It has been my own personal project to follow H5N1 for the last 3 years simply because it interests me. Attracted to this type of information like a magnet, I've been watching this relatively new influenza virus to see where it will go, how it will change itself, and possibly change our world. I have followed its country by country outbreaks, and watched for the important viral mutations such drug resistance or changes that allowed it to more specifically target mammals.
Keeping in mind at all times that we will be cleared impacted as HCW, as well as being members of our communities, and having families of our own to care for, I wanted to start the new year by opening a single focused pandemic thread that would also look at what we are doing nationally to prepare for a future pandemic. Is this the virus to spark the next pandemic? No one can answer that question. We can look back at the past to the last few pandemics, and in particular to the most devastating one in 1918, and extrapolate useful information about them, but we can not predict the future. We can only make comparisons with our situation now, and learn what worked to lessen morbidity and mortality in those past events. And, we can look at those other viruses, and compare them with what we are seeing now. For example, H5N1 is a Type A virus. We know that all pandemics are caused by Type A viruses. It is also an avian virus. The deadly 1918 virus, H1N1 was also an avian virus.
For this thread, as in the previous threads, I will be making use of news sources, scientific studies, govt bulletins such as the MMR, as well as flu forums and blogs devoted to this subject for my sources. Because press information, particularly the foreign press, is not always available for later access when I am looking back to check recent historical information, the use of these blogs and forums are important because archived information quoting the media and all other sources is always fully and easily available there with no worries about information disappearing or no longer being available. They also fully document their sources or I would not be using them.
With this link from Avian Flu Diary, a well researched source that I highly recommend, we can read the words of outgoing HHS Secretary Leavitt on our state of preparedness. Leavitt has done an admirable job during his tenure, but admits that there is much left to do.
A scant 33 months ago, I sent my first message about a race that HHS had just begun. As I said then, it was a race against a fast-moving virulent virus with the potential to cause an influenza pandemic. Since then, we have mobilized experts and resources across the country and around the world. I now send you this final message, as I look back at the unprecedented progress we have made in energizing a national pandemic influenza preparedness movement in those 33 months.
Today, many people mistakenly think influenza pandemics are a thing of the past, but influenza has struck hard in the era of modern medicine – much harder than most people realize. And it will strike again. Pandemics are hard things to talk about. When one discusses them in advance, it sounds alarmist. After a pandemic starts, no matter how much preparation has been done, it will be inadequate.
It was my understanding that the slaughter was carried out to 'keep the peace', as it were, since the non-Christian community views pigs as unclean, thus a path of disease. The meat was to be frozen and preserved, and later sold back to the Christian community so that the pig farmers would not have complete losses.
That could be, and I read that the pigs were reservoirs for the mutated swine-avian virus, which wasn't widely known, in the effort to avoid hysteria......
The Muslims and Jews have been told since the beginning of (original, not common era) time, that pigs had trichonosis (not necessarily by that name) which caused the disease in humans, and was not "kosher" (for Jews), therefore it was forbidden as food for them, along with "bottom feeding" fish such as shellfish and catfish (not that the latter 2 had trichonosis, there were other things found to be caused by them - probably serious allergies).
Once better hygiene was used for the care and slaughter of pigs; and allergies were found to be the cause of anaphylactic shock from one or more type(s) of shellfish in some people, Reform Jews were allowed by their Rabbis to eat pork, shellfish, and catfish.
Bird flu cases continue to occur in children in Egypt, and we have heard nothing from the WHO on their investigation into why this is so. They were supposed to have sent a team in two months ago to investigate the changing demographics of bird flu in Egypt. At this time, the disease has been mild in toddlers, but still seems to kill some of the the children in older age groups as well as any adults infected.
Meanwhile, the first diagnosed case of swine flu has just been announced. Of course, this does not mean that there have not been other cases of swine flu that have gone undetected. Margaret Chan of the WHO has said more than once that there is concern about how H5N1 will behave under pressure of a pandemic of swine flu. It is well known that flu viruses can exchange genetic material when co-infecting the same host. The CFR of bird flu is much higher than that of swine flu, but swine is far more transmissible. A recombination of the two would be alarming.
The case is a 4-year old female child from the Kefr El Sheikh District of Kefr El Sheikh Governorate. Her symptoms started on 30 May 2009 with fever, cough and sore throat.
She was admitted to Kefr El Sheikh Fever Hospital on 31 May 2009. The patient received oseltamivir and is in a stable condition.
A girl who had travelled from the United States has been confirmed as having Egypt's first case of swine flu, Health Minister Hatem el-Gabali said on Tuesday.
The 12-year-old with US and Egyptian nationality was quarantined by health workers at Cairo airport on Monday after she showed symptoms of the flu, Gabali said in a statement aired on state television.
