ONE
“To begin at the beginning, and I think it was the beginning,” Dr. Henry F. Long wrote in his 1898 report to the North Carolina Board of Health, “the first smallpox experience we, of Iredell, had, was when the negro Perkins made his way from Neal’s camp, on the M & M Railroad, to Charlotte.”1
Henry Long was the superintendent of health of Iredell County, an area of low ridges and valleys known for its loamy soil and its many creeks. Most of the citizens were North Carolina natives, like their mothers and fathers before them. Long himself carried on the medical practice established by his father in Statesville, an old town of wide, elm-lined streets that served as the county seat. In the past twenty years, the hum of industry had altered the rhythm of life in the Piedmont. Farming families and respectable townspeople like the Longs had had to accustom themselves to growing numbers of wage earners and outsiders. Apart from farming wheat, the people now spent their days making furniture, processing tobacco, tending textile machines, working on the railroads, and, as ever, raising families. Until the winter of 1898, most folks in Iredell County had never seen a case of smallpox. Then that, too, changed.2
Harvey Perkins was fifty-seven years old that February, when he left his home in Pelzer, South Carolina, and traveled some one hundred and fifty miles north and east to seek work on the Mocksville & Mooresville extension of the Southern Railway. He arrived, the fever already upon him, at Neal’s Camp, one of the turn-of-the-century South’s ubiquitous railroad construction camps. He spent the night in a hut with two other laborers. As Long explained, patients in the preeruptive stage of smallpox already battled their unseen foe: “The pulse is strong, full and bounding. . . . The patient is restless and distressed and when sleep is possible has frightful dreams.” When morning broke, Perkins noticed the first spots on his face. Guessing at their significance, and fearing that his new bosses would confine him in quarantine, he left camp without a word and slipped into the woods.3
All Harvey Perkins wanted was to get home to Pelzer, maybe by picking up a train in Charlotte, forty miles south of Neal’s Camp. By the time Perkins walked the twelve miles to Mooresville, in southern Iredell County, the eruption was visible to anyone who cared to look him in the face. But a sick old black man did not usually attract much notice, especially from white people. Perkins spent the night. He resumed his journey the next day. He was just two miles from Charlotte when his strength finally gave out and he “fell by the wayside.” A pair of bicyclists found him in the woods, his face and body covered with pocks. Perkins warned them not to come near. Local authorities transported him to the city pesthouse, a makeshift isolation hospital on the outskirts of Charlotte in Mecklenburg County, where Perkins discovered he was not alone. Dr. Long had not, in fact, begun at the beginning.4
Smallpox had been stalking North Carolina’s southern border for months, maybe longer. Health officials in the lower South thought the disease confined to the African American sections of a few cities and to the dispersed settlements of black farmers, laborers, and families. Since the end of slavery, the white medical profession had paid African Americans little notice and offered little aid. Within the past year or so, smallpox had broken out, seemingly without warning, in parts of Florida, Alabama, Georgia, South Carolina, Tennessee, Kentucky, and Virginia. Some white physicians and laypeople dismissed the disease as a peculiar negro malady: “Nigger itch,” they called it. But Dr. Long and other seasoned public health officials knew better. “So far the disease has been almost exclusively confined to negroes,” said the Kentucky Board of Health, in a circular titled “Warning Against Smallpox,” “but this exemption of the white race cannot long be hoped for if it continues to spread.”5
In late January, the North Carolina Board of Health issued a smallpox bulletin. The “justly dreaded disease” had crossed the state line. Wilmington, the state’s largest city, had the dubious honor of reporting the first case, in “a negro train hand of the Atlantic Coast Line whose run was into South Carolina.” Soon after, Charlotte health authorities discovered a case in a black railroad hand named William Jackson. He had recently returned from a run to Greenville, South Carolina, the very place Perkins had caught his train north. By the time Perkins arrived at the Charlotte pesthouse, there were three other people detained there. Within twenty-four hours, there would be four more. All of them were African American. Three of them were broken out with pocks, including William Jackson’s four-year-old son Frank. Jackson himself was already dead. The remaining five inmates showed no symptoms, but since they had come into contact with the others they would be detained for two weeks.6
Charlotte was in a state of turmoil. The physicians who examined the pesthouse patients disagreed about whether the cases were smallpox at all. At the request of the state authorities, Surgeon General Walter Wyman of the United States Marine-Hospital Service, the federal government’s civilian health corps, dispatched an officer to Charlotte. For Dr. Charles P. Wertenbaker, a surgeon in command of the service’s station in Wilmington, diagnosing smallpox was fast becoming a specialty. In the quasi-military argot of the corps, Wertenbaker held the rank of “passed assistant surgeon,” meaning he was a midlevel officer who had passed the service’s famously rigorous examination for promotion. He told the mayor of Charlotte that all four patients had smallpox. The quarantined inmates would almost certainly develop the disease, too. Instead of segregating suspects from patients, pesthouse officials had put suspects to work nursing the sick.7
