Kirsten Weir

This isn’t the first big pet food recall to come down in recent years. In December 2005, more than 100 dogs died of liver failure after eating food manufactured by Diamond Pet Foods. The products contained corn tainted with aflatoxin, a toxin released by a naturally occurring crop fungus. Aflatoxin should have been detected at any number of testing points along the way from cornfield to finished product, says Donald Smith, dean of the College of Veterinary Medicine at Cornell University. “For some reason, something didn’t happen in the testing process,” he notes.

Unlike the aflatoxin outbreak, the latest recall involved chemicals that no one knew to look for. The products produced by Menu Foods contained wheat gluten and rice protein concentrate contaminated with the industrial chemical melamine, a flame retardant and component of some plastics. Earlier this month, government officials reported evidence that the foods may also have contained cyanuric acid, a chemical often found in swimming pools. The chemicals apparently triggered kidney failure in dogs and cats that ate the tainted foods.

The Chinese companies that produced the wheat and rice proteins allegedly spiked the products with chemicals in an attempt to dupe buyers; high in nitrogen, the chemicals made the products appear to contain more protein than they actually did. It’s safe to say that American pet food manufacturers didn’t intend for melamine to wind up as an additive in their kibble. “The problem was a toxin,” says Tony Buffington, a professor of veterinary clinical sciences at the Ohio State University. “If you put arsenic in someone’s tea, it’s not the tea’s fault.”

Maybe not, but the recalls have served to highlight vulnerabilities in the manufacturing of processed foods — both pet and human foods. Weaknesses in pet food regulation may have contributed to the recalls, says Smith. Or, he says, it may have been a matter of luck that this time, the melamine ended up in the dog’s bowl and not your own. “This has been a canary in the mine,” he says. “It’s a wake-up call.”

Pet owners like Melissa Hull, a small-business owner in southern Maine, have certainly taken notice. Hull admits she and her husband “were definitely aware of potential scary things” in their cat Smokey’s commercial pet food, even before the recall. But the incident drew new attention to the fact that so many pet food ingredients originated on the opposite side of the globe, in countries like China that “have no FDA,” she says. “It definitely opened our eyes to just how poor the quality is.”

Earlier this month, Sen. Dick Durbin of Illinois and Rep. Rosa DeLauro of Connecticut introduced legislation to upgrade the country’s food safety system, both for humans and their pets. Among other things, the legislation would give the FDA authority to order mandatory food recalls and would establish uniform federal standards for pet food. As it stands now, pet food falls into something of a regulatory gray area.

Most states follow pet food guidelines published by the Association of American Feed Control Officials. These regulations touch on everything from labeling to contaminant testing to nutritional requirements. But the guidelines are only suggestions, and AAFCO itself has no regulatory authority. “Most of the routine day-to-day pet food regulation is performed by the states,” explains AAFCO Pet Food Committee chairman David Syverson, and state laws and enforcement programs vary. At the federal level, the FDA’s Center for Veterinary Medicine requires that animal feed be “pure and wholesome” and “safe to eat,” but there’s currently no requirement that pet foods have FDA approval before they hit store shelves.

Another weakness, Smith points out, is the lack of a federal agency to monitor outbreaks of illness or disease in pets. The Center for Veterinary Medicine has received thousands of complaints from pet owners who believe their dogs and cats were poisoned by melamine. But tracking disease, Smith says, isn’t part of the agency’s mandate. Even if it were, it simply doesn’t have the budget to do it. “We don’t have an equivalent of the Centers for Disease Control in companion animals,” he says.

While pets may not have their own CDC, they do have a place in our hearts. Sixty-three percent of U.S. households own cats or dogs, and people drop more than $15 billion each year on pet food. They’re a loyal bunch, says Duane Ekedahl, president of the Pet Food Institute, a lobbying group that represents the manufacturers of 98 percent of the dog and cat food produced in the United States. According to Ekedahl, Pet Food Institute surveys found that consumers are more loyal to their pet food brand than to any other products in the supermarket, with the notable exception of soda.

So what, exactly, is in those cans and bags we pet owners buy so loyally, month after month? “Protein is really the most important ingredient in the nutrition of a carnivore,” says Jean Hofve, a Denver veterinarian and former official liaison to AAFCO. But not all protein is created equal, and therein lies the problem.

Consider that checkerboard classic, Purina Dog Chow. Ingredient No. 1 is ground corn, followed by poultry byproduct meal, animal fat and corn gluten. Purina Cat Chow is similar, with poultry byproduct, corn meal and corn gluten taking the top three spots on the ingredient list. Real meats like chicken, beef or lamb are nowhere to be found. “There aren’t enough high-quality ingredients to make all the pet food sold in this country,” Hofve says. “Somebody is using the crap.”

Traditionally, much of the protein in pet food comes from animal byproducts. The pet food industry nicely parallels the human agricultural industry, providing a convenient way for food producers to use up the spleens and bones and chicken feet that American consumers don’t have the palate for. Even diseased and dying animals are allowed in pet food, as long as they’re processed in such a way to destroy any microorganisms, Syverson says. All of those myriad pieces and parts end up as appetizing ingredients like “poultry byproduct meal,” “meat-and-bone meal,” and “animal digests.”

Pet food is also a handy way for meat processors to get rid of brains and spines from cows and sheep — the parts with a high risk of housing prions, the rogue proteins that cause bovine spongiform encephalopathy, or mad cow disease. While such parts are banned from human foods and from animal feed intended for cows and other ruminants, they’re A-OK for the family pet. No dog has ever been diagnosed with a mad cow-like disease, but as many as 90 cats in the U.K. are known to have contracted feline spongiform encephalopathy. Most of those cats are thought to have snacked directly on raw scraps from butchers, and according to Syverson, the FDA considers the threat to American cats “minimal.”

The good news for pets and owners is that animal byproducts in pet food may not be as gruesome as feared. For years the pet food industry has been, well, dogged by persistent rumors that meat from horses and from euthanized cats and dogs finds its way into pet food. “They do not use horse meat,” Ekedahl says, and “as a condition of membership, [Pet Food Institute members] affirm that none of their rendered material will contain cats and dogs. The public just wouldn’t stand for it.”

So we’re probably not feeding cats and dogs to our cats and dogs. Of course, a quick glance at the ingredient lists of that Dog Chow (and most other major brands) reveals that much of the protein doesn’t come from animals at all. “Glutens and soybeans and rice protein concentrate — those are cheap substitutes for real meat,” Hofve says. “Protein is the most expensive ingredient, and it’s the one that’s going to get shortchanged.”

Hofve takes issue with grain-based pet foods for nutritional reasons. But she also notes that, whether it’s a coincidence or not, most of the major pet food recalls have been associated not with the poor-quality meat byproducts used in pet food, but with grains.

In the case of melamine, the contaminated grain products slipped across the border undetected. The 2005 aflatoxin contamination, on the other hand, involved corn grown on American soil during an unusually wet and fungus-prone summer. According to Ekedahl, most of the meats and grains used in pet foods are produced in the U.S. But “there are some ingredients that come in from overseas, because that’s where they’re available,” he says.

Certain vitamins and additives are generally imported. The amino acid taurine, for example, is almost exclusively produced in China. Taurine is an essential additive for cats; they must get the amino acid from their diet or risk suffering blindness and heart damage. Other ingredients, particularly vegetable proteins, are also frequently imported. “Take wheat gluten — that’s not an inexpensive ingredient,” says Ekedahl. “The primary availability of wheat gluten is in China, and we get a very fine product from China.”

But Cornell’s Smith points out that availability and price go hand in hand. In fact, he says, U.S. producers of wheat gluten “have not been working at full capacity because they’ve been outbid by foreign suppliers.” Despite the recent scandal, Ekedahl says most pet food manufacturers plan to continue doing business with those foreign companies. “For the most part, they have great confidence and long-term relationships with their suppliers,” he says.

Pet food manufacturers have been running scared since the recent recall. A spokesman for Natural Balance Pet Foods said the company, besieged by calls, had stopped speaking to the media. Repeated phone calls to other major manufacturers, including Purina, Procter & Gamble (the makers of Iams), Hill’s Pet Nutrition and Menu Foods were not returned.

To be fair, even those critical of the major pet food manufacturers, such as Hofve, admit the melamine contamination was something of a fluke. No one tested for it because no one expected it to ever turn up in food products. Most American pet food manufacturers generally “do a pretty good job of testing,” she says. Human foods are recalled much more frequently than are pet foods, she notes. “When I started looking at pet food, I became really afraid about what was going into pet food, but I was even more afraid about what goes into human foods,” she says.

While pet food may not be uniquely vulnerable to contaminants, however, cats and dogs themselves may be more sensitive to them. Our pets are usually a lot smaller than we are, and they eat the same thing day after day. “Because we eat a lot of different foods, toxins that come in are diluted,” Hofve says. “If we ate one thing all the time like most pets do, we’d be in a lot more trouble. Variety really is the spice of life, and our pets should eat variety too.”

