COLUMN ONE : Hunting a Mysterious Deer Killer : Scientists and game wardens are tracking an elusive quarry. In one of the animal world’s biggest whodunits, they seek clues to the deadly virus believed to have claimed thousands of animals.

When the first deer dropped dead in Jill Ballas’ yard, she didn’t give it much thought. But six weeks later, when a fawn keeled over in her flower bed, Ballas knew something was wrong.

One sweltering afternoon in August, Ballas gazed out her kitchen window and watched the leggy, white-spotted fawn nuzzling a doe and dashing across the woods. An hour later, when she looked again, it had collapsed into a soft mound of fur the color of damp sand.

Oddly enough, the fawn looked perfectly healthy. Except it was dead.

“It was just a baby,” said Ballas, 78, who had watched the 2-month-old frolic in her acre of oaks and pines since it was born. “They have the most beautiful faces with big, brown eyes. Just like Bambi.”

Ballas rounded up a neighbor, who loaded the body into a wheelbarrow. Then she called the game warden.

When Ron Colombani hung up the phone, he knew he had more than an oddity on his hands.

In just three weeks, 20 deer had died mysteriously within a two-mile radius in this little Mother Lode town on the western slope of the Sierra Nevada. Was someone poisoning deer to keep them from gnawing on rosebushes? Had some toxic chemical, perhaps buried long ago by a gold mine operation, seeped to the surface?

Gruff and unflappable after 23 years as a state Fish and Game warden, Colombani can tell all sorts of bizarre critter tales. But whatever was killing Sonora’s bucks, does and fawns was the biggest mystery he’d ever encountered.

It turned out the outbreak was not confined to Sonora. Wild deer began dropping dead by the hundreds--almost as if on cue--all over the northern half of California in late July.

By mid-August, California’s deer die-off had become one of the biggest whodunits in the animal kingdom, baffling everyone until a sharp-eyed pathologist dissected the fawn that died in Ballas’ yard and noticed an odd mark in the center of a cell.

The culprit turned out to be a virus--a nasty, DNA-mutating strain never encountered before. With the fawn as their “Patient Zero”--the first deer to be diagnosed--state wildlife investigators began tracking the epidemic, searching for clues to its cause, or better yet, its cure.

The death toll remains unknown, but it is believed to be in the thousands. Since July, the carcasses of at least 500 deer--mostly fawns--have been found in 17 counties, from the redwood forests of Yreka to Yosemite National Park to the coast of Marin County. The body count has slowed to 20 or 30 a week, but officials suspect that the corpses represent a fraction of those that are dying in the wild.

“It spreads like a cancer,” said Bradd Barr, one of several UC Davis veterinary pathologists investigating the virus. “We’ve got what looks like a massive die-off of animals in a short period of time.”

Although there is some dispute over the long-term legacy of the epidemic, California’s stock of wild deer, estimated at 700,000 to 800,000 strong, is not likely to disappear. However, signs are emerging that populations might be decimated in some parts of Northern California, especially in the High Sierra towns and backcountry of Tuolumne and Nevada counties.

This fall, some hunters reported nearly as many dead mule deer as live ones in the mountains, and some residents say the black-tailed does and fawns that nibbled on their gardens have vanished.

“Is it a catastrophe? Probably not,” said David Jessup, an animal disease expert with the state Department of Fish and Game, which is handling the investigation. “Most of these diseases are fairly self-limiting. That’s not to say it’s not important. Especially with new viruses, the effects can be profound.”

Still, the killer virus is unnerving. Although humans and other animals seem immune, it infects deer herds with the ease of a cold, spreading through a sneeze or a lick of the tongue.

But instead of flowing like a slow wave from animal to animal, the disease has struck hundreds of miles apart, seeming to rapidly cross cities, interstates and mountain ranges--obstacles no deer can easily ford. “That’s a helluva lot of deer rubbing noses,” one wildlife biologist said.

Investigating a wildlife epidemic is similar to tracking a human virus, except the quarry is more elusive. After all, a deer cannot fill out a questionnaire: Who was your last sex partner? Where have you been during the past 48 hours?

“It is very difficult to go in reverse and figure out why an animal died when all you have is a pile of bones,” said Bill Clark, director of Fish and Game’s Wildlife Investigations Laboratory.

