Date: 08-14-02 06:11
CWD: Report From Ground Zero
Did the push for a bigger. better buck create the conditions for a tragic epidemic?
By Mike Irwin Special to The Capital Times July 20, 2002
TOWN OF VERMONT - One chilly evening in the winter of 1990 a group of local deer hunters - farmers, neighbors and kin - gathered for a chili supper at a farmhouse here to brainstorm about how to build a better buck.
Out of the conversation came a pact. They agreed to a long-term plan to refine the white-tailed herd in their area, including 12 square miles in the northwestern part of the town of Vermont, in western Dane County.
Beginning that year, they would shoot many does but spare young bucks. They would give the males three to five years to develop the big bodies and splendid antlers that could qualify them as trophy candidates for the Pope and Young and Boone and Crockett record books.
So Part 1 of the pact was selection. Part 2 was nutrition.
"We'd come from dairy farming families, so we took our cues for improving the herd from that background," recalled a woman who took notes after the chili supper.
"We asked: 'What do the animals need that they might not be getting from the environment?' " Their ground was flinty, she noted, and forest soils were not high in calcium or phosphorus, the stuff that nursing does and fast-growing bucks "in velvet" need.
Deer were ruminants, like sheep or cattle, they reasoned. Why not supplement their diets, as farmers did for livestock, with pasture lots and licks? "Couldn't hurt, might help," one farmer said at the meeting.
So the group agreed to start - or, since some had already started, continue - a long-term program of supplemental mineral feeding of wild deer aimed at doe-fawn and buck health and the making of big antlers.
Within a few years, the results began to appear in the trophy books.
Of 152 Dane County bucks earning enough total points for registration between 1980 and 2000 in the Pope and Young Club's "Bowhunting: Big Game Records of North America," 136 were registered between 1990 and 2000.
Of the 136, 84 were killed between 1996 and 1999. Bucks with the highest scores for antlers dominated the years 1996, 1997 and 1998.
Clearly, something was working. Then, this year, something horrible appeared.
Eleven cases of chronic wasting disease - a devastating brain disease not before seen east of the Mississippi River - showed up in deer specimens taken by the Wisconsin Department of Natural Resources from land, including one DNR-owned parcel, in the 12 tightly clustered square-mile sections of the town of Vermont. This was the area where the chili supper group was working.
DNR epidemiologist Julie Langenberg said in an interview that the cluster "suggests original cause. We're gathering data and asking questions."
Do the questions include whether the innocently begun nutrition and selection practices of local hunters may have created the conditions for the introduction of the disease and given it the years it needs to develop?
The DNR did collect feed samples in the days immediately after the first cases were reported. Thomas Solin, chief of special operations in the DNR Bureau of Law Enforcement, said Thursday that wardens canvassed the area "to get a snapshot" of conditions. Part of that involved collecting feed blocks from farmers and hunters and also purchasing blocks from local suppliers.
"A lot of people there were actively feeding. Once we captured the information we turned it over to the Department of Agriculture, because they regulate the feed. If they want to test, we have samples available."
But Eric Nelson, feed program manager for the state Department of Agriculture, Trade and Consumer Protection, says there are no procedures to test feed products for the presence of CWD. "With feed microscopy you can tell the difference between mammals and birds and that's about it," he said in an interview Friday.
"We did inspect feed manufacturers and deer feeders and found all products to be in compliance with the federal regulation banning rendered ruminant materials. There were no prohibited materials in any materials we inspected."
Thirty-five years of scientific study show that epidemics of the fatal brain diseases of the class known as transmissible spongiform encephalopathies (TSEs) have been largely bred by human behavior and spread by animal behavior.
Chronic wasting disease (CWD), like its cousins mad cow disease and sheep wasting disease or scrapie, is caused by a protein fragment called a prion, not a bacterium or a virus but a chain of amino acids that lives in the brain and nervous tissue. As was found in England, it can be introduced from dead animals to living ones through feed containing rendered meats and bones of diseased animals.
To do its full damage to a living animal, it must have years to develop. Studies report the incubation period between first contact and visible symptoms in deer is between one and a half and five years.
