Rabid
After the meeting, Janice drove over to the clinic in her Jeep. Thirty years on the island had assimilated her to the pell-mell driving style of the natives. She zipped around motorbikes, dodged dogs in the road, all at a velocity that was rather unnerving to an American visitor. On arriving, she set out to find the dog that had caused such a stir. It was nighttime, and only a dim fluorescent bulb lit the spot where it was being kept, in a little black wire kennel perhaps two feet wide. For all the fuss about rabies in Bali, you can spend a week reporting on the vaccination campaign—to say nothing of two years researching a book on rabies, or ten years as a U.S. veterinarian—without actually witnessing a rabid dog in the flesh. But here, finally, was one: its head wrenched back on its neck, eyes rolling morbidly in their sockets.
This was not a Bali dog. It was a little “breed dog” (as the locals called them), a black-and-tan Pekingese. It stumbled about like an angry drunk, attacking its cage bars and yowling—a long, mournful, strangled-sounding howl, ending in a wet desperate gurgle. Periodically, the poor dog would slump over in a haze, as if finally spent from its mad exertions. But all of a sudden it would start up again, groaning and snarling, stumbling and biting. It seemed antagonized by our presence, and yet it never seemed fully to recognize we were there.
It’s an odd thing to interact with dogs your whole life and yet never see one laid low by this most ancient of canine curses. And in a strange way, it was less terrifying to see in the flesh than to brood upon as a prospect, a threat, a phantom. Just as the needle has become scarier to us than the bite, the reality of the rabid dog cannot quite measure up to the myth. Far more arresting than its rage is its sickness, its absentness.
Many people forget that in the original children’s book version of Old Yeller, published in 1956, the dog never even develops symptoms of rabies. We are made to understand that the disease is sweeping through the area—afflicting the family’s bull, for example, which “reeled and staggered like he couldn’t see where he was going…. He scrambled to his feet and came on, grunting and staggering and moaning, heading toward the spring.” But after Old Yeller gets bitten while tussling with a clearly rabid wolf, the boy shoots the wolf and then, on the hard-spun advice of his pioneer mother, shoots the dog, too, right there and then. It’s all over within just a page and a half of junior-reader, large-print type.
To this day it remains shocking that Walt Disney, of all movie moguls, agreed to make Old Yeller into a film—and that he didn’t find some way to save the dog. The book’s author, Fred Gipson, was even hired to write the screenplay. Bill Anderson, a longtime Disney producer who was vice president of studio operations when the film was made, claimed in an interview that a second, more experienced screenwriter, brought in to work with Gipson, had floated the “gutless approach” of saving the dog.
“But Walt could see the drama,” Anderson recalled. “Walt knew that—showman that he was—we had to kill the dog to have a story.”
At Disney’s instigation, though, the writers did make a subtle but extremely important change. To the boy’s last-ditch suggestion in the book—that they “tie him or shut him up in the corncrib or some place until we know for sure”—the mother in the film assents, though reluctantly. The dog is confined until, in fact, it becomes mad, snarling at the children, its foaming mouth clearly visible through the wooden gate. For the film, as Anderson put it, they changed the story such that “there was no out but to kill the dog.”
For all the generations of children scarred by the movie—Anderson said that his own daughter, many years later, “still doesn’t forgive us for killing the dog,” and one critic bluntly called the ending “child abuse”—one has to see Walt Disney’s subtle amendment as a strange sort of mercy. As brutal as it was for kids to see that mad dog get shot, how much crueler the world would have seemed if its killing had been necessary only because it might go mad. Rabies, frightening though its ravages may be to see up close, has about it the comfort of certainty. However much the furious dog was once loved, it cannot be saved.
Dogs’ bond with humans is bred into their very cells, their genes; it’s written through their entire history, a chronicle that can be read in their eyes. But inside this black wire cage, in the lolling eyes of what remained of a Pekingese, there was nothing legible at all. One could hardly grieve for the dog, because the dog was already gone. To euthanize it—which a BAWA vet mercifully did, moments later, with the customary overdose of anesthesia—was merely to acknowledge its departure.
