PROLOGUE
A House Boarded Shut
The flies had been swarming around the house for days. As he walked the exterior, he tried to peer into the boarded windows where flies crawled through starbursts of broken glass. Shielding his eyes with cupped hands, he could not see anything through the black splinters of darkness but a gray, dim light. He had no name, at least not one that survived in the family records; he was an old slave who continued to live with the Angevine family as a servant long after he had been legally freed. The family owned a 4,000-acre farm outside of Grenada, Mississippi, where Mrs. Angevine had been born and raised before marrying a New York attorney and moving to Memphis. A graduate of Harvard Law, Mr. Angevine worked in the Memphis offices of Harris, McKissick and Turley. When the Civil War broke out, he fought for the South against his brothers fighting for the North.
The family left Memphis and boarded themselves inside of the plantation house when the 1878 yellow fever epidemic struck. The measure may have seemed drastic to others, but Mr. Angevine understood the toll of yellow fever better than most; his wife had died of the fever the previous summer.
As far as the servant could see, the front door was locked, and the flies seemed to have the only access to the house. He pried open the shutters and broke the glass, letting loose a plume of repugnant air. In the stale, dark rooms he saw the corpses of the Angevine family, many in advanced stages of decomposition. Even in the darkness, he could see their yellow skin, the color of unpolished brass. Mary Louisa, the eldest, had been the first to go, and five others had followed. Mr. Angevine lay dead among his children.
No one can really imagine those final days in the fever-ridden house. The fever attacked each person in the Angevine family, one after the other, until none were well enough to help the others. It hit suddenly in the form of a piercing headache and painful sensitivity to light, like looking into a white sun. At that point, the patient could still hope that it was not yellow fever, maybe just a headache from the heat. But the pain worsened, crippling movement and burning the skin. The fever rose to 104, maybe 105 degrees, and bones felt as though they had been cracked. The kidneys stopped functioning, poisoning the body. Abdominal cramps began in the final days of illness as the patient vomited black blood brought on by internal hemorrhaging. The victim became a palate of hideous color: Red blood ran from the gums, eyes and nose. The tongue swelled, turning purple. Black vomit roiled. And the skin grew a deep gold, the whites of the eyes turning brilliant yellow.
The servant climbed through the window and made his way through the rooms where other servants and guests had died. Finally, he found a body not yet rotting; it was the youngest daughter, nine-year-old Lena. He knelt down, brushing away flies and maggots. Lifting her weightless frame, he carried her out of the family mansion that had now become a tomb, into the fresh air. He placed her body in a nearby house, resting a piece of raw bacon across her lips, and watched as Lena began to suck on the first bite of food she had had in days. It was then that Lena, more dead than alive, began to make her way back.
In the coming weeks, she would recover and tell of the horrors trapped inside of the house. Men from the countryside came into the city, robbing the dead and stepping over the bodies of the dying. “My own father, while ill with the fever, was choked, robbed and left alone to die: I was too ill to even cry out for help, but witnessed the entire affair.”
With no surviving family, Lena went to live with her grandparents in Memphis to attend St. Mary’s School. After graduation, and against the wishes of her grandparents, she enrolled in a nursing school at the Maury and Mitchell Infirmary, where she worked under the tutelage of Dr. Robert Wood Mitchell.
The remainder of Lena Angevine’s time in the South was a patchwork of nursing, ambition and marriage to a St. Louis man by the name of E. C. Warner. Warner, whose name Lena Angevine would take from that point forward, died of a heart attack just four months after the marriage. At least that was the generally accepted story; family rumors also alluded to a divorce. As it was far better to be a widow than a divorcée in the 1890s, Lena Warner would naturally opt for a dead husband over an estranged one.
Lena Angevine Warner’s experience with yellow fever would continue to sear her, and in 1898, with the outbreak of the Spanish-American War, she answered an ad in the newspaper. The surgeon general of the United States Army was looking for nurses immune to yellow fever. Warner would receive fifty dollars per month, and in 1900, she was stationed in Cuba as chief nurse under a doctor of some distinction, Major Walter Reed.
