by The Pandemic Century- One Hundred Years of Panic, Hysteria
This is a book about these events and processes, and the reasons why, despite our best efforts to predict and prepare for them, they continue to take us by surprise. Some of these epidemic histories, such as the panic over the 2014–2016 Ebola epidemic or the hysteria over AIDS in the 1980s, will be familiar to readers; others, such as the pneumonic plague outbreak that erupted in the Mexican quarter of Los Angeles in 1924, or the great “parrot fever” panic that swept the United States a few months after the Wall Street Crash, less so. Whether familiar or not, however, each of these epidemics illustrates how quickly the received medical wisdom can be overturned by the emergence of new pathogens and how, in the absence of laboratory knowledge and effective vaccines and treatment drugs, such epidemics have an unusual power to provoke panic, hysteria, and dread.
Far from banishing panic, better medical knowledge and surveillance of infectious disease can also sow new fears, making people hyperaware of epidemic threats of which they had previously been ignorant. The result is that just as lifeguards now scan the sea for dorsal fins in the hope of forewarning bathers, so the World Health Organization (WHO) routinely scans the internet for reports of unusual disease outbreaks and tests for mutations that might signal the emergence of the next pandemic virus. To some extent this hypervigilance makes sense. But the price we pay is a permanent state of anxiety about the next Big One. It’s not a question if Apocalypse will occur, we’re repeatedly told, but when. In this febrile atmosphere it is not surprising that public health experts sometimes get it wrong and press the panic button when, in reality, no panic is warranted. Or, as in the case of the West African Ebola epidemic, misread the threat entirely.
To be sure, the media plays its part in these processes—after all, nothing sells like fear—but while 24/7 cable news channels and social media help to fuel the panic, hysteria, and stigma associated with infectious disease outbreaks, journalists and bloggers are, for the most part, merely messengers. I argue that by alerting us to new sources of infection and framing particular behaviors as “risky,” it is medical science—and the science of epidemiology in particular—that is the ultimate source of these irrational and often prejudicial judgments. No one would wish to deny that better knowledge of the epidemiology and causes of infectious diseases has led to huge advances in preparedness for epidemics, or that technological advances in medicine have brought about immense improvements in health and well-being; nevertheless, we should recognize that this knowledge is constantly giving birth to new fears and anxieties.
Each epidemic canvassed in this book illustrates a different aspect of this process, showing how in each case the outbreak undermined confidence in the dominant medical and scientific paradigm, highlighting the dangers of overreliance on particular technologies at the expense of wider ecological insights into disease causation. Drawing on sociological and philosophical insights into the construction of scientific knowledge, I argue that what was “known” before the emergence event—that water towers and air conditioning systems (“Legionnaires’ disease”) don’t present a risk to hotel guests and the occupants of hospitals, that Ebola doesn’t circulate in West Africa and can’t reach a major city, that Zika is a relatively harmless mosquito-borne illness—was shown to be false; and I explain how, in each case, the epidemics would spark much retrospective soul-searching about “known knowns” and “unknown unknowns” and what scientists and public health experts should do to avoid such epistemological blind spots in the future.¶
The epidemics canvassed in this book also underline the key role played by environmental, social, and cultural factors in changing patterns of disease prevalence and emergence. Recalling Dubos’s insights into the ecology of pathogens, I argue that most cases of disease emergence can be traced to the disturbance of ecological equilibriums or alterations to the environments in which pathogens habitually reside. This is especially true of animal origin or zoonotic viruses such as Ebola, but it is also true of commensal bacteria such as streptococci, the main cause of community-acquired pneumonias. The natural host of Ebola is thought to be a fruit bat. However, though antibodies to Ebola have been found in various species of bats indigenous to Africa, live virus has never been recovered from any of them. The reason, most likely, is that as with other viruses that are adapted to their hosts as a result of long evolutionary association, the Ebola virus is quickly cleared from the bloodstream by the bat’s immune system, but not before, presumably, it has been transmitted to another bat. The result is that the virus circulates continually in bat