A few days later, a van containing samples of Muhumuza’s blood—triple-packaged inside plastic coolers—rolled through the guarded gate of the Uganda Virus Research Institute. A modest collection of stucco and brick buildings, it spreads across verdant lawns overlooking Lake Victoria in Entebbe. Founded as the Yellow Fever Research Institute by the Rockefeller Foundation in 1936, the UVRI has in recent years conducted scientific research on several other communicable diseases, including HIV/AIDS. Two years ago, the CDC opened a diagnostic laboratory at the institute for Ebola, Marburg and other viral bleeding fevers. (During previous outbreaks in Uganda, health officials had to send samples from suspected cases to laboratories in South Africa and the CDC.) A security fence is being constructed around the compound, where blood specimens brimming with Ebola virus and other deadly diseases are tested. The new layer of protection is a consequence of the U.S. government’s deepening concerns about bioterrorism.
Wearing biohazard suits, pathologists removed Muhumuza’s blood samples from their containers inside a containment laboratory. Fans vent air only after it has been HEPA-filtered. The researchers subjected the samples to a pair of tests to detect the presence of the virus and then detect antibodies in the blood. Every virus is made of genetic material enclosed in a protein coat or “shell.” A virus survives by entering a cell, replicating itself and infecting other cells. This process, repeated over and over, is fundamental for the pathogen’s survival. In the first test, scientists added a disruptive agent called a lysis buffer, which breaks down the virus and renders it harmless. Virologists then added a fluorescence-tagged enzyme to the now-denatured mixture, which helps identify strands of the virus’s ribonucleic acid (RNA). By heating, then cooling the mixture, scientists amplify a segment of the virus’s genetic material. They make multiple copies of a small piece of the genetic sequence, which makes it easier to see and study the virus’s genetic code, and thus identify it. The test identified the virus as Ebola Sudan.
The second test detects specific antibodies in the blood produced by cells in an attempt—usually futile—to beat back the Ebola virus. Droplets of blood, mixed with a reagent, were placed into little wells on plastic trays. When a colorless dye was added, the mixture turned a dark blue—a telltale sign of the presence of Ebola antibodies. On July 28, Ugandan health officials announced at a press conference and via the Internet that Uganda was facing its second outbreak of Ebola Sudan in two years.
At the time that epidemiologists confirmed the Ebola outbreak, health workers were tending about two dozen patients in the general ward at Kagadi Hospital. Several of these patients, including Claire Muhumuza’s infant daughter, and Muhumuza’s sister, were fighting high fevers and displayed other symptoms consistent with the virus. The administration called a staff meeting and urged the employees not to panic. “They told us what we were dealing with, that it is contagious, and they pleaded with us to stay,” says Pauline Namukisa, a nurse at the hospital. But the mere mention of the word “Ebola” was enough to spread terror through the ranks. Namukisa and nearly all her fellow nurses fled the hospital that afternoon; any patient who was mobile left as well. Days later, with the facility nearly abandoned, Jackson Amone, who had coordinated the response to Ebola outbreaks in Gulu in 2000, Bundibugyo in 2007 and Luwero in 2011, arrived to take charge of the crisis.
Amone, a tall, bespectacled physician with a baritone voice and an air of quiet authority, reached out to staff members who had fled and implemented a strict disinfection regimen to protect them from the contagion. He also asked a team from Médecins Sans Frontières (Doctors Without Borders) in Barcelona, veterans in the Ebola wars, to assist in the treatment and containment of the outbreak.
After a decade, Ugandan health officials and MSF have developed the skills, manpower and resources to stop contagion quickly. The team set up a triage station and an isolation ward for suspected and confirmed Ebola cases, and applied supportive care—including rehydration, oxygen, intravenous feeding and antibiotics to treat secondary infections—to four people who had tested positive for Ebola. These treatments “keep patients alive for the immune system to recover,” I was told by one MSF doctor. “Intensive care can put the patient in a better condition to fight.”
The quick reaction by the health authorities may have prevented the outbreak from spiraling out of control. Health workers fanned out to villages and methodically tracked down everyone who had close contact with the family in which nine had died. Those showing Ebola-like symptoms were given blood tests, and, if they tested positive, were immediately isolated and given supportive treatment. Four hundred and seven people were ultimately identified as “contacts” of confirmed and suspected Ebola cases; all were monitored by surveillance teams for 21 days. The investigators also worked their way backward and identified the “index patient,” Winnie Mbabazi, although they were unable to solve the essential mystery: How had Mbabazi acquired the virus?
Jonathan Towner is the head of the virus host ecology section of the CDC’s Special Pathogens Branch. He specializes in the search for viral “reservoirs”—passive carriers of pathogenic organisms that occasionally leap into human beings. Towner earned his reputation investigating Marburg, a bleeding fever that can be 80 percent lethal in humans. The virus got its name from Marburg, Germany, where the first case appeared in 1967. Workers were accidentally exposed to tissues of infected African green monkeys at an industrial laboratory; 32 people became infected and seven died. Virologists eliminated the monkeys as the primary source of Marburg, because they, like humans, die quickly once exposed to the virus. “If the virus kills the host instantly, it’s not going to be able to perpetuate itself,” Towner explained, as we sat on the patio of the Hotel Starlight. “It has to adapt to its host environment, without killing the animal. Think of it as a process taking thousands of years, with the virus evolving along with the species.”
Between 1998 and 2000, a Marburg outbreak killed 128 workers at a gold mine in Congo. Seven years later, two more gold miners died at the Kitaka mine in Uganda. In 2008, a Dutch tourist who had visited a cave in Uganda became ill and died after returning to the Netherlands. Towner and other scientists captured hundreds of Egyptian fruit bats (Rousettus aegyptiacus) in the mines and found that many were riddled with Marburg. “Every time we’ve captured decent numbers of these bats, and looked for the virus, we’ve found it,” he says. A bat bite, contact with bat urine or feces, or contact with an infected monkey—which often acts as the “amplification host” in virus transmissions to humans—were all possible means of infection, says Towner.
Ebola is considered a “sister virus” to Marburg, both in the family of filoviridae that biologists believe have existed for millennia. They have similar genetic structures and cause nearly identical symptoms, including external bleeding in the most severe cases. “Marburg is one of the strongest arguments that bats are the reservoir for Ebola,” said Towner.