To Wertenbaker’s eye, Perkins presented a “typical” case, in the “fifth day of the eruption.” But in an old man smallpox was especially cruel. Perkins died in the pesthouse ten days later. He was buried in a nearby woods, more than a hundred miles from home.8
The citizens of Charlotte had dodged a bullet, Wertenbaker announced in a bulletin issued by the state board of health to drum up support for vaccination. Had Perkins been stronger, “he would have come into the city; he might have stood next to any one in a crowd and infected him, he might have come in contact with one of your servants, and in this way sent the disease into your homes.”9
Dr. Henry F. Long learned the truth of these words. From the “seeds” of smallpox Perkins sowed at Mooresville arose the largest outbreak North Carolina had seen in years. An itinerant black preacher named A. B. Smoot unknowingly carried the disease from Mooresville to Statesville. More than sixty cases were eventually reported in Iredell County. It was anybody’s guess how many more people suffered, as Perkins had aimed to, in the privacy of their own homes. Dr. Long set up a hospital and detention camp in the woods outside Statesville. He hired the recovered Reverend Smoot to drive the ambulance wagon. When Long tried to organize a county-wide vaccination campaign, he ran up against fierce opposition, most of it “from the whites.” The city council gave Long power to vaccinate the citizens, with or without their consent. One state health official reflected, “The unreasoning prejudice of ignorance is extremely difficult to meet, and sometimes requires a resort to methods that are very obnoxious to Americans.”10
As the summer heat climbed into the Piedmont, the Iredell County epidemic of 1898 ran its course. But as Long put the finishing touches on his report, the fetid odor of smallpox, “insupportable and tenacious,” continued to haunt him. He was not going to escape that smell anytime soon. The North Carolina Board of Health, facing a widening epidemic in counties across the state, was about to create a full-time position for him: State Smallpox Inspector.11
The age of AIDS did not invent the notion of “Patient Zero.” Epidemics are dramatic events of cultural as well as scientific meaning, and the hunt for an outbreak’s first case has ever served needs and purposes other than those of medicine. One Alabama health officer reached all the way back to Genesis 3:15—the story of the serpent in the garden—to launch his narrative of the Greene County smallpox epidemic of 1883. The epidemic, he said, had begun with the arrival on an evening train from Birmingham of one Eliza Burke, the “colored woman ‘who brought death and all our woe.’ ”12
Narrative accounts of smallpox outbreaks—whether recounted aloud to neighbors, scratched into a letter, or prepared, like Dr. Long’s history, for a government report—rarely failed to include a few words about the first case. These sketches of suddenly infamous men and women cast flashes of light on obscure figures, most of them otherwise untraceable. The way these stories were told reveals at least as much about their tellers: their forensic certitude, their fixed ideas about race and place, and their faith that buried somewhere in the human wreckage of an epidemic lay the stuff of larger moral reckonings. The desire to begin at the beginning, with a cognizable first case, was particularly strong at a time when the actual agents of so much misery and loss—the unseen, unseeable particles of the variola virus—were so imperfectly understood.13
After the fashion of Harvey Perkins, or the minstrel actor who stayed over on All Nations Block, the alleged source of infection was typically an outsider or a marginal local figure whose work or wanderings brought him in promiscuous contact with strangers. Consider three first cases reported by county physicians to the Kentucky Board of Health during the outbreaks of 1898 and 1899: smallpox invaded Boyd County in the body of a deckhand who worked on a “steamboat plying between Pittsburgh and St. Louis”; the disease was spread around Clay County by “a young girl of bad reputation”; and it struck Lincoln County in the person of a peripatetic real estate salesman named Joseph Sowders, a white man whose taste for the “biled juice of the cereal corn” had landed him in a smallpox-ridden Catholic mission in Columbus, Ohio, before he stumbled home to Lincoln. When smallpox struck Los Angeles in the winter of 1899, infecting thirty-five people and killing seven, officials blamed unnamed “tramps or trainmen from Arizona.” In port cities from New York to San Francisco, anyone arriving by boat, especially in steerage, loomed as a potential threat. North and south of the Mason-Dixon line, itinerant African Americans were the most prime of suspects: laborers “traveling afoot,” performers in “Uncle Tom’s Cabin” shows, missionary preachers, Pullman porters, coal miners, roustabouts, even, in the case of Columbia, South Carolina, a “runaway student” from a black college.14
Other reports attributed the spread of smallpox not to a single individual but to the undifferentiated inhabitants of entire encampments of people on the move: railroad camps, mining camps, logging camps, Army camps, convict labor camps, African American revival meetings, fairs, lodging houses, and any other short-lived settlement where strangers crowded in an unfathomable mass. “The camp as a focus of disease is more potent than all others,” wrote Dr. James N. Hyde, a smallpox expert at Chicago’s Rush Medical School. In such places, Hyde argued, people who had become adapted to the particular microbial environment of their distant homes were thrown together, “under subjection,” unable to choose where or with whom they slept. “The chances of thus begetting disease are enormously multiplied.”15
The United States was not just a nation of farms, small towns, and industrial cities. For the country’s poorest working people, America was a vast archipelago of camps. Nothing did more than smallpox to reveal this rarely mentioned fact about American society at the turn of the twentieth century.
