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DNA Pollution May Be Spawning Killer Microbes

Copyright Jessica Snyder Sachs

Originally published in Discover magazine, March 2008

Rogue genetic snippets spread antibiotic resistance all over the environment.

On a bright winter morning high in the Colorado Rockies, a slight young woman in oversize hip boots sidles up to a gap of open water in the icy Cache la Poudre River. Heather Storteboom, a 25-year-old graduate student at nearby Colorado State University, is prospecting for clues to an invisible killer.

heather_storteboom_photo_by_JSS.jpgHeather Storteboom on the Poudre, photo by JSSachs

Storteboom snaps on a pair of latex gloves and stretches over the frozen ledge to fill a sterile plastic jug with water. Then, setting the container aside, she swings her rubber-clad legs into the stream. "Ahh, no leaks," she says, standing upright. She pulls out a clean trowel and attempts to collect some bottom sediment; in the rapid current, it takes a half dozen tries to fill the small vial she will take back to the DNA laboratory of her adviser, environmental engineer Amy Pruden. As Storteboom packs to leave, a curious hiker approaches. "What were you collecting?" he asks. "Antibiotic resistance genes," she answers.

Storteboom and Pruden are at the leading edge of an international forensic investigation into a potentially colossal new health threat: DNA pollution. Specifically, the researchers are seeking out snippets of rogue genetic material that transforms annoying bacteria into unstoppable supergerms, immune to many or all modern antibiotics. Over the past 60 years, genes for antibiotic resistance have gone from rare to commonplace in the microbes that routinely infect our bodies. The newly resistant strains have been implicated in some 90,000 potentially fatal infections a year in the United States, higher than the number of automobile and homicide deaths combined.

Among the most frightening of the emerging pathogens is invasive MRSA, or methicillin-resistant Staphylococcus aureus. Outbreaks of MRSA in public schools recently made headlines, but that is just the tip of the iceberg. Researchers estimate that invasive MRSA kills more than 18,000 Americans a year, more than AIDS, and the problem is growing rapidly. MRSA caused just 2 percent of staph infections in 1974; in the last few years, that figure has reached nearly 65 percent. Most reported staph infections stem from MRSA born and bred in our antibiotic-drenched hospitals and nursing homes. But about 15 percent now involve strains that arose in the general community.

It is not just MRSA that is causing concern; antibiotic resistance in general is spreading alarmingly. A 2003 study of the mouths of healthy kindergartners found that 97 percent harbored bacteria with genes for resistance to four out of six tested antibiotics. In all, resistant microbes made up around 15 percent of the children's oral bacteria, even though none of the children had taken antibiotics in the previous three months. Such resistance genes are rare to nonexistent in specimens of human tissue and body fluid taken 60 years ago, before the use of antibiotics became widespread.

In part, modern medicine is paying the price for its own success. "Antibiotics may be the most powerful evolutionary force seen on this planet in billions of years," says Tufts University microbiologist Stuart Levy, author of The Antibiotic Paradox: How the Misuse of Antibiotics Destroys Their Curative Powers. By their nature, antibiotics support the rise of any bug that can shrug off their effects, by conveniently eliminating the susceptible competition.

But the rapid rise of bacterial genes for drug resistance stems from more than lucky mutation, Levy adds. The vast majority of these genes show a complexity that could have been achieved only over millions of years. Rather than rising anew in each species, the genes spread via the microbial equivalent of sexual promiscuity. Bacteria swap genes, not only among their own kind but also between widely divergent species, Levy explains. Bacteria can even scavenge the naked DNA that spills from their dead compatriots out into the environment.

The result is a microbial arms-smuggling network with a global reach. Over the past 50 years, virtually every known kind of disease-causing bacterium has acquired genes to survive some or all of the drugs that once proved effective against it. Analysis of a strain of vancomycin-resistant enterococcus, a potentially lethal bug that has invaded many hospitals, reveals that more than one-quarter of its genome-including virtually all its antibiotic-thwarting genes-is made up of foreign DNA. One of the newest banes of U.S. medical centers, a supervirulent and multidrug-resistant strain of Acinetobacter baumannii, likewise appears to have picked up most of its resistance in gene swaps with other species.

So where in Hades did this devilishly clever DNA come from? The ultimate source may lie in the dirt beneath our feet.

For the past decade, Gerry Wright has been trying to understand the rise of drug resistance by combing through the world's richest natural source of resistance-enabling DNA: a clod of dirt. As the head of McMaster University's antibiotic research center in Hamilton, Ontario, Wright has the most tricked-out laboratory a drug designer could want, complete with a $15 million high-speed screening facility for simultaneously testing potential drugs against hundreds of bacterial targets. Yet he says his technology pales in comparison with the elegant antibiotic-making abilities he finds encoded in soil bacteria. The vast majority of the antibiotics stocking our pharmacy shelves-from old standards like tetracycline to antibiotics of last resort like vancomycin and, most recently, daptomycin-are derived from soil organisms.

Biologists assume that soil organisms make antibiotics to beat back the microbial competition and to establish their territory, Wright says, although the chemicals may also serve other, less-understood functions. Whatever the case, Wright and his students began combing through the DNA of soil microbes like streptomyces to better understand their impressive antibiotic-making powers. In doing so the researchers stumbled upon three resistance genes embedded in the DNA that Streptomyces toyocaensis uses to produce the antibiotic teicoplanin. While Wright was not surprised that the bug would carry such genes as antidotes to its own weaponry, he was startled to see that the antidote genes were nearly identical to the resistance genes in vancomycin-resistant enterococcus (VRE), the scourge of American and European hospitals.


"Yet here they were in a soil organism, in the exact same orientation as you find in the genome of VRE," Wright says. "That sure gave us a head-slap moment. If only we had done this experiment 15 years ago, when vancomycin came into widespread use, we might have understood exactly what kind of resistance mechanisms would follow the drug into our clinics and hospitals." If nothing else, that foreknowledge might have prepared doctors for the inevitable resistance they would encounter soon after vancomycin was broadly prescribed.

Wright wondered what else he might find in a shovelful of dirt. So he handed out plastic bags to students departing on break, telling them to bring back soil samples. Over two years his lab amassed a collection that spanned the continent. It even included a thawed slice of tundra mailed by Wright's brother, a provincial policeman stationed on the northern Ontario-Manitoba border.

By 2005 Wright's team had combed through the genes of nearly 500 streptomyces strains and species, many never before identified. Every one proved resistant to multiple antibiotics, not just their own signature chemicals. On average, each could neutralize seven or eight drugs, and many could shrug off 14 or 15. In all, the researchers found resistance to every one of the 21 antibiotics they tested, including Ketek and Zyvox, two synthetic new drugs.

"These genes clearly didn't jump directly from streptomyces into disease-causing bacteria," Wright says. He had noted subtle variations between the resistance genes he pulled out of soil organisms and their doppelgangers in disease-causing bacteria. As in a game of telephone, each time a gene gets passed from one microbe to another, slight differences develop that reflect the DNA dialect of its new host. The resistance genes bedeviling doctors had evidently passed through many intermediaries on their way from soil to critically ill patients.

Wright suspects that the antibiotic-drenched environment of commercial livestock operations is prime ground for such transfer. "You've got the genes encoding for resistance in the soil beneath these operations," he says, "and we know that the majority of the antibiotics animals consume get excreted intact." In other words, the antibiotics fuel the rise of resistant bacteria both in the animals' guts and in the dirt beneath their hooves, with ample opportunity for cross-contamination.

Nobody knows how long free-floating DNA might persist in the water.

A 2001 study by University of Illinois microbiologist Roderick Mackie documented this flow. When he looked for tetracycline resistance genes in groundwater downstream from pig farms, he also found the genes in local soil organisms like Microbacterium and Pseudomonas, which normally do not contain them. Since then, Mackie has found that soil bacteria around conventional pig farms, which use antibiotics, carry 100 to 1,000 times more resistance genes than do the same bacteria around organic farms.

"These animal operations are real hot spots," he says. "They're glowing red in the concentrations and intensity of these genes." More worrisome, perhaps, is that Mackie pulled more resistance genes from his deepest test wells, suggesting that the genes percolated down toward the drinking water supplies used by surrounding communities.

Pig farm waste lagoon

An even more direct conduit into the environment may be the common practice of irrigating fields with wastewater from livestock lagoons. About three years ago, David Graham, a University of Kansas environmental engineer, was puzzled in the fall by a dramatic spike in resistance genes in a pond on a Kansas feedlot he was studying. "We didn't know what was going on until I talked with a large-animal researcher," he recalls. At the end of the summer, feedlots receive newly weaned calves from outlying ranches. To prevent the young animals from importing infections, the feedlot operators were giving them five-day "shock doses" of antibiotics. "Their attitude had been, cows are big animals, they're pretty tough, so you give them 10 times what they need," Graham says.

The operators cut back on the drugs when Graham showed them that they were coating the next season's alfalfa crop with highly drug-resistant bacteria. "Essentially, they were feeding resistance genes back to their animals," Graham says. "Once they realized that, they started being much more conscious. They still used antibiotics, but more discriminately."

While livestock operations are an obvious source of antibiotic resistance, humans also take a lot of antibiotics-and their waste is another contamination stream. Bacteria make up about one-third of the solid matter in human stool, and Scott Weber, of the State University of New York at Buffalo, studies what happens to the antibiotic resistance genes our nation flushes down its toilets.

Conventional sewage treatment skims off solids for landfill disposal, then feeds the liquid waste to sewage-degrading bacteria. The end result is around 5 billion pounds of bacteria-rich slurry, or waste sludge, each year. Around 35 percent of this is incinerated or put in a landfill. Close to 65 percent is recycled as fertilizer, much of it ending up on croplands.


Weber is now investigating how fertilizer derived from human sewage may contribute to the spread of antibiotic-resistant genes. "We've done a good job designing our treatment plants to reduce conventional contaminants," he says. "Unfortunately, no one has been thinking of DNA as a contaminant." In fact, sewage treatment methods used at the country's 18,000-odd wastewater plants could actually affect the resistance genes that enter their systems.

Wastewater treatment

Every tested strain in a dirt sample proved resistant to multiple antibiotics.

Most treatment plants, Weber explains, gorge a relatively small number of sludge bacteria with all the liquid waste they can eat. The result, he found, is a spike in antibiotic-resistant organisms. "We don't know exactly why," he says, "but our findings have raised an even more important question." Is the jump in resistance genes coming from a population explosion in the resistant enteric, or intestinal, bacteria coming into the sewage plant? Or is it coming from sewage-digesting sludge bacteria that are taking up the genes from incoming bacteria? The answer is important because sludge bacteria are much more likely to thrive and spread their resistance genes once the sludge is discharged into rivers (in treated wastewater) and onto crop fields (as slurried fertilizer).

Weber predicts that follow-up studies will show the resistance genes have indeed made the jump to sludge bacteria. On a hopeful note, he has shown that an alternative method of sewage processing seems to decrease the prevalence of bacterial drug resistance. In this process, the sludge remains inside the treatment plant longer, allowing dramatically higher concentrations of bacteria to develop. For reasons that are not yet clear, this method slows the increase of drug-resistant bacteria. It also produces less sludge for disposal. Unfortunately, the process is expensive.

