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The mild winter was nice for us, but it was also ideal for the mosquitoes that carry the deadly Eastern equine encephalitis virus. Last year, EEE struck 11 people in Massachusetts and New Hampshire. So what happens now to our barbecues, soccer games, and camping trips?

By Mary Carmichael  |  May 7, 2006 |  The Boston Globe

LAST AUGUST, RICHARD LABELL, a detective with the Raymond, New Hampshire, police, got word of a killer on his beat. The warning came by e-mail from the chief: All officers should take caution while patrolling outside, especially as shadows grew long at dusk. But guns and nightsticks would be inadequate protection, because the new menace was no criminal. It was a rare but lethal virus, Eastern equine encephalitis, and although it hadn’t killed anyone in New Hampshire in a quarter century, it was circulating in the local mosquito population. The chief told his officers to cover their arms with sleeves or DEET. Labell skimmed the e-mail. “I remember clicking on it clear as a bell and thinking, `Yeah, what are the chances of that?’ ” he says. “And then I deleted it and didn’t think about it again.”

Less than a month later, Labell’s 20-year-old daughter, Kelly, started complaining of a fever and pain in her back, neck, and ears. On the third day of symptoms, doctors at a local hospital told her she had the flu and an ear infection. Kelly knew something more serious was wrong; she told her father she thought she might die. On the fourth day, she became incoherent, and the hospital admitted her. The next morning, she had a seizure. The detective watched as the doctors stuck a needle into her spine and tried to identify the culprit.

When Kelly’s brain started swelling, the local medical team sent her to Beth Israel Deaconess Medical Center in Boston. The doctors there had a new plan: They put her in a coma, trying to “cool down” her now dangerously inflamed brain, with the hope of bringing her slowly back to consciousness. But the organ strained against her skull. Surgeons bored into her head to relieve the pressure, but it was too late. Kelly was brain-dead. On September 9, Richard Labell and his wife, Donna, made the decision they’d been dreading and pulled her off life support. It was only later, after an autopsy, that the doctors could tell Richard what had killed his daughter: EEE, the same mosquito-borne disease he had casually disregarded as a threat to himself.

By the first frost in October, the end of mosquito season, New Hampshire and Massachusetts had seen 10 more cases of EEE, three of them also fatal. Two of the dead were men in their 80s, already weak. But Kelly, blonde and vivacious, and Adreanna Wing, a 5-year-old girl from Halifax, were headline material. Town councils across the region sent out calls for emergency meetings, and schools canceled outdoor activities. Though EEE had been entrenched in New England for decades, it suddenly seemed like a new enemy – strange, insidious, and deadly.

Now, as mosquito season starts up again this month, cities and towns all over New England are preparing for more EEE cases. There is no consensus as to how to prevent them and no reliable way to estimate how many there will be. The past winter, wet and warm, was ideal for the main mosquito species that harbors EEE, but that is just one factor in a complex cycle that scientists don’t fully understand.

“Mosquitoes don’t pay much attention to our forecasts, nor do they necessarily behave in ways that we believe they should,” says Richard Pollack, a Harvard professor who researches infectious diseases. “Anyone who would offer you a firm prediction regarding risk has, in my estimation, delusions of his own abilities.” The one thing we know for sure, he says, is that we don’t know enough.

With that in mind, the families of last year’s victims are plotting a better-safe-than-sorry strategy for this year, and some have joined public health officials in pushing for more pesticide use.

But they have to convince their neighbors that pesticide spraying is a threat only to mosquitoes; that it’s worth the cost, even though nothing in the public-health arsenal can eradicate EEE or its carriers; and that in an era of bird flu, AIDS, and terrorism, a disease that kills five people nationwide in an average year is a threat to be taken seriously. And they are working against a clock. The time to start is now, before mosquito season gets underway. They must convince people that, if ignored, EEE could be a problem — before it has a chance to prove them right.

