On march, 1918, US army recruits at Fort Riley in Kansas began complaining of headaches, fever and aching joints. The disease quickly spread through the camp’s 50,000 soldiers, then jumped the fence to turn up in military camps in Georgia and South Carolina. By March 11, it had reached Queens, New York. Flu was nothing new in the United States, and this one appeared to follow the standard MO: while it killed the elderly, or the immuno-compromised, young people soon shrugged it off.
Nevertheless, within a month, the disease appeared in transit camps across the Atlantic at Brest and Bordeaux, after US soldiers were shipped to the Western Front. By June, it was afflicting every major European centre. Throughout spring and early summer, it cut a swathe through entire battalions on both sides of the lines, then it seemed to abate.
But by August, it or something like it was back, and this time the flu had transmogrified into something more lethal. In the trenches, army medics found themselves dealing with a new horror: young men practically suffocating to death in their cots, their faces blue with cyanosis. Post-mortems revealed sodden, bloody lungs.
By now, people misled by erroneous media reports—were calling it the “Spanish flu’, (we now know it as H1N1), but it was already cosmopolitan, hitching a ride on troopships and trains to such diverse destinations as Sierra Leone, and back to the United States, where, in Philadelphia, it killed more than 12,000 in a single month 759 in one day in October. By then, the flu was truly global. As Jeffery Taubenberger, a researcher at the Armed Forces Institute of Pathology in Maryland, told National Geographic: “Everybody on Earth breathed in the virus, and half of them got sick.’
In New Zealand, some noticed that the flu of October seemed a different beast from the one that had swept the country the previous month. The most vulnerable appeared to be young, healthy adults, and it cut them down in record numbers; corpses piled up in the Auckland Domain, awaiting twice-daily trains to take them to Waikumete Cemetery, where an extra 33 grave diggers were hired to cope with up to 70 burials a day.
In all, that ‘second wave’ killed more than 8600 New Zealanders (Maori were particularly hard-hit) in less than two months.
Influenza is caused by a suite of tiny viruses, of the family Orthomyxoviridae. They infect only birds and mammals, as far as we know. There is almost nothing to a virus: just genes wrapped up in a coat of protein. Unlike most other life, virus cells cannot divide; instead, they force the victim’s own cells to manufacture thousands of identical copies of them.
Viruses are just one of the raft of disease-causing agents we call pathogens, or what your mum would have called ‘germs’. Together with bacteria, protozoans, prions, fungi and worms, they perpetuate some of the most virulent contagious diseases on the planet.
Most have a preferred target, or host, but every now and then, either by coincidence or aberration, a pathogen jumps the species barrier from non-human to human (and sometimes back the other way).
Often, it will either fail to establish or infect only the single individual it enters. But should that pathogen secure a toe-hold and find a way to its next host, you have the makings of a pandemic. Ebola, anthrax, mad cow disease, rabies, bubonic plague, yellow fever, monkey pox, bovine tuberculosis, Lyme disease, West Nile fever, Ross River fever all originated in other creatures before jumping to humans, a phenomenon we call zoonosis. And it’s far more common than you think; around 60 per cent of contagious diseases shift between humans and other species.
Viruses might be rudimentary, but they’re supremely, you could even say beautifully, fit for purpose. Their simple genetics a typical influenza virus has just eight genes—mean they can mutate on a dime. In addition, RNA enzymes, common in viruses, often make mistakes, leading to new strains, vastly outpacing our own ability to evolve defences. Antibiotics are useless against them (although new anti-viral drugs, such as those developed to fight HIV, are showing some promise).
Above all, viruses are consummate stow- aways, equally at home in the gut of a mosquito, macaque or mechanic. Some employ a ‘reservoir host’—an intermediary that may suffer few or no ill effects, but is merely employed as a way of getting from A, through B, to C. Bats are a common choice, and therein lies the true beauty of viral ecology bats have been around for a long time, and their power of flight means they’ve populated almost every suitable habitat on Earth. Some gather in roosts of thousands, making viral transfer a doddle, and their habit of wide foraging, from forest floor to canopy, puts them in contact with a plethora of other creatures, some of which could be ideal end hosts.
