, Greg Rogers summed up honey production in the Smokey Mountains for me this way: “We know where, but we don’t know why.” In getting rid of the treatments in your apiary, you don’t always have to know why in order to know how.

After watching this process go on for more than ten years, and listening to and observing others as they go through it, I think it’s possible now to recommend a more specific, 4-year plan to other commercial beekeepers who want to continue with beekeeping in the future, and who understand that the underlying health, stability and resilience of their bees is the only really stable foundation for such a business in the long run. Short-term profits (sometimes very large ones) have been made in the past by exploiting the bees and using them as hard as possible. In the future, and over a working lifetime, the largest profits (in both money and a decent lifestyle) will go to those who abandon the focus on profit and concentrate instead on the “wild” health and resilience of their bees, while resolving to live themselves on the by-products of this process. The self-organizing, creative power of Nature needs to be tapped as the primary energy source, and this is accomplished by working with the four essential elements of “Wild Farmers Getting Horizontally Minded” (explained last month).

If Nature is willing to move from point A to point B, she always has more than one way to make the journey. There are undoubtedly more ways than one to eliminate the treatments from an apiary, but I’m describing here a way that has already been pioneered by myself and others. I made the transition without going into debt, but I made many mistakes, and the overall economic trajectory of the apiary was disrupted while the transition was in progress. Some income was lost as the mites carried off the poorly adapted bees, but this income has been largely or entirely recovered in recent years as the industry in general declines, and the value of bees, queens and honey from untreated colonies increases. With what is now known and available, I have no doubt that many apiaries could go through this process with a much smaller immediate economic disruption, or even none at all. The key is to re-organize the apiary around the principles outlined above, and take advantage of the growing demand for untreated bees, and the queens that produce such bees.

Preparation:
There are six things an apiary must have at the outset in order to successfully make the transition to non-treatment. I would be afraid of investing time and money in this direction if any one of these six were missing or unobtainable.
1. Good Food for the bees.
2. Clean Combs and/or the ability to draw new combs quickly.
3. Resistant Bees—Stock that already has proven itself capable of surviving and thriving in untreated situations for at least two years.
4. Mating Control—one way or another, at least 75% of the drones mating with your queens must come from your own colonies.
5. The ability to Raise All Your Own Queens and Requeen all your colonies annually.
6. A good Attitude.

Now let’s go back through these in reverse order, starting with the most critical one—having a positive Attitude: I remember hearing a radio spot about an Iowa farmer who consistently produced the highest per-acre yield of corn in the state, by quite a wide margin. Eventually he was persuaded to give a series of workshops about his methods. He always began by stating: “The most important thing in growing a good crop of corn is having a good attitude…” After a few more minutes of talk like this you could hear the pencils snapping in the background as the assembled farmers broke them with their hands or their teeth in frustration. They came to find out how deep to plow or how many pounds of this or that to spray on the crop in order to achieve a record yield. But instead most of what they heard was about how important it was to imagine what it’s like to be a corn plant, and what’s necessary to keep growing rapidly through changing extremes of moisture, heat and drainage. When he finally mentioned his choices of varieties and fertilizers, it was almost identical to what most people in the room were already using. It was his genuine love of the corn plant, and his constant attention to his plants and all aspects of the growing environment over many years that enabled him to consistently produce a record crop.

Commercial beekeeping without treatments is only for people who love Nature and their bees, who personally manage and work with their bees every day, and want to stick with beekeeping over the long haul. It’s important to be a farmer first, and a broker of bees and bee products second. Embracing the methods of Nature can mean opposing or ignoring the recommendations of the larger community or their spokespeople, who may have something to sell and are still operating on the assumption that pesticides and other agricultural chemicals are and always will be essential. Let’s not forget that beekeepers have always been among the most inventive and independent-minded people in every society.