The girl and her mother had arrived to spend the summer in Egypt. Her mother was not infected, the minister said.
No other passengers on the flight showed signs of infection with the A(H1N1) virus, he added...
Right now, my nightmare scenario is H5N1 and H1N1 combining. I think we can probably get through H1N1, even if it's severe in the fall, but H5N1 still has, what, a 60% CFR? H1N1's case fatality rate is still higher than seasonal but lower than 1918, so cause for some concern with all eyes turned toward the immediate, murky future. But together, life would get rough for a little bit.
However, pandemics are a "normal" part of life and not just for humans. The grand cycle of life goes on for all things. Even with an uncertain future, I am far more focused on the aftermath and renewal that will happen after we come through this particular point in history, and all the knowledge that we will gain that will help make us stronger and perhaps safer when we face another pandemic in 30 or 40 or 50 years.
And btw, those masks are expensive - but I happened through Walmart the other night for shampoo and other stuff, and saw a box of 2 for $2.82. If you go over to the house/remodeling section, the masks are the regular price. I just plan to carry a box in my bag when I go to work, and if the bug has become more severe and if there are starting to be concerns about PPE shortages in some LTCs.
the english press has yet to pick up on this story, but commonground at flutrackers has posted a story from the arabic press announcing that a 5 year-old from the damietta governorate has been found to be infected with the h5n1 bird flu virus.
this makes the 28th such infection detected this year, a considerable jump from last year's total of only 8. in addition to the increase in the number infected, they are also seeing a much lower mortality rate than in years past.
while ostensibly good news, a milder bird flu virus - one that doesn't immediately incapacitate its victim - is more likely to be spread in a community. and that could give the virus more opportunities to mutate.
dr. abdel rahman shahin, official spokesman of the ministry of health on thursday, no. 79 on the infection of bird flu, a child, ahmed fathi, ahmed issa, aged 5 years and months of "albesartp" damietta governorate.
sahin said that the onset of symptoms the child was the first of this month, which on their impact on income, the hospital admitted damietta, which is suffering from high temperature after being nominated for the birds suspected of being infected with bird flu, he said, adding that once suspected of being infected with the disease have been given the drug tamiflu, the condition is stable and is being transformed to a hospital in the capital bakrie.
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, I am going to link to several of Dr. Racaniello's posts. He is a wonderful teacher. I have already posted this first link elsewhere.
As professionals, we are going to be dealing [a lot, I think] with this illness because it does not seem to be going away. The virus is seeding itself throughout the globe just about everywhere. It's very mildness helps it to spread. The pattern is very reminiscent of 1918 as everyone knows by now. We have also seen just how ill some people can get. Not all of them had prior existing conditions. More worrisome is the fact that much of our population does seems to have prior existing conditions. The situation could be very bad if this virus returns in a big way in the fall even if it does not become more severe.
According to the CDC, one of the indications that a flu victim's situation is becoming more serious is that flu-like symptoms start to improve only to return later with a fever and a worsening cough. Why is that? Why would someone seem to be better than suddenly get worse?
I think that the answer may be addressed in this link. Also explained is why it takes so long to recover.
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 (which we'll discuss in later posts) 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.
He's talking about cytokines now. Laying the ground work for understanding the "cytokine storm" perhaps? I hope so.
In response to viral infection, many organisms mount a remarkable defense known as the immune response. This response to viral infection consists of an innate, or nonspecific component, and an adaptive, or specific defense. The innate response is considered the first line of immune defense because it is active even before infection begins....within minutes to hours after infection.
A key property of the innate immune system is the ability to recognize viruses as ‘foreign’. Viral proteins and nucleic acids are distinguished from cellular counterparts by cellular proteins called pattern recognition receptors...These are proteins present either in the cell cytoplasm or on cellular membranes, where they detect viral components.
Viral proteins and nucleic acids are distinguished from cellular counterparts by cellular proteins called pattern recognition receptors ...These are proteins present either in the cell cytoplasm or on cellular membranes, where they detect viral components. For example, the cytoplasmic protein RIG-I detects double-stranded RNA (dsRNA) or single-stranded RNA (ssRNA) with a 5′-triphosphate. These types of RNAs are usually not found in the cytoplasm of unifected cells; rather they are typically products of viral replication. When RIG-I binds these viral RNAs, a series of reactions occur which lead to the synthesis of cytokines, the primary output of the innate defense system. Other detectors of viruses are the membrane-bound toll-like receptors (TLRs), which sense viral glycoproteins, dsRNA, ssRNA, and the sequence CpG in viral DNA. Engagement of TLRs by these virus-specific ligands also leads to the synthesis of cytokines, albeit by different pathways.
The presence of cytokines in the blood is typically one of the earliest indications that the host has been infected with a virus.
Cytokines function locally by binding receptors on other cells. For example, IFN produced by infected cells engages receptors on neighboring cells. Those cells then produce hundreds of cellular proteins which have antiviral activities. When cytokines enter the circulation, they elicit symptoms typical of many viral infections, including fever, sleepiness, lethargy, muscle pain, loss of appetite, and nausea.
Another key component of the innate response are the so-called sentinel cells: dendritic cells and macrophages... Sentinel cells patrol the body, seeking signs of infection. Dendritic cells bind cytokines produced by virus-infected cells, and also take up viral proteins released from dying virus-infected cells. They respond by producing more cytokines to amplify the original response.
In many viral infections, the early action of cytokines produced by infected cells and dendritic cells is sufficient to eliminate the pathogen. If innate defenses are overwhelmed and virus replication continues unabated, then the second-line defenses are mobilized to ensure host survival. These comprise the adaptive immune response - antibodies and immune cells. Days to weeks are required to mount an adaptive immune response that is specifically tailored to the infecting virus. The innate response therefore serves as a crucial rapid response that provides sufficient time for the activation of the adaptive immune system.
Yes, I know this is a little complicated. Well, more than a little perhaps so just skim through it. I trimmed it down quite a bit. This is the truncated [abbreviated] version. We are just hitting the highlights here...
Ubiquitin is a regulatory protein. To be ubiquinated is to be modified or degraded by the attachment of ubiquitin molecules.
The fact that viruses routinely and frequently cause disease shows that our defense mechanisms are imperfect. This occurs in large part because nearly every viral genome encodes one or more countermeasures to modulate host defenses. Influenza virus is no exception. One of the viral proteins, called NS1, is particularly adept at impairing the synthesis of interferons (IFN) by cells.
The influenza NS1 protein, which is encoded by viral RNA 8, inhibits the innate and adaptive immune responses by multiple mechanisms. The protein blocks expression of type I IFN and inflammatory cytokines, and interferes with T-cell activation. Viral mutants with a truncated NS1 protein cause less severe disease [in mice, pigs, horses, and macaques]. Such viral mutants induce higher levels of IFN synthesis, and better T-cell activation... It has been suggested that viruses with truncated NS1 proteins might be good candidates for infectious, attenuated vaccines against influenza.
The main sensor of influenza virus infection is the cytoplasmic protein known as RIG-I...This protein resides in the cytoplasm and senses the presence of viral RNA... When these RNAs bind RIG-I, a signaling cascade is initiated which culminates in the production of IFN. The IFNs in turn activate the synthesis of nearly a thousand cellular proteins which have antiviral properties.
In order to function in the pathway leading to IFN induction, RIG-I must be ubiquinated...Attachment of ubiquitin to RIG-I is accomplished by a cellular enzyme called TRIM25. In cells infected with influenza virus, RIG-I is not ubiquinated, and therefore IFN is not produced. ...by binding to TRIM25 and preventing it from forming multimers. A specific amino acid sequence in NS1... is involved in binding to TRIM25.
He is addressing experiments in mice infected with bacteria. Flu victims in Mexico, and here also, I think were coming down with viral, not bacterial pneumonia. Does this make a difference?
The results seem inconclusive to him. His final note about a possible drug treatment is interesting. I am wondering if he is going anywhere else with these virology lessons...
Secondary bacterial pneumonia occurs after the patient has begun to recover from influenza infection, and often influenza virus can no longer be isolated. The reasons why influenza virus infections may lead to pneumonia are not understood. One group studied this problem by using mice inoculated in the trachea with a mouse-adapted strain of influenza virus, A/PR/8/1934 (H1N1). Five days later, Streptococcus pneumoniae bacteria are administered by the same route. The bacteria multiplied to high levels in mice that had been previously infected with influenza virus, but not in saline-treated control mice. Furthermore, significant mortality was observed in the doubly-infected mice but not in mice infected with virus or bacteria alone.
The same experiment was then repeated, using mice that lack the genes encoding cell surface receptors for type I IFNs (IFN-α and IFN-β). These mice can produce IFN, but they cannot synthesize the hundreds of antiviral proteins that are made in response to IFN, because the receptor for this cytokine (illustrated) is absent from cell surfaces. These mice were resistant to secondary bacterial pneumonia. When infected with influenza virus and then S. pneumoniae, the mice had no higher bacterial burden in the lung, and no more mortality, than mice infected only with bacteria.
Why does type I IFN predispose mice to secondary bacterial pneumonia? Two cytokines, called KC and Mip2, appear to be the culprits. After secondary challenge with S. pneumoniae, these cytokines were detected at higher levels in the lungs of type I IFN receptor deficient mice than in the lungs of wild type mice. These observations indicate that type I IFNs appear to inhibit the production of KC and Mip2 chemokines.
