Emerson, Day, and Wood spent the rest of the night trying to respond to the short-term consequences of the catastrophe. Order had to be restored to the city and thousands of terrified people, who were already under armed guard, had to be fed, housed, and resettled. As a smoldering glow illuminated drifting nighttime clouds, the three physicians began to face the fact that a policy they initiated in the name of public health had produced the worst civic disaster in Hawaiian history. The long-term consequences of what had happened could hardly be contemplated.
Next to the attack on Pearl Harbor in 1941, the Chinatown fire remains not only the worst civic disaster in Hawaiian history but one of the worst disasters ever initiated in the name of public health by American medical officers anywhere. This book looks at how that catastrophe came about and how the people of Honolulu dealt with it. At its core lies the enduring dilemma of making public health policy in times of crisis on the basis of limited medical knowledge. The three physicians in charge-Emerson, Day, and Wood-rightly remain at the center of this story, and their actions are essential to an understanding of what happened in Chinatown. But this book also demonstrates that their actions and the actions of everyone else involved in this dramatic tale were deeply embedded in a context of racial tensions, cultural assumptions, economic interests, ideological conflicts, medical revolutions, professional rivalries, and American territorial visions. Neither the public health policies developed by the three physicians nor the consequences of those policies can be understood outside their historical context.
Chinatown after the fire with the ruins of Kaumakapili Church in the distance. Hawaii State Archives
ew people realize that the world's last major epidemic of bubonic plague occurred quite recently: it began circling the globe at the end of the nineteenth century and killed tens of millions of people worldwide before it receded in the early years of the twentieth century. The disease that Emerson, Day, and Wood were fighting with fire three weeks into the twentieth century had broken out in south-central China sometime before 1870- Severe influenzas and other plague-like diseases were common in that region, but most previous outbreaks had been confined to the interior or had disappeared quite quickly. This new illness, however, seemed to expand and strengthen over time.'
By the late 1870s, the disease had decimated most of the provincial villages of south-central China, and by the early i 89os it began appearing along trade routes that led down river valleys toward the coast. Breaking out of the interior, the disease struck the bustling commercial city of Canton with deadly force in 1893, and tens of thousands of people died "like plum blossoms in a late frost." Eyewitnesses remembered that "the dead were buried by the living-and then the living died." Gaining momentum, the epidemic raced rapidly down the heavily traveled Pearl River corridor in 1894 to the port city of Hong Kong, where it began killing the residents of that British coastal colony by the thousands.2
The illness typically began with a sudden wave of high fever, headache, chills, and nausea. In many cases, those initial symptoms tapered off after several hours, encouraging victims to hope they had escaped with a mild case of whatever this affliction was. But sometime within the next two daysand often quite quickly-the same symptoms returned more forcefully than before. As their fevers soared to life-threatening levels, victims experienced a crushing combination of overall body pain and almost complete loss of energy. Sufferers often lay limply in a fetal position. Diarrhea, vomiting, lethargy, and mental stupor were common, but not always present, and a bewildering array of other symptoms occasionally appeared as well, including insomnia, speech disorders, delirium, a racing pulse, liver and spleen discomfort, seizures, ruptured blood vessels, and open sores on the skin. Some patients experienced toxic shock and died suddenly after the major onslaught began; others hung on for as many as five unspeakably horrible days, either in semiconscious agony or in a coma, as their internal organs ceased to function and death finally ensued.;
The 1894 Hong Kong epidemic had two distinctive traits that seemed to distinguish it from the many previous plague-like diseases and severe influenzas that had regularly appeared there through the nineteenth century. The first was a frighteningly high death rate. Fewer than a quarter of those who came down with the new disease managed to survive. In the British hospitals of Hong Kong, 95 percent of the patients succumbed. Even allowing for the fact that Chinese families took people to those hospitals only as a last resort, that was a devastating death rate for an ailment that now seemed to be spreading so relentlessly and so widely.
The other distinctive symptom of the epidemic was the presence in most victims of badly swollen and exquisitely painful lymph glands, most commonly along the inner thighs and under the armpits. In some patients the swelling at the top of their thighs made their upper legs appear to be inflated. In others the swelling under their armpits gave the impression that a hen's egg was trying to emerge from beneath their shoulder joints. Any pressure on the affected glands-even in cases where the swelling was barely discernible-produced excruciating pain. The few victims who attempted to walk often staggered about in an almost crablike manner to avoid aggravating the pain.
