In Kenya in 2004, spring became the rainy season that wasn’t. March turned into April, and then May, and still the rains didn’t come. The once lush countryside began to parch and drinking water slowly evaporated. Women used to fetch small buckets of water from nearby streams and ponds, but the drought forced them to travel farther. To save themselves from trudging for hours each day in the blazing equatorial heat, women began to gather several days’ worth of water in multi-gallon containers, which they stored outside their homes. What the women didn’t know was that these vessels would spark a worldwide outbreak of a viral disease unfamiliar to most Westerners—for now.
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In the Makonde language of eastern Africa, “chikungunya” means “that which bends over.” The chikungunya virus causes joint pain so excruciating victims can’t stand or even sit upright for weeks or months at a time. It has existed in southeastern Africa for centuries, passed from person to person by the Aedes aegypti mosquito. The mosquito has adapted to living alongside humans, happily breeding in human houses and water containers. The drought increased the number of drinking water containers, the population of Aedes aegypti and the incidence of chikungunya cases. After infecting most of the susceptible people in the drought-afflicted area, the outbreak flickered out.
Chikungunya has usually been confined to Africa, but in early 2005, embers of the Kenyan outbreak spread to the Seychelles and Comoros islands in the eastern Indian Ocean. By June of that year, cases of chikungunya had been reported on the island of Réunion, a French protectorate 550 miles east of Madagascar and a popular European tourist destination.
A few cases of chikungunya didn’t overly worry public health officials on Réunion. The spraying of DDT decades earlier had all but eliminated Aedes aegypti on the island. The Asian tiger mosquito (Aedes albopictus), a close relative of Aedes aegypti, lived on Réunion and could potentially carry chikungunya, but it didn’t transmit the virus well enough to cause a major outbreak. During the second half of 2005, reports of chikungunya continued to trickle in. Then, in the beginning of 2006, case reports spiked. Public health officials noted 13,000 cases in the first week of March alone. By the end of the year, around 266,000 people on Réunion had been infected with chikungunya, more than one-third of the island’s residents. Epidemiologists were at a loss to explain the epidemic.
A group of French scientists sequenced the genetic material of the chikungunya virus from Réunion and compared it with chikungunya viruses from Africa. The researchers found that a single mutation had occurred on Réunion, a mutation that slightly changed the shape of one of the proteins that studded chikungunya’s surface. Previous studies showed that this protein helped similar viruses enter host cells and cause infections, which led the scientists to hypothesize that this small shape change was enough to let the virus infect the Asian tiger mosquito and use it as a ready vector.
A follow-up study showed that the mutation on Réunion let chikungunya infect the Asian tiger mosquito extremely efficiently—100 times more efficiently than the non-mutated strain infected Aedes aegypti. Chikungunya enters a mosquito’s body when it bites someone with large amounts of virus in the bloodstream. The blood enters the mosquito’s gut, where the virus pries open the gut cells and makes copies of itself. The shape of proteins on the outside of the virus determines whether it can get inside. For the older strains of chikungunya, trying to enter the gut cells of the Asian tiger mosquito was like trying to shove a square peg in a round hole. The mutation from Réunion changed the virus from a square peg to a round one.
After the virus multiplies in the mosquito’s gut cells, it travels to the salivary glands. When the mosquito bites its next victim, it squirts saliva into the bite to prevent clotting, saliva laden with the chikungunya virus. After three to seven days, the next human victim would have large amounts of virus in his or her own blood, causing fever and the agonizing joint pain for which the disease is so famous. The victim could then pass the virus to the next biting mosquito. The best way to prevent chikungunya infection, says Erin Staples, a medical epidemiologist at the Centers for Disease Control and Prevention (CDC) in Fort Collins, Colorado, “would be to avoid contact with mosquitoes.” But that’s easier said than done.
Over the past 30 years, the Asian tiger mosquito, a native of Southeast Asia and India, has spread to every continent. It travels in used tires, which are usually stored outdoors before being shipped around the world. The tires collect rainwater, the perfect location for a female mosquito to lay her eggs. Even if rainwater evaporates during the voyage, that’s no problem for the desiccation-resistant eggs of Asian tiger mosquitoes.
“When the tires get dumped in their new location and it rains on them, it’s like growing sea monkeys,” says Dina Fonseca, an entomologist at Rutgers University in New Jersey.
The Asian tiger mosquito first arrived in the United States by way of a used tire shipment to Houston in 1985. From there, it spread across the country by way of shipping routes and interstates. Although Aedes aegypti also lives in the United States, it can’t survive cold northern winters, and its presence is limited to the Southeast. The Asian tiger mosquito, however, has adapted to cooler temperatures and can live as far north as Wisconsin and New Hampshire. A widespread population of Asian tiger mosquitoes combined with globe-trotting humans means that chikungunya can arrive in the United States at any time.