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Yellow Jack: How Yellow Fever Ravaged America and Walter Reed Discovered Its Deadly Secrets

Yellow Jack: How Yellow Fever Ravaged America and Walter Reed Discovered Its Deadly Secrets

by John R. Pierce, James V. Writer, James Writer

The end of a scourge

"The prayer that has been mine for twenty years, that I might be permitted in some way or some time to do something to alleviate human suffering, has been answered!"
—Major Walter Reed, writing to his wife, New Year's Eve, 1900

As he wrote to his wife of his stunning success in the mission to identify the cause of yellow fever and


The end of a scourge

"The prayer that has been mine for twenty years, that I might be permitted in some way or some time to do something to alleviate human suffering, has been answered!"
—Major Walter Reed, writing to his wife, New Year's Eve, 1900

As he wrote to his wife of his stunning success in the mission to identify the cause of yellow fever and find a way to eradicate the disease, Walter Reed had answered the prayers of millions. For more than 250 years, the yellow jack had ravaged the Americas, bringing death to millions and striking panic in entire populations. The very mention of its presence in a city or town produced instant chaos as thousands fled in terror, leaving the frail, the weak, and the ill to fend for themselves.

Yellow Jack tracks the history of this deadly scourge from its earliest appearance in the Caribbean 350 years ago, telling the compelling story of a few extraordinarily brave souls who struggled to understand and eradicate yellow fever. Risking everything for the cause of science and humanity, Reed and his teammates on the U.S. Army Yellow Fever Board invaded the heart of enemy territory in Cuba to pursue the disease—and made one of the twentieth century's greatest medical discoveries. This thrilling adventure tells the timeless tale of their courage, ingenuity, and triumph in the face of adversity.

Editorial Reviews

From the Publisher
"A fascinating examination of how science works in the real world.   This book may inspire future Walter Reeds to solve tomorrow's medical mysteries." (Journal of College Science Teaching)
Publishers Weekly
There isn't much new in this workmanlike examination of yellow fever, which focuses on the American impact of this deadly hemorrhagic disease closely related to the West Nile virus. While mostly a tropical disease, yellow fever reached as far north as Philadelphia in 1793. But particularly in the South, deadly plagues were the norm year after year. Pierce, a physician and retired colonel with the U.S. Army, and coauthor Writer describe the debates over the cause of the disease, which many thought originated in the Caribbean, and the work to determine the mode of transmission. In 1900, after the Spanish-American War, Walter Reed headed the Yellow Fever Board sent to Havana and rather quickly confirmed earlier suspicions that mosquitoes were responsible; in remarkably short order the board rid the entire island of yellow fever. But the disease's virulence and the harsh working conditions threatened the researchers themselves. The authors explain this in their hyperbolic style: "Eight loyal and fearless soldiers in the war against an invisible foe had, in the noblest sentiments of the profession, died in hopes of saving others.... [N]o other virus in the history of laboratory research has taken away so many of those working to solve its mysteries." B&w illus. (Apr.) Copyright 2005 Reed Business Information.

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Read an Excerpt

Yellow Jack

By John R. Pierce

John Wiley & Sons

ISBN: 0-471-47261-1

Chapter One

Yellow Fever Comes to America

Yellow fever is an acute viral hemorrhagic disease caused by the yellow fever virus. The virus belongs to the flavivirus group, which includes the West Nile and dengue fever viruses. Infection results in a wide spectrum of disease, from mild symptoms to severe illness and death, making the disease difficult to diagnose. Doctors may confuse it with malaria, typhoid, rickettsial diseases, other arthropod-borne viral fevers, viral hepatitis, and even some poisonings.

While some infections will have no symptoms, most people with yellow fever will experience an acute illness normally characterized by fever, muscle pain, backache, headache, shivers, loss of appetite, nausea, and vomiting. Their eyes may be bloodshot and their tongue fuzzy. While in many febrile illnesses a high fever is accompanied by a rapid pulse, in yellow fever, the pulse is often slowed down, a phenomenon called Faget's sign. During the acute phase, which lasts about three days, there is virus circulating in the patient's blood and that person can be a source of infection. In most patients, the illness will not progress beyond these symptoms, and most victims will improve and recover. However, about 15 percent will enter a "period of intoxication" within two to twenty-four hours after the acute phase appears to be resolving. In these patients, fever reappears and jaundice develops along withsevere abdominal pain and vomiting. Bleeding can occur from the mouth, nose, eyes, and stomach. Digested blood may appear in the feces or vomit. The Spanish were struck by this feature and named the disease el vomito negro. It often heralds death. Kidney function may be affected, ranging from abnormal protein levels in the urine, called albuminuria, to complete kidney failure with no urine production, called anuria. Half of the patients in the toxic phase die within ten to fourteen days after becoming ill.

