by The Pandemic Century- One Hundred Years of Panic, Hysteria
PASTEURELLA PESTIS, or Yersinia pestis to give the bacillus its proper name, is one of the deadliest pathogens known to man. Named for the Swiss bacteriologist, Alexandre Yersin, who isolated the microbe during the third plague pandemic in Hong Kong in 1894, Y. pestis is conservatively thought to have been responsible for 100 million deaths throughout history, perhaps as many as 200 million. Yet for all the horror evoked by the word plague, human infections are only incidental events in the life cycle of the parasite. The bacillus’s natural reservoir is wild rodents, such as marmots, ground squirrels, and rats. Transmitted by the bites from infected fleas that live in the rodents’ burrows, Y. pestis circulates for the most part harmlessly in these rodent populations. It is only when the relative immunity of rodent populations wanes, and there are sudden die-offs, leaving fleas temporarily homeless, or diseased rodents are brought closer to human habitations, that the existence of the zoonosis becomes visible and there is a risk of transfer of the infection to humans or some other animal host. From the point of view of the parasite and its survival, however, this is not a great strategy, as this “accidental” transfer usually results in the death of its new host, preventing further onward transmission of the bacillus.
The human disease takes three forms: bubonic, septicemic, and pneumonic. The bubonic form occurs when a flea jumps from a rat or some other rodent and bites a human, injecting the plague bacilli under the skin (afterwards, human fleas or body lice may transmit bubonic plague to other individuals). As the victim scratches the site of the wound, the bacilli multiply and spread to the lymph glands in the groin (in the case of a flea bite to the leg) or the armpits (in the case of a bite to the arm). As the immune system struggles to contain the infection, the lymph glands become swollen and inflamed, giving rise to the painful egg-shaped “buboes” from which the disease takes its name. On average, plague takes three to five days to incubate, and another three to five days before the victim dies (untreated, bubonic plague is fatal in around 60 percent of cases), the final stages being marked by extensive hemorrhaging and organ failure. In the most toxic form of bubonic plague, known as septicemic plague, the skin becomes mottled with dark blue patches and the extremities may turn black, hence one possible derivation of the disease’s name, “Black Death.” In the last stages of the infection, victims often fall into a delirium and are unable to bear the slightest touch to their sores. The only mercy is that this form of plague usually kills quickly and is only transmissible by bites from fleas.
By contrast, the pneumonic form can be spread directly from person to person and can arise either from inhalation of Y. pestis or septicemic spread of bacteria from the bubonic form of the disease. Typically, an originating case of pneumonic plague occurs when some of the bacilli escape the lymph system and migrate to the victim’s lungs, causing edema and secondary infection (this is particularly common when a bubo forms in the neck region). During this time, the victim is noninfectious but may exhibit a fever and rapid pulse. Within one to four days, however, the victim’s condition suddenly deteriorates as the edema spreads, triggering necrotizing pneumonia throughout the lungs and violent paroxysms. At this stage, the victim typically coughs or “spits” blood, causing the bed sheets to become spotted and stained crimson. Unless treated within twelve hours of the onset of fever, pneumonic plague is invariably fatal. Suspended in cough droplets or sputum, the bacilli can also be expelled as far as twelve inches, making it easy for someone lying on a nearby sofa or an adjacent bed to catch the disease. In cold weather and cool, humid conditions the bacilli can also become attached to water droplets and linger in the air for minutes or hours at a time. The bacteria can also survive for up to three days on hard surfaces, such as glass and steel, and for much longer in the soil and other organic material.
