Story by Patrick McGuire
From witnesses hundreds, even thousands, of years ago to recent research observations, a theory begins to take shape about the origins of ka-dinga pepo.
Some 2,000 years ago in the Nile region of Egypt, a deadly pathogen confined within a specific species of mosquito found a way to thrive in a new host: human beings. Curiously, a legend among peoples in those ancient times bears striking parallels. In it, Allah punishes a sinful leader called Nimrod by inserting a mosquito into his brain. Driven mad by the insect’s buzzing, Nimrod begs a servant to crack open his skull, allowing the mosquito to fly free.
Ka-dinga pepo, marked by its bright red rash, first appeared in isolated epidemics in tropical and subtropical regions. But as the centuries passed, the mosquito that transmitted the virus stowed away with slave traders and rum-runners, slowly taking hold in new surroundings across the world. By the 17th century, it reached the docks of Boston and Philadelphia.
Everywhere, it infected humans—most frequently children—with spiked fevers, terrible pain in joints, muscles, bones and behind the eyes. It could even cause blood to ooze through the pores. It acquired a variety of graphic names, the best known of them attributed to Dr. Benjamin Rush, a signer of the Declaration of Independence. Rush treated an outbreak in 1780 Philadelphia and, observing the misery afflicting its victims, called it “Break Bone Fever.” In Swahili, however, it was still known as ka-dinga pepo, a disease of the devil. It was but a short linguistic jump for it to become known worldwide as dengue fever.
Whatever its origins, scientists, medical professionals and disease control experts are concerned now with the most recent history of dengue (pronounced DEN-ghee). Before 1950, a typical world map depicting affected regions contained few flecks of color. A dab in Africa, a small glob in Southeast Asia, a sliver of color in South America. Today, it’s as if a can of paint spilled across the bottom half of the map.
As it has spread, the most dangerous form of the disease—dengue hemorrhagic fever (DHF)—has appeared with alarming regularity. According to Anna Durbin, MD, an associate professor in International Health, the often-fatal DHF causes vascular leak syndrome where fluid in the blood vessels leaks through the skin and also into spaces around the lungs and belly. Blood pressure falls, shock sets in and death often follows.
DHF ran rampant in Southeast Asia in the 1960s and 1970s, and has increased its presence ever since. The WHO estimates that 2.5 billion people are at risk annually for dengue infections. Between 50 million and 100 million contract the disease each year. More than half a million of those are diagnosed with DHF.
Compared to malaria, dengue has a relatively low mortality rate. Malaria, caused by a parasite transmitted by a different mosquito species, infects up to 400 million people each year and causes 1 million deaths. While dengue’s annual mortality rate is about 26,000, it’s the dengue morbidity rate that causes widespread concern. WHO reports a 30-fold increase in cases since 1960. It has become the world’s most common viral disease spread by blood-sucking insects. Editors of the recent book Frontiers in Dengue Virus Research call it “an old disease spreading with a new vengeance.”
Many trace the spread of dengue to the upheavals of World War II. Fighting in the Pacific meant more mosquitoes were transported via wartime shipping. It was also during the war that scientists used a potent chemical against the Anopheles gambiae mosquito that transmits malaria. In the mid-’50s this chemical—DDT—became the main tool of a worldwide malaria eradication program promoted by WHO. It killed not only the malaria-carrying Anopheles gambiae but the Aedes aegypti mosquito that carried the dengue pathogen, effectively eliminating malaria and dengue fever through Central and South America.
By the late ’60s, however, DDT became anathema for health and environmental reasons. This fact coupled with the decline of malaria eradication programs allowed the mosquitoes and dengue to return.
The only way dengue can spread is when the Aedes aegypti mosquito bites someone who is infected and then bites a second human who is not. The more people who live in close surroundings where mosquito control is weak or nonexistent, the more likely a mosquito will transmit the virus to others.
Dengue has reached endemic status, says the CDC, in many tropical and subtropical regions. It reappears annually during the rainy season when mosquitoes breed.
According to the WHO, dengue is the leading cause of hospitalization among children in eight tropical Asian countries. It often overwhelms the national health budgets and fragile health care systems of developing countries. Many scientists refer to it as a disease of poverty.
That doesn’t mean that a wealthy nation like the U.S. is immune. In fact, a small outbreak of dengue fever was reported in the Texas border city of Brownsville in 2005. But generally, dengue is rare in the U.S. even though Aedes aegypti is common in the South. Experts attribute that to infrequent contact between people and the mosquito, due to better sanitation conditions in American cities, as well as window screens and central air conditioning.
“We don’t think actual transmission will happen in the next year or two in the U.S., but we recognize that it could happen,” she says.
Durbin is conducting clinical trials in Baltimore—and later this summer in Brazil—with an experimental dengue vaccine created by NIH. She is also part of the Pediatric Dengue Vaccine Initiative (PDVI), an international consortium of scientists, drug manufacturers and public health institutions. It was founded in 2003 by Scott Halstead, MD, a world authority on dengue research and an adjunct senior scientist in the W. Harry Feinstone Department of Molecular Microbiology and Immunology (MMI).
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