Yellow fever is an arboviral disease, meaning that it is transmitted to humans by an arthropod vector. Arthropods include insects and ticks. Adult female mosquitoes pick up the virus from infected individuals while feeding. Males do not feed and cannot carry the disease. Humans and monkeys are generally the only animals that can be infected.

After the mosquito ingests infected blood, the virus is carried to the mosquito's midgut. There it reproduces or replicates in the cells lining the midgut wall. The virus is then released into the mosquito's hemolymph, or blood, and travels to her salivary glands. The virus is now ready for release into the mosquito's next victim. The time needed for the virus to complete this part of its life cycle is about seven to seventeen days and is called "extrinsic incubation." The mosquito cannot transmit the virus until after this time.

The female mosquito can also pass the virus via infected eggs to its offspring. These eggs can lie dormant through dry conditions, hatching when conditions are right. Therefore, the female mosquito and its eggs are the true reservoir of the virus, ensuring transmission from one year to the next.

Today scientists recognize three different transmission cycles for yellow fever: sylvatic or jungle, intermediate, and urban. All three cycles exist in Africa, but in South America, only sylvatic and urban yellow fever occur. Until the 1930s, only the urban cycle was known. Each cycle has its own specific ecology and may involve several different species of Aedes and Haemagogus mosquitoes.

In jungle yellow fever, monkeys in tropical rain forests are infected by wild mosquitoes that may bite humans entering the forest, resulting in sporadic cases of yellow fever. Intermediate yellow fever occurs in the humid or semihumid savannas of Africa, where small-scale epidemics occur. In this cycle, semidomestic mosquitoes infect both monkey and human hosts in areas where their habitats intersect. Urban yellow fever has historically been the type most associated with the large-scale deadly outbreaks in the United States, the Caribbean, and Central and South America. In this setting, the tiny black-bodied silver-striped domestic mosquito, Aedes aegypti, which prefers to breed in man-made containers, carries the virus from person to person. It also stays close to home, having a flight range of only about a thousand feet.

There is no specific treatment for yellow fever, but several strategies are used to prevent the disease or control an outbreak. The most important and effective is vaccination. Also important, especially in urban settings, but perhaps less effective over the long term, is mosquito control.

Some four hundred years after the first cases of the disease were described in Mexico and the Caribbean, the mystery surrounding the origin of yellow fever remains unsolved. Among the many theories of its origin is one that claims the yellow fever virus existed in the rain forests of the New World but needed the African Aedes aegypti mosquito to carry it to humans. The consensus among virologists and disease ecologists, however, is that both the disease and the Aedes aegypti mosquito arrived in the Western Hemisphere from Africa as a consequence of the early slave trade. Molecular biology may end the debate. The case for an African origin of the disease is supported by recent work in the evolutionary genetics of the yellow fever virus. There is more genetic variation in the African strains than in the South American strains, pointing to a longer evolutionary history for the virus in Africa. Therefore, Africa is most likely yellow fever's ancestral home.

There is little or no question that the mosquito has its roots in Africa. On that continent, there are many mosquito species closely related to A. aegypti. As with the virus, this suggests a common evolutionary path. In the Western Hemisphere, this particular mosquito has no close relatives, making it likely that it was recently introduced. In Africa, Aedes was primarily a forest-dwelling pest that bred in water-filled tree holes. Over time, it adapted itself to life in close proximity to human habitats and became domesticated. By the middle of the twentieth century, it was found in many of the world's tropical and subtropical regions and even made its way into the more temperate zones of North America, North Africa, and the Middle East. Since that time, aggressive mosquito control efforts, especially in the Western Hemisphere, have greatly reduced its range.