One of the extremely important and powerful tools that Nature uses to help insects recover from a serious shock is the process of rapid decline and then expansion in a population in order to change the genotype and activate defenses that were not functioning previously. This is one of the most difficult things for production and profit-oriented beekeepers to embrace in a positive way; but so far all the evidence says there is no way to move to a stable and resilient beekeeping future without using it to our advantage. Look at the way varroa mites recovered over and over, after out most determined efforts to kill every last one of them, and how they adapted and became immune to even the most deadly poisons. Honeybees have the same ability to adapt, rebound and become stronger than they were at the beginning of the process; but only a few people have so far made good use of this principle. With what we know now, the process can be controlled, and the declines kept to a manageable level. There still needs to be planning and preparation for a possible loss of production and income, but this is no different than having contingencies ready for poor weather or low prices—things farmers and beekeepers have always had to deal with. Over the last few years several beekeepers have told me they’d like to give up their treatments, but they could never withstand a 40-50% loss of their colonies. The trouble is that many commercial beekeepers have now experienced losses on this scale (sometimes more than once) and have not been able to use the situation to create better bees and beekeeping for the future.

The second prerequisite for moving away from treatments is having the ability to Raise Your Own Queens and Requeen at least 75% of your colonies each year. This is important for “pulsing” new stock rapidly through the apiary as treatments are withdrawn. The first couple of years when colonies are left unprotected are the most difficult, and having all young queens of a tested stock is the best offense here. Embedded in this suggestion are two important principles: The first is to reduce the number of colonies per beekeeper—in large part to make sure all colonies can be requeened every year, at least for the first few years. In the end this will lead to greater intensity of production (explained in the March 2008 ABJ) and much more enjoyable and profitable beekeeping. The second is to utilize Nature’s ability to recover after a shock by increasing the rate of reproduction when conditions are favorable. In practical terms this usually means increasing the rate of making new colonies. A powerful way of doing this is to start two nucs in each box instead of one. Then, when mites and parasites weed them out, even a 50% loss will only take a few boxes out of productive use. I’ve described my methods for doing this in detail in the past, and so have several others.

Mating Control is the third essential ingredient in this recipe. Your new queens must mate with your breeder queens from the previous year (via drones from the daughters of those breeders). Any of the three methods of mating control (Instrumental Insemination; Natural Mating in Isolation; and Drone Saturation) can be used to produce bees that don’t need treatments. It’s interesting that each of these three schemes will lead your apiary off in a somewhat different direction genetically, over several generations, even if they start with the same breeders. Drone Saturation shifts the apiary genotype more slowly than the other two options, but this method yields the most stable and diverse gene pool in the long run, and is in any case the only practical option for most commercial beekeepers.

Most of my own bees are located in the Champlain Valley of Vermont, where it’s very crowded with bees belonging to several different owners, each pursuing a different program. I first set up an isolated mating yard in the mountains above the valley when tracheal mites came, and I planned to use it for breeding bees resistant to this parasite. The extra time and effort required to mate queens in isolation proved unnecessary in this case because most stocks already present in the valley already had the ability to adapt quickly to this new pest, after recovering from the initial shock and after the most susceptible colonies had perished. Few treatments were applied, and soon the open mated daughters of outstanding survivors were doing just as well as sister queens mated in isolation. But the experience gained in setting up that first isolation apiary served me well later when varroa came and it became clear that queens grafted from proven survivor stock had to mate with drones representing other proven survivors in order to eliminate treatment pressure on the mites, and make steady progress from one generation to the next. I’d be afraid to start on this now unless I was quite sure that at least 75% of the drones mating with my new queens were coming from my own selected colonies.

