by The Pandemic Century- One Hundred Years of Panic, Hysteria
In Los Angeles, by contrast, no plague-carrying rats had been found in the immediate vicinity of the harbor. However, by the end of December thirty-five had been retrieved from ranches within a mile of the port, and nearly twice as many again from other areas within a forty-mile circumference of San Pedro. In addition, survey squads had established that 64 percent of rats in the Los Angeles area were colonized by squirrel fleas and, although hunting parties had failed to turn up any infected squirrels in or around the city, eight squirrels retrieved from a ranch in San Luis Obispo that had been the focus of previous plague epizootics also tested positive for Y. pestis. At the same time, ranchers reported having observed epizootics of squirrel plague in San Benito and Monterey Counties the previous summer, suggesting that, as Meyer put it, 1924 had “truly [been] a sylvatic plague year in California.” However, it was the reports from Europe of a new outbreak of rat plague at several Mediterranean ports that persuaded Cumming the PHS was facing a worldwide recrudescence of the disease and prompted him to finally institute quarantines at San Pedro and other “plague-infected” American ports.
Cumming’s decision prompted a subtle but significant shift in the medical language. It was no longer the threat of domestic American squirrels transmitting the pneumonic form of the disease that was to be feared, so much as foreign introductions by “bubonic rats.” That hysterical conjunction was sufficient to panic Congress into voting an emergency appropriation of $275,000 to support the PHS’s renewed campaign against its old enemy. At first, Los Angeles’s chamber of commerce protested the decision, accusing Cumming of “discriminatory” action since no plague rats had been found at San Pedro. In any case, it argued, while the harbor was the Fed’s fiefdom, the port was the jurisdiction of the state and the city health department. For a while Cryer tried to argue the case for his new appointee, city health officer George Parrish. However, when Cryer got his wish and the city council authorized Parrish to take over the eradication campaign from Dickie, it also slashed his budget, forcing Cryer to swallow his pride and go cap in hand to President Calvin Coolidge to request that the PHS be allowed to assume responsibility for the plague cleanup work. As far as Cumming was concerned, there was only one man for the job, his predecessor Rupert Blue, who was promptly recommissioned into the Service and dispatched to Los Angeles. For Blue it was an opportunity to finish the work he had begun in 1908, and by July he was once again in his element, probing Los Angeles’s downtown rat runs, overseeing the concreting over of basements and taking other abatement measures. “Nine suspicious rats and five ground squirrels have been found since June thirteen in widely separated sections, extending from Hollywood north to West Washington Street south,” he wired Cumming on June 26. “Should these prove positive for plague we may expect several human cases to occur at any time. Seasonal conditions highly favorable for a return of the epidemic.”
It is hard to say who deserves most credit for the eventual eradication of plague in Los Angeles, Blue or Dickie. The last reported case of pneumonic plague occurred on January 12, 1925, and, despite Blue’s ominous telegram, the last plague-infected rat was recovered from eastern Los Angeles on May 21, in other words two months before Blue took charge. And while Dickie may have been guilty of colluding in the press cover-up, he never doubted that the outbreak was serious. Moreover, his prompt action in quarantining Macy District and directing the plague cleanup efforts, however harsh and unfair the measures must have seemed to the area’s Mexican residents, ensured that pneumonic plague did not spread to other parts of the city. Indeed, it could be argued that the Board’s response might have been even more effective had the city health department alerted Dickie to the outbreak sooner, rather than waiting for him to learn about it from a newspaper. As Dickie observed in his official report on the outbreak, physicians and bacteriologists at County General were also culpable in failing to recognize the symptoms of plague in Jesus Lajun.§ Though official figures probably did not reflect the full extent of the outbreak, in total there had been just forty-one cases of pneumonic plague and thirty-seven fatalities. In addition, there had been seven cases and five deaths from bubonic plague and a single fatal case of septicemic plague. Most important of all, perhaps, it was the last recorded outbreak of pneumonic plague anywhere in North America.
