Stopgap measures against H5N1 bird flu can only go so far

In the summer of 2023, I connected with an epidemiologist from Kerala. A lush sliver of land along the Indian peninsula’s southwestern edge, it is a place of sleepy backwaters and rolling hills of spices. It is also known for its forests. There, a man from the leafy village of Maruthonkara had died from Nipah virus.

Outbreaks of Nipah virus are alarmingly common: They occur seasonally in parts of Bangladesh and nearly as often in Kerala, where there have been six since 2018. Borne of frugivorous bats — and, on occasion, passed between people who become ill — the virus causes encephalitis, inflaming the brain’s tissues in a process that is fatal in as many as 70% of those who become infected. In a string of WhatsApp messages and voice notes, I was getting this epidemiologist’s perspective on the latest outbreak at the time. And what I took from him surprised me.

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It was not simply the belief in a diligent surveillance of the virus’ motions. Rather, it was the paradox of having a system in place to detect outbreak after outbreak, to contain them, all while having little means to prevent them. Which gave rise, recently, to a troubling thought: Will our efforts against H5N1 — or bird flu, as we know it — bind us to a similar Sisyphean-like struggle?

After initial reports in Texas dairy cattle last March, H5N1 has come to be identified in 964 livestock herds across 17 states. Meanwhile, the Centers for Disease Control and Prevention has confirmed 67 infections in humans — mainly in dairy workers. All had manifested mildly until an older man in Louisiana, after tending to dead birds in a backyard flock, became both the first person in the U.S. to become critically ill from bird flu and the first to succumb to its effects. In California, the ramping up of the virus’ proclivity for human and bovine hosts seemed to culminate in a decision to declare a state of emergency.

It’s reasonable to have faith in solutions that aim to stem the virus’ spread. Bolstering testing and monitoring measures, building vaccine stockpiles, and providing personal protective equipment to agricultural laborers who, for now, are most at risk are stopgap fixes that are critical to the moment.

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But alone, they dismiss an outsized advantage we possess over bird flu — one that is greater, arguably, than our standing with any other pathogen we have come to know.

Influenzas of avian origin have plagued humanity for almost a century and a half, and are therefore neither novel nor understudied. In the wake of their periodic wreckages, we have picked up knowledge of them down to their very minutiae — enough to fashion reliable treatments that disrupt the function of the microscopic proteins that stud their surfaces; to know when companion viruses wriggle their way into the same cell, shuffling segments of their genomes to generate new adaptations of themselves, each can be virulent in new and different ways. Today, we can even predict the prospect of a pandemic down to the nanometer of a single, imperceptible mutation in a virus’ genetic code.

Larger and more conspicuous forces also lift a contagion into prominence. We happen to know about these, too. Countermeasures need not come only in a vial or a swab. In fact, they can help the virus not become the virus altogether.

We can explain how the range of pathogens expand under the turmoil of a changing climate. As is the case for bird flu, the strain of H5N1 now circulating in North America arrived during the winter of 2021, after a swelling of the virus among European wild birds and amid a set of some of the most active Atlantic hurricane seasons on record. The ripples of such effects are felt keenly by the natural world, including by wild waterfowl, which harbor bird flu most effectively. Their migratory patterns and behaviors, in response, are prone to change.

Infected birds intermingle with uninfected ones. States of stress or mismatches between the green-ups of vegetation and the arrival of migrations, as a consequence of extreme weather events, lead to suppressed immune systems; and, in turn, higher burdens of virus in their bodies. Birds then carry it over great distances. There it spreads — among other birds, then on to foxes, seals, polar bears, cats big and small.

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Evolution is a game of odds. And as it is, each infection gives bird flu a spin at the wheel to become something utterly terrible. But, if it does, it likely does so far from any gathering of animals in the wild.

Instead, as the global appetite for animal products grows, so do our concocted congregations of them. H5N1 had its origins on a small chicken farm in Scotland in 1959. Such a farm may be hard to recognize these days. Authorities on the subject of intensive livestock production estimate that over 10 billion land animals are now raised annually for human consumption in the United States. Virtually every one is wholly confined in a highly concentrated factory farm.

Such places harbor a potpourri of pathogens from their crowding of homogenous animals, unyielding use of antibiotics, and alterations of natural environments. And so, they are a bridge between universes: those of microbes and our own. Brushing with unwitting wildlife and the people who tend to them, a single facility can house more than 5 million animals. In a manner of speaking, that’s 5 million pathways for one to be brought, ultimately, to a human. The gargantuan industries of animal husbandry and the small markets that peddle local wildlife may seem operationally distinct. But the common ground they share is a lack of meaningful regulatory oversight related to a patchwork of policies that govern them. It is why, altogether, more than 50% of infections that spill over from animals come to do so in agricultural settings.

In another chapter of a similar story, a mysterious wave of fever and neurological symptoms befalls Malaysian pig farmers. Scientists are puzzled. Eventually, they trace the farmers’ illnesses to the Nipah virus, which swine acquire from ingesting the virus-laden excreta of bats who had encroached onto their feedlots.

Before future studies would uncover a link between Nipah outbreaks and the felling of native forests for the purposes of fruit plantations, more than 1 million pigs are culled to quell an outbreak that leads to the deaths of 105 people.

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Efforts in the decades since to contain the Nipah virus — which now might coat the fallen areca and cashew nuts some might handle, or float in the date palm sap others might drink — to keep it from unspooling into something larger than a handful of tragic cases, have been a recurring mission for the epidemiologist I spoke to. But “tests and treatments have a linear [relationship] to outcomes,” he told me. Preventing infections remained his ambition, except this required parsing through the messiest data of all: how we live.

It means looking not at a virus for answers — but to ourselves. Environmental and agricultural reforms to protect us from a virus that moves from one species to the next, looming over us the possibility of a pandemic, mean asking why, as people, we desire the things we do, and what a world from which we take so much from will eventually return to us.

Arjun Sharma is an infectious diseases physician in Toronto.