I was very near the center of the 1993 outbreak of a "new" disease, hantavirus pulmonary syndrome, in the Four Corners, so I'm not quite as prone to panic over the swine flu as many people seem to be. Here are excerpts from a presentation I sometimes gave to a university class back when avian flu was the big concern. It is still relevant now that we are focusing on swine flu. I'll leave it up for a limited time, because of the copyright issues, but I do think it's extremely relevant. It also speaks to the xenophobia that can be provoked by poorly understood diseases.

The idea of “emerging diseases” is one that’s much more familiar to us now than it was 14 years ago, because we know of quite a few, and we think we know where they emerge from. We, in the United States, are accustomed to thinking that bad germs come from someplace else: deepest, darkest Africa, for example, or the jungles of South America or southern Asia, or at least south of the border.

There are several reasons that’s logical to believe. We don’t have the environmental or socioeconomic conditions that cause large numbers of people to have a very poor baseline level of health, and we have better health care here than is available in many regions of the world. We don’t have many big epidemics.

Modern travel is very quick and relatively cheap, so it’s possible for us to contract diseases to which no one we know has ever even been exposed, and which no one in our area is experienced in diagnosing or treating..

And it’s easy for us to know that some of them didn’t originate here because of their names. Often viruses are named after the place in which the sentinel cases of the diseases they cause were first observed: Hong Kong flu, West Nile virus, Rift Valley fever. Ebola is the name of a river in Zaire. But an emerging serious disease is not the kind of accomplishment a community or region wants to be famous for. Norwalk virus, for example, is often called “the cruise-ship virus” and you probably don’t know that the Norwalk in question is not a ship but a town in Ohio, where the disease first appeared in an elementary school. There’s a related gastroenteritis, Snow Mountain virus, named after a resort camp in Colorado, and I bet you’ve never heard of it, because they don’t want you to.

Still, most of our really serious new diseases, emerging diseases, appear somewhere else, or appear here in someone who arrived very recently, so when a new, fatal, disease, an unknown hantavirus, first appeared in northern New Mexico, it presented a challenge we really hadn’t faced before. 

The first case to come to anyone’s attention, in 1993, was a Native American from near Chaco Canyon, and it appeared especially worrisome because he was a young, healthy athlete — he was a distance runner — who succumbed very quickly to symptoms that generally strike people who are very old, very young or chronically ill. Medical personnel discovered that his fiancé had died several days before, after exhibiting similar symptoms. Researchers, beginning with the New Mexico Office of Medical Investigations and reaching out to the CDC, state health departments, the Indian Health Service, the University of New Mexico, and so on, began to look for other cases, and very quickly an IHS doctor from Gallup had located five.

All those cases had several factors in common: All the patients were young, healthy, and Native American. And they all died.

So those looked like the parameters: A 100% fatal disease that struck young, healthy Native Americans.

That’s where the tale starts. Then it branched out in many dimensions: temporal, spatial, racial, theoretical.

Dr. William Osler, a 19^th-century Canadian physician who is considered one of the fathers of modern medicine, wrote, "The good physician treats the disease; the great physician treats the patient who has the disease." The great physician, then, has to understand the patient and the context of that patient's illness, and that was the challenge of this new disease.

Fairly early on, it came to be called Adult Respiratory Distress Syndrome, a name that describes the symptoms.  That was an upgrade from “Mystery Disease,” which is what the national press had been calling it, and definitely an improvement over “Navajo Flu,” which we heard also heard frequently. No one on the Navajo Nation wanted to be associated with it, any more than we would. One big reason was the cultural belief system about death, but also on everyone’s mind was the tremendous cost in tourism dollars if everyone avoided the Navajo Nation and the entire Southwest, which many people did that year. Tour buses that came through that summer issued surgical masks to everyone; we could see them through the windows as they drove through without stopping, and those were the people who apparently couldn’t get refunds on their trip plans.

When confronted with an emerging disease, we have two urgent questions: What causes it? What cures it? Immediately, epidemiologists began working on the first question, and doctors and clinical researchers began working on the second. 

