Skip to comments.More Effective Treatment For Pneumonia Following Influenza Found, Study Shows
Posted on 06/17/2009 4:51:43 PM PDT by grey_whiskers
Scientists at St. Jude Children's Research Hospital have demonstrated a more effective treatment for bacterial pneumonia following influenza. They found that the antibiotics clindamycin and azithromycin, which kill bacteria by inhibiting their protein synthesis, are more effective than a standard first-line treatment with the "beta-lactam" antibiotic ampicillin, which causes the bacteria to lyse, or burst.
The finding is important because pneumonia, rather than the influenza itself, is a principal cause of death from influenza in children and the elderly. During pandemicssuch as the one that may arise from avian influenzaup to 95 percent of influenza deaths are due to pneumonia. A bioterrorism attack using the influenza virus would likely result in the same high percentage of pneumonia deaths, according to the researchers.
(Excerpt) Read more at sciencedaily.com ...
""Traditional first-line therapy has been based on the belief that the bacteria are bad, so we have to get rid of them as quickly as possible," McCullers said. "But what we are finding is that maybe it is the inflammation we need to worry about first, and the bacteria second. Protein synthesis inhibitors shut down the bacterial protein-making factory, and they can avoid the inflammatory burst by killing them over days instead of quickly lysing them."
This may help limit deaths due to pneumonia following infection by flu...
Some good news from an unexpected quarter...
Thanks, Grey_Whiskers. Another article that might be of interest.
Miracle Man Survives Deadly Virus With New Surgical Procedure
Local Houston Man, Darren Pangle, Survives Rare Pneumonia Virus; Recently Saved At St. Luke’s Hospital
HOUSTON June 10, 2009 — In February, doctors and medical personnel at St. Luke’s Hospital were amazed at the results of an ongoing research project that saved the life of a 43 year old Darren Pangle.
Headed by cardiologist, Dr. Pranav Loyalka, of St. Luke’s Hospital, a machine was attached via tubes surgically placed in his groin, to aide in the oxygen exchange in the lungs, which then provided time in the healing process of a mutant strain of pneumonia virus.
This procedure, relatively new to the medical world, has a survival rate of only 38%.
This has some problems. To start with, secondary bacterial pneumonia is more typical of normal influenza, and they specify young children and the elderly-infirm which again are typical.
However, the radically different influenza for which there is little or no immunity or partial immunity, has different rules. Its primary victims are those from about age 20-45, with healthy and strong immune systems. This is because their immune system itself attacking the virus, not secondary bacteria, is what is destroying their lungs.
For these young and healthy people, it is essential that lethal Acute Respiratory Distress be prevented in the first place. And there are some very positive things that can be done right now to fend off ARD during an epidemic.
The first thing is to eliminate possible sources of Arsenic from your environment. Small amounts of Arsenic, over time, have been found to inhibit the immune system pathogen recognition system. So in the case of influenza, first the body doesn’t recognize the disease, and then it overreacts to it, causing ARD.
Fortunately, the EPA has strict limits on Arsenic in city water, so only rural wells present a drinking water - influenza risk. But 90% of the other Arsenic in our environment is used as wood preservative.
Statin drugs, normally used for high cholesterol, like Lipitor and Crestor, have been found to strongly inhibit ARD.
I appreciate your taking the time to correct me courteously.
Also--if I may be so bold as to ask--do you have any further information on the role of arsenic in the CFR for H1N1? I had read of such about a month or so ago, but have found no follow-ups.
I knew about the statins, but I am not on them...
I may have led you astray there. I would imagine a strong likelihood of lethal secondary pneumonia infections from novel influenza; however, these will be so horribly overwhelmed by the cytokine storm mortality numbers as to be almost unnoticeable.
Arsenic and influenza:
I would also add that there is a four-drug recipe targeting some of the major components of the (about 150) cytokine response elements, which may be enough to settle down the immune system until the threat is passed. Only one of the four is prescription, and it has an OTC substitute.
The first is an ACE-2 inhibitor, normally prescribed for hypertension. Its substitute is 15,000 IU of Vitamin D for two weeks.
The second drug is a Histamine-1 blocker. Ordinary Benedryl.
The third drug is a Histamine-2 blocker. Tagamet, usually used for acid reflux.
The fourth drug is Advil, Ibuprofen. It is a prostaglandin blocker.
Importantly, all four drugs have to be taken for the hoped for effect of stabilizing the immune response.
And, of course, the fifth drug, which is independent of the recipe, is a statin drug, such as Lipitor or Crestor, which according to data mining from a 16,000 person medical records sample group, makes somebody 40% less likely to die from Acute Respiratory Distress *and* Pneumonia.
Do you take the 4 OTC medications as a prophylactic, or shortly after infection -- except for the Vitamin D, which you should do for two weeks?
Turmeric (in the form of high potency curcuminoids) has a pronounced anti-cytokine effect. Many published papers returned on a search of curcumin+cytokine. Curcumin is resident in my flu kit.
A couple of months ago I posted the statin study showing the protective effect against ARDS. An anti-psychotic drug has also been used for its anti-cytokine effect but at the moment which one escapes me.
Typically, ARD happens about 5 days into avian influenza. But when and for how long the treatment should be conducted optimally is still unknown. However, all else being equal, going maximum dose for 5 days would be my choice.
The study results seem to mirror the advice for treatment of anthrax as well. A slow, steady kill of the germinated organisms achieves the objective without dumping a large volume of toxins into the patient at one time. The antibiotics that cause a breach of the bacterial wall dump the endotoxins out in one broad step. Many of the fever producing toxins are endotoxins. That likely explains my own experience.
Have a caution with the regular consumption of Vitamin D. Unlike other vitamins, it is a hormone, and your body will adjust itself accordingly, producing less natural Vitamin D. Instead of a supplement, I would recommend a natural light sun lamp. Just 15 minutes should give you a whopping natural dose.
As far as Ibuprofen for pain, I’m one of those individuals who never profited from conventional NSAIDs. However, I was eventually prescribed Celebrex, which I found to be the first pain reliever I had ever taken that worked. A different class of drug entirely.
Other things of potential interest. Researchers in Africa made the interesting discovery that people who had very low levels of Vitamin A, due to dietary deficiency, also had unusually high levels of Tumor Necrosis Factor alpha (TNF-1), which is often a major part of arthritis.
Just bringing up their Vitamin A to normal levels as much as halved the amount of TNF-1 in their blood. Importantly, even with severe deficiency, they had to be careful how much of the Vitamin to give, and over what time period, because it is so easy to overdose.
Details, (or more precisely, source), please?
I may have to invest in a sun lamp, living in Minneapolis.
Pneumonia occurring as a secondary infection after influenza is a major cause of excess morbidity and mortality, despite the availability and use of antibiotics active against Streptococcus pneumoniae. We hypothesized that the use of a bacteriostatic protein synthesis inhibitor would improve outcomes by reducing the inflammatory response. BALB/cJ mice infected with influenza virus and superinfected with S. pneumoniae were treated with either the cell-wall-active antibiotic ampicillin or the protein synthesis inhibitor clindamycin or azithromycin. In the model, ampicillin therapy performed significantly worse (survival rate, 56%) than (1) clindamycin therapy used either alone (82%) or in combination with ampicillin (80%) and (2) azithromycin (92%). Improved survival appeared to be mediated by decreased inflammation manifested as lower levels of inflammatory cells and proinflammatory cytokines in the lungs and by observation of less-severe histopathologic findings. These data suggest that beta-lactam therapy may not be optimal as a first-line treatment for community-acquired pneumonia when it follows influenza.
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