Before you start eliminating treatments across the board, you want to stock your equipment with Resistant Bees—daughters of proven survivors if possible. Even here you want to be careful and seriously consider what to start with. Some colonies that can live without treatments with no problems do not pass on that ability to their daughters, even when carefully mated to other survivors. It’s safest to get your foundation stock from a large pool of bees, collectively managed and succeeding without treatments—or at least with very infrequent treatments—over several years. This is evidence that the ability to co-exist with mites and viruses is both present and heritable. The only bees of this sort that I can recommend based on experience are the Russian stocks, which are soon to be available from an expanded network of certified breeders. They already have a large enough gene pool to prevent inbreeding depression, and a carefully worked out mating scheme—so you can purchase unrelated stock every season for several years if necessary. The Russians have advantages and disadvantages for most beekeepers. On the plus side I put first of all their strong and easily heritable ability to co-exist with mites and virus, as well as their overall resilience and “wildness”. They are at the same time very gentle, frugal bees that winter exceptionally well with small clusters. The main buildup starts later than with most other bees, but then proceeds very rapidly, and they are extremely good honey gatherers. The only things I don’t like about them are the frequency of swarming, and a relatively weak desire to draw comb in the spring. (It’s not an issue for me, but they also don’t mix with other, non-Russian bees as well as Italians do). The people who are doing well with these bees and really like them are all removing brood in the spring, creating a smaller brood nest during the swarming season; and then producing a honey crop in mid-summer or later. Beekeepers who need a lot of bees in the spring or depend on an early honey flow have difficulty dealing with the strong swarming urge. I hope there are other broad-based survivor stocks out there that are suitable for others to use for beekeeping without treatments. A few are being advertised—you should question both the producers and some of their customers closely if possible before devoting a lot of space to them in your apiary. The purpose of writing this is so that you can create your own uniquely adapted stock of healthy and resilient bees—so this gene pool of untreated bees can continue to grow.

Clean Combs are the next requirement for any kind of healthy beekeeping. This implies the ability to draw new combs rapidly—at least 20% of your total comb number per year, and more is better. The source of wax for your foundation is a concern, but the truth is I don’t know of the best plan for dealing with this problem, or how important it really is. I devoted a huge amount of time, energy and money setting up a system to make the small number of sheets (2,000-4,000) that I need every year, from my own wax. Now that it’s done I consider it a vital and fascinating part of the apiary but I’ll be the first to admit that it takes a lot of time. Finding a manufacturer who will make foundation for you directly from your cappings wax would be theoretically the best of both worlds, but this is hard to arrange. According to the folks at Penn State, there may be some effective techniques for filtering contaminates out of wax, so this may recede as a problem as time goes on. I don’t like plastic foundation, but I do keep some of it on hand for emergencies, and buying it unwaxed and rolling on wax of your own sounds like a workable compromise to me.

I should say at this point that it is not necessary to have some certain cell size in your combs in order for bees to adapt to non-treatment. Now, if I am found dead with a stake driven through my heart shortly after you read this you will know where to find the murderer—among the small-cell people. I tried to work with smaller comb size, but my breeding program progressed much faster than my ability to change combs. Now I have combs with worker cells throughout the natural size range (5.1-5.4 mm), and my foundation mill prints out a 5.2 size pattern. It’s far more difficult and costly to establish a large number of existing colonies on small-cell combs than it is to propagate promising stock and survivors, and step up the rate of colony reproduction to offset heavier than normal losses during the “collapse” phase. As far as I can tell, every commercial apiary that is functioning successfully without treatments went through exactly the same pattern of collapse and recovery—no matter what size combs they were using. They did share one thing when they made the transition however: They all had combs that were not seriously contaminated. So, replacing your combs and stabilizing mite control with formic or oxalic acid are important things to accomplish before the transition to non-treatment.

The last requirement for that transition is the most obvious of all; Good Food and a healthy environment for the bees—as essential to their health as it is to ours. Having the opportunity to visit with beekeepers from several different parts of the U.S. and Canada has made it very clear that I have better, natural food, and a more healthy environment for my bees than many commercial beekeepers have access to. This is partly because I live in a relatively clean, dairy farming region with a wide variety of good nectar and pollen sources, and partly because my bees are not subjected to the stress of moving. A lot of research and work has been done recently around supplemental feeding, and hopefully this can fill some of the gaps in our environment that industrial farming has created. But I don’t think there’s any real substitute for clean, bee-gathered nectar and pollen, and I’d be afraid to try weaning bees off their crutches and props if they couldn’t stay in one place, with good nectar and pollen, for at least six months of the year. So now, after all this preparation, the actual 4-year transition process is fairly straightforward. Be prepared for a period of comparative chaos as unselected stocks are mixed together in the first two years and losses increase in the third and possibly fourth year.

Year 1: Management can vary, according to location and whether you migrate or not, but the goal is the same: Requeen all colonies with queens raised by yourself from promising survivor stock you obtained from elsewhere. Graft from several different queens and raise extra small nucs to replace queens that fail later in the season. Keep track of which queens came from which breeders, and continue treating the apiary with formic and/or oxalic acid.