Drying sewage sludge into pellets-which kills the sludge bacteria-is another way to contain resistance genes, though it may still leave DNA intact. But few municipal sewage plants want the extra expense of drying the sludge, and so it is instead exported "live" in tanker trucks that spray the wet slurry onto crop fields, along roadsides, and into forests.

Trolling the waters and sediments of the Cache la Poudre, Storteboom and Pruden are collecting solid evidence to support suspicions that both livestock operations and human sewage are major players in the dramatic rise of resistance genes in our environment and our bodies. Specifically, they have found unnaturally high levels of antibiotic resistance genes in sediments where the river comes into contact with treated municipal wastewater effluent and farm irrigation runoff as it flows 126 miles from Rocky Mountain National Park through Fort Collins and across Colorado's eastern plain, home to some of the country's most densely packed livestock operations.

"Over the course of the river, we saw the concentration of resistance genes increase by several orders of magnitude," Pruden says, "far more than could ever be accounted for by chance alone." Pruden's team likewise found dangerous genes in the water headed from local treatment plants toward household taps.

Presumably, most of these genes reside inside live bacteria, but a microbe doesn't have to be alive to share its dangerous DNA. As microbiologists have pointed out, bacteria are known to scavenge genes from the spilled DNA of their dead.

"There's a lot of interest in whether there's naked DNA in there," Pruden says of the Poudre's waters. "Current treatment of drinking water is aimed at killing bacteria, not eliminating their DNA." Nobody even knows exactly how long such free-floating DNA might persist.

All this makes resistance genes a uniquely troubling sort of pollution. "At least when you pollute a site with something like atrazine," a pesticide, "you can be assured that it will eventually decay," says Graham, the Kansas environmental engineer, who began his research career tracking chemical pollutants like toxic herbicides. "When you contaminate a site with resistance genes, those genes can be transferred into environmental organisms and actually increase the concentration of contamination."

Taken together, these findings drive home the urgency of efforts to reduce flagrant antibiotic overuse that fuels the spread of resistance, whether on the farm, in the home, or in the hospital.

For years the livestock pharmaceutical industry has played down its role in the rise of antibiotic resistance. "We approached this problem many years ago and have seen all kinds of studies, and there isn't anything definitive to say that antibiotics in livestock cause harm to people," says Richard Carnevale, vice president of regulatory and scientific affairs at the Animal Health Institute, which represents the manufacturers of animal drugs, including those for livestock. "Antimicrobial resistance has all kinds of sources, people to animals as well as animals to people."

The institute's own data testify to the magnitude of antibiotic use in livestock operations, however. Its members sell an estimated 20 million to 25 million pounds of antibiotics for use in animals each year, much of it to promote growth. (For little-understood reasons, antibiotics speed the growth of young animals, making it cheaper to bring them to slaughter.) The Union of Concerned Scientists and other groups have long urged the United States to follow the European Union, which in 2006 completed its ban on the use of antibiotics for promoting livestock growth. Such a ban remains far more contentious in North America, where the profitability of factory-farm operations depends on getting animals to market in the shortest possible time.


On the other hand, the success of the E.U.'s ban is less than clear-cut. "The studies show that the E.U.'s curtailing of these compounds in feed has resulted in more sick animals needing higher therapeutic doses," Carnevale says.

"There are cases of that," admits Scott McEwen, a University of Guelph veterinary epidemiologist who advises the Canadian government on the public-health implications of livestock antibiotics. At certain stressful times in a young animal's life, as when it is weaned from its mother, it becomes particularly susceptible to disease. "The lesson," he says, "may be that we would do well by being more selective than a complete ban."

McEwen and many of his colleagues see no harm in using growth-promoting livestock antibiotics known as ionophores. "They have no known use in people, and we see no evidence that they select for resistance to important medical antibiotics," he says. "So why not use them? But if anyone tries to say that we should use such critically important drugs as cephalosporins or fluoroquinolones as growth promoters, that's a no-brainer. Resistance develops quickly, and we've seen the deleterious effects in human health."

A thornier issue is the use of antibiotics to treat sick livestock and prevent the spread of infections through crowded herds and flocks. "Few people would say we should deny antibiotics to sick animals," McEwen says, "and often the only practical way to administer an antibiotic is to give it to the whole group." Some critics have called for restricting certain classes of critically important antibiotics from livestock use, even for treating sick animals. For instance, the FDA is considering approval of cefquinome for respiratory infections in cattle. Cefquinome belongs to a powerful class of antibiotic known as fourth-generation cephalosporins, introduced in the 1990s to combat hospital infections that had grown resistant to older drugs. In the fall of 2006, the FDA's veterinary advisory committee voted against approving cefquinome, citing concerns that resistance to this vital class of drug could spread from bacteria in beef to hospital superbugs that respond to little else. But the agency's recently adopted guidelines make it difficult to deny approval to a new veterinary drug unless it clearly threatens the treatment of a specific foodborne infection in humans. As of press time, the FDA had yet to reach a decision.

Consumers may contribute to the problem of DNA pollution whenever they use antibacterial soaps and cleaning products. These products contain the antibiotic-like chemicals triclosan and triclocarban and send some 2 million to 20 million pounds of the compounds into the sewage stream each year. Triclosan and triclocarban have been shown in the lab to promote resistance to medically important antibiotics. Worse, the compounds do not break down as readily as do traditional antibiotics. Rolf Halden, cofounder of the Center for Water and Health at Johns Hopkins University, has shown that triclosan and triclocarban show up in many waterways that receive treated wastewater-more than half of the nation's rivers and streams. He has found even greater levels of these two chemicals in sewage sludge destined for reuse as crop fertilizer. According to his figures, a typical sewage treatment plant sends more than a ton of triclocarban and a slightly lesser amount of triclosan back into the environment each year.

For consumer antibacterial soaps the solution is simple, Halden says: "Eliminate them. There's no reason to have these chemicals in consumer products." Studies show that household products containing such antibacterials don't prevent the spread of sickness any better than ordinary soap and water. "If there's no benefit, then all we're left with is the risk," Halden says. He notes that many European retailers have already pulled these products from their shelves. "I think it's only a matter of time before they are removed from U.S. shelves as well."

Consumers may contribute to the problem of DNA pollution whenever they use soaps and cleaning products containing antibiotic-like compounds.

Finally, there is the complicated matter of the vast quantity of antibiotics that U.S. doctors prescribe each year: some 3 million pounds, according to the Union of Concerned Scientists. No doctor wants to ignore an opportunity to save a patient from infectious disease, yet much of what is prescribed is probably unnecessary-and all of it feeds the spread of resistance genes in hospitals and apparently throughout the environment.

"Patients come in asking for a particular antibiotic because it made them feel better in the past or they saw it promoted on TV," says Jim King, president of the American Academy of Family Physicians. The right thing to do is to educate the patient, he says, "but that takes time, and sometimes it's easier, though not appropriate, to write the prescription the patient wants."

Curtis Donskey, chief of infection control at Louis Stokes Cleveland VA Medical Center, adds that "a lot of antibiotic overuse comes from the mistaken idea that more is better. Infections are often treated longer than necessary, and multiple antibiotics are given when one would work as well." In truth, his studies show, the longer hospital patients remain on antibiotics, the more likely they are to pick up a multidrug-resistant superbug. The problem appears to lie in the drugs' disruption of a person's protective microflora-the resident bacteria that normally help keep invader microbes at bay. "I think the message is slowly getting through," Donskey says. "I'm seeing the change in attitude."

Meanwhile, Pruden's students at Colorado State keep amassing evidence that will make it difficult for any player-medical, consumer, or agricultural-to shirk accountability for DNA pollution.

Late in the afternoon, Storteboom drives past dairy farms and feedlots, meatpacking plants, and fallow fields, 50 miles downstream from her first DNA sampling site of the day. Leaving her Jeep at the side of the road, she strides past cow patties and fast-food wrappers and scrambles down an eroded embankment of the Cache la Poudre River. She cringes at the sight of two small animal carcasses on the opposite bank, then wades in, steering clear of an eddy of gray scum. "Just gross," she mutters, grateful for her watertight hip boots.

Of course, the invisible genetic pollution is of greater concern. It lends an ironic twist to the river's name. According to local legend, the appellation comes from the hidden stashes (cache) of gunpowder (poudre) that French fur trappers once buried along the banks. Nearly two centuries later, the river's hidden DNA may pose the real threat.

Jessica Snyder Sachs is the author of Good Germs, Bad Germs: Health and Survival in a Bacterial World, published in fall 2007 by Hill & Wang, a division of Farrar, Strauss and Giroux. Her last feature for Discover looked at how antibiotics affect the body's bacterial ecosystem.


For every cell in your body, you support 10 bacterial cells that make vitamins, trigger hormones, and may even influence how fat you are. Guess what happens to them when you pop penicillin?

Copyright Jessica Snyder Sachs, as first published in DISCOVER magazine


ALAN HUDSON likes to tell a story about a soldier and his high school sweetheart. The young man returns from an overseas assignment for their wedding with a clean bill of health, having dutifully cleared up an infection of sexually transmitted chlamydia.

Image of Chlamydia by Judith Whittum Hudson

"Three weeks later, the wife has a screaming genital infection," Hudson recounts, "and I get a call from the small-town doctor who's trying to save their marriage." The soldier, with obvious double standard, has decided his wife must have been seeing other men, which she denies.

Hudson pauses for effect, stretching back in his seat and propping his feet on an open file drawer in a crowded corner of his microbiology laboratory at Wayne State Medical School in Detroit. "The doctor is convinced she's telling the truth," he continues, folding his hands behind a sweep of white, collar-length hair. "So I tell him, 'Send me a specimen from him and a cervical swab from her.' " This is done after the couple has completed a full course of antibiotic treatment and tested free of infection.

"I PCR 'em both," Hudson says, "and he is red hot."

PCR stands for polymerase chain reaction-a technique developed about 20 years ago that allows many copies of a DNA sequence to be made. It is often used at crime scenes, where very little DNA may be available. Hudson's use of the technique allowed him to find traces of chlamydia DNA in the soldier and his wife that traditional tests miss because the amount left after antibiotic treatment is small and asymptomatic.

Nonetheless, if a small number of inactive chlamydia cells passed from groom to bride, the infection could have became active in its new host.

Hudson tells the tale to illustrate how microbes that scientists once thought were easily eliminated by antibiotics can still thrive in the body. His findings and those of other researchers raise disturbing questions about the behavior of microbes in the human body and how they should be treated.

For example, Hudson has found that quiescent varieties of chlamydia may play a role in chronic ailments not traditionally thought to be related to this infectious agent. In the early 1990s, he found two types of chlamydia-Chlamydia trachomatis and Chlamydia pneumonia-in the joint tissue of patients with inflammatory arthritis. More famously, in 1996, he began fishing C. pneumonia out of the brain cells of Alzheimer's victims. Since then, other researchers have made headlines after reporting the genetic fingerprints of C. pneumonia, as well as several kinds of common mouth bacteria, in the arterial plaque of heart attack patients. Hidden infections are now thought to be the basis of still other stubbornly elusive ills like chronic fatigue syndrome, Gulf War syndrome, multiple sclerosis, lupus, Parkinson's disease, and types of cancer.