I want to read you a brief section of the book that describes the difficulties in researching this disease:

“It is irresponsible to lump all Native American religions into one doctrine, but a theme that runs through many of them is the concept of “emergence,” of progressing spiritually, as a people, from one world into the next. The local inhabitants believed they had emerged upward into the deserts of the Southwest.

“Therefore, the topic of “emerging diseases” was politically difficult to introduce. This was not the time for science and religion to clash. … In order to understand the outbreak, however, it was important to understand the events that had led up to it.

“… Some social scientists hoped that by working backward through Native Americans’ oral traditions, they might find some clues about the outbreak. The Navajo had lived in the area for hundreds of years and as yet accounted for most of the cases. However, they have a traditional reluctance to talk of the recently dead, and they had been deeply offended by much of the media coverage, which seemed to blame them for the outbreak they were suffering. They believed that to speak of something bad was to risk bringing it down on their own heads. They were also private individuals, understandably suspicious of outsiders, and sensibly reluctant to have their lives examined closely by strangers.”

And so on.

The Navajo didn’t want to talk to the researchers — the US secretary of health and human services had to appeal to Navajo President Peterson Zah to encourage cooperation.

I couldn’t blame them, because the racism was obvious. In border towns, we were shown cartoons about smoke signals and of mice with slanted eyes and big teeth, reminiscent of World War II propaganda. We were warned that we were putting ourselves at risk by going onto the reservation — as if we weren’t at the same risk on the other side of the line. And behind it all was a very real fear of a disease that’s fatal at least 40 percent of the time.

One of the discussions to which I was privy in 1993 involved the knowledge that Native Americans do have traditions about keeping mice out of their dwellings. Was that knowledge relevant to hantavirus? On one side were sociological researchers, mostly not from here, who were convinced that all of Native American lore — some of which I’m convinced is invented on the spot to get researchers to go away, and I don’t think that’s unique to Native Americans — taps into some deep well of universal knowledge with which “less primitive” people have lost touch. That perspective was interesting because it was at the same time complimentary and insulting.

At the other extreme were some condescending scientists who said, “You know, we’re assuming a taxonomy that Native Americans may not have. When they say “mouse” they probably just mean any rodent smaller than a breadbox.”

Then the first set would argue, “No no no! These are people who are intuitively in touch with nature!”

Off to the side were some down-to-earth people who said, “Yeah, you know what? NOBODY wants rodents in their food or in their beds.”

There is some evidence that a disease with similar symptoms was known to the Navajo and/or the Hopi — I heard it more from the Hopi, and that it was associated with mice. It’s really difficult to judge the validity of that information in retrospect. On one hand, there are clearly documented health practices among those groups that do serve very well in preventing exposure to rodent-borne disease, which would also include plague. I don’t know if there is an other hand, but I would respectfully suggest that figuring out such a link to a relatively rare disease with an incubation period that ranges from 9 to 33 days and averages more than two weeks, would be a pretty impressive deduction.

People, even locals, did begin avoiding contact with Native Americans, and you can imagine how comfortable the Navajo themselves were when researchers sealed themselves head to toe into biohazard suits before even venturing into the region. That practice was soon abandoned, and now the CDC will tell you it never happened, which is insulting to the people who witnessed it.

Fear causes people to act in ways they otherwise might not. Racism was an unfortunate manifestation of that early panic. But it’s important to remember that for some very tense days that that first spring and summer, no one knew first what was killing people, or later, how they were being exposed. The biohazard suits made sense — it’s not logical to expose and perhaps kill the researchers who offer the best hope of identifying, preventing and curing the disease. It also wasn’t logical to remove local residents from that setting unless it became clear that the environment was the risk factor and that the people themselves weren’t carrying the disease and so wouldn’t expose everyone with whom they came into contact.

It was just very unfortunate that all the first victims, and nearly all the residents of the area where the disease first appeared were Native American, and that the disease became so closely associated with them so quickly.

Early on, no one could be sure that there wasn’t a genetic risk factor associated directly with Native Americans. I don’t want to wander into a discussion of whether race is a valid construct, but that question wasn’t all prejudice. We’re learning a lot about genetics and why some diseases are more prevalent in certain groups of people; it has to do with human leukocyte antigens, which are protein groups that help control immune responses, and some types are more common in different genetic groups. Specific HLAs have been identified in association with malaria, and more relevantly, with a type of hantavirus in northern Europe. But human genetics couldn’t even come into play until the cause of the disease was identified.