Hercules Capturing Cerberus by Hans Sebald Beham, 1545.
CONCLUSION
THE DEVIL, LEASHED
Walking the streets of Manhattan, one encounters spitting, staggering, and convulsing on a daily basis, but the offenders generally perambulate on two legs, not four. In July 2009, though, a suspiciously erratic animal was spotted on Payson Avenue, just outside Inwood Hill Park at the island’s northern tip. It tested positive for rabies: not an unprecedented occurrence in the borough, but one that officials at the health department felt they should monitor closely. Later that summer, on August 27, 2009, a second case was found, this time along the northern border of Central Park. Then, in December, after more than four months of quiet, ten more were found to be infected, eight of them in Central Park. As 2010 began, the situation started to spiral out of control: twenty-two gone mad in January, twenty-nine in February, with two people bitten. New York’s favorite dog-walking destination had quite suddenly become infested with rabies. Yet all the beloved poodles and French bulldogs and bichons frises were not vectors but potential victims.
The perpetrator was a wild animal, but one that nevertheless lives nearly as close among us as our dogs do. Most North Americans, upon being awoken by the characteristic rattle and crash of a trash can lid, will guess the culprit immediately. It is Procyon lotor, or the common raccoon, identifiable by its masked face, its shuffling gait, its light- and dark-ringed tuft of tail. During the past twenty years, raccoons have become the U.S. species most frequently found to be infected with rabies. And although their range covers nearly the whole continent, from Canada to Panama, raccoons thrive more today in urban and suburban locales than they do in pristine forests; the highest density of raccoons in New York State is not in the Catskills or the Adirondacks but in New York City. They come, like many human visitors to New York, for the food. One of the most omnivorous animals on earth, the raccoon eats everything—earthworms and acorns, minnows and bluebird nestlings—but it especially enjoys trash, from corncobs to cat chow to cheesecakes. Urban environments, inhospitable to much of the wild kingdom, offer up tons of delectable food for raccoons every day, conveniently presented to them in plastic bags or in cylindrical serving containers that their nimble hands can pry open easily. Sated at this buffet, raccoons can bunk down just about anyplace, whether an abandoned burrow or a sewer, a treetop or a fire escape.
The spread of rabies among raccoons has been described by the CDC as “one of the most intensive wildlife rabies outbreaks in history,” and a human blunder seems to have been at least partly to blame. Before the mid-1970s, raccoon rabies—a strain adapted to the raccoon, such that the animal is generally able to survive infection long enough to transmit the virus to another—was confined to Florida and neighboring states, spreading very slowly through the Deep South at a rate of eighteen to twenty-four miles per year. But starting in 1977, more than thirty-five hundred raccoons were legally trapped in Florida and shipped to private hunting clubs in Virginia, where they were released as prospective game. Seeing as how raccoons do not respect the lines of private property, the creatures were effectively being released into the wild. The mid-Atlantic saw its first case of raccoon rabies in 1977, near the Virginia–West Virginia line, far from the existing margins of the southern outbreak. Now there were two loci of infection: one emanating out from Florida, another from the Virginias. Within three decades, rabid raccoons had been observed throughout the entire eastern United States, with a few cases sighted as far
west as Ohio.
