Spillover

by David Quammen

A larger outbreak occurred in Paris in 1892, after two animal dealers received a shipment of five hundred parrots imported from Buenos Aires. The dealers became infected, several of their customers became infected, and then so did relatives, friends, and one doctor in attendance. Sixteen people died. Soon the disease had cropped up also in Germany, in New York, and at a department store (which sold birds) in Wilkes-Barre, Pennsylvania. In 1898 it struck the annual exhibition of the Berlin Union of Canary Fanciers, demonstrating that parrots and their kin weren’t the only birds capable of carrying this “parrot fever” microbe, whatever it was. (Canaries belong to the order Passeriformes, not to the Psittaciformes.) Half a dozen canary fanciers fell ill and, by an account in a Berlin newspaper, “three died in agony.”

  Then came a hiatus, if not in the incidence of parrot-borne infections at least in the attention they received. The Great War, followed immediately by the great influenza, gave people a surfeit of death and disease to engage their sorrows and fears. The 1920s were decidedly more cheerful and carefree, until they weren’t. “The year 1929 marked a turning point in the revival of interest concerning the etiology of human psittacosis,” according to one historical survey of the disease. Etiology, that was the crux. Outbreaks might come and go. What differed in 1929, besides the Crash and a general lowering of spirits, was a sufficiency of parrot-fever cases to make studying the cause not only more practical but also more urgent.

  Lillian Martin of Annapolis had been among the first of this new wave, and though she eventually recovered, others weren’t so lucky. The Washington Post continued to track the story, reporting parrot-fever fatalities in Maryland, Ohio, Pennsylvania, New York—and Hamburg, Germany. On January 13, the Surgeon General telegraphed health officials in nine states, asking for help in tracking the situation. Two weeks later, with cases now reported also from Minnesota, Florida, and California, President Hoover declared an embargo against imported parrots. The director of the Bureau of Bacteriology within Baltimore’s health department, who had been doing necropsies on infected birds, got sick and died. A laboratory technician at the Hygienic Laboratory, which was part of the US Public Health Service, got sick and died. That technician had been assisting a researcher, Charles Armstrong, with bird-to-bird transmission experiments in the laboratory basement. Their working conditions were less than ideal: two small basement rooms full of distressed parrots held in garbage cans, wire mesh over the tops, feathers and bird shit flying out, curtains soaked in disinfectant to contain the airborne drift. It wasn’t BSL-4. Charles Armstrong got sick but did not die. Nine other personnel of the Hygienic Laboratory also became infected, none of whom had even entered the basement bird rooms. The laboratory director, realizing that his building was broadly contaminated with whatever wafting agent caused psittacosis, closed the place down. Then he descended to the basement himself, chloroformed all the remaining parrots, chloroformed the guinea pigs and pigeons and monkeys and rats involved in the same experimental work, and threw their dead bodies into the incinerator. This forthright man, this hands-on administrator, described in one source as “tall with a gnarled Lincolnian face,” was Dr. George W. McCoy. For reasons explicable only in terms of the wonders of the immune system and the vagaries of fortune, Dr. McCoy didn’t get sick.

  The psittacosis epidemic of 1930 was winding down, and probably also, though more slowly, the psittacine panic. On March 19, the Acting Secretary of the Navy issued a general order for sailors on shipboard to get rid of their parrots. George McCoy reopened the Hygienic Laboratory, Charles Armstrong returned from convalescence, and the search for a cause of the disease continued.

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  Within a month, a culprit had been identified. It was a small bacterium with some unusual properties, seemingly similar to the agent that causes typhus (Rickettsia prowazekii) and therefore given the name Rickettsia psittaci. Where did it come from? Argentina had been implicated as a source of sick birds at the start of the 1930 outbreak; President Hoover’s embargo would have stanched that source. But then latent psittacosis was detected in some commercial California aviaries, where parakeets for the domestic pet trade were produced—meaning that American breeders were harboring an endemic reservoir of the infection and distributing it by way of interstate commerce. So a proposal was made to destroy all those infected flocks and then reestablish the trade with healthy birds from Australia. This seemed to make sense on two counts. First, what we Americans call a “parakeet” is a native Australian bird, widespread and abundant in the wild, known to Australians as the budgerigar. Second, Australia itself (despite a high diversity of psittacine birds) was thought to be psittacosis-free. Starting over with wild birds might free the American bird trade of psittacosis. That was the idea, anyway.