It is difficult to be certain what proportion of deaths that occurred during historical outbreaks were due to the bubonic as opposed to the pneumonic form of the disease, because prior to modern bacteriological tests diagnosis was uncertain and rested on the interpretation of clinical symptoms and signs. The first plague pandemic that began during the reign of the Byzantine emperor, Justinian I, and which is estimated to have killed some 25 million people throughout the Mediterranean basin between 541 and 750, is thought to have been largely bubonic. However, the second pandemic appears to have been a mixed outbreak. Colloquially known as the Black Death, the pandemic began in 1334 in China before spreading along the great trade routes to Constantinople, Florence, and other European capitals in the middle decades of the fourteenth century, reducing Europe’s population by approximately one-quarter to one-half between 1347 and 1353 and killing at least 20 million people, possibly as many as 50 million. To judge by contemporary accounts, buboes and swellings, called gavocciolo by Italian chroniclers, were ubiquitous. However, in 1348, the first year of the Black Death in Europe, so were pneumonic symptoms. “Breath,” wrote one Sicilian chronicler, “spread the infection among those speaking together . . . and it seemed as if the victim[s] were struck all at once by the affliction and [were] shattered by it. . . . Victims coughed up blood, and after three days of incessant vomiting for which there was no remedy, they died, and with them died not only everyone who talked with them, but also anyone who had acquired or touched or laid hands on their belongings.”
The news that a deadly pathogen from the Middle Ages had arrived in the City of Angels was not something anyone in Los Angeles wanted to hear in 1924, least of all business leaders. As William Deverell, a historian of California and the West, puts it, at a time when Los Angeles was selling itself as a hygienic retirement destination, “plague was not the sort of thing expected in the proud city of tomorrow.” Plague’s presence in Los Angeles was also a considerable blow to the prestige of the US Public Health Service (PHS) and the Californian State Board of Health. Just ten years earlier, health officials had confidently declared that all “discoverable” plague had been eradicated from California. This announcement was based on the new knowledge of plague’s ecology that had been acquired following the outbreaks of bubonic plague in San Francisco in the early years of the century.
Introduced to the city in around 1900, most likely from black rats that had hitched a ride to San Francisco on a steamship from Honolulu, the plague was at first confined to Chinatown, where it killed 113 people. However, following the earthquake and fire that struck San Francisco in 1906, rats were displaced from their downtown runs and dispersed throughout the city, sparking new outbreaks in 1907–1908 over a much wider urban area. In response, US Assistant Surgeon General Rupert Blue launched a massive rat extermination campaign. Whereas in 1903 Blue had concentrated on demolishing houses in Chinatown and baiting rat holes with arsenic, now he ordered his men to hunt down and kill rats wherever they found them. By January 1908, when the last two cases of bubonic plague were seen in the city, some two million rats had been exterminated and many thousands had been autopsied, giving Blue, and his chief laboratorian, George McCoy, new insights into the transmission of plague and its persistence in rodent reservoirs in interepidemic periods. Unlike in India and Asia, where the principal vector of plague was the black rat, Rattus rattus, Blue and McCoy discovered that in San Francisco the main vector had been the brown sewer rat, Rattus norvegicus. A prolific breeder, the brown rat’s preferred habitat is sewers and cellars where it likes to lay out its run in the shape of a Y, with its food store hidden at one branch and its nest at the other—evidence, according to Blue, of the rodent’s “sagacity” at evading predators. This strategy had served the brown rat well, enabling it to spread from the waterfront in northeast San Francisco as far as the County Hospital in the southwest.
Although in 1908 no one had definitively demonstrated that fleas living on rats were vectors of plague, their incriminating role was widely presumed, and Blue routinely ordered his men to comb rats for fleas and count the number of ectoparasites. He found that in winter his men could comb twenty rats and recover only one flea among them, but in warm weather
the flea numbers multiplied, such that a healthy rat could harbor twenty-five fleas, while a sick one might host eighty-five. As long as these fleas fed on rats, they hypothesized, they posed little threat to human populations. It was only when rats were evicted from their runs and came into contact with people, or when plague-infected fleas killed their rodent hosts and began looking for a new blood meal, that humans risked being infected. However, there was much more to the ecology of plague than just rats and fleas.
