The Pandemic Century

by The Pandemic Century- One Hundred Years of Panic, Hysteria

  All told, between January 25 and March 15, eleven people at the Hygienic were hospitalized with psittacosis. Despite drawing a floor plan of the infections, McCoy could discern no pattern in the cases, leading him to speculate that psittacosis may have been transferred to the upper floors by mice or cockroaches. The other possibility, of course, was that the organism had been aerosolized and the building was full of infectious fomites. Either way, drastic action was needed. So it was that on March 15 McCoy ordered everyone to evacuate the building and shut the laboratory. Experimental animals not involved in psittacosis research were removed to temporary lodgings. Then McCoy entered the basement for the last time and exterminated all those that remained—a menagerie of parrots, guinea pigs, mice, rats, pigeons, and monkeys. Next, he burned their bodies in the incinerator and scrubbed their cages with creosol, and methodically worked his way through the building to seal the windows on each floor. Finally, when he was sure there was no living thing left inside the Hygienic, he ordered a fumigation squad to blitz the building with cyanide. The legend goes that so much gas was used that sparrows flying fifty feet above the Hygienic stopped in mid-flight and plummeted to Earth. The next day, the headline in the Sunday edition of the Washington Post read, “Parrot Fever Panic Seizes Laboratory.”

  McCoy was not the only one panicking. By now, Roscoe Spencer was rushing up and down the East Coast in search of serum. The flasks of blood he brought back to Washington were used to treat the Hygienic personnel, and by April all the building’s staff had recovered, Armstrong included. Others were not so fortunate, however. Stokes got two transfusions of Roscoe’s serum but died on February 9, the day after Anderson. For those stricken with psittacosis there was good reason to be afraid. The infection often proved fatal, with thirty-three deaths recorded in the United States between November 1929 and May 1930. Of the 167 cases where the sex of the victim was known, 105, or two-thirds, had been women. Another badly affected country was Germany, with 215 cases and 45 deaths. Indeed, at one point Berlin Zoo had been forced to bar its gates to frightened parrot owners desperately looking for a temporary refuge for their birds. In all, some fifteen countries were affected. By the time the pandemic ended in May 1930, eight hundred cases had been recorded worldwide, with an average mortality rate of 15 percent.

  Armstrong and McCoy were not the only researchers puzzled by the sudden appearance of psittacosis and the failure to find Nocard’s bacillus. Soon, researchers in other countries were also convinced the pathogen must be a filter passer and that Nocard had mistaken it for salmonella, the bacterium that causes typhoid. The first to succeed was a team led by Samuel Bedson, a senior researcher at the London Hospital. Taking parrots associated with human cases, Bedson and his colleagues emulsified the dead birds’ liver and spleen, passed the material through a Chamberland filter, and then inoculated budgerigars with the filtrate. The budgerigars died within five days. Next, Bedson’s group showed that by passaging filtered material from diseased budgerigars every few days, the organism gradually lost its virulence. Bedson’s conclusion was unequivocal: “the aetiological agent of psittacosis in parrots is a virus which cannot be cultivated on ordinary bacteriological media, and which is capable of passing through some of the more porous filters.”

  Soon after, Charles Krumwiede, a researcher at the New York Board of Health, demonstrated that the virus could be readily transferred from parakeets to white mice. This greatly facilitated laboratory study of psittacosis as white mice were far less infectious than birds. Nevertheless, Krumwiede was forced to suspend his studies when he fell ill, resulting in his research being taken up by Thomas Rivers. Aware that psittacosis was highly infectious, the Rockefeller researcher left nothing to chance, insisting that his team wear full body suits, with glass goggles in the helmets and rubber gloves attached to the sleeves—precautions that foreshadowed measures that would become standard in Biosafety Level Four laboratories used to study Ebola and other hazardous pathogens sixty years later. Rivers also demonstrated that psittacosis could be transferred to rabbits, guinea pigs, and monkeys. However, in monkeys the infectious material only produced typical pneumonia if introduced via the trachea. To Rivers, this suggested that the principal transmission route in humans was via the respiratory tract, not through scratches or parrot bites—a view soon adopted by other researchers.