populations, without leading to the destruction of either. A similar process occurs with pathogens that have evolved so as to infect only humans, such as measles and polio, with a first infection in childhood usually resulting in a mild illness, after which the subject recovers and enjoys lifelong immunity. However, every now and again these states of immunological balance are disrupted. This may occur naturally if, for instance, sufficient numbers of children escape infection in childhood to cause herd immunity to wane, or if the virus suddenly mutates, as occurs frequently with influenza, leading to the circulation of a new strain against which people have little or no immunity. But it can also occur when we accidentally interpose ourselves between the virus and its natural host. This is presumably what happened with Ebola in 2014 when children in Meliandou began taunting long-tailed bats roosting in a tree stump in the middle of their village. And it is thought that something very similar may have prompted the spillover of the HIV progenitor virus from chimpanzees to humans in the Congo in the 1950s. Tracing the precise genesis of these epidemics is the subject of ongoing research. In the case of AIDS, there is little doubt that the inauguration of steamship travel on the Congo River at the turn of the twentieth century and the construction of new roads and railways in the colonial period were important contributing factors, as was the greed of loggers and timber companies. However, social and cultural factors also played a part: were it not for the practice of consuming bushmeat and widespread prostitution near the camps supplying labor to the rail and timber companies, the virus would probably not have spread so widely or been amplified so rapidly. Similarly, were it not for entrenched cultural beliefs and customs in West Africa—in particular, people’s adherence to traditional burial rituals and their distrust of scientific medicine—it is unlikely that Ebola would have morphed into a major regional epidemic, let alone a global health crisis.
However, perhaps the most important insight medical history can bring is of the long association between epidemics and war. Ever since Pericles ordered Athenians to sit out the Spartan siege of their harbor city in 430 BC, wars have been seen as progenitors of deadly outbreaks of infectious disease (this was certainly the case in West Africa in 2014, where decades of civil war and armed conflict had left Liberia and Sierra Leone with weak and underresourced health systems). Though the pathogen responsible for the plague of Athens has never been identified and perhaps never will be (candidates include anthrax, smallpox, typhus, and malaria), there is little doubt that the decisive factor was the crowding of upwards of 300,000 Athenians and refugees from Attica behind the Long Walls of the Greek city. That confinement created the ideal conditions for the amplification of the virus—if virus it was—turning Athens into a charnel house (as Thucydides informs us, as there were no houses to receive the refugees from the countryside “they had to be lodged at the hot season of the year in stifling cabins, where the mortality raged without restraint”). The result was that by the third wave of the disease in 426 BC, Athens’s population had been reduced by between one-quarter and one-third.
In the case of the Athenian plague, for reasons that are unclear, the disease does not appear to have affected the Spartans, or spread far beyond the borders of Attica. But 2,000 years ago, towns and cities were more isolated and there was far less passage of people and pathogens between countries and continents. Unfortunately, this is not the case today. Thanks to global trade and travel, novel viruses and their vectors are continually crossing borders and inter
national time zones, and in each place they encounter a different mix of ecological and immunological conditions. This was nowhere more true than during World War I, when the congregation of tens of thousands of young American recruits in training camps on the eastern seaboard of the United States and their subsequent passage to and from Europe provided the ideal conditions for the deadliest outbreak of pandemic disease in history.
* The species of shark or sharks responsible for the attacks has never been identified. Some experts believe they were the work of a juvenile great white, Carcharodon carcharias; others that they are consistent with the feeding pattern of bull sharks, which are known to favor shallow coastal waters.
† An epidemic is the rapid spread of infectious disease to a large number of people in a given population within a short period of time. By contrast, a pandemic is an epidemic that has spread across a large region, for instance, multiple countries and continents. This spread may be rapid or may take many months or years. The World Health Organization defines a pandemic simply as the “worldwide spread of a new disease.”