  A pair of American scientists got permission, despite the embargo, to import a consignment of two hundred Australian parakeets lately captured in the vicinity of Adelaide. They wanted to do an experiment. Their plan was to infect the imported birds, whose immune systems were assumed to be naïve, with American strains of psittacosis. But when one of the imports fell dead, not long after arrival, the scientists opened it up and found Rickettsia psittaci. They also noticed that some others of their birds, seemingly healthy, carried the bacterium as a latent infection, like the birds in those California aviaries. That raised fresh concern about what might be lurking in other aviaries, in zoos, and in pet shops around America, and strongly suggested that Australia might not be as clean as it seemed.

  This is where Frank Macfarlane Burnet, a great figure in Australian science, enters the story. Burnet was a complicated, brilliant, crotchety man and a signal character in the study of infectious diseases. Eventually he would earn a knighthood, a Nobel Prize, and a number of other fancy honors, but long before those he had made a name for himself in zoonoses. Born in 1899, second child among an eventual seven, he was a solitary, opinionated schoolboy who read H. G. Wells, disapproved of his own father’s shallow morality, preferred beetle collecting to more sociable activities, despised his roommates, read about Charles Darwin (who became one of his heroes) in an encyclopedia, forced himself (despite an inaptitude for sports) to achieve competence as a cricketer, and became an agnostic during his undergraduate years. Unfit for a career in the Church, ambivalent toward the law, he chose medicine. He trained as a doctor in Melbourne but then, recognizing his lack of empathy with patients, went to London for a PhD in virology. Declining a chair at the University of London, he returned to Australia to do research. He was a nationalist, stoutly Aussie. Much later in life, laden with honors and fame, Burnet kept his edge by publishing cranky pontifications on a wide range of subjects including euthanasia, infanticide for handicapped babies, Aboriginal land rights, population control, tobacco advertising, French nuclear testing in the Pacific, the futility of trying to cure cancer, and the merits (low, in his view) of molecular biology (as distinct from his discipline, microbiology). Burnet received his Nobel, in 1960, for helping illuminate the mechanisms of acquired immune tolerance. His role in understanding zoonotic diseases began much earlier. In 1934, as a young microbiologist based at the Walter and Eliza Hall Institute, back in Melbourne, he got interested in psittacosis.

  Keying off the American study, Burnet ordered himself a crate of parrots and cockatoos from Adelaide. He found that a third of them were infected. He ordered another dozen from Melbourne. At least nine of those were probable carriers. Another two dozen from Melbourne yielded still more positives. So much for the myth of Australia as a prelapsarian psittacosis-free Eden.

  But if the country’s wild bird populations were riddled with this bacterium, how could the country’s people—so many of whom doted upon their pet budgerigars and talking cockatoos—be entirely as unaffected as they seemed? The likely answer, Burnet guessed, was not some magical form of immunity but ignorance and underdiagnosis. Australian doctors didn’t know psittacosis when it wheezed in their faces. To test that guess, Burnet started chasing down cases of human illness that looked like psittaco
sis but might have been diagnosed as influenza or typhoid. He and a co-investigator found seventeen people, sick with fever, cough, headache, pneumonia, et cetera, all of whom had been exposed to pet birds—either captive-bred budgerigars or parrots and cockatoos lately caught from the wild. His most interesting cluster was a group of twelve people infected from one batch of sulphur-crested cockatoos.

  Those birds, all forty-nine of them, had been sold by the bird catcher to a Melbourne man, a laborer, who dabbled in bird dealing for a bit of seasonal income. Burnet called the man Mr. X, giving him the usual medical anonymity. Mr. X kept his avian merchandise in a small, dark, backyard shed. The first signal of disease in the birds, several weeks after their transfer to his “aviary,” was that eight or nine of them died. But by then Mr. X, wasting no time, had sold seven others to people in the neighborhood and sent his twelve-year-old son off to the local market with twenty more. Mr. X’s son got sick, and his daughter, and his wife, and his mother-in-law. Five neighbors and three other people, each of whom lived in a house with a cockatoo bought from Mr. X or his son, also fell ill, some of them severely. Nobody died. Mr. X himself didn’t sicken, not on this occasion—possibly because there is no justice in the world, though more likely because exposure to Rickettsia psittaci during his earlier bird dealings had given him some acquired immunity.