During his tenure as state smallpox inspector, Dr. Long developed his own theory about the origin of the great wave of epidemics that struck the southern states beginning sometime in 1897: it all started in a single labor camp in Mexico. A few years before the southern epidemics, Long explained, a railroad contractor from Birmingham had taken a crew of African American railroad workers across the border to do a job. They contracted smallpox in the camp there and brought the disease back home with them. From Birmingham smallpox had slowly made its way, in the bodies of itinerant black workers, to the east and north, unnoticed or at least unremarked by the white public health authorities. Maybe the narrative of the North Carolina outbreaks properly began there. 16
Epidemiological uncertainty made moral certainty easier. A common, cautionary theme pervades this accumulating archive of smallpox narratives: “The pestilence that walketh in darkness” travels unseen in the bodies of the strangers and outliers who move among us. And it is fearful indeed.17
At the end of the nineteenth century, smallpox still reigned as the most infamous and loathsome of infectious diseases. Since the 1870s, serious epidemics of smallpox had grown relatively uncommon in the United States, but that did not lessen the fears attached to the disease. Nor did the fact that Americans of the period were far more likely to fall ill or die from diphtheria, influenza, scarlet fever, typhoid fever, or consumption. Smallpox occupied a special place in the hall of human horrors. As J. N. McCormack, secretary of the Kentucky Board of Health, put it, “One case of smallpox in a tramp will create far more alarm in any community in Kentucky than a hundred cases of typhoid fever and a dozen deaths in the leading families.”18
The 1898 outbreaks coincided with the centennial commemorations of the invention of vaccination. In 1798, the English physician Edward Jenner had published his first paper on his experiments with smallpox vaccination (which he had conducted in 1796). Newspaper articles, magazine stories, and public speeches across the United States regaled Americans about the horrors of smallpox and the scientific triumph of Jennerian vaccination. In a speech to the “plain people” of Winston, North Carolina, “Colonel” A. W. Shaffer of the state board of health proclaimed that smallpox had been a “vile destroyer” since before “the first century of the Christian era.” “Great kings and royal princes, stately women of high degree and matchless beauty, and babes at the mother’s breast fell alike before its destroying blast and were disfigured and deformed for life, or thrust into the same hole with the filthy carcasses of their meanest subjects.”19
Shaffer did not exaggerate. The variola virus had been entangled with human history, to devastating effect, for millennia. No one knows when or how the virus first infected human beings. The earliest unequivocal descriptions of smallpox date to the fourth century A.D. in China, but scientists have long believed that the pustules found on the cheeks of Egyptian mummies from the twelfth century B.C. were caused by smallpox. Smallpox may have emerged as early as six thousand years ago—when the introduction of irrigated agriculture enabled human civilizations to grow large and dense enough to sustain the disease. By the time of Christ, smallpox was probably commonplace in the thickly populated valleys of the Nile and Ganges rivers, spreading from there across southwestern Asia. An inveterate camp follower, variola hitchhiked in the bodies of traders, soldiers, and other migrants. It spread east along the Burma and Silk roads and into China. In the eighth century, Islamic armies carried it through North Africa into the Iberian Peninsula. By the end of the tenth century, its expanding territory included much of southwestern Asia and the Mediterranean littoral of Africa and Europe. Many places had yet to be touched by the disease. But during the next six hundred years, smallpox became endemic in much of Europe, from whence it spread to most inhabited regions of the world. By the end of the eighteenth century, when Jenner first introduced vaccination in England, 400,000 Europeans were dying each year from smallpox.20
If the early history of smallpox remains mysterious, the origin of the variola virus itself is murkier still. The most plausible theory holds that the virus originated in a rodent, made the species leap to humans, adapted to its new host, and never went back. This much is certain: the variola virus has a special affinity for humans. Variola is one species in a larger genus of disease agents—the orthopoxviruses—that infect diverse members of the animal world. There is cowpox, monkeypox, raccoonpox, camelpox, and so on. Many of those poxviruses infect multiple species. Cowpox, for example, has naturally occurred in cows, gerbils, rats, large cats, rhinoceroses, elephants, and humans. But the natural host range for variola is decidedly more narrow. It only infects people.21
The bond between variola and humans is not merely a virological curiosity. It is a fact of epidemiological and even world-historical significance. It is perhaps the essential fact about a virus that killed at least three hundred million people during the twentieth century alone—more than all of the century’s wars. There is no animal reservoir or vector for smallpox. It cannot be transmitted by mosquitoes (as with malaria) or lice (typhus) or rat fleas (bubonic plague) or domestic animals (anthrax). Nor, for that matter, can smallpox infect people through their sewage-tainted water supplies (as does cholera) or contaminated food (typhoid fever). Smallpox can spread only from one person to another, normally through face-to-face contact.22
Smallpox is, as George W. Stoner observed in his Handbook for the Ship’s Medicine Chest (1900), a “self-limited disease.” An attack followed a distinctive clinical course for which there could be but two outcomes: smallpox either killed its victim or left the survivor immune for life. Although particles of the virus could persist for long periods in scabs on the bodies of the dead, variola did not remain in a living body after convalescence. There was no chronic recurrence, as in many herpes viruses. Smallpox survivors did not become symptomatic and infectious time and time again. They could never again get or spread the disease. This, rather than an appreciation for the poetry of the situation, was why Dr. Long hired Reverend Smoot to drive the pesthouse wagon.23
Human beings appear to be universally susceptible to the variola virus. Unless they have been made immune by a previous infection with variola or another orthopoxvirus—such as cowpox or vaccinia, the principal viruses used in vaccination—they will almost certainly develop smallpox if the virus particles enter their respiratory tracts.
Together these facts about the variola virus begin to explain the epidemiology of smallpox—its behavior in human communities. When the virus entered a population, smallpox tended to be passed around until most people had been infected. In small, relatively isolated populations, such as most towns of colonial North America, the virus would soon die out. The virus particles did not normally survive for long outside the human body, and when the ranks of vulnerable humans were exhausted, variola had no place to replicate. For smallpox to become endemic in a given population (prevalent for a long period at a relatively low level), there had to be a steady influx of susceptible bodies, whether through significant levels of in-migration or by natural reproduction. This is why in societies where endemic smallpox existed, such as European or English cities in the eighteenth century, small-pox was known as a disease of children. Most children born in London had smallpox before their seventh birthdays; the disease was a rite of passage. In English towns, nine out of ten fatal smallpox cases occurred in children under five. It was endemic smallpox that the nineteenth-century British historian Lord Thomas Macaulay famously called “the most terrible of all the ministers of death.” “The smallpox was always present,” he wrote, “filling the churchyard with corpses, tormenting with constant fear all whom it had not yet stricken, leaving on those whose lives it spared the hideous traces of its power, turning the babe into a changeling at which the mother shuddered, and making the eyes and cheeks of the betrothed maiden objects of horror to the lover.”24
Of course, the “speckled monster” earned its worldwide infamy by its horrific epidemics. Major smallpox epidemics arose in two distinct epidemiological situations. In a so-called virgin soil population, one that had never been afflicted with smallpox or had been spared the virus for many years, a single epidemic could be devastating. In 1241, the people of Iceland had such an encounter with variola: some twenty thousand of the island’s seventy thousand people died. The experience of indigenous populations of the Americas with epidemics of smallpox after the arrival of the Europeans in 1492 is well known if not easily fathomed. Many factors may have contributed to the extraordinarily high susceptibility of sixteenth-century American Indians to smallpox, including malnutrition, dislocation, and poverty—problems caused or exacerbated by the violent process of European colonization. But the likelihood that American Indians and their ancestors had no previous contact with the disease helps explain mortality rates that ran from 50 to 80 percent. Variola was the deadliest killer in a terrible onslaught of alien microorganisms that, by some historical estimates, may have decimated as much as 90 percent of the precontact population of the Americas.25
A different sort of epidemic occurred in well-populated places where smallpox was more or less always present, such as parts of late eighteenth-century Europe and England. The number of susceptible individuals in a community gradually built up over time, creating fodder for an “epidemic year,” when smallpox became suddenly widespread and lethal. In this situation, where a majority of the adult population, including most of the breadwinners, was immune from previous infection, an epidemic could cause untold misery without seriously threatening the population’s subsistence. 26
As with many infectious diseases, the incidence of smallpox rose and fell with the seasons. Climate, social factors, and the traits of the virus itself conspired to make smallpox a disease of the winter and spring. Variola remained viable longer at cooler temperatures. And the tendency of humans to crowd together indoors during the winter months made the virus’s journey from person to person a short one.