By 2009, raccoon rabies had already hunkered down in the New York suburbs; it even kept a semipermanent residence in the Bronx. Now, finally, it had swept furiously into Manhattan. Every week, as the city made updates to its online rabies map, the red dots—denoting spots where afflicted raccoons were found—sprayed across Central Park and the vicinity like bullet wounds from a tommy gun. On February 16, 2010, with a total of forty cases identified, the city health department announced a daring plan. It was a scheme that involved, as one rabies expert puts it, “thinking like a raccoon.” Based on an understanding of their habitats and behaviors, teams would set collapsible cage traps around the affected areas at night, baiting them with food. The traps would then be checked at dawn and the rabid animals destroyed; those that appeared healthy would be sedated, tagged, vaccinated, and released, on the principle (just as with feral dogs in Bali and elsewhere) that moving or killing healthy animals only invites the population to fill out again with potentially sick ones. Central Park being one of the most popular parks in the world, traps needed to be kept away from the curious hands of children and noses of dogs. Thus the teams had to set traps in out-of-the-way locales, working quickly under cover of darkness: set, sedate, vaccinate, collapse the traps, and go.
Even as this heroic undertaking got under way, rabid raccoons were staggering out with frightening regularity through the green spaces of upper Manhattan, even venturing into the tony neighborhoods nearby. March saw nearly as many cases as February, and April saw nearly as many as March. But by that summer, the reported cases had slowed to a coon-like creep. In the eight months beginning on December 1, 2009, there had been 124 rabid raccoons confirmed, but in July, August, and September 2010 there were only 6; since then, as of the fall of 2011, only 1 more case has been reported. For all the arduousness of trapping and vaccination, the effort seems to have paid off, with the urban jungle of Manhattan left to its more customary ravages.
How, then, to understand the great Manhattan Rabies Outbreak of 2009–10? It was a far cry from the rabies paranoias that racked New York and the great cities of Europe near the end of the nineteenth century. All the way into the twentieth, with Pasteur’s cure on the march, rabies lurked as a constant menace in streets and lanes, even in the developed world. The agent of infection was the familiar—the all-too-friendly dog, sometimes even one’s own pet—and the consequence of a bite was routinely a horrible death. By contrast, at the beginning of the twenty-first, our dogs are largely vaccinated, our bites are nearly always treated; the threat, meanwhile, lingers among creatures not adapted to our companionship, such as raccoons and foxes, skunks and bats. Rabies has receded to become a sort of spectral presence, a ghost story. It’s gone until it isn’t.
As we saw in the last two chapters, the struggle of science against rabies seems to have arrived at a frustrating stalemate. Through his innovative, last-ditch protocol for human cases, Rodney Willoughby has broken the 100 percent fatality rate of the world’s deadliest virus. But reliable rescue of patients through his methods has proven elusive. By the same token, in the fight to control the exposure rate, the path for government health agencies is clear: with diligent and mandatory vaccination of dogs, human cases can be brought down to near-negligible levels, even in poorer countries where strays are a problem. And yet as the tale of Bali makes clear, beating back the virus can be extremely costly, in both capital and effort, and gains can be quickly reversed if government vigilance flags.
Despite the terrible manner in which it kills, and despite the fact that prevention through dog vaccination is far more cost-effective than treating bites after they happen (to say nothing of managing the fatal cases)—despite all this, the small number of human deaths from rabies means that money for prevention is hard to come by. Charles Rupprecht, chief of the rabies unit at the CDC and still arguably the world’s preeminent expert on the virus, calls this the “cycle of neglected diseases.” Rupprecht is an odd combination of a soft speaker and a tough talker, rarely conversing for more than ten minutes without touting his New Jersey roots. Growing up in Trenton, he cultivated a deep love for animals, but also for science fiction, and so he sees the course of his career as having been in some sense inevitable. “When you put the two together—reality and fantasy, animals and monsters—you can’t get much closer than rabies,” he says with a chuckle. One particularly vivid childhood memory is a face-to-face encounter with a bat, which his brother had inadvertently scared out into view by throwing a basketball against the side of their house. While in graduate school in zoology at the University of Wisconsin, he studied bat ecology; that took him to a summer fellowship in Panama, where he studied bats at the Smithsonian Tropical Research Institute. While he was in veterinary school at the University of Pennsylvania, his interest in bat-borne disease brought him to the Wistar Institute, a biomedical research group on campus, where—his curiosity piqued by the garish medical oddities in the building’s front windows—Rupprecht knocked on the door of Tad Wiktor, head of the institute’s rabies unit, and introduced himself as a bat specialist. “Ah, bats,” Wiktor replied gravely, sucking on his pipe. “I’ve always wanted bats. How do you grow them?”