PART ONE
Plague: A widespread affliction or calamity, especially one seen as divine retribution.
—The American Heritage Dictionary
The rain came in West Africa. A massive wind blew in from the Atlantic coast bringing the deluge of water known as the southwest monsoon. It swelled the Niger and Benue rivers; it spilled into the braided streams of the Niger Delta; it filled the flood-plains and swamplands of southeastern Nigeria. It purpled the sky and saturated the country.
Towering oil palms dripped water from their feathered branches, and the brush-marked trunks of rubber trees were streaked with rain. The broad, bush-topped cocoa trees moistened. And the forests of Nigeria grew heavy and humid. Water is nourishing, and it enriched the plant life emerging from West Africa’s dry season. It also nourished something else—dry, oval-shaped eggs clinging to life inside the hollows of trees. Once the rain fell, those eggs grew, and soon, mosquitoes hatched. In the natural world, a string of events had been set into motion.
The rains falling in Africa did not deter men from entering the forest and felling trees for timber. As the trees fell, their canopy of dense green fell with them, often bringing a swarm of gnats and mosquitoes with it. Some of those mosquitoes would bite.
The native Africans who worked the forests noticed an eerie silence in the trees. Usually alive with the piercing sound of birds, the hum of insects and the calls of monkeys, tree canopies in some areas were still, a haunting contrast to the living, breathing rain forest—a sign that something was not right in the ecosystem. The monkeys had grown ill, their shrill chatter quieted. Unknown to the men, the rain forest, teeming with smells, sounds, color and life, was also home to something much smaller. Microscopic. A tiny, thriving life-form.
No one knows for sure how the yellow fever virus first came into existence. No records of it in early history exist, nor is it among the biblical plagues. But then, how does any new life emerge? There is a creation and a birth and eventually a discovery in the dark forests of Africa.
A virus is one of the smallest beings in evolution’s survival of the fittest, mutating and coalescing in order to thrive, its ultimate goal being epidemic. Viruses affect nearly every life-form on earth from flora to fauna, but a virus in its own right is not actually alive—it only becomes alive by possessing something living. The virus seeks out a healthy cell, overtakes it, impregnating it, forcing the body’s cells to produce thousands of the new offspring. This rapacious battle will eventually allow the virus, something as small as one-ten-thousandth of a millimeter, to conquer something the size of a human.
It is uncertain whether viruses evolved from a single cell, becoming more complex, or whether they devolved into something simpler, more efficient, gracefully infectious. Either way, a virus is an evolutionary masterpiece; since it does not have the ability to have sex or reproduce on its own, it must constantly change, adapting to other life-forms—from something as small as bacteria to something as large as mammals. Taking it a step further, once the virus has mastered something like a mosquito in the case of yellow fever or a bird in the case of influenza, it may spread to other species. There, it adapts again and again until there is a seamless transition between certain species—perhaps a monkey to a mosquito to a man.
Once inside the bloodstream, a virus is programmed with elegantly simple genetic material, its DNA or RNA, to produce certain symptoms that will spread it further. In the common cold, sneezing and a runny nose spread the virus. In smallpox, open sores on the skin act as the vehicle for infection. With influenza, coughing expels the virus into the air. In the case of HIV, the virus uses one of the most basic functions in human life— reproduction—to spread through the population of men, women and children.
Yellow fever is what is known as a flavivirus, a group of viruses spread by mosquitoes that includes West Nile, dengue and Japanese encephalitis. As a virus, yellow fever is not one of the stronger ones. It cannot live outside of the body for more than a few hours. It does not spread through the air or by touch. It does not mutate as easily as some viruses. In fact, its most telling symptom—fever—is really just the body’s own attempt to kill the virus. What makes yellow fever unique is its choice of vector. What the virus lacks in evolutionary prowess, the mosquito makes up for.
In the African rain forest, mosquitoes carry the virus, this finely evolved life-form looking to conquer. The mosquito feeds off of the monkeys in the tree canopy, and a small epidemic erupts, foreshadowing the larger one to follow.
Of course, none of this would be known until well into the twentieth century. For the Africans and Europeans, and later for the Americans, a virus would remain an invisible, unknown entity. No one would even know how yellow fever spread from one person to the next until 1900.