Turn-of-the-century medical experts, well versed in the germ theory, assumed that some life form, invisible to the naked eye, caused smallpox. But they could only guess at its nature. “The contagious principle, probably a microbe, has not been discovered,” declared an authoritative 1899 pamphlet, prepared by Marine-Hospital Service scientists for Surgeon General Wyman. Since the introduction of the germ theory, European and American scientists had hunted for the disease agent under their microscopes. A few reported seeing traces of smallpox “germs.” Orthopoxviruses are among the largest known viruses, but they are still extremely small. According to one modern writer, it would take three million of them, laid out in rows, to pave over a standard typographic period. An actual sighting would not be possible until the invention of the electron microscope in the 1930s. In 1947 Canadian and American scientists finally viewed the particles, or virions, of variola.27
Since that time, variola virions have often been called bricks, because of their shape: a three-dimensional rectangle with slightly rounded edges. The name fits for other reasons as well. Each virion is made up of a combination of a hundred different proteins, which interlock in a structure so durable that it enables the virions to survive for a time in the open air. The knobby protein exterior of each brick protects the genetic jewel within: a molecule of double-stranded DNA. By attaching itself to and then penetrating a susceptible cell, usually in the mucous membranes of the throat or lungs, a single virion has the power to trigger an unstoppable process of genetic replication that can turn a healthy person into a corpse.28
For all of its mysteries, the clinical features of smallpox were fairly well understood in January 1899, when Surgeon General Wyman issued his “Précis upon the Diagnosis and Treatment of Smallpox.” The timing was significant. The disease was invading communities, mostly in the South, where neither the laypeople nor the physicians had seen a bona fide case of smallpox in many years, if ever. The “Précis” was, in no small measure, a political document. Wyman aimed to remind people of the necessity of vaccination, to shore up confidence in the nation’s vaccine supply, to clarify the national government’s limited responsibilities, and to spur the fiscally conservative local and state governments to take action.29
Wyman’s officers in the Marine-Hospital Service disseminated the “Précis” widely, especially in the South. The report reflected state-of-the-art American medical knowledge about smallpox. Wyman’s description of the clinical course of smallpox squares with descriptions of the disease found in medical treatises and journals from the period, as well as the accounts of local cases written by physicians such as Dr. Henry Long. The vast scientific literature on smallpox produced since that time has generally confirmed that clinical picture, while shedding new light on the virological and pathological processes that underlay the disease. Unlike the vast majority of physicians alive today, these turn-of-the-century experts had firsthand experience with smallpox. For them smallpox was not a frozen stockpile preserved, like ancient DNA sealed in amber, in a carefully guarded government laboratory vault and read about in medical journals. For them small-pox was still a part of the known world.30
Perhaps the most significant misunderstanding about smallpox shared by the authors of the “Précis” and many of their scientific contemporaries had to do with the mechanics of disease transmission. They understood correctly that smallpox could be spread by the passage of “the microbe” from one person’s respiratory system to another’s. In fact, a person suffering from smallpox shed virions in each droplet of saliva. A single breath, cough, laugh, sigh, or spoken word was enough to launch the virions into the air. When one or more particles touched down upon the mucous membrane of another person’s mouth, nose, throat, or lungs, the process of viral replication began within hours.
