My father was a man of deep convictions.
He even sneezed with conviction.
He’d fumble in the hip pocket of his green work trousers—his face rapidly turning a deep shade of crimson—and produce a giant red handkerchief just in time to deliver an earsplitting “HUPSWAAAA!!!!!!!” into its depths.
I have a lasting memory of standing outside with my Dad one bright spring morning as one of his legendary eruptions frightened a long row of starlings—assembled neatly on the power line strung between our house and barn—skyward in chaotic disarray.
I’m every inch my father’s son. Fifty percent of my DNA came from my mom—but as far as sneezing goes, all my talent comes from Dad.
For decorum’s sake I suppress my explosions in public, just as my father did in church back in the day. (I can only imagine how his blood pressure spiked as he sat in his pew, desperately keeping the lid on his volcanic compulsions.)
At home—like my father before me—I let ‘er rip. Window-rattling iterations of “ACHA–WACHA–HASHAAA–HOOEY!!!!!” send my kids into gales of laughter followed by comical attempts to imitate me.
Sneezes, of course, are a protective reflex, convulsive expulsions of air from the lungs designed to blow out foreign particles that irritate our nasal passages. They’re triggered by all sorts of things: tobacco smoke, perfume, mold, dander, dust, and so on.
For some, sneezes are prompted by looking at the sun, an oddity labeled, appropriately enough, ACHOO: Autosomal Compelling Helio-Ophthalmic Outburst.
I spend my days immersed in the world of sneezery, working as I do in a pediatric emergency department, a setting in which sneezes are mostly instigated by viral respiratory infections. Roughly fifty million viral particles blast into the air with every sneeze before settling nicely in the vicinity for other little humans to collect. It’s a diabolically efficient way for respiratory viruses to spread their joy.
These days, as is the case every year when cold and flu season is in high gear, our waiting room is jam-packed with families waiting long hours for a physician’s assessment. Kids are practically hanging from the rafters, trailing rivulets of snot, coughing and sneezing and spraying payloads of virus-packed mucous in every direction and making a mockery of our efforts to limit infectious spread.
We provide protective masks to all of our “customers”. But it’s easier to lick one’s elbow than to keep a mask on the average two-year-old’s face for hours on end—not to mention keeping little fingers out of streaming noses.
During flu season, if you don’t have the flu upon arrival to the ED there’s a decent chance you—or your child—will carry it home (pro tip: WASH YOUR HANDS). After incubating the virus for a few days you get sick, expose your family members and classmates or coworkers to the disease, and more often than not trundle back to the ED for care, whereupon the contagious cycle begins all over again.
It’s a great way to amplify infectious outbreaks. And it’s good for business—for my business, that is: the flu virus pays off a good chunk of my mortgage every year. But it’s not so good for people, particularly not when pandemics (like the current coronavirus threat) march their way around the world.
All of us remember the 2009 H1N1 scare: the “swine flu” pandemic infected, by some estimates, 1.3 billion people. At the outset scientists were deeply worried that the outbreak could prove as deadly as the Spanish flu pandemic of 1918, which killed between 50 and 100 million people—up to five percent of the world’s population at the time.
Fear of H1N1 drove record amounts of traffic to our emergency department in 2009. The dire forecasts that sparked parental angst were further inflamed by the fact that the virus—in contrast to typical influenza—disproportionately infected young people. Every cough and sniffle, seemingly, prompted a trip to the ED by families seeking reassurance.
We staggered under the burden. We worked more and longer shifts, created extra spaces, and recruited extra personnel to help us cope with the stupendous volume.
Thankfully, although it was extraordinarily contagious, the 2009 H1N1 virus was much less deadly than first feared: “only” two or three hundred thousand of the world’s people died, well below the 600,000-person death toll exacted by an average seasonal flu.
After the H1N1 outbreak finally burned itself out, there were kudos all around at my hospital, much high-fiving and backslapping in recognition of how we collectively rallied to meet the crisis. Deservedly so, perhaps.
But the unvarnished truth is this: if the 2009 H1N1 virus had been anywhere near as lethal as its 1918 “Spanish” predecessor, there would have been no cause to celebrate.
