On Pandemics

WESTERN EQUINE ENCEPHALITIS, TELEVISION, AND AIR CONDITIONING

IN 1967, U.S. surgeon general William Stewart declared that “because [they] have been largely controlled in the United States, we can now close the book on infectious diseases.” He was not the first person to confuse his country with the world, or his state of knowledge with knowledge in general, nor will he be the last.

Stewart’s declaration of victory over infectious diseases, from the helm of the smallpox eradication aircraft carrier, was premature. The world seemed so much simpler then. We had the microscopes to find the problem-causing microbes, and the big guns—the antibiotics, the vaccines, the disinfectants—to kill the microbes or at least prevent them from causing disease. Smallpox was retreating before our superior weapons, and diseases such as polio and measles were lined up in the eradication queue. Other scourges such as leprosy and tuberculosis seemed to have just fled large parts of the world, leaving few explanations behind. The best guesses for what got rid of them are better food, cleaner water, and good housing—nothing really spectacular, nothing to patent.

Globally, infectious diseases really did seem to have taken a holiday; most people were more likely to die from accidents, suicides, heart disease, or strokes than from infections. But the microbes were still there, as anybody not living in suburban enclaves in North America, Europe, and Australia could have told us. In a 1990 study of causes of death worldwide, heart disease and strokes were number one and number two, respectively, but right behind them were respiratory infections and diarrhea.

The more scientists look, and the better the detection technology, the more microbes there seem to be. In the late seventeenth century, Anton van Leeuwenhoek saw what he called “animalcules,” tiny a nimals, through his microscopes. Now there are electron microscopes, which can take pictures not only of bacteria but also of viruses and even those impossible disease makers, the prions. Viruses are thin bits of DNA (deoxyribonucleic acid) or RNA (ribonucleic acid), covered with distinctive jackets of protein. They move long distances quickly. They are the ultimate cool, athletic anorexics. There are uncountable numbers of viruses jostling around. They get into a bloodstream through a nostril or a gut or by being mainstreamed through the good graces of a blood-feeding arthropod. Once inside, they take over the host cells and use the organism’s machinery to reproduce themselves. Mostly, they shuffle and sneeze and poke their way around pretty quietly, bird to mosquito to bird to mosquito to mouse. Viruses are probably as old as the oldest ancestors of the animals they infect, so there has been a long time to co-evolve and learn how to be good neighbors. Usually no one gets hurt.

In the southern United States, west of the Mississippi, there is a virus called western equine encephalitis (WEE). The virus multiplies in the blood of a variety of birds and in certain mosquitoes (Culex tarsalis). The original homeland of the virus was in a community of marsh-dwelling mosquitoes and birds such as blackbirds and swallows. It lived there for a long time without causing any serious problems in the animals it infected. As people moved in and, through drainage, irrigation, and land cultivation, destroyed some of that habitat and modified what was left, the viruses and the birds adapted. The birds found new sources of food, such as grain in fields or in grain bins, and the viruses found new hosts with cells to hijack.

On the one hand, the viruses needed some warm-blooded species with fast population turnover, so that there was always a fresh, non-immune crop to invade; house sparrows, which emigrated from Europe in the mid-nineteenth century, seem to fill that role in many areas. On the other hand, the viruses also needed mosquitoes willing to feed on both birds and mammals. With more than 150 species of mosquitoes in the United States (several thousand in the world), feeding at different times of day on a variety of species, everywhere from deep mine shafts to high mountains, the odds were pretty good that appropriate mosquito carriers could be found. The life cycle expanded so that wee virus could now infect wild rodents, chickens, and pigs without, apparently, making them ill.

Not all animals were as lucky as pigs and chickens. In the summer of 1930, about six thousand horses in the San Joaquin Valley, in California, came down with a mysterious brain disease. They became uncoordinated, somnolent, and fatigued. Half of the horses died. The disease was WEE. From the 1930s to the 1970s, outbreaks and epidemics of WEE occurred in people and animals all through the western United States and north into Manitoba, Saskatchewan, and Alberta, in Canada; thousands of horses and hundreds of people got sick. Although birds and their attendant mosquitoes can maintain the virus in nature, mammals are apparently a so-called dead-end host: they can get the disease but usually don’t get enough viruses in the blood to pass on.

From my memory of growing up in Winnipeg, Manitoba, hot, muggy weather, migratory birds, and great veils of mosquitoes drifting across the back lawn are staple features of the prairies. The question is not so much why the disease occurred, but why it didn’t occur every year, and why it only attacked in some places and not others, when the birds and damned mosquitoes were everywhere. Could any of the outbreaks be predicted?

In the first instance, investigators used the fact that chickens get infected, and hence develop antibodies to WEE, without getting sick. For many years, putting cages of chickens outside in strategic locations and periodically collecting involuntary blood donations from them to look for antibodies provided a reasonable way to anticipate a coming epidemic. Rainfall and temperature conditions could be used to project mosquito populations; as the number of mosquitoes, and, if the virus was present, the rate of infection in chickens, increased, the probability of a serious epidemic could also be anticipated. This kind of epidemic prediction required a fair amount of intensive monitoring and still left unanswered the big questions: where did the viruses come from before they got to the chickens, and could the disease be stopped or predicted earlier?