Year 2: Same as year one, except graft from different promising stock obtained from elsewhere. This year your new queens are getting mated (75% or greater) with your breeder queens from the year before. By the time your new queens are laying their second round of brood, your apiary is filling up with worker bees that have promising survivors for both mothers and fathers. Keeping track of the families is more important this year because these queens will be the foundation stock of your own untreated families in year three. Decide whether to make one last treatment in the spring of Year 2. Carefully evaluate the necessity of artificially lowering the mite population on more time against the possible damage to your new, extremely valuable queens and a longer wait before being able to tell for certain which colonies are really thriving without treatment. Begin propagating nucs at a faster rate to compensate for the increased loss of colonies in Year 3.

Year 3: Now you’ve reached the really chaotic part. Your bugs may be a hybridized mix of stocks you were not familiar with in the past, and their behavior is all over the map. Even worse, colonies are starting to fail, and you will feel like someone trying to quit smoking and have to force yourself not to get out the heavy artillery and kill the mites another time. Don’t panic. You’ve allowed the element of Wildness to come into your apiary, and now is your chance to get it to work for you. This year you should graft principally from your own stock—the best of what you raised the year before. This is when keeping track of the families is important to avoid inbreeding depression in the future. Resist the temptation to graft entirely from just a few of the best looking colonies and try to find at least two good daughters from each of the breeders you used the year before. From this point on, each time you choose a grafting mother you are potentially starting a new family that could be very important in your apiary for many years to come. In year 3 you are mating the best of the crosses you made from imported, untreated stock, with the total gene pool you have so far imported. I recommend that in Year 3 you do about 20-30% of your grafting from more imported, promising stock—as a source of new, unrelated families, and because your own bees are not fully tested yet; not enough time has elapsed since the last treatment. Year 3 is also when you really see the importance of increasing nuc production and/or starting two nucs in each box. The extra queens and colonies keep most of the equipment in production as the apiary goes through the “collapse” part of the natural cycle, while bees and mites begin adapting to continuous co-existence.

Year 4: With a little luck from the weather, during Year 4 you should start to see and feel some really positive momentum resulting from all your hard work, as the apiary calms down and enters the “recovery” part of the natural, insect-challenge cycle. By the end of the year, the great majority of your worker bees will have both fathers and mothers selected by a joint committee consisting of yourself, the two mites, viruses and all the other known and unknown parasites and challenges that are part of the environment where you live. Mites and other factors select for survival, vigor, overall fitness and resilience; and you finish the process by selecting again for the desirable economic and beekeeping characteristics. Over the next few years, the bees will become much more uniform, as you have “boiled down” your gene pool until only combinations that are both good survivors and good economic producers remain. The important thing now is to start the gene pool growing again, first by maintaining at least 12-15 families, founded upon unrelated, or only slightly related, breeder queens; and second by starting a new family each year from a small amount of outside stock. This provides a constant source of unrelated genetic material “bleeding” slowly into your apiary to compensate for that which is lost as you continue to select for your favorite traits. Hopefully in the future there will be many more untreated apiaries to buy and trade stock with.

There will be other downturns and challenges in the future—but now you have a way of dealing with them, and also benefitting from them. By selection, rapid turnover of queens and the acceleration of nuc production, many difficulties can be overcome. After the bees recover from a shock, the work habits already in place will yield a surprising number of extra colonies, queens and queen cells. The sale of these products can equal or exceed the income lost during the “collapse” years of the cycle. These extra bees and queens can help reverse the nationwide downward trend in colony numbers and serve as the foundation for a more stable, healthy and satisfying beekeeping in the future.

As long as this essay has become, the information and advice it contains still needs to be amended and adapted to each new situation. You can get suggestions and hear about the experiences of myself and others, but only you can figure out the best way to run your apiary without treatments. We’re not using the healing and creative power of Nature in commercial beekeeping now; and we never will until more people stop treating their bees and propagate good stock out of that new environment.

