Re: CDC Reports Additional 572 Deaths This Week
The most disconcerting thing is the decision to "roll" pneumonia and H1N1 deaths into the same categories for reporting purposes. Previous historical data allowed separate analysis of these two different kinds of infections. See the pdf file in this thread:
http://www.flutrackers.com/forum/showthread.php?t=126629
When I read Laidback Al's comment, I began wondering why they would merge the two categories. I went back to Barry's "The Great Influenza" and took the following notes that relate to cause of death during that pandemic.
You can draw your own conclusion, but I think the reason they are combining the two is that many of the pneumonias are either a direct result of the H1N1 virus penetrating deep into the lungs or the result of opportunistic bacterias causing bacterial pneumonias because of the immune system having been weakened by the H1N1 virus. Likely they are merging them because most of the pneumonia cases being seen are either directly or indirectly related to H1N1.
The notes below indicate that in the 1918 pandemic, the H1N1 virus contributed to death in several major ways:
Causes of Death from 1918 Viral Influenza
1) Viral pneumonia when virus directly killed lung cells (rapid onset of death)
2) Acute Respiratory Distress Syndrome, basically death because of massive immune response (organ failure due to too little oxygen, drowning in own fluids in lung, die from exhaustion) (death one or two days or so after infected) (Note: see Flutracker entries on "cytokine storms")
3) Opportunistic bacterial pneumonias after H1N1 weakens immune system; death occurs 1, 2, 3 weeks after infection; patient may have started to recover
4) Heart or other organ weakened by influenza
Relevant Notes from John M. Barry's "The Great Influenza", Penguin
p. 242 It was the lungs that had attracted attention from pathologists first. Physicians and pathologists had many times seen lungs of those dead of pneumonia. Many of the deaths from influenzal pneumonia did look like these normal pneumonias. And the later in the epidemic a victim died, the higher was the percentage of autopsy findings that resembled normal pneumonia, bacterial pneumonia
p. 243 Those who died very quickly, a day or even less after the first symptoms, however, most likely died of an overwhelming and massive invasion of the virus itself. The virus destroyed enough cells in the lung to block the exchange of oxygen. This alone was unusual and puzzling. But the lungs of the men and women who died two days, three days, four days after the first symptom of influenza bore no resemblance to normal pneumonias at all.
p. 244 In bronchopneumonia, bacteria?invade the alveoli (tiny sacs in the lungs responsible for the transfer of oxygen from the lungs into the blood) themselves. Immune-system cells follow them there, and so do antibodies, fluid, and other proteins and enzymes. An infected alveolus becomes dense with this material, which prevents it from transferring oxygen to the blood.
p. 245 Roughly two-thirds of all bacterial pneumonias and an even higher percentage of lobar pneumonias are caused by a single group of bacteria, the various subtypes of the pneumococcus. (The pneumococcus is also the second leading cause of meningitis.)
In 1918 pathologists did see at autopsy the normal devastation of the lungs caused by the usual lobar and bronchopneumonias. But the lungs from those who died quickly during the epidemic, the lungs that so confused even Welch, those lungs were different?..The pathological picture was striking, and was unlike any type of pneumonia ordinarily seen in this country?.In bacterial pneumonias, normally the infection rages inside the alveoli, inside the tiny sacs. In 19918, while the alveoli were also sometimes invaded, the spaces between the alveoli were filled. This space, which makes up the bulk of the volume of the lung, was filled with the debris of destroyed cells and with every element of the immune system, from enzymes to white blood cells. And it was filled with blood?.
p. 246 Victim?s lungs were being ripped apart as a result of, in effect, collateral damage from the attack of the immune system on the virus.
p. 247 But when the lungs do become infected, other defenses, lethal and violent defenses, come into play. For the immune system is at its core a killing machine. It targets infecting organisms, attacks with a complex arsenal of weapons ? some of them savage weapons ? and neutralizes or kills the invader.
The balance, however, between kill and overkill, response and overresponse, is a delicate one. The immune system can behave like a SWAT team that kills the hostage along with the hostage taker, or the army that destroys the village to save it.
