Smiths? deaths caused by ARDS

[JimO]

Smiths? deaths caused by ARDS

A Knox County mother and father are placed on life support at a southeastern Kentucky hospital. Then they?re flown to a Tennessee medical center, where they are diagnosed with the same disease.

The mother, Marilyn Hurley Smith, dies on Jan. 7. She was 50.

Four days later, her husband, Dorman Smith, would also pass away. He was 64.

Both died from ARDS ? Acute Respiratory Distress Syndrome.

- See more at: http://www.thetimestribune.com/x1724....imwEuYVy.dpuf

[alert]

Re: Smiths? deaths caused by ARDS

It actually says later in the article that both patients were thought to have flu. It would be interesting to know if the influenza virus had been subtyped or sequenced. Two linked deaths due to seasonal flu, even H1N1pdm09 is fairly rare.

[curiosity]

Re: Smiths? deaths caused by ARDS

2009 Flutrackers Post

Similar event in Indiana during pH1N1's first pass through the population.

[JimO]

Re: Smiths? deaths caused by ARDS

Wouldn't it also be unusual for two people to die within days of one another from ARDS unless there was some contagious pathogen involved?

It actually says later in the article that both patients were thought to have flu. It would be interesting to know if the influenza virus had been subtyped or sequenced. Two linked deaths due to seasonal flu, even H1N1pdm09 is fairly rare.

[Emily]

Re: Smiths? deaths caused by ARDS

Wouldn't it also be unusual for two people to die within days of one another from ARDS unless there was some contagious pathogen involved?

This research indicates there could be a genetic mutation involved in these rare cases where multiple family members succumb to flu:
Lethal influenza virus A H1N1 infection in two relatives with autosomal dominant GATA-2 deficiency
Natural History Study of GATA2 Deficiency and Related Disorders

The 2 victims in the 2009 case that curiosity brought up were siblings, though there was apparently a shared environmental exposure prior to infection that could have irritated their lungs and sinuses along with the weight risk factor in those cases. They could have had 2 strikes against them when the flu came along.

In the current case, the 2 victims were unrelated genetically, but their son thinks that ARDS, rather than the flu was the primary cause of death (from Jim's link):

Both my mom and dad had the flu, but ARDS was more of a factor in their deaths,? said Eric Smith, who is 24 years old, and stayed with his parents at their home in the Cannon community of Knox County.

Eric noticed the problems when his parents were taken to Pineville Community Hospital last month.

?My dad had pneumonia and started developing the flu. My mom had bronchitis and a double ear infection. - See more at: http://www.thetimestribune.com/x1724....KsbMLxyV.dpuf

So it sounds like they were already ill when the flu came along, perhaps there was a lung/sinus-irritating environmental factor precipitating all of this.

[NS1]

Re: Smiths? deaths caused by ARDS

Wouldn't it also be unusual for two people to die within days of one another from ARDS unless there was some contagious pathogen involved?

2009 ReDux
pH1N1 ~= Causality
ARDS = Mechanism

Exactly, Jim.

ARDS is not a disease, but is a mechanism of biological failure. That biological failure is generally caused by an external toxin or pathogen, although human genetics including variant proteonomic expression may be a considerable factor.

The ARDS designation during flu season is typically an attempt to reduce the count of pH1N1 category fatalities. That clinical sleight of hand swiftly moves the emphasis away from causality.

Most pH1N1 human cases that are severe or fatal invoke an ARDS type biological outcome . . . the lungs fail. ARDS is a sadly convenient and mysterious explanation delivered to family members when the causal pathogen has not been averted by the clinician.

Deep Lung Involvement, many times with rapid deterioration, typically translates to an ARDS designation. pH1N1 since 2009 has demonstrated the singular ability to kill from direct viral-induced lytic activity and the associated Cytokinic Dysregulation, rapidly destroying masses of cells of its own accord without the involvement of secondary infection.

That ARDS designation should be an adjunct Diagnosis at most, not the Primary Dx.

Causality obviously should rule the day if the medical community is seeking current and future beneficial outcomes.

[NS1]

Re: Smiths? deaths caused by ARDS

pH1N1
Data Sparsity
Egg Passage
Winter 2013

2014-01-18-21:30
At the WeekEnd, Atlanta

A December Void

During the minimal pH1N1 case count in the Northern Hemisphere's 2012 season and post-season, the US CDC demonstrated the experimental importance of Egg Passage strategies. Variant polymorphisms known to drive deep lung involvement in humans were surfaced repeatedly from quasi-species. That egg-based experimentation was considered valuable and was pursued throughout much of 2013, but evidently not to quantify the actual circulating pH1N1 viral population . . . because the production came to a full halt at the moment that the US flu season's high fatality rates became public due to an unexpected re-emergence of pH1N1.

Prior to the beginning of the present US season, experimental devotion was clear with seventeen sequences published on Egg Passaging having sample dates BETWEEN seasons, a much-appreciated and long overdue analysis bed. That high interest from the depositing organisation, however, waned just as the infective period of actionable usefulness began. After the four mid-November US samples from egg-based passages (concentrated six day period), no further information has been provided.

Silence is NOT Golden

Few explanations satisfy the fact of publication quiescence . . .

Few indeed, unless we consider that the intent of this egg-based benchwork may have been to suggest that the dangerous polymorphisms were "artifacts", a managed message stream flowing from these agencies since 2009 via all outbound portals. Even a passing view of their results shows genetic incongruity to that hypothesis. The public health monopoly's campaign to marginalise the experimental evidence with their tiresome, "artifact of egg passaging" explanation cannot be supported by their genetic outputs.

Flashfires of dominant pH1N1 populations carrying accumulations of those dangerous polymorphisms began as early as the summer of 2013 and then impacted with full force in December 2013. The High-CFR Upsilon subclade's polymorphic set re-emerged. As individual geographies moved into the highest fatality and severity yet seen since modern records have been collected, the public health leaders responded by markedly reducing usable surveillance.

Eight Weeks

During the period from November 19, 2013 to today, no sample has been published with a sequence generated upon an Egg-Based Passage strategy.

During this predictable epidemic with geographically-focal high severity and high fatality, the most relevant information has been withheld for eight weeks.

By those we've trusted to protect our children's lives.

During 4 weeks of fatality intensity, only one sequence has been deposited covering the geography and time period of the high intensity events.

Are we able to measure intent from these actions? Are we satisfied with political utility being the primary measure of our public health organisations?

More importantly, is mission failure driving this silence?

WHO decides. We'd like to see.

And it can't wait another eight weeks.