The virus that killed Kelly Labell had been lurking in the swamps of coastal New England long before she was born. For decades, possibly centuries, it has ridden in the bodies of mosquitoes, infecting the occasional bird or mammal and largely escaping human notice. Unlike West Nile virus, which appeared in Massachusetts in 2000 just one year after its debut in the Western Hemisphere, EEE is native to the Eastern seaboard and may have originated in New England. It was near Boston that farmers first described the virus in 1831. EEE has appeared in animals in Connecticut and Maine but has never, to anyone’s knowledge, infected a human in either state. Massachusetts and New Hampshire are not so lucky; together, they accounted for half of last year’s deaths nationwide and 11 of 20 total confirmed human infections.

The virus rides along in the saliva of a mosquito called Culiseta melanura, a pest that finds an especially fertile breeding ground in the Hockomock Swamp. Local lore says the swamp, a vast, acidic wetland in the southeast corner of Massachusetts, is haunted by evil spirits. But what really makes it creepy are Culiseta larvae that spend the winter in protective “crypts” formed by frozen pockets of water beneath the roots of white cedar trees. While the larvae of other species can be taken out with pesticides, there’s no way to kill an infant Culiseta. It hides until the crypt thaws, typically in mid-April. Then it hatches and takes wing.

If humans don’t like Culiseta melanura, the feeling is mutual; the species rarely bites people. “They may get sloppy from time to time,” says Pollack, but the mosquitoes much prefer to bite birds. For a few days after a bird has been newly infected, it carries high levels of the virus in its blood. During that short window, females of more than 20 other species of mosquito can catch the virus by biting the sick bird, which by then may have traveled a considerable distance from where it was infected by Culiseta. These “bridge vector” mosquitoes also take their blood meals from humans and can pass the virus on. This is why people who never go anywhere near infested wetlands can still catch EEE.

“My daughter wasn’t an outdoor enthusiast. She wasn’t camping or fishing or horseback riding,” says Richard Labell. “She just got bitten, and it could have been anywhere. It could have been in this house.”

The disease is not always a death sentence for humans; if the virus does not reach a patient’s central nervous system, symptoms are little worse than those of the flu. (These cases are rarely diagnosed and therefore are not usually included in official statistics.) But when EEE does reach the brain, it kills a third of its victims. There is no vaccine and no cure — the disease is too rare for most pharmaceutical companies to chase – and for about half of those who live, survival does not equal recovery. “We’ve gotten better at keeping people alive, but the scary thing about EEE is the lingering effects,” says David Henley, a superintendent of the East Middlesex Mosquito Control Project since 1982. Had Kelly Labell lived, she might have been blind, deaf, paralyzed, or permanently brain-damaged.

By the time the virus infects a person, its travels are effectively over. Humans cannot transmit EEE; they don’t carry high enough viral loads in their blood. For that reason, barring a radical mutation, the virus will never cause a pandemic. But mosquito bites alone can be enough to cause an epidemic or, as it’s called in animals, an epizootic.

That’s almost certainly what happened when the virus is first known to have reared its head, in the summer of 1831. According to reports in the New England Farmer, several dozen horses in rural Massachusetts started lurching through the pastures, paralyzed and spastic. People took to calling the illness “brain fever” or “sleeping sickness” or, after its most distinctive symptom, “the blind staggers.” But it remained undescribed by scientists for more than a century, until in 1938 it infected almost 300 horses near its Hockomock hiding grounds and, this time, 34 people. Three-quarters of the human victims died (as did all the horses), and only one fully recovered. At the epidemic’s peak, five Massachusetts children living within a few miles of one another fell fatally ill. By the end of the outbreak, Harvard doctors examining the children’s brains had named the disease.

EEE appeared in regular two- or three-year cycles after that, killing a few people on average each year, and although small epidemics and epizootics broke out in the 1950s and ’70s, they never reached the scale of 1938. Local mosquito-control programs were put in place across New England during the mid-1990s, but the goal of those was to make the region more attractive for tourists, not to prevent disease. At the start of this decade, some counties began to let their programs lapse. And even though health officials started publicly worrying in 2003 that the state might be overdue for an outbreak, Massachusetts had no known human cases of EEE that year.