Hofve practices both traditional and holistic veterinary medicine for cats. She’s convinced that the ingredients in most commercial pet foods are harming our animals, contributing to conditions such as diabetes and obesity. “The amount of carbohydrates and the quality of the protein [in most commercial diets] are damaging to health over time,” she says. “Our pets are carnivores.”

AAFCO’s Syverson acknowledges that proteins aren’t entirely interchangeable. Lamb and wheat gluten contain different sets of amino acids. But along with the glutens and the bone meals, commercial pet foods contain additives (such as the taurine imported from China) to ensure that they are “complete and balanced,” Syverson says. That’s good enough for him. The Syverson family dog lived to age 18 on an inexpensive diet of grain-and-beef-byproduct kibble.

Buffington, the Ohio State veterinarian, also believes that most pet food is nutritionally complete. “Many people are concerned about ingredients. I think those concerns are misplaced,” he says. He suspects that some dogs and cats, like some humans, may have genetic predispositions to certain diseases. In pets as in humans, those diseases may be “unmasked” by something in the environment or the diet. But American pets being fed sufficient quantities of commercial pet food are hardly malnourished, he says. “From a nutritional point of view, deficiencies are nonexistent [in pets] in North America.”

With disagreement even among vets, it’s no wonder many consumers resign themselves to buying the same old bags of pet foods time and again. A trip down a supermarket’s pet food aisle is a lot like a trip down the cereal aisle — dozens of choices, Technicolor packaging, and big, bold marketing claims. You can find pet foods that minimize hairballs, keep your cat’s urinary tract squeaky clean, or protect your pooch with vitamin-packed spinach and beets.

It goes without saying that Rover and Tiger aren’t selecting their own food. Health-conscious humans stocking up on blueberries and pomegranates for their antioxidant punch naturally want to do good by their furry family members. Yet any given ingredient — carrots, for example — only needs to make up 3 percent of the pet food’s total weight for the phrase “with carrots!” to appear in colorful block letters on the front of the bag.

“Many companies will put a token amount of vegetables in to have a label presence,” says Peter Atkins, president and co-founder of Natura Pet Products, one of a growing number of small “holistic” pet food producers. “Does it do anything for the dog or cat? The answer is no.”

While ingredients like antioxidants probably are beneficial in high enough quantities, “most haven’t been fed in trials to understand what effects they have,” says Quinton Rogers, a professor of veterinary medicine at the University of California at Davis, and a member of the National Academy of Sciences’ Committee on Nutrient Requirements of Dogs and Cats. “There is so much faddism in human food as well as pet food,” Rogers says. And despite the bevy of health claims listed on pet food labels, only two FDA standards for pet foods actually exist: growth formulas for puppies and kittens, and maintenance formulas for adults. “Everything else is fluff and marketing,” Hofve notes.

Don’t tell that to Natural Balance’s Dick Van Patten or to Natura Pet Products’ Peter Atkins, who whips out an analogy of his own to describe the difference between average pet food and small niche brands like his. “It’s like buying a Hyundai or buying a Mercedes,” Atkins says. “You can get basic nutrition or you can get top-of-the-line holistic nutritional support.”

For pet owners who want nothing but the best and have money to burn, top-of-the-line nutritional support may be out there. But let’s face it. The average American doesn’t have a great record of questioning the ingredients in his own food (Olestra, anyone?), let alone those in his pet’s.

A wild cat might not eat oats and wild dogs may not crave corn, but after thousands of years of domestication, our pets aren’t truly wild. A feral cat might subsist on birds or chipmunks, but it probably won’t sleep on your feet or live to age 20. “There have been a lot of cats and dogs raised on various pet foods their whole lives, without any observable problems,” Rogers notes.

That doesn’t mean there isn’t room for improvement. McDonald’s now serves salads, after all, and the $15 billion pet food industry, too, may have to change if customers demand it. Although the Menu Foods scandal is only the latest in a line of recalls, its size and scope have placed pet foods on the public’s radar screen. “This is a catharsis for the industry,” Atkins predicts. “At the end of the day I think it will be for the better; we’ll take a real strong look at where ingredients originate and make sure companies are vetted and ingredients checked very thoroughly.”

Hofve hopes the latest recall will force change, but she’s skeptical that the government will put its money where our mouths are. The entire annual budget of the FDA is around $2 billion; only a fraction of that is spent on inspecting the foods eaten by people and their pets. Food safety hasn’t been a priority for the feds, Hofve says, yet the recent outbreak of toxins in pet food “is nature’s way of saying: Pay attention.”

During the last year, geoscientists have held several workshops and conferences to discuss what is known — and the great deal that isn’t — about the “deep carbon” cycle. Next week, at the annual meeting of the American Geophysical Union, scientists plan to hold a special session devoted to one potentially frightening aspect of that cycle: a strange little substance known as methane hydrate.

Methane hydrates, or clathrates, are icelike gas deposits buried under permafrost and deep below the seafloor. Some researchers fear that the hydrates are on the verge of melting en masse and belching out a cloud of methane gas that will send global temperatures skyrocketing.

The doomsday scenario goes something like this: If global temperatures keep rising, some methane hydrates will melt, sending methane gas bubbling up through the ocean and into the atmosphere. Like any good greenhouse gas, the methane will trap heat close to Earth’s surface, causing temperatures to climb even higher. Hotter temperatures will melt more hydrates, and on and on. In other words, methane hydrates could trigger the mother of all feedback loops. The story, says David Archer, a geophysicist at the University of Chicago, “has a great apocalyptic side to it.”

Methane is the same natural gas that we burn for fuel. Under the right combination of intense pressures and chilly temperatures, the gas becomes trapped inside icy cages of hydrogen bonds. These methane hydrates look like chunks of ice, with the nifty difference that they eagerly burst into flame when sparked. Methane hydrates are also a lot less stable than your average ice cube. If the temperature rises or pressure eases, the hydrates essentially melt to form methane gas.

Methane hydrates aren’t unusual, astronomically speaking. They exist on Mars, inside comets, and on at least a couple of Saturn’s frosty moons. Here on Earth, they form deep below permafrost and under seafloor sediments, where temperature and pressure conspire to keep the structures stable. It’s not certain how much methane is locked up in hydrates, but some estimates put the total as high as 10,000 gigatons, says Gerald Dickens, a professor of earth sciences at Rice University. To put it in perspective, he says, “the estimates for all of the oil, gas, and coal [on Earth] is about 5,000 gigatons.”

As a greenhouse gas, methane is in the big leagues, some 20 times as potent as carbon dioxide. If all the methane trapped underground were to wind up in the atmosphere, you could kiss your winter boots goodbye. “There is so much [methane hydrate] in the ocean that if you gave the planet a big shake and it came out all at once, it would be a climate disaster far worse than anything we have with carbon dioxide,” Archer says.

Are we giving the planet that kind of shake? To predict the future, climate scientists begin by peering into the past. Human-induced global warming may be a new trend, but Earth has certainly experienced rapid and dramatic climate changes in its ancient history. Methane hydrates may have played a role in a period of abrupt warming 635 million years ago, according to a paper published in Nature last spring. The researchers, from UC-Riverside and Flinders University in Australia, point to high levels of methane present in the atmosphere at that time.

Around 55 million years ago, Earth again shifted abruptly from snowy to steamy. Many researchers have fingered hydrates in that warming spell, too. “Methane hydrates may not be the only explanation, but very likely played a large role,” says Carolyn Ruppel, a research geophysicist with the U.S. Geological Survey, who will co-chair with Dickens the upcoming American Geophysical Union panel on hydrates.

James Kennett, a professor of earth sciences at UC-Santa Barbara, is a vocal proponent of the idea that methane hydrates have played a role in past climate changes. He also fears they are poised do so again. “The gas hydrates are inherently unstable with warming of the oceans. I can’t see why [melting hydrates] would not be inevitable,” he says. “The question is just how sensitive the system is.”

Kennett argues that much of the geological research community has turned a blind eye to the evidence of methane hydrate’s role in climate change. “It’s a paradigm problem. The community is not prepared at this time to make a paradigm shift,” he says. “[Climate change] is the biggest issue of our time. I think we need to look at this.”

He suggests we start by taking a cold, hard look at the Arctic, where a great deal of methane hydrate exists in permafrost and under the continental shelf. Because of the extreme cold, hydrates are stable at shallower depths in the Arctic than anywhere else on Earth. Warm up the Arctic a bit, and these shallow hydrates will be the first to come apart, Kennett warns. “Is this already happening? Are we living in it now?”

Kennett has valid reasons for wondering. Inside the Arctic Circle, the ocean is reportedly bubbling like a freshly uncorked magnum of Dom Perignon. In September, scientists aboard a Russian research vessel described methane gas fizzing up from the seabed in several areas of the Arctic. Just a few days later, British scientists exploring the ocean west of the Norwegian island of Svalbard reported hundreds of these methane plumes.

It all sounds pretty ominous, but researchers aren’t ready to attribute the recently observed methane bubbles in the Arctic to melting hydrates. Scientific reports of the plumes have not yet been published or peer-reviewed. Although Kennett is fearful of a methane catastrophe, he’s not yet sure this is it. “I need to be convinced,” he says.