THE LOS ANGELES OUTBREAK upset the assumptions of Kellogg and other plague experts, challenging the wisdom that California’s mild, year-round Mediterranean climate was a protection. Instead, it demonstrated that conditions of low humidity and warm weather made little difference to the transmission of the pneumonic form of the disease and that in Southern California the pathogen could assume as deadly a form as plagues during earlier historical periods. Indeed, the crucial factor was not the weather but the close proximity of the sick to the healthy. In the overcrowded conditions of the Mexican quarter the bacillus had found the ideal conditions for spread via respiratory droplets. Plague’s explosive potential had been further amplified by burial rituals—in particular, the Catholic custom of holding open wakes—which brought mourners into close contact with infectious cadavers and those who might be incubating the infection. The Los Angeles outbreak had another legacy too: it shattered the belief that plague was largely a rat-borne disease of urban areas and that to eradicate it all you needed to do was clean up the places where rats bred. Though it was never proven that squirrels were the source of the 1924 outbreak, the discovery of squirrel fleas on rats recovered from the greater Los Angeles area, together with the fact that no plague-infected rat was found between the port and the Mexican quarter, suggested that Meyer had been right and that the disease had most likely found its way to the Mexican quarter from the hinterland. Looking back, the signs had been there in 1908 when the boy in Elysian Park, thirty miles from the port, had died of plague after handling an infected squirrel in his backyard. It was around this time that squirrel die-offs had been reported in San Luis Obispo, a phenomenon that was repeated in 1924 when similar epizootics were observed in several counties in southern and northern California. Perhaps squirrels had originally caught the bug from rats rummaging in garbage dumps in Oakland, or that had hitched a ride south on the Southern Pacific Railroad. Or perhaps ground squirrels and other wild rodents had been harboring the plague bacillus for decades without anyone noticing. Whatever had been the case, the Los Angeles outbreak prompted Meyer and others to take a closer look at the role of squirrels in the persistence of plague between epidemics and the role of their fleas in the transmission of the disease to rats and other wild rodents. With Dickie’s help Meyer examined the records of previous outbreaks, trying to see if there was a relationship between epizootics observed in squirrels and human outbreaks. In 1927, when the state resumed responsibility for plague control work, Meyer and Dickie joined forces to survey ranches and woodlands suspected of harboring plague-infected squirrels. By the mid-1930s, state survey crews had trapped tens of thousands of squirrels and combed their fur for fleas, returning the rodents and their ectoparasites to Meyer’s laboratory at the Hooper Foundation. Although many of these squirrels appeared perfectly healthy, Meyer discovered that some harbored latent infections and that their ground-up organs could be used to communicate plague to guinea pigs. Many were also infested with plague fleas. In addition, crews recovered diseased fleas from burrows that were known to have harbored infected squirrels twenty years previously but which were now occupied by other rodents, suggesting that in certain parts of the state ground squirrels constituted a hidden “reservoir” of disease. It was the beginning of a new ecological approach, one that by the mid-1930s would see Meyer adopt the term sylvatic plague to describe the preservation of the disease by forest-dwelling rodents.
By 1935, the PHS had joined the survey effort and established that sylvatic plague was endemic to eleven Pacific coast and Rocky Mountain states and that its reservoirs included eighteen species of ground squirrel, plus chipmunks, prairie dogs, marmots, wild rats, white-footed mice, kangaroo rats, and cottontails. By 1938 m
ore than 100,000 squirrels had been trapped and shipped to the Hooper Foundation for examination. However, when Meyer came to autopsy the rodents he found that only a small percentage were infected with Y. pestis. He also observed that no sooner had the squirrels been eliminated than field mice took up residence in the empty burrows where they promptly became infested with the same plague fleas and “peddled” the infection to other rodents. Eradication was doomed to failure because sylvatic plague was “independent of the usual lines of communication,” he concluded. The challenge was to keep sylvatic plague at a low level by periodically culling the squirrel populations that harbored Y. pestis. Of course, every now and again, someone might be bitten by a squirrel flea and contract the disease, but such events were rare, and as long as squirrels were prevented from infecting urban rat populations, sylvatic plague posed little threat to people living in built-up areas.