But of course, the disease has never really gone away.

The mystery is why it came back now.

The damp, warm winter of 2004-2005 provided ideal conditions for Culiseta, but that’s not enough to explain the rash of EEE cases in New Hampshire, a state that hadn’t seen a fatality in 25 years. “Overall, last year in New England wasn’t nearly as bad of a year as we’ve experienced in the past,” says Pollack. “[But] New Hampshire certainly had a banner year.” Scientists don’t agree on why; they have pinned the blame on everything from global warming to a statistical anomaly. It’s also possible that EEE cases have gone undiagnosed in New Hampshire and elsewhere for years. “Maybe,” says Henley, “they just weren’t looking hard enough before.”

Even more difficult than explaining why one year was bad is divining whether the next one will be worse. Pollack’s lab runs computer simulations every year, but no model can predict a season with great accuracy. Though they’re based on years of experience and reams of data, they require at least one notoriously unreliable input: weather predictions. That makes them “a forecast based upon a forecast,” Pollack says.

EEE’s life cycle depends on dozens of factors. Some are controllable, usually related to conservation. In 1938, for example, the year of Massachusetts’s biggest outbreak, loggers stopped clearing the white cedar swamps, and the snowy egret, a disease carrier, started making a comeback. Other factors are up to nature. Rain is important, but only at certain times of year, and overall weather conditions must suit both Culisetaand the bridge-vector species that bite humans — even though what’s good for one isn’t always good for the other. Dry weather can suppress Culiseta, but a summer drought can increase the “organic load” in standing pools of water, creating an ideal habitat for Culex pipiens, a double-trouble species that can transmit both EEE and West Nile.

And those are just the factors that affect insects. The disease also requires a vulnerable bird population, one that hasn’t armed itself with antibodies. This may explain why the virus seems to burn itself out in short cycles, only to reemerge. Once most birds in an area are immune, the virus must wait for a fresh generation to infect. As for what happens to it during its dormant years — not to mention winter — researchers are baffled. It may die out in one region only to be brought back by migratory birds from another, or it may mutate into a form that tests can’t detect. Either way, says Henley, it survives. “I don’t think you can wipe it out,” he says. “EEE is something we’re always going to have to deal with.”

OK, so how do we deal with it?

The first step is to identify the virus in the wild. Massachusetts’s surveillance system compares favorably with any other state’s, although agencies sometimes disagree on what to do with the results, causing gridlock. But the real controversy arises on the local level, where many of the efforts to control mosquitoes are carried out. At the beginning of mosquito season, public health officials remind residents to take easy and effective precautions: Stay indoors at dawn and dusk, wear long sleeves and pants, and don’t forget the bug spray, especially a variety that contains DEET. But as Richard Labell learned last August, those precautions are easy to ignore. And the only other practical way to tamp down the virus is to shoot the messenger — to spray pesticides.

The process has already begun in some areas. Early last month, when the first broods of several mosquito species emerged, Henley started covering Middlesex County wetlands with BTI, a bacterium that destroys the digestive tracts of mosquito larvae. As the season wears on, he will send out college students on bikes to drop more bacteria and methoprene, which mimics a hormone that stops the larvae from maturing, into tens of thousands of storm drains. By late May, all of the spring mosquitoes that remain will be on the wing. To take them out, he’ll spray a chemical called a synthetic pyrethroid.

Mosquito control is a literal NIMBY for many people — spray the rest of the town, sure, but not my backyard. “Many people seem to believe that any pesticide either will clear the landscape of all life forms or induce mutations that cause their children to develop extra arms and heads,” says Pollack. This, of course, is wildly exaggerated. The EPA says the methods used in the Northeast are safe for humans. BTI is found naturally in soil, and synthetic pyrethroids are similar to a chemical found in chrysanthemums. Of the latter, Henley says, “you can use a very small amount — we’re talking a few thousandths of a pound of active ingredient.” And neither method appears to have the deleterious environmental effects of DDT.