He’s not the only one. For one thing, says Archer, “there weren’t observations before, so it’s hard to say if it’s a new phenomenon.” Perhaps methane has been sputtering up from the Arctic for decades, with no one around to see it. What’s more, many potential sources of methane exist. As bacteria break down thawing organic matter, they release the gas as a byproduct. “There’s all this juicy organic carbon preserved in these areas,” Archer points out. “These methane escapes could be from decomposing peat.”

Ruppel, too, is a long way from ringing any alarm bells over the Arctic bubbles. “Perhaps people are jumping to conclusions before the story is really clear in the Arctic,” she says. “My suspicion is that almost all of that methane has nothing to do with gas hydrates.”

But let’s imagine, for the sake of argument, that the Arctic gas plumes do turn out to be from methane hydrates. Does that mean it’s curtains for life as we know it? Not necessarily.

“Methane beneath the permafrost is probably the most sensitive to change, but it’s a small component of the total amount [of methane hydrates],” Dickens says. The vast majority is buried deep below the seafloor, he notes, and would be considerably harder to unlock. “At deep water depths, temperature would have to change 10 or 15 degrees Celsius to remove all the methane,” Dickens estimates. “It would be very difficult for all of it to come out.”

For that matter, adds Archer, it would be very difficult for even a portion of it to come out. “It would be arrogant to say it’s impossible, but nobody has come up with a mechanism to get even 10 percent of this methane into the atmosphere,” he says.

Even if methane hydrates did start melting, the gas would have to travel through hundreds of meters of mud and thousands of meters of water before it could mix with the air. “A lot of methane would dissolve in ocean waters,” Ruppel says. “The ocean is very undersaturated with methane. It could accommodate a whole lot before the methane would get out into the atmosphere.”

Furthermore, Dickens adds, it’s not enough to show that methane can travel from the deep ocean to the atmosphere. One also has to consider the rate. “It is possible in the future that large amounts of methane can come out of these systems,” he says. “Is it probable that significant amounts will come out in the next 100 years? Probably not.”

Archer is also skeptical of the importance of methane hydrates in ancient global-warming events. “The evidence for these things being important for climate change in the past, I think, is kind of dodgy,” he says. True, something released a lot of carbon into the atmosphere 55 million years ago. But maybe, he suggests, that something was a volcanic event that spewed methane gas, or a bunch of carbon-rich sediments that were suddenly lifted above sea level and exposed to the air. “There’s no real clear smoking gun that it was methane hydrates,” he says.

Ruppel says there’s definitely more to learn. “I think the jury is still out on this,” she says. But she doesn’t see any reason for panic. The story that methane hydrates are a looming catastrophe “is a position some of us are working hard to counteract,” she says.

In fact, much of the effort put into studying methane hydrates isn’t focused on global warming at all, but on energy. The U.S. Department of Energy is taking a close look at mining methane hydrates for fuel, and they aren’t the only ones. Countries including Japan, China and India are also exploring ways to turn hydrates into usable energy. “It is getting to the point now that methane hydrates could definitely become a viable commercial source for natural gas within the next 10 years,” Ruppel says.

As a fuel, methane hydrate has some advantages. It’s more accessible than conventional natural gas resources, Ruppel points out. And it is cleaner to burn and emits about half as much carbon dioxide as does coal. “Natural gas is probably the greenest of the fossil fuels,” adds Archer.

But it is a fossil fuel, after all, and human-induced global warming is still a very real phenomenon. So will methane hydrates fuel our future, or destroy it? That may be the ultimate question, but not an easy one to resolve. For those willing to try, “it is a very interesting time in this field,” Ruppel says. “We need more good science. I think we’re moving in that direction, but it will be a few years before we have the answers.”

In the meantime, panic over methane hydrates is probably premature. “There is a tendency in some quarters to latch on to a catastrophism scenario,” she says. “That may sell newspapers, but it may not be the most responsible way to portray the science.”

If you’re the publisher of a sensationalist newspaper, take heart. There’s still a good deal to fear when it comes to climate change. “I think the trajectory we’re on with CO2 is very likely to lead to droughts that would be destabilizing to civilization. Another thing I worry about is sea-level rise,” Archer says. “I think we have plenty to worry about with CO2. We don’t need methane hydrates in order to be very reasonably frightened about the future of our climate.”

Biologists named the syndrome for the unusual white fungus growing on the muzzles and bodies of many of the dead and dying bats. But most bat biologists believe the fungus is a symptom of WNS rather than the cause — an opportunistic infection running amok in an already weakened bat. What’s behind the deaths? Scientists don’t know exactly, but they know the condition’s deadly. Indeed, it looks as though WNS is to bats what colony collapse disorder is to bees, another baffling lethal syndrome.

“This is the worst crisis I’ve ever seen,” says Merlin Tuttle, founder and president of Bat Conservation International. “I think anytime you have animals as ecologically essential, and as distantly related, as bees and bats dying en masse, it should send a canary-in-the-coal-mine signal.”

Bat experts are working hard to decipher that signal. So far, they have more questions than answers. More than a few wildlife biologists have raised concerns that the bat deaths may stem from the way humans are treating our shared habitat. They are taking a close look at the impacts of pesticides, pollutants and possibly even climate change on the miniature mammals. “Bats are very good at living in high-stress environments,” says Elizabeth Buckles, a wildlife pathologist at Cornell University College of Medicine. “But they’ve reached some kind of threshold where they can’t adapt anymore.”

Insect-eating bats fluttered around North America for millions of years before humans appeared on the scene. The winged mammals don’t get the love that birds and bunnies do, but they fill a crucial environmental niche. A bat can eat half its weight in insects every night; if the female bat is lactating, it swallows twice that.

Bats have three favorite food groups: flies, moths and beetles. Mosquitoes (a member of the fly family) carry disease like West Nile virus, which has killed hundreds of species of birds in the United States and infected some humans, too. Many moths and beetles, and particularly their larvae, are serious agricultural pests that can destroy crops from apples to zucchinis.

“Bats are major ecological role players,” says Tuttle. “They keep vast numbers of insects in check — insects that cost farmers and foresters billions of dollars in losses every year.”

The first signs that bats were in trouble showed up in New York two winters ago. The animals normally spend the winter months tucked inside caves and mines known as hibernacula. During routine surveys in 2007, staff from the New York State Department of Environmental Conservation discovered unusually large numbers of dead and dying bats lying in the snow outside the caves. The bats were thin, and many had an unusual white fungus growing on their faces. “It was very obvious to me that this was something new,” says Al Hicks, the mammal specialist at the department who sent out the first warning cry.

By this winter, the mysterious malady had spread beyond New York to Vermont, Massachusetts, Connecticut and, most likely, Pennsylvania. Tens of thousands of bats perished. In the New York caves where WNS was first identified, 80 to 100 percent of the hibernating bats were lost. Of the six species that hibernate in colonies in the Northeast, WNS has struck five, including the federally endangered Indiana bat. The sixth species in the area, the big brown bat, is on the “suspicious” list.

It’s all too easy to identify an afflicted cave, says Hicks. The ground outside the entrance is often littered with dead bats, and the white fungus is visible on many, though not all, of the animals. The bats are also extremely thin. They awaken and leave the caves months ahead of schedule, apparently because they lack the necessary fat stores to sustain them through their winter slumber. “The animals that have been recovered have been devoid of fat reserves,” Hicks says. “They’re starving to death.”

Cracking the mystery is proving particularly challenging because scientists know so little about healthy bats. “We haven’t known much about basic bat biology before this,” Darling says. “That is science’s little secret: We really don’t know a lot of what people think we know, or what people think we should know.”

Back in the woods, Darling identifies his squirming catch as a male little brown bat, the most common species in the area, and the hardest hit by WNS. “This bat looks pretty healthy,” he says, sounding pleased and somewhat surprised. Just then, he gets a call on his cellphone. His colleagues at another site down the road report they’ve already snared 10 bats, so he sends me over to take a look.

When I arrive I meet up with Kristen Brissee, an enthusiastic wildlife technician in her mid-20s. She’s removing bats from cotton storage bags strung up along the back of the Fish and Wildlife truck. She checks their body condition and attaches tiny metal I.D. tags to their wings. She gently spreads the wings of an Indiana bat and points out small white spots indicating scar tissue on the wing membrane. Another bat has several small holes in its wing.

Scientists suspect this wing damage is somehow connected to WNS. Some have theorized it may be caused by cold exposure when bats leave the caves prematurely and encounter icy winter temperatures. Others suggest the damage is caused by the fungus itself. Early studies turned up many different kinds of fungi growing on the bats, suggesting they were secondary infections thriving on already compromised bats. Recently, though, a common fungus species has been isolated from the sick bats. Ward Stone, a wildlife pathologist at New York’s Department of Environmental Conservation, is growing the fungus in his lab. It seems to thrive in cold environments, like the chilly caves where bats spend the winters. “We think it’s a brand-new species,” he says.

