The Coming Plague: Newly Emerging Diseases in a World Out of Balance

Having already examined the outbreaks of three other hemorrhagic viruses, Garrett introduces the most famous representative of the group: Ebola. A 1976 outbreak in a Catholic mission hospital in Yambuku, Zaire, became the epicenter for the spread of a lethal new virus. Yambuku lay in the Bumba Zone, a remote and difficult-to-access area of central Africa, but word of the outbreak spread rapidly, pushed on by stories of victims who died within days, their skin stretched tight and bleeding from every orifice. Word was relayed to Dr. William Close, who had previously worked in Zaire, and he, in turn, notified the CDC. Soon an international team of doctors and researchers was assembling to tackle the virus, led by Karl Johnson (see Chapter 1) and including Joe McCormick, whom Johnson recruited (see Chapter 3). The challenge facing them was significant, not only because the outbreak was in such a remote area but because word of another similar outbreak was trickling out of an even more remote region in southern Sudan. If the two outbreaks were related, then it meant that the virus had already achieved a massive spread. By the time the team reached Yambuku, the outbreak’s initial wave had died because locals started taking precautions and avoiding the hospital.

It was immediately apparent that they were dealing with something new; the Belgian doctor Peter Piot analyzed the virus under a microscope and saw it arranged in a unique question-mark shape, unlike any known virus. Much of the virus’s transmission in the hospital was tied to reusing syringes in up to 600 patients a day without proper sterilization. The cases derived from the mission hospital had a lethality rate of more than 90% and had claimed many of the mission workers themselves.

McCormick, meanwhile, had begun an investigation into the south Sudanese outbreak, and while it appeared to be a strain of the same virus, there were no connecting cases in the hundreds of miles between the two outbreaks. The outbreaks were not connected, but they were the same virus, which suggested that researchers were dealing with the amplification of a naturally occurring, endemic virus spread over the area, which had somehow achieved high rates of lethality and transmissibility in these two breakthrough spots. Despite having to wrestle against fear and governmental incompetence at multiple stages (taking the form of pilots who would refuse to take researchers on their planes and villagers who refused them access), the scientists succeeded in finding some answers. In addition to transmission via undersupplied hospital facilities, the two outbreaks had expanded due to cultural practices of cleaning dead bodies before funerals. However, searching for an animal reservoir of the virus proved fruitless: “The source of both horribly lethal viruses—Marburg and Ebola—remains a complete mystery” (148).

After focusing on outbreaks in South America and Africa, Garrett turns her attention to the USA, where in 1976, two outbreak scares shook the nation. It began with a young army recruit in New Jersey suddenly falling ill and dying of what appeared to be influenza. This sparked fears of a long-predicted emergence of a highly lethal flu strain like the one that caused a global pandemic in the wake of World War I. Early indications showed that it could be a version of swine flu, and the Gerald Ford administration stepped in with a massive effort to prepare for the coming onslaught of disease, which it identified as a resurgence of the old pandemic strain. As it turned out, no epidemic ever materialized, and the government was left to reckon with the effects of what looked in retrospect to be a case of letting panic, rather than medical research, set the agenda. Garrett quotes Dr. Harvey Finberg reflecting on the situation: “In this case the consequences of being wrong about an epidemic were so devastating in people’s minds that it wasn’t possible to focus properly on the issue of likelihood” (163).

In the same year, there was an authentic outbreak of real concern in the US. A group of American Legion members, who had celebrated the nation’s bicentennial together in Philadelphia, suddenly began falling ill of pneumonia and dying. Researchers ran into difficulties early on: “The epidemiologists couldn’t figure out how, whatever the culprit was, people got sick. They couldn’t even narrow the clues enough to tell whether the killer was a chemical or a microbe” (175). The investigators’ slow progress, combined with the government’s massive spending on the false alarm over swine flu, led to a rupture in national confidence in public health officials. That was only worsened when the government-promoted vaccination project against swine flu led to a sharp rise in Guillain-Barré syndrome. Eventually, though, results began to appear in the search for Legionnaire’s disease. Two researchers, Joe McDade and Shep Shepard, isolated a bacterium that caused the condition, previously unnoticed because it would not grow under normal laboratory conditions. This microbe, adapted to living in the nearly anoxic environments of pond scum, had found a new habitat in cooling towers and large air-conditioning systems. In this case, an advance in human technology (primarily air recirculation systems) had brought a bacterium into a new environment, where its effects proved toxic to the humans around it.