  Although psittacosis was beyond the magnification range of optical microscopes at that time, by now Walter Levinthal of the Robert Koch Institute in Dahlem, Germany, A. C. Coles of the Lister Institute in London, and Ralph Lillie at the Hygienic Laboratory, were reporting distinctive clusters of inclusion bodies in the cytoplasm of patients who had died of psittacosis. Dubbed “Levinthal-Coles-Lillie” or “LCL” bodies, these could be observed through an ordinary optical microscope, where they appeared as microcolonies on the surface of the cell, making the diagnosis of psittacosis and the development of agglutination tests far easier. The only point that remained uncertain was the exact mode of transmission. Handling an ill or dead bird was certainly a risk, but there were also plenty of cases in which patients had merely been in the same room or house as a sick parrot. There were even cases in which people had contracted psittacosis after visiting a pet shop or, in the case of baggage handlers, sharing a railway carriage with a sick bird. This was not a message that pet shop owners or bird breeders wished to hear. On the contrary, many refused to accept that the reports of pneumonia and typhoid-like illness were due to parrots or parakeets at all, much less that psittacosis could be spread via the atmosphere from bird to man. Otherwise, they claimed, breeders and people who worked in pet shops would be ill all the time, but according to dealers the opposite was the case. “So far as it is aware,” declared the newly formed Bird Dealers Association of America at a meeting held in New York’s Commodore Hotel at the height of the pandemic, “no bird dealers whose hourly contact with feathered pets would render them likely to contract psittacosis if it is communicable to humans, have been affected.” Nor could reports of pet owners catching psittacosis directly from imported birds be believed as “any one putting his face near enough a newly imported parrot to catch a disease would sure to be bitten by the untrained bird.” In short, the parrot fever “scare” was down to “the active imagination of a Baltimore newspaper man.”

  One can hardly blame bird dealers for wanting to fight back. America’s six leading pet dealers, all of which were based in either New York or Philadelphia, stood to lose $5 million annually from Hoover’s import ban. And, in many ways, they were right, for as the panic over imported parrots subsided, foreign birds no longer constituted the principal threat. Instead, it was home-reared birds—parrots and parakeets raised in backyard aviaries—that posed the biggest risk to pet owners, particularly in Southern California where conditions were perfect for breeding birds outdoors year-round. This time it would not be a newspaperman who would spot the danger, however, but a Swiss-trained veterinary pathologist whose laboratory sat near the summit of a chilly, fog-shrouded hill overlooking the Golden Gate Bridge.

  IN THE SUMMER OF 1930, while researchers on the East Coast were developing tools for visualizing psittacosis and refining agglutination tests, Karl Friedrich Meyer was focused on a mysterious “sleeping sickness” affecting horses in southern California and other western states. Educated in Basel and Zurich, Meyer’s interest in animal diseases bridged by multiple insect and arthropod vectors was born in 1909 in South Africa, when, as an assistant at Arnold Theiler’s (the father of the Nobel Prize winner Max Theiler) Veterinary Bacteriological Institute in Pretoria, he became the first person to elucidate the life cycle of the plasmodium of East Coast Fever, a tick-borne disease of cattle. Soon after, Meyer contracted malaria and was forced to return to Europe, but he did not stay long. By 1911 he had secured a teaching position at the University of Pennsylvania’s veterinary school. There, Meyer became acquainted with the leading lights in American pathology and bacteriology, including Theobald Smith, whose groundbreaking study of Texas
Cattle Fever was to provoke a rethinking of germ theory and the role of parasitical infections generally, and Frederick Novy, the director of the University of Michigan’s Hygiene Laboratory, who had headed the official inquiry into the 1901 bubonic plague outbreak in San Francisco. Through Smith, Meyer was also introduced to Simon Flexner, the director of the Rockefeller Institute. But rather than take a job in New York, Meyer decided to head west, lured by the offer of an assistant professorship at Berkeley and the prospect of a research position at the newly formed George Williams Hooper Foundation for Medical Research in San Francisco.

