Spillover: Animal Infections and the Next Human Pandemic

by David Quammen

An atypical pneumonia can be any sort of lung infection not attributable to one of the familiar agents, such as the bacterium Streptococcus pneumoniae.

superspreader is a patient who, for one reason or another, directly infects far more people than does the typical infected patient.

Finding an entirely new pathogen is more difficult. You can’t detect a microbe by its molecular signature until you know roughly what that signature is. So the lab scientist must resort to a slightly older, less automated approach: growing the microbe in a cell culture and then looking at it through a microscope.

the virus became known as SARS coronavirus, inelegantly abbreviated as SARS-CoV. It was the first coronavirus ever found to inflict serious illness upon humans.

Eating wild, Greenfeld explained, was only one aspect of these new ostentations in upscale consumption, which might also involve patronizing a brothel where a thousand women stood on offer behind a glass wall.

By the time that paper appeared, the SARS epidemic of 2003 had been stopped, with the final toll at 8,098 people infected, of whom 774 died.

“consensus primers,” meaning generalized molecular jump-starters that would amplify RNA fragments shared commonly among coronaviruses, not just those unique to the SARS-like coronavirus that Guan Yi had found in his civets.

It meant that horseshoe bats are a reservoir, if not the reservoir, of SARS-CoV. It meant that civets must have been an amplifier host, not a reservoir host, during the 2003 outbreak.

What have we learned from the SARS experience? One thought that turns up in the latter sort is that “humankind has had a lucky escape.” The scenario could have been very much worse. SARS in 2003 was an outbreak, not a global pandemic.

One further factor, possibly the most crucial, was inherent to the way SARS-CoV affects the human body: Symptoms tend to appear in a person before, rather than after, that person becomes highly infectious.

That order of events allowed many SARS cases to be recognized, hospitalized, and placed in isolation before they hit their peak of infectivity.

If SARS had conformed to the perverse pattern of presymptomatic infectivity, its 2003 emergence wouldn’t be a case history in good luck and effective outbreak response. It would be a much darker story.

When the Next Big One comes, we can guess, it will likely conform to the same perverse pattern, high infectivity preceding notable symptoms. That will help it to move through cities and airports like an angel of death.

(An ordinary bacterium differs from a virus in several obvious ways: It’s a cellular organism, not a subcellular particle; it’s much larger than a virus; it reproduces by fission, not by invading a cell and commandeering the cell’s machinery of genetic copying; and it can usually be killed by antibiotics.)

Lyme disease, psittacosis, Q fever: These three differ wildly in their particulars but share two traits in common. They are all zoonotic and they are all bacterial. They stand as reminders that not every bad, stubborn, new bug is a virus.

intracellular bacterium, meaning that it reproduces within cells of its host—as does a virus, though by dissimilar mechanisms—not out in the bloodstream or the gut, where it could be more easily targeted by immune response.

The Netherlands is a crowded country, containing 16 million people within an area half the size of Indiana, and many of those high-density goat farms are sited near towns and cities.

one genotype present in 90 percent of all samples. And that is what we call the CbNL-01.” CbNL-01 seems a fancy cryptogram but it connotes simply “Coxiella burnetii, Netherlands, genotype #1.”

no matter by what method a parasite passes from host to host, an increased density of the susceptible population will facilitate its spread from infected to uninfected individuals.”

“Deer ticks” of the species Ixodes scapularis do not draw their crucial sustenance from deer.

Larval ticks are minuscule and even a tiny masked shrew, weighing only five grams (about the same as two dimes), carried on average fifty-five ticks, the researchers found.

The unchanging fact is that Borrelia burgdorferi infection doesn’t pass vertically between blacklegged ticks. In plainer language: It is not inherited. Of those million baby ticks, all derived from the female ticks that fed on a single deer, none will be carrying B. burgdorferi when they hatch

“reservoir competence.” This is the measure of likelihood that a given host animal, if it’s already infected, will transmit the infection to a feeding tick.

White-footed mice love acorns and, because the mice reproduce quickly and mature quickly, responding to food abundance with bursts of heightened fecundity, big masting events are often followed (after a two-year lag) by big increases in the mouse population.

More acorns, more mice, more infected ticks, more Lyme.

