Spillover: Animal Infections and the Next Human Pandemic

Quammen describe a 1993 caterpillar infestation near his Montana residence. The “tent caterpillars” stripped virtually all leaves from the area trees. This memory illustrates what ecologists call an “outbreak […] any vast sudden population increase by a single species” (495). One example, as it turns out, is humanity’s own population explosion since roughly the end of the Black Death. No animal has grown in comparable numbers.

Ecological outbreaks, Quammen warns, typically end. Viruses play a significant role in this, including in his personalized case study of tent caterpillars. He corresponded with an entomologist who identified a line of viruses “called nuclear polyhedrosis viruses, known collectively as NPVs, which ‘may be the long-sought driving force of population cycles in forest Lepidoptera’” (498).

Later, when attending a conference on infectious disease as part of his book research, Quammen met a mathematical ecologist who used NPVs as an example of how outbreaks work. Caterpillars infected with NPV literally “melt” onto leaves, leaving this residue behind to infect other caterpillars. Some also remains on eggs, so baby caterpillars can be born and infected. Quammen asked Dwyer if humans faced a similar threat, given their own abundance, and found himself in a discussion of influenza.

While influenza has long been known, the strain that caused the 1918-1919 pandemic was not identified until 2005. By the 1950s, it was clear that flu infected many animals but not yet clear whether the disease was zoonotic or had a reservoir host. In 1961, a wild tern in South Africa was found to contain influenza. Not long after, two friends, an Australian and a New Zealander, went for a walk, observed some dead seabirds, and began to ask questions. Those friends, Graeme Laver and Robert Webster, applied for various research grants to study birds in the Great Barrier Reef to search for influenza and found some.

Webster became a flu expert and spent his career at St. Jude’s Research Hospital in Memphis. As an RNA virus, flu has a high mutation rate. But it also engages in “swapping” of genomic segments due to its “segmented” structure. This explains why the flu changes every year and is so difficult to vaccinate against. This also has implications for animal flus—while some only infect one animal, pigs can be infected with both bird and human types, leading to even more “recombination.” So far, only some types of flus infect humans, and when humans are infected via blood exposure, the viruses do not spread well. However, this is likely to be a temporary state of affairs.

Bird flus are of particular concern since a 1997 outbreak in Hong Kong. This was particularly poor timing for a health crisis, as it coincided with Hong Kong’s political transition back to China from the UK. Webster relied on some of his own experts to verify that the virus was present in poultry markets, which the government promptly shut down. The virus continued to “lurk” in ducks, not infecting or killing them but allowing them to spread it. It reached a waterfowl site known as Qinghai Lake, where the birds got as far as Egypt and wreaked chaos in poultry there. Webster sees this as a potential political disaster, given Egypt’s inability to cope well with outbreaks, but an even more likely public health one, as the virus will only continue to mutate and may eventually transmit from person to person with ease.

Quammen notes that when asked if we are all going to die, he always answers yes—all humans are mortal, even if most are unlikely to die of a rare or emerging zoonotic disease. Experts debate the likelihood of the “Next Big One,” but none of them dispute that it will be zoonotic (512). An epidemiologist named Donald Burke similarly stressed “evolvability” and “proven ability to cause epidemics in non-human populations” and specifically mentioned viruses similar to Hendra and SARS as likely candidates (512-13).

Burke stresses that no preparation can be perfect, but it is possible. Being ready and alert for the next zoonosis requires careful preparation to study possible zoonosis in the wild before it emerges, and the laboratory technology to identify and treat viruses. Various governmental and non-governmental bodies are focused on these issues, including the WHO and the US Department of Defense.

As a species, we humans require these experts to be on guard, but Quammen insists that we have a similar responsibility to recognize that zoonosis happens because of our choices. Humanity’s population continues to grow, we continue to invade environments, raise animals for food, and import and export animals from place to place. We continue to travel on a global scale.

Humanity’s growth has coincided with gradual interdisciplinary connections in science. Evolution has been gradually applied to germ theory and viruses and applied in turn to the study of habitats. Molecular biology was crucial to truly understanding viruses. Quammen remains pessimistic about the eradication of zoonotic disease, coming back to his original point that smallpox was only eradicable because it does not exist in animals. To conclude, Quammen comes back to Greg Dwyer, who focused his thoughts on epidemics on the role of individuals: AIDs has been more contained because human behavior has changed. SARS worsened because of superspreaders. Individual choices matter.