To counteract these killers, some physicians have turned to lengthy or lifelong courses of antibiotics. At the same time, other researchers are counterintuitively finding that bacteria we think are bad for us also ward off other diseases and keep us healthy. Using antibiotics to tamper with this complicated and little-understood population could irrevocably alter the microbial ecology in an individual and accelerate the spread of drug-resistant genes to the public at large.

THE TWO-FACED PUZZLE regarding the role of bacteria is as old as the study of microbiology itself. Even as Louis Pasteur became the first to show that bacteria can cause disease, he assumed that bacteria normally found in the body are essential to life. Yet his protege, Elie Metchnikoff, openly scoffed at the idea. Metchnikoff blamed indigenous bacteria for senility, atherosclerosis, and an altogether shortened life span-going even so far as to predict the day when surgeons would routinely remove the human colon simply to rid us of the "chronic poisoning" from its abundant flora.

Today we know that trillions of bacteria carpet not only our intestines but also our skin and much of our respiratory and urinary tracts. The vast majority of them seem to be innocuous, if not beneficial. And bacteria are everywhere, in abundance-they outnumber other cells in the human body by 10 to one. David Relman and his team at Stanford University and the VA Medical Center in Palo Alto, California, recently found the genetic fingerprints of several hundred new bacterial species in the mouths, stomachs, and intestines of healthy volunteers.

"What I hope," Relman says, "is that by starting with specimens from healthy people, the assumption would be that these microbes have probably been with us for some time relative to our stay on this planet and may, in fact, be important to our health."

Meanwhile, the behavior of even well-known bacterial inhabitants is challenging the old, straightforward view of infectious disease. In the 19th century, Robert Koch laid the foundation for medical microbiology, postulating: Any microorganism that causes a disease should be found in every case of the disease and always cause the disease when introduced into a new host. That view prevailed until the middle of this past century. Now we are more confused than ever. Take Helicobacter pylori. In the 1980s infection by the bacterium, not stress, was found to be the cause of most ulcers. Overnight, antibiotics became the standard treatment. Yet in the undeveloped world ulcers are rare, and H. pylori is pervasive.


"This stuff drives the old-time microbiologists mad," says Hudson, "because Koch's postulates simply don't apply." With new technologies like PCR, researchers are turning up stealth infections everywhere, yet they cause problems only in some people sometimes, often many years after the infection.

Helicobacter pylori

These mysteries have nonetheless not stopped a free flow of prescriptions. Many rheumatologists, for example, now prescribe long-term-even lifelong-courses of antibiotics for inflammatory arthritis, even though it isn't known if the antibiotics actually clear away bacteria or reduce inflammatory arthritis in some other unknown manner.

Even more far-reaching is the use of antibiotics to treat heart disease, a trend that began in the early 1990s after studies associated C. pneumonia with the accumulation of plaque in arteries. In April of 2007, two large-scale studies reported that use of antibiotics does not reduce the incidence of heart attacks or eliminate C. pneumonia. But researchers left antibiotic-dosing cardiologists a strange option by admitting they do not know if stronger, longer courses of antibiotics or combined therapies would succeed.

MEANWHILE, MANY RESEARCHERS ARE ALARMED. Infectious-diseases specialist Curtis Donskey, of Case Western Reserve University in Cleveland, says: "Unfortunately, far too many physicians are still thinking of antibiotics as benign. We're just now beginning to understand how our normal microflora does such a good job of preventing our colonization by disease-causing microbes. And from an ecological point of view, we're just starting to understand the medical consequences of disturbing that with antibiotics."

Donskey has seen the problem firsthand at the Cleveland VA Medical Center, where he heads infection control. "Hospital patients get the broadest spectrum, most powerful antibiotics," he says, but they are also "in an environment where they get exposed to some of the nastiest, most drug-resistant pathogens." Powerful antibiotics can be dangerous in such a setting because they kill off harmless bacteria that create competition for drug-resistant colonizers, which can then proliferate. The result: Hospital-acquired infections have become a leading cause of death in critical-care units.

"We also see serious problems in the outside community," Donskey says, because of inappropriate antibiotic use.

The consequences of disrupting the body's bacterial ecosystem can be minor, such as a yeast infection, or they can be major, such as the overgrowth of a relatively common gut bacterium called Clostridium difficile. A particularly nasty strain of C. difficile has killed hundreds of hospital patients in Canada over the past two years. Some had checked in for simple, routine procedures. The same strain is moving into hospitals in the United States and the United Kingdom.

JEFFREY GORDON, a gastroenterologist turned full-time microbiologist, heads the spanking new Center for Genomic Studies at Washington University in Saint Louis. The expansive, sun-streaked laboratory sits above the university's renowned gene-sequencing center, which proved a major player in powering the Human Genome Project. "Now it's time to take a broader view of the human genome," says Gordon, "one that recognizes that the human body probably contains 100 times more microbial genes than human ones."

Color-enhanced intestinal bacteria

Gordon supervises a lab of some 20 graduate students and postdocs with expertise in disciplines ranging from ecology to crystallography. Their collaborations revolve around studies of unusually successful colonies of genetically engineered germ-free mice and zebra fish.

Gordon's veteran mouse wranglers, Marie Karlsson and her husband David O'Donnell, manage the rearing of germ-free animals for comparison with genetically identical animals that are colonized with one or two select strains of normal flora. In a cavernous facility packed with rows of crib-size bubble chambers, Karlsson and O'Donnell handle their germ-free charges via bulbous black gloves that serve as airtight portals into the pressurized isolettes. They generously supplement sterilized mouse chow with vitamins and extra calories to replace or complement what is normally supplied by intestinal bacteria. "Except for their being on the skinny side, we've got them to the point where they live near-normal lives," says O'Donnell. Yet the animals' intestines remain thin and underdeveloped in places, bizarrely bloated in others. They also prove vulnerable to any stray pathogen that slips into their food, water, or air.

All Gordon's proteges share an interest in following the molecular cross talk among resident microbes and their host when they add back a component of an animal's normal microbiota. One of the most interesting players is Bacteroides thetaiotaomicron, or B. theta, the predominant bacterium of the human colon and a particularly bossy symbiont.

The bacterium is known for its role in breaking down otherwise indigestible plant matter, providing up to 15 percent of its host's calories. But Gordon's team has identified a suite of other, more surprising skills. Three years ago, they sequenced B. theta's entire genome, which enabled them to work with a gene chip that detects what proteins are being made at any given time. By tracking changes in the activity of these genes, the team has shown that B. theta helps guide the normal development and functioning of the intestines-including the growth of blood vessels, the proper turnover of epithelial cells, and the marshaling of components of the immune system needed to keep less well behaved bacteria at bay. B. theta also exerts hormonelike, long-range effects that may help the host weather times when food is scarce and ensure the bacterium's own survival.

Fredrik Backhed, a young postdoc who came to Gordon's laboratory from the Karolinska Institute in Stockholm, has caught B. theta sending biochemical messages to host cells in the abdomen, directing them to store fat. When he gave germ-free mice an infusion of gut bacteria from a conventionally raised mouse, they immediately put on an average of 50 percent more fat although they were consuming 30 percent less food than when they were germ-free. "It's as if B. theta is telling its host, 'save this-we may need it later,' " Gordon says.

Justin Sonnenburg, another postdoctoral fellow, has documented that B. theta turns to the host's body for food when the animal stops eating. He has found that when a lab mouse misses its daily ration, B. theta consumes the globs of sugary mucus made every day by some cells in the intestinal lining. The bacteria graze on these platforms, which the laboratory has dubbed Whovilles (after the dust-speck metropolis of Dr. Seuss's Horton Hears a Who!). When the host resumes eating, B. theta returns to feeding on the incoming material.

Gordon's team is also looking at the ecological dynamics that take place when combinations of normal intestinal bacteria are introduced into germ-free animals. And he plans to study the dynamics in people by analyzing bacteria in fecal samples.

Among the questions driving him: Can we begin to use our microbiota as a marker of health and disease? Does this "bacterial nation" shift in makeup when we become obese, try to lose weight, experience prolonged stress, or simply age? Do people in Asia or Siberia harbor the same organisms in the same proportions as those in North America or the Andes?

"We know that our environment affects our health to an enormous degree," Gordon says. "And our microbiota are our most intimate environment by far."

A COUPLE HUNDRED miles northeast of Gordon's laboratory, microbiologist Abigail Salyers at the University of Illinois at Urbana-Champaign has been exploring a more sinister feature of our bacteria and their role in antibiotic resistance. At the center of her research stands a room-size, walk-in artificial "gut" with the thermostat set at the human intestinal temperature of 100.2 degrees Fahrenheit. Racks of bacteria-laced test tubes line three walls, the sealed vials purged of oxygen to simulate the anaerobic conditions inside a colon. Her study results are alarming.

Salyers says her research shows that decades of antibiotic use have bred a frightening degree of drug resistance into our intestinal flora. The resistance is harmless as long as the bacteria remain confined to their normal habitat. But it can prove deadly when those bacteria contaminate an open wound or cause an infection after surgery.

"Having a highly antibiotic-resistant bacterial population makes a person a ticking time bomb," says Salyers, who studies the genus Bacteroides, a group that includes not only B. theta but also about a quarter of the bacteria in the human gut. She has tracked dramatic increases in the prevalence of several genes and suites of genes coding for drug resistance. She's particularly interested in tetQ, a DNA sequence that conveys resistance to tetracycline drugs.

When her team tested fecal samples taken in the 1970s, they found that less than 25 percent of human-based Bacteroides carried tetQ. By the 1990s, that rate had passed the 85 percent mark, even among strains isolated from healthy people who hadn't used antibiotics in years. The dramatic uptick quashed hopes of reducing widespread antibiotic resistance by simply withdrawing or reducing the use of a given drug.

Salyers's team also documented the spread of several Bacteroides genes conveying resistance to other antibiotics such as macrolides, which are widely used to treat skin, respiratory, genital, and blood infections.

As drug-resistant genes become common in bacteria in the gut, they are more likely to pass on their information to truly dangerous bugs that only move periodically through our bodies, says Salyers. Even distantly related bacteria can swap genes with one another using a variety of techniques, from direct cell-to-cell transfer, called conjugation, to transformation, in which a bacterium releases snippets of DNA that other bacteria pick up and use.

"Viewed in this way, the human colon is the bacterial equivalent of eBay," says Salyers. "Instead of creating a new gene the hard way-through mutation and natural selection-you can just stop by and obtain a resistance gene that has been created by some other bacterium."

Salyers has shown that Bacteroides probably picked up erythromycin-resistant genes from distantly related species of staphylococcus and streptococcus. Although neither bug colonizes the intestine, they are routinely inhaled and swallowed, providing a window of 24 to 48 hours in which they can commingle with intestinal flora before exiting. "That's more than long enough to pick up something interesting in the swinging singles bar of the human colon," she quips.

