Coronavirus COVID-19 - Global Health Emergency #5

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Crazy? thought about how coronavirus might travel to Iran from China or anywhere- without direct person to person contact...
Could the virus droplets be rising into the atmosphere, "riding" in the smog, moving along and released?
Obviously complete speculation, imo.

Neat real-time pollution map..
AirVisual Earth - 3D Real-time Air pollution map

Watch air pollution flow across the planet in real time | Science | AAAS
''China’s air is notoriously toxic: Each year, it contributes to the premature deaths of some 1.6 million people. Concerned about how such pollution was affecting his family, Beijing-based data scientist Yann Boquillod founded AirVisual Earth, an online air pollution map that uses data from satellites and more than 8000 monitoring stations to display global air pollution in real time. The AirVisual Earth interactive maps prevailing wind patterns and shows color-coded concentrations of PM2.5—airborne particulate matter less than 2.5 microns in diameter that can penetrate deep into the lungs. Users can zoom in, tilt, and spin the globe for better viewing''
rbbm
 
Coronavirus Live Updates: South Korean Cases Spike, and Fear Builds

Nine South Korean tourists who spent a week visiting some of Israel’s most popular religious sites have tested positive for the coronavