Real killer maybe opportunistic infections that follow flu.

  1. http://www.post-gazette.com/pg/09166/977499-114.stm
  2. Visit oramar profile page

    About oramar

    Joined: Nov '98; Posts: 7,097; Likes: 5,244
    returned nurse

    3 Comments

  3. by   indigo girl
    Very good article, oramar! Let's look at this a little more...

    http://www.post-gazette.com/pg/09166/977499-114.stm


    Remember, the CDC says to watch for signs that your child is feeling better but then relapses after a few days. It's a very bad sign, and parents need to know that this is an emergency situation, and get the child to the ER.

    Also, CDC is now recommending the pneumovax for adults and kids with any of the known risk factors including smoking. This is directly in response to the hospitalizations of swine flu victims. Personally, I think that all of us could benefit from getting the pneumovax if only because as HCW we are going to be exposed. We are already getting report of nurses becoming infected from taking care of some of these cases in many countries.

    Quote from www.post-gazette.com

    ...many children who die from flu complications, the virus paralyzes the part of their immune systems designed to protect them against bacterial invaders.

    She estimated that in one-third of the children who die after flu infections, the virus immobilizes cells known as toll-like receptors, which are designed to alert the rest of the immune system to attack bacterial pathogens.

    A common pattern in those children, she said, is that they seem to be recovering from the flu. Then, about a week after their first symptoms appear, they suddenly get much sicker and rapidly weaken -- a sign of the bacterial onslaught.

    http://www.virology.ws/2009/06/02/pa...nza-in-humans/

    Now, I do understand that maybe micro was not your favorite subject in school, but this is for the most part decipherable. For those who do want to understand more about how, and why influenza can make people sick enough to kill them,

    Quote from www.virology.ws

    When influenza virus is introduced into the respiratory tract, by aerosol or by contact with saliva or other respiratory secretions from an infected individual, it attaches to and replicates in epithelial cells. The virus replicates in cells of both the upper and lower respiratory tract. Viral replication combined with the immune response to infection lead to destruction and loss of cells lining the respiratory tract. As infection subsides, the epithelium is regenerated, a process that can take up to a month. Cough and weakness may persist for up to 2 weeks after infection.


    Influenza complications of the upper and lower respiratory tract are common. These include otitis media, sinusitis, bronchitis, and croup. Pneumonia is among the more severe complications of influenza infection, an event most frequently observed in children or adults. In primary viral pneumonia, the virus replicates in alveolar epithelial cells, leading to rupture of walls of alveoli and bronchioles. Influenza H5N1 viruses frequently cause primary viral pneumonia characterized by diffuse alveolar damage and interstitial fibrosis. Primary viral pneumonia occurs mostly in individuals at high risk for influenza complications (e.g. elderly patients) but a quarter of the cases occur in those not at risk, including pregnant women.


    Combined viral-bacterial pneumonia is common. In secondary bacterial pneumonia, the patient appears to be recovering from uncomplicated influenza but then develops shaking chills, pleuritic chest pain, and coughs up bloody or purulent sputum. Often influenza virus can no longer be isolated from such cases. The most common bacteria causing influenza associated pneumonia are Streptococcus pneumoniae, Staphylococcus aureus, and Hemophilus influenzae. These cases can be treated with antibiotics but the case fatality rate is still about 7%. Secondary bacterial pneumonia was a major cause of death during the 1918-19 influenza pandemic, during which antibiotics were not available.
    Last edit by indigo girl on Jun 15, '09
  4. by   indigo girl
    http://www.post-gazette.com/pg/09166...xzz0IYUnrORR&D

    The link following oramar's article explains more about the toll-like receptors.

    Quote from www.post-gazette.com

    Dr. Kathleen Sullivan, chief of allergy and immunology at Children's Hospital in Philadelphia, published a study this month in the Journal of Leukocyte Biology showing that in many children who die from flu complications, the virus paralyzes the part of their immune systems designed to protect them against bacterial invaders.

    She estimated that in one-third of the children who die after flu infections, the virus immobilizes cells known as toll-like receptors, which are designed to alert the rest of the immune system to attack bacterial pathogens.

    A common pattern in those children, she said, is that they seem to be recovering from the flu. Then, about a week after their first symptoms appear, they suddenly get much sicker and rapidly weaken -- a sign of the bacterial onslaught.

    Viral evasion of innate host defenses

    http://www.virology.ws/2009/06/12/vi...host-defenses/

    IFNs refers to interferons.

    Quote from www.virology.ws

    Host defense mechanisms are imperfect because the genomes of every known virus encodes proteins that can block nearly every step of the immune response. For every host defense, there is a viral offense. Let's consider the different ways that viruses are known to evade the early, or innate, host defenses.

    When a virus enters a cell, the infection is sensed and the cell responds by producing IFNs. These cytokines bind to specific receptors on the cell surface, causing the production of hundreds of proteins encoded by interferon-stimulated genes, or ISGs. These proteins have anti-viral activity, and can stop a viral infection.

    ...Viral infections antagonize the sensing of infection, production of IFN, and synthesis and activity of ISGs.

    Viral gene products interfere at nearly every step of the innate immune pathway...the cytoplasmic proteins RIG-I and MDA5 detect double-stranded or single-stranded RNA, leading to a series of reactions and the synthesis of cytokines such as IFN....each step of these pathways is carried out by proteins...viral proteins are known to interfere with these pathways.

    ...many viruses encode proteins that interfere with this sensing pathway...The viral proteins interfere with recognition of viral RNA, the individual steps (mainly phosphorylation events) carried out by the multiple proteins, and synthesis of IFN mRNA in the cell nucleus.

    What's more amazing is that this is only one of the pathways by which viral infections are sensed by cells. Other detectors of viral infection include the toll-like receptors, which sense viral RNA, DNA or proteins. And yes, you guessed it - viruses have also evolved ways to antagonize those pathways. And we haven't yet discussed the adaptive immune response to virus infection!
  5. by   lamazeteacher
    I sent this email to the author of the article recommended in the OP.

    Congratulations on writing an excellent, comprehendable article about the facts regarding the agent causing the present pandemic. The explanation you gave regarding secondary infections, allows the public to consider what their appropriate actions should be, following the mild illness that appears first, and possibly changing their plans to go on a trip (or whatever) within a month of recovering from the flu. Curbing its spread is of primary importance, and limiting exposure to the organisms that cause secondary infections is the next priority.

    Thank you.

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