Stone is working to put a name on the fungus and learn more about its biochemistry. The white stuff seems only to infect the surface of the bats’ skin. So far, Stone hasn’t found evidence that the fungus is infecting the bats internally. Nor has Buckles, who is also working to characterize the fungus at her Cornell pathology lab. Some investigators have suggested it may be an itchy irritant that prompts bats to wake up and groom themselves when they should instead be hanging around in a state of suspended animation. Yet that hypothesis doesn’t fully explain the dramatic loss of fat reserves in the animals.

One possible explanation for the skinny bats is simply that they’re entering hibernation in poor shape in the fall, without the fat they need to get through the long Northeastern winter. Perhaps there’s a problem with their insect prey base, or an illness preventing them from putting on weight. “The other alternative is that they’re coming in fat and happy, but something is happening while they’re hibernating that causes them to burn up their fat reserves really quickly,” Hicks says.

To Stone, that “something” is people. “We are involved — oh, yes, we are involved,” he says. Human-induced climate change is at the top of his suspect list.

Stone hypothesizes that dry summers over the past few years may have caused a decrease in the bats’ insect prey, and that warm spells in recent winters may have triggered bats to awaken and burn up energy, which they couldn’t replenish. “It would appear they were burning a lot more energy than they were taking in,” he says. Climate change may have also allowed for the spread of the white-nose fungus, which may have been hiding under our noses for years, he says.

Despite his strong convictions, Stone can’t explain how a warming climate would favor the spread of a cold-loving fungus, and he doesn’t yet have evidence to directly link climate change to any of the symptoms of WNS. Stone has some respectable achievements under his belt; he was the first person to identify West Nile virus in the United States. But he’s something of a contrarian, and hasn’t convinced many other scientists of his theory. At a recent meeting of bat biologists, Darling says, the majority of attendees agreed that global warming was not a leading hypothesis.

That doesn’t mean humans are off the hook. Many researchers say it’s likely there is no WNS silver bullet, and that the syndrome may be caused by a thorny combination of factors. “Are they exposed to a new fungus? Is there a toxin depressing their immune system? Is there a problem in their food supply?” Buckles wonders. “Most diseases are multifactorial. We’re not in a situation where we can rule anything out.”

Buckles has looked for high levels of contaminants like lead and PCBs, and for chemicals from pesticides or other environmental toxins. The Northeast is downwind from the rest of the country’s pollution, and all manner of agricultural pesticides are introduced into the landscape each year. Again, though, no obvious suspects have emerged. However, a pair of researchers in the Midwest recently uncovered intriguing data that hints pesticides may be involved.

John Whitaker is a biologist at the Center for North American Bat Research and Conservation at Indiana State University. Several years ago, he and collaborator Kathleen Dannelly, a microbiologist at ISU, discovered an enzyme called chitinase in the guts of bats. This enzyme breaks down chitin, the major component of insect exoskeletons. But mammals weren’t known to produce chitinase. Digging deeper, the pair discovered a garden of chitinase-producing bacteria in the bats’ intestines. The scientists concluded that the beneficial bacteria were helping bats draw energy from otherwise indigestible insect parts.

Whitaker dissected some hibernating bats. He found no fresh food in their stomachs — not surprising in the middle of winter. But he did find pieces of chitin, presumably left over from the bats’ summer meals. Whitaker and Dannelly believe the chitin pieces stored in the bats’ guts are slowly digested over the winter, giving the bats extra energy to get through the season. So when they heard about a new syndrome causing bats to waste away while they hibernated, they were eager to take a look.

Whitaker and Dannelly examined 12 little brown bats from New York, all found dead in caves where WNS was rampant. Inside the bats, they found plenty of chitin. “We could see bug legs and wings,” says Dannelly. But the chitinase-producing bacteria were harder to come by. She took multiple samples from each of the bats, up and down the intestinal tracts. She found extremely low numbers of the beneficial bacteria in one bat. In the remaining 11, she found none at all.

Dannelly’s hunch is that a toxin may be killing off the symbiotic bacteria in the bats’ intestines. “Maybe they’re using a new pesticide [in the Northeast] and it’s becoming more widespread,” she suggests. Theoretically, bats could take in traces of a pesticide with their food or drinking water. If the chemical wiped out the beneficial bacteria, the bats couldn’t break down the chitin in insect parts. It’s the energy from that chitin, Whitaker believes, that may give bats the boost they need to survive the winter.

According to Dannelly, at least one relatively new pesticide is known to be toxic to chitinase-producing bacteria. “So far nobody has been able to tell me if it’s used in the New York area,” she says. She declines to give pesticide names, since she doesn’t have evidence implicating any specific chemical. And she and Whitaker admit their data isn’t perfect. They examined only 12 sick bats, and they weren’t able to examine healthy bats from the Northeast to use as a control. Instead, they compared the gut bacteria of sick bats with those of healthy little brown bats from Indiana. Their findings are “a powerful clue” that the disease may be linked to a loss of beneficial bacteria, Whitaker says. But it’s not an answer. “We haven’t proved it yet.”

He and Dannelly are hoping to get their hands on more bats to boost their sample size. Meanwhile, they’re attempting to calculate exactly how big a role chitin plays in the bats’ total energy needs, in both summer and winter. Whitaker adds, with slightly detectable disappointment, that his idea hasn’t gotten much attention from his colleagues. The theory “hasn’t risen to the top of the pile,” admits Hicks, who has emerged as the de facto leader of the WNS investigation. Then again, he says, “nothing much has. We’re fishing now. Anything that shows potential, we’ll pursue.”

While lab scientists such as Buckles and Stone continue to pursue the fungal clues, field biologists like Darling are keeping tabs on the health of the bats, hoping to have a better sense of the animals’ condition when they enter hibernation this fall. By Darling’s count, more than 25 agencies and institutions are contributing to the effort.

They may not all see eye to eye on which angles to pursue, but nearly everyone agrees the syndrome could be disastrous to the bat population. Bats can live up to 30 years, and females give birth to just one pup per year. At that rate, it could take a very long time for a broken bat population to recover. The animals migrate hundreds of miles between hibernacula and summer foraging grounds, mingling with bats of other species and from many states. In its first year, WNS spread between 80 and 130 miles from the apparent epicenter in Albany, N.Y. “I’m afraid it could spread right across the country,” says Hicks.

Darling worries that caves that appeared healthy last winter may have been in the early stages of the syndrome. “It may progress in such a way that it takes a couple of years for sites to be maximally affected,” he says. If that’s true, “we might be facing a really traumatic winter for the bats.”

On the evening I spend bat-trapping with Darling, his primary mission is to catch a female Indiana bat and fit her with a radio transmitter. If all goes as planned, the transmitting bat will lead him and his team to the maternity roost, a tree where a mass of mother bats and their pups sleep off the daylight hours. If he can find the tree, he can better estimate the size of the endangered bats’ reproductive population.

On this night, the team is energized by success. Two female Indiana bats land in the net within the first two hours. Both are lactating (a fact that wildlife technician Brissee establishes by squeezing the tiny bats’ even tinier teats to look for milk), and will likely be heading to the maternity roost as day breaks. The biologists carefully glue the minuscule transmitters to the animals’ backs and, one at a time, set them free.

It’s just after midnight and the cloudless Vermont sky is overflowing with stars. We watch the last bat fly off, beeps from the transmitter antenna growing fainter as the female flutters away into the darkness. It’s a magical moment, and I want to be optimistic for this bat and its kin. But white-nose syndrome hasn’t offered much reason for optimism. “It could be years before we have an answer,” Darling had told me earlier, as he trudged through the tall meadow grass with a squeaking bat in his hand. “I’m not sure the bats have that long to wait.”

Thompson grew into a wildly affectionate, completely lovable, moderately rotund adult cat. He outgrew most of his extreme behaviors, but one trait persisted. Thompson is a biter. He bites frequently and hard. As I climb into bed at night, he’ll dart from a dark corner and lock his jaws around my ankle, ears back and eyes wide, like a lion taking down a wounded gazelle. But five minutes later, all is forgotten. He pads clumsily back to bed, tucks his head under my chin and stares up at me with an expression of pure, unwavering love. He purrs, so happy he drools, until we both fall asleep.

Thompson’s nearly 7 now, and we’ve moved on from that speck-size studio to a large Maine loft that we share with my husband and our dog. Much in our lives has changed, but the biting has remained a constant — one for which I’ve become adept at making excuses. Yes, Thompson has the jaw force of a puma, but he never uses his claws. So I simply stocked up on Band-Aids, bought red bedsheets that would mask the bloodstains, and resolved to suck it up and take the bad with the good.

And then I discovered the Cat Whisperer.

OK, so that’s not really her title. Mieshelle Nagelschneider is a cat behaviorist who is in no way affiliated with Cesar Millan, the trainer-star of the television phenomenon “The Dog Whisperer.” Nagelschneider is, however, working with a major television network to develop an upcoming cat behavior show of her own. She can’t reveal too much about it yet, since the network people are still hashing out the details. Alas, it probably won’t be called “The Cat Whisperer.” But given that there are 13 million more pet cats than pet dogs in this country, she may very well be poised for Cesar Millan-style fame and glory.