GROW YOUR OWN
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by Kirk Webster /

Now, I had been warned, but I was still not prepared for the difference in attitude and ambiance I would encounter at the 2nd Annual Treatment-Free Beekeeping Conference in Leominster, Massachusetts in late July 2010. If you are genuinely looking hard for a positive new vision of beekeeping for the future–this is an event you must attend. Most of the 100 or so attendees were hobby beekeepers and some wanna-beekeepers. So there was plenty of naive, positive energy there, to be sure. (We need a certain amount of that sort of energy.) But there was also, among both presenters and attendees, an astonishing variety and depth of practical and successful experience with bees kept without treatments of any kind. Aside from this meeting’s overall ambiance, the thing that struck me most was the balance somehow maintained between an overall awareness of the gravity of current beekeeping problems, and the simplicity, ease and elegance of the solutions arrived at in very different locations and circumstances. Almost all of these solutions, however, were only won after a very difficult struggle; and all of them required the cultivation of an open mind and learning how to allow Nature’s multifaceted powers of resilience and recovery to function without impediments. All of those who have achieved this with bees are pioneers at this point. Many of them have been ignored, ridiculed, harassed or even worse, as part of their reward for achieving something deemed “impossible” by “experts”; or by those who are always trying to co-opt the end result while other people do the work. (As in all other worthwhile endeavors, it’s not possible to have real, long-term success with honeybee health without doing the work.) All of this makes our pioneers all the more determined to share what they know with all honest and genuine comers– making it easier in the future than it was in the past. The completely open nature of all the conversation, the willingness to help and share, and the absence of competitive and proprietary feelings were all very striking at the Leominster meeting.

At the same time, it must be stressed that there were no special recipes or any single, infallible road to success revealed. In fact, some of the presenters have completely opposed views on certain points. The overall message of the conference I would summarize in three statements:
1. There are now both commercial and hobby beekeepers succeeding with untreated bees, in many parts of the world and using an astonishing variety of equipment, stocks and techniques.
2. There are good examples, shared experience and guidance available to help people who want to move toward non-treatment; or to start off that way from the beginning.
3. Many of the non-treatment beekeepers have had similar experiences, but in the end each beekeeper discovers his or her own combination of stock, equipment and management that works for them in their situation. There is no substitute for steady attention and work– applied in your own location.

As the presenters got up to give their talks, one after another spontaneously burst out with what a huge relief and pleasure it was to be at a meeting entirely devoted to a healthy future for bees and beekeeping, with everyone freely sharing whatever they have to contribute. The gravity of beekeeping’s current plight was kept always in mind, but the shared convictions about destructive agricultural practices and the correct way to overcome them created a huge sense of relief and shared energy for just about everyone who came to this meeting.

Here’s the cast of “characters” who presented at the 2010 Leominster meeting, and a brief description of their work and message:

Dee Lusby‘s name is known to everyone who has made even a half-hearted search for knowledge about treatment-free or “organic” beekeeping. As far as I know, she has the only commercial apiary in Europe or North AmErika that has been completely free of treatments since before the varroa invasion. Her bees are in Arizona’s Sonora Desert, between Tucson and the Mexican border. She and her late husband Ed, (a descendent of one of the oldest beekeeping families in the U.S.) pioneered the use of small-cell sized foundation and combs for control of parasitic mites and overall bee health. Their pioneering work–which was so far ahead of its time– their independence and long-term success, and their outspoken defense of their practices have generated a huge amount of controversy that continues up to the present. Dee’s talks are sometimes hard to follow due to the many esotErik references cited, and frequent mentions of the fights she’s had to wage with an Establishment with different aims and methods than her own. But if you can separate the “heat” from the “light”, what lies beneath is a very broad understanding of honeybee health, and one of the best blueprints so far available for keeping bees healthy in the long run. Her assertion that the solution to our honeybee problems is one third genetic, one third management, and one third environmental is, in my experience, completely bulletproof. Let the detractors say what they want, she still maintains 800 colonies with minimal help and produces several varieties of beautiful desert honey. She helps to organize a treatment-free conference every year in Arizona, and invites the attendees to see for themselves that her bees are healthy and vigorous in a difficult environment. Some of the major equipment manufacturers are now making and selling small-cell foundation, so the cell-size controversy is likely to be resolved as more people try it out and weigh in. I’d been in touch with Dee and Ed off and on by phone for many years, and it was a great pleasure to meet her in person for the first time last summer. My own untreated apiary has evolved into something quite different from Dee’s, but she and Ed provided a lot of the initial inspiration and courage necessary for me to pursue this path.