Most disturbing is Salyers's discovery that antibiotics like tetracycline actually stimulate Bacteroides to begin swapping its resistance genes. "If you think of the conjugative transfer of resistance genes as bacterial sex, you have to think of tetracycline as the aphrodisiac," she says. When Salyers exposes Bacteroides to other bacteria such as Escherichia coli under the disinhibiting influence of antibiotics, she has witnessed the step-by-step process by which the bacteria excise and transfer the tetQ gene from one species to another.

Nor is Bacteroides the only intestinal resident with such talents. "In June 2002, we passed a particularly frightening milestone," Salyers says. That summer, epidemiologists discovered hospital-bred strains of the gut bacterium enterococcus harboring a gene that made them impervious to vancomycin. The bacterium may have since passed the gene to the far more dangerous Staphylococcus aureus, the most common cause of fatal surgical and wound infections.

"I am completely mystified by the lack of public concern about this problem," she says.

With no simple solution in sight, Salyers continues to advise government agencies such as the Food and Drug Administration and the Department of Agriculture to reduce the use of antibiotics in livestock feed, a practice banned throughout the European Union. She supports the prescient efforts of Tufts University microbiologist Stuart Levy, founder of the Alliance for the Prudent Use of Antibiotics, which has been hectoring doctors to use antibiotics more judiciously.

Yet just when the message appears to be getting through-judging by a small but real reduction in antibiotic prescriptions-others are calling for an unprecedented increase in antibiotic use to clear the body of infections we never knew we had. Among them is William Mitchell, a Vanderbilt University chlamydia specialist. If antibiotics ever do prove effective for treating coronary artery disease, he says, the results would be "staggering. We're talking about the majority of the population being on long-term antibiotics, possibly multiple antibiotics."

Hudson cautions that before we set out to eradicate our bacterial fellow travelers, "we'd damn well better understand what they're doing in there." His interest centers on chlamydia, with its maddening ability to exist in inactive infections that flare into problems only for an unlucky few. Does the inactive form cause damage by secreting toxins or killing cells? Or is the real problem a disturbed immune response to them?

Lately Hudson has resorted to a device he once shunned in favor of DNA probes: a microscope, albeit an exotic $250,000 model. This instrument, which can magnify organisms an unprecedented 15,000 times, sits in the laboratory of Hudson's spouse, Judith Whittum-Hudson, a Wayne State immunologist who is working on a chlamydia vaccine. On a recent afternoon, Hudson marveled as a shimmering chlamydia cell was beginning to morph from its infectious stage into its mysterious and bizarre-looking persistent form. "One minute you have this perfectly normal, spherical bacterium and the next you have this big, goofy-looking doofus of a microbe," he says. He leans closer, focusing on a roiling spot of activity. "It's doing something. It's making something. It's saying something to its host.

|Science writer Jessica Snyder Sachs is the author of Good Germs, Bad Germs: Health and Survival in a Bacterial World (FSG/Hill&Wang) and Corpse: Nature, Forensics, and the Struggle to Pinpoint Time of Death (Perseus Books).

"Jessica Snyder Sachs successfully weaves story--telling, history, microbiology and evolution into an exciting account of the two aspects of microbes for humankind -- the good and the bad. The book is a wonderful read." --Stuart B. Levy, M.D., author of The Antibiotic Paradox: How the Misuse of Antibiotics Destroys their Curative Powers


A Maggot for the Prosecution

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Copyright Jessica Snyder Sachs, as first appeared in Discover magazine

Insects can help solve murders but their testimony is being attacked in the courts. Pigs in stockings may help make the bugs respectable.

In the cow town of Stroud, Oklahoma, no one thinks twice about a junk pile alongside a neighbor's driveway. But people paid attention to the pile by Aureliano Cisneros's house, thanks to the thick swarm of shiny, fat flies and a ripening stench. On August 8, 1994, police discovered within that junk pile the decaying, maggot-packed body of Cisneros himself. Apparently, after being stabbed in the chest and neck, he had collapsed in front of his house; a short drag mark in the lawn suggested that someone then tried to move the 220-pound corpse before hiding it beneath the heap of dresser drawers, suitcases, and blankets.


Suspicion quickly fell on Cisneros's wife, Linda Howell. The previous Thursday night, August 4, witnesses saw the couple storm out of a local bar, with Howell saying, "You son of a bitch, I'm gonna kill you!" When investigators came to Howell's door, though, she said she'd been wondering where Cisneros was. Yes, they'd argued Thursday night, she acknowledged, but they'd made up before morning. She hadn't seen her husband for two days, since the evening of Saturday, August 6, when he left home to join some buddies.

The police didn't buy her story and arrested her for the murder of her husband. Yet when Jackie Johnson, a deputy inspector at the Oklahoma State Bureau of Investigation, looked over the forensic evidence, she wasn't very confident about the case. None of the reports gave her anything to refute Howell's claim that Cisneros was still alive two days after their public brawl.

Ironically, it was Howell's defense attorney, Frank Muret, who led Johnson to the evidence she needed. When she was handing over the forensic reports to Muret, he asked if they had looked at the maggots on the corpse. If they had, he was entitled to know what they'd found. As soon as Muret walked out the door, Johnson picked up her phone. Two calls later, she had located Neal Haskell, one of North America's most unusual private investigators. Haskell is a forensic entomologist--a scientist trained in gleaning criminal information from insects. He is, in fact, the world's only full-time forensic entomologist, though he counts as his colleagues a dozen or so other researchers who pursue forensics as a sideline. Haskell earned his Ph.D. from Purdue back in 1993. Now he crisscrosses the continent in a dusty white van with the Indiana license plate MAGGOT, consulting with the police in homicide cases and conducting research of his own.

Johnson asked Haskell if he could testify about Cisneros's time of death based on photographs, case reports, and a few vials of maggots--that is, fly larvae--collected from the body. "No problem," Haskell replied.

Haskell identified the larvae as belonging to two common flies: the black blowfly and the secondary screwworm. He then determined that these maggots were in their third developmental stage, or instar, the last before they would crawl away from the corpse to pupate and mature into adult flies. Since temperature influences the pace at which flies develop, he consulted the temperature records from the nearest weather stations, then calculated that the maggots had come from eggs laid on the body 72 to 96 hours before discovery. In other words, Cisneros could have died no later than the morning of August 5--a day earlier than Howell claimed she had last seen her husband alive.


Howell's lawyer did not exactly cave in when faced with the scientific evidence. Instead he tried to have it suppressed. During the pretrial hearings, Muret pointed out that much of the research on how blowflies develop has been conducted not on human cadavers but on dead pigs or cows' livers, and that, he argued, makes the findings inapplicable to homicides. Haskell replied that, as a matter of fact, he was preparing to publish some of his own research on human corpses, done in Tennessee. The results were consistent with nonhuman experiments.

Next Muret objected to Haskell's reliance on research done outside Oklahoma. He questioned whether developmental charts created in Tennessee are accurate enough for flies in, say, Oklahoma. This leap of faith--that blowflies in different regions grow at the same rate--is generally accepted by entomologists but remains unproved. "I've collected maggots at hundreds of workshops from one end of this country to the other," Haskell countered gruffly. "I've never seen significant variation in their growth rates outside of that determined by temperature."

Which led Muret to his next and final objection. Haskell had relied on weather readings that had been recorded miles away from Cisneros's house. Since temperature is a powerful influence on how quickly larvae grow, police should have recorded the temperature at the scene of the crime. Pulling out a field manual that Haskell himself had published, the defense attorney pounced on a passage detailing the proper procedure for determining temperature at the scene of a murder. "Did the police at the scene take ambient air temperature readings at one-foot and four-foot heights in close proximity to the body?" he asked, repeating Haskell's own instructions. "Did they take ground surface temperatures, body surface temperatures, and maggot-mass temperatures?"

Haskell granted that they had not. In making his calculations, he had used a composite of temperatures taken at weather stations miles from Stroud. Muret objected, calling the calculations guesswork, and urged the judge to rule Haskell's testimony inadmissible.

"Fortunately," recalls Haskell, "that judge was also a rancher, a no-nonsense kind of guy. When he finally made his ruling, he basically said, `When it's hot in Oklahoma City, it's hot in Stroud.'"

The judge admitted Haskell's testimony. Soon afterward Howell accepted a plea bargain.

Disputes like these over the courtroom legitimacy of entomological evidence are becoming more frequent and more pointed. In the coming years, says forensic anthropologist Bill Bass, of the University of Tennessee, such challenges will largely determine whether forensic entomology can take its place alongside such established practices as DNA fingerprinting, fiber analysis, and ballistics. Even his own science, says Bass, the identification of victims from recovered bones, "is ten years or so ahead of entomology in terms of acceptance in the courtroom."

Some forensic entomologists welcome this trial by fire. It's worth the struggle, they say, because their science offers the most reliable way of determining the time of death at a crime scene, short of an eyewitness. "Medical examiners have never been comfortable determining time of death," admits Amy Fantaskey, a pathologist with the University of Hawaii Medical School. In the first 72 hours, pathologists can make crude estimates based on rigor mortis, blood-pooling patterns, and body temperature. "But these are iffy determinations, more art than science," says Fantaskey. And beyond 72 hours, as the body cools, blood-pooling patterns fade, and rigor mortis melts away, these methods become useless.

This is exactly why some judges have been so receptive to forensic entomology. Insects populate the human corpse--or any carcass--in predictable waves over the course of weeks. The first to arrive are the husky bombardiers known as blowflies, or bottle flies, distinguished by their metallic sheen. Though cold weather and closed doors can delay their arrival, in warm weather they materialize within minutes of a body hitting open ground. "Just leave a steak uncovered by the barbecue," notes entomologist Gail Anderson of Simon Fraser University in Burnaby, British Columbia. "You'll see how fast they pull in."

Entomologists suspect that the first blowflies to find a corpse lay down chemical signals that draw kin from miles around. Within hours, the body crawls with flies. The females pack their eggs, like a paste of Parmesan cheese, around wounds and orifices such as eyes, nose, and mouth. Eggs typically hatch 12 to 72 hours later, depending on the temperature and the species of blowfly. The squirming maggots begin life the size of a pen nib. As they feed, they secrete enzymes that enable them to slice through soft tissue like butter. As their numbers swell into the tens of thousands, they move through the corpse in roiling, crackling packs, all of them growing quickly through their instars in a matter of days or weeks.

After reaching a fat third instar, the satiated larvae--about half an inch long--crawl away from the corpse and bury themselves in soil or debris. If they are in a house, they will seek dark crevices such as the folds of bedsheets. Their larval skins shrink and harden into pupa cases. The adults emerge 6 to 14 days later. Unable to fly for several hours, they skitter around the corpse like hyperactive spiders, waiting for their wings to expand.

The development of various species of blowflies has been so well documented that blowflies have become the most reliable postmortem insect clock. Once these flies depart, it becomes harder to determine time of death with precision. An entomologist must then knit together the arrival and departure of several other kinds of insects that visit the body in a more or less orderly succession.

