Rabid

by Monica Murphy

  At the same time, though, even as the oldest animal infection receded as a public menace, the pioneering work of microbiologists was establishing that a whole host of other diseases were, in fact, linked to similar diseases in beasts. This includes, of course, the titan of them all, the bubonic plague. (The flea-borne pathogen that Alexandre Yersin isolated in 1894 was later renamed in his honor—Yersinia pestis—and in 2010, using skeletons from plague pits, it was proved beyond doubt that this pathogen had been the cause of the Black Death.) All of human history prior to the twentieth century had been haunted by rabies as an unforestallable and invariably fatal infection from animals. In the twentieth century, as rabies receded, it was replaced by a rapid succession of equally horrific and, in many cases, far more dangerous zoonoses.

  The most fatal of these struck like a tsunami between 1917 and 1920, when some 50 to 100 million people worldwide—roughly 3 percent of the global population—died of a particularly nasty strain of influenza, the so-called Spanish flu. At the time, medicine believed influenza to be a uniquely human malady. But throughout 1918, during the height of the epidemic, reports trickled in about uncommon animal ailments that seemed to mirror the symptoms of flu. At a veterinary hospital of the French army, a shocking number of horses had been laid low with such a syndrome. In South Africa and Madagascar, it was primates, baboons, and monkeys felled by the hundreds; in northern Ontario it was moose, dead in the brush. But most ravaged of all was the Iowan pig. First noted at the Cedar Rapids Swine Show in the fall of 1918, flu-like symptoms spread over the succeeding months to literally millions of hogs. The veterinarian J. S. Koen, who tracked the disease while in the employ of the federal Bureau of Animal Industry, reported its toll in stark terms. “Sudden and severe onslaught. Patient very sick and distressed…. Muscular soreness, nervous and excitable. Congestion of eyes. Watery discharge from eyes and nostrils…. Temperatures usually high, many instances up to 108°F. Rapid loss of flesh, may lose as much as five pounds per day. Extreme physical weakness. Very rapid progress through herd. Lasts four or five days and patient begins to recover about the time death is expected.” But recovery never arrived for the thousands of pigs, or roughly 1 to 2 percent of cases, that perished from the infection.

  Just calling this pig malady a “flu” was enough to invite skepticism from scientists and hand-wringing from the pork industry, which worried that reports of a deadly human flu in pigs could turn the public stomach against its products. But Koen stood his ground. “I believe I have as much to support this diagnosis in pigs as the physicians have to support a similar diagnosis in man,” he wrote, and went on:

  The similarity of the epidemic among people and the epizootic among pigs was so close, the reports so frequent, that an outbreak in the family would be followed immediately by an outbreak among the hogs, and vice versa, as to present a most striking coincidence if not suggesting a close relation between the two conditions. It looked like “flu,” it presented the identical symptoms of “flu,” it terminated like “flu,” and until proved it was not “flu,” I shall stand by that diagnosis.

  It was, as the historian Alfred W. Crosby later wrote, “a peroration…worthy of Luther standing before the Emperor at Worms.”

  Over the course of the next twenty years, four scientists working on both sides of the Atlantic—Richard Shope, based in Princeton, New Jersey, at the laboratories of the Rockefeller Institute for Medical Research, and a team of three in the United Kingdom (Wilson Smith, Christopher Andrewes, and Patrick Laidlaw)—endeavored to prove Koen’s intemperate assertion correct. In 1928, Shope was back in his home state of Iowa investigating so-called hog cholera (in fact, unrelated to the human virus of that name) when he started looking into Koen’s theory. The following fall, when the swine infection hit the herds again in full force, Shope returned to collect tissue samples and mucus secretions, and by 1931 he and his mentor, Paul Lewis, had isolated what would later be confirmed as the swine flu virus.