‡ In fact, polio is spread principally via the oral-fecal route and nonparalytic polio had been endemic to the United States for several decades prior to 1916.
§ Coronoaviruses primarily infect the respiratory and gastrointestinal tracts of mammals and are thought to be the cause of up to one-third of common colds.
¶ The concepts of “known knowns” and “unknown unknowns” were infamously introduced into public discourse by the former US secretary of defense Donald Rumsfeld at a Pentagon news conference in 2002 (see endnotes for further discussion).
CHAPTER I
THE BLUE DEATH
“Ordinariness is what strikes one first about the town of Oran.”
—ALBERT CAMUS, The Plague
It was an unassuming village, much like any you would have encountered on a rural tour of New England in 1917. Blink and you might have missed it. Set in drab scrubland thirty-five miles northwest of Boston, Ayer comprised fewer than three hundred cottage-like dwellings, plus a church and a couple of stores. Indeed, were it not for the fact that the village sat at the junction of the Boston and Maine and Worcester and Nashua railroads and boasted two stations, there would have been little to recommend it. But in the spring of 1917, as America prepared to go to war and military planners began looking for suitable sites to train thousands of men responding to the draft, those railroad stations and empty fields marked Ayer out as special, unusual even. Perhaps that is why in May 1917 someone in Washington, DC stuck a pin with a red flag in a map of Lowell County, Massachusetts, and designated Ayer as the site of the cantonment of the new Seventy-Sixth Division of the US Army.
In early June leases were signed with owners of some 9,000 acres of treeless “sprout” land adjacent to the Nashua River, and two weeks later engineers arrived to transform the site into a camp fit for Major General John Pershing’s doughboys. In the space of just ten weeks, engineers constructed 1,400 buildings, installed 2,200 shower baths, and laid sixty miles of heating pipes. Measuring seven miles by two, the cantonment contained its own restaurant, bakery, theater, fourteen huts for reading and fraternizing, plus a post and telegraph office. Arriving from Ayer—a short half-mile walk that led across the tracks of the Fitchburg railroad—the first sight to greet newly drafted men was the huge YMCA auditorium and the barracks of the 301st engineers. To the right lay the barracks of the 301st, 302nd, and 303rd infantry divisions, and nearby, those for the field artillery, depot brigade, and machine-gun brigade. Beyond that lay fields for practicing drill and bayoneting skills, and an eight-hundred-bed hospital, also run by the YMCA. In all, the cantonment was capable of housing 30,000 men. But over the next few weeks, as raw recruits arrived from Maine, Rhode Island, Connecticut, New York, Minnesota, and as far south as Florida, the rough wooden barracks would be filled with in excess of 40,000 men, forcing engineers to erect tents for the overflow. In recognition of its importance to the northeastern military command, the cantonment was named Camp Devens in honor of General Charles Devens, a Boston lawyer turned Civil War commander whose Union troops were the first to occupy Richmond after its fall in 1865. As Roger Batchelder, a propagandist for the War Department, put it, admiring Camp Devens from a hill outside Ayer in December 1917, the cantonment resembled nothing so much as a “huge city of soldiers.” What the observer did not say was that Devens also represented an unprecedented immunological experiment. Never before had so many men from so many different walks of life—factory workers and farmhands, machinists and college graduates—been brought together in such numbers and forced to live cheek by jowl.
Camp Devens was not the only camp to be hastily constructed that summer, nor was it the biggest. In all, draftees destined for the American Expeditionary Force would be sent for training to forty large camps across the United States. Some, such as Camp Funston, built on the site of a former cavalry station at Fort Riley, Kansas, accommodated as many as 55,000 men. Meanwhile, on the opposite side of the Atlantic at Etaples in northern France, the British had constructed an even larger facility. Built on low-lying meadows adjoining the railway line from Boulogne to Paris, Etaples had bunks for up to 100,000 British and Imperial troops and hospital beds for 22,000. In the course of the war, it is estimated that one million soldiers passed through Etaples en route to the Somme and other battlegrounds.