Whether it was the vector and disease or the vector alone that was brought from Africa, there is no debate on how they came to meet in the Americas-trade. In much the same way that the global economy of the twenty-first century facilitates the movement of diseases like SARS or West Nile around the world, the opening of trade routes in an earlier time resulted in the movement of disease. Yellow fever was not the only disease on the move. Spanish conquistadors brought measles and smallpox to the Inca and Mayan societies and the Carib Indians. In turn, the Spanish probably took home syphilis. Most likely it was the trafficking in human cargo that delivered yellow fever to the Americas.

Infectious diseases love social upheaval. War, mass migrations of people, changes in climate, and other events that alter human ecology often create incubators for illness. The American Revolution and a continent-wide smallpox epidemic were joined in time and place. The 1918 influenza pandemic that took 20 million lives worldwide began at the tail end of World War I. HIV/AIDS took advantage of changing sexual mores. Yellow fever was born of the mating of slavery and sugar.

At the midpoint of the 1600s, significant changes came to Caribbean agriculture and the labor pool that supported it. Until this time, indentured servants from Europe mainly worked the small farms that dominated colonial West Indian agriculture. These laborers exchanged three to five years of their lives for passage to the Americas; some voluntarily, some at the point of a sword. But the indentured labor pool was shrinking, and many of these workers, it was discovered, were not up to the backbreaking work and hardships of tropical farming. A new source of cheap labor was needed.

The Spanish-Portuguese monopoly on the African slave trade that had been in place since the early 1500s was also coming to an end. Dutch, British, and French slavers were increasingly taking over the trade-sometimes by force. The Dutch were among the most aggressive and seized Spanish-controlled slave ports on the west coast of Africa. With more players in the trade, the number of slaves transported to the Americas dramatically increased.

The typical slave ship of the time may have been similar to a Dutch flute: a small three-masted wooden ship with two decks, top and below. The crew of about twenty would sail from Europe to slave-trading outposts such as Benin and Old Calabar on Africa's west coast. There, ship and crew plied coastal Africa for many months, cutting their best deals for slaves who were hunted down and sold by other Africans and Islamic traders. Before departing, the ships loaded up on provisions. Sweet potatoes and other native African fare were put up for the journey across the Atlantic. These foods were for the slaves. Many captains had learned that a European diet, especially one of dried meats and hardtack, could not sustain their human cargo. Too much of their high-priced inventory was lost to dysentery and other digestive disorders during a crossing without native foods.

Water was also essential for the trip. Casks of water were loaded in Africa for the three-month journey. It can be assumed that a few days out of port, wigglers, or mosquito larvae, danced just below the surface of the water. Several days later, the mature mosquitoes would have emerged. Slaves and crews provided the blood meals female mosquitoes needed to produce eggs. The sated females returned to the water casks and cisterns to lay their eggs. During the voyage across the Middle Passage, as the Africa to America journey was called, the mosquitoes could pass through several generations.

Between the time they left Africa and the time they docked in Pernambuco, Guadeloupe, or Barbados, a ship's crew was likely reduced by 20 percent, almost entirely by sickness. The extent to which yellow fever contributed to this mortality rate will never be known; such things were kept "conveniently dark." The death rate among the ship's human cargo, due to disease, suicide, and murder, was about the same in this period. It is very likely that only the mosquito population had increased on the crossing.

Slaves and mosquitoes disembarked into the New World. Slave labor was desperately needed to work the new large plantations that were displacing the smaller family farms. In Barbados in the mid-1600s, the tenacre plot worked by a family and a few indentured servants was disappearing, replaced by large plantations averaging three hundred acres; some stretched over a thousand acres. As the plantations grew, the number of property holders fell from over 11,000 to under 800. The demand for a huge slave labor force also grew, and the slavers were ready to comply. Barbados had 5,600 black slaves in 1645, up from near zero a few years earlier. By 1667, there were more than 82,000 Africans working the island's plantations.

Many of the shifts in land use and the labor force were the result of a major change in West Indian agriculture. Europe and the European colonies to the north had developed a sweet tooth. Where cotton and tobacco were once grown, the green spiky leaves of sugar cane now waved in the Caribbean trade winds. Whether it was packed into cones of sugar, turned into molasses, or fermented into rum, demand was high, prices were higher, and the incentive to forsake other crops in favor of cane was even higher.

While the slaves went to work in the fields and plantation homes of the Caribbean, Aedes aegypti mosquitoes, now freed from their water casks, went in search of blood meals. And while blood was essential for laying eggs, it was not required for sustenance. Sugar water, now abundant on the islands, could sustain them quite well until they happened on a warm-blooded mammalian feast.