Another presenter, Sam Comfort, is a beekeeping tycoon. Well… he’s the biggest top-bar beekeeper in the Northeast. Actually, he’s not very tall or heavy, but he does have more top-bar colonies (around 200) than anyone I know of except maybe Wyatt Mangum in Virginia, or Les Crowder in New Mexico. I always thought it would be great to have a top-bar hive or two and see what the bees would do inside; but I shuddered at the thought of trying to make a living from them. But Sam seems to be doing well selling top-bar boxes and top-bar nucs in the Hudson Valley.

Just out of college, Sam cut his teeth working for a couple of Vermont beekeepers, and later learned how to raise queens for them in South Carolina. He worked for another couple of outfits in Florida, before heading to Montana to work for a honey and pollination business based there. As Sam tells it, he worked pretty hard for a couple of years, and also built up a hundred or so colonies of his own– which he was allowed to bring along on the trucks to the almonds, and collect the pollination fee. I guess he always lived in the company trailers, and didn’t have much opportunity to spend money. So his back wages built up for quite awhile, and when he left and his employers bought out his bees, they had to pay him in one shot what a new doctor or a tenured professor might make as an annual salary. This allowed Sam to “retire” for awhile, and try to figure out an easier way to live around bees. That’s when he came back to his old haunts in the Hudson Valley, reverted to his hippy ways, and started his top-bar apiary (anarchyapiaries.com)– keeping it completely untreated from the beginning. Sam brought some top-bar hives to the conference, and enjoyed manipulating them for us in his shorts and sleeveless T-shirt, without shoes or even a smoker. Some of us think Sam should be a little more responsible, but he does have a very large and entertaining store of beekeeping experience for someone as young as he is… Oh yes, he’s also written some great songs about what it’s like to be a worker, drone, or queen; and to be honest some of us strongly resent the fact that, no matter how smelly or dirty he is, the young women all cluster around him like flies around molasses…

Corwin Bell, another top-bar beekeeper from the Denver/Boulder Colorado area, has a wonderful and hilarious presentation about how he became a beekeeper, and all the painful lessons he had to endure in order to unlearn his initial training and allow the bees to thrive on their own. He now oversees a huge swarm “rescue” network of volunteers who save unwanted swarms and establish them in top-bar hives. His other career is in computer mapping, so he has a computer map of the location and status of all these semi-feral colonies, now numbering in the hundreds. Many of these hives are continuously occupied for several years, with almost no care or interference. Some of his apprentices are now starting spin-off programs in other western locations. (backyardhive.com)

Erik Osterlund has been one of my earliest, most steadfast and best friends during the years of struggling toward treatment-free beekeeping. Many long phone conversations have occurred between my home in Vermont and his in Sweden. Last summer marked the fourth time I’ve had the privilege of meeting him in person– each time here in the U.S. Erik works part-time as editor of the Swedish beekeeping magazine (Bitiningen), and part-time as a commercial beekeeper. In both of those capacities he has travelled to many distant countries to observe and report on bees, mites and beekeepers who have managed to live together in harmony. He was a long-time associate and disciple of Brother Adam, and still follows closely the breeding protocols of his mentor. The bees he has now are derived from Buckfast stock (which is quite popular in Sweden) with the addition of apis mellifera monticola, which he obtained on an expedition to Kenya together with other Scandinavian beekeepers.

I’ve described Erik many times as “the best prepared for the varroa invasion of any beekeeper I know, or can imagine.” Varroa didn’t reach his part of Sweden until three years ago, so he had to observe, test and select his bees in other mite-infested locations before the parasite reached his home apiary. He also downsized all of his combs to 4.9 size cells before the mite invasion. (More on this next month). Erik’s wide experience in both research and practice, his calm demeanor and deep religious faith gave the meeting a wonderful grounded quality, which might have been impossible to achieve by the rest of us AmErikan iconoclasts.

