We Need to Rethink Our Food System to Prevent the
Next Pandemic
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Agricultural laborers spray
against insects and weeds inside the orchards of a fruit farm in Mesa,
California.
Brent Stirton—Getty Images
Ideas
By Laura Spinney
April 13, 2020
Spinney is the author of Pale
Rider: The Spanish Flu of 1918 and How it Changed the World.
Once a dangerous new pathogen
is out, as we are seeing, it can be difficult if not impossible to prevent it
going global. One as contagious as SARS-CoV-2 has the potential to
infect the whole of humanity. Eighty per cent of cases may be benign, but with
such a large pool of susceptible hosts, the numbers who experience severe
illness and die can still be shockingly high. So the only sensible answer to
the question, how do we stop this from happening again, is: by doing all we can
to prevent such pathogens infecting humans in the first place. And that means
taking a long, hard look at our relationship with the natural world, and
particularly with the animals that sustain us.
SARS-CoV-2,
like the influenza virus and many other disease-causing microbes, initially
infected an animal – probably a bat in the case of SARS-CoV-2. The term for
when such a microbe jumps the species barrier into humans is “spillover.”
Spillover has always happened, but it was accelerated by the introduction of
farming around 12,000 years ago, which brought humans and the animals they
domesticated into close proximity – making the jump easier.
The last
century saw a lull in spillover, largely due to improved nutrition and hygiene,
but it has been increasing again in
recent decades. This is partly to do with the sheer number of us, and the
extent to which we’re connected through global travel and trade, but there is
growing evidence that it is also connected with the way we produce our food –
and in particular, the novel ways in which modern farming forces humans,
animals and microbes together. The problem goes way beyond food markets in
China, implicating food production systems on all continents.
Addressing that problem won’t
stop this pandemic, but if the world’s experience of Covid-19 has a silver
lining, it could be that it galvanizes us to take seriously our role in
manufacturing our own diseases.
The list of exotic-sounding
diseases that have recently become human problems is impressive. “This century
we’ve already trainspotted novel strains of African swine fever, Campylobacter,
Cryptosporidium, Cyclospora, Ebola, E. coli O157:H7,
foot-and-mouth disease, hepatitis E, Listeria, Nipah virus, Q fever,
Salmonella, Vibrio, Yersinia, Zika, and a variety of novel influenza A variants,
including H1N1 (2009), H1N2v, H3N2v, H5N1, H5N2, H5Nx, H6N1, H7N1, H7N3, H7N7,
H7N9, and H9N2,” wrote evolutionary biologist Rob Wallace of the
Agroecology and Rural Economics Research Corps in Saint Paul, Minnesota, on 29
January. “And near-nothing real was done about any of them.”
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Wallace is the author of Big
Farms Make Big Flu (2016) and an outspoken critic of agribusiness, but he’s
not the only one to have noticed that farming practices are shaping our disease
ecology – and not in a good way. Spatial epidemiologist Marius Gilbert of the
Université Libre de Bruxelles in Belgium, and colleagues, have clearly demonstrated
a link between intensive poultry production and the emergence of highly
pathogenic forms of avian flu, for example. And a 2015 study published
by Martha Nelson of the U.S. National Institutes of Health, and colleagues,
demonstrated that Europe and the U.S. – the world’s biggest exporters of swine
– are also its biggest exporters of swine flu. A swine flu that spilled over
into humans is what caused the most recent flu pandemic, in 2009, the first
cases of which were recorded in California.
Normally, when a new pathogen
emerges in a host population, and assuming it is transmitted directly from host
to host, it gradually moderates its virulence in order to keep those hosts
alive for long enough to spread it far and wide. But in a factory farm – where,
say, chickens, are densely packed together and host-to-host transmission is
easy – the evolutionary pressure on the pathogen to moderate its virulence is
relieved. And because those chickens tend to be near genetic clones of each
other – due to decades of selection for desirable traits such as lean meat – a
pathogen introduced into that chicken population can race through it without any
genetic “firebreak” to slow its progress. Experiments and field observations
have both demonstrated that such serial passage through a host
population can ratchet up the pathogen’s virulence.
Two relatively new and
dangerous forms of avian flu, H5N1 and H7N9, are thought to have first spilled
into humans in China, whose poultry industry underwent rapid industrialization
from the 1980s on. But similar mechanisms may have been at work in swine herds
far beyond China. Porcine reproductive and respiratory syndrome (PRRS), a
disease of pigs that was first described in the U.S. in the late 1980s,
has since spread to herds across the world. Strains of PRRS detected recently
in China are more virulent than the early American ones.
Though the
original animal reservoir for SARS-CoV-2 was probably a bat, scientists think
the virus passed through an intermediate animal host before it spilled over
into humans. That animal – possibly the spiny mammal called a pangolin – was
probably sold as food in a market in China.
Most of the animals sold in
such markets are produced by smallholders, not large industrial concerns, but
the two are not easily separable. Many smallholders took up the
cultivation of “wild” animal species after they were pushed out of livestock by
the big farming conglomerates – and their exodus was accelerated by the
economically disastrous appearance of diseases such as PRRS in their herds. As
the large-scale farms took over more and more land, the smallholders were also
displaced geographically – closer to difficult-to-cultivate zones such as
forests, where bats lurk. The risk of a bat virus spilling into a pangolin or
other mammal, and from there into humans, increased.
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In other words, Wallace says,
the causes of the spillover of SARS-CoV-2 lie in a complex web of relationships
and the way they have shifted over time and space. The forces shaping our
disease ecology – and driving the emergence of new infectious diseases – can be
traced back to a growing, increasingly wealthy and increasingly urbanised human
population, and the behavioural choices that population makes. Infectious
disease is not the only downside of that growth or those choices either. Others
include antimicrobial resistance and elevated greenhouse gas emissions.
Though it may not feel like it
now, we have been let off lightly with SARS-CoV-2. Experts suggest that its
case fatality rate – the proportion of those who fall sick who go on to die –
will likely settle around 1 to 2 per cent, once all the data are in. It is
undoubtedly a dangerous pathogen, but H7N9 kills close to a third of the humans
it infects, and H5N1 an even higher proportion. Neither of those have caused a
pandemic – yet – but the prospect of their global spread doesn’t bear thinking
about, and meanwhile new
zoonoses continue to emerge. We can prevent or at least slow them, but to do so
we need to start talking about our lifestyle choices and the industries that
satisfy them. The time to do that is now.
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