  Meanwhile, the three English scientists, also at work on the problem of flu, employed a domesticated animal that until then had stayed on the sidelines of the quandary: namely, the ferret. In the mid-1920s, Laidlaw had coauthored some pathbreaking research on distemper, a nasty respiratory illness in dogs that he and his collaborator demonstrated could easily be spread to ferrets. Now he and his collaborators on flu were attempting to pass the human strain of the disease to ferrets. In 1933 they succeeded, isolating a virus from diseased humans that created a comparable illness in twenty-six ferrets. Perhaps more important, they also demonstrated that Pfeiffer’s bacillus, a bacterium that for decades had been suspected as the cause of influenza, had no effect at all.

  That same year Shope, with whom the three were now working in excited collaboration, used his swine virus to produce flu in ferrets. And this was not just any flu; it was a horrific, Spanish-style flu, characterized by the same bloody pneumonia that had swept away millions in the global pandemic. By May 1935, in a lecture at St. John’s College, Laidlaw was able to state confidently his opinion—one borne out by all subsequent discoveries—that “the virus of swine influenza is really the virus of the great pandemic of 1918 adapted to the pig and persisting in that species ever since.”

  This retrospective understanding of the 1918 pandemic was just the first such awakening in a century replete with terrifying zoonoses. U.S. soldiers returned from the Korean War with a sinister strain of hantavirus, a nasty hemorrhagic fever acquired from rats. In the late 1960s, Africans were falling ill from Lassa fever, also the handiwork of rats. The 1980s saw the emergence not just of AIDS but of the terrifying Ebola, also a disease from monkeys that, at its most acute, can induce terrible death involving bleeding from all bodily orifices. More recently, two strains of animal influenza—the onset of the avian flu and the robust return of the swine flu—killed thousands of people and prompted thousands more to hide for months behind surgical masks. Despite the slow ebb of rabies as a killer of men, the preceding century nevertheless supplied humans with countless reasons to eye their animal neighbors warily.

  By the 1930s, rabies in America had largely subsided in humans, though their dogs were a different matter. This was especially the case in the South; a report from late in that decade put the infection rate among the dogs of Birmingham, Alabama, at 1 percent—a shocking number for a virus that kills all of its canine hosts. Though the canine vaccine was by then widely available, whites in the region vaccinated just 40 percent of their dogs, and African Americans only one in ten. The human death rate had been brought low but remained real: more than 250 deaths were logged in the American South during the 1930s, a per capita rate not dissimilar to the pre-Pasteur hysterias in eighteenth-century England.

  That decade also saw the publication of a seminal novel, one of the most important of the twentieth century, whose denouement hinges on a spectacular demise in the jaws of rabies. Their Eyes Were Watching God, by Zora Neale Hurston, details the life and romantic entanglements of Janie Crawford, a black woman from a modest upbringing in western Florida. After being raised by her grandmother, a former slave, Janie marries a much older farmer; is seduced away from him by a soon-to-be politician and entrepreneur; then finally (after the death of this brutal and abusive second husband) falls in love with a much younger man named Vergible Woods, known to all as Tea Cake, whose fraught and tempestuous marriage to Janie consumes the second half of the book. The pair move first to Jacksonville and then to the Everglades, where they live happily in a shack, planting and picking beans by day and socializing at night, as Tea Cake entertains guests with his guitar and then takes their money (or vice versa) in dice games.

  Their reverie is eventually shattered by the arrival of a hurricane, the ravages of which on their little shack prove to be the least of their troubles. Far more consequential, though neither is aware of this at the time, is the bite that Tea Cake receives—on his face, no less—from a shivering, furious dog they encounter while fleeing to safety. Perched improbably on the back
of an almost wholly submerged cow, the dog “growled like a lion,” with “stiff-standing hackles, stiff muscles, teeth uncovered as he lashed up his fury for the charge.” Tea Cake wrestles with the dog and eventually drowns it, but not before it has clamped its slavering jaws upon his cheekbone.

  Three weeks later, after the pair has fixed up a house in the Everglades and (they believe) resumed their life together, Tea Cake starts to complain of a headache. In the dead of night he wakes up in a “nightmarish struggle with an enemy that was at his throat.” The next morning, offered a glass of water, Tea Cake gags on it, dashes the glass to the floor. “Dat water is somethin’ wrong wid it,” he exclaims. “It nelly choke me tuh death.”

