The Pandemic Century

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

  Concerned that as many as 40 percent of birds raised in backyard aviaries and professional breeding pens might be carriers of psittacosis, Meyer warned that California could be harboring a huge reservoir of infection. He urged health officials to take action. In particular, he worried that when Californian parakeets were packed into crowded containers and shipped across state lines, the stress caused them to shed the virus, running the risk that they would reignite the epidemic. In other words, Argentine parrots were no longer the main danger: it was Californian birds that now posed the principal threat.

  The State Department of Health had previously been blissfully unaware of the extent of California’s bird breeding industry and the implications for public health. Now, it declared it was imposing a quarantine and placed an embargo on the transportation of lovebirds across state lines. The measure sparked uproar among California’s breeders, particularly as Hoover’s embargo on imported parrots the previous year had led to pent-up demand for parakeets, and pet stores in the East were increasingly looking to California to supply the market. Estimates as to the value of this market varied: breeders put it at $5 million; Meyer thought it was worth one-tenth of that. What was not in doubt was that Southern California’s temperate year-round Mediterranean climate provided the ideal conditions for bird breeding and that upwards of 3,000 individuals now depended on the trade. What was needed was a system of inspecting pens and checking the condition of birds. However, it was a completely unregulated industry, and no one seemed willing to assume responsibility. Meyer scented an opportunity. When the botulism scare had hit the sales of Californian sardines and other canned foods in the 1920s, the canners had hired Meyer to advise on heat sterilization, establishing safety procedures that soon became standard across America. Now, he proposed a similar technological solution for Californian bird breeders.

  His opening came in March 1932 when 125 leading breeders were summoned to a meeting at the Associated Realty Building in Los Angeles. Opening the proceedings, Dr. Giles Porter, the director of the State Department of Public Health with whom Meyer had previously collaborated during the pneumonic plague outbreak in Los Angeles, introduced Meyer as a world authority on psittacosis and someone who could “prove to you, that this is not just a ‘scare’ but . . . a really serious matter.” Meyer began with a review of medical knowledge of psittacosis prior to 1930, then presented the evidence obtained during the pandemic that psittacosis was a filterable virus. “Probably there is a lot of ‘hokus-pokus’ talk about psittacosis that is not true,” he told breeders, but there was no doubt that it was a “highly contagious infection” that could be spread aerially from bird to man via droppings or mucal discharges. This had been proven by the “sad experience” at the Hygienic Laboratory, where nine people had contracted psittacosis merely after passing along a corridor close to cages containing desiccated material. “Probably the wind blew the dust from these cages through a crack in the door and in this way the contact was made,” he said. Next, he briefly detailed his own investigations in San Francisco. Then, pointing to a chart, he directly addressed the problem of infections in bird breeding establishments.

  Let us say, for the sake of argument, we have one hundred birds. In this group of one hundred birds, the disease, parrot fever, breaks out. Probably—let us say—ten of the birds will die. Now these ten birds should have been examined. Unfortunately, nothing of this sort is usually done, but so far, we examine these birds and find ten have the parrot fever. There are ninety birds left. You would probably assume that these ninety birds . . . are practically safe. My answer is NO! NO!

  The difficulty was that every pen contained a certain percentage of “carriers”; that is, birds whose spleens showed evidence of prior infection but who did not appear sick or visibly diseased. These healthy-looking birds might harbor the virus for six months or longer without infecting other birds in the same pen. However, if such birds were exposed to cold or sudden climatic changes, then these infections could “become activated,” and the birds might “secrete the virus,” infecting other birds with whom they were confined. In particular, Meyer speculated, there was a good chance they would pass the virus to young birds or “runts.” Nor was that the end of the danger. “Convalescent birds,” that is birds recovering from infection, might also secrete the virus for between four to six weeks. In all probability, the only birds that were safe were those with inherited immunity, or older birds that had acquired immunity during previous outbreaks or through exposure to the virus in the nest.