Where the “Précis” went wrong was in its insistence that such face-to-face contacts constituted a lesser threat than did the scabs and crusts of dried pus that fell from the skin of a convalescent patient. “The contagion is tenacious,” the “Précis” stated, “and may be conveyed by persons and by fomites, such as hair, clothing, paper, letters, furniture, etc., or it may be spread through the air by means of the wind blowing the dust containing the virus.” This belief in the infectious power of “fomites,” contaminated objects of countless variety, led to the conclusion that smallpox was what nineteenth-century sanitarians called a “filth disease”—dangerous to all but spread chiefly by the lower orders. As the “Précis” put it, smallpox was “more common among the colored races, probably on account of their condition of living in small, crowded rooms, with slight regard for cleanliness.”31
The “Précis” got the infective nature of variola about half-right. The crowded sleeping quarters that the world’s poorest people called home—be it a sharecropping family’s one-room cabin or a bamboo hut—were prime variola territory. It surprised no one when, two weeks after Harvey Perkins shared a hut with two other workers at Neal’s Camp, reports reached Charlotte that two cases of smallpox had broken out in the encampment. There were obvious obstacles to maintaining personal hygiene and health under such circumstances. Still, scientists now believe that “filth” had little to do with the spread of smallpox. Laboratory tests have shown that the virions in smallpox scabs can, under optimal conditions, retain their infectivity for years. But the virions are so tightly bound within the hard fibrin mesh of the scab that it takes heavy grinding to release them. For this reason, many experts have concluded that fomites were “relatively unimportant” transmitters of infection, compared with the spread of virions in sneezes and coughs. This does not mean that infection by fomites never occurred—contaminated bed linen, in particular, readily transmitted infection—but the long-standing association of smallpox with the filthy poor was grounded more in class and racial bias than in medical reality.32
Once the first virion penetrated the first cell in a person’s respiratory tract, the incubation period began. During this period, most people presented no symptoms—perhaps a little malaise or gastric discomfort. Meanwhile, the variola bricks silently but explosively replicated and spread in the host’s lymph nodes, spleen, and bone marrow. Over time, the virions piling up in the patient’s cells would number in the quadrillions. The incubation normally lasted from ten to fourteen days. The “Précis” gave twelve days as the norm. Such medical facts determined the politics of smallpox control. Conservative health officials enforced two weeks as the term a smallpox “suspect,” showing no symptoms, could be held against her will in a quarantined house or detention camp.33
When the symptoms finally came, they struck with such unexpected force that the “Précis” called the onset the “Invasion.” The patient felt a sudden chill, followed by severe pain in the loins and lower back, a splitting headache, and a high fever, in some cases surging to 106 degrees F. The pulse raced. Many patients vomited. The tongue grew thick with a brown coating; the appetite vanished, but the thirst was unquenchable. Some adults grew delirious. Some children were rocked by convulsions.34
In this early phase, as Dr. Long learned while attending to patients in the Iredell County pesthouse, smallpox remained inscrutable even to the trained medical eye. It could be typhoid fever, malaria, la grippe, or dengue. For the patient, these feverish days felt like a bad case of the flu, and some managed to carry on with their work. President Abraham Lincoln is believed to have been fighting the preeruptive fever of smallpox when he delivered the Gettysburg Address on November 19, 1863. One listener described the president’s appearance as “sad, mournful, almost haggard.” The rash appeared two days later.35
Smallpox patient from the Cleveland epidemic of 1901–03. This photograph was taken by Dr. Homer J. Hartzell, who headed the city’s smallpox hospital. COURTESY OF THE DITTRICK MEDICAL HISTORY CENTER, CASE WESTERN RESERVE UNIVERSITY
In a typical case, the fever fell by the second or third day. The constitutional symptoms abated. The patient felt better. So much so, a nineteenth-century nurse’s manual noted, that he might “suppose himself convalescent.” Unknown to the patient, the lesions had already begun rising, about twenty-four hours earlier, on the mucous surfaces of the mouth, the back of the throat, and more generally throughout the alimentary and respiratory tracts. Modern virologists call this eruption the “enanthem.” The enanthem turned the patient into a veritable mist machine of infection. The lesions evolved rapidly and broke down within two or three days, releasing virions in vast quantities into the saliva. For the next week or more, the patient’s every breath might launch a fusillade of invisible infective particles into the air. Although the patient could remain infectious for weeks, twentieth-century studies concluded that smallpox sufferers were most likely to infect others during the first week of their skin rash.36
From the perspective of the patient, and the turn-of-the-century physician, the true horror—and the real danger—of smallpox resided on the outside of the body, in a rash so spectacular and explosive it was universally called “the eruption.” It was the eruption that ancient commentators had described, and that peoples around the globe had painted, with pointillist precision, on the images and figurines of smallpox sufferers. It was the eruption that had caused a medieval bishop to give the disease its Latin name, variola, meaning “spotted.” (In England, the disease was known simply as “the pox” until the late fifteenth century, when the term “smallpox” was adopted to distinguish it from syphilis, the “great pox,” or the French pox.) For physicians working at the turn of the twentieth century, it was still the eruption, above all else, that defined and signified smallpox.37
The eruption appeared on the skin just as the fever broke, caused by the infection of the epidermal cells. The rash appeared first as small red dots (called macules) on the forehead and scalp, and often around the mouth and the wrists. Patients often got a “worried face,” a disturbing contraction of the facial muscles that some experienced doctors recognized as a diagnostic sign of smallpox. Within twenty-four hours the lesions spread over the body. They appeared so rapidly that even the most attentive patients found it difficult to track the order of their appearance. In the worst cases it would become difficult to distinguish the rash from the skin, but smallpox was, in its way, an orderly disease. It distributed itself in a characteristic centrifugal pattern that distinguished it from other skin diseases: it was most dense on the face, hands, and feet, though it also covered broad areas of the chest, back, trunk, arms, legs, and genitals.38
Over the next two weeks, the lesions followed a well-known clinical course. Wyman’s “Précis” ticked off the stages: “macule, papule, vesicle, and pustule, ending in desiccation and desquamation.” By the second day of the rash, a small raised bump (the papule) formed atop each red macule, rising just above the skin as the papule filled with fluid. Physicians described the papules as “shotty,” because they could be rolled between thumb and forefinger, as if shot from the blast of a hunter’s gun had become embedded under the skin.39
In a few more days, the papules evolved into vesicles, blisters with navellike depressions in their centers. (Physicians called the vesicles at this stage “umbilicated.”) The depressions gradually rounded out as the vesicles became filled with a pressurized fluid that started opalescent and gradually turned opaque. When that process was completed, after a few days, the lesions were called pustules. The puffy pustules had a yellowish gray color encircled by a red border. They reached their full size, like blood-engorged dog ticks, by the tenth day of the eruption. In the most common form of smallpox cases, the rash remained “discrete”: normal skin could still be seen between the lesions. But in more severe, “confluent” cases, there were so many pustules that they fused together, especially on the face. Dr. Long found it “almost impossible to paint a pen-picture” of the “terrible faces” of confluent patients.40
Throughout the eruption, the patient suffered. As if to trumpet the ascendance of the pustules, the fever returned, as did many of the symptoms that had attended the fever the first time around. By this time, the patient’s face was normally swollen and disfigured, the hands puffy and aching, the skin inflamed. Ulcers burned the mouth and throat, growing so large in some cases that the patient had the sensation of suffocating.