The flip side of the Navajo association was that it turned out that a reservation might have been the best possible case for this disease to emerge from hiding, because the Indian Health Service has a much better communication network than private-practice physicians do. The IHS jumped on it much faster, and got the CDC involved much sooner, than might otherwise have happened. IHS physicians also have experience in identifying and treating illnesses that are rarely seen by city physicians. Plague is one; we deal matter-of-factly with plague out here, but it still causes panic in cities because people think of it as a medieval disease that killed perhaps a third the population of Europe. If you’re going to catch the plague, catch it in the rural West, because a city doc might not recognize it before it’s too late.

Anyway, my point was that the public health system in this region did work well. Now both government and private industry are developing data-mining systems designed to identify outbreaks very quickly by looking for patterns of symptoms in aggregated patient data, and the CDC hopes to institute a national syndromic surveillance system, thanks in no small part to Osama bin Laden, but back then, luck and location had a lot to do with the relatively quick identification of a the virus.

Figuring out what caused the disease itself was difficult because by the time people developed symptoms, the virus had cleared from the body and it was the overwhelming immune response to that initial viral presence that ultimately killed them. That’s why healthy adults with strong immune symptoms are mostly likely to die from the disease; children do not seem to contract this particular hantavirus.

So it was really difficult to isolate the pathogen, and in fact, the first researchers could not even be sure that this was a microbial illness. An unknown virus was the top suspect from the very beginning, but they had to look at a wide variety of possible causes, and the fact that they were looking in all those directions caused considerable fear.

What if, instead, the risk was broadly environmental? Was it related to atomic testing west and/or south of here? Nuclear fallout spreads from west to east; that makes us downwinders. We know that radiation causes mutations. Or did it have to do with power-plant emissions?

Was it related to chemical weapons that people suspected were stored at a depot east of Gallup at Fort Wingate? That wasn’t as unreasonable as it sounds. Exposure to phosphene, a chemical used to control prairie dogs, produces similar symptoms. The spring of 1993 had been wet, so rodent numbers were increasing. Phosphene is closely related to another chemical compound, phosgene, the common name of carbonyl chloride, which was responsible for 4/5 of all the gas casualties in World War I. It kills through massive lung inflammation. There was actually a small clue in that line of investigation, although it was visible only in retrospect. The investigators also considered herbicides and other pesticides.

Then, again looking at a viral or bacterial illness, or possibly a fungal infection, what if it was a biological weapon, either part of an attack by someone else or a test of one of ours. That idea wasn’t as farfetched as it seemed to some people, because our own government has, of course, not always treated minorities well in using them in medical research. This was before the anthrax scare, but remember the suspicion then that it had originated in a government lab.

This is another example of cultural context. In the West — and I know this specifically about some parts of my own county — quite a few people are deeply distrustful of the government. They have reasons they believe are valid. Like other groups, they immediately began to suspect that what came to be known as hantavirus was somehow being caused by the government, or at least by politics, and they — being on the libertarian end of conservativism — suspected the Democrats. One man later told me that hantavirus had been part of a plot to convince Americans of the need for a nationalized health care system. That makes some sense, because it did show the Indian Health Service in a positive light, but it’s revisionist history in that Hillary had not yet unveiled her plans for health-care reform in the spring of 1993. Was it part of a plot to take land from rural westerners who tend to be conservative? Was this, as HIV had been rumored to be, a way of eliminating a population segment?

People were suspicious, partly because the Four Corners region seems, just by looking at it, to be a very old landscape and a fairly pristine environment, and the Navajo to be an ancient people — although they’re not, in terms of settlement of the Southwest — and so it seemed very unlikely, to some, that a new disease would emerge here, of all places. It was much more likely, many local people believed, that such diseases would be introduced by immigration, and that is indeed a risk, although not related to hantavirus.

And here’s the punch line for that particular story: In the end, most of that group concurred that the Democrats probably weren’t responsible — because they weren’t smart enough to do that, but they were indeed weasely enough to capitalize on it. They hadn’t done it; they’d just lied about it.