Noting the combination of high death rates and dramatically inflamed glands, which earlier physicians had classically called "buboes," alarmed public health officials in Hong Kong declared the scourge of 1894 to be a return of the legendary bubonic plague, the same affliction that was thought to have killed more than a quarter of the planet's human population dur ing the middle decades of the fourteenth century. From that time through the end of the eighteenth century, recurring waves of the so-called black death-a nickname it acquired because internal hemorrhaging often left dark blotches on its victims' corpses-subsequently killed an estimated fifty million additional people in Europe alone. Though the dreaded disease had apparently never reached the central Pacific or the Western Hemisphere, and for unknown reasons had lapsed into relative quiescence throughout the world near the end of the eighteenth century, it now seemed to be back. Chinese physicians, who knew the black plague as "the great eternal sorrow illness," agreed. Whether this was exactly the same bubonic plague that had ravaged the globe in previous centuries is open to serious debate, but public health officials in the i 89os believed that it was.4
The multitude of different symptoms that showed up in different individuals led to widespread medical debates about the fundamental nature of the disease. Was it an intestinal ailment, a skin disease, another of the many fever diseases, or something else altogether? Those debates, in turn, fueled arguments over how best to treat the disease. In the past, plague doctors had tried almost everything, and they were now doing so again. Some attempted to purge their patients' bodies with emetics, hoping to help the body expel whatever was causing the difficulties; some lanced and drained the swollen glands, hoping to relieve the pain and create an exit for internal poisons; some applied salves to inflamed skin as they would for a skin disease; many attempted various methods of fever reduction; and most offered whatever their culture's traditional strengthening and rejuvenating agents might be, which typically included such items as herbal broths, botanical extracts, strong teas, or special foods. But the world's healers all knew full well that they could ultimately do little in the face of bubonic plague except watch and wait helplessly, as their predecessors had done for millennia and the English doctors were still doing in Hong Kong, while the disease ran its horrific and usually fatal course through their patients.
One new development in medical science offered at least some physicians of the 189os reason to hope-after centuries of frustration-for the possibility of a genuine breakthrough against plague: the rise of bacteriology. During the late i 86os, investigators led by Robert Koch in Berlin and Louis Pasteur in Paris had begun to explore systematically the long-suspected possibility that infectious diseases were caused by extremely tiny creatures that somehow invaded human bodies and disrupted the ability of various organs to function properly. Armed with modern microscopes,
investigators were actively searching for such disease-causing microorganisms, all of which were then called bacteria, since the existence of viruses was still unknown. Once identified and isolated, the culprits could be grown in laboratory situations outside the human body, where scientists could work on vaccines, serums, antitoxins, and antidotes to counteract the organisms.
During the i 88os and i 89os, Europeans had used the new bacteriological approach to develop the world's first successful laboratory-produced vaccines and antitoxins, initially and famously against rabies and then even more effectively against diphtheria, which had long been a potent killer of children, and against brucellosis (or undulant fever), a persistent flu-like disease that farmers caught from livestock and city dwellers got from infected milk. Especially for physicians trained in laboratory-oriented medical schools during the last three decades of the nineteenth century, those well-publicized bacteriological triumphs were nothing short of revolutionary. The prospect of more victories to come made scientific medicine in the late i89os a more optimistic and exciting field than it had ever been before.
Bacteriological investigators around the world were steadily working on many other diseases when the epidemic of 1894 appeared in Hong Kong. Anxious to see if their promising new approach might be applicable to the world's most legendary killer, two prominent investigators rushed to the British colony. One of the two was Kitasato Shibasaburo, who had been sent from his native Japan to work with Koch in Berlin; the other was Alexandre Yersin, who had emigrated from his native Switzerland to France in order to study with Pasteur. Since both of them openly coveted the potential glory of being the first person in history to discover the cause of bubonic plague, the two did not cooperate. Kitasato, for example, tried to prevent Yersin from obtaining bodies to work on. But their rivalry intensified an already frantic research pace. Within months the two scientists more or less simultaneously isolated variations of the same bacterium, which they confirmed to be responsible for the epidemic. Laboratory experiments with animals and pathological reports from the field confirmed the contentions of Kitasato and Yersin that their newly identified pathogen was indeed the perpetrator of bubonic plague.'
International public health journals quickly disseminated news of the bacterial discovery that Kitasato and Yersin had made in Hong Kong. The culprit they identified was formally named pestis-the plague-producing bacterium-and descriptions of the microorganism circulated the globe, in drawings not unlike wanted posters. Even Honolulu's English-language newspapers published cartoon-like illustrations of what the pestis would look like through the lens of a microscope.'
Among bacteriologists, the discovery of pestis was both exhilarating for its own sake and full of promise for the future. For the first time, physicians knew definitively what was causing bubonic plague, the disease regarded as humankind's most fearsome long-term scourge. By testing for the presence of pestis in their patients, physicians could now determine with accuracy whether a suspicious case was that disease. Actual samples of pestis were dispatched by ship from Hong Kong to laboratories throughout the world, where medical scientists immediately began trying to produce vaccines, serums, antitoxins, and antidotes to counteract this most recently unmasked bacterial enemy. Physicians and medical students working on the front lines of the global pandemic did the same.
Despite the possibility of long-term progress, however, the discovery of pestis in and of itself offered little practical help in the short run for the rank-and-file physicians who actually had to deal with the disease at hand. To make a positive identification, for example, a physician would need a reasonably sophisticated microscope, along with the chemical staining agents that rendered bacteria visible. The physician would also have to know how to obtain and handle human tissue samples, how to prepare those samples properly on a thin pane of glass, and how to discern with confidence exactly what appeared, often dimly and imperfectly, through the eyepiece. In fact, bacteriological equipment and bacteriological skills remained limited around the world through the end of the nineteenth century, so the vast majority of healers continued to diagnose the plague epidemic by its symptoms.