Assuming, of course, that cats can be trained. And plenty of people, including me, were skeptical. Dogs wag and slobber and will do just about anything to please us, whether it’s chasing down a tennis ball 27 times in a row, or dragging an unconscious master from the crackling flames of a burning bedroom. Cats, if you’re lucky, might sit on your lap and purr. Our feline companions don’t exactly have a reputation for malleability.

Think again, Nagelschneider said. “You don’t use the same techniques on a cat as you do on a dog, but they’re definitely trainable,” she assured me the first time we spoke. “Cats are motivated by what’s in it for them.”

Nagelschneider, now 37, studied psychology in college but never finished her degree. She worked as a veterinary technician and cat sitter and, over time, developed a protocol for modifying cat behavior. In 1999 she officially opened her Cat Behavior Clinic, in Portland, Ore. Nagelschneider has six cats of her own, not to mention three dogs and what must be one very anxious cockatiel.

Nagelschneider has boned up on behavior theory, flying across the country to take animal behavior classes at Harvard. She estimates that over the years, she’s consulted with tens of thousands of clients, mostly by phone. Nagelschneider is no pet psychic, and she doesn’t necessarily need to meet a cat in person to diagnose its problem. Her goal isn’t to train cats, per se, but to teach their owners to get inside the minds of their feline friends.

I started my consultation by filling out a questionnaire about Thompson’s behavior and home environment. I described in detail his two main issues: the biting, of course, and also his need for attention. In the hour or so I spent filling out the form, Thompson jumped onto my desk and lap no fewer than five times. I finally shooed him away long enough to send off the questionnaire, and scheduled an hour-long phone call with Nagelschneider for later in the week.

In the meantime, I wanted to find out what scientists might say about the behavioral experiment I was about to embark upon. Could a middle-aged cat really change his stripes? I called up Stephen O’Brien and Carlos Driscoll for some insight into the feline brain.

O’Brien and Driscoll research the cat genome at the National Cancer Institute’s Laboratory of Genomic Diversity. Last summer, they published a report on the origin of domestic cats in the journal Science. “Cats are actually fairly well trainable,” Driscoll told me.

In their study, Driscoll and O’Brien concluded that domestic cats evolved from the wildcat Felis silvestris in the Near East, probably around 10,000 years ago. The way they see it, cats domesticated themselves. Wandering humans were settling down in the Fertile Crescent and establishing agriculture. Cats were drawn to the settlements to feed on mice that had shacked up in the grain stores. Natural selection favored the tamer cats, which could take better advantage of the spoils produced by our budding society. “They chose humans at the right time and the right place,” O’Brien said.

Driscoll took the comparison a step further. We artificially selected dogs to be useful to us; they guarded our homes, hauled our sleds, retrieved our dead ducks, and, in the case of poodles, allowed themselves to be pruned like hedges for our amusement. But we didn’t select cats to be useful to us. They were selected by nature to use us. “It’s best to think of cats like mice or cockroaches or pigeons,” Driscoll said, the weed species of the animal kingdom, thriving wherever humans traipse in and muck up the environment.

OK. Listen, Driscoll. Thompson may be a pest, but that’s my pet you’re comparing to a cockroach. Before I could defend my poor kitten, though, Driscoll distracted me with another important difference between Felis and Canis. “Cats are a strange domesticate. They’re the only domestic animal that, in the wild, is solitary,” he explained. “All other domestic animals live in groups in the wild, [and] people harnessed their natural proclivity toward following along.”

So now I know what I’m up against: a solitary hunter who doesn’t play nicely with others, and who, for thousands of years, has been evolving a skill set designed to take advantage of me. But at least my foe is predictable. According to Nagelschneider, most cat behavior problems fall into one of a handful of predictable categories. Not surprisingly, some of her most frequent complaints involve cats that take issue with the litter box. (When Nagelschneider mentioned the cat that urinated at night on his sleeping owner’s face, Thompson’s problems suddenly seemed very minor indeed.) In any event, aggression is also fairly common, and Nagelschneider has turned around her fair share of violent cats. She was optimistic that Thompson could be fixed.

On the day of our consultation, Nagelschneider called right on time. She was friendly and easy to talk to, but also professional. She got right down to business, running through a laundry list of potential explanations for Thompson’s toothiness. He might have been taken away from his mother and litter mates too early, before learning appropriate social boundaries. He might be acting out to assert his territorial dominance, or to satisfy his prey drive, or because he doesn’t like the way we pet him. Or he may just be genetically predisposed to aggression. But as we discussed his habits and quirks, one theory emerged above the others as a likely diagnosis: Thompson had low self-esteem.

As Nagelschneider described it, Thompson’s apparent lack of confidence could explain his dizzying alternations between clinginess and viciousness. When he followed me from room to room and jumped on my desk 15 times a day, he was looking to be reassured of my affections. When he attacked, he was acting out in an attempt to control me, like a playground bully knocking the skinny kid down to boost himself up. “He may be worrying excessively,” she explained.

She tried to soften the blow. “It’s not unusual,” she said. “I had a client once with a cat actually named Jekyll-Hyde.” Regardless, I felt horrible. I’d failed as a mother. Part of me wanted to ring up the vet and get him on anxiety meds, stat. But Thompson is already saddled with asthma medication that he must take every other day, puffed from a human-variety inhaler through a bonglike plastic tube. The treatment is highly amusing to observers, but much less so to the cat; I wasn’t eager to pump him full of kitty Xanax on top of all that. I committed to boost his confidence the old-fashioned way.

It wasn’t going to be easy, but Nagelschneider would be there to help me through it. Her $165 fee included the initial one-hour phone consultation and four weeks of regular e-mail follow-up. If we followed her instructions, she said, we should begin to see results in two weeks. It was just like whitening my teeth or using new wrinkle cream. I’d have to be patient, but I should know in a few weeks if the whole thing was a big waste of time and money.

Reprogramming Thompson would require a multifaceted approach. We’d already admitted we had a problem, so I figured the hardest part was out of the way. Next step: detox. For five days, we had to stop petting him completely. No scratching his ears, no dragging him into my lap to keep me warm while I watched “Project Runway.” Once Thompson felt confident he could trust our touches, we’d slowly ease him back into petting.

Next up, reinforcing Thompson’s good behavior. Nagelschneider suggested I buy a little clicking device, which I found at the local pet shop. It was originally designed for teaching dolphins, but has since become popular among dog trainers. Every time Thompson did something good, I was supposed to mark the behavior with a click of the clicker, then feed him a treat.

While I understood the overall concept, it wasn’t so easy figuring out what “good” cat behavior was. It wasn’t like I was training him to roll over or to sit. So I clicked for anything that wasn’t bad. If Thompson was sleeping on top of the washer-dryer instead of bugging me at my desk, I’d click. Lounging in the sun, click. Kissing the dog, click. It didn’t take long for him to figure out how to earn a much-adored Whisker Lickin’s Dreamy Duo, and soon he was licking his lips in anticipation each time he hopped onto his cat bed.

We’d covered how to get Thompson to trust us again, and how to teach him what behaviors we liked. Our next step was more hands-on: We had to make Thompson feel like the successful predator that he is not. At least once a day, but preferably twice, we must trick Thompson into believing he’s successfully slaughtered a small animal.

I tried a variety of toys for this process, but soon zeroed in on the perfect tool of deception: Da Bird. Just a bunch of feathers on a string tied to the end of a wand, it appears no different than any other cat toy. Yet when Da Bird flies through the air, its neon feathers rustling, Thompson is instantly and utterly mesmerized.

The idea is to mimic a hunt sequence. I start by fluttering Da Bird energetically as Thompson darts frantically around the room. As the hunt drags on, Da Bird loses steam, and I let Thompson catch it more easily. As the toy’s end draws near, I tug lightly on the wand a few last times — Da Death Throes. Finally the toy stops moving, and Thompson sinks his teeth in. When he does this, he actually makes a low, guttural growling sound I’d never heard before. At this point, I feed him a handful of treats. Satisfied and satiated, he flops down and goes to sleep.

One thing that I immediately liked about Nagelschneider’s approach was her assertion that we focus on rewards, not punishment. She suggested a few “aversive techniques” to try when Thompson misbehaved, but they were pretty mild — rattling a soda can filled with quarters to startle him, or simply ignoring him altogether. “We don’t want to traumatize him,” she explained. “The idea is to achieve the desired results with the least amount of invasive measures possible.”

This pro-active approach made sense to Alice Moon-Fanelli, a clinical assistant professor of animal behavior at Tufts University. “Cats are very responsive to positive reinforcement,” she said. “Usually what happens is the pet gets attention when it’s doing something wrong.”

Guilty. I’d spent years shrieking “no” whenever Thompson attacked, but had done virtually nothing to assure him of his self-worth. Of course, I certainly hadn’t intended to raise my poor, innocent kitten to be a wheezy, anxious cat with a pitiable self-image. Scientists know little about how the ancestral Felis silvestris lives in the wild, and I’d argue that few pet owners realize what’s going on in the minds of their cats. Nagelschneider hopes her show will give second chances to troubled cats. I don’t know how cooperative her feline clients will be under the bright studio lights, but I hope her show succeeds.