Now that seems like an amusing sidebar, but at the time, such beliefs, and such distrust, did hamper efforts to investigate the new disease because investigators spent time listening to a lot of implausible ideas and chasing some that seemed not entirely impossible.

Very quickly, though, most of the research centered on viruses, and this one was difficult to identify. If you know what you’re looking for, you can find its tracks, so to speak, but in those first cases, no one knew what they were seeking. You can read the book to learn how it was first identified; there’s a lot of science there, and I admit I’ve forgotten a lot of it, because microbiology, let alone molecular virology, is not my field — although I had to learn a lot really quickly. The short answer is that the immune response appeared to epidemiologists to resemble the symptoms of Asian hantaviruses, and assays for hantavirus antibodies were positive. It took only four days after the first specimens arrived at the CDC. But four days is more than long enough for a hantavirus patient to die.

Identifying the virus didn’t immediately lay all the political suspicions to rest, because it was a hantavirus — a genus of viruses named for the Hantaan River in Korea — and we know about hantaviruses because of their prevalence in Asia. How did this one get to the American Southwest?

Also mysterious was the fact that this one didn’t act like Asian hantaviruses, which cause hemorrhagic kidney disease; this one causes hemorrhagic lung disease. Antigens are deposited on lung tissue, antibodies attack them, lung cells are disabled and destroyed, and the lungs and chest fill with fluid.

Until 1993, there had been no hantavirus identified in the New World. Epidemiologists have come to believe that hantavirus probably spread across the Americans the same way that plague did after arriving on our shores with rodents, but in 1993, no one had any reason to suspect a hantavirus and they were really surprised to find one. Once they had, they knew the carrier was likely to be a rodent.

The actual virus was first confirmed under an electron microscope in the November 1993, isolated from the tissue of a deer mouse trapped near the home of a person who had contracted the disease. Remember the first patient died in May; that’s six months. Shortly afterward, researchers at USAMRIID — the Army Medical Research Institute of Infectious Diseases — managed to grow the virus from a human patient, so it’s possible, but clearly that’s not going to be a useful diagnostic tool. 

The big risk factor, we now know, is exposure to Peromyscus maniculatus — deer mice, which are endemic to much of the United States. They excrete the virus in urine and feces, and humans inhale it when it’s aerosolized — for example, by sweeping or walking, as well as at the time it’s excreted. A mouse can get into your house through a gap the size of a dime. Deer mice aren’t very shy; if you prop a door open, they’ll come in. You may not know they’re there. You won’t see those tombstone-shaped holes in your baseboards. Several epidemiologists told me that all of us should assume we have mice in our house; we’re all at risk.

However, there’s a caveat here: There have been patients for whom it was never possible to identify an exposure to mice or their droppings. We simply don’t know how or where they contracted the disease.

Fortunately, “Navajo Flu” didn’t stick as a name. For a brief time, the virus was called Muerto Canyon virus after the locale near Chaco, and if you speak Spanish you know why that wasn’t a very good name; it didn’t give patients the impression that they were likely to survive. Eventually scientists settled on Sin Nombre Virus — No Name Virus — because no one wanted to claim it, and the disease became known as hantavirus pulmonary syndrome, but for the whole first summer of panic, it was called ARDS.

Some big questions remained: Why here? Why now? The answers to those questions came not from medical researchers but from field biologists studying mice, primarily the deer mouse. Although other rodents carry the virus, in this region they rarely transmit the disease to humans, just because they don’t come into contact with humans. There’s an Andean hantavirus spread by a different mouse. There’s a hantavirus along the Gulf Coast spread by the cotton rat, and one in New York transmitted by the white-footed mouse. In Europe, hantavirus is also transmitted by voles. In the United States, Sin Nombre seems to be the most virulent, but the South American viruses are worse. None of that was known in 2003, but once researchers associated the deer mouse with the virus and the patients, they could begin to unravel what had happened in the summer of 1993.

