She was bleeding from everywhere. There was blood in her urine, blood in her stool. She had blood-streaked sputum and bloody vomit. As we doctors huddled around her bed, blood was trickling from her nose.We were not gathered around a patient in some hushed room in an intensive care unit. Outside, I could hear children screaming, laughing, and the sounds of diesel trucks laboring down the nearby road. I was working for the medical relief group World Vision in St. Mary's Hospital Lacor, a 460-bed missionary hospital in the small farming town of Gulu in northern Uganda. Everything was different here. And I had no idea what was wrong with this woman. Doctors base their diagnosis on what's common in the community. In the United States, a doctor finding an enlarged spleen in a reasonably healthy young woman would suspect mononucleosis. In South America, a doctor might consider Chagas' disease; in Ethiopia, Ewing's tumor. Most likely, each would be right. But put an American doctor in the sub-Sahara or a Saudi doctor in Minneapolis, and suddenly each doctor is clueless. On the other hand, the post-9/11 threat of unfamiliar pathogens used as bioterrorist weapons has only highlighted this weakness. Now physicians in American emergency rooms are quietly studying up on symptoms of rare, deadly diseases such as anthrax and smallpox. Before I came to work in Uganda for a summer, I pictured myself teaching the ins and outs of cutting-edge Western medicine. As it turned out, I was the one who needed educating.
Day one: A resident arrived a little early for morning rounds. He had come to request a day off. "I'm aching all over, I've got a fever, I'm nauseated," he said. "Sounds like the flu," I said. "No," he said with a sigh. "It's just my malaria acting up again." After a month or so on the job, I got better at dealing with common complaints. I had learned that you do a rectal biopsy for belly pain. That's because the likely cause is schistosomiasis, a parasitic worm found in the drinking water; the best way to diagnose it is with a "rectal snip." Still, every day I would stumble over differences in medical practice. One day a resident diagnosed kidney failure in a 29-year-old man with two wives and four children. When I said the patient needed dialysis, the resident laughed. "There are maybe 10, maybe 12 dialysis patients in all of Uganda," he said. "That's how many people can actually afford it." He turned to the patient and patted his shoulder. "Go home and make your will," he said in English. The nurse translated. "And go make your peace with God. You are going to die." My boss was Dr. Matthew Lukwiya, the director of the hospital. He was Acholi—born and raised in the Gulu district, dirt-poor like everyone else here. Dr. Matt was a brilliant student, though, and somehow someone found enough money to send him to Kampala to study medicine. He graduated at the top of his class in 1983—the only Acholi tribesman to become a medical doctor. Not only that, he was later appointed medical director of St. Mary's Hospital Lacor, the best hospital in northern Uganda. Some said it was the best hospital in all of Uganda. He was much like all the other physicians I had worked with in the States, and like all doctor-administrators I have known, he wore an air of terminal exasperation. Day after day, he dealt with the nuns who ran the hospital, the residents who rotated through their clinical clerkships, the patients and their unremitting parade of AIDS-related diseases and other ailments, and on occasion, even expatriate doctors like me. Dr. Matt endured us all. Normally, after seeing a patient so mysteriously ill, I would have gone to find him, but he was in Kampala working on a research project. I was on my own.