Stoner’s Handbook for the Ship’s Medicine Chest offered a concise description of the final clinical stages of smallpox, which occurred by the end of the eruption’s second week. First came the desiccation: “The pustules break, matter oozes out, crusts form, first on the face and then over other parts of the body following the order of the appearance of the eruption.” The secondary fever gradually abated. Then came the desquamation, or scaling off: “The crusts rapidly dry and fall off, leaving red spots on the skin.” This could take two or more incredibly itchy weeks. Given the reigning scientific beliefs, all scabs and crusts had to be carefully collected and incinerated.41
From the onset of fever to the separation of the scabs, smallpox typically lasted three to four weeks—though sometimes much longer. Throughout, there was not much an attending nurse or physician could do but try to ease the suffering. “As regards treatment, there is little to say,” wrote Dr. Long. Cold compresses and cool drinks for the fevers. Morphine for the back pain. Vaseline ointments for the exfoliating scabs. A few ounces of whiskey sometimes bought the patient a moment’s peace. Dr. Llewellyn Eliot, who ran the District of Columbia Smallpox Hospital during the winter epidemic of 1894–5, said he tried every treatment regimen he could think of: “the expectant, the bitartrate of potash, the salicylic acid, the antiseptic, and, finally, the do-nothing.” Still, good nursing care could make all the difference. As late as the 1970s, studies showed that in developing countries, where hospital facilities were typically “poor” and “grossly overcrowded” (a fair description of most American smallpox hospitals circa 1900), smallpox patients cared for by devoted family members, in their own homes and villages, had a higher chance of survival .42
In a run-of-the-mill case of smallpox, as it had been known from time immemorial until the twentieth century, the sufferer had about a one-in-four chance of dying from the disease: a case-fatality rate, in epidemiological parlance, of 25 percent. Beneath this historical average lay wide variation, caused by differences in viral strains and the particular susceptibilities and immune responses of different individuals and groups. In cases of discrete smallpox, the case-fatality rate could be as low as 10 percent; in confluent cases, it could run to 60 percent or higher. Age also affected the prognosis. Mortality was highest in infants, lowest for young children, and from there it tended to rise with age. Smallpox was especially severe in pregnant women. It often caused miscarriages or stillbirths, and fetuses could be infected in utero.43
Some outbreaks were so sudden and severe as to defy comprehension. In March 1900, the Atlanta Constitution reported that the small community of Jonesville, Mississippi, was “honeycombed with smallpox of the most virulent and loathsome form.” The case-fatality rate was 75 percent. Nearly one hundred people died. Entire families perished. It all happened so fast that city officials could do little more than order coffins .44
When death came, it usually occurred around the tenth or eleventh day of the disease. Scientists still do not know exactly how smallpox killed. By the tenth day, the variola bricks had piled up in cells throughout the body, including many of the vital organs. Still, the disease did not normally destroy the organs. The slow, painful death from smallpox was usually caused by severe viral toxemia—a generalized poisoning of the body. In the final moments, most patients suffered respiratory failure.45
It could be worse. Discrete and confluent smallpox were subtypes of “variola vera,” or true smallpox. (“Ordinary type” is the preferred term today.) In a small percentage of cases, smallpox presented in far more severe forms. If a particularly virulent strain of the virus met with an extremely weak immune response at the cellular level, as sometimes occurred in children, the lesions remained flat, turned black or purple, and were said to feel “soft and velvety to the touch.” The patient’s body looked charred. This form of smallpox (now called “flat type”) was almost invariably fatal. Rarer still, and almost always fatal, were the various forms of “hemorrhagic” or “black smallpox,” in which the virus caused explosive bleeding. Through it all, patients suffering from hemorrhagic smallpox were said to exhibit “a peculiar state of apprehension and mental alertness.” They seemed to know exactly what was happening to them.46
The best thing to be said about smallpox was this: when the disease was done with a person, it was done. The virions did not persist in the body. Smallpox survivors were forever immune. In most cases of variola vera, though, the skin never fully recovered. From 65 to 80 percent of patients bore deep scars on their faces, the pitted “pockmarks” that made smallpox unforgettable.
During the Cleveland smallpox epidemic of 1901–3, in which 266 people died, Dr. William T. Corlett, a professor of dermatology and syphilology at Western Reserve University medical school, kept a photographic record of patients in the smallpox hospital. After poring over Dr. Corlett’s photos of patients—their cobblestoned faces, their blistered nakedness, the distant stares of those who can open their eyes—it should come as a relief to find one of a fully recovered man. It does not. He could be thirty. Or forty-five. He wears a heavy woolen suit, with a gold watch pin at the top buttonhole of his vest. He stands erect, chin up, his body squared off to the camera. But his face is just a few degrees askew, as if he can’t quite look the camera in the eye. His forehead, cheeks, nose, and chin are a dermatological rubble. The survivor’s proud, clamped mouth carries the weight of the photograph. But the unforgiving eyes command the viewer’s attention.47
The scars of smallpox might fade with time, but they never went away. In the patent medicine marketplace of early twentieth-century America, unscrupulous purveyors touted newfangled procedures and ointments which, they promised, would make pockmarks disappear. In the same newspapers where the patent hucksters hawked their wares, the police blotters printed notices about wanted criminals. On any given day, the reader might be advised to keep an eye out for any number of physical markers in the hustle of the urban crowd—one suspect’s height, another’s build, yet another’s race. But one trait in particular—the smallpox marks tattooed indelibly on the suspect’s face—told the vigilant reader that the fugitive had a history of escaping tight situations.48
Dr. William T. Corlett of Cleveland’s Western Reserve University took this photograph of a recovered smallpox patient. The scars were permanent. COURTESY OF THE DITTRICK MEDICAL HISTORY CENTER, CASE WESTERN RESERVE UNIVERSITY
Not all “germs” are alike. Bacteria, which are much larger than viruses, are single-celled microorganisms, capable of reproducing on their own and metabolizing nutrition. Since the advent of penicillin in the 1940s, scientists and pharmaceutical companies have developed a widening range of antibiotics that work by killing or inhibiting the life-sustaining activities of various disease-causing microorganisms. Viruses are impervious to antibiotics. They are difficult to kill because they are not exactly alive. A virion is essentially an inert package of genetic information, encased in proteins. It can only replicate when it penetrates a vulnerable host cell. At that point, the virion sheds some of its protective layer and begins to convert the cell into a virion factory. The best way to help a human body beat a virus like variola is to teach the cells to recognize the virions and to respond quickly with a powerful immune response. For some viral diseases physicians artificially immunize patients by exposing their bodies to an inactivated (“killed”) or attenuated (“live” but weakened) form of the virus; for other diseases, a related virus does the trick. When preventive immunization works, the body reacts to an invasion of virus with an immune response that will prevent infection, or at least reduce the damage the virions can do.
