A pandemic "Big Bang?"
Bangladesh H5N1 human positive begs more questions
The recent disclosure from the Bangladesh government and the CDC that a toddler was positive for H5N1 when originally certified negative opens the door to a multitude of questions. Read with me the capsule, as digested by Dr. Henry Niman:
The DGHS, as part of its routine surveillance, sent a swab with samples from naso-pharyngeal of the 16-month-old boy to the Centres for Disease Control and Prevention in Atlanta which confirmed the H5N1 infection Wednesday.
http://www.recombinomics.com/News/05220806/H5N1_Dhaka_Mild.html
"When the child came to us it was diagnosed with strain A positive but the H5 was found negative. However, one and a half months later when we sent the sample to Atlanta, as part of our routine surveillance, it was confirmed after culturing the virus that it was H5 positive,"
The boy, who lives in Kamalapur in Dhaka, was cured without any medicine for Influenza. He was provided with medicines for respiratory infection for 14 days... (bold mine)
This one small snippet of the news story is quite revealing. First, why did it take six weeks to send the virus sample to the WHO and CDC? Is this routine? Second, why the false negative for H5? What test was used that produced the false negative? Thank the God of your faith that the Bangladesh government did its due diligence and sent a negative sample ahead to the WHO and CDC.
A significant case can be made for the global junking of the test that produced the false negative. The unanswered question is, How many false negatives have been misdiagnosed across the globe using this and other tests since 2003?
The odds say that this 16-month old should not have survived. By the way, I do like to play the odds, and got four horses right in the only two Preakness races I participated in last week. Not bad.
But I digress. The odds say this toddler should have died. Since the child is recovering without the aid of antivirals, this means that we are probably looking at a very mild Qinghai clade 2.2 H5N1. This implies that if one toddler contracted high-path H5N1, then we need to assume others in the region bordering and including east India (a region the size and shape of the state of Maine) have also contracted H5N1. Since we have not seen a massive die-off of humans in the region, my suspicion is this mild H5N1 is being misdiagnosed as seasonal flu. If it is not tipping the scales on influenza tests, it is not evoking concern. This hypothesis is bolstered by the false negative and subsequent discovery of H5N1 by the CDC six weeks later, in the culturing of the virus.
We have read about cases where Indian cullers have experienced flu-like symptoms. I hope somebody is following up with those cullers to see if they exhibit antibodies to H5N1. Certainly mass suggestion could also be a culprit, and I tip my cap to that theory as being entirely possible. Just as possible now, however, with the Bangladesh disclosure, is the chance we are seeing mild human H5N1 (once again) go completely undiagnosed. It is not an unfamiliar refrain.
I blogged not too long ago that perhaps Qinghai will not become the pandemic strain of H5N1. I theorized that Fujian Clade 2.3 would be the trigger. But I am also reminded of the words given to me by Dr. Richard Webby, protege of the Pope of Influenza, Dr. Robert Webster. Dr. Webby said to me in 2006 that we would be surprised how little we really know about influenza.
Perhaps this is exactly how influenza becomes pandemic. We see three or four substrains of a particular virus circumnavigate the globe. We see the virus move from wild birds to poultry and back again; or we see the virus move from poultry to wild birds and back again. The sequence really does not matter. The "Three P's" (poultry, pigs, people) help move the viral goulash along in its evolution and help the virus substrains acquire -- slowly, maybe agonizingly so -- the necessary genetic elements for pandemic activity.
This evolution cannot be stopped, only slowed. .
Then, quite suddenly, these subtypes all recombine with each other. A pandemic "Big Bang," if you will, ensues. Since influenza A plays King of the Mountain, the strongest (most lethal?) substrain accepts other substrain's acquired genetic characteristics and takes its victory lap around the world a few times.
It is at that point that a pandemic occurs. This theory is not far removed from that of one of my heroes. The late Dr. R. Edgar Hope-Simpson theorized that asymptomatic carriers of novel influenza were at least partly responsible for pandemics. He also sprinkled in doses of sunspots and solar radiation -- kind of a Pandemic Theory of Everything.
What if he was right? Perhaps those "asymptomatic" carriers were not so asymptomatic, but were actually carrying a milder form of a novel strain that no one picked up on. That 16-month old toddler could be one such asymptomatic carrier. So could thousands of Indian, Chinese, Vietnamese, Russian, Thai, Pakistani and Turkish carriers. This also would explain the sudden appearance of pandemic influenza all over the world simultaneously. There are too many stories of historic pandemics where the virus' travel was much too quick for any of the conventional transportation mechanisms of the day. Pandemic influenza outran sailing ships and other ocean-going vessels. It outran horseback, wagon, carriage and train. It did so because it was with us already for years, festering, smouldering, waiting for that simultaneous worldwide genetic addition that caused it to spark.
Only antibody testing of tens of thousands of people in bird flu hot spots all over the world will reveal any fact or truth to this hypothesis. It certainly does underscore the prevailing belief that we won't know that we are in a pandemic until after it starts. There are simply too many holes in surveillance to guarantee early warning.
But in one remote area of one struggling nation, we may have found a very important clue to solving this riddle. And we found it courtesy of due diligence and surveillance.
If only other nations (are you listening, Indonesia?) would do as well.
Reader Comments (2)
The stunning fact is that the boy illness date back January 2008.
If a transmissible virus circulated in a overcrowded setting as a Dakka slum is, with a number of communicable diseeases already in place and malnourished people, with faecal waste everywhere... a disaster resulted.
But perhaps there is a missing link.
The search of this missing link should be carried out.
If the old idea of professor Edwin Kilbourne is true! That's N1 component of H1N1 human influenza virus may trigger a cross-reactive immune response, at least in some population, due to particular strain... Perhaps.
No one know for certainty, the extent of previous exposure of Asian people to H1N1 variants and the research of a some level of cross-neutralizing antibody activity against H5 may be advisable.
"waiting for that simultaneous worldwide genetic addition that caused it to spark."
I don't disagree that something like this accounts for the rapid spread in 1918. Would you say more, though, about how you see this change happening almost simultaneously around the world? Seems that if a mutation or reassortment is required to to the thing into pandemic, then THAT would still have to travel the globe. Maybe I'm missing something.
Thanks