"What happened?" I asked the girl sitting at the head of the bed. She couldn't have been more than 13 or 14—probably a daughter taking care of her dying mother. "She got sick on Friday night," the girl told me through the translator. Today was Sunday. I bent over to examine the multiple blue blotches on the woman's hands. "What are those?" I asked the residents. "Purpura," someone said. Purpura is a subcutaneous hemorrhage—bleeding under the skin. It is a sign that the clotting mechanism has gone awry. I checked her wrist for a pulse. Nothing. When I felt her neck, even her carotid pulse was weak. Context didn't matter here. Africa or America, the woman was in shock. If nothing was done, only death could follow. Back in the States, this woman would be in some intensive care unit with tubes and catheters, monitors and ventilators, and a whole swarm of health-care professionals. Here there was just a cot with a plastic sheet. We could do so little. "Okay," I said. "What are the common causes of shock associated with this kind of bleeding?" By this I meant "bleeding from every pore." There weren't many. "End-stage liver disease," one of the residents said. I nodded. But that kind of liver failure takes time to develop. This patient had gotten sick overnight. "What else?" Silence. "How about DIC?" I asked. Disseminated intravascular coagulation is a paradoxical disease that causes a patient to bleed and form clots simultaneously. The residents responded as they do in the States. You could see the little light go on: "DIC. Oh, yeah." Certain diseases, for reasons that aren't well understood, can set off the first few steps in the blood-clotting cascade. The reactions then spread to involve blood everywhere in the body. Platelets clump and intravascular micro-clots form. Blood begins to sludge, and no-blood-flow regions spring up all over the body. As the process continues, clotting factors get used up until the patient can no longer make clots when or where they are really needed. End result: chaos and death. "Now, what is the most common cause of DIC?" I asked. The correct answer is "bacterial sepsis," which means an infection, usually by a class of pathogen known as gram-negative bacteria. The infection overwhelms the body's defense mechanisms and trips the wire on the clotting cascade. "Snakebite," one of the residents said. This brought me up short. Bacterial sepsis was the most common cause of DIC in the United States. In Africa, snakebite could cause 90 percent of all cases for all I knew. "Snakebite," I said nodding. "Not the first thing I would think of. What else?" "Abruptio placentae," another resident said. This occurs when, late in pregnancy, the placenta pulls away from the intrauterine wall. The amniotic fluid activates the blood-clotting mechanism, resulting in the downward spiral of DIC. "How do you make the diagnosis?" I asked, and then regretted it. In the United States you could run a dozen different tests. Here all we could measure was a platelet count. Except, of course, today—Sunday—when the hospital laboratory was closed. I moved on quickly. "And how do you treat it?" Again, silence. In Africa there is no treatment for this disease. I could see each resident wondering what miracle Western medicine had dreamed up. Unfortunately, the West has no magic potions for this condition either. Some experts recommend heparin, which may prevent clotting, but it doesn't seem to be particularly effective. One resident spoke up. "You treat the underlying disease." "Correct," I said. Then it occurred to me that there was a difference between Africa and the United States. We in America didn't have a cure, but we did have a "promising new therapy." The latest experimental drug prevents the first step in the chain reaction of DIC—but so far, only in the laboratory. I knelt down next to the patient and took her feverish hand in mine. Her eyes had rolled back so that not much more than the whites showed through narrow slits. For a moment, looking at her prunelike fingers, I thought, This woman has cholera. But no, it was just that she had entered the final common pathway of all diseases—the collapse of all the smoothly integrated organ systems. I squatted there helplessly for a moment, patting her hand clumsily as her daughter looked on. "Well," I finally asked, in order to say something, "what did her malarial preps show?" In Africa, when in doubt, think malaria. We could do little more than start fluids and administer a blast of antibiotics in hopes of arresting any infection. We moved on to other patients and to other diseases we couldn't cure. The next afternoon, her bed was empty, and the rubber mat that served as a mattress had been pulled outside and was drying in the waning sun. A little spooky, though, was the woman's neighbor, there with pneumonia, who had developed a nosebleed that wouldn't stop. By the time Dr. Matt returned from Kampala the following day, she had died as well. I told him about the two cases: "Classic gram-negative sepsis." "How about something viral?" he said. "What about one of the viral hemorrhagic fevers?" "Oh," I said. "Yeah, of course." I mentally kicked myself. I had completely forgotten the little I knew about hemorrhagic fevers. These are a distinct class of viral infection that features massive