Did any of the patterns of this disease have to do with where the virus stayed in the winter? Where did it stay in the winter? When I was in veterinary college, our instructor, John Iversen, had us take Richardson’s ground squirrels out of the walk-in cooler and watched them slowly wake up. Iversen, a scientist who could suddenly switch his costume and, it seemed, his personality, from a three-piece suit to a white laboratory coat to rugged field gear, had a theory that the virus overwintered in these abundant rodents. After all, they do harbor a whole lot of other microbes. In the spring, when the last dirty patches of snow disappeared and chunks of floating ice clogged up canals and creeks, mosquitoes came alive in puddles by the road and migrating birds arrived from the south, initiating a cycle of amplification. By the time lovers strolled bare-armed through the woods, leading their horses behind them, the mosquitoes were singing in the sweet prairie air, and the epidemics could start in earnest. Other scientists suggested that the virus overwintered in frogs or snakes or that it just lived through the winter in the gut of the hibernating mosquitoes (the way West Nile virus does).

At the time WEE was being investigated, researchers were asking the same questions about a similar, less common, but more serious disease—eastern equine encephalitis (EEE). This one, sickening a few horses a year at most, occurs sporadically from Louisiana north into Michigan, Ontario, Connecticut, and Quebec. It also appears to kill ring-necked pheasants and a few other birds as well as the occasional horse or person, but it is otherwise a little beast similar to the WEE virus.

One of the most plausible and intriguing theories is that these viruses don’t overwinter in the north at all. Like many weary northerners, they spend the winter quietly reproducing in warm southern areas, along the Gulf Coast for WEE and Florida for EEE.

In the 1980s, two Canadian researchers, Robert Sellers and Abdel Maarouf, published a series of papers in which they asked: between 1980 and 1983, did WEE-infected mosquitoes ride the wind currents up from the Gulf of Mexico into Manitoba, Minnesota, and North Dakota? They found that a northward movement of warm air, meeting a cold front with rain, could well have carried infected mosquitoes and then dropped them at various locales in stages as summer crept its way farther north. It is a difficult theory to prove absolutely, given that mosquitoes are hard to microchip and that unstable weather patterns, vaccination of horses, changing landscapes, and changing habits of people all contribute to transforming a probability into an event.

Still, I am reminded of the time I was working on developing an animal-disease-monitoring system in the Caribbean in the late 1980s. One of my colleagues called me into his office one day to show me a giant locust in a jar of alcohol on his desk. “It’s an African locust,” he said. “I picked it up on the beach, right here in Trinidad.” He paused. “Thank God they don’t have enough space to swarm here.” One of the Trinidadian women laughed. “Typical,” she said in her slow lilt. “The big males fly over and then just lie on the beach all day.”

It occurred to me to wonder: if those big lugs can blow over from western Africa and flop down on the beach in Trinidad, how hard can it be for a mosquito infected with WEE to get from, say, Texas to Manitoba? This also occurred to me later, when West Nile virus exploded into North American consciousness. A lot of other individual events have to fall into a particular pattern for an epidemic like that of West Nile virus to occur, but with the ecological, climatic, and social world in constant, rapid flux, and nobody really paying very close attention, it was bound to happen sooner or later.

The long-term patterns of WEE, like those of so many other mosquito-borne viruses, are puzzling. Although St. Louis and eastern equine encephalitis both make their periodic, sporadic appearances, the once-feared widespread epidemics of western equine encephalitis have all but disappeared. The CDC has suggested that the intensity of the natural cycle for WEE increases every five to ten years, leading to a higher probability of epidemics, yet the last epidemic in horses or people was in 1987. But the lack of disease in horses shouldn’t be a surprise.

We take care of our horses. There’s money in doing so. Effective vaccines against equine encephalitis were developed quickly, advertised widely, and rapidly made available to veterinarians. There are no similar vaccines for people. Who would pay? Who bets on people running around a dirt track? Vaccines are good for the horses (and the vets and the people who make vaccines), but the antibodies produced by the vaccine often interfere with our ability to differentiate animals that got the real infection from those that were vaccinated. Furthermore, if horses are vaccinated, there is no use monitoring them for infection or disease, so where do we look to find out if the virus is still out there, looking for another opportunity? We can monitor the sentinel chickens and look for antibodies in them, and we can search for the virus in mosquitoes. But if there haven’t been any cases of serious disease reported recently, there is less pressure on government agencies to maintain monitoring programs. Money gets directed to other priorities until the next outbreak occurs.

People tend to get sloppy about vaccination, or cavalierly oppose it, especially when the vaccine works and the disease disappears. It is the general problem of preventive health programs, to which I referred earlier, that if they are successful, nothing happens, so governments and individuals are always tempted to disinvest in the most successful of them. Why would a horse owner pay someone a lot of money to stick a needle into her horse if there’s no disease around? In 1987, there was a northward wave of WEE from the Rio Grande; starting in April and continuing into June, the virus moved north through the Texas Panhandle, New Mexico, and Oklahoma; in July, it headed farther north across the Great Plains; by August, it was in North Dakota, Manitoba, and Minnesota. Thirty-seven people and 132 horses were reported sick. In the Imperial and Sacramento valleys of California, the sentinel chickens developed antibodies to the virus, demonstrating that it was in the wild mosquito and bird populations, but no horses or people got sick. The sentinel chickens were the scientific equivalent of omens, but what was the message? What should be done?