  Housed in a three-story brick building in the former veterinary school on Mount Sutro in Parnassus Heights, the Hooper Foundation had been established by Hooper’s widow in 1913 with a generous $1 million bequest and was the first private medical research institution to be attached to any American university. Although Flexner warned Meyer that in joining the Hooper, he risked “disappear[ing] in the Pacific Ocean, because the intelligentsia of the United States lives within a hundred miles from New York,” the Hooper offered Meyer a degree of intellectual freedom that would have been impossible in the East. Besides, as Meyer acknowledged, he was a “typical Basel squarehead” with a stubborn streak as wide as the Rhine. In his interactions with colleagues and other scientists, this stubbornness could come across as arrogance—an impression not helped by Meyer’s Teutonic bearing, thick German-accented English, and intolerance of errors, particularly ones that occurred in his laboratory. However, when it came to tracking and identifying the source of new diseases there was, apparently, no more indefatigable opponent of microbes. Indeed, in a special tribute published in Reader’s Digest in 1950, de Kruif hailed Meyer, then in his 60s, as “the most versatile microbe hunter since Pasteur.” In a career spanning three decades, Meyer had helped eradicate brucellosis from Californian dairy herds; had demonstrated that botulism, a deadly food-borne pathogen, was a highly resistant spore found in soils across America; and had shown how sylvatic plague was endemic to ground squirrels and other wild rodent populations across the western United States. In short, declared de Kruif, Meyer was “an outdoor scientist living in a state of permanent outdoor emergency . . . [and a] master among the world’s microbe hunters.”

  History does not record whether Meyer was pleased or embarrassed by de Kruif’s gushing tribute—interviewed in the 1960s, Meyer said that his former wife suspected de Kruif of trying to “belittle” and “besmear” him. However, although de Kruif was an alcoholic and had a turbulent personality, he and Meyer maintained a friendship for more than three decades, and twice a year de Kruif would make a point of visiting Meyer in San Francisco, where the pair enjoyed solitary moments hiking together on Mount Tamalpais, discussing the latest medical breakthroughs, and exchanging gossip about their bacteriological colleagues.

  A member of the Sierra Club, Meyer traced his fascination with infectious disease to his boyhood excursions in the Swiss Alps, where he fell into conversation with British climbers recently returned from the plague spots of India; de Kruif was right to link his passion for microbe hunting with his enthusiasm for adventure and outdoor living. So it is little wonder that when reports reached the Hooper of a massive horse epizootic in the San Joaquin Valley, Meyer raced from his laboratory to investigate. There, he found horses wandering aimlessly in circles or listing from side to side. Meyer’s veterinary colleagues thought the horses’ staggering symptoms were the result of “forage poisoning” due to botulism. However, the San Joaquin epizootic had broken out in June—the wrong time of year for botulism—and vets who visited affected ranches noted that the majority of the victims of “staggers,” as the disease was known, were free-ranging horses, not those that had been fed on silage or stacked hay. At autopsy Meyer noted that the horses’ brains were inflamed and scarred by microscopic hemorrhages, leading him to suspect that the neurological impairment was caused by a virus. Unfortunately, by the time he came to examine the horses, the virus had disappeared. What Meyer needed was to autopsy the brain of a recently infected horse. His opportunity came later that summer when one of his colleagues located a sick horse on a ranch in Merced. The rancher wanted nothing to do with Meyer’s experiment, so Meyer bribed his wife with $20 and, when she signaled that her husband was asleep, snuck into the stable and decapitated the horse in the middle of the night, hot-tailing it back to San Francisco with its severed head sticking out of the trunk of his car. That very same morning, Meyer extracted the horse’s brain, mashed it up, and injected the material into guinea pigs. Soon the guinea pigs’ bodies were racked with tremors. Next, they curled up into balls or hunched up like cats, dying four to six days later. After repeating the experiment in rabbits, monkeys, and horses with the same results, Meyer and his colleagues announced that they had isolated a new filter-passing virus. It would be several years before researchers would confirm that, as Meyer had suspected, the virus was a type of encephalitis communicated to horses by mosquitoes breeding in nearby irrigation ditches, and would be able to divine its arboreal life cycle.