  The only way to know for sure whether a flock was infected or not was for breeders to turn over 10 to 20 percent of their stock so that Meyer could examine them for latent infections. In this way, Meyer would be able to give those aviaries that were free of disease a clean bill of health, and there would be no need for further embargos or quarantines. However, Meyer warned, autopsying the birds was dangerous and expensive work, and, in return, he would expect breeders to pay him for his services. $10,000 should be sufficient.

  This is a disease which has caused in every laboratory they work with cases of psittacosis; and we have to almost put our foot in the grave, so to speak, in order to solve the problem. I took this responsibility to work with you. I therefore solicit from you your earnest cooperation—or, I give it up. It is not my business to die for a disease like psittacosis.

  Not surprisingly, the breeders balked at Meyer’s offer, feeling his price was too steep. Instead, they tried to convince health officials that such tests were unnecessary and that once birds reached the age of four months they no longer presented a health risk. Next, they proposed that officials introduce a permit system. Porter refused to budge, but the breeders lobbied the governor, who relented and lifted the embargo. As the trade resumed in the summer of 1931 and parakeets were sent from California to markets in the East, Meyer feared a revival of the pandemic. Once the parakeets reached dealers in New York, there was no telling how many flocks might be infected or in which state or country a psittacosis carrier might turn up next. By the end of the year, Californian lovebirds had been scattered to every state in the union. They proved particularly popular at country fairs in Wisconsin and Minnesota, where they were raffled as prizes. Then, on September 22, 1932, came the news that Mrs. William E. Borah, the wife of the senator from Idaho, was seriously ill at her home in Boise, Idaho. On investigation, her physician discovered she was a collector of parakeets and had recently acquired a set of lovebirds from California. Suspecting parrot fever, her husband, the senator, wired Washington to send serum immediately. Thus began another extraordinary chapter in the history of the Hygienic.

  TWO MONTHS AFTER McCoy’s fumigation of the north building, Congress had passed an act changing the laboratory’s name to the National Institute of Health (NIH) and establishing fellowships for research into basic biological and medical problems. The Randsell Act, named after Senator E. Randsell, a Democrat from Louisiana, was seen as a reward for the PHS’s investigations of psittacosis and the heroism of its research staff, and marked a sea change in American attitudes to the public funding of medical research.§ Unfortunately, when Senator Borah’s request arrived on McCoy’s desk, the NIH’s stores of serum had been exhausted. It was at this point that Armstrong volunteered his services. Having made a full recovery, it was likely his blood still contained antibodies. Why not make use of it? Armstrong’s personal physician performed the phlebotomy, then stayed up all night separating out the serum. Because of the urgency, there was no time to check that it was sterile. Instead, the serum was dispatched directly to a waiting plane. The story of the mercy flight was a media sensation, with the Associated Press and national and local newspapers publishing hourly logs of the serum’s progress from Washington to Boise, Idaho. By now Mrs. Borah was close to death and her doctors were doubtful the serum would make a difference. But they decided it was worth a try and administered all twelve ounces (350 ml) in a single transfusion. Five days later she was on the road to recovery and by the following Fe
bruary she was fit enough to travel to Washington. Her first stop was the NIH. “I came to thank you for saving my life,” she told Armstrong. “I have some of your blood flowing through my veins.”

  If Mrs. Borah’s recovery was good news for the NIH, it was bad news for Californian bird breeders, as no sooner had his wife recovered than Senator Borah urged President Hoover to reinstate the embargo, but this time on Californian rather than Argentine birds. Hoover forwarded the request to PHS, prompting Cumming to issue an order banning the interstate transport of Californian parakeets. However, he indicated that if California could find a procedure for demonstrating that its birds were free of psittacosis then he might make an exception. The previous March, breeders had done everything they could to avoid submitting their birds to testing. Now, as the embargo bit, denying them access to lucrative markets in the East, they came around to Meyer’s proposition.