As the disease develops, the animals may spread it through many kinds of contact. It may go from deer to fawn. If wild herds are concentrated rather than dispersed - in areas such as Mount Horeb, where urban development narrows their range and feeding intensifies contact - it may be spread through saliva on food blocks, and in areas where deer bed down and leave their droppings. The prions can contaminate the soil where deer congregate.
One study in 1999 showed that feed itself can transmit the disease. In the study, mule deer fawns were fed a preparation of brain tissue taken from a mule deer with CWD. The protein marker, evidence of infection, was found in the lymph tissue of the digestive tract after fawns were sacrificed. At 42 days the first fawn autopsied showed infection. All of the fawns showed infection after 53 days.
Wisconsin's Eric Nelson scoffed at that study Friday. "They were using raw brain material and it wasn't natural feeding," he said. "If it had been rendered, the infectivity would have been greatly reduced."
He adds flatly: "There is no evidence to support the idea that CWD can be spread by feeding."
Researchers have found TSE prions to be nearly indestructible. They can remain viable on sterilized surgical tools. Clinical studies report that heats of 680 degrees Fahrenheit are required to kill these agents. Controlled studies have shown them to live in soils for seven or more years.
Richard Marsh, a renowned UW-Madison researcher, once warned a statewide farming audience that Wisconsin was especially vulnerable to TSE outbreaks because "we have so many animals here and so much rendering of them."
In 1982-83, Marsh asked Blair McMillan, a post-doctoral researcher and Madison-based epidemic microbiologist, for some help. McMillan's mentor then was UW epidemiologist Robert Paul Hanson. The three sought to understand transmission of the TSEs, but also the makeup of their infectious agents.
"I looked at this tiny, tiny fragment of protein - nucleic acid, this prion or virino, from a sheep scrapie-infected brain," McMillan said in an interview. "What I learned above all was that it was so small you couldn't kill it. It took intense heat. Even if you tried to irradiate it, you had to find it first."
McMillan, now a senior microbiologist and epidemiology specialist teaching at Madison Area Technical College, approaches the town of Vermont CWD outbreak with the caution of a scientist.
"You've got a true disease cluster out there. You've got your index (the first case) identified. Maybe the disease was there first, but now science has seen it," he said. "The geographic boundaries and timeline of the outbreak suggests a sole source of infection."
Still, to settle on a single cause for transmission makes McMillan very uncomfortable. Was that source deer feed containing animal byproducts? Or was it animal-to-animal contact? Or prions lurking in the soil at feeding stations where animals also had contact?
"You have science showing soil contact is possible, science that doe and fawn eye-to-mouth or afterbirth contact is possible. Moving across species to a new form, sheep to deer or cattle to deer is possible, but less likely. Next, you show me that deer are eating with infected deer, or eating rendered, infected deer" - and you'll have it."
But until then? He shakes a handful of pepper grains into his palm and tosses them toward the sidewalk just as a breeze comes up. "There are your infectious prions. They're out there. Go find them," he says.
The feed barns
As early as 1991, the U.S. Department of Agriculture created a voluntary ban on feeding rendered sheep byproducts to cattle.
On Aug. 4, 1997, in the wake of Britain's mad cow epidemic, the federal Food and Drug Administration placed a more extensive ban on ruminant-to-ruminant feeding. Ruminants included cattle, sheep, elk, buffalo, goats, antelope and deer, according to the rule.
But between 1991 and 1997, before the ban and while the deer feeding program was under way in the town of Vermont, Wisconsin deer carcasses and body parts did go to rendering plants. There they were processed into meat meal and bone meal and could legally be fed back to healthy deer.
In the 1994-95 fiscal year alone, just under 26,500 road-killed or seized white-tailed deer were picked up statewide by contractors for disposal at rendering facilities, according to 1995 DNR Bureau of Law Enforcement statistics.
A Wisconsin Meat Trades Association official, who asked not to be identified, recalled that before 1991, all his slaughterhouse offal and body parts went "down the road together" to rendering plants. After that, he said, unused sheep parts were rejected. But until August 1997, deer, cattle and other mammal body parts continued to be collected together for rendering in the same containers, dumpsters and vats.