  Though preoccupied by equine encephalitis, Meyer had followed the parrot fever outbreaks, and Armstrong and McCoy’s efforts to passage the virus. However, it was not until the following year that he had reason to initiate his own studies and became interested in the involvement of bird breeders. The impetus came when three elderly women, who had attended a coffee club in Grass Valley in the Sierra Nevadas shortly before Thanksgiving in 1931, died. Local physicians were baffled as to the cause, attributing the women’s deaths to, variously, typhoid fever, dysentery, and “toxic pneumonia.” However, on reviewing the medical reports and learning that the husband of the woman who had convened the gathering was also ill, Meyer realized that the common denominator was the room where they had gathered. He instructed the local health officer to see if there was a sick or dead parrot there. Meyer’s intuition was partially correct: there was no parrot, but on going to the woman’s home in Grass Valley the health officer discovered a healthy shell parakeet still in its cage, and another one which had recently died. Meyer immediately ordered the official to disinter the parakeet and send its carcass to the Hooper, together with its live mate. That same evening, at around 10 p.m., Meyer’s was astonished to see a driver in a face mask pull up outside his laboratory. It was the official, and on the back seat was the surviving parakeet chirping in its cage. “He was scared out of his wits that he might pick it up,” Meyer recalled, “because it was generally known that because it was air-borne this was a highly contagious disease.”

  To verify his hunch that the bird was infected, Meyer began with a simple exposure test, taking a healthy Japanese ricebird (finch), which he had read was highly susceptible to psittacosis, and placing it in a bell jar with the parakeet. Within two to three weeks the ricebird was dead. The parakeet, meanwhile, appeared “perfectly normal” and continued to shed sufficient virus such that if it was transferred again to a clean bell jar with another ricebird, that bird also became ill and died. When Meyer finally sacrificed the parakeet on January 16, 1932, and inoculated the bird’s mashed-up spleen into mice in his laboratory, the mice died within three to four days, suggesting that the “agent was exceedingly virile.” To be sure, Meyer repeated the experiment, removing the parakeet from the glass jar every time a finch died and transferring it to a new jar with another finch. After six months, Meyer had his proof: it was the desiccated droppings from the parakeet that were spreading the infection.

  In the meantime, in January, the woman’s husband had also died. Concerned that there might be a statewide problem, Meyer had pressed the health department to issue a press release. The resulting publicity brought further reports of suspicious deaths involving parakeets from as far south as Tehachapi. Questioning itinerant peddlers who made a living selling parakeets door-to-door, Meyer and his assistant Bernice Eddie discovered that most of the birds had come from backyard aviaries in the Los Angeles area. Many of these breeding establishments belonged to war veterans and had b
een funded by the bonuses they had received under Depression relief. It was a low-tech and highly profitable business as the birds bred astonishingly fast. All an amateur breeder needed was lumber, wire netting, and a breeding box. Within weeks the pens were full of young hatchlings or “crawlers.” These young birds were very popular with pet owners; they could be trained to sit on their fingers and pick seeds. Rather than allow the nestlings to mature, amateur breeders had quickly sold them on to the trade. Indeed, over the Thanksgiving period and in the run-up to Christmas, Meyer discovered peddlers had crisscrossed the state offering lovebirds as gifts for housewives and widows.

  Meyer put out a call to pet shops throughout California requesting that they send him other birds that were visibly sick or were associated with a householder who had recently been hospitalized with psittacosis. Soon, birds were arriving at the Hooper Foundation from as far north as Santa Rosa and as far south as San Luis Obispo. At first glance, the parakeets appeared perfectly healthy, but when Meyer examined their spleens he discovered their organs were swollen and scarred with lesions characteristic of psittacosis. The final proof came when he inoculated mice with the mashed-up bird spleens and the rodents fell ill. The more Meyer and Eddie quizzed peddlers and pet shop owners, the greater became their fear that birds all over California might be harboring these asymptomatic, latent infections. From Pasadena, they obtained twenty-two birds, only to find that nine had enlarged livers and spleens. In some of the breeding pens, Meyer reported, the birds were visibly diseased and “so weak that they were actually crawling on the floor.”