Now that Swine Flu has gone from the Dire Plague That Will Kill Each And Every One Of Us to the butt of forwarded e-mail jokes, it may be time to take a look at this latest mutation of the influenza virus and compare it to its big, moustache-twirling older brother, “La Grippe”, the Spanish Flu that caused 50 million deaths in 1918 and 1919. What can we draw from the development and spread of the first truly global pandemic?
This latest instalment in the viral franchise belongs to the H1N1 family, that family of bugs that circle the globe each year, spread by that annoying jackass in the office who refuses to stay home and killing about 0.1% of those they come into contact with. It is an airborne virus, spread by coughing and sneezing, making transmission incredibly easy in crowded environments such as urban areas, schools, public transport and aircraft.
The Spanish Flu that erupted in Europe and spread across the rest of the globe was also a member of this same family. Back in 2007 a group of scientists at Canada’s National Microbiological Laboratory, pondering the dangers posed by an outbreak of Avian Flu exhumed the preserved body of a flu victim buried in Arctic permafrost. Having extracted RNA, the genetic material needed to work out the structure of the 1918 virus, they brought it to life by combining it with modern strains of the flu. In a horrible turn of events, monkeys infected with the strain had to be put down within a matter of days as they began to drown in their own blood — a distinctive marker of the 1918 pandemic. For the first time, scientists had a picture of one of the greatest killers in history — it was a clear precursor to the H1N1 virii prevalent today.
In many ways the Spanish Flu arrived on the scene like the flu of every other year and that may have been one of the reasons it managed to end up destroying so many lives.
Virii are fickle things. They dump or modify the proteins they use to bind to healthy host cells and soon, new, stronger, more insidious strains will emerge from the body’s destroyed cells. The Spanish Flu provides a prime example of a viral mutation leading to a much deadlier package altogether.
The first wave of the Spanish Flu was much like the flu of every other year. Those who succumbed comprised mostly of the very old and very young across America and Europe. The virus ravaged their upper respiratory tracts, making them an easy target for a secondary infection — bacterial pneumonia, which killed them — but not in numbers greater than any other outbreak. Outbreaks were reported in Fort Riley, Kansas and Queens, New York, but not in the alarmed, panic tones that later outbreaks would bring. It was the winding down of hostilities in World War One that would create an environment that would give birth to two more waves of a much stronger, deadlier virus.
Soldiers who caught the flu in the mud and filth of the French trenches were restricted to their fighting positions or hospitals in the rear, where the virus had more time to mutate amongst the weakened, exhausted fighting men into a deadlier pathogen that had the ability to kill normal, healthy adults. It did this in exactly the same way as it had the young and the elderly during the first wave, but it was stronger and able to more fully damage the respiratory tissues of those with healthy immune systems. Once again, once the influenza had attacked the lungs, bacterial pneumonia would strike the weakened organ, working quickly to kill the patient.
This tag team of disease would result in otherwise healthy people heading to work with a mild fever, growing ill over the course of the day and dying in a hospital bed in the evening, projectile-vomiting blood across the room, like something out of your worst 28 Days Later-induced nightmares. Hospitals and morgues were kept full as the dead piled up. Those working as nurses, hospital staff and morgue attendants would often inadvertently lead to the spread of the contagion as they returned home from their place of employment.
It was this development that made the Spanish flu a viral serial killer — children and the elderly can be sequestered fairly easily, but when healthy adults become infected, they will inevitably still try to go about their daily work, spreading the virus with every tram ride and trip to the shop.
One theory that might also explain the extraordinary amount of deaths states that that healthy adults in their 20s and 30s died so quickly from the pandemic because they were born following the last great epidemic in 1889 — their bodies simply did not contain the antibodies that would allow them fight the virus and subsequent infection. There you go parents, another argument in favour of letting your kids play in the muck to pick up all manner of bugs.
The Swine Flu will not able to spread as far and as quickly to as many victims as its predecessor due to the advances in medicine, quarantine and public hygiene since the second decade of the 20th century. The development of antibiotics, assisted by Australia’s own Howard Florey, has lowered pneumonia from the level of “call the undertaker” to “two weeks in hospital”. The secondary infection, the major killer, simply isn’t the threat it once was. Cleaner, better designed hospital environments, MRSA aside, give far fewer places for the virus and bacteria to breed and be transmitted. Anyone who watches Border Security can tell you that rampantly xenophobic narration aside, Australian Customs do an effective job at monitoring who and what comes into the country.
But it’s not time to relax just yet. Some of the advances made in the last century may end up as channels for a supercharged form of the virus and an unstoppable bacterial infection. The overabundant use of antibiotics has led some bacteria to becoming resistant to its effects. Should strains of drug resistant pneumonia become more common at a time when a virus mutates, the potential for a high number of deaths is very real. Affordable, fast air travel means that carriers of the virus can move thousands of miles in a number of days, spreading the infection to thousands of people, unlike the lengthy sea voyages of 1918 — it is also a lot harder to quarantine a 747 than it is an ocean liner. Paradoxically, tighter borders mean that the ill will try harder to cross the border by illegal means, hiding channels of infection into a country.
In many ways, the world of 1918 was a harder one for the influenza virus to thrive in. The world was more enclosed to the average man or woman and overseas travel less accessible. It took a particular set of conditions to give rise to a truly devastating pandemic — namely, the First World War. Could it be that future conflicts around the world, coupled with a much more connected society result in another disastrous pandemic?
Mike Stuchbery works with cultural institutions to make their collections accessible to students, teachers and the general public. He is also the Editor of Macabre Melbourne.