In China, it had long been suspected that marmots acted as reservoirs of plague in interepidemic periods. However, until Blue, McCoy, and William Wherry, a bacteriologist with the San Francisco Board of Health, began studying sporadic outbreaks of plague in counties on the east side of San Francisco Bay in 1908, no one had suspected that Californian ground squirrels and other wild rodents indigenous to the western United States might be similarly susceptible to infection with Y. pestis or might play a similar role in maintaining transmission of the parasite in interepidemic periods. Blue’s suspicions had first been aroused five years earlier when a blacksmith from Contra Costa County died of bubonic plague at a hospital in San Francisco. On questioning his friends and family, Blue learned that the blacksmith had not visited the city in over a month, but that three to four days before the onset of his illness he had shot and killed a ground squirrel in the hills near his home. By July 1908 Blue was certain that there were no more infected rats in San Francisco. However, that same month he learned that the son of a rancher from Concord in Contra Costa County had contracted plague and died, prompting Blue to dispatch his top rat catcher, William Colby Rucker, to investigate. The scene that greeted Colby at the ranch had all the hallmarks of a classic epizootic, with bodies of dead rats littering the ground. In a barn on the ranch near where the boy had died, Colby also recovered a dead squirrel. Blue immediately ordered Colby and his men to collect squirrels from other ranches in the region and discovered that several were infected with Y. pestis. As Blue later wrote Washington, DC, this was “perhaps the first demonstration of the occurrence in nature of bubonic plague in the ground squirrel (Citellus beecheyi) of California.” McCoy speculated that the squirrels must have caught the plague from rats that had migrated from San Francisco to Oakland and had mingled with wild rodents in the hills behind Berkeley, exchanging ectoparasites in the process. Evidence for this hypothesis was supported by his discovery that the California ground squirrels were heavily infested with two species of flea, Hoplopsyllus anomalus and Nosopsyllus fasciatus. The latter was commonly found on rats and, together with Xenopsylla cheopis, the oriental rat flea, was thought to have been the principal vector of bubonic plague during the 1906 San Francisco outbreak. However, McCoy observed that the squirrel fleas also readily attacked humans, writing that at one point his “squirrel stock room became so heavily infested that upon going into the room one was certain to be bitten by many of the parasites.” McCoy also found that in the laboratory it was easy to transmit plague by means of the H. anomalus flea from squirrels to guinea pigs and rats, and vice versa, leading him to conclude that “it is not improbable that the conveyance in nature is in the same way.”
The discovery that squirrels might act as reservoirs of plague between rat epizootics and that their fleas might also be capable of transmitting the infection to humans caused Blue “considerable apprehension.” However, it was thought that as long as the risk was confined to Contra Costa and Alameda Counties, there was little to worry about. Then in August, a report reached McCoy of the death of a ten-year-old boy in Elysian Park, in northeast Los Angeles, some four hundred miles to the south. On arriving at the boy’s home, McCoy discovered that seven days before the onset of illness, the boy had come across a ground squirrel in his backyard and it had bitten him on the hand. Both the boy and a dead squirrel recovered from the property subsequently tested positive for plague. The boy’s home, McCoy noted, was just two miles from city hall and backed onto the yards of the San Francisco–Los Angeles line of the Southern Pacific Railroad.*
This was alarming news and prompted the PHS to cast its net wider. After writing Washington for more rifles and ammunition, Blue sent hunting parties into nearby woodlands and hillsides to collect squirrels and bring them to McCoy’s laboratory. By 1910, McCoy had examined 150,000 ground squirrels across ten California counties and discovered that 402, or 0.3 percent of them, were infected with plague. These diseased squirrels had been recovered from as far south as San Luis Obispo and the San Joaquin Valley, many miles from the sea and the presumed original ports of entry to the United States. In response, Blue focused his efforts on the areas where infected squirrels had been found, poisoning their burrows with carbon bisulfide and sending hunting parties into the woods to shoot stray rodents. Blue’s war on rodents made him a household name, and in 1912 he was elevated