  Macfarlane Burnet, as a biologist as well as a physician, was interested in the birds and the bacterium, not just in the people. He knew that the sulphur-crested cockatoo nests in tree holes, producing two or three eggs in a clutch, and that bird catchers typically raided the nest holes just before fledging. He suspected that almost all the young became infected with the bacterium as hatchlings, before leaving (or being taken from) the nest. “If the young cockatoo, after capture, is kept under good conditions,” he and his coauthor wrote, “it remains healthy and presents no danger to human beings.” Likewise, the wild bird populations might carry a high prevalence of infection but suffer little impact in terms of damaged health or mortality. “When, on the other hand, birds are crowded into small spaces, with inadequate food and sunlight, their latent infection is lit up.” The bacterium multiplies and “is excreted in large amounts.” It floats out of the cages along with downy feathers, powdered dung, and dust. It rides the air like a Mosaic plague. People inhale it and become ill. Burnet acknowledged that no government in Australia was likely to prohibit the sale of cockatoos, not in those days, nor even to insist they be kept under decent conditions. But that’s what is needed, he added gruffly. Then he turned to another disease.

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  The other disease was Q fever. Remember those abattoir workers in Brisbane, during the early 1930s, who suffered mysterious, feverish ailments resembling typhus? The job of investigating that cluster of cases fell first to a man named Edward H. Derrick, newly appointed as director of the microbiology laboratory at the Queensland Health Department. Using guinea pigs inoculated with patients’ blood to start a sequence of infections and then infecting one guinea pig from another, Derrick established the presence of “a distinct clinical entity,” a new sort of pathogen, not recognizable by any of the standard lab tests for typhus, undulant fever, or other familiar possibilities. But he couldn’t see the new thing through a microscope, nor could he get it to grow in a dish. That led him to suspect it was a virus. So he sought help from Macfarlane Burnet.

  In October 1936, Derrick sent Burnet a sample of guinea-pig liver, infected experimentally with whatever had been raging through the abattoir workers. From that sample, Burnet and a laboratory assistant continued the chain of infection in more guinea pigs, and also in a series of inoculated mice. Like Derrick, Burnet and his assistant checked for bacterial pathogens and found none. So they suspected “a filterable virus,” meaning an agent so small it would pass through a fine filter designed to screen out bacteria. They took a thin smear of puréed spleen from an infected mouse, stained it for microscopy, and looked through the scope. Thirty years later, Burnet recalled: “Most significant discoveries just grow on one over weeks or months. Recognition of Q fever as a rickettsiosis was, however, an exception datable to the minute.” What he saw were tiny rod-shaped “inclusions” within some of the spleen cells. For a better view, he tried another slide of spleen using a different stain. This one showed an abundance of the rods, some within spleen cells and some floating free. “From that moment, there was no doubt in my mind about the nature of the agent responsible for Q fever.” It was another new rickettsia, he concluded, not too unlike the one that caused parrot fever.

  In his later recollection, characteristically blunt, Burnet told how the disease got its name:

  Problems of nomenclature arose. The local authorities objected to “abattoir’s fever”, which was the usual name amongst the doctors in the early period. In one of my annual reports I referred to “Queensland rickettsial fever”, which seemed appropriate to me, but not to people concerned with the good name of Queensland. Derrick, more or less in desperation, since “X disease” was preoccupied by [sic, meaning “already applied to”] what is now Murray Valley encephalitis, then came out for “Q” fever (Q for “query”). For a long time, however, the world equated Q with Queensland, and it was only when the disease was found to be widespread around the world that “Q fever” came to stand firmly in its own right as the name of the disease.

  For the scientific binomial, Derrick proposed Rickettsia burnetii, to honor Burnet’s role in finding and identifying the bug. The genus name, Rickettsia, would eventually change due to a taxonomic revision, but Burnet’s half stuck.