In forest patches containing a full cast of ecological players—medium-sized predators such as hawks, owls, foxes, weasels, and possums, as well as smallish competitors such as squirrels and chipmunks—the populations of white-footed mice and shrews are relatively small, held in check by predation and competition.

Bear in mind that any patch of forest, surrounded by pavement and buildings and other forms of human impact, is to some degree an ecological island. Its community of land animals is insularized because, when individuals try to leave or to enter, they get squashed.

When assaulted with antibiotics, for instance, B. burgdorferi seems to retreat into a defensive, impervious form, a sort of cystlike stage known as a “round body.” Round bodies are resistant to destruction and very difficult to detect. A patient who seems cured of Lyme disease by the standard two-to-four-week course of amoxicillin or doxycycline might still be harboring round bodies and therefore subject to relapse.

a swirl of late-nineteenth-century ideas that commonly get lumped as “the germ theory” of disease, which marked a movement away from older notions of malign vapors, transmissible poisons, imbalanced humors, contagious putrefaction, and magic.

But the first viral infection recognized in humans wasn’t smallpox; it was yellow fever, in 1901.

A virus won’t grow in a medium of chemical nutrients because it can only replicate inside a living cell. In the technical parlance, it’s an “obligate intracellular parasite.” Its size is small and so is its genome, simplified down to the bare necessities for an opportunistic, dependent existence. It doesn’t contain its own reproductive machinery. It mooches. It steals.

So a genome of just two thousand code letters, or even thirteen thousand (as for the influenzas) or thirty thousand (the SARS virus), is a very sketchy set of engineering specs.

Viruses face four basic challenges: how to get from one host to another, how to penetrate a cell within that host, how to commandeer the cell’s equipment and resources for producing multiple copies of itself, and how to get back out

The individual viral unit, one particle, standing intact outside a cell, is called a virion. The capsid also defines the exterior shape of a virus. Virions of Ebola and Marburg, for instance, are long filaments, which is why they’ve been placed in a group known as filoviruses.

Many viruses are wrapped with an additional layer, known as an envelope, comprising not only protein but also lipid molecules drawn from the host cell

Across the outer surface of the envelope, the virion may be festooned with a large number of spiky molecular protuberances,

Those spikes serve a crucial function. They’re specific to each kind of virus, with a keylike structure that fits molecular locks o...

The specificity of the spikes not only constrains which kinds of host a given virus can infect but also which sorts of cell—nerve cells, stomach cells, cells of the respiratory lining—the virus can most effectively penetrate, and therefore what sort of disease it may cause.

viruses are impervious to antibiotics—chemicals valued for their ability to kill bacteria (which are cells) or at least impede their growth.

Tetracycline works by interfering with the internal metabolic processes by which bacteria manufacture new proteins for cell growth and replication. Viruses, lacking cell walls, lacking internal metabolic processes, are oblivious to the effects of such killer drugs.

Inside the viral capsid is usually nothing but genetic material, the set of instructions for creating new virions on the same pattern. Those instructions can only be implemented when they’re inserted into the works of a living cell.

The different attributes of DNA and RNA account for one of the most crucial differences among viruses: rate of mutation.

RNA viruses, coded by a single-strand molecule with no such corrective arrangement, no such buddy-buddy system, no such proofreading polymerase, sustain rates of mutation that may be thousands of times higher.

The basic point is so important I’ll repeat it: RNA viruses mutate profligately.

Mutation supplies new genetic variation. Variation is the raw material upon which natural selection operates.

RNA viruses therefore evolve quicker than perhaps any other class of organism on Earth. It’s what makes them so volatile, unpredictable, and pesky.

Of course, positive results on antibody tests meant only that those eleven monkeys had been exposed to the virus, not that they were presently infected, let alone shedding herpes B.

To understand why some outbreaks of viral disease go big, others go really big, and still others sputter intermittently or pass away without causing devastation, consider two aspects of a virus in action: transmissibility and virulence.

Transmission is travel from one host to another, and transmissibility is the packet of attributes for achieving it. Can the virions concentrate themselves in a host’s throat or nasal passages, cause irritation there, and come blasting out on the force of a cough or a sneeze?

In fact, virulence is such an iridescent, relativistic concept that some experts refuse to use the word. They prefer “pathogenicity,” which is nearly a synonym but not quite. Pathogenicity is the capacity of a microbe to cause disease. Virulence is the measurable degree of such disease, especially as gauged against other strains of similar pathogen.