With this chapter, Garrett varies from her recent string of narrating outbreaks of new diseases and returns instead to the source-animal investigations that ran in the aftermath of Lassa fever and Ebola. In 1976, after the first response to Ebola was complete, Joe McCormick went to West Africa to test how widespread Lassa fever might be. Far from a rare rate of occurrence, he found that this previously unknown disease showed evidence of widespread endemicity throughout sub-Saharan Africa. It could be easily treated through an antiviral drug, ribavirin, but the low levels of economic development meant that most African governments simply could not afford to provide a reliable drug supply for their people.

Many African countries were trapped in cycles of poverty that were only exacerbated by global interventions. Global market conditions had encouraged them to switch from domestic agriculture to cash crops, but rich western nations controlled those markets, ensuring that conditions remained at merely a subsistence level for most workers. Development initiatives from the global community provided high-profile projects like dams and airports but left none of the means of maintaining them in the hands of the African governments, which led to a continual breakdown in the continent’s infrastructure. Under those conditions, maintaining a reliable network of public health was nearly impossible. Some development projects led to ecological catastrophes for local populations, such as when the creation of the Aswan High Dam in Egypt caused an increase in schistosomiasis cases because of the expanded habitat that the dam provided to the schistosome parasite. By the 1980s, governments realized that far from eradicating disease microbes, many development projects had led to resurgences in some diseases, as was the case for sleeping sickness, river blindness, and Chagas’ disease. Garrett quotes Nobel laureate Sir MacFarlane Burnet, who said, “[…] [W]hen we attempt to remold any such [stable] ecosystem, we must remember that Nature is working against us” (214).

After his Lassa work was done, McCormick was asked to investigate another suspected Ebola outbreak in Sudan, this time in the remote town of N’zara. He found a situation reminiscent of Yambuku, where an undersupplied hospital became a major avenue of transmission. Though a full survey of local animals was undertaken, none were found to be the virus’s reservoir, leaving the question of when and where Ebola might resurface unanswered.

Chapter 8 traces yet another arc from scientific optimism to a more realistic interpretation of the dangers inherent in biological complexity, but here the arc follows the story of our progress in genetic science rather than our ambitions to eradicate disease. In the 1970s humanity’s understanding of genetics was expanding at a whirlwind pace as scientists plumbed the secrets of DNA and RNA. Seeing what was happening in the genes of microbes might, they thought, give humanity another advantage in the war against disease. However, what they found was that far from being a possible weakness, genetics revealed the microbes’ greatest strength in new depth:

They soon discovered that microbes could share genes with one another that made them more formidable human enemies; […] some microbes possessed the ability to chemically manipulate the human immune system to their advantage; and there were viruses that could hide for years on end inside human DNA (225).

Bacteria, like all living things, had genetic sequences that governed their cellular life, but they could also move genes from one spot to another (“jumping genes” or transposons), exchange genes with other bacteria, or even keep backup strands of unused but potentially advantageous DNA (plasmids) floating around in their cytoplasm until they needed them.

Some of the new discoveries about microbial genetic abilities were alarming. One class of viruses—retroviruses—could invade a cell and read their own genetic programming backward to create a DNA strand that would then be incorporated into the human cell’s DNA. Such viral interactions with host DNA were discovered to lay at the root of some cancers. Areas on the human genome in which viruses could interact to cause cancer were labeled “oncogenes,” and it was gradually revealed that human and viral genetics existed in a complex, entangled relationship with one another. Various theories as to the mechanism and frequency of these viral-genetic interactions were debated, but the basic picture was already becoming clear: “[…] [I]t was an accepted tenet of biology by 1982 that viruses could directly, or perhaps through intermediary chemicals or host genes, cause the changes in cells that were the hallmarks of cancer” (233).