“And the bottom line is there is not a damn thing we can do about it. The virus is going to run its course. There is no way to treat it, or vaccinate, or do anything to all the individual animals out there.”

*

Ron Colombani was sitting down for Sunday dinner Aug. 15, but as soon as he heard about a fawn dropping dead in Ballas’ yard, he jumped into his pickup truck and drove the mile to her house.

Colombani wanted the mystery solved quickly because rumors about poison were starting to spread. The fawn was exactly what he had been waiting for. He knew the pathologists needed a fresh carcass to make a diagnosis.

Colombani packed the deer on ice--its 15-pound frame fit perfectly in an ice chest--then loaded it into his pickup. The next morning, he drove the 120 miles to the state’s wildlife lab near Sacramento, which promptly turned to nearby UC Davis for help.

When the deer was carried into the university’s Veterinary Diagnostic Laboratory, Leslie Woods was intrigued. A pathologist for 10 years, Woods had diagnosed plenty of animal diseases--parasites in cattle and hepatitis in turkeys. But most of her experience was with livestock, not wild animals.

Logging the deer in a specimen book, Woods was alarmed to read the warden’s hand-scribbled notes: “Apparently healthy fawns mostly 2 months old have died from unknown causes.” A crudely drawn map showed 20 deaths, nine within yards of a mobile home park near Ballas’ home.

The instant Woods sliced into the corpse with her scalpel, she knew the deer’s healthy looks were deceiving. Its lungs were filled with a white foamy fluid. Vessels in the brain were enlarged. The small intestines were hemorrhaging.

Woods tested for all the usual suspects. “When we didn’t know what we were dealing with, we looked for everything,” she said.

All tests were negative. No poisons, no pesticides, no abnormal bacteria and no bluetongue disease, which is spread by insects.

Woods was puzzled. She slipped tissue from the deer’s ravaged lung under her microscope, magnifying it 400 times. A cluster of nuclei, dyed bright pink on the slide, caught her eye, and she focused her scope on one cell. She noticed an abnormality so subtle she almost missed it--a tiny particle in the nucleus, called an inclusion.

That could mean only one thing--a virus had attacked this deer’s DNA, the building block of life. Finding the odd mark took a combination of skill and luck because such telltale signs appear only during a certain stage of a virus’s activity before vanishing forever.

Woods was surprised and still dubious because she had never heard of a DNA disease in a deer, let alone one that was deadly.

Bob Nordhausen, who operates the lab’s high-powered electron microscope, prepared the tissue for closer examination. Bathed in the green phosphorous light of his microscope, he magnified the cell 80,000 times. He photographed the image, studied the abstract patterns, and walked the pictures over to Barr, the UC Davis pathologist.

Nordhausen then uttered one word that touched off a flurry of interest: Adenovirus. He was 99% certain.

Adenoviruses--a broad category of infectious viruses that alter DNA and cause respiratory disease--are ubiquitous, even in humans. If you remove your tonsils you’ll probably find an adenovirus. But they are not usually fatal. This one, however, had taken a much nastier form.

As Barr studied the photos, he remembered that six years earlier, a deer carcass was sent to his lab from an animal rehabilitation center in Sonoma County. At the time, Barr had not noticed any abnormal cells, and there was just one dead deer. The case was quickly closed.

But the memory gnawed at him, so Barr rummaged through the long-forgotten file and found some old tissue. The same pockmarked nucleus was there--meaning that the virus had lingered dormant in California’s deer population since at least 1987. Either it suddenly became more virulent this summer, or some environmental condition changed that made it more deadly.

One theory is rain. The Sonoma deer had died after a wet winter, and then the virus subsided for six dry years. Coincidence? Woods wondered. “This is just my theory,” she said, “but this is the first years of drought.”

*

For those living in the western shadow of the Sierra Nevada, the third Saturday in September--the start of deer hunting season--was marked on most calendars. Dave Townsend, who had not missed a season in 33 years, was riding on horseback in the Emigrant Wilderness, a land of unpretentious beauty with golden meadows and endless firs. Just off the trail, he saw a dead doe. It was just the beginning.

Over the next two days, Townsend’s party counted 18 live mule deer and 13 dead ones. They had heard tales of the virus in the more populated foothills, but were stunned to see deer stricken in the remote national forest.