to surgeon general, the top medical position in the country. In his absence, others carried on the eradication work he had begun, and by 1914 ground squirrels had been recovered from twenty-one infected ranches and their burrows so thoroughly poisoned that officials were only able to find one infected squirrel when they repeated the survey, prompting Colby to claim that “danger of its further spread has been removed.” But Colby and his colleagues were wrong. The ecology of plague was far more complex than they could have anticipated—as one expert put it, writing in 1949, plague was “like following the different voices in a Bach fugue,” the difference being that while the structure of a Bach fugue is known, with plague “the basic design is unknown.” The fact is, plague never entirely disappears from wild rodent populations. Rather, the pathogen circulates continually between fleas, squirrels, and other wild mammals, including chipmunks, marmots, and prairie dogs.† Many of these rodents have genetic or acquired immunity so are resistant to illness. However, every few years, this resistance wanes and the host population crashes, leaving fleas without a source of food. It is at this stage that the fleas seek a new host, seizing upon whatever animal happens to stray into the vacant rodents’ burrows. This could be another species of ground squirrel or it could be a wild rat or a field mouse, or even a rabbit. Regardless, the transfer usually results in a violent epizootic as these new and highly susceptible hosts fall victim to the disease for the first time—hence the rats that Colby found littering the grounds of the ranch in Concord.
Nonetheless, there was good reason why, by 1924, California health officials should have been on their guard, not only against renewed outbreaks of the bubonic form of the disease, but of pneumonic plague, too. Indeed, bacteriologists only needed to recall the outbreak of pneumonic plague that had occurred in Oakland five years earlier, killing thirteen people. The outbreak began in August 1919 when an Italian man named Di Bortoli went hunting in the foothills of Alameda County, returning with several squirrels for the table of his rooming house in Oakland. Within days, Di Bortoli was complaining of fever and pain in his right side and had reported to a doctor. Unfortunately, the physician attributed Bortoli’s symptoms to influenza and even after Di Bortoli developed a painful bubo on his neck, the doctor did not think of plague. Most likely, it was septicemic spread of plague from this bubo that sparked a tonsillar infection and secondary pneumonia. The result was that by the time Di Bortoli died at the end of the month, five other people, including his landlady and a nurse, had been infected and by September 11, thirteen more people had contracted plague. In all, only one survived. Fortunately, thanks to the rapid hospitalization and isolation of the patients, the outbreak was self-limiting. Nevertheless, the fact that thirteen people had died and that the outbreak had begun following contact with a squirrel was extremely alarming, suggesting that, as with Siberian marmots, Californian squirrels might harbor fleas infected with highly virulent and potentially pneumotrophic strains of the bacillus. As William Kellogg, the director of the State Board of Health Bureau’s communicable disease division, observed, “Until plague-infected ground squirrels are entirely eradicated from California we shall always have a sword of Damocles hanging ov
er our heads.”
Kellogg’s concerns were born of bitter experience. In 1900 when plague had announced itself in San Francisco, it had been he who had taken samples from the lymph gland of the first presumed plague patient to Joseph Kinyoun at the United States’ Marine Hospital laboratory on Angel Island for testing. After Kinyoun demonstrated that the tissues contained the plague bacillus, and that that organism caused guinea pigs to sicken and die, Kellogg then found himself thrust into the uncomfortable position of having to defend Kinyoun against a vitriolic campaign orchestrated by California’s governor, Henry Gage, and local business interests. Angered by the imposition of the quarantine around Chinatown, Gage and his allies called into question Kinyoun’s methods and findings, and alleged that the quarantine measures were a “scare.” They also proposed that “it be made a felony to broadcast the presence of plague.” Kinyoun’s findings were subsequently upheld by a commission of prominent bacteriologists appointed by the US Treasury, but Kellogg, whose competence came in for similar scrutiny and who faced similar vilification, felt that “for unexampled bitterness, unfair and dishonest methods” the campaign “probably never had been and never again will be equaled.”