bleeding, whether by DIC or other mechanisms. I'd never seen a case because the hemorrhagic fevers, such as Lassa fever and Crimean-Congo fever, are found primarily in the tropics. The only hemorrhagic fever someone in America might ever see would be hantavirus pulmonary syndrome, an illness that was identified in outbreaks in Arizona and New Mexico. "Yeah," Matt said. "Lassa fever . . . yellow fever . . ." Yellow fever, the other hemorrhagic viral fever. I had forgotten about it too. "Well," I said lamely, "there's not much more we could have done for her even if we knew she had yellow fever." Actually, there is an antiviral agent, ribavirin, for treating yellow fever. But it's expensive, and needless to say, no one at St. Mary's Hospital could afford that drug. "No, no." Matt shook his head over me. "You've got to make the diagnosis. That's the only way you know if you've got a public-health problem. You need to know what's out there." Why was I always looking in the wrong direction? Matt slapped my back, laughing. "I'll make you an tropical disease expert. Just give me another 10 years." The following Saturday, though, I had my chance to show my stuff. A patient came in with new-onset diabetes and diabetic ketoacidosis—a life-threatening imbalance in the blood that results when the body lacks enough insulin to metabolize sugar. He was a young soldier, diagnosed as malarial the Friday before and only dragged into the hospital now because his buddies had noticed the antimalarial pills didn't seem to be working. His honey-sweet smell was enough for me to make a diagnosis. The bedside glucometer (the only one, I think, in all of northern Uganda) confirmed it. At last a disease I knew. We started him on an insulin drip, gave him saline to rehydrate him, and sent off for multiple blood tests—modern medicine in action. And then he abruptly and inexplicably died. He just stopped breathing. No CPR here. We all just stood around looking at his inert body—his corpse. He was 32. Not long after that, my time was up, and I returned to the United States and to an emergency room full of sore throats and runny noses. The tropical diseases, the dying patients, the dusty town of Gulu all became so distant that when I saw the word Gulu on the front page of The New York Times, I didn't really recognize it as something I knew about firsthand. Once it registered, though, I was so startled I couldn't read the article. I just scanned it until I saw another word: Lacor. I finally picked out the point of the story: Ebola. Ebola, the classic hemorrhagic fever. An outbreak of Ebola virus had occurred; the epicenter seemed to be St. Mary's Hospital Lacor. Personnel from the World Health Organization (WHO) were camping out all over Gulu. I scanned the article to find out when the WHO personnel thought the epidemic started. I was thinking of that woman bleeding from everywhere. Had I touched her? Had I treated a woman with Ebola? The only reliable way to get messages in and out of Gulu was through the World Food Bank satellite mail system. I tried to get through but couldn't reach anyone. I ended up following the epidemic through the newspapers, helpless. WHO identified the index case, the first human case confirmed, as a woman who lived in a village about a mile from Gulu. She had died suddenly. No one knew—or even really wondered—why. As was customary in Gulu, her daughters washed her body prior to burial. Then the daughters got sick. One died immediately, but the other made it to the hospital. Apparently Dr. Matt had been suspicious enough to send some blood samples off to the reference lab in Kampala. The result came back positive for Ebola. There had never been an outbreak of Ebola in Uganda. The organisms, or vectors, that carry other hemorrhagic-fever viruses are known, but no one knows the vector for Ebola. Researchers suspect that its natural reservoir is some creature of the forest, and that outbreaks occur when the virus somehow spreads into another host, such as a monkey or a chimp. Contact with infected, sickened animals could begin the chain of infection in humans. A case appears and an epidemic ignites, blazes through a population, and eventually burns itself out. The virus then returns to its hiding place, its secrets intact. St. Mary's Hospital remained the center of the outbreak. Within two weeks there were 71 suspected cases, including 35 deaths. WHO had recognized immediately that the epidemic had international implications, and they sent out the troops. Their field personnel began gathering data about the outbreak and helped guide hospital care for victims. They instituted barrier nursing methods at the hospital and provided the necessary supplies. (When I was there we washed and reused gloves many times, not a satisfactory arrangement in an epidemic.) The disease spread through Gulu Town, then on to the Masindi and Mbarara districts and north toward Kitgum. All are meaningless names unless you've been there. Every time I read them in a newspaper, they stung like a whip. WHO officially proclaimed the epidemic over on February 28, 2001, some 150 days after it began. Agencies disagreed over how many had died, but the Centers for Disease Control and Prevention in Atlanta gives the total as exactly 425. The case fatality rate was calculated at 53 percent.