  A doctor, summoned to Tea Cake’s bedside, warns Janie that rabies is the likely diagnosis. The only thing she can do now is to leave him at the County Hospital, where the staff can “tie him down and look after him.”

  “But he don’t like no hospital at all,” Janie replies. “He’d think Ah wuz tired uh doin’ fuh ’im, when God knows Ah ain’t. Ah can’t stand de idea us tyin’ Tea Cake lak he wuz uh mad dawg.”

  “It almost amounts to dat,” says the doctor, forebodingly. “He’s got almost no chance to pull through and he’s liable to bite somebody else, specially you, and then you’ll be in the same fix he’s in.”

  By the very next morning, Tea Cake has descended into a paranoid fury. Seized with suspicions of his wife, he returns from the outhouse and draws his pistol on her. She has prepared herself for this turn with a rifle. She plants a fatal shot in Tea Cake just as he lunges and bites her on the arm. She is forced to pry her slain husband’s jaws from her own flesh.

  Given the doctor’s explicit warning, we are left to wonder: Has Janie herself contracted rabies from Tea Cake’s bite? Today’s rabies experts believe that the virus is unlikely to be passed from human to human via biting. But as the Hurston scholar Robert Haas points out, that possibility was often emphasized by doctors in Hurston’s time, and the doctor in her own book raises it. If Janie has been infected, we aren’t given any sense that a similar madness is settling on her. And yet it’s impossible to tell whether the window for infection has passed. The book both begins and ends at some unspecified time after the incident, when Janie returns to the town (Eatonville, Florida, Hurston’s own hometown) where she and her second husband had lived and prospered. At her trial for Tea Cake’s death—before, in a heavy irony, Janie is acquitted by an all-white jury that simply doesn’t believe killing a black man to be a crime—the doctor testifies to finding her “all bit in the arm, sitting on the floor and petting Tea Cake’s head.” Probably we are supposed to conclude, somewhat reasonably, that he treated Janie then for her possible exposure.

  The other lingering question, of course, is how Hurston came to use rabies as a plot point in the first place. Critics and biographers have found the choice somewhat bewildering. Robert Haas points out that Hurston’s brother and first husband were both doctors, and her family had seven hounds while she was growing up; either of these might have lodged rabies in her brain, as it were.

  But he also offers up a more intriguing and ultimately more plausible theory. At the beginning of 1936, as Hurston was writing her novel, a surprisingly popular movie about science played on screens all across the country. Its title? The Story of Louis Pasteur. Based on its gross of $665,000, Haas estimates that thirteen million Americans, or a full tenth of the population, would have seen the film—the entire last half of which is devoted to Pasteur’s formulation of the rabies vaccine. In New York, where Hurston was living at the time, it ran for the whole month of February and also received reviews in the daily papers. It’s only circumstantial evidence, to be sure; but we take a strange pleasure in the thought that the great Pasteur, while alleviating the terror of rabies in the streets, at the same time helped to inject a dollop of that terror into one of the century’s great works of fiction.

  It was also during the mid-1930s that the man who would revolutionize our ideas of the undead got his first taste of big-screen terror. The movie was Werewolf of London, and Richard Matheson was nine. “Somehow, I talked my mother into taking me,” he recalled. “And when Henry Hull”—who in the film played a biologist, Wilfred Glendon, bitten by a strange animal while conducting research in Tibet—“changed into a werewolf, I freaked! Fell out of my seat and crawled up the aisle.” The son of Norwegian immigrants, Matheson grew up in Brooklyn and excelled at science and music during high school, at the city’s prestigious Brooklyn Tech. But after seeing combat in World War II and then graduating from the University of Missouri, he charted an entirely different course as a writer. He began with short stories in various genres—sci-fi, mystery, western—and then moved on to novels. To pay the bills, he worked days at the post office and later at an aircraft plant. At the time of his marriage, he had made only five hundred dollars from writing. “Those were very bad years,” he later recalled, during which time his financial anxieties began to play into his fiction: “My theme in those years was of a man, isolated and alone, and assaulted on all sides by everything you could imagine.”

