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Lessons in History: what we can learn from… the Spanish flu
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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. |
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13 Comments
The plural of virus is viruses!
Also, whilst it is true that the flu is an airborne pathogen that can be picked up through inhalation, many scientists believe that this is not the most common method of transmission. Touching surfaces that have had the virus deposited on them, and then touching one’s mouth, eyes or other mucous membranes, or one’s food, is considered by many to be the greatest risk.
So, a person with the flu covers their mouth when coughing, to avoid spreading it, but then touches the handrail on the train, and manages to potentially spread the disease further than if they had just coughed openly.
The good news is that good personal hygiene and avoiding touching your face, can help to keep you healthy. Keep that in mind in case of a pandemic!
Goddamit man, virii sounds more sinister. I’m a hack, not a doctor!
Hack?
Look out, he’s got the swine flu!
A nice article, ruined by a rather critical factual error.
The 1918 flu killed young healthy adults not by secondary bacterial infection, but by a thing called “cytokine storm”. Cytokines are the shock troops of your immune system, they are designed to kill invaders. Unfortunately pandemic flus often provoke such a strong immune response that the rest of the body gets caught in the crossfire. The immune response is so brutal that it kills the host as well as the invader (this is not the same as auto immune disease where the immune system turns on the body, this is just the body over-reacting, literally to death). The old and the young don’t get to experience the joys of a cytokine storm, their weaker immune systems aren’t up to the task of self immolation. Plain old bacteria still get to knock them off.
So what I hear you say. Well we have lots of high tech (and some not so high tech) antibiotics to help kill bacteria and treat secondary bacterial infections but we have very little that will damp down a cytokine storm (there are a few things, but no magic bullet and effectiveness is unclear). If this happens to you all doctors can do is admit you to intensive care (and that is a very very finite resource) and hope your body can ride out the storm.
If (and that’s a very big if) on a second or third iteration this flu causes this sort of response things might get very interesting.
Jackson
(a doctor, not a hack)
PS H1N1 is only one of several “regular strains” that are circulating at any time, and at the moment both the regular or garden variety as well as “Novel H1N1” are out and about.
Reading this article made me join Crikey. Very well-written, interesting and engaging. Really enjoyed it, thank you Mr. Stuchbery!
Has it been verified that cytokine storms have been identified as the culprit, rather than merely suggested? I’ve seen it discussed in rather hysterical terms in some other articles I’ve read, prior to researching this piece.
Perhaps that is what makes a more lethal flu pandemic a much deadlier prospect- deaths are not due to a singular factor, but a number of reactions or opportunistic infections?
Jackson, here is my source - ‘Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic Influenza: Implications for Pandemic Influenza Preparedness’. I would be very interested to hear if there’s been a study or a journal article published that sheds new light on the predominant cause of death for victims in 1918.
Mike,
It’s not quite as simple as it seems, Morens’ paper has reviewed histopathological samples and shown that the damage is the same as that seen in bacterial infection. While bacteria were seen they is no proof that they are the cause of the problem. The haemorrhagic pneumonitis that was seen in 1918-19 is not typical of bacterial infection, the rapid progression to lung haemorrhage is something that appears to be something that only occurs in some strains of influenza (other illnesses also cause cytokine storms, notably malaria, measles and some cases of HIV). Morens et al don’t even mention cytokine storm, something I find odd. They also fail to consider the very likely possibility that cytokine storm causes severe lung damage predisposing to massive bacterial overgrowth.
This link http://www.ncbi.nlm.nih.gov/pubmed/18697437?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=5&log$=relatedreviews&logdbfrom=pubmed discusses the role of cytokines and makes the point that the histological changes are similar to those seen in severe infection. This is to be expected, after all these are the chemicals the body uses in fighting infection, they cause inflammation and it’s not surprising that the collateral damage they cause is found in both cases. Unfortunately I can only access the abstract, the original article is in a Bulgarian journal and in Turkish, the Western European medical orthodoxy tend to shun these journals and pay them scant regard, often for no good reason. A better journal (Chest, the leading pumonology and critical care journal) has also published this one: http://www.ncbi.nlm.nih.gov/pubmed/16424427?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum It deals mostly with H5N1 infections but presumably H1N1 produces a similar result.
Then there remains the issue of why did the 1918-19 strain kill young adults in such unusually high numbers. Cytokine storm still seems to be the likely root cause, the havoc it causes allowing the massive bacterial overgrowth, and then the demise of the patient. This leads to 2 further problems. Firstly antibiotics are good, but they are not magic bullets and not all patients respond. Then from the logistic point of view I see many patients with severe bacterial pneumonia, it is a common cause for admission to ICU. You need the advanced respiratory support while the antibiotics work and your body recovers. There just aren’t that many ICU beds, and other demands on them (such as road trauma and other severe illnesses) won’t go away during a pandemic.
Jackson
This one also deals with cytokine storm http://www.ncbi.nlm.nih.gov/pubmed/19218453?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_PMC&linkpos=2&log$=citedinpmcarticles&logdbfrom=pubmed (although it’s in non-human primates)
Jackson
So, aside from the ‘the immune system eats you’ description of a cytokine storm, what do you see in a patient in the midst of one of these immune reactions? Does this account for the arcing nosebleeds and vomiting?
Very interesting article AND feedback comments, but now I’m not feeling very well!
Mike,
Yes it does. The whole cytokine system is incredibly complex (there are many identified substances, and probably even more as yet unidentified) and they are responsible for modulating much of the immune response, fighting off the array of bugs were are assailed with every minute of every day and most critically modulating the response to serious incursions by nasty pathogens. In simple laymans terms with cytokine storm you see all manner of effects often unrelated to the primary site of infection, direct lung damage leading to pulmonary haemorrhage (which is where the blood was coming from with the 1918-19 flu if the descriptions of the reconstituted virus in other primates is any guide), kidney damage, direct cardiac effects including reduced pumping ability, leaking of body fluids from the vascular system into tissues causing swelling, increased ability of all the bugs that live in your bowel (and your body usually keeps at bay) getting into the circulation, and most critically a lack of oxygen getting into your blood via your lungs for several reasons, not least of which is your lungs filing up with fluid and possibly blood. The lack of oxygen causes other cells to become stressed and possibly even to die. One of the bodies responses to this insult is to release more cytokines, which can then make things worse.
Back and forward here is probably not the most efficient way of doing this. I’ll ask the editors to forward you my email and if you are interested we can discuss this elsewhere.
Jackson
@Jackson, Mike
I don’t know if this has been an efficient way of discussing this, but it certainly has been interesting. Thank you both.