Hawaii entomologist Lee Goff has made good use of this puzzle-piece approach. In 1996 he handled a particularly grisly case in which the decomposed corpse of a Marine--with an execution-style bullet wound--was found in a rain forest just off the Old Pali Highway on Oahu. By the time Goff arrived (in his usual mariner, aboard a Harley-Davidson, with his collecting bottles and a collapsible butterfly net tucked into a side pouch), most of the blowflies had already come and gone, but a host of other insects were still busy with the corpse. "We had clerid beetles and hide beetles, both of which like their bodies slightly dried. I also found larvae of a rove beetle--it arrives early, but you don't see its larvae until a couple weeks into decomposition. Then I had hairy maggot blowfly; this was neat because it takes at least 17 days to emerge, and all I had were empty puparia." Goff also found cheese skippers, flies that arrive no later than a week after death. "The trick to cheese skippers," says Goff, "is that after a month, they pop off the corpse to pupate in the soil. So the fact that I find larvae means we're under 34 days." Finally Goff found soldier flies. "This one's pretty definitive for my time estimate because they let the body age for about 20 days before coming in. And the ones I collected were fifth instars, between 9 and 11 days old."

Goff thus placed time of death at 29 to 31 days before the body's discovery. Military police confronted two Marines seen with the victim 30 days earlier, and they confessed.

Part of what makes the method work so well for Goff, though, is Hawaii's isolation and its relatively limited number of insect species. Experts on the mainland find it harder to make such definitive analyses. They often encounter dozens of different cadaver-loving insects, only the most common of which have been studied adequately. "It's not unusual to find ourselves estimating the developmental time of a lesser-known insect based on that of a close relative that's been better studied," admits forensic entomologist Robert Hall of the University of Missouri. This kind of deduction is an easy target for legal attack. "On cross-examination, a good lawyer will say, `So, Dr. Hall, what you're telling us is you're guessing.'"

For forensic entomologists to answer such challenges requires thousands of hours of more research and legions of graduate students, but these are hard to come by in their underfunded field. A noticeable exception has been a program set up by Gail Anderson of Simon Fraser University, largely funded by the Canadian Police Research Center. Anderson's students camp out across the rugged landscape of British Columbia year-round, each baby-sitting the carcasses of several dozen pigs. To simulate real-life homicides, some of the victims lie buried in soil or partially submerged in streams or lakes.

In 1995, Anderson's students began clothing some of their pigs. "In Canada, at least, most of our murder victims are dressed," she explains. "We needed to document whether this altered insect behavior." The research raised eyebrows across North America when a school newspaper intercepted a grad student's e-mail request for used panties and bras.

Wire services quickly spread the story:


"I was sure I was going to get kicked out of the program for that one," recalls Leigh Dillon, now a coroner. "But certain things you can't find at Goodwill." In fact, by studying pigs in underwear, the entomologists learned some important things--that clothing, for instance, helps conserve moisture in a corpse, so that it will remain attractive to blowflies longer than if it is naked, and that maggots tend to eat the skin when a body is clothed but not if it is unclothed.

Then there are greater barriers between a fly and its host, which pose an even greater puzzle for forensic entomologists. It's one thing to say that blowflies will find an exposed corpse within minutes. But what if the body lies indoors, in a car mink, or wrapped in garbage bags? Because of such uncertainties, entomologists are only willing to offer estimates of the minimum time elapsed since a death, leaving open the possibility that the flies were delayed in reaching the body. Haskell will add 48 to 72 hours to death estimates for bodies found in closed spaces. "If a fly hasn't found the body by then, it's not going to," he says.

A better approach is to replicate the murder, says Goff, who recently did just that by wrapping a pig carcass in blankets and dropping it in his backyard. His impromptu experiment gave the court a convincing postmortem interval for a woman found in similar circumstances. "But things got a little twitchy with my neighbors," he admits.

Forensic entomologists also know that their science will be reliable only if police and medical examiners recognize the value of the bugs they encounter. Lamar Meek of Louisiana State University grumbles about one case in which the only specimen he was given was a photograph of a mass of eggs on a victim's ear. Since the body was indoors and had been found in the late morning, he testified that for the blowflies to have had enough time to find the corpse, the murder must have happened at least a day earlier--and possibly a day and a half earlier, on the evening the suspect admitted burglarizing the home. In response, the defense made their own estimate from the photograph of how old the eggs were, which they claimed pointed to the murder's taking place the following night. Meek knew their reasoning was poor but couldn't categorically refute it because he didn't have the actual eggs to analyze. "I couldn't disprove it with a picture."

Researchers like Meek wish that a forensic entomologist could be part of every crime-scene investigation, but with so few experts in the country, the next-best approach is for homicide investigators to be trained to do the necessary fieldwork. Some police departments are beginning to send their officers to "police entomology" courses held at universities around the country. Among them is the annual spring workshop directed by K. C. Kim at Penn State. This year found Kim, Haskell, and grad student David Skipper leading a line of detectives, pathologists, and coroners through the woods behind the Penn State campus.

"In the seventies or eighties, my superiors would have laughed at this," said Pennsylvania state trooper Jim Shubzda as he traipsed through the forest. "Maggots were just something we pushed aside to look at other Stuff."

As the group approached a forested area, the breeze grew perfumed with a sweet, skunklike smell. The more jaded in the group grinned at the familiar scent. "We've got some stinkers," someone cracked. Pushing aside branches, the group followed a deer trail leading to Joe Pig 1, 2, and 3. Spaced about 100 feet from each other, the victims lay in three different stages of maggot-infested decay. (The pigs had been killed by injection before being brought to the forest.)

Pig 1 was especially ripe that morning. The group's arrival dispersed a thick cloud of chunky black flies. Not so easily disturbed was a swarm of plump maggots churning inside an open wound on its flank. Masses of smaller maggots packed themselves into the pig's mouth and nostrils. Dusty patches of empty egg cases still clung to the wiry hairs around the cavities.

"Listen," whispered Skipper. Bending close to the open flank wound, students could catch the crackling of feeding maggots. Then a cascade of maggots tumbled out, pouring onto the ground. "Periodically they have to come up for air to cool off," Skipper explained. "A big maggot mass can generate a lot of heat."

The class broke into three groups, each assigned to a pig whose time of death they had to determine based on the insect evidence. "I want a nice sample of maggots from each wound and orifice," Skipper told his students. "Then get me at least one of everything else you can find." He supplied everyone with alcohol vials for preserved specimens and "maggot motels" (icecream cups with beef liver) for rearing live ones.

"All these things we're teaching you are to keep us from getting beat up in court," added Haskell. He launched into a diatribe on botched collections. "Once all we had were some squished maggots on a bloody blouse. I mean, for Christ's sake, they'd been stuffed in a paper bag and left in an evidence locker for over a year!"

Haskell reached for a long-handled butterfly net and then waited for a half-dozen blowflies to settle on Joe Pig 1's rump. He skimmed the net gracefully over the carcass and then gave the net a twist to trap several flies. After transferring the specimens into a vial, he handed the net to a pathologist to catch some flies of her own. She whacked the pig on the rump and came away empty.

Meanwhile, a monarch butterfly drifted down from the trees to settle on the white hairs of a pink ear on Pig 3. A student reluctantly poised himself to capture it, but Skipper called out, "Not of forensic value."

Later, in the lab, the students examined their maggots under microscopes. "Identifying species is the entomologist's job, not yours," Kim said, "but we want you to see what we look for so you can appreciate the importance of proper collection."

Specifically, the entomologist distinguishes different species of blowfly maggots by features such as the arrangement of the hooks lining their mouth and structures around their anus known as spiracles. Resembling a pair of sand dollars, the spiracles serve as breathing organs when the maggots bury their heads in putrefying flesh. The spiracles also reveal a maggot's stage of development--it starts life with one slit on each spiracle, and with each instar it adds another slit.

As forensic entomologists struggle to make determining time of death court-proof, recent work has begun to push the science's powers in new directions. At the FBI's National Center for the Analysis of Violent Crime in Quantico, Virginia, entomologist Wayne Lord has figured out how to use maggots to help medical examiners detect drugs or poisons in their hosts' bodies. "We've taken the you-are-what-you-eat scenario to its limit," says Lord. Recently he was asked to help determine the cause of death of a nearly skeletonized male body that had been found by hikers in a wooded area of Connecticut. He plucked blowfly larvae from the clothing and body cavities, made a puree of them, and from it detected high levels of cocaine. Combining Lord's results with the victim's case history, the medical examiner concluded that the man had died of an overdose.

In another case, Lord was faced with even less evidence: the mummified remains of a middle-aged woman who had died in her New England home two and a half years earlier. (Her death had gone unnoticed until foreclosure agents entered her house.) Instead of actual maggots or beetles, Lord could collect only empty blowfly pupae and beetle droppings. But even with these scant materials, he was able to detect an antidepressant. The woman's death was ruled a fatal overdose.

Most remarkable of all, Lord is now perfecting a method for tracing DNA found in bloodsucking insects to the humans on which they have fed. "It's only a matter of time before we put this research to work in an actual case," Lord says. "Most likely it will involve a rape and murder, in which the suspect's blood is retrieved from crab lice left on the victim." At the moment, Lord is still determining the feasibility of this approach, but he is confident it will work. If he's right, then someday one more previously mute witness will speak for the dead.

JESSlCA SNYDER SACHS ("A Maggot for the Prosecution," page 102), former editor of, Science Digest, is a science writer from the Atlanta area. "During the course of this assignment I inadvertently sickened and completely alienated the film processor at our local photo shop," she says. "I had a roll of film that was half family vacation pies, half maggot-infested body pies. My husband, not knowing, took them in to be developed without warning her. Boy, did she tell him off when he picked them up!" Sachs is now the proud owner of a black T-shirt that reads ENTOMOLOGY AND DEATH.

Jessica Snyder Sachs, a regular contributor to National Wildlife magazine, is the author of Good Germs, Bad Germs: Health and Survival in a Bacterial World (Hill&Wang/FSG) and Corpse: Nature, Forensics, and the Struggle to Pinpoint Time of Death (Perseus/Basic Books).

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The Fake Smell of Death

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Teaching dogs to sniff out corpses or drugs or bombs has traditionally been more craft than science. But some novel synthetic substances may soon change that.

copyright Jessica Snyder Sachs, as originally published in Discover magazine

FOUR YEARS AGO, standing under the Arizona sun, Detective Mark Green thought about the search ahead and felt a little queasy. Four eyewitnesses had each told the police a similar tale of young children murdered, eight years earlier, on a moonlit desert night. On this day the Phoenix police would search for their remains, reportedly buried somewhere on this desolate plateau southwest of the city.

His partner, Green remembers, was far more enthusiastic--his shiny brown coat was twitching with excitement, his tail whacking against Green's leg as they stood side by side. Judge, a chocolate Labrador retriever, was accustomed to sniffing out dope, but recently he'd been learning a new scent, that of a human corpse. His education, though, was somewhat experimental: he had learned this scent not from real bodies but from an artificially concocted perfume that purportedly captured the smell of death. Green now broke open an ampoule of that perfume and gave Judge a whiff. "Back!" he commanded--as in, "Here's what I want; now bring it back!"