  By 1933 Meyer and Eddie had inspected sixty-six aviaries containing nearly 2,000 lovebirds. In these aviaries, they found that anywhere from 10 to 90 percent of birds classed as healthy by their owners might be carrying latent psittacosis. However, they observed that while many of these infections were of an “eminently chronic character,” they did not spread to parakeets in adjacent pens. Contrary to breeders’ claims that they never fell ill, Meyer and Eddie discovered many had antibodies to psittacosis, suggesting they had been previously exposed and had suffered mild infections which had been misdiagnosed. The principal risk came from handling dead birds or direct contact with their nasal discharges and excreta, or from bite wounds. However, on occasion, psittacosis could be contracted simply by inhaling desiccated droppings. Indeed, Meyer found that such droppings were highly efficient aerosols and could be scattered over a wide area simply by the flapping of a bird’s wings when it became agitated. In such circumstances, the environment is “charged with virus and becomes a menace to human beings who inhale it.” For this reason, they warned, psittacosis presented a particular threat to bird breeders and pet store owners, or those with close attachments to lovebirds.

  They also found that the LCL bodies of psittacosis could be readily observed on a microscopic slide simply by taking a smear from the spleens of diseased birds and adding an appropriate stain. In other cases, the size of the spleen provided a rough-and-ready approximation of the degree of a latent infection in a pen. In particular, medium-sized spleens measuring three to five millimeters were more likely to produce “a typical, acutely fatal, or latent” illness in inoculated mice than spleens measuring seven to ten millimeters. Meyer and Eddie also found proportionately more enlarged spleens (six millimeters or greater) in young, immature birds than in the older capped birds, suggesting that parakeets typically contracted psittacosis early in their development and that enlarged but noninfective spleens in the older caged birds was evidence of an old sterilizing infection. Their conclusion was unequivocal: “In general, ‘noncapped’ immature birds are more frequently carriers of the virus than the ‘capped’ old birds.” The implications were clear: birds needed to be observed until they were at least four months old to be sure that they had cleared the infection and no longer presented a danger of transmitting the mycobacterium.

  By 1934 Meyer and Eddie had tested nearly 30,000 parakeets and certified 185 Californian aviaries as psittacosis-free. The program was a valuable source of income for the Hooper Foundation, and soon Meyer was using the funds to investigate other scientific questions. Meyer was not only a bacteriologist and veterinary pathologist, he also considered himself a biologist and nascent ecologist. Though trained in the German tradition, by the 1930s he was growing disenchanted with bacteriology’s narrow focus on microbes. Instead, as he considered the phenomenon of latent infections, he found himself drawn to the language of “hosts” and “parasites” and wider evolutionary questions about the relationship between virulence and immunity to disease. In particular, he wished to discover whether wild parakeets showed the same susceptibility to psittacosis as birds bred in captivity. To find out, Meyer paid a barber on a Pacific liner to bring him two hundred wild shell parakeets from the Australian bush. As psittacosis had never been reported in Australian parakeets before, Meyer assumed that these birds would possess a high susceptibility to the virus and lend themselves to comparative exposure and immunity tests. Imagine his astonishment, then, when within four weeks of his quarantining the Australian parakeets, one of them died. On examination he found its spleen riddled with the same lesions as those in the Californian birds. Perhaps the most significant finding, however, came when Meyer allowed the Australian birds to mingle freely with Californian parakeets, half of whom he knew to be latently infected: none of the Australian parakeets died of the disease, and when he sacrificed the birds and performed autopsies, Meyer was unable to recover virus from the birds’ spleens.