There would have been no time for high-fiving or backslapping. Those of us still alive would have been too busy stacking bodies in the morgue. (In pandemics, health care workers die at substantially higher rates than the general public).
It’s fair to say, I think, that we didn’t properly respect all three limbs of the “epidemiologic triangle”. The triangle— a tool employed by epidemiologists to predict and control the spread of disease—consists of an external agent (i.e. a virus); a host (i.e. a person); and an environment that brings the agent and host together. All three are necessary for disease to spread; the extent of spread depends on their characteristics, the overlaps, and interactions between them.
We usually know (at least eventually) what the agent is, but we may have little ability to influence its behaviour. The agent will simply do what it’s programmed to do, be it Ebola, the Spanish flu, or 2019-nCoV, the new coronavirus menace. And that program can mutate rapidly, which may explain why the second wave of the Spanish flu was far more deadly than the first.
When humans are the host, we have some ability to protect and fortify ourselves: by immunization, if a vaccine is available; by washing our hands; by avoiding sick people; by eating well, getting plenty of rest, and staying fit.
Ultimately, to suffocate the spread of disease one limb of the triangle must be broken; and the environment is the limb most amenable to effective intervention.
If a highly pathogenic strain of bird flu arises in poultry, for instance—like the H5N6 variant discovered this week in China’s Sichuan province—we immediately cull entire flocks to remove the virus from the environment and prevent its spread to humans.
We don’t cull humans in similar circumstances, obviously. But we limit contamination by isolating sick patients and donning protective gear while we’re around them. China is attempting to do this on an unprecedented macro scale in the face of the 2019-nCoV outbreak, locking down Wuhan and at least 15 other major cities and quarantining more than 60 million people in the process.
The jury is still out as to whether the Chinese cordoned off the epicenter in time, or whether this sort of epic quarantine can even work as well as hoped.
We achieve the opposite of quarantine, however, by habitually crowding sick patients together for hours on end in emergency department waiting rooms, not just during pandemics but during each and every influenza season. Rather than breaking the environmental side of the epidemiological triangle we inadvertently strengthen it.
There is a better way.
In 2009 amidst the H1N1 pandemic Dr. Eric Weiss and his colleagues at Stanford University Hospital devised a far superior process, elegant in its simplicity: the drive-through emergency department.
Patients were screened while still in their cars. Those presenting with a flu-like illness were directed to a “drive-through ED” parking structure; physicians and nurses in full PPE (personal protective equipment) teamed up to assess patients ensconced within their four-wheeled “isolation” chambers. If needed, patients exited briefly to receive a more complete examination on car-side stretchers before returning to their vehicles. Most patients, following receipt of advice and simple treatments, then simply drove home.
The results were impressive. Mean length of stay plummeted. Patient satisfaction skyrocketed. Much more importantly: patients with respiratory illness remained naturally isolated from others, rather than spending hours in a waiting room potentially infecting dozens of other patients.
It remains to be seen how serious the 2019-nCoV new outbreak will be. In my February 1 piece about the emerging contagion I recorded: “Almost twelve thousand people infected. More than 250 dead.”
Ten days on those numbers have jumped considerably. As I write these lines, more than 1,000 people have died from the virus, with more than 42,000 infected, the vast majority in China’s Hubei province. (SARS, by comparison, infected 8,000 people globally and killed 774 during its entire run.)
Perhaps the coronavirus outbreak has already crested and will peter out with a whimper. Perhaps it’s just getting started. No one really knows: there is much conjecture, but not much certainty.
Either way, it’s best to be properly prepared.
It’s a great time to adapt the “drive-through ” model of care delivery pioneered by Dr. Weiss and his colleagues in California to the cold environs of Canada.
We should build it, road test it, and work out the bugs—and then polish it every year during flu season.
Then one day—when we REALLY need it in the face of a full-blown lethal pandemic—we’ll be ready. All we’ll need to do is press “START”.
It’s a very good idea—an idea, you’ll pardon me for saying, that is nothing to sneeze at.