Nor were the facilities at many of these camps always as good as war supporters suggested. Indeed, in many cases mobilization had been so swift that engineers had been unable to complete the construction of hospitals and other medical facilities in time, and barracks were often so drafty that men were forced to huddle around stoves in the evening to keep warm and to sleep in extra layers of clothing at night. Some, such as Batchelder, saw this as a way of toughening recruits and preparing them for the hardships of trench warfare in northern France. “At Ayer it is cold, but . . . the cold weather is exhilarating; it inures the men who have always lived in hot houses to the out-door life.” However, others criticized the War Department for selecting a site so far north, saying it would have been better if Devens had been located in the South where the weather was more hospitable.
In truth, the principal danger was not the cold so much as the overcrowding. By bringing together men from so many different immunological backgrounds and forcing them to live at close quarters for weeks on end, the mobilization greatly increased the risk of communicable diseases being spread from one to another. Wars have always been incubators of disease, of course. What was different in 1917 was the scale of the call-up and the intermixing of men raised in very different ecological settings. In urban areas, where populations are denser, the chances of being exposed to measles or common respiratory pathogens, such as Streptococcus pneumoniae and Staphylococcus aureus, is far higher and usually occurs in childhood. By contrast, in an era before cars and buses, when children raised in rural areas tended to be educated at grade schools close to their homes, many avoided exposure to measles. Nor would many have been exposed to Streptococcus pyrogenes and other hemolyticus bacteria that cause “strep throat.” The result was that as the US Army grew from 378,000 in April 1917 to a force of 1.5 million by the turn of 1918 (by the war’s end, in November 1918, the combined strength of the US Army and Navy would be 4.7 million), epidemics of measles and pneumonia erupted at camps all along the eastern seaboard, as well as in several southern states.
Prior to the introduction of antibiotics, pneumonia accounted for roughly one-quarter of all deaths in the United States. These pneumonias could be triggered by bacteria, viruses, fungi, or parasites, but by far the largest source of community-acquired outbreaks were pneumococcal bacteria (Steptococcus pneumoniae). Under the microscope these pneumococcal bacteria resemble any other streptococcus. However, one of S. pneumoniae’s unusual features is that it possesses a polysaccharide (sugar) capsule that protects it from drying out in air or being ingested by phagocytes, one of the immune system’s principal cellular defenses. In
deed, in moist sputum in a darkened room, pneumococci can survive on surfaces for up to ten days.
Worldwide, there are more than eighty subtypes of pneumococcal bacteria, each one differing from the others in terms of the constitution of its capsule. For the most part, these bacteria reside in the nose and throat without causing illness, but if a person’s immune system is impaired or compromised by another disease, such as measles or influenza, the bacteria can get the upper hand, triggering potentially fatal lung infections. Typically, such infections begin as an inflammation of the alveoli, the microscopic sacs that absorb oxygen in the lungs. As the bacteria invade the alveoli, they are pursued by leukocytes and other immune cells, as well as fluids containing proteins and enzymes. As the air sacs fill they become “consolidated” with material, making it harder for them to transfer oxygen to the blood. Usually, this consolidation appears in patches surrounding the bronchi, the passages which branch from the bronchus, the tube that carries air from the trachea into the right and left lungs. When this consolidation is localized it is known as bronchopneumonia. However, in more severe infections, this consolidation can spread across entire lobes (the right lung has three, the left two) turning the lungs into a solid, liverlike mass. The effect on lung tissue is dramatic. A healthy lung is spongy and porous and a good conductor of sound. When a doctor listens to the breathing of a healthy patient through a stethoscope he or she should hear very little. By contrast, a congested lung conducts breathing sounds to the wall of the chest, resulting in rattling or cracking sounds known as rales.