UPDATE: I got some more info from a doctor I know well. He told me that there were reports of flu patients going from seemingly healthy one day to seemingly very much dead the next. DIC from infective agents doesn’t happen that fast. He informed me that there are three diseases generally known to cause such sudden death: cholera, plague and meningococcal meningitis. Meningococcal meningitis is caused by Neisseria meningitidis. It is normal flora in many people’s nose and throat region but can cause devastating infections if it gets in the wrong site under the wrong circumstances. Not only does it fit the bill, I suspect, for the sudden deaths but meningococcal septicemia can produce a purplish rash – explaining the heliotrope cyanosis (along with actual cyanosis from fluid in the lungs). So DIC might not be needed to explain some of these strange symptoms though it may occur in some patients who get a different opportunistic infection due to the effects of the flu virus. The rest of the post continues as first posted.
The more I learn about this swine flu and previous flu outbreaks the more interesting the subject becomes to me.
When I had previously heard about the concept of novel flu viruses causing what is referred to as a cytokine storms, I had the impression that they were causing a massive overreaction by the immune system to the unfamiliar viral infection which (after getting the jump on the body’s defenses) provoked fluid in the lungs which helped to nurture the bacterial pneumonia that these flu patients often die from – or with, depending on your point of view. But it seems to be more subtle than that. One of these groups of cytokines, called interferons, are used to inhibit viral reproduction inside cells and helps keep them from gaining access in the first place. These interferons also have other effects like telling bacteria-eating cells such as neutrophils that the infection is viral in nature and their services are not needed or wanted.
Hey, that’s fine when the flu is in the upper respiratory tract since there are normal flora living there – helpful bacteria which can out compete potential pathogenic species which might land in the area and keep each other in check. And the tissue of the upper respiratory tract is harder for bacteria to colonize than the tiny little air sacks of the lungs. But when the virus is in the lungs, for the immune system to tell all bacteria-fighting cells to clear out is asking for trouble. Now, even some of the beneficial normal flora in the upper respiratory tract can ride down on an aerosol, a globe of phlegm or some misdirected trickle of spit and start planting its flag. “I claim these aveoli in the name of Streptococcus pneumoniae!” All the neutrophil are out of the area and the virus is raising a ruckus that leaves the region filled with blood, cell proteins and mucous. Whatever bacteria land in the environment think they have died and gone to prokaryote heaven. The immune system is making a mistake that Stalin made at the onset of WWII. He was so obsessed with threats like Japan and his own paranoia that he couldn’t imagine that the Nazis would break the non-aggression pact; to the point that he didn’t believe it even while his own forces were frantically trying to tell him that the Nazis were on the move east.
Another interesting feature of the 1918 flu is the colour it left its corpses. The term, “heliotrope cyanosis” was often used to describe victims and some of the dead had been turned black, leading some of the survivors to term it the “black flu”. I have heard of claims of similar effects on bird flu victims but I have yet to see a reference to back this up. The cyanosis was, I suspect, due to the fluid in the lungs causing the body to shunt blood away from the skin to the vital organs to maintain their oxygen but this usually causes a blue tinge. This could be pushed into the purple and even black range if the damage in the lungs was causing D.I.C. – distributed inter-vascular coagulation. Many things can cause DIC but when it happens, tiny clots form through the blood and cause microscopic strokes in the capillaries of the tissue, usually leading to organ failure and death in about 90% of DIC sufferers. The tiny clots would probably cause the blue of the cyanotic skin to become purplish and DIC also uses up coagulation factors and platelets meaning that bruising and bleeding can occur which could cause a blackening of the skin. Wikipedia states that bleeding from the mucous membrane occured in some cases which would be consistent with DIC.
The fact that some called it the “black flu” is rather appropriate. I remember someone noting that, while everyone learns that the black plague killed about a third of Europe, it did so over the course of a few decades. The 1918 flu seems to have killed a similar number of people in one year but since there were so many people on earth its proportion of fatalities is less impressive unless one realizes how short a time it took to do it. This would not be the best time to be sitting back and gloating over how worked up everyone got over a simple flu. Now would be the time to be stocking up on antibiotics to fight the bacterial pneumonia and stocking the supplies needed to monitor for early signs of DIC while working diligently to get the vaccine ready.
This might not be a “herald wave”.
But it is acting like one so it would be wise to plan for a deadly second wave so as to minimize the damage.