Because the thing is, her method worked. We started to see a difference in around two weeks, just as Nagelschneider predicted. Now, just over a month later, Thompson almost never bothers me at my desk while I’m working. After almost seven years of weekly, if not daily, stealth attacks, I have been free of bite wounds for more than four weeks.

I admit that Thompson isn’t completely cured. If I pet him too long, he might try to bite (though it’s more of a warning, without the wide-eyed intensity he once possessed). But by and large, for the few minutes of effort we must make each day, the change in his behavior is striking.

When I began this experiment, part of me wondered if I’d miss the scrappy old Thompson. I need not have worried. He’s still the same cat, charming and strange and overflowing with character. He still chases his tail, stalks water droplets in the shower, and enjoys lying on top of the washing machine for a hearty shake during the spin cycle. He’s just a slightly upgraded, nicer — dare I say, more confident — version of himself.

And this is where the story might have ended, had I not gone out of town for three nights. Although my husband dutifully engaged Thompson with Da Bird, the attention did not, apparently, make up for the fact that I had abandoned him for a long weekend. My first night back, as I was climbing into bed, I saw him lurking in the shadows. His ears went back, his eyes grew wide. Fortunately we had a coin-filled Diet Coke can stashed near the bed. I lunged for the can and jingled it just in time, startling Thompson only milliseconds before his fangs made contact with my flesh. I escaped unbitten, but barely.

The lesson, I suppose, is that we have to remain vigilant. I consider it a minor setback. After only a month, I have seen marked improvement in Thompson’s behavior. Buoyed by progress, we’ll keep clicking, keep birding, keep assuring Thompson that he is a capable and valued member of the household. Confident cats are made, not born, and we have more esteem to build.

Foremost among the finger-pointers is Republican Sen. Tom Coburn of Oklahoma, who blocked bills to honor Carson and name a Pennsylvania post office for her. Coburn’s Web site links visitors to Rachel Was Wrong, a site hosted by the Competitive Enterprise Institute (a free-market think tank known for, among other things, disputing evidence that human activity is driving climate change). Beside a grim photo gallery of malaria victims, the site claims “millions of people around the world suffer the painful and often deadly effects of malaria because one person sounded a false alarm. That person is Rachel Carson.”

Novelist Michael Crichton has a front seat on the bandwagon. He took on DDT and climate change in his footnote-studded 2004 novel, “State of Fear.” “Banning DDT killed more people than Hitler,” his protagonist alleges. “And the environmental movement pushed hard for it.”

The Coburn/Crichton talking points have infected the mainstream press. In his New York Times Science column this month, John Tierney thrashed Carson’s warnings about insecticides and argued that her voice still “drowns out real science.” Over at the Pittsburgh Tribune-Review, Bill Steigerwald blamed “environmentalists spooked by Rachel Carson” for banning a “miracle weapon” that is “like Kryptonite to the mosquitoes.”

Malaria’s burden is enormous. Each year, the disease infects 350 to 500 million people and kills at least a million — the vast majority in Africa, mostly children under 5. As decades have passed, science has shown that Carson was wrong about some of the dangers she associated with DDT. It’s also true that the insecticide can be a valuable tool in the arsenal against malaria. But blaming Carson and the environmental movement for malaria’s death toll is not supported by evidence from generations of scientists and malaria researchers.

“Groups are latching onto the emotional impact of the malaria story, which is truly a human tragedy, to discredit environmentalists,” says John M. Balbus, chief health scientist with Environmental Defense. “Are there places where DDT may have been beneficial? Probably, yes.” But is the 1970s DDT ban “the cause for rampant malaria and millions of deaths? Absolutely not.”

Historians and scientists have shown that despite some benefits of DDT, few African countries made the pesticide a part of their malaria control efforts over the past quarter century. Many factors led to the decreased use of DDT — factors that had nothing to do with Carson. In fact, the decline in DDT use coincided with a drop in malaria rates.

Socrates Litsios, a historian and former scientist for the World Health Organization (the agency that has headed global malaria control efforts since the 1960s), says the assertion that “Silent Spring” and the DDT ban led to millions of deaths is “outrageous.” May Berenbaum, head of the Department of Entomology at the University of Illinois at Urbana-Champaign, who has studied mosquitoes and malaria, says that “to blame environmentalists who oppose DDT for more deaths than Hitler is worse than irresponsible.”

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DDT was first created, for no practical purpose, in 1874 as a science project of a German chemistry student. It earned little attention until 1939, when Swiss scientist Paul Hermann Muller discovered that the chemical was deadly to insects. During World War II, Allied soldiers were dusted with DDT to rid them of the lice that spread typhus. Around the same time, governments in Europe and elsewhere began using the compound to control the mosquitoes that carried malaria. DDT was so successful at killing disease-carrying insects that Muller was awarded the 1948 Nobel Prize in medicine.

In 1955, an anti-malaria crusader named Fred Soper launched the Global Malaria Eradication Program with backing from the World Health Organization. He’d successfully battled malarial mosquitoes in countries such as Brazil years earlier, before DDT was available. Now, DDT was his weapon of choice. Sprayed on the inside walls of homes, it repelled many mosquitoes and killed those that lingered too long. With Soper’s help, malaria rates plummeted in countries around the world, including Taiwan, India, Australia and large parts of the Caribbean.

Advocates of DDT often argue that the chemical was instrumental in eliminating malaria from the United States as well. “The U.S. and western European countries all used DDT in the mid 20th century to eliminate malaria from their territories,” Coburn has said, “but then banned the substance for use by poor countries today to combat their number one health threat.”

In fact, malaria “was pretty well gone” from the United States before DDT appeared on the scene in the 1940s, says Jay Ellenberger, associate director of field and external affairs for the U.S. Environmental Protection Agency. Improvements in sanitation and a higher standard of living played a big role, as did public health measures such as installing window screens and draining the swamps where mosquitoes bred. Insecticides, including DDT, did help deal the disease a final blow, and by 1952 malaria had been eradicated from the country.

Meanwhile, DDT continued to be used widely to control agricultural pests in the United States. Mass quantities were dumped from airplanes onto crops, and more was sprayed in forests to exterminate the beetles that spread Dutch elm disease. The indiscriminate use of the chemical caught the eye of Carson, a former marine biologist who worked as a publications editor at the U.S. Fish and Wildlife Service.

Carson wasn’t the first to sound the alarm about DDT. In the 1950s, various lawsuits, brought by ornithologists, beekeepers and concerned citizens, sought court injunctions to end DDT spraying. But Carson’s passionate and poetic treatise, “Silent Spring,” captured the public’s attention. Carson warned that man-made chemicals spelled nearly certain doom for the environment and human health, and that DDT was among the chief villains. “The most alarming of all man’s assaults upon the environment is the contamination of air, earth, rivers, and sea with dangerous and even lethal materials,” she wrote. In a chapter titled “Elixirs of Death,” she described DDT in no uncertain terms. “Dissolved in oil, as it normally is, DDT is definitely toxic,” she wrote.

The author filled most of her pages by describing the harm that chemicals such as DDT can inflict on wildlife and human health. She only briefly mentioned DDT’s role in fighting diseases transmitted by insect vectors. Yet she allowed that insecticides could play a role in the fight against disease. “No responsible person contends that insect-borne disease should be ignored,” she wrote. “It is not my contention that chemical insecticides must never be used. I contend … that we have allowed these chemicals to be used with little or no advance investigation of their effect on soil, water, wildlife, and man himself.”

Mark H. Lytle, a professor of history at Bard College and author of “The Gentle Subversive,” a biography of Carson, explains that context is key to understanding why “Silent Spring” had the power it did. In 1959, mild panic had ensued when the U.S. government announced, just days before Thanksgiving, that cranberries were contaminated with a weed-killing chemical. Over the next few years, the public witnessed the disaster of thalidomide (a drug prescribed to treat morning sickness that resulted in thousands of babies born with birth defects) and a scare over the radioactive element strontium 90 (which was found to have accumulated in people’s bones in the years following nuclear testing). “When Carson wrote, there had been a whole series of environmental events that were scary,” Lytle says. “It made her all the more credible.”

In 1972, the EPA banned DDT in America. Carson’s solid reputation may have contributed to the decision, Lytle says. But Carson was by no means the sole reason for the ban. According to the EPA’s Ellenberger, the decision was backed by sound science, with evidence of DDT’s negative effects on wildlife continuing to mount. At the same time, after years of dumping DDT on agricultural pests, insects were becoming increasingly resistant to the chemical. “The risks were increasing, and the benefits were declining,” Ellenberger says. “If risks exceed benefits, EPA is supposed to take action.”

Overseas, DDT was being phased out of the fight against malaria, but Carson and budding environmentalists were not the reason. In the 1950s, when the Global Malaria Eradication Program was launched, the U.S. had been a major financier of it. But as the years ticked by, eradication remained a distant dream, says Litsios, the retired World Health Organization scientist. (His book, “The Tomorrow of Malaria,” was published in 1996.) He explains that the global program “oversold the possibility of eradication” and Congress tired of its promises. By the early ’60s, the money Congress had pledged to the program dried up. In 1969, the WHO officially abandoned the eradication effort.