Judge traced a switchback pattern across the baked red earth, his nose jumping like a rabbit's. He paused to smell the flattened remains of something furry, then moved on. After 30 minutes, he slowed, swept his snout back and forth, and started furiously digging. "Good boy!" said Green, bouncing a red chew-toy in front of his partner's nose. The Labrador bounded away with his reward.

Green brushed over Judge's scratch marks and took the dog several hundred yards downwind to repeat the search. Within a few minutes Judge returned to the same spot, again scratching and barking. Now the humans dug. They found old diapers and shreds of rotted clothing.

Unfortunately, the site was ground zero for an overpopulated pack-rat colony. It looked as if any flesh and bone, had it been here, had been eaten or carried away. Still, the human odor remained, according to Judge, who returned to claw, bark, and bite at the unearthed clumps of clay.

A forensic pathologist from the University of Arizona in Tucson arrived and pointed out a subtle depression in the desert floor. Not natural, he said, but more like the settling that would follow the filling of a wide hole. The digging continued with backhoes, and the police combed through the clay for more evidence. One of the alleged victims, a preschooler, had been described as wearing cowboy boots. Even if the leather was gone, the metal shanks should have remained. The police found nothing, but by finding those scraps of cloth, Judge became one of the first dogs in the ranks of the pseudoscent-trained.

In the wake of the Oklahoma City bombing and the Kobe earthquake, sniffing dogs have become a common sight on television. What the pictures don't communicate, though, is how difficult it is to train a dog to track a given scent. The dogs have to be worked at least once a week, and if the scent in question is that of a corpse, the trainer's life can get complicated. Carrying around the odor-laden ooze from a corpse is not a great way to win friends. "When I'm on a three-day trek in the desert, the real stuff will get me kicked out of camp pretty quick," says Green. Even training a dog to recognize a drug like heroin is problematic.
To acquire and use illegal drugs, a trainer has to plow through mountains of paperwork; moreover, a dog can easily overdose if it gets a snoutful of the stuff.

Trainers have therefore tried to replace the real stuff with substitutes. "For heroin and cocaine, we mixed up a paste of powdered milk, vinegar, and a little quinine," says Texan Billy Smith, who began training drug-sniffing dogs in the 1970s. Similarly, dogs slated for search-and- rescue missions are trained on everything from roadkill to hair and nail clippings to their trainers' own blood. Sometimes the substitutes work. But just as often, they don't.

A small cadre of chemists and biologists believe that science can make the training of dogs easier and more reliable. Their most visible handiwork, commercially available pseudoscent, is manufactured by the Sigma Chemical Company in St. Louis. Over the past five years, Sigma has developed a unique product line that now includes Pseudo Corpse I (for a body less than 30 days old), Pseudo Corpse II (a formulation designed to mimic the dry-rot scent cadavers attain after a month), Pseudo Distressed Body, and Pseudo Drowned Victim. Pseudo Burn Victim is in the planning stage. Sigma also sells a pseudo powder explosive and a line of pseudo illegal drugs.

Pseudoscent Variety Pack


"In theory, the pseudoscent is the way to go," says Larry Myers, a sensory biologist and veterinarian at Auburn University in Alabama, "because the truly difficult thing about training a dog to a scent is stimulus control." The ideal compound, he says, should capture an odor signature common to everything you want a dog to find, but nothing else. "You don't want a dog trained to find explosives hitting on a can of shaving cream." Even given the amazing sensitivity of a dog's sense of smell, such things do happen. For example, Myers tells of a narcotics officer who had trained his dog on drugs kept in plastic storage bags. "I'll be damned if that dog didn't start alerting to the scent of Ziploc bags," says Myers. A dog trained on street drugs can likewise get distracted by cutting agents, homing in on baking powder in the fridge and ignoring uncut cocaine in the pantry.

"Reliability is crucial," says Myers, "because today search dogs are being used in life-and-death situations." Among those who rely on such dogs is the Federal Aviation Administration, which deploys roughly 100 canine search teams to check suspicious-looking air cargo for explosives. The faa might be interested in using pseudoexplosives in the future--one reason being that real explosives have a nasty way of actually exploding-- and so it sponsors research on dog olfaction, including Myers's. But before he or anyone else is going to be able to come up with a reliable pseudo bomb scent, Myers says, there's a lot of basic science that needs to be discovered.

Researchers know that when a dog sniffs deeply and odor-carrying molecules flow into its nasal cavity, the shape of the cavity changes so that the molecules are focused onto a yellow, rippled, mucus-covered membrane, called the sensory mucosa, toward the back of the snout. So convoluted is the canine mucosa that if it were smoothed flat it would be several times larger than the dog's head. Because it has so much surface area, the mucosa can carry a vast number of odor-sensitive, hairlike cilia- -ten times more than are found in a human nose.

But beyond that, researchers know very little. They have yet, for instance, to define the limits of a dog's sense of smell. A dog may be able to track the day-old trail of a fugitive, yet when it comes to certain smells, such as that of acetone (the sweet smell of nail polish), a dog's nose is no better than a human's. No one has yet systematically sorted out just what a dog can smell and exactly how it does so.

Against this background of meager knowledge, Sigma chemists Thomas Juehne and John Revell created their first pseudoscents in 1989. Dog handlers working for federal agencies had come to Sigma asking for compounds for training narcotics dogs. Revell began with heroin and cocaine, each of which consists of a single big complex molecule. "With such pure, large compounds," he explains, "we knew we had to find some outer piece to work with, a little active site that might break off from the main molecule." Such a piece would probably be safe--that is, nonnarcotic--yet present in the air around the drug, so a dog could be trained with it to recognize the drug.

Fortunately, U.S. Customs had already done a lot of Revell and Juehne's work for them, analyzing the gases that float above both heroin and cocaine and isolating a variety of alcohols, alkanes, esters, and acids. All were readily available in Sigma's catalog of 35,000 laboratory chemicals. Revell and Juehne could proceed directly to a game of mix and match: they developed several test batches for each drug and sent them to six handlers with dogs already trained on real narcotics. Each handler was asked to try to have their dogs find a hidden sample. The dogs completely ignored some samples while showing keen interest in others, and from these Sigma created refined formulas.


Search dogs assist diving team in body recovery.

After a confirmation round with the veteran dogs, Revell sent the most promising signature for each drug to a second set of handlers, asking them to use it to train new dogs not yet exposed to the scent of actual drugs. Reports came back that these pseudo-trained dogs were then able to locate the real stuff. VoilĂ : Sigma had its first pseudos.
Developing a pseudomarijuana has been more complicated, says Revell. "Instead of a single pure compound, now we're working with a whole plant." To isolate the molecules in marijuana and determine their abundance, he uses both gas chromatography, which can separate chemicals based in part on how quickly they evaporate from a liquid, and mass spectrometry, which identifies compounds according to their atomic mass and charge.

Revell looks in particular for substances that will become gaseous even at low temperatures, since these would be the compounds most likely to waft from a hidden stash. "Unfortunately, we discovered that not all dogs alert to the same thing," he says. Though all the dogs had been trained on whole marijuana, they had apparently selected different signature chemicals to use for identification. Revell was able to produce a commercial pseudomarijuana by taking several of the most popular compounds and combining them in a scent cocktail, on which all the dogs hit. Still, he wants to tinker with the formula more, since Sigma has received occasional reports of the cocktail's not working. "The first came from Saudi Arabia," says Revell. "My hunch is there may be differences between marijuana varieties worldwide."

In 1990 dog handlers let Sigma know about the troubles they had training their dogs on corpses. Because this type of work comes in irregular spurts, handlers need to train their dogs continually--at least once a week, preferably more. Their substance of choice is dirt collected from under a corpse, which becomes infused with its putrid smell. Reflecting the callousness probably essential to the job, the handlers refer to this training aid by a number of names: "dirty dirt," "Mr. Sousa," or "Fred," as in "Fred B. Dead." Nobody likes handling the stuff. Trainer Carl Makins, of the Greenville, South Carolina, sheriff's office, keeps his double wrapped in plastic and locked inside a vapor-proof munitions cache. When he opens the box even for a second, he saturates the room with a sickeningly sweet smell. (Think skunk meets Montezuma's revenge.) But that's the least of a trainer's worries--there's also the threat of infection associated with hiv, hepatitis, and other diseases transmitted through body fluids.

Hearing such complaints, Patricia Carr, Sigma's liaison to the dog handlers, went to Revell and Juehne and said, "Give me body in a bottle." At first they looked at Carr as if she were crazy, but eventually they warmed to the idea. That's not to say that they allowed any ooze in their lab, let alone in their gas chromatograph. "That would have been difficult for me," Juehne says with an audible shudder. Instead he searched through scientific journals and found that the human body had been well quantified in various states of decomposition.

Five to fifteen minutes after death, protein synthesis in the body grinds to a halt. With nothing to maintain the protective lining of the gut, digestive enzymes eat the body from the inside out, splitting proteins into amino acids. At the same time, the body's resident bacteria, unhindered by an immune system, feast on the amino acids and skyrocket in number. As the bacteria produce chemicals such as ammonia and ptomaines (with such apt names as putrescine and cadaverine), they produce the distinctive smell of decaying flesh. Each stage of decomposition produces distinct peaks and ebbs in the levels of various chemicals, including the ptomaines, which is a great help to both the pathologist who wants to determine the time of death and the chemist trying to emulate the smell of it.

Juehne cataloged the chemicals most likely to be in the air or soil around a decaying human body--both fresh (Pseudo Corpse I) and well aged (Pseudo Corpse II). Among these, he looked for chemicals that might set the smell of a human corpse apart from that of an animal. "I needed something unique about the human body versus a dead animal," says Juehne.

Juehne's preliminary guinea pig was Revell. Revell had joined up with Sigma after seven years in a forensics lab, where he often worked alongside coroners at autopsies and crime scenes. "Basically," says Revell, "once Tom had a list of potential compounds, he began running them by my nose and asking, 'Does this smell like a corpse?' I'd say, 'Yeah, that's close,' and he'd disappear back into his lab to refine it."

Juehne diluted his scents to a level indiscernible to humans and sent them to a half-dozen dog handlers. The first batch was well received; a more refined brew drew raves. "I started out their biggest skeptic," says Billy Smith, "but as soon as we hid this stuff in a sandbar, the gators stole it. Then we put some in a tree, and the coons stole it; in a log stump, and the buzzards stole it."

Another tester was Caroline Hebard, a New Jersey mother of four who has been honored internationally for her canine search-and-rescue work. "Yes, this works," she told Sigma. "Now give me something for live folk."

But not just ordinary live folk. Over the years, as Hebard and her dogs sifted through the rubble of earthquakes and explosions, she saw that she needed to train her dogs to tell her if they were smelling buried trauma victims or the workers around them. "There's a certain scent, kind of sour and sweaty, around someone in shock," she says. "Anybody who's familiar with the smell in an ambulance knows what I mean." To fill the request, Juehne hit the journals again. There he found detailed analyses of compounds our bodies secrete onto the surface of our skin. "I needed to find a universal human scent, something nondiscriminatory with respect to a person's diet, sex, or age--from that baby-fresh smell of a newborn's head to the musty odor of Grandpa in the nursing home."