Processing and rendering industries' common practices help explain how the CWD agent could have ultimately entered animal feeds and mineral supplements.
Larry Meicher, a hunter since 1976 who lives on the eastern side of the town of Vermont, outside the cluster, remembers seeing "deer blocks with animal products" ingredients on the label in 1995 at a suburban feed outlet west of Madison. If deer were accidentally fed contaminated feeds or minerals between, say, 1991 and 1997, the CWD disease symptoms clearly would be showing up now.
Between the mid to late 1980s until Aug. 4, 1997, it was legal and everyday practice in Wisconsin farm co-ops and private feed mills to blend ruminant feeds to include dry, prepared, rendered animal products. These specifically included meat meal, bone meal or both.
They used rendered materials because they were inexpensive compared, for example, to soybean meal. The rendered meat meal contained an average of 50 percent protein. The rendered bone meal contained 8 percent to 12 percent calcium and 4 percent to 6 percent phosphorus.
For deer muscle and antler growth, the bone meal seemed a good supplement. One of the women in the town of Vermont quality-deer group happened to work at a local co-op during the pre-ban years. "I was one of the promoters," she said. "We recommended 4 percent bypass (rendered) protein. We'd put it in dairy rations," she said, and recalled that pasture minerals had bone meal in their recipes as well.
"But even before we came in 1987, they were feeding mineral supplement out here," her husband said. "It's what farmers did. We all were doing it. People out here were putting together their own formulas. The whole community was doing it."
In talking with local residents and hunters, this reporter collected three firsthand, eyewitness "sick deer, skin-and-bones deer" stories going back four to five years.
DNR wardens no doubt heard some of the same stories and acted on them. Well before the 2001 hunting season, through deer brain sampling at the Mount Horeb deer registration station, DNR specialists had formed a working hypothesis that the disease was present -- at least in western Dane County.
Last year, they bore down on the Mount Horeb station. Of all deer brain testing done statewide during last falls gun hunt across Wisconsin, fully a quarter of all samples, 82 out of 345, were from the Mount Horeb station and from Management Unit 70A. Three positives for CWD appeared. They came from Sections 19 and 21 in the northwest part of the town of Vermont. The first positive, what epidemiologists call "the index case," came from Section 21.
This information prompted the March-to-May shoot of this year that added 416 samples from other Dane and Iowa County towns abutting the town of Vermont. It also eventually established a fully identifiable disease cluster, with 11 of 18 total cases, 63 percent, appearing in 12 abutting square-mile sections of the town of Vermonts northwest corner.
With the cluster identified, what would the next logical step be? Harvard University epidemiologist Melissa Perry suggested in an interview: "Your state people might find the mineral feeding sites in the disease cluster and try to correlate them with sites where they found deer testing positive" for the disease.
The DNR did just that.
"I never had thought about feeding as a possible way to spread the disease until a warden came over this spring and asked, Whats in your mineral supplement? " one landowner said in an interview. "I never thought about animal byproducts being in our mineral supplements before 97. Maybe mineral feeding was a link."
The DNR responded to what it found with a proposal to ban baiting and feeding in the CWD outbreak study area. On June 25, the Wisconsin Natural Resources Board, despite intense opposition, imposed a statewide ban on deer feeding as part of its emergency policy to halt the epidemic.
DNRS Solin said Thursday: "We do know that feed concentrates the herd, and thats why the ban was put in place. Feed concentrates animals, and if a lateral transmission occurs through saliva, stopping feeding reduces the chance of spreading it. Its going to take research and time to figure out what happened."
Today, the group that met a dozen years ago with dreams of cultivating awesome trophy bucks feels devastated, as the order has gone out to kill the entire wild herd in their area and in an expanded area around them, an estimated 25,000 deer.
"Out here, we are a community that is grieving. We know our lives will never be the same again," one of the hunters said in a phone conversation late in May. "We've loved and respected the deer so much."
But the man, whose wife described him as the kind of sportsman who is "awestruck over the greatest buck or the tiniest fawn," is doing his part to stop the spread of CWD. With his DNR-issued special landowner permit, he has taken up his rifle.
"I shot eight deer for the DNR this past month, and by the eighth I was numb," he said. "I had no feeling at all."