During that period, the fight against malaria in Africa never picked up steam. Robert Snow, head of the malaria group at the Wellcome Trust/Kenya Medical Research Institute in Nairobi, has done considerable research and number crunching in an attempt to quantify the true burden of malaria in Africa over the last century. In an article published in 2001, in Trends in Parasitology, he wrote, “Despite the successes of the WHO eradication campaign in many parts of the world following the Second World War, most of Africa was regarded as a lost cause, and in practice the eradication of malaria in Africa was never attempted.”

In the 1960s and 1970s, colonialism in Africa was ending and several countries were undergoing major changes. “Many African countries realized they couldn’t really expect to progress with malaria at all if they didn’t have some kind of infrastructure,” says Litsios. The WHO couldn’t afford to launch a massive insecticide-spraying program and help countries build up basic health services at the same time. It chose the latter, Litsios says.

Better public health services helped improve childhood mortality in Africa, but malaria programs faltered. Malaria is a complex disease caused by a parasite with a complicated life cycle. “For malaria control, you need to have a really good understanding of mosquitoes, the malaria parasite and human behavior,” says Richard Tren, chairman of the board of Africa Fighting Malaria, an advocacy group that has lobbied for increased use of DDT. In the ’70s, many health programs were ill-equipped to handle that complexity.

Tren, who is allied with libertarian and free-market think tanks, such as the Institute of Economic Affairs, believes that anti-insecticide sentiment scared donors away from DDT programs. “By the late 1960s and early 1970s, the donor nations were starting to withdraw support from insecticide-spraying programs and from the use of DDT,” Tren says. “I am confident in saying that the anti-DDT crusades harmed malaria control and cost lives.”

That is misleading, say Litsios and Clive Shiff, a malaria researcher at the Johns Hopkins Bloomberg School of Public Health who has participated in malaria programs in Africa for decades. They stress that aid organizations weren’t anti-DDT during that period, they were pro-medicine. Through the ’70s and ’80s, most countries, on the advice of the WHO, “changed their approach to malaria control from insecticide treatment to treating people with chloroquine” — which kills the parasites that cause malaria — “because that was a way they could impact the mortality of the disease,” Shiff says. “I don’t think the ban of DDT in the U.S. had any impact on malaria control programs in Africa, certainly not in southern Africa where I was working.”

According to Snow’s research, malaria was responsible for 18 percent of deaths in Africa before 1960 and 12 percent of deaths between 1960 and 1989. In other words, deaths from malaria decreased during the period that treatment shifted from insecticides to medicine.

Still, DDT can be a boon to malaria control. The chemical is sprayed onto the inside walls of houses, where it has little chance of accumulating in the environment. What makes it bad for wildlife makes it good for mosquito control: It’s extremely persistent. DDT crystallizes onto the walls and stays there for a year or more, repelling some mosquitoes and killing others. Of the 30-40 species of Anopheles mosquitoes that carry malaria, most bite after dusk, so protecting people in their homes can have a big impact.

South Africa — one of the few African countries that could afford a spraying program without help from aid organizations — continued to use DDT after it was banned in the United States. By 1996, South Africa reported fewer than 10,000 malaria deaths annually. That year, it switched from DDT to another insecticide. The new chemical was also sprayed to control agricultural pests, and mosquitoes quickly developed resistance to the widely used chemical. By 2000, the number of annual malaria deaths had spiked to more than 60,000.

Elsewhere in Africa during the 1990s, the focus shifted to insecticide-treated bed nets that protect sleeping children from malarial mosquitoes. The nets have good success rates when used correctly, but even with their help, malaria was still winning the war. From 1990 to 1995, deaths caused by malaria soared to 30 percent. But the jump had nothing to do with DDT or any insecticide-spraying program. Deaths increased, Snow concluded, because the malaria parasite was evolving resistance to chloroquine.

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In 2006, the WHO announced it would actively back DDT and indoor residual spraying as a tool for controlling malaria. For Tren, that was good news. “In the last 10 years, almost all of the attention has been going to bed nets,” Tren says. “I think indoor residual spraying will have an increased role, and there will be more of a balance now.”

Public health workers generally agree that balance is the best approach: spraying houses, hanging bed nets, tracking outbreaks and treating those infected with malaria. DDT has a place in that strategy, but it is not the silver bullet it’s often made out to be. Today, a variety of insecticides are available for indoor residual spraying. DDT, says Shiff, “is just one important tool.” And not always the best tool.

Mosquitoes can evolve resistance to any insecticide. In India, DDT-resistant mosquitoes were reported as early as 1959. “Insects will develop resistance to insecticides,” says entomologist Berenbaum at the University of Illinois. “This is one sure thing you can count on.”

Mosquitoes, Berenbaum says, can develop resistance in any number of ways — biologically, biochemically, even behaviorally. In some regions, mosquitoes might develop resistance by becoming physically immune to the effects of DDT. In other populations, mosquitoes might evolve new behaviors, such as avoiding inside walls and resting on the unsprayed outer walls of homes after biting their victims.

Relying on insecticide alone to control malaria ignores big pieces of the puzzle, Berenbaum says. Mosquitoes may be the carrier, but it’s the Plasmodium parasite that causes malaria. “It’s not just the mosquito. There’s a pathogen involved, and there are people involved. To reduce this extremely complicated situation to one bad guy is beyond simplistic,” she says.

That oversimplified argument seems to suit Coburn, Crichton and their cohorts in the press. In his Tribune-Review column, Steigerwald claimed that “environmentalists are still outraged” over the use of DDT. That’s not so. Most prominent environmental organizations, including the Sierra Club and Environmental Defense, support indoor spraying of DDT for malaria control, at least until safer alternatives are found.

In his New York Times column, Tierney blasted Carson’s “junk science.” It’s true that some of her claims sound foolish to modern readers, like the case she cited of a woman who sprayed DDT to kill spiders in her basement in August and September and was dead from leukemia by October. She also raised concerns that DDT could be linked to liver disease and central nervous system damage.

But many of the dangers Carson warned about, such as the detrimental effects of DDT on birds, have held up. It is now well accepted that when DDT accumulates in the environment, it causes eggshells to thin and crack, leaving predatory birds such as ospreys and other raptors especially vulnerable. DDT is also toxic to many fish. “In retrospect, the facts have borne out the concerns,” says Environmental Defense’s Balbus.

While DDT’s detrimental environmental effects have stood up to scrutiny, repeated studies have found no evidence that DDT exposure increases the risk of cancer. That’s not to say that the chemical is benign. DDT appears to have a hormonal effect on humans, and exposure to high levels is linked to a shortened period of lactation among nursing mothers. A study led by scientists at the National Institute of Environmental Health Sciences, published in the medical journal Lancet in 2001, found that heavy DDT exposure in the 1940s and 1950s was linked to an “epidemic” in the 1960s of premature births — a significant risk factor for infant mortality.

Today, to many environmentalists, Carson is still a hero for encouraging people to treat the planet with care. “She taught people how to change their mind-set,” Lytle, her biographer, says. “Her major legacy was that she taught the public to think ecologically.” But for better or worse, her legacy will probably always be bound up with the story of DDT. What her critics seem unwilling to admit is that Carson was just one person, and DDT is just one tool. DDT plays a part in the fight against malaria, but it’s one drop in a very big puddle.

As for the DDT debate in vogue at the moment, Berenbaum says, “it’s all emotional and not rational.” She fully agrees that malaria is an international tragedy, and she doesn’t “place the lives of ospreys above the lives of people,” she says. But neither would Berenbaum pin her hopes on one insecticide — a point Carson herself understood half a century ago. “Carson’s point wasn’t that DDT was evil,” Berenbaum says. “It was that if you put all your eggs in one basket, that basket’s going to break.”

“It would be really hard to replicate the life experiences that made Shadow who she is today,” says Schlegelmilch, of Homer, Alaska. “Still, if I could clone her when she reaches old age, I might be tempted.”

Schlegelmilch is not alone in her desire to keep her canine companion around indefinitely. In recent years, a trio of pet-cloning companies, Genetic Savings & Clone, ForeverPet and Perpetuate, have sprung up to meet the growing demand for carbon copies of Rex and Fluffy. Already the companies have a backlog of customers who have paid to store their pets’ genes in the companies’ freezers. So far, Genetic Savings & Clone is the only company that has cloned kittens for clients. (Recently it dropped the price from $50,000; a cat clone can now be had for just $32,000.)

Beneath the utopian science are some unsettling ethical questions about animal welfare and health. With city pounds across the country filled with homeless dogs and cats, should a person pay tens of thousands of dollars to essentially manufacture a new pet? Given that cloning is not a perfected science, is it premature to clone dogs and cats that could later suffer a bevy of medical problems?