As the men made their way back to the Niger Delta and the coast of West Africa where the timber would be sold for ships carrying palm oil, ivory, salt, gold and slaves, they might run a mild fever or feel lethargic, but it was nothing compared to what the white Europeans would feel in the coming weeks. Through this cycle of men entering the forests, mosquitoes biting men and the virus spreading among small tribal villages, most native Africans had encountered the yellow fever virus at one time or another. They acquired immunity to it, and the virus began to run out of the kindling that kept the flames of fever alive. When white Europeans landed on the coast of West Africa, it was like a fresh burst of oxygen in a waning fire.
The Nigerian coast had been booming with the slave trade since the fifteenth century, providing the Middle Passage across the Atlantic with 30 percent of its human exports. As the ships of the Portuguese, Spanish, Dutch and English pitched in the ocean swells along the coast, they waited for the cargo making its way from the interior down the river delta to the coast.
The port towns were filled with the smells of Africa: sweet oil from the palms, spices, yams and dates sold at local markets. There was fire smoke and the poignant scent of rainwater mixed with human sweat where the next shipment of slaves sat chained to one another in thatched sheds, waiting to board the ship. Fearful of tropical diseases, the Europeans might even taste the sweat of slaves to try to determine if he or she carried disease. The smells would worsen in the next few months at sea when hot air, sweat and human excrement would be trapped beneath deck with the slaves. When the ships encountered squalls, and the sea and sky would join, the tumbling ship would induce vomit to add to the amalgam of human smells.
As the ship traversed the waters of the Atlantic, the virus made its way through the bloodstream of the passengers as succinctly as it had made its way through the rivers of West Africa to the coast. In the blood, yellow fever looks something like a fuzzy snowflake, but it is actually round with twenty smooth sides that protect the virus’s single strand of RNA at the center. The coating of the virus is made up of proteins, and human cells are attracted to those proteins—the virus doesn’t need to look for healthy cells; they look for it. Once the two make contact in the bloodstream, a process with a technical name known as receptor-mediated endocytosis begins—sort of a molecular Trojan horse. The healthy cell eventually enfolds the virus, taking it in and closing the door behind it. Once inside, the virus hijacks the cell and its basic machinery, using the cell’s internal makeup to replicate the viral proteins and RNA, until the new particles burst through the cell. A body that was once filled with healthy cells is now filling up with cells carrying the yellow fever virus. That is why a virus cannot be treated by antibiotics; human cells give it refuge, and anything that could destroy the virus might also destroy the cell.
Soon, the filth, lack of nutrition, dehydration and rapid-fire spread of disease turned the transatlantic journey into a death voyage, with bodies being tossed overboard in the wake of the ship. In fact, slave ships were often trailed by sharks, which quickly learned that the vessels served as a source of food.
It was through this journey from the interior of West Africa, down the Niger and Benue rivers, to the coast, onto ships and into the blood of Europeans that yellow fever first made its way from the Old World to the new one.
Yellow fever, more than any other disease, would seem conjured by God and divinely directed. When the slave trade first began, every European country that profited from the purchase and sale of Africans would soon see a yellow fever epidemic: the United Kingdom, France, Germany, the Netherlands, Spain, Portugal. Though Asia had the ideal climate and the right mosquito, it has never had an epidemic of yellow fever. It also never participated in the African slave trade.
As the European powers crossed the Atlantic to establish West Indian colonies, which quickly became horrific holding pens for slaves, yellow fever settled its roots in the western hemisphere and proliferated. The first epidemic on this side of the world occurred in 1648. After that, the slave trade increased fivefold in the West Indies. And by 1702, as the trade of flesh spread to North America, yellow fever blossomed on the continent. From 1700 to 1750, the slave population in America doubled and then doubled again. As each slave ship arrived into the ports of the New World, bringing over ten million slaves to this hemisphere, yellow fever made a giant, evolutionary leap. It adapted. It spread. As one historian put it, “When the disease invaded the Atlantic and Gulf States, it struck with a force more powerful than the one which bombed Pearl Harbor more than two centuries later.”