In 1918 especially, this question of balance played a crucial role in the ware between virus and immune system, and between life and death. The virus was often so efficient at invading the lungs that the immune system had to mount a massive response to it. What as killing young adults a few days after the first symptom was not the virus. The killer was the massive immune response itself. (Note: Is there a clue to treatment here?)
p.247 Meanwhile, the virus is also attacking the immune system directly, undermining the body?s ability to protect itself; the virus inhibits the release of interferon, and interferon is usually the first weapon the body employs to fight viral infection. In 1918 the ability to inhibit the immune system was so obvious that researchers, even while overwhelmed by the pandemic, noticed the influenza victims had weakened immune responses to other stimuli; they used objective tests to prove it.
p. 249 Routinely, the body fights off the influenza virus before it gains a solid foothold in the lungs themselves. But in 1918 the virus often succeeded in infecting epithelial cells not only in the upper respiratory tract but all the way down the respiratory tract into the inner most sanctuaries of the lungs, into the epithelial cells of the alveoli. This was viral pneumonia.
The immune system followed the virus into the lungs and there waged war. In this war the immune system held nothing back. It used all its weapons. And it killed. It killed particularly with ?killer T cells?, a white blood cell that targets the body?s own cells when the are infection with a virus, and it killed with what is sometimes referred to as a ?cytokine storm,? a massive attack using every lethal weapon the body possesses.
The same capillaries that moved blood past the alveoli delivered this attack. The capillaries dilated, pouring out fluid, every kind of white blood cell, antibodies, other elements of the immune system, and cytokines into the lung. Then these cytokines and other enzymes virtually obliterated the capillaries. Even more fluid poured into the lung. The cells that line the alveoli were damaged, if they survived the virus itself. Pink glassy membranes, called hyaline membranes, formed on the insides of the alveoli. Once these membranes formed, ?surfactant? ? a slippery, soap-like protein that reduces surface tension and eases the transfer of oxygen into red blood cells ? disappeared from the alveoli. More blood flooded the lungs. The body started producing fiberlike connective tissue. Areas of the lung became enmeshed in cell debris, fibrin, collagen, and other materials. Proteins and fluid filled the space between cells.
p. 249 The immune system changes with age. Young adults have the strongest immune system in the population, most capable of mounting a massive immune response. Normally that makes them the healthiest element of the population. Under certain circumstances, however, that very strength becomes a weakness.
In 1918 the immune systems of young adults mounted massive responses to the virus. The immune response filled the lungs with fluid and debris, making it impossible for the exchange of oxygen to take place. The immune response killed.
p.250 Acute Respiratory Distress Syndrome. Almost anything that puts extreme stress on the lung can cause ARDS: near drowning, smoke inhalation, inhaling toxic fumes (or poison gas)?.or influenzal viral pneumonia. Doctors today looking at pathology reports of lungs in 1918 would immediately designate the condition as ARDS.
Whatever the causes of ARDS, even today there is no way of stopping the process of disintegration in the lung once it begins. The only care is supportive, keeping the victim alive until he or she can recover. This requires all the technology of modern intensive care units. Still, even with the best modern care, even with for example dramatically more efficient and effective administration of oxygen than in 1918, the mortality rate for ARDS patients in different studies ranges from 40 to 60 percent. Without intensive care ? and hospitals have few beds in intensive-care units ? the mortality rate would approach 100 percent.
In ARDS, death can come from many causes. Organs outside the lungs fail because they get too little oxygen. The lungs can so fill with fluid that the right ventricle of the heart cannot empty it so the victim drowns. The strain of trying to pump blood out of the lung can cause heart failure. Or the victim can simply die from exhaustion: he or she must breathe so rapidly to get enough oxygen that muscles become exhausted. Breathing just stops.
ARDS by no means accounts for all the influenza deaths in 1918 and 1919, or even for a majority of them. It explains only those who died in a few days, and it explains why so many young healthy people died. Although influenza almost certainly killed some people in ways that had little to do with the lungs ? for example, someone whose already weak heart could not stand the additional strain of fighting the disease ? the overwhelming majority of non-ARDS deaths came from bacterial pneumonias.
The destruction of the epithelial cells eliminated the sweeping action that clears so much of the respiratory tract of bacteria, and the virus damaged or exhausted other parts of the immune system as well. That gave the normal bacterial flora of the mouth unimpeded entry into the lungs. Recent research also suggests that the neuraminidase on the influenza virus makes it easier for some bacteria to attach to lung tissue, creating a lethal synergy between the virus and these bacteria.
Bacterial pneumonias developed a week, two weeks, three weeks after someone came down with influenza, including even a seemingly mild case of influenza. Often influenza victims seemed to recover, even returned to work, then suddenly collapsed again with bacterial pneumonia.
It is impossible to know what percentage of the dead were killed by a viral pneumonia and ARDS and how many died from bacterial pneumonias. ?..The conclusion of the army?s pneumonia commission?found signs of what would today be called ARDS in almost half the autopsies.