The same was true for treatment. Though bacteriologists in laboratories around the world were already working with their newly acquired samples of pestis to develop effective counteragents, no one knew for sure whether their experimental efforts would ever produce useful results, much less how long those efforts might take. In the interim, doctors desperately trying to help actual patients could do nothing more than they were already doing before the discovery.
Nor did the positive identification of pestis by itself provide an answer to the question immediately pressing all of the world's public health officers: how and why was this plague continuing to spread? Even if Kitasato and Yersin were right that the disease resulted from the proliferation of pestis bacteria inside human bodies, how did the bacteria get there? Did they travel on foul air currents inhaled by unsuspecting victims? Were they ingested with particular foods or bad water? Did they enter human orifices after stowing away on clothing or merchandise? Could they penetrate skin? Might they spread by personal contact?
More than a decade after its appearance in Hong Kong in 1894, scientists would demonstrate that bubonic plague was principally a disease of rodents, especially rats, that was spread from them to humans by the bite of a flea. Whenever a flea sucked blood from a rat that had pestis in its bloodstream, the ingested bacteria produced what might be thought of as a throat blockage in the flea. In order to clear its own passageways for fresh blood, the flea essentially vomited the bacterial clot into its next victim, thereby spreading the disease. But no one understood that process in the final years of the nineteenth century.'
To be sure, centuries of observation had established a correlation between rat deaths and human deaths in plague epidemics, including this one. Some medical authorities suspected that rats could somehow spread plague once it was underway, perhaps through their fecal matter. That was one of the reasons why British colonial public health officers urged people to wear shoes during the epidemic and one of the reasons why public authorities around the globe had sometimes conducted anti-rat campaigns when plague appeared in past centuries. But most observers either withheld judgment or had concluded that rats, like people, were probably co-victims of plague rather than mobile reservoirs of the disease.
W. J. Simpson, the British public health officer who conducted the British colonial campaigns against plague, maintained through the end of the nineteenth century that rats were no more likely to convey the disease than many kinds of food and many other animals. Walter Wyman, the U.S. federal government's highest-ranking public health officer, published an influential report in 1897 arguing that pestis bacteria probably traveled from person to person on dust or foodstuffs; hence rats commonly got the disease because they encountered more dust and more discarded foodstuffs than people did. In a widely circulated magazine that appeared around the English-speaking world in December 1899, a British public health analyst concluded there was "no evidence that rats have been an important factor in spreading infection" during the plague pandemic of the previous five years. After all, reasoned such observers, rats and humans interacted almost everywhere and practically all the time, yet epidemics were infrequent and appeared some places but not others.'
Ominously for the rest of the world, the plague that Kitasato and Yersin had studied in Hong Kong soon began to appear in other places as well. With local officials unable to stop it, the disease spread rapidly along trade routes through Southeast Asia. By 1895, people across the Indian subcontinent began dying in record numbers. When major outbreaks of bubonic plague reached the Middle East the following year, nervous European nations began separately to implement quarantines and sanitary measures. Trying to block the epidemic at the border was an ancient and historically ineffective tactic, but it still seemed to be the only defensive strategy available to them. Consequently, the European powers organized an international medi
cal congress in Venice in 1897 to discuss measures that might keep the scourge out of Europe. Since none of the authorities knew exactly what they should be turning away, the protocols allowed for a general scrutiny of goods and people and granted local inspectors a great deal of arbitrary discretion. Even England, a maritime trading nation that had spent the preceding fifty years trying to restrict the use of international quarantines, now ratified the Venetian protocols.'
Inside their borders, the European governments launched cleanup campaigns. Public health experts meeting in Berlin to share antiplague strategies reiterated the long-standing categorization of bubonic plague as one of the so-called filth diseases, afflictions that were thought to breed and spread in unclean conditions. Patterns of death throughout China, India, and the Middle East, after all, seemed to reconfirm that opinion, since the dirtiest cities seemed to suffer the highest death rates and people residing in the least sanitary slums of those cities contracted plague in far greater numbers than those living in cleaner neighborhoods.
European public health officials also noticed another characteristic of the epidemic of the i 89os that gave them some hope of avoiding a repetition of what happened when plague devastated their continent in the Middle Ages. Even as hundreds of thousands of Chinese, Southeast Asians, and Indians were dying, European colonial personnel living in the same areas had suffered almost no deaths from the disease. Since even experts did not yet know how plague was transmitted, they did not know that people living in neighborhoods where rats proliferated were more likely to contract the disease than people living in well-manicured areas, such as colonial compounds, or that people wearing long pants and boots, such as colonial officers, were safer from the bites of infected fleas than the urban poor, who generally wore short pants and went about barefoot. Instead, European public health officials drew a conclusion consistent with the pseudoscientific racial theories of that period: they decided that Asians were more susceptible to bubonic plague than Europeans. For that reason, the international protocols ratified at Venice permitted governments to impose separate travel restrictions on some categories of people, such as incoming immigrants from China or India, who seemed more likely to be carriers of the disease, than on other categories of people, such as upperclass whites returning from the same areas.10
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