We know all of this because of the exponential growth of scientific knowledge that has occurred since the introduction of the germ theory of disease during the second half of the nineteenth century. In the 1860s and 1870s, laboratory pioneers such as the French chemist Louis Pasteur and the German physician Robert Koch marshaled increasing evidence behind an idea that we now take for granted. Overthrowing long-held medical beliefs, the new theory proposed that contagious and infectious diseases arose neither from the grossly deficient “constitutions” of their sufferers nor from atmospheric “miasmas” arising from stagnant water; rather, specific diseases were caused by particular microorganisms. From the late 1870s into the early twentieth century, laboratory scientists identified one pathogenic “microbe” after another (including the bacteria that caused cholera, consumption, gonorrhea, and typhoid). As scientific knowledge of bacteria, viruses, and other “germs” accumulated, so did understanding of the mechanisms and pathways by which those germs circulated across populations: contaminated food and water, casual contacts, insect vectors, and so on. From these new understandings of the etiology of infectious diseases arose new strategies for policing them. To the ancient practices of isolation and quarantine were added antispitting ordinances, food and milk regulations, and a growing arsenal of vaccines, antitoxins, and serums. In the United States, where many physicians had been slow to embrace the germ theory (and laypeople had been slower still), health officials of the local, state, and federal governments approached the twentieth century with a greatly enlarged sense of their duties and powers.49
The history of smallpox vaccination has a special but curious relationship to this scientific revolution. Smallpox was the granddaddy of infectious diseases: the deadliest scourge in recorded history and the one upon which the field of immunology was founded. Smallpox variolation (using live variola virus) and vaccination (using the live viruses of cowpox or vaccinia) were the oldest practices of preventive immunization. In fact, they were practiced long before the germ theory took shape. Both techniques had been developed without the benefit of microscopes and laboratory smears, through experiments based upon everyday observations about the disease. Pasteur himself saluted this lineage when he proposed, in 1881, that the term “vaccination” be universalized to apply to preventive inoculation with other infectious agents.50
Variolation was practiced in China and India as early as the tenth century. It probably originated in the commonplace observation that people with pockmarks never contracted smallpox. The practice entailed introducing a small amount of material from the pustules or scabs of a smallpox patient into the body of a healthy person. In China, the common method was nasal insufflation: scabs were ground into a fine powder and then snorted. In India, the pus material was inserted into the skin. Variolation normally produced a mild attack of smallpox, followed by long-lasting immunity. The practice spread far and wide from its Asian (and perhaps African) origins. By the early eighteenth century, variolation spread into Europe from the Balkans and from Turkey into England. Called “inoculating the smallpox” or simply “inoculation” by the English, it grew increasingly common in Britain and the colonies—especially when epidemics threatened. In the terrible Boston epidemic of 1720–21, Reverend Cotton Mather and Dr. Zabdiel Boylston caused a public firestorm by promoting inoculation. In 1777, as North American smallpox epidemics took more than 100,000 lives, General George Washington ordered the compulsory variolation of all new recruits into the Continental Army. The wide adoption of variolation during the eighteenth century is perhaps all the evidence one needs of the severity of smallpox, for the practice carried serious risks. The artificially induced attack was not always mild: as many as one in fifty died. Even worse, during the infection the inoculated person could infect others with full-blown smallpox.51
Vaccination descended directly from variolation, and it came about in much the same way. In the late eighteenth century, it was a commonplace observation among the country people of smallpox-ridden parts of England and Europe that milk hands and milkmaids rarely had pockmarks. An English country doctor named Edward Jenner, who had himself suffered a harsh bout of smallpox following his childhood inoculation, had trouble persuading dairy workers to take the pox. The workers, Jenner later explained, had the “vague opinion” that they had been protected by their exposure to diseased cows. Some of the workers had pocklike ulcers on their hands, gotten by milking cows whose teats were broken out with cow-pox. From one such ulcer, on the hand of a milkmaid named Sarah Nelmes, Jenner extracted the pus that he inserted, just beneath the surface of the skin, on the arm of a young servant named James Phipps on May 14, 1796. Jenner later repeated the experiment on several other children. After several months, he inoculated the children with smallpox. In every case, it failed to take. The children’s bodies resisted the variola virus. Vaccination, which takes its name from the Latin word for cow, was born. The new technique had neither of the limitations of variolation: it did not give people smallpox, and it did not cause them to spread it either.52
When Jenner published his first results in a 1798 paper, his claims bred skepticism and controversy among medical men and laypeople. An English political cartoon from the period depicts a gaggle of country bumpkins lined up to get jabbed in the arm by the bewigged Dr. Jenner. The right half of the frame is a riotous scene filled with men and women who have already taken the vaccine. Horns, hooves, and entire cows spring forth from their arms, faces, and rear ends. The cartoon is titled, “Cow Pock—or—the Wonderful Effects of the New Inoculation!” Despite opposition, vaccination spread far and wide with remarkable speed. Jenner estimated that within three years, 100,000 people had been vaccinated in England. By that time, Professor Benjamin Waterhouse of Harvard University had brought vaccination to the United States.53
More than half a century before the germ theory, then, the fundamentals of preventive immunization were in place. And yet at the turn of the twentieth century, smallpox remained full of mystery. The causative agent had not been identified, the process of human transmission was imperfectly understood, and the exact nature and biological effects of the vaccine strains in circulation were largely matters of conjecture and debate. What scientists and physicians could say for certain, based upon a century of medical experience, was that vaccination worked. Wyman’s “Précis” summed up the medical consensus: “The most efficient means for preventing the spread of smallpox is by vaccination. The protection, provided the [vaccine] virus is pure, is believed to be as complete against contagion as is that of smallpox against a second attack.” Unlike a bout with actual smallpox, the authors cautioned, vaccination conferred only a temporary immunity, perhaps five years or more. Accordingly, the “Précis” advised that communities encourage revaccination, whenever smallpox became prevalent, to “continue this protection indefinitely.”54
