Pandemic: Tracking Contagions, from Cholera to Coronaviruses and Beyond

by Sonia Shah

Thus the WHO’s activities, the agency’s director-general Margaret Chan admitted in an interview with The New York Times, are no longer driven by global health priorities but rather by donor interests.83 And those interests have introduced a pronounced distortion into the WHO’s activities. While the agency’s regular budget is allocated to different health campaigns in proportion to their global health burden, according to an analysis of the agency’s 2004–2005 budget, 91 percent of the WHO’s voluntary contributions were earmarked for diseases that account for just 8 percent of global mortality.84

Of course, even if political leaders are corrupt and political institutions are rotten, people can still cooperate with each other. They can take matters into their own hands, launching their own cooperative efforts to contain pathogens. For example, when city leaders failed to alert New Yorkers to the spread of cholera in the nineteenth century, private physicians banded together and issued their own bulletins. Such actions make sense. And extreme events do tend to bring people closer together. Think of New Yorkers after the September 11 terror attacks or in the wake of recent hurricanes. But that’s not what tends to happen when pandemic-causing pathogens strike. Unlike acts of war or catastrophic storms, pandemic-causing pathogens don’t build trust and facilitate cooperative defenses. On the contrary, due to the peculiar psychic experience of new pathogens, they’re more likely to breed suspicion and mistrust among us, destroying social bonds as surely as they destroy bodies.

Another popular antivaccine claim is that drug companies push vaccines solely to make more money. This too is contrary to fact. Corporate influence on vaccine promotion is relatively slim. Indeed, drug companies have considered vaccines so unprofitable that during the 1990s and 2000s, many abandoned the vaccine business altogether. Between 1998 and 2005, nine vaccines required for routine childhood immunizations suffered chronic shortages as a result.62

Epidemics are sparked by social conditions as much as they are by introductions. Whether it’s deforestation and civil war in West Africa, the lack of sanitation and modern infrastructure in Haiti, or the crowding and filth of nineteenth-century New York City, without the right social conditions, epidemics of cholera and Ebola would have never occurred. Should health-care workers in West Africa, UN soldiers in Haiti, or Irish immigrants in nineteenth-century New York be held responsible for those, too?

Drug development is slow and constrained by the economic concerns of the for-profit pharmaceutical industry. If the market for a new drug is modest, it doesn’t matter how big the public-health need for it is, or how solid the scientific evidence supporting its effectiveness: that drug is unlikely to get to market. There are precious few drugs developed for diseases, like malaria and Ebola, that selectively afflict the poor. Malaria sickens hundreds of millions of people every year, but since most of those victims have less than $1 a year to spend on health care, the market for new malaria drugs is vanishingly small.

Disease is intrinsic to the fundamental relationship between microbes and their hosts. All it takes to confirm that is a brief tour through the history of microbial life and a peek inside our own bodies. Humans dominate the planet in modern times, but in the past, it was the microbes that ruled. By the time our earliest ancestors, the first multicellular organisms, clambered out of the sea around 700 million years ago, microbes had been colonizing the planet for nearly 3 billion years. They had radiated into every available habitat. They lived in the sea, in the soil, and deep inside Earth’s crust. They could withstand a wide range of conditions, from temperatures as low as 14°F to as high as 230°F, feeding on everything from sunlight to methane. Their hardiness allowed them to live in the most extreme and remote places. Microbes colonized the pores inside rocks, ice cores, volcanoes, and the ocean’s depths. They thrived in even the coldest and saltiest seas.

Grasping this rather counterintuitive notion requires a brief digression into what’s called the “selfish gene theory” of evolution. The basic idea is that genes—or, rather, the genome, which is the entire complement of genes in a given individual—are the movers and shakers of evolution. The genome consists of long twisted molecules of DNA (or RNA), which are carried around in each of our cells, bits of which (the genes) provide instructions for a wide range of biological traits, from eye color to nose shape to the sound of one’s voice. According to the selfish gene theory, all of evolution can be boiled down to their machinations. Some genes, by dictating or “coding” for traits that help them spread more widely, become dominant. Others, which code for traits that are useless or harmful to their own dissemination, die out.

But senescence and death are not inevitable facets of life. There are examples of immortality all around us. Microbes live forever. Trees don’t deteriorate with time. On the contrary, as they age they get stronger and more fertile. For microbes and many plants, immortality is the rule, not the exception. There are even some animals that don’t age: clams and lobsters, for example. Death, for them, is caused solely by external factors, not internal ones.

The discovery of these genes dates back to the 1970s, when scientists found that removing certain glands from a female octopus could postpone her otherwise inevitable death. Normally, a female octopus will stop eating and die, like clockwork, ten days after she finishes tending her eggs. But surgically removing the glands that control maturation and breeding resulted in an octopus that behaved quite differently. After laying her eggs, she resumed eating and survived for another six months.9 Scientists have similarly pinpointed genes with no known purpose other than to trigger deterioration and death in worms and flies. When those genes are experimentally inactivated, death is delayed. The worms and flies live on.

That force may be pathogens causing repeated cycles of epidemics. To cause repeated epidemics in the same population, a pathogen must switch between different strains to evade detection, like a thief using different disguises to repeatedly rob the same bank. Retaining a large number of pathogen-detection genes among us ensures that there’ll always be a few individuals who can suss out the latest disguise. Each pathogen-detection gene variant thus neither fully dies out nor sweeps into dominance. We carry them around with us, like a treasure chest full of specialized detection tools handed down from generation to generation.15

The disease historian William McNeill hypothesizes that these highly localized immune behaviors contributed to the development of the caste system in India, in which strict rules limit contact between castes, and there are elaborate rules for purifying the body if contact occurs. These may be the result, in part, of each group having specific immune behaviors tailored to its local pathogens, McNeill speculates, and the resulting need for a system that policed group boundaries.