  In an example of Meyer’s use of international scientific networks, he immediately shared his findings with the Australian virus researcher Frank Macfarlane Burnet, prompting Burnet to launch a parallel study in which he found that psittacosis was an endemic infection of wild Australian parakeets and had probably been “enzootic amongst Australian parrots for centuries.” Burnet hypothesized that it was most likely Australian parrots and parakeets from Japanese dealers, not Argentine parrots, that had been the source of the outbreaks of psittacosis in California in 1931. In a letter to Meyer, Burnet explained that in the wild, young birds were typically infected in the nest, but these natural, mild infections could also flare up under the stress of close confinement, resulting in the birds’ losing their acquired resistance and shedding the virus. By questioning importers, Meyer established it was common practice for shippers to mix wild unbanded birds with clean birds, greatly facilitating the spread of the virus. He concluded that in the wild, these virus strains were highly adapted to their avian hosts, but conditions in shipping containers and Californian aviaries had greatly increased the virulence of psittacosis and, as he put it, “shifted the balance in favor of the virus”—hence the spillovers of enzootic psittacosis infections seen in Californian birds and people in the early 1930s.

  TODAY, PSITTACOSIS no longer presents a pressing health threat and parrot fever has once again disappeared from public view. The disease’s retreat from popular consciousness is due in large part to Meyer. Following the discovery of Aureomycin in 1948, Meyer approached the Hartz Mountain Distribution Company, then the largest supplier of milled bird seed in the United States, to develop a line of medicated millet. By the middle 1950s another easy-to-administer antibiotic, oral tetracycline, had also become available and chlortetracycline-impregnated seed had become standard in the bird breeding industry. To be sure, there were still occasional outbreaks, but these tended to occur on turkey farms or in poultry processing plants, where exposure to psittacosis was, and still is, an occupational hazard. In most cases, all it took was a properly administered course of tetracycline to clear human infections and return a flock to health.

  Unfortunately, today, as in the 1930s, some breeders refuse to believe their aviaries are latently infected. Instead, they dilute the seed or fail to administer a full course of antibiotics, resulting in the persistence of subclinical infections of psittacosis in domestic bird flocks. Should these birds be shipped to a pet store and mingle with imported birds emerging from quarantine, there is a risk they will communicate the organism and spark fresh outbreaks of parrot fever. Indeed, the principal lesson of the 1930 pandemic is that imported birds were merely the fall guys. The main culprits were domestic lovebirds bred in Californian aviaries. Once this was realized, parrots and parakeets ceased to be a source of fear and hysteria, and the control of psittacosis became a largely veterinary problem. However, without the simultaneous worldwide outbreaks sparked by Argentinian parrots and the press coverage that accompanied it, it is unlikely that anyone would have noticed the unusual pattern of pneumonia deaths, and Nocard’s error that psittacosis was due to a type of salmonella would have taken longer to dispel.

 
There was another lesson, too, one that would become increasingly apposite in the second half of the twentieth century as other little-known or neglected pathogens emerged to spark new epidemic scares. And that is that in nature parrots and parakeets pose little threat to human populations. Sure, there might be occasional mass die-offs deep in the Amazonian rain forest or the Australian bush, but, in Burnet’s words, psittacosis was “not intrinsically a very infectious disease.” On the contrary, he argued, the parasite’s primary function was to return wild bird populations that had grown too large or too dense for their ecological niches to a state of equilibrium. The problem was that when man disrupted these biological and ecological processes by packing parakeets into overcrowded crates, he created the ideal conditions for the propagation of the virus and its transfer from bird to man. “It is reasonably certain that cockatoos, left to a natural life in the wild, would never have shown any symptoms of their infection,” Burnet observed, following an outbreak in Melbourne in 1935. “In captivity, crowded, filthy and without exercise or sunlight, a flare-up of any latent infection was only to be expected.”

  Indeed, by the 1940s Burnet was worrying that these spillover events were becoming more common and that overpopulation, coupled with international trade and jet travel, was disrupting natural ecologies in new and unpredictable ways, leading to virulent outbreaks of vector-borne diseases such as yellow fever. While a world in which everyone and everything was more closely linked in a biological sense should favor a “virtual equilibrium” between humans and microbial parasites, Burnet warned that “man . . . lives in an environment constantly being changed by his own activities, and few of his diseases have attained such equilibrium.”