This is pretty much the approach employed by the CDC today. From its wildlife station in Fort Collins, Colorado, the CDC monitors the incidence of plague in prairie dogs, thought to be a key reservoir of plague in the western United States, and the spillover of the disease into squirrels and other wild rodents. In the Pacific Coast and Rocky Mountain states the principal vector is a species of flea called Oropsylla montana. Unlike in the rat flea X. cheopis, the midgut of O. montana gets blocked only rarely when it takes a blood meal, but it is known to unleash rapidly moving epizoonotics among Californian ground squirrels and rock squirrels through an “early-phase” transmission system.¶ When plague levels are considered dangerously high, warnings are posted in state parks and campgrounds showing a squirrel in a red circle with a diagonal slash through it. At such times hikers are warned not to feed squirrels and pet owners are advised to keep an eye on cats and other domestic animals lest they cross paths with a squirrel and accidentally become infested with their fleas. In spite of these precautions, every year about three people in the United States are infected with plague and in some years, as in 2006, there have been as many as seventeen infections. Prompt treatment with a powerful antibiotic, such as doxycycline or ciprofloxacin, is usually sufficient to clear the plague bacillus from the system.# Nonetheless, newspapers continue to run panicked headlines about the deaths of Americans from “bubonic plague” and the threats posed by squirrels and other wild rodents, as occurred in 2015 when an elderly Utah man died from the disease.
No one is sure what causes these periodic flare-ups, but climate and topography are thought to be important factors. Plague persists in relatively small geographical pockets, such as the high plateaus and grasslands of New Mexico, Utah, and Colorado, and the coastal fog belts of northern California, where the weather tends to be cool and damp year round. Indeed, in California, only the dry, central desert region is completely free of sylvatic plague. By contrast, in Yosemite National Park and other wilderness and coastal areas, plague is nearly always present. In such locales, it finds the ideal ecological balance between climate, flea vectors, and rodent hosts. It is only when unusual rainfall levels boost plant growth or some other factor increases the rodent and flea populations, that the balance between parasite and host is disturbed and plague risks spilling over into other animals.
Indeed, with the ongoing encroachment of residential developments into these wild habitats, the animal that most threatens to disturb this balance today is humans, which is why in the future we should expect further small outbreaks of plague, in its bubonic form at least. However, it is highly unlikely that Los Angeles or any other American city will ever again be confronted with an epidemic of pneumonic plague, much less a pandemic on the scale of the Black Death.
* Though McCoy states that the squirrel had bitten the boy on the hand, he goes on to say that it is uncertain whether the boy contracted plague this way, speculating that he may have contracted it from infected fleas, which is the more usual transmission route of plague from squirrels to humans.
† Rabbits, pigs, coyotes, bobcats, badgers, bears, gray foxes, and skunks can also be infected with plague, though they rarely exhibit symptoms. By contrast, domestic cats are highly susceptible.
‡ Mercurochrome is the brand name for dibromohydroxymercurifluorescein, sometimes called merbromin. Its use was discontinued by the FDA in 1998 because of fears of potential mercury poisoning.
§ The swelling in Jesus’s groin was almost certainly an inguinal bubo that had been allowed to drain for three weeks before anyone thought to examine it for plague bacilli. A culture subsequently revealed “bipoloar organisms,” and when a laboratory animal was inoculated with the culture it died within twelve hours.
¶ Plague bacilli multiply rapidly in X. cheopis, sometimes causing blockages that prevent ingested blood from reaching the flea’s midgut. These blockages cause the flea to feed more voraciously, thereby increasing the chances it will retransmit the infection.
# In patients treated with antibiotics the average fatality rate is 16 percent. In the untreated, it ranges from 66 to 93 percent.
CHAPTER III
THE GREAT PARROT FEVER PANDEMIC
“What men against death have done.”
—PAUL DE KRUIF
On January 6, 1930, Dr. Willis P. Martin paid an urgent house call on a family in Annapolis, Maryland. Lillian, her daughter Edith, and Edith’s husband Lee Kalmey, the owner of a local auto repair shop, had begun to feel feverish shortly after Christmas, and all three were now deathly ill. At first, they attributed their symptoms to influenza and the depressive effects of the recent stock market crash, which had hit Kalmey’s business as hard as any, but in the first week of the new year their condition had taken a decided turn for the worse. To the chills and generalized aches and pains typical of influenza was now added an irritable dry cough, accompanied by constipation and exhaustion that alternated with headaches and insomnia. For large parts of the day, Lillian, Edith, and Lee lay somnolent as logs, the silence broken only by their intermittent mutterings. By contrast, when awake they would be restless and prone to fits of violent excitement. The most worrying symptom of all, however, was the rattling sound coming from deep within their lungs.