Mike Palmer is a very accomplished honey producer from Vermont who now has a rapidly growing queen and nuc production branch of his apiary as well. He is still using treatments on his bees, but we have hope for Mike, and he has fully embraced the principles of selection and rapid mid-summer propagation of nucleus colonies, which were essential to the success of myself and others who no longer treat. Mike likes nothing better then sharing what he knows, and he gave some great lectures and demonstrations about his methods, as well as his take on the current state of the honey market.

As part of the Vermont contingent, I put in my two cents, but my biggest contribution to the meeting may have been to convince Chris Baldwin to stop fretting over grasshoppers for a few days and join us in Leominster. Chris is a honey producer who raises his queens and nucs in Texas in the spring, and produces honey in S. Dakota during the summer. Aside from the Weavers, he has the largest apiary of untreated bees that I know of–1500-2000 honey producing colonies– and is also my best example of how larger apiaries can move to eliminate treatments. Chris got on board with the Russian bees a couple of years after I did, and just like all of us early converts, he endured some serious losses along the way, including an episode in July 2006 when two-thirds of his bees died in one day in S. Dakota when the temperature reached 124 degrees (F). But, by propagating his best survivors, flooding his mating area with his own drones, and rapidly propagating new colonies, his bees are now not just survivors of mites and virus, but also record high temperatures and even trips to the disease cesspool of California almonds. Unfortunately, despite his great success with breeding and propagating bees, his apiary has been held hostage for several years now by a terrible weather cycle in his part of S. Dakota. In addition to being a great beekeeper, Chris is a great guy who loves to share and help others, and we hope he can come to the meeting again next year. (southbeekota.com)

The cast of presenters was rounded out by Julian Wooten of N. Carolina, who gave an impromptu and entertaining talk about supplying the bees and training the actors for making the film: The Secret Life of Bees. And the last official talk was given by James Fearnley of Nature’s Laboratory LTD in England. Just as we were starting to become jaded by too much of a good thing, James roped us all in again with his fascinating accounts of a long career with beehive and botanical pharmaceuticals, and how these things are going to be absolutely essential to maintaining human health in the future. We all hope to see and hear more of him in the future as well.

Now, there’s one more show to report on, and I saved the best for last. These great presentations, the wonderful atmosphere and special camaraderie would never have come together in the same place if it wasn’t for Dean Stiglitz and Ramona Herboldsheimer. As far as I can tell they did 99% of the event planning and organization; and even with a good sized crew of family and friends helping out, they still managed to do about 60% of the work during the conference– including teaching a two-day beginners course and giving presentations themselves on management and hive microbes.

Dean and Ramona started out as many hobby beekeepers do now, struggling for years to keep their new package colonies alive, despite following all the standard advice. After hearing about, and then working with Dee Lusby, the bee fever really descended on them and took over their lives as they abandoned the “shoot-em-up” defensive school of beekeeping, and embraced a more positive and pro-active approach. Now they are basically trying, with their own bees, to find out how many of Dee’s management ideas are suitable for New England. They also have started bottling and selling different honeys from treatment-free apiaries. It’s noteworthy that they were sought out by the Penguin Group (of publishers) to write the beekeeping volume for the “Complete Idiot’s Guide” series. Penguin, on their own, decided this was the best way to portray beekeeping in general, and this is the only post-varroa book I know of entirely devoted to treatment-free beekeeping. (Other than needing more photos, it’s very good.) And then, in their spare time, they organize the conference…

It would be hard to imagine anyone doing a better job of organizing an event than these two did. The venue was beautiful, set in a preserved tract with footpaths thru the surrounding forest and fields. There were nice airy rooms inside and plenty of outdoor tables for eating and visiting. The food was wonderful, and anyone with the nerve to complain about the cost of the meeting should just save their money for a few trips to McDonalds– since the food by itself was worth more than the fee for the entire meeting. The talks were arranged so that a story line emerged and built on itself as the meeting progressed, and every evening people relaxed around the campfire, visiting, singing songs and telling stories into the wee hours…

Earlier I recommended this meeting to everyone searching hard for a more positive vision of beekeeping’s future. Dean and Ramona have found a new venue for the 2011 meeting that can accommodate both more people and more bees. So make your reservation soon (at beeuntoothers.com). It’s OK to be concerned and upset about the plight of the honeybee, but please bring an open heart and mind, and leave your pessimism and proprietary notions at home.