The spotlight on cloning also illuminates the seldom acknowledged fact that, in many ways, cloning dogs and cats is redundant. We’ve more or less accomplished with breeding what cloning aims to create — animals nearly identical in appearance and temperament. Since domesticating dogs from wolves more than 10,000 years ago, we’ve engineered the species to suit our needs and our whimsies — border collies for herding sheep, malamutes for hauling sleds, teacup Chihuahuas for accessorizing starlets.

When it comes to dogs, “we’ve been doing seat-of-the-pants genetics for at least 12,000 years,” says Stanley Coren, a psychology professor at the University of British Columbia and author of numerous books on dogs. We did so, for the most part, with little knowledge of the underlying genetics. Today, sophisticated geneticists are tinkering with dog DNA in all sorts of ways. Some experiments are resulting in key cures for canine afflictions. And cloning, which at first glance may seem a quintessential act of human vanity, could become a reliable method for duplicating ideal pets.

Snuppy was created by somatic cell nuclear transfer, the same technique that produced Dolly the sheep. The genetic material is sucked out of donor eggs and replaced with DNA taken from skin cells of the clone “parent.” The resulting embryo is stimulated to divide with chemicals or electricity, then implanted into a surrogate mother.

From nearly the moment Snuppy was born, groups such as the American Anti-Vivisection Society, People for the Ethical Treatment of Animals and the Humane Society of the United States expressed their opposition. “There are millions of animals who are euthanized every year simply because they don’t have a home,” says Stephanie Shain, director of outreach for the Humane Society. “To clone a pet when there are so many animals that need homes, we think it’s a technology that’s completely unnecessary.”

Not only is the technology unnecessary, Shain says, but it’s imperfect and potentially dangerous. Cloning is extremely inefficient. To produce the first dog clone, the Korean team implanted multiple embryos into more than 100 surrogate dogs; only Snuppy survived. The lifespan and health of cloned mammals has also been called into question. Dolly, the famous first mammal to be cloned from an adult, suffered from lung disease and arthritis and was put down at a relatively young age. Whether her health problems were related to cloning is unknown.

Critics also contend that commercial cloning is consumer fraud, given that a clone won’t be identical to the original pet. Although they will look alike and share the same genes, clones will grow up in different environmental conditions than the original animals, and have their own personalities and behaviors. Clones are essentially identical twins displaced in time. “There’s no way to replicate an animal’s personality,” Shain says. “They’re toying with these people’s emotions.”

Autumn Fiester is a senior fellow at the Center for Bioethics at the University of Pennsylvania Medical School and the owner of a purebred bichon frisé. She believes the jury is still out on pet cloning and will be until we know more about the health of the clones. But, she says, “it seems like Genetic Savings & Clone, for its part, has produced healthy animals.” In the meantime, she says, “the preliminary arguments made by the opposing camp are not strong arguments.”

Fiester points out that spending $30,000 on an animal that may live 15 years works out to just a couple hundred dollars a month. We often spend that on other so-called luxury items, like going to the movies or dining out. And at the end of a month of fine dining, you aren’t even left with an object — let alone one that loves you unconditionally. “In principle it is not irrational to want a later-born twin of a beloved pet,” Fiester says. “Clients can say, ‘At least I have something left, a little bit of my animal for me to cherish.’”

For some pet owners, replacing a lost pet with an animal from a shelter isn’t an acceptable alternative. “Pet owners do not want any old pet,” Fiester says. “They are after a certain genetic constellation, a certain cat or certain dog.”

One such owner is Kathleen McNulty, from Long Valley, N.J. She has banked her dog Riley’s genes with Genetic Savings & Clone and has posted a testimonial on the company’s Web site. “I am very sympathetic to homeless cats and dogs,” she wrote. “I have a barn full of cats that have been adopted from shelters. But I had this one very special relationship with this one dog, and I know that I’m not going to find that relationship with a dog that I get out of a shelter.”

According to the American Pet Products Manufacturers Association, more than 43 million U.S. households keep nearly 74 million dogs as pets and de facto family members. We love our dogs and are often willing to spend exorbitant sums for the perfect pup. The American Kennel Club estimates that one in four dogs are purebreds.

Individual dog breeds are so familiar to us, it’s easy to forget that they are just races of a single species — races that we’ve invented. In the wild, nature selects for particular traits and behaviors. In dogs, we’ve stepped in for Mother Nature and made our own selections.

Those selections have produced a species that comes in shapes and sizes that are all over the map. English mastiffs tip the scales at up to 200 pounds, while Chihuahuas weigh in at less than six. The faces of a bulldog and a basenji give no hints that they belong to the same species. “Some people design dogs like it’s an art form,” says Coren.

Unfortunately, those art forms often beget health problems, linked not to genetic diseases but to the dog’s body shape. We’ve selected for physical traits in dogs that would never have originated in nature because they’re not adaptive. The English bulldog is a classic example, says Raymond Coppinger, an evolutionary biologist at Hampshire College in Amherst, Mass., and co-author (with his wife, Lorna) of “Dogs: A Startling New Understanding of Canine Origin, Behavior, and Evolution.”

Bulldogs’ heads are so big that they cannot fit through the birth canal, and their puppies must be delivered by cesarean section. And their radically flattened faces lead to deformed respiratory machinery, Coppinger says. As anyone who’s come into contact with a snorting, snoring bulldog knows, they have a hard time breathing. Such a hard time, in fact, that they often have abnormally low levels of oxygen in their bloodstreams. “The dog isn’t adapted to be that shape,” he says. “The biology can’t go there.”

Some of our aesthetic choices have no apparent bearing on a dog’s well-being; chances are, fur color doesn’t much matter to a dog that doesn’t have to camouflage itself in the wild. But in other cases, our choices could very well affect a dog’s quality of life. Is it animal cruelty to create teacup breeds that are so small their mouths can’t support a healthy set of teeth? Or to engineer Chinese Shar-Peis whose absurdly wrinkled skin harbors ulcers and mange?

Breeders themselves sometimes debate where to draw the line in shaping a dog’s anatomy, says Patrick Venta, a professor of veterinary medicine at Michigan State University and a collaborator on DogMap, one of several canine genome projects. “If you breed to the extreme, you enhance the features of the breed, but if you push too far, it can create some type of health problem for the dog,” he says. “There will be gray areas.”

While much of current genetic research aims to benefit human medicine, a large number of scientists are working to improve the health of our favorite pet. Dogs suffer from an impressive collection of genetic diseases and disorders, thanks to a high incidence of inbreeding. Breeds such as Labrador retrievers and Afghan hounds are crippled by hip dysplasia, golden retrievers are prone to a specific type of cancer, and narcoleptic Dobermans fail as watchdogs when they topple over into a deep and sudden sleep.

Those and other health issues may very well be resolved with genetics research, but cloning isn’t likely to play much of a role in identifying and eliminating genetic disorders. “Cloning is incredibly expensive … and extremely inefficient,” says Venta. “There are so many things people involved in canine genetics can do without whole-organism cloning.”

In 2001, scientists at Cornell announced a gene therapy technique to cure congenital blindness in Briards, a type of French herding dog. Traditional genetics work has so far produced tests for as many as 30 canine diseases, Venta says, allowing breeders to avoid carriers of conditions like narcolepsy and hip dysplasia.

Animal rights activists often condemn genetic tinkering as well as cloning. But whether a dog was conceived by breeding or by cloning, maybe they have it made. Sure, they suffer a little manipulation, but they get food and healthcare and a warm place to sleep. While we’ve exterminated the wolf from much of its original habitat, we’ve made sure to ferry our pampered dogs into this millennium and probably the next.

“We wouldn’t have any dogs if humans over the course of thousands of years hadn’t selected certain characteristics,” Venta says. “We’d be living with wolves.”

Coren agrees and even calls dog breeds vital. “My wife and I recently got a beagle and we knew he’d be sweet and kissy-faced and dumb as a stone,” he says. “Predictability is what you’re paying for when you pay for a purebred dog, and it’s a good thing. You don’t want to have to roll the dice.” Cloning would take that purebred predictability and bump it up a notch.

Schlegelmilch first fell in love with the Afghan hound when one ran by her house more than 30 years ago. “I had never seen any animal quite so elegant and graceful,” she says. Within six months she owned one, and she and her husband have kept them ever since. With each new dog, they know just what to expect: a graceful, athletic, independent dog that doesn’t necessarily obey commands.

Schlegelmilch now deals with a trusted breeder who tests for genetic disease and produces healthy puppies. Not all breeders are so responsible. Schlegelmilch’s first Afghan hound Desiree died at age 3 from the canine version of Huntington’s disease, a genetic disorder. “In retrospect, I think she came from a puppy-mill type of breeder,” she says.

The irony of cloning, says bioethicist Fiester, is that it may prove more ethical than breeding, as there’s no dearth of evidence that breeders can be irresponsible. Commercial cloning companies can also be fairly certain that a person spending thousands of dollars on a clone will pamper her pet. The average dog breeder has much less reassurance that clients will be loving owners. “Our initial reaction [to cloning] may be a yuck factor against Frankenpets,” Fiester admits. “But ethically, cloning may have a leg up.”