Yellow fever became the most dreaded disease in North America for two hundred years. It did not kill in numbers as high as some of its contemporaries like cholera or smallpox, and it was not contagious; yet it created a panic and fear few other diseases, ancient or contemporary, can elicit.
During its tenure in this country, yellow fever would inflict 500,000 casualties and 100,000 deaths. The fever would stretch the length of North America, afflicting Massachusetts, Rhode Island, New Hampshire, Connecticut, New Jersey, Pennsylvania, New York, Delaware, Maryland, Illinois, Missouri, Ohio, Kentucky, Virginia, North Carolina, South Carolina, Georgia, Alabama, Tennessee, Mississippi, Arkansas, Louisiana, Florida and Texas.
The U.S. capital would move from Philadelphia to Washington, D.C., after a devastating yellow fever epidemic in 1793. Alexander Hamilton suffered the fever, while George Washington, John Adams and Thomas Jefferson fled the city; the United States government was paralyzed.
In New York, Greenwich Village would become known as “the Village” because it was the safe haven outside of the city during yellow fever epidemics.
Napoleon would abandon his conquests in North America after losing 23,000 of his troops to yellow fever in the colony of Haiti. He made a hasty and fearful retreat from this pestilent hemisphere, selling his large Louisiana holdings for cheap to Thomas Jefferson.
During the Civil War, yellow fever would serve as one of this country’s first forms of biological warfare. And the Spanish-American War, at the close of the nineteenth century, would be fought more against this fever than against the Spanish.
For the first century of its siege in the United States, yellow fever marked for destruction the heavily populated, northern port cities of Boston, New York and Philadelphia. Then, in 1807, the Atlantic slave trade was abolished, and the fever suddenly retreated from the North. By 1850, no other epidemics of yellow fever would occur in those major cities. As the North weaned itself from the slave trade, its southern counterpart absorbed the slave labor and the accompanying yellow fever. In the South, where slavery became deeply entrenched, yellow fever found its lifeblood.
The 1878 yellow fever epidemic, the worst in history, started with the rains in West Africa. February, the wet season, arrived, the mosquitoes hatched, the monkeys grew ill, the loggers stared up at the silent tree canopy. This time, the ships moored off the coast would not carry slaves across the Atlantic; they would carry ivory, gold, copper, salt—and mosquitoes.
But this year would be different for two reasons: Nature had afforded the virus with the perfect environment. An El Niño cycle turned the American South that winter into a tropical region with warm temperatures and rainfall 150 percent above normal. Insects, usually deterred by the winter freeze, proliferated. The significance of the weather phenomenon meant nothing to nineteenth-century observers, but 100 years later, scientists would link El Niño to most major outbreaks of yellow fever. As southerners cut hyacinth blooms in January and waded through waterlogged streets, they complained about the number of mosquitoes beginning to swarm.
American progress was the virus’s other ally. A great influx of immigrants—Irish, German, eastern European—had been migrating south since the Civil War. Just like the white Europeans descending upon Nigeria and other parts of West Africa, they served as fuel for a fever fire, a fresh source of nonimmune blood for the virus.
Transportation had paved the way for these immigrants. Trains connected every corner of America for the first time—east to west, north to south. And paddleboats and steamers snaked their way north from the Gulf of Mexico up the Mississippi River. At the center of this web sat a city 400 miles inland from the Gulf, ready to take its place as one of the largest, most successful cities in the South.
Memphis, Tennessee, was poised for greatness in 1878. By the end of that year, it would suffer losses greater than the Chicago fire, San Francisco earthquake and Johnstown flood combined. The devastation to the Mississippi Valley would cost over $350 million by today’s standards. And the U.S. government would create the National Board of Health, which would report: “To no other great nation of the earth is yellow fever so calamitous as to the United States of America.”
As the southwest monsoon pelted the Niger Delta in February 1878, hatching mosquito eggs and giving birth to a virus, people on the other side of the world could not have known what awaited them. In Memphis, Tennessee, their attention was turned not toward disease or death, but just the opposite: a carnival.