Sporadic cases of yellow fever probably occurred for many years before the virus and the vector were sufficiently established to cause a devastating epidemic. Historians have reported several disease outbreaks before 1648 as yellow fever. Among those were an epidemic that ravaged Christopher Columbus's troops and the Carib Indians they engaged at the 1495 battle of Vega Real in Hispaniola. Much later, in 1643, an illness dubbed the Coup de Barre struck Guadeloupe. Four years later, a mysterious illness visited Bridgetown, Barbados. Both this outbreak and Coup de Barre have been called the first reports of yellow fever. It is uncertain whether any of these were yellow fever.

The Vega Real outbreak is too poorly documented for us to know its cause. The Coup de Barre, described by the French priest Pere Duptertre and named for the extreme muscle pains that accompanied it, was unlikely to be yellow fever. It was similar to a previously known disease and had too low a death rate for yellow fever. While conditions may have been right for yellow fever on Barbados in 1647, not enough is known about the outbreak to name it. Whatever it was, it was devastating. Writing to Governor Winthrop of New England, a correspondent described "an absolute plague, very infectious and destroying." In the writer's parish, twenty people were buried in one week, and in many weeks during the epidemic there were fifteen or sixteen burials.

The first relatively certain occurrence of yellow fever was in the Spanish stronghold on the Yucatan in 1648. Writing in his Historia de Yucathan, Lopez de Cogolludo noted that conditions that year were ripe for a great calamity. In March, one of the signs of impending disaster was the arrival of a fog so dense that for several days the sun appeared eclipsed. For the old Mayan Indians the fog was "a sign of great mortality of people in this land, and for our sins." The first cases of the mystery illness appeared in Campeche in June. Cogolludo said the city was "totally laid waste." The peste, as he called it, continued throughout the summer. The Spanish established roadblocks around Campeche in an effort to confine the contagion. But the disease spread. There was little confidence in the authorities' ability to halt the sickness. After all, many reasoned, what good were human barriers if their Lord God did not protect the city? Moving from Campeche, its apparent place of origin, to Merida, the peste appeared to jump over the villages between as if carried directly from one city to the other. A resident of Merida, where the epidemic hit in August, wrote in a letter, "With such quickness it came on great and little, rich and poor, that in less than eight days almost the whole city was sick at one time and many of the citizens of highest name and authority died."

Accounts describing the spread and symptoms of the disease leave little doubt that it was yellow fever. Indians fell ill a few days after arriving in the city of Merida. Initially, only friars who left their cloisters to care for the sick became ill. But soon cases of the peste appeared in the cloisters seventeen to twenty days after the first friars fell ill. This timing is in keeping with the now known time needed for the virus to reproduce in the infected mosquito, the extrinsic incubation, and for symptoms to develop in people. Henry Rose Carter, who discovered and described the extrinsic incubation period, wrote in his exhaustive 1931 History of the Origin of Yellow Fever, published after his death, that the known epidemiology of yellow fever dovetails so perfectly with that reported from the Yucatan "as to almost compel of the diagnosis of it or some other host-borne disease."

Cogolludo's recounting of the malady's symptoms almost certainly confirms it as yellow fever. Victims of the peste were "taken with a very severe and intense pain in the head and of all the bones of the body, so violent that it appeared to dislocate them or to squeeze them as a press." Many but not all of the sick progressed to a "vehement fever" often accompanied by delirium. The truly unfortunate began vomiting "putrefied blood and of these very few remained alive." Those who worsened often died on the fifth day. Except for dying two or more days earlier than most yellow fever patients today, the descriptions of the peste symptoms offered by Cogolludo mirror what is now known of the disease.


Excerpted from Yellow Jack by John R. Pierce Excerpted by permission.
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

Meet the Author

JOHN R. PIERCE, M.D. (Col. MC, U.S. Army, Ret.), wrote the series of articles on which this book is based for Stripe, a publication for Walter Reed Army Medical Center (WRAMC) personnel and included on dcmilitary.com, a Web site for military personnel in the Washington, D.C., area. Pierce recently retired after thirty years of active duty, a significant portion of that spent at WRAMC. With Pierce, JIM WRITER coedited a supplement to the journal Military Medicine on the 1900 Yellow Fever Board.

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