The chemokines KC and Mip 2 are believed to be essential for recruiting neutrophils, the most abundant type of white blood cell in the blood. Neutrophils are attracted to sites of bacterial infection, where they engulf and destroy the microbes. As expected, more immune cells were detected in the lungs of mice lacking type I IFN receptors than in the lungs of wild type mice.
These observations may explain why secondary bacterial infections occur after influenza in humans, according to the following model. During infection with influenza virus, type I IFN is produced, as the host innate defenses attempt to clear infection. Type I IFNs inhibit the production of the chemokines KC and Mip 2. Because these chemokines are essential for recruiting bacteria-destroying neutrophils into the lung, bacteria that enter the lung cannot be effectively cleared, and pneumonia occurs.
This is an interesting hypothesis, but it fails to explain two important observations. First, it does not explain why secondary bacterial pneumonia only occurs in a subset of influenza virus infected humans. And if the influenza virus NS1 protein inhibits the production of IFN, as we discussed yesterday, there should be no defect in the recruitment of neutrophils to the influenza virus-infected lung.
An intriguing observation is that influenza virus does not replicate any better in the lungs of mice lacking the IFN receptor than in the lungs of wild type mice. Perhaps the type I IFN system is redundant for limiting viral replication: when it is missing, other systems take its place. I don't understand this finding, given the role of the viral NS1 protein in blocking IFN production. Nevertheless, it might be possible to avoid secondary bacterial pneumonia by treating influenza patients with drugs that inhibit type I IFN.
...an interesting question is whether the 2009 H1N1 influenza virus could mutate into something more lethal... Of course it could - but is it beneficial for the virus?
A fundamental principle of viral evolution is that viruses must spread from host to host to maintain the viral population. A virus spreads only if an infected individual passes the virus on to more than one new host. Furthermore, infection can spread only if population density exceeds a minimal value.
Some scientists believe that increased viral virulence reduces transmissibility.
According to this hypothesis, virulence is selected against as the virus spreads in humans.
Why is reduced lethality equated with being better adapted to humans? And how could the virus become better adapted to humans when human to human transmission has been minimal?
There is insufficient evidence to conclude that increased viral virulence leads to reduced transmission. For example, the 1918 influenza virus strain was extremely virulent, yet spread very efficiently among humans.
It seems more likely that increased viral virulence could lead to better transmission.
Perhaps we should focus on transmissibility, not virulence, as the property that drives viral evolution. Viruses evolve so they can be efficiently transmitted to other hosts. According to this hypothesis, any other properties that accompany transmissibility, such as virulence, are secondary effects. If this idea were true, then all viruses would evolve to be maximally infectious and avirulent. But this is not the case. Perhaps, as Peter Palese said, viral virulence has unknown benefits:
"Look, I believe in Darwin. Yes, the fittest virus survives. But it's not clear what the ultimate selection parameter is." A mutation that confers lethality, he explained, may confer another advantage scientists have not pinned down.
I'm Dave. One of the folks at www.pfiforum.com provided me with a link to your site. Over at PFI we are all pretty concerned about how our health care professionals will fare during a pandemic. I have read a lot of the posts by Indigo Girl, so it looks like you have access to good information, but you might benefit from a little .pdf pandemic planning guide that I put together a few years ago. It is called "Becoming Self-Sufficient". The most recent revision, which dates back to 2008, does not specifically address A/H1N1. It was written in response to the threat from H5N1; however, you might still find it useful. It has sections that provide guidance on food, water, personal protection equipment, and undertaking a "shelter-in-place" exercise without the benefit of modern utilities. I will admit that my document is a little dark, but an influenza pandemic is a serious threat.
If you have specific concerns about pandemic planning, I will be happy to contribute what I know.
I did have a link to to your guide somewhere in one of the older threads, but that was some time ago.
Even though our current pandemic is considered moderate at this time, this could change. We can still benefit from your thoughtful work. Thank you for thinking of us.
lamazeteacher
2,170 Posts
That could be, and I read that the pigs were reservoirs for the mutated swine-avian virus, which wasn't widely known, in the effort to avoid hysteria......
The Muslims and Jews have been told since the beginning of (original, not common era) time, that pigs had trichonosis (not necessarily by that name) which caused the disease in humans, and was not "kosher" (for Jews), therefore it was forbidden as food for them, along with "bottom feeding" fish such as shellfish and catfish (not that the latter 2 had trichonosis, there were other things found to be caused by them - probably serious allergies).
Once better hygiene was used for the care and slaughter of pigs; and allergies were found to be the cause of anaphylactic shock from one or more type(s) of shellfish in some people, Reform Jews were allowed by their Rabbis to eat pork, shellfish, and catfish.