For many of the same reasons, birds are extremely effective agents.
Pathogen-host relationships have endured for millennia, but new diseases, or different strains of a known one, break out routinely. This often happens when, for some reason, the pathogen switches reservoir hosts, a development known as ‘spillover’. We don’t know exactly what prompts spillover, but it typically happens when historically disconnected creatures come into contact, as when farmers cut deep into rainforest. Or it may be a result of habitat loss forcing species into co-existence.
For something like a virus, the risk of leaving a comfy, functional relationship for unfamiliar territory carries huge risks. It might, for instance, kill its new host before finding a vector for its onward journey an evolutionary brick wall. But the rewards are great: a vast new opportunity for range expansion and population growth.
Ever the opportunists, pathogens will exploit any confluence of man and beast. Simian foamy virus (SFV) infects monkeys and humans in Asia, seizing the moment when Buddhist and Hindu monks make offerings to semi-tame macaques. But the big payout for SFV comes when international tourists come to visit. Pathogens now travel at the speed of an Airbus.
It’s tempting to imply that a speck of protoplasm makes deliberate choices, employing well-considered and sinister life strategies, but pathogens are no less bound by evolutionary forces than the rest of us they’re simply more flexible under their influence. Consider again the influenza virus. In a normal urban environment, people really sick with flu those afflicted with a virulent strain stay in bed, limiting that strain’s chances of transmission.
On the other hand, the mildly ill (or the martyrs) continue to go to work, greatly facilitating a lesser strain’s spread. Selection pressures have favoured that strain.
On the Western Front, those evolutionary pressures were reversed: soldiers with a mild strain stayed in the trenches, while the critically ill were packed into trains bound for crowded field hospitals a gift for the deadlier ‘second wave’ virus, which went on to kill between 50 and 100 million people.
There’s speculation that the second wave that struck New Zealand that fateful October was a hybrid, the product of an unholy marriage between a ‘domestic’ strain and the Spanish flu. It’s an easy matter for different flu strains to swap genetic material should they meet. Ordinarily, a bird flu can’t infect humans it’s not adapted to survive in our cells but if it should somehow fraternise with a human flu (called re-assortment). their ‘progeny’ might inherit the capabilities of both strains.
But first, they have to infect the same animal. Very few creatures are susceptible to both viruses, but there is one, and it can be found the world over. Any pig could conceivably catch flu from the ducks it shares a barnyard with and the farmer who tends it.
If those two strains re-assort, the resulting hybrid could infect human cells, bringing with it bird-virus genes our immune systems have never encountered. Because we have no defence against hybrid flus, they’re especially deadly: two separate re-assorted pandemics H2N2 ‘Asian’ in 1957 and H3N2 ‘Hong Kong’ in 1968—killed around two million people. Since H5N1 ‘Avian influenza’ appeared in 2003, it’s killed more than half the humans it’s infected. The only thing standing between us and disaster is the fact that, while H5N1 has figured out how to jump from birds to humans, it hasn’t yet found a way to transmit from human to human, at least not on an epidemic scale.
Many infectious disease experts believe it’s simply a matter of time.
Nothing, not even World War I, killed as many New Zealanders in such a short space of time as Spanish flu. Globally, it may have killed more people than the plague. In 1996, Taubenberger went looking for reasons. He delved into lung tissue preserved from a victim who died in 1918, in South Carolina, and found bits of H1N1’s genes still intact.
More clues later came from the corpse of a young woman, hurriedly buried in a mass grave in Alaska the same year, but the strands have yet to reveal any smoking gun. Interestingly, though, pigs were widely observed to fall ill during the pandemic, and an epizootic the following year laid waste to swine herds across the US Midwest.
H1N1’s deadly secret remains just that, but a comparison of five of the eight RNA segments with today’s workaday strains confirmed a long-held suspicion: without doubt, the Spanish flu originated in some other creature, then jumped into humans who had no defence.
At the head of Eucalyptus Way in Waikumete stands a single granite headstone, a memorial to the many who lie in unmarked graves to this day. It might also remind us not to underestimate a nanometric speck of protein and eight genes.