  In 1953, Matheson turned this trope into what is probably the most influential horror novel of the twentieth century. I Am Legend tracks the lonely existence of Robert Neville, who apparently stands as the only human survivor of a terrible virus that has killed off most of the people and turned the remainder into vampires. But these vampires are far from the becloaked aristocrats who haunted the dreams of the nineteenth century. They are insensate monsters who sleep all day in their lightless hovels and then roam at night in search of fresh blood. Immune to the virus, Neville becomes desperate in his loneliness, brought to the brink of self-destruction by the psychological ravages of his ceaseless routine: his home must be constantly fortified, and supplies replenished, in order to withstand the nightly onslaught. During the daylight hours he also drives around his city, a postapocalyptic Los Angeles, breezing down its abandoned avenues to stake as many vampires as he can find.

  The slightest slip in this routine can lead to terrible consequences. One day, while making his rounds, Neville realizes that his watch has stopped; dusk is near, and he is at least an hour from home. At the intersection of Western and Compton he begins to see the vampires, rushing out of buildings as his station wagon passes. By the time he reaches his house, a mob of them await in front. He careers straight into the crowd, watching them fall like bowling pins, their pale, contorted faces crying out in agony. He heads past his house, and the remaining vampires make chase behind him, allowing him to dart around the block, park in front of his house, and dash to his door before they catch up.

  We never learn the precise nature of the virus, though we do know that it afflicts dogs as well as people. Indeed, Matheson’s description of a dog, dying in its agonies, gives us a sense that it bears an acute resemblance to rabies. Neville is amazed to see a live dog walking around, and so he begins to feed it. Soon, though, the dog succumbs: its expression begins to glaze, its tongue lolls out. Neville reaches for it, and its lips pull back in a threatening grimace. It begins to violently shake, with “guttural snarls bubbling in its throat.” The dog dies a week later.

  With I Am Legend’s evocation of a pandemic, and its intimations of nuclear devastation—World War III, we discover, has recently transpired, possibly helping to create the virus—the novel somehow managed to take the moribund vampire genre, still ruled even then by dour gothic Slavs in musty castles, and to reinvent it for the cold war era. One of Matheson’s prime innovations was its setting: contemporary, suburban. But even more revolutionary was the nature of his “vampires.” Far from the sophisticated loners of vampire literature to date, this was a mob of undead creatures whose threat lay not in their cunning but in their animal ferocity and, most important, their sheer numbers. “He was going out and staking vampires every day, finding them at the cold counter at Stop and Shop, laid out like lamb chops or something,” Stephen King once said, in citing Matheson’s book
as a tremendous influence on his own work. “I realized then that horror didn’t have to happen in a haunted castle; it could happen in the suburbs, on your street, maybe right next door.”

  Although I Am Legend calls its ghouls “vampires,” the book actually was instrumental in jump-starting an entirely different genre: the zombie tale. The term “zombie” derives from Haitian religious belief and has been appropriated by American fiction authors since at least the late 1920s; Hollywood began making zombie movies in the 1930s. But in the mid-1960s, Matheson’s story inspired George Romero, then a TV-ad director in Pittsburgh, to conceive of a more vital sort of zombie. In a short story that he eventually called “Anubis” (though never published), Romero “basically ripped off” Matheson’s vision in describing a dystopian world where the dead have come back to life. Eventually, chafed by the constraints of television and unable to get funding for a feature, Romero and his friends decided to fund themselves in bringing his story to life. They pooled six hundred dollars apiece, from ten of them; a few of the other producers took roles in the film, the rest all pitched in as miscellaneous crew, and Romero directed. The result was a low-budget masterpiece called Night of the Living Dead, which grossed millions as a cult classic and also set the template for all zombie movies that would follow. Like the “vampires” in Matheson’s story, Romero’s zombie undead were not individual malefactors, not some garden-variety Draculas or wolf-men. They were an insatiable horde, eating their way through a society where all order has broken down. Zombies became synonymous with apocalypse.