In the best scenario, vaccination prevented a person exposed to smallpox from getting the disease at all. Even when a previously vaccinated person did contract the disease, the vaccination accelerated the clinical course of smallpox, producing a milder form of the disease called “varioloid.” The patient remained infectious until recovered: “The most virulent form of smallpox may rise from exposure to varioloid,” the “Précis” warned. But fatalities were rare and pockmarks uncommon. Physicians found that if they vaccinated a person infected with smallpox during the first five or six days of the incubation period, the patient would normally suffer a mild case of the disease.55
Despite the power of this revolutionary scientific technology, England and America did not rush to embrace compulsion. Some European governments established compulsory vaccination of infants in the first decades of the early nineteenth century: Bavaria in 1807, Denmark in 1810, Norway in 1811, Bohemia and Russia in 1812, Sweden in 1816, and Hanover in 1821. But England, the birthplace of Jennerian vaccination, did not enact its first compulsory measure until 1853. It applied only to children.56 Until the mid-nineteenth century, the thorny legal question regarding vaccination in the United States concerned the right of local communities to use tax money to provide free vaccination for the poor. Things began to shift after England adopted compulsion. In 1855, Massachusetts became the first American state to require public schoolchildren to get vaccinated. Between the end of the Civil War and the turn of the twentieth century, public officials and lawmakers gradually built a legal regime of compulsory vaccination in America. By the 1890s, that regime included federal inspection of immigrants at the nation’s borders, some form of compulsory vaccination for public schoolchildren in most states, and general vaccination orders issued by county courts, city councils, and local boards of health during epidemics.57
Sol Ettinge, “Vaccinating the Poor.” The engraving pictures a New York City police station house during the 1872 smallpox epidemic. From Harper’s Weekly, March 16, 1872. COURTESY ROBERT D. FARBER UNIVERSITY ARCHIVES AND SPECIAL COLLECTIONS DEPARTMENT, BRANDEIS UNIVERSITY
For Surgeon General Wyman, the case for compulsion was simple: it worked. He reminded Americans of the lesson of the Franco-Prussian War of 1870–71. As the French and Prussian armies collided, the war unleashed a pandemic of smallpox that killed more than half a million people in Europe, including some 143,000 German civilians. Both France and Prussia had poorly vaccinated civilian populations. But the armies differed dramatically. The thoroughly vaccinated Prussian army, 800,000 men strong, suffered only 8,463 cases of smallpox and just 457 deaths (a case-fatality rate of 5.4 percent). The smaller, sparsely vaccinated French army counted 125,000 cases and 23,375 deaths (18.7 percent). After the war, many European countries enacted new legislation compelling vaccination (and in some places subsequent revaccination) as a basic duty of citizenship.58
As epidemics broke out in the United States during the next few years, American state and local governments responded with measures of their own. Again, the German example proved irresistible. By an 1874 law, the unified German state required all citizens to submit to vaccination and revaccination. In 1899 the disease took only 116 lives in Germany, a nation of 50 million people. For Wyman, the success of vaccination imposed a clear moral responsibility upon American citizens and their governments. “Smallpox is a disease so easily prevented by vaccination that the smallpox patient of to-day is scarcely deserving of sympathy,” he wrote in December 1899, as the wave of epidemics that had begun in the South moved across the country.59
But vaccination carried its own well-known health risks, and compulsory measures clashed with medical beliefs, religious tenets, the rights of parents, and dearly held notions of personal liberty. As nations tightened their smallpox vaccination laws in the late nineteenth century, those efforts ran up against strong, even violent, antivaccination movements, in the metropoles and in their overseas colonies. Antivaccination riots rocked Leicester, Montreal, and Rio de Janeiro. Since the 1870s American antivaccination leagues had challenged compulsory measures in the statehouses; after 1890, they began turning to the courts as well. Across the United States, citizens resisted public health authority by burning down pesthouses built in their neighborhoods, running away from vaccinators, fighting with police, forging vaccination certificates, or, perhaps most commonly, by quietly taking care of their sick loved ones in their own homes, instead of surrendering them to the authorities.60
American supporters of compulsory vaccination—including public health officials, the rising professional class of physicians, and the editorial writers for major newspapers such as The New York Times—often dismissed the opposition as an insignificant coterie of “imbecile cranks” who had fallen under the spell of foreign ideas. But the opposition was far more broad and complicated than that. It did not arise solely from a transatlantic critique of modern state medicine. Nor did it spring, fully formed, from American traditions of rugged individualism and constitutional liberty. The turn-of-the-century epidemics in particular would reveal that opposition to government-mandated smallpox vaccination grew up in the same soil from which had sprung compulsion itself: the conflict-laden realm of everyday social and political life in local communities.61
The variola virus itself played no small role in the vaccination controversies that embroiled communities across the United States. As reports of outbreaks reached Washington from communities across the South during 1898 and 1899, many local physicians, public health officers, and political leaders commented that smallpox did not seem its old self. And the more people smallpox struck, the bigger the “kick” the public put up against vaccination. 62
Dr. Henry F. Long was one of the first southern medical men to report on this unprecedented new situation. Harvey Perkins had died as expected. But something peculiar happened to the sixty-two others who landed in Dr. Long’s pesthouse during the months after Perkins made his long walk through the woods of Iredell County: every last one of them survived.