The previous couple years had been uncharacteristically wet. The primary food source of P. maniculatus is piñon nuts. We know that piñons have big crops every few years — some people will tell you 3, others will say 7, and the scientific research tilts toward 3 or 4 — and when a genetically big-crop year combines with a wet point in the weather cycle at the time when the nuts are setting on, occasionally really, really big crops are produced. That had happened in 1992. The deer mice had been well fed, and well-nourished deer mice can multiply very rapidly: litters of 4 or 5 but up to 10 in times of plenty, and those mice are ready to reproduce at 5 weeks. Going into the winter, there were a lot. They spent the winter in close proximity to one another, which is how the virus spreads among mice. Male mice also spread it by fighting. The higher the population density, the greater the percentage of infected mice.

Climate change wasn’t a big part of the discussion in 1993 or when we were writing the book; epidemiologists are now looking closely at it, although they don’t get much government funding to do so. Regardless of the politics, climate shifts do occur, and precipitation is still our best predictor of mouse population and therefore risk, so we need to keep looking at it. If, for example, most of our precipitation began to fall in the warm months, in torrential thunderstorms, instead of as snow during the winter, that would have a lot of implications for rodent populations. If the average annual temperature shifts just a few degrees, plants that now are significant food sources may no longer be able to survive here, other plants may move in, and that has effects all way up the food chain. Mice aren’t picky eaters, but they do have preferences. And even if, as global warming opponents tell us will happen, the change swings the other way, the ecological effects may not be reversible quickly or perhaps even at all. How long will it be before we have healthy piñon forests again, or aspen forests? Not in our lifetime. So regardless of where you stand politically on climate change, I think it’s important to model some of those changes as they might affect the species that affect us, and disease risk is one of the ways in which humans are affected.

The CDC Website will tell you that in the spring of 1993, there were 10 times as many deer mice as there had been in the spring of 1992. That wasn’t true anywhere, not at a single one of their trapping sites, and in fact some sites had fewer mice. I don’t know why they’re still saying it; that piece of misinformation frustrates researchers here and contributes to distrust of the government. But what you need to know is that there were a lot of mice. The summer, though, was dry. The mouse population outpaced the food supply and mice, in much larger numbers than usual, started looking in human habitations for food.

An astute student recently asked whether this disease had emerged because of human population growth and development. Yes and no. Obviously, as more people live here, more will come into contact with mice. Usually, when we talk about the human/wildlife interface, it’s in the context of habitat degradation. There’s no longer enough terrain or food for mountain lions, bears, whatever, so they move into town and into conflict with humans.

Hantavirus isn’t an example of that; it’s more complex, because humans often improve mouse habitat, not only with buildings but with irrigation. It’s not that they’ve been displaced; mice are incredible hard to displace. They’re very adaptable; they survive the famines because they can capitalize on any available feast. Some publications in 1993 put a very anthropomorphic spin on it — “Mice refuse to be banished”  — and attributed Monty-Pythonesque behavior, as though, in revenge, deer mice pee in your general direction and kill you. No. They’re just there; they’re everywhere.

Peromyscus is the most prevalent mammalian species in North America, and they’re field mice. The house mouse is an entirely different species; lab mice are related to house mice. Deer mice are less shy than some other mice, including the white-footed mouse (Peromyscus leucopus) that also harbors the virus. Deer mice moved into people’s houses, sheds, woodpiles, cars — you name it. They shed the virus in their urine. Hantaviruses are encapsulated viruses, which means they have a long shelf life. The urine soaked into the dust, and when humans stirred it up, perhaps in their spring cleaning, they inhaled it. And they died.

I need to say a little bit here about viruses and how they differ from bacteria. Bacteria are living organisms. Kill them and they’re rendered harmless. Viruses are not, strictly speaking, alive. Their ability to infect involves injecting a small bit of genetic coding — in this case, ribonucleic acid, RNA, although there are DNA viruses too — into an animal’s cells. The virus then replicates. It produces antigens, the body responds with antibodies, and the fight is on.

Some viruses deteriorate quickly without a host. Hantavirus is relatively stable in a wide range of temperatures — it seems viable for at least two or three days, and perhaps more under certain conditions — but sunlight, ultraviolet light, kills it very quickly. So does bleach; that’s why we tell people to spray the floor of their sheds, etc., with a chlorine-bleach and water solution before they sweep. 