Dr. Martin suspected pneumonia, possibly mixed with typhoid fever. However, Lillian’s husband, who had eaten the same meals as the rest of the family, was perfectly well, which tended to rule out a food-borne illness. The only other member of the household who had been sick was a parrot that Lillian’s husband had purchased from a pet store in Baltimore and which Edith and Lee had kept at their home in the run-up to the Yuletide festivities so as to present the bird to Lillian as a surprise on Christmas Day. Unfortunately, by Christmas Eve the parrot’s plumage had grown ruffled and dirty and the creature was showing signs of listlessness. Come Christmas Day the parrot was dead.
Dr. Martin was baffled by the family’s symptoms and shared his bewilderment with his wife. At first, Mrs. Martin was similarly puzzled. Then Dr. Martin mentioned the dead parrot. It might be a coincidence, she said, but the previous Sunday she had been reading about an outbreak of “parrot fever” in a theatrical troupe in Buenos Aires. According to the newspaper report, the disease was being blamed for the death of two members of the company, who, in common with other members of the cast, had been required to interact with a live parrot on stage. That bird was now dead and pet owners throughout Argentina were being warned to report sickly psittacines—birds in the parrot family—to the authorities.
It sounded unlikely, ridiculous even, but Martin was not the type to take a chance. Instead, he sent a telegram to the PHS in Washington, DC:
REQUEST INFORMATION REGARDING DIAGNOSIS PARROT FEVER . . . WHAT INFORMATION AVAILABLE REGARDING PREVENTION SPREAD OF PARROT FEVER. . . . CAN YOU PLACE SUPPLY PARROT FEVER SERUM OUR DISPOSAL IMMEDIATELY. WIRE REPLY.
Martin was not the only doctor puzzled by the sudden appearance of mysterious pneumonias accompanied by typhoid-like symptoms in the United States that winter. By now similar telegrams were arriving at the PHS from Baltimore and New York, and health officials in
Ohio and California were fielding similar requests for information. Like Martin’s telegram, these communications ended up on the desk of Surgeon General Hugh S. Cumming, who passed them on to his subordinate, Dr. George W. McCoy, the director of PHS’s Hygienic Laboratory. A veteran of the bubonic plague investigations in San Francisco, McCoy was renowned for discovering tularemia, dubbed the “first American disease” because the bacterium was first identified in McCoy’s lab in California, and was then the most celebrated bacteriologist in America.* If anyone could solve the outbreak, Cumming figured, it was McCoy. But when McCoy read Martin’s telegram he could not help smiling. Parrot fever? It sounded like the sort of diagnosis you might encounter in the medical columns of the yellow press or a joke in the funny pages. Certainly, McCoy had never heard of parrot fever. But then McCoy was a busy man—America was in the grip of an influenza epidemic, a recrudescence, it was feared, of the Spanish flu, and he and his deputy, Charlie Armstrong, were working day and night on a serum for postvaccinal encephalitis, a “sleeping sickness” that affected some individuals who’d received the smallpox vaccine. Nevertheless, McCoy thought it best to check with his colleague.
“Armstrong, what do you know about parrot fever,” McCoy demanded. “What do I know about it? I don’t know a thing about it,” Armstrong admitted.
Within days, however, McCoy and Armstrong would come to rue their ignorance as one by one laboratory workers tasked with investigating whether parrots were implicated in the outbreaks seen in Annapolis and elsewhere, fell ill. Indeed, by February Armstrong and several other personnel at the “Hygienic,” as the ramshackle red-brick laboratory overlooking the Potomac was known, had been removed to the nearby US Naval Hospital. By the time the outbreak concluded in March, Armstrong’s longtime assistant, Henry “Shorty” Anderson, was dead. In the end, it fell to McCoy to conduct the critical passage experiments on parrots in the basement of the Hygienic in an attempt to isolate the “virus” of psittacosis and develop a serum. But the tests were inconclusive and in the end McCoy had been forced to chloroform the birds and fumigate the Hygienic from top to bottom to prevent the putative virus from escaping the building. As the science writer Paul de Kruif put it in his book Men Against Death, McCoy “never smiled nor even muttered” as he performed this grim task, “but just killed and killed and at the end of it swashed out every last cage with creosol, and gave all the dead bodies of those assorted unhappy experimental creatures a decent and thorough burning in the laboratory incinerator.”