  Meanwhile, nine thousand miles away, the same pathogen came under scrutiny by a much different route, when two bacteriologists at the Rocky Mountain Laboratory, in Hamilton, Montana, found it in ticks from a place called Nine Mile, a Civilian Conservation Corps camp in the mountains northwest of Missoula. These two weren’t looking for abattoir fever. Gordon Davis, the first on the hunt, had brought the ticks into his lab for research on the ecology of two other diseases, Rocky Mountain spotted fever and tularemia. Setting the ticks onto guinea pigs, he watched one guinea pig become sick with something he couldn’t identify. For a while it was simply “the Nine Mile agent.” Herald Cox, joining the laboratory a year later, helped Davis isolate it and recognize that it was probably a rickettsia. Then another man entered the fray, an infectious disease expert who was also a powerful administrator at the National Institutes of Health, with supervisory responsibility for Cox, Davis, and their colleagues at the Rocky Mountain Laboratory. His name was Dr. Rolla Dyer. Dr. Dyer seems to have been a bit of a bullhead, but not irredeemably so. Strongly skeptical of Cox’s claim to have found that the Nine Mile agent was a rickettsia, he stormed out to Montana and into Cox’s lab. Cox showed him evidence on a microscope slide. Dyer reversed himself, acknowledged the discovery, and stayed around in Hamilton just long enough, assisting Cox with the work, to catch a dose of Q fever himself. Ten days after returning to Washington, he felt “sharp pains in the eyeballs,” followed by chills, followed by fever and night sweats for a week. Maybe there’s some justice to zoonotic diseases after all. But probably not, just a high degree of infectiousness in Q fever, because by that time Macfarlane Burnet had caught it too. Both he and Rolla Dyer recovered.

  As for Herald Cox, he was further vindicated when, in 1948, the pathogen was recognized as different enough from all other Rickettsia to deserve its own genus and was renamed Coxiella burnetii, honoring him as well as Macfarlane Burnet. That name remains today.

  “There is no disease to match Q fever for queer stories,” wrote Burnet, in the little memoir he published in 1967. First, he claimed, it was “a record-breaker” for producing laboratory infections, such as his own, Dyer’s, and similar illnesses in two secretaries at the Hall Institute. (He may have wrongly ignored the laboratory-infection claims of psittacosis.) Second, he noted the high incidence of what had been called “Balkan grippe” during the Great War, especially among German troops in Greece and New Zealande
rs in Italy. Furthermore, a shipload of American soldiers had been assembled “for a night or two near Bari in southern Italy, prior to embarkation,” more than half of whom took sick by the time their boat reached home. “Sooner or later, all these episodes were established as Q fever.” After the war, research showed “the extraordinary versatility of C. burnetii as a parasite,” infecting dairy cows in California, sheep in Greece, rodents in North Africa, and bandicoots back home in Queensland. It passed from one species to another in the form of minuscule airborne particles, often dispersed from the placenta or the dried milk of an infected female animal, inhaled, and then activated through the lungs, or taken directly into the bloodstream from the bite of a tick. As he said, it was versatile.

  “One of the more bizarre episodes concerns an English class of art students,” Burnet recounted with some enthusiasm. “Around 1950, a collection of casts from classic statuary was ordered from Italy. The crates arrived with the casts packed in straw, and everyone in the class lent a hand in unpacking. Most of them got Q fever, but no one knows how the straw was contaminated.” All of this, Burnet wrote, “was the beginning of an ever-widening recognition of Q fever across the world.” He was right. Though Coxiella burnetii is now known as a bacterium, not an anomalous form halfway between bacteria and viruses, its impact on human health didn’t disappear with the development and mass production of antibiotics during the 1940s. As recently as 2007, Q fever caused serious trouble in a modern European country, far removed from both Queensland and Montana: the Netherlands.

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  Fifty miles southeast of Utrecht, amid the flat landscape and tangled roadways of the Dutch province of Noord-Brabant, lies a little back-road village called Herpen. It’s a tidy place, largely assembled from red brick: redbrick farmhouses on the outskirts, redbrick cottages in town, cobbled sidewalks, and a handsome old redbrick church. The farmhouses, some shielded behind pruned hedges and prim gardens, command fields of hay and corn, grown for fodder to feed livestock that shelter in large, low, redbrick barns. Although it looks like a farm village, Herpen nowadays is a bedroom community for laborers and contractors in the building business. A few workhorses stand idle in pastures, kept company by a modest number of cows, sheep, and pigs. But the agricultural component of the local economy, insofar as it still exists, is committed more heavily to dairy goats. They seem to have been the source of the problem in 2007.