Humans are an end-stage host because, it turns out, the virus is eliminated before they get sick enough to pass it on. Infecting a human is a viral dead end. It can’t get out. In the few cases where more than one family member contracted Sin Nombre, it’s been determined that they were all infected from the same source. Sin Nombre is not communicable from person to person, although that’s not true of some of the South American pulmonary hantaviruses, and the fear, of course, is that through antigenic shift and drift — the same processes that concern us about avian influenza — that could change.

I want to get back to the socio-cultural aspects of this. The first victims were Native Americans, and it turns out they were victims because they were in the wrong place at the wrong time. They lived in proximity to mice — and I’m talking about regional proximity rather than living conditions — at a time the mouse population boomed. So immediately, the assumption — not among scientists but among the non-local media and the public — was that it was because they lived in “dirty” conditions.

There’s some validity to that risk factor — the better we can seal out mice, the safer we are — but those “dirty conditions” include everyone who has a woodpile, a garden shed, a crawl space. I don’t know about you, but that includes me. Ironically, it’s now the dusty boxes of hantavirus records and notes in my basement that now put me at risk.

I’m not going to tell you that politics and poverty don’t have anything to do with it. There’s a reason the Navajo nation is where it is and Manhattan Island isn’t reservation land. Worldwide, poverty is a risk factor for hantavirus and a large number of other diseases. It does cost money to keep mice out of a dwelling, just as it costs money to purify water, acquire healthy food, etc. In hantavirus, though, the link seems to be circumstantial, and being Native wasn’t the risk factor. It just happened to be Native people who were there at the time.

Many of the next cases weren’t. Once clinicians knew what to look for, hantavirus it began to be identified in rural areas throughout the Rocky Mountain West, and then across the country. One man in Montana died because he hopped in a pickup he’d parked in a barn for the winter, turned on the heat and got a blast of dust and viruses and straw from a mouse nest built in the heating ducts. A camper contracted it when a mouse ran across his sleeping bag. A woman who was able to walk into the emergency room in Colorado deteriorated so rapidly that she could not be stabilized to fly out, and she died after only four hours in the hospital. None of those people were Native American.

Medical practitioners also began looking backward through their records and identifying cases that had been called acute respiratory distress syndrome that might be attributable to the newly identified virus. In some cases, blood was identifiable to be tested. The CDC has identified cases of HPS as far back as 1959; it just took 34 years for a cluster of cases to appear in a way that enabled someone to see the pattern.

Some people are exposed but don’t contract the disease, or have a subclinical case that confers immunity but doesn’t make them sick. We know that a certain percentage of people have been exposed to the Sin Nombre virus because researchers were able to study immune factors in samples of blood collected at Northern Navajo Medical Center for a separate research project and preserved.

I especially want to emphasize that the stigma associated with hantavirus are misplaced and can delay or deter people from seeking treatment. All these years later, we still hear that hantavirus only strikes Indians, or people who are poor housekeepers — in other words, someone other than us, because it’s a scary disease and we don’t want to believe we can catch it. At first it looked like it was 100% fatal. Now it’s between 35% and 60% fatal, because of some limited success with drugs to halt the immune response and a technique called ECMO — extracorporeal membrane oxygenation, which involves taking your blood out of your body and giving it the oxygen it can’t get when your lungs are flooded with fluid. It’s still a horrendous disease; there aren’t many diseases with 35% mortality rates. There are some — rabies kills nearly everyone who actually contracts it. But for comparison, West Nile kills at most between 3 and 10 percent of those who actually get sick from it; last year in Colorado for this year it’s a little more than 1 percent. Plague, in the United States, kills fewer than 15 percent of its victims, depending on the form they contract.

 I don’t want to get into treatments, because I’m not qualified to discuss that. If you have the symptoms and are aware that you’ve been exposed to mice, get to the doctor fast and say so. The University of New Mexico hospital is the best place to go. This is a serious disease, and immediate, appropriate treatment is crucial. And again, if you’re going to get it, you’d better hope you’re in the Southwest when the symptoms show up, because our doctors have a far better chance of recognizing it.