After another game of chemical mix and match, Juehne sent Pseudo Distress for field-testing. It reportedly sailed through all trials, with claims that dogs trained on the stuff were proving their worth in actual rescue situations. And not only did Pseudo Distress help dogs track people in shock: handlers report that it's good for finding frightened children in the wilderness and adrenaline-charged escapees in prison air ducts.

The company added its most recent pseudoscent--Drowned Victim--by reformulating its corpse tinctures into a granulated capsule that sinks in water. "The first batch was like Alka-Seltzer," comments Hebard. "It had the dogs jumping to bite overhanging branches." What trainers needed was a scent that would collect in a thin film just on top of the water's surface- -as true cadaver scent does--so dogs could follow its concentration gradient to the source. Accordingly, researchers at Sigma made a slower- dissolving capsule and filled it partly with salt grains to make it sink. "That did the trick," says Hebard.

For all the testimonials to the pseudoscents' effectiveness, there is still plenty of room for skepticism. There are no statistics from a controlled test of pseudoscents with large numbers of handlers who themselves did not know where the samples were hidden. Nor has the accuracy of dogs trained on pseudos been reliably compared with that of dogs trained on the real thing.

"We need to separate the science from the mumbo jumbo," says Myers. To begin with, he says, nobody yet knows what a dog is physiologically capable of smelling. A simple analysis of a drug or a decaying body won't tell you which chemicals are of canine interest.

That question is among those Myers is trying to answer at Auburn's Institute for Biological Detection Systems. Myers founded the institute in 1989 to study everything from actual canaries in coal mines to microbes that glow when exposed to pollutants. But for now, 90 percent of his grant money arrives earmarked for studying canine detectors.

The work begins in the sensory lab: wrapped in a baby-blue blindfold, a tan cocker mix lies on a padded table. Two students murmur reassuringly as they clip to the dog's scalp electrodes that will pick up general patterns of brain activity when she is presented with a test smell. They also focus an overhead camera on her head. One student then lifts a test tube suspended from a two-foot glass handle. As the tube nears the cocker's nose, an electroencephalograph across the room traces eight jagged lines to record a spark of brain activity. The overhead camera captures the slight movements of a sniff.

Myers's students are determining the limits of the cocker's sense of smell with a dilution of eugenol, one of the odor-producing molecules in cloves. Myers employs eugenol as a standard for determining whether his test dogs are having an off day, since dogs, like people, experience a range of colds and allergies that can interfere with smell.

If the cocker's sense of smell is up to snuff, the students test her ability to detect vanishingly small amounts of an explosive and then several of its volatile ingredients. Ultimately, Myers would like to isolate just one or two key chemicals that dogs can use to recognize the entire explosive. The result could be a safe, reliable pseudo.

Enlisted in the effort are two men that Myers admiringly calls the institute's control freaks: chemist Mark Hartell, an eager young doctoral student with a passion for ferreting out contaminants, and experimental psychologist Jim Johnston. Skinnerian to the bone, Johnston is likewise obsessed with purging contaminants--the type that creep in when humans bring subjectivity to the study of dog behavior.

To begin with, says Hartell, "what's in the list of ingredients is not necessarily what's in the air around an explosive. If the guy down the hall is wearing Polo, that doesn't mean the explosive you're studying is made by Ralph Lauren." Today Hartell is fueling his gas chromatograph and mass spectrometer with air drawn from the explosive under study. He's already identified dozens of airborne compounds, many of which were contaminants from the institute's house air. ("Dirty stuff," he comments.) Many of the other compounds break down too quickly for a dog to notice. That leaves a dozen or so worth examining.

The researchers use conditioning experiments to test these remaining chemicals. Their subject dogs do their work in the isolation of six wooden chambers--oversize Skinner boxes--in a room slung with computer wires and plastic air tubes. No human handlers here. "Uncontrollable variable," says Johnston--humans have a habit of unconsciously affecting the response of dogs by subtle changes in their appearance. Johnston prefers the objectivity of a computer program. Each chamber is equipped with a nose cup attached to an olfactometer, a glorified air pump that delivers a precisely calibrated flow of clean or scented air. Inside the chamber, slightly above the cup, are three levers. The dogs have been trained to press the right lever when they smell the explosive under study, the left lever when they get a puff of clean air, and the middle lever when the air contains a scent other than the explosive.

In chamber two, a white shepherd named Columbus begins her eight- hundredth session. (Each dog works one hour a day.) At the sound of a tone, she inserts her snout in the cup. At a second tone, she removes it and paws the middle lever: in other words, she smells something, but not one of the explosives she has been trained on.

So far, admits Johnston, none of the dogs trained to recognize the explosive have responded to any one isolated ingredient. But only a few chemicals have been tested as yet. If no one ingredient evokes a response, they will try two- or three-chemical mixtures. Developing a pseudoscent in this way is time-consuming, Myers admits, but it may help reveal the classes of chemicals to which dogs are most sensitive. To know whether dogs are indeed more attuned to certain compounds, and to identify which ones, would elevate canine training to a new and reliable height.

Till then, 1,850 dog handlers will continue to use Sigma's fascinating but sketchily tested perfumes. According to the company's customer logs, sales have more than doubled in the last three years. Often the trainers who buy them use them in combination with more traditional materials. "I like to mix it up," says Smith, who trains dogs initially with corpse pseudoscent, then graduates them to dirty dirt. Hebard combines pseudoscent with human hair for "a very strong response."

Many handlers, though, steer clear of the scents. "Using pseudos is like going to the firing range with blanks," argues David Frost, canine training supervisor for the Tennessee Public Service Commission. "The strongest thing we have going for us is the dog's amazing power to discriminate one thing from another. So why muck that up with anything but the real thing?" Using real drugs means leaping over a long series of bureaucratic hurdles, he admits, "but sometimes to do something right isn't convenient."

Still, the stories of success linger and tantalize. Out in Arizona, Detective Frank Shenkowitz, who inherited Green's grisly case, remains haunted. "I still go back there fairly often," he says of the plateau where the pseudoscent-trained Labrador Judge uncovered the decayed clothes. "You never know what the desert is going to toss back at you." A while ago, not far from Judge's find, Shenkowitz came across a tiny faded cowboy boot--the size a four-year-old might wear. "It doesn't prove murder," he says. "But I know Judge is reliable."

Science writer Jessica Snyder Sachs is the author of Good Germs, Bad Germs: Health and Survival in a Bacterial World (Hill&Wang/FSG) and Corpse: Nature, Forensics, and the Struggle to Pinpoint Time of Death (Perseus Books).

Converting Landfills

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At Play on a Field of Trash

Hastily converted landfills can be unruly dragons, belching garbage, gas, and fire. But done right, a dump can be a thing of beauty.

Copyright Jessica Snyder Sachs (first published in Discover)

During his 12 years at Englewood Golf Course in Colorado, superintendent David Lee has seen some goofy things pop out of the ground--wigs, bowling balls, even car bumpers. The course sits on a curvaceous mound of trash some 40 feet deep, and in some places, all that separates the velvety green from the garbage is a few inches of sod. Two years ago, at another converted landfill--Charlotte, North Carolina's Renaissance Park--a soccer mom went after a stray ball that disappeared into a hole at the base of a light pole. To see in the shadows, she pulled out a pocket lighter, igniting a methane fireball that blew her several feet through the air. Fortunately, she suffered little more than minor burns.


The city of Charlotte has since posted "no smoking" "no open flame" signs at all of its several converted-landfill parks. But the waste that lies just inches below the Renaissance landfill cover continues to make itself known in other tangible ways.

Renaissance Park Golf Course.

On an afternoon after a gentle rain, the ground at the park's 18-hole golf course crackles like the sound of Rice Krispies. The noise comes from large patches of mud bubbling with gas. "It looks like polenta boiling on the stove," observes retired course superintendent Robert Orazi. But it smells like rotten eggs. Last year, Orazi gave up after six years of coaxing the grass and trees to grow on two feet of soil baked dry from the heat of rotting garbage below.

The course is also plagued by uneven settlement that dimples the fairways, tilts putting greens, breaks irrigation pipes, and turns cart paths into rolling "whoop-de-doos" only a dirt biker would love. Then there's the Blob, a foot-tall lump of wiggly amber-colored ooze creeping out of the fourth fairway. "We tried shoveling it; we tried covering it. It just comes back," says Orazi. Tests show "it" to be a kind of alga that feeds on the iron-rich liquid that seeps up from below. And pop-up waste? Among the scariest finds, says Orazi, are blood bags and syringes. More typical are the tires and rubber hoses that literally float up through the soil.

The hazards don't end with belches of garbage and gas. The heat of decaying trash can itself ignite the gases a landfill releases. That may have been the case when a six-foot flame shot from a crack near Renaissance's sixth green in 1989. Workers quickly doused it. But such landfill fires can spread underground for miles.

Several years ago, in Mountain View, California, an open-air amphitheater built over a landfill erupted in smoke during a Grateful Dead concert. The landfill was equipped with a gas extraction system, but the city had turned over the system's maintenance to the production company that ran the concert. When the production crew saw the smoke coming out of a crack in the ground, they cranked up the suction. The smoke disappeared, but the suction drew the fire underground and fueled it. Luckily, engineers arrived before anyone was hurt.

Closed structures, of course, are particularly susceptible to landfill gas. Without proper sealing and venting, methane can seep inside a building on or near a landfill and rise to explosive levels. That's what happened two years ago in a snack bar under construction on a landfill driving range in North Hempstead, New York. One night the water heater kicked on, igniting a fireball that knocked down the walls.

Despite the scare stories, over the past 20 years hundreds of municipalities and landfill operators have fashioned closed landfills into golf courses, parks, ball fields, playgrounds, even ski slopes. There is no national tally--largely because dumps, especially closed dumps, are considered local domain. And there is little regulation. "You don't need an EPA permit to play ball on a landfill," says Allen Geswein, of the Environmental Protection Agency's office of solid waste. "And given the current political climate, I wouldn't expect any moves in that direction."

Yet the need for more and bigger dumps won't go away. The United States generates some 209 million tons of municipal waste each year, over four pounds per person per day. Although no one knows exactly how many landfills reach capacity each year, the number is probably well over a hundred, and these monuments to waste cost money to maintain. Since 1993, for example, EPA regulations have required landfill operators to prevent their sites from leaking gas or polluted water for at least 30 years after they're closed (by then, according to theory, most of the gases from the decomposing garbage will have been released). The associated maintenance costs can reach hundreds of thousands of dollars an acre, which makes conversion to a revenue-generating facility like a golf course attractive-- but problematic.