But that’s not to say pesticides are perfect. To cover a single town can cost tens of thousands of dollars. There is ecological risk as well. Synthetic pyrethroids can be toxic to fish; methoprene, used to fight West Nile in 1999, may have contributed to a die-off of lobsters that year in Long Island Sound. And the pesticides now used to control mosquitoes could eventually become ineffective. Because mosquitoes breed quickly, they can evolve resistance to particular pesticides.

A new method of mosquito control, one without serious environmental impacts, may be on the horizon. At American Biophysics Corp. in Rhode Island, chief technology officer Emma Durand hatches mosquitoes to study as they fly through wind tunnels and bite a dummy. The lab’s biggest breakthrough has been figuring out why “some people get bit unmercifully at family picnics, and others don’t get bit at all,” she says. The reason, it turns out, is skin chemistry: Those unlucky enough to have high levels of certain chemicals in their perspiration are mosquito buffets.

Eventually, Durand hopes to use her lab’s research as a tool to screen for those at high risk of being bitten. But for now, the findings are applied in the Mosquito Magnet, a machine that lures the insects with carbon dioxide and skin emanations into what Durand calls “the Zone of Doom.” The traps can kill several thousand mosquitoes in a week, and 800,000 have been sold. But the buyers are shoppers at Home Depot and Ace Hardware, not town councils. Durand says that selling the traps to public health authorities is her next goal, but at about $300, the cheapest trap can cover just a half an acre. Even more than spraying, widespread trapping could be wildly expensive.

At what point does the cost of saving a human life, in both dollars and possible public-health risks, outweigh the benefits?

FOR THE LAST EIGHT MONTHS, TOWNS across New England have sought an answer. Some have put spraying measures in place where there were none. Labell’s hometown of Newton, New Hampshire, had budgeted $15,000 for spraying; after Kelly’s death, Labell says, it added $20,000. (Private citizens have come forward with their own money, albeit for medical research rather than spraying. Fund-raisers expect The Kelly Labell EEE Research Fund to sell out of tickets for its October 14 benefit for AlphaVax, a firm working to develop a viral encephalitis vaccine.) Labell would like to see more towns follow Newton’s lead. In recent months he has been testifying in support of a state bill that would help New Hampshire towns pay for spraying and put pesticide-permit applications on a faster track — in a classic example of events moving faster than government, the process currently takes six to 10 months, longer than the actual mosquito season.

Not all town councils agree that mosquito control offers enough bang for the buck. Take Concord, New Hampshire, about 35 miles northwest of Newton. As the state capital and third-largest city, Concord has more cash than many of the surrounding towns for projects like mosquito control, but in recent years, the city has been reluctant to spend the money. Although last summer’s EEE outbreak prompted an emergency city council meeting, the group ultimately decided against spraying, 9 votes to 5. Katherine Rogers, a longtime councilor, voted nay because the city couldn’t spray everywhere. Private lands would go unprotected, as would a patch of public land in her area near the home of an endangered butterfly. “My concern all along was `Who tells the mosquitoes where they can and can’t go?’ You know, they do fly,” she says dryly. “You’d still be leaving a huge number of people vulnerable. If they could offer me a 100 percent guarantee that [after spraying] this disease would never hurt another person, I would consider it.” Rogers also notes that funds spent on mosquito control are funds not spent on road construction, libraries, or other projects. “Not to minimize the fact that people have died, but … there are a lot of other things that need money,” she says. “If you’re going to gamble with money, you’d better make sure you’ve got the best odds.”

In the end, this is what the debate comes down to: a bet. EEE has a high fatality rate, but the odds of catching it are vanishingly small. The chance that pesticides will completely eliminate EEE is nil. And there is not an infinite supply of money.

“It’s expensive to spray, I’ll give you that,” Richard Labell says. “But you’re talking about human life. And I don’t think we should put a dollar-and-cent value on human life.” You want to talk about price? “One or two or three lives,” Labell says, “is a huge price to pay for being bitten by a mosquito.”