Since then, Rupprecht has had a hand in nearly every important advance in rabies management during the past twenty-five years. At Wistar, he played a role in developing a recombinant oral rabies vaccine for wildlife, which helped beat back a nasty outbreak among Texas coyotes in the 1990s. He was involved with the first trap-vaccinate-release campaigns among raccoons, on the mid-Atlantic’s Delmarva Peninsula and in Philadelphia’s Fairmount Park. It was Rupprecht, after moving to the CDC, who consulted with Willoughby when he was scheming a rescue plan for Jeanna; he also was one of the experts that Janice Girardi consulted in devising BAWA’s vaccination plan. (“The CDC is a service organization,” explains Rupprecht. “It’s like The X-Files.”) It’s charming to talk to a virus hunter who speaks with such deep respect for his quarry. An “exquisite parasite,” Rupprecht calls rabies, citing all the ways that it has perfectly adapted to its mammalian hosts. “We love to lick, we love to suck, we love to bite,” he points out, and so rabies “exploits what mammals do naturally.”
Like many other rabies experts, Rupprecht believes that dog rabies—the type responsible for the vast majority of human deaths worldwide—can be eradicated during his lifetime. Unfortunately, though, any concerted effort to do so would require a fairly precise understanding of what the rabies “burden” is: an epidemiologically sound tally of canine infection (which often goes unnoticed or unreported) and human death from rabies (which, if counted at all, often get misclassified as some other encephalitis). This census never gets made, precisely because the number of definitive infections and deaths doesn’t seem to justify the spending. “We don’t have an effective surveillance system, because there are no resources,” Rupprecht says with exasperation. “And there are no resources because there are no cases!” Together with his peers at other health departments worldwide, along with a nonprofit called Global Alliance for Rabies Control, Rupprecht has helped to popularize World Rabies Day, an annual affair designed to build awareness and keep health officials informed about strategies against the disease. If you’d like to mark your calendar, the date each year is September 28—in honor of Louis Pasteur, who died that day in 1895.
There is one realm in which one might say rabies has been conquered during the past ten years—even, in a strange way, enslaved. If this most ancient of viruses can never be eradicated from animals, molecular biologists have hit upon the next best outcome: they are harnessing its uniquely diabolical properties in an attempt to resolve one of our thorniest medical problems. Rabies still knows how to infect us, but at the molecular level we have learned how to infect it.
To see how this is possible, we need to understand what neuroscientists call the “blood-brain barrier.” This barrier is not, as the word might imply, a solid wall or even a discrete membrane. Capillaries, just as they do elsewhere in the
body, feed every cell in the brain with blood directly; there are nearly four hundred miles of capillaries in the brain alone, each lying less than two-hundredths of an inch from one another. These brain capillaries, however, prohibit most types of molecules from passing through their walls. Oxygen, carbon dioxide, and hormones make it in and out, but larger bodies—including, thankfully, most pathogens—are unable to enter easily.
The existence of the blood-brain barrier was first hinted at by the work of Paul Ehrlich, a German biologist best known for discovering a cure for syphilis. (An unlikely 1940 Hollywood film about that feat, Dr. Ehrlich’s Magic Bullet, starred Edward G. Robinson as the good doctor.) In dyeing experiments on animals, Ehrlich showed that certain pigments, introduced into the bloodstream, would soon stain all the internal organs—except the brain. Soon, one of his students thought to carry out the opposite side of the equation: injecting the same dye directly into the brain. What he discovered was that the dye stained the whole brain but nothing else. Something unique was happening at the boundary between brain and body.