“I’ve been going to the Sierras all my life,” said Townsend, 45, of Sonora, “and I’ve seen the deer herd hurt by real heavy winters, but never anything like this.”

So many hunters called Jim Maddox, the senior-ranking Fish and Game biologist in Tuolumne County, he spread out a map of the Emigrant Wilderness and drew a red dot where each deer had died.

By that Monday, his map looked like it had a bad case of chicken pox. There were more than 100 dots.

Since mid-summer, Maddox had become accustomed to finding dead deer under people’s porches. But those areas, he rationalized, were overpopulated with deer anyway because people feed them. It was another matter when carcasses turned up in remote areas; hunters found the first ones Sept. 18 in the Emigrant Wilderness, where several of the state’s largest herds converge every summer as if it were an annual convention.

“That one was a whole new red flag because we knew it came from migrant deer country,” Maddox said.

He started to tick off the names of the migrating herds that meet in that stretch of backcountry, then stopped, as if silently calculating how quickly the disease could spread throughout the Sierra.

“I suspect that this die-off is significantly greater than what we know,” he said. “The indications are at this point that there are less deer out here than in recent years. As populations get lower and lower, somewhere down there is a threshold and below that, it’s hard for the deer to come back.”

*

A month after deer season started, on a brisk October afternoon, the phone rang at Fish and Game’s investigations lab in Rancho Cucamonga. Sitting on a desk, dressed in a green surgeon’s tunic with a stethoscope draped around her neck, Pam Swift listened intently to a worried woman calling from Nevada County.

“Does he look pretty bad? They don’t all die. Drooling? OK,” said Swift in the soothing voice of a country doctor.

She listened, then laughed. “Pepto Bismol on bread? Well, you’re trying. Pepto Bismol won’t hurt him, but it’s best not to feed him. . . . Since we’re overloaded here, let’s just let him be.”

As a veterinarian, Swift’s job is to document and investigate the reports of deer deaths and assist UC Davis pathologists as they try to culture and identify the virus. But her most time-consuming duty is answering questions from people who will do anything to nurse the dying deer, even administering pink diarrhea medicine.

“It’s what we call the Bambi syndrome,” Swift said. “People don’t realize deer die and get disease, just like people do. . . . It’s just that we can’t do much for deer.”

Swift takes the turmoil in stride. “Whenever there is a new disease, the population takes a little while to adapt, but I think they will adapt. Deer snap back,” she said.

Most diseases in the wild start as large outbreaks, gradually subside as animals build up immunity, then return periodically. Forty years ago, dire predictions were made when a disease swept through white-tailed deer in New Jersey, but now the animals are so plentiful there that homeowners are plotting ways to get rid of them to save their gardens.

Compared to other natural causes of death in deer, the virus has had a minor impact, said Ken Mayer, California’s deer management coordinator. Every year, half a million fawns in the state die, mostly victims of starvation or predators, he said. Of every 100 fawns born each spring, 30 die by fall.

“It would have to be a chronic disease, year in, year out, to wipe them out,” Mayer said. Still, to animal lovers, such reassurances are like saying: “Don’t worry about AIDS--human beings are unlikely to go extinct.”

UC Davis veterinarians have made the outbreak their priority as they try to isolate the virus in a live cell. If they succeed, researchers can try a novel technique called retro epidemiology. Deer tissues collected over the past 15 years could be tested for antibodies to the virus, determining how long deer have been infected. That is a major step toward finding a cause, understanding how it spreads and learning why some adult deer carry low-level infections without dying.

“We’re still in the praying mode,” said Jim MacLachlan, an immunologist at UC Davis’ veterinary school. “This one is not an easy one to isolate from what we’re seeing. Some viruses are highly selective with the cells they will grow in. The most famous case of that was the AIDS virus. It’s hit and miss, but eventually we’ll get it.”

In the meantime, the Fish and Game Commission must decide whether to more tightly restrict deer hunting, a popular and profitable sport in California. How many hunters will be allowed in each region next fall will mainly depend on deer counts that determine how deep the die-off has been.

The statewide census began in October, but before the results trickle in, even avid hunters such as Townsend are encouraging tighter hunting limits to let the creatures recover.

“It looks to me like the deer have had enough,” Townsend said. “There are some things you have to give up to let it get better.”