In 1993 the EPA also set some minimum standards for the design and operation of new landfills. Though aimed at reducing off-site pollution, these rules have the side effect of improving safety and stability on top of landfills as well. They require operators to screen waste for obvious chemical hazards and to refuse medical or toxic waste. Bulk liquids--such as sewage--are acceptable only if they have been solidified with soil or other stabilizers. Operators must also cover each day's garbage with a six-inch layer of dirt, which reduces the blowing away of trash and odors. The landfill's final cap, in turn, must consist of at least two feet of compacted soil.

But only last year did the EPA make a move to control some of the gases that bubble to the surface of closed landfills. These gases are produced by the microbial food chain in the anaerobic, or oxygenless, environs of a landfill. Some bacteria, for example, degrade cellulose into sugar. Others eat the sugar, producing the acid that feeds gas-releasing bacteria. The result of their feast is a mix of methane (50 percent), carbon dioxide (40 percent), and nitrogen (9 percent), plus the trace contaminants that produce the foul smell of decay. None of these gases are particularly hazardous when allowed to dissipate in open air, says Martha Smith of the EPA's office of air quality planning and standards. It's the remaining 1 percent that includes some scary stuff.

When bacteria degrade household cleaning products, solvents, paints, and pesticides, they generate vapors that include such nasty carcinogens as benzene, toluene, vinyl chloride, and a half dozen others. Vinyl chloride is a particularly toxic and persistent gas--persistent because it kills the very microbes able to dechlorinate and so detoxify it. The EPA's new rules require landfill owners to monitor and control these dangerous vapors in the air just above the landfill cover, keeping them within a safety margin of 500 parts per million. Control measures usually include an underground venting system that sucks toxic vapors and other landfill gases aboveground and burns them off.

Unfortunately, EPA regulations apply only to large landfills-- typically those serving more than 100,000 households--that have been opened or modified since 1991. "This isn't to say that smaller and older landfills aren't of concern," says Smith. The EPA encourages individual states to set higher standards. California, for one, actually does, she adds. Moreover, whether from civic-mindedness or fear of liability, some of the nation's garbage giants are pioneering new designs for landfills and landfill parks that far exceed government standards.

The 188-acre live Oak Landfill and Recycling Center on Atlanta's outskirts is a far cry from the haphazard dumps of the past.

Roughly the size of several football fields, it is one of the Southeast's largest landfills--handling some eight tons a minute, 4,500 tons a day. Opened in 1986 by Waste Management--which is the world's largest waste-disposal company, with some 140 landfills--Live Oak will reach capacity in 2001. After that it may begin a new life as a recreational facility with soccer fields and horseback-riding trails.

Last December trash compactors at the Live Oak site were still spreading refuse on top of two of the three trash heaps that will end up 160 feet high. The first two mounds sit astride a central pit, where the operation's next phase will begin. Garbage will ultimately fill this pit, then start piling up and out like an inverted mountain against the sides of its sister peaks. The result will be a single flattened pyramid with a playable tabletop some five acres in size.

At the bottom of the still-empty central pit are seven layers of protective barriers for gathering and removing leachate--the polluted liquid from the decaying waste. The uppermost layer is a two-foot blanket of glistening white sand; not ordinary sand but grains manufactured to a specific size. If the grain sizes varied, they would pack together under the weight of the landfill, and smaller grains would fill in the holes between larger ones, preventing the runoff of leachate. Buried within this permeable, carefully milled sand is a horizontal pipe that will carry the leachate to a low-lying area. From there it will be pumped out of the landfill for disposal.

Directly beneath this layer of sand is a thin--.06 inch--sheet of high-density polyethylene (HDPE) plastic. Below the plastic lies a quarter- inch geosynthetic clay liner consisting of two fabric layers filled with a dry granular clay called bentonite. When wetted by, say, a leak in the overlying plastic sheet, the bentonite swells to form a tight, highly impermeable barrier.

The next layer down is the landfill's drainage system--a thick screen of heavy HDPE perforated pipes. Should any leachate reach this grid, it will drain to a low-lying pit. Leachate filling the pit will lift a float, which sounds an alarm signifying that the primary liner system has been breached. Live Oak operators can then draw the leachate out of the pit by applying suction. An added safeguard is a bottom layer of high-density polyethylene, which in turn lies on top of six inches of compacted clay.

Above these protective barriers, daily operations begin. Unlike the casually heaped dumps of the past, Live Oak conserves space by squeezing every last bit of air out of the garbage, creating a tightly compressed landfill structure. The garbage is sorted and distributed by size and compressibility, then ironed flat by 100,000-pound trash compactors that grind along on broad, cleated rollers. The compacting continues in two-foot layers until some 1,400 to 1,700 pounds of waste have been compressed into every cubic yard of space. Uncompacted, the same cubic yard would hold just 500 pounds.

At day's end, an eight-to-ten-foot stack of smashed waste is covered with dirt and crushed once more into a "cell." Imagining the landfill in cross section, the daily cells form continuous rows called lifts, which in turn become the landfill's horizontal tissues.

Trash compactors grade the landfill's outer slopes to a 30 to 33 degree angle to maximize the structure's stability. The continuous grading and compacting will greatly reduce the settling of garbage after the landfill is closed. More important, the compaction helps ensure that settlement is smooth and even. Though Live Oak Landfill may eventually settle by a dozen or so feet over the next 30 years, the overall shape and surface contours should remain roughly the same.

At five acres, Live Oak's upper surface is too small to be converted into a golf course, but had that been the plan, bulldozers would have shaped the top layer of refuse into berms, curving fairways, and flattened greens. For the more modest plan of a ball field or equestrian center, the landfill's upper surface will be graded into a broad, gentle crown with just enough grade, about 5 degrees, to quickly slake off rain.

Before capping the landfill, Live Oak operators will install vertical pipes down through some 140 feet of trash to collect methane-rich gas. Other landfill operators have fashioned even more detailed gas collection systems, including a grid of flexible horizontal perforated pipes that snake through the trash, absorbing gas and feeding it to the vertical gas collection pipes.

Although the EPA requires only that the gas vented from a landfill be flared, Waste Management is considering another plan for Live Oak. The gas might be drawn off to an on-site power plant and used to generate electricity. In this speculative scenario, the company estimates that for some five to ten years after closure, Live Oak could generate .8 to 2.4 megawatts of power, enough continuous energy to serve perhaps 1,200 to 3,600 homes.

The crowning touch, of course, will be the landfill's cap, the crucial barrier between its waste and park visitors of the future. At Live Oak, plans call for a composite cover combining natural and synthetic liners. The layer that lies directly above the waste will be an 18-inch layer of compacted clay. Workers will iron the clay with 60,000-pound drum rollers until it's virtually impermeable to water.

Above this layer they will install a synthetic membrane like the plastic that lines the bottom of the landfill. High-density polyethylene is a popular landfill liner because it consists of strings of polyethylene molecules (CH2-CH2) thousands of carbon atoms long. The extreme length and stability of polyethylene's carbon backbone allows the molecules to pack tightly together like a crystal and so resist the assault of corrosive landfill leachate. However, this extreme density comes at the expense of flexibility. HDPE's brittleness is not an issue at the bottom of the landfill, where the membrane lies on top of solid ground. But the landfill cover must be able to flex as the garbage beneath it decays and shifts in its bed.

A little chemical manipulation provides the answer: add hexene (C6H12) to the polyethylene. Hexene's molecular structure prevents it from folding up into the neat, crystalline structure of the polyethylene, thus creating "lumpy," disorganized patches in the polyethylene matrix. This extra elbowroom between the tightly packed carbon chains produces a more flexible, less dense polyethylene. By adding pigments and stabilizers to the polyethylene, chemists can ensure that the membrane lasts upwards of 200 years.

To prevent water from pooling onto--and possibly breaking--the landfill cover, Live Oak engineers will install a drainage net just above the surface membrane. Rainwater seeping into this open grid will flow to the landfill's edge. The drainage net, in turn, will be covered with a synthetic textile, over which will be heaped two feet of soil, seeded with grass. The entire cover system, from compacted clay to top soil, is designed to achieve an impermeability of a ten millionth of a cubic centimeter of water--a leakage rate of less than 147 gallons per acre a year.

When the landfill cover is finished, the top and bottom liners will be sealed together like a gigantic plastic bag. Post-closure maintenance, such as sealing up fractures or repairing leaks, will be costly. Although Waste Management is reluctant to confirm details concerning revenue, the cost of constructing and operating Live Oak-- including buying the land and converting it into a recreation area--will reportedly total some $400,000 an acre. That's about $75 million, and it sounds staggering until one calculates revenues for the 188-acre landfill. With tipping fees of $32 to $35 a ton, that's as much as $157,000 a day.

In reality, few landfill parks in this country are as well-financed and state-of-the-art as Live Oak. The typical scenario has been that of a cash-poor local government trying to convert an old, unregulated dump into landfill that can be used as a park. "All too often,
County engineers simply dump dirt on the landfill, plant some grass, and say here's your recreation area," says Morton Barlaz, an environmental engineer at North Carolina State University. "Without a properly engineered cover and a methane collection system, you're going to have big problems."

Stories like these strike fear in the hearts of municipal attorneys. "The idea of putting people on a landfill makes me shudder," says Ann Moore, an assistant city attorney for Chula Vista, California. As a land-use expert, Moore has followed the landfill conversion trend for many years. "It was real fashionable a while back, and now a lot of cities are experiencing big problems," she says. Adds Barlaz, "There's always the risk that local governments won't have money for the high maintenance these parks demand. When budgets get cut, parks are the first to go."

Others argue that active use may simply be incompatible with the idea of keeping landfills sealed tight within a "dry tomb" of plastic. Bill Sheehan, director of environmental biology for a landfill engineering company in Lawrenceville, Georgia, warns that even the most durable synthetic covers are likely to be punctured by plant or tree roots. The irrigation needed to keep parks green is another bugaboo. If the added water penetrates the landfill cover, it can overload leachate collection systems. This is a particular problem when irrigation pipes break under the strain of uneven settlement, as they often do.

Still, with dumps filling and open space dwindling, landfill conversions are probably here to stay. And waste disposal companies can point to several thriving examples. Take Mount Trashmore Park in Virginia Beach. Created in 1973 from a 68-foot-high, 650,000-ton garbage heap, the park is now one of the area's most popular--especially with young children, who flock to the colossal wooden playground at its base. Another success is a 600-acre resort in Industry Hills, California, home of two championship golf courses. Methane from the underlying landfill is used to heat two Olympic-size pools and a hotel laundry in the adjacent Sheraton Conference Center. Then there's Riverview Highlands, a ski and golf resort built on a 600-acre garbage mound south of Detroit.

Some communities, in fact, have apparently overcome their reluctance and are ready to embrace their trash wholeheartedly. With nearly 6 million tons of refuse already in place, Virginia Beach is now drawing up plans for another landfill-based park to keep Mount Trashmore company--one more than twice as high and 18 times as voluminous as the original. After its makeover, the landfill will be dubbed City View Park, for an obvious reason--from its crest you will be able to see all there is to see. It's the biggest thing in town.

Jessica Snyder Sachs is the author of Corpse: Nature, Forensics and the Struggle to Pinpoint Time of Death (Perseus Books) and Good Germs, Bad Germs: Health and Survival in a Bacterial World (FSG).

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