John M. Marzluff—

Charles Darwin started his treatise on natural selection by reminding readers of how human action has transformed domestic animals. Domestication occurs because artificial selection imposed by humans causes exceptionally rapid evolution. The domestic animals we house in agricultural settings also provide a new theater for the development of deadly disease organisms. As an international team of disease ecologists and public health investigators put it: “The intensification of agriculture in the twentieth century transformed the landscape for the infectious agents of farm animals.” The results of this evolution are evident in diseases that plague swine and poultry and, increasingly, in disease outbreaks that move from farm to table. The emergence and spread of disease remind us that evolution is not merely of theoretical or economic importance; at times, it is a matter of our life and death.

Perhaps you remember the swine flu pandemic of 2009 or more recent, seemingly annual, eruptions of bird flu. As many as two hundred thousand people died from respiratory complications resulting from swine flu, most in Mexico, Argentina, and Brazil. Bird flu was mostly confined to poultry, resulting in the culling of millions of chickens, ducks, and turkeys in efforts to limit the spread of the disease to humans. Still, several hundred people died, mostly in China. Those were relatively mild outbreaks, considering that the similar Spanish flu of 1918 killed 2 to 5 percent of the entire human population (fifty to one hundred million people). Each of these flu viruses is a form of the influenza A virus that is continuously evolving within its hosts. The movements and interactions of wild birds, people, and our farm animals, especially pigs and poultry, stoke the flu’s evolution.

The cells in the upper respiratory tract of pigs are naturally able to bind influenza viruses from both pigs and humans. In this way, the RNA of human and pig flu can end up in the same pig cell. (The characteristics of viruses are encoded in the structure of their RNA, which like DNA is composed of repeated subunits that encode both the identity and assembly order of specific amino acids, the building blocks of proteins.) As the pig and human viral RNA replicates, infected pig cells house vast numbers of each type of RNA, and because this RNA is not confined in a viral nucleus and is broken up into eight small segments, it is very prone to swapping bits and pieces during replication. Exchange even occurs between pig and human viral RNA. Frequent mutation and trading of genes creates new flu strains at an alarming rate, an estimated one million times faster in viruses than in organisms such as ourselves, where mutation rates are low and merging of DNA segments from different species is virtually nonexistent. Rapid viral evolution within hogs produces strains that can bind with human cell membranes, strains that are increasingly virulent, and strains that are both. When a pig infected with the latter strain sneezes near a farmworker, pandemics, such as the Spanish flu, can result.

As we move farm animals and ourselves around the world and as birds migrate, we increase the potential for viruses to combine into new and deadly mixes. Influenza A viruses are widespread in migratory ducks, geese, swans, and shorebirds. As a result, rapidly evolving strains of flu are moved around the world seasonally as birds migrate. As humans, farm animals, and wild birds intermingle, contacting each other’s waste or sharing a breath of contaminated air, they increase the potential to share viruses and evolve strains able to infect new hosts. In this way, variants of influenza A viruses once confined to wild birds can bind to and infect the cells of pigs and chickens, while those formerly limited to horses can infect dogs. We threaten our health and food security by stoking the flames of viral evolution.

Sometimes in our desire to control disease and to increase food production, we inadvertently play right into a virus’s evolutionary gambit.

Humanity’s collective appetite for chicken is staggering. Worldwide we eat about two hundred billion pounds of it annually, according to the Food and Agriculture Organization of the United Nations. Americans seem especially fond of the bird, eating more—an average of ninety-two pounds per person in 2017—than is consumed in any other country. Farmers have been able to keep pace with our increasing demand for poultry in large part by increasing the speed at which animals grow. The time it takes to produce a five-pound broiler chicken on an industrial farm, for example, has been halved (from ten to five weeks) since the 1950s. Shortening the lifespan of a broiler chicken allowed farmers worldwide to produce more than sixty billion birds in 2016. The United States is the worldwide leader in chicken farming, bringing nine billion broilers to market in 2017, for example, according to the National Chicken Council. Just the fact that we have a National Chicken Council ought to clue us in to the prominence of this bird!

The short lifespan of a broiler chicken not only quickly fills our larders but also directs the rapid evolution of chicken viruses in a novel way. Typically, the killing power, or virulence, of a disease that remains within a host for long periods is reduced to an intermediate level by natural selection. One theory posits that viruses are of intermediate virulence because those that are overly potent kill their hosts before they can infect others, while benign viruses produce few offspring and enable hosts to develop immunity. Throttling down virulence seems consistent with a pattern exhibited by the virus that produces Marek’s disease in chickens. In response to the halving of broiler lifespans over the past sixty years, the losses from Marek’s disease have also substantially increased. Increasingly virulent strains of the Marek’s disease virus cause cancer and death in the chickens they infect. As losses have mounted, farmers have vaccinated their flocks, but immune strains have quickly evolved, and virulence has continued to climb. Losses of chickens to Marek’s disease have become so severe that now nearly every broiler is vaccinated while still in the egg or within its first day of life.

It is likely that the rapid evolution of highly virulent strains of Marek’s disease virus resulted from the use of vaccines as well as from the shortened lifespan of broilers. Vaccination prolonged the life of infected chickens, and while it controlled the spread of viral strains of low virulence, it afforded resistant and increasingly virulent strains a haven where they could survive and reproduce in a host kept alive by artificial means. In addition to this benefit, the typical cost of high virulence—killing the host and therefore shortening the period of disease transmission—was also relaxed because broilers lived just seven weeks before slaughter. The intensification of chicken production, while providing protein to a growing and increasingly affluent human population, has inadvertently increased the pathogenicity of a killer virus. Marek’s disease hasn’t yet jumped from chickens to other species, but just as it evolved increased strength, so too it may develop the ability to infect a broader range of hosts by bumping into a pig or human virus and swapping a bit of RNA. That possibility keeps public health officials up at night.

From In Search of Meadowlarks by John M. Marzluff. Published by Yale University Press in 2020. Reproduced with permission.

John M. Marzluff is professor of environmental and forest sciences at the University of Washington and is the author or coauthor of several books, including In the Company of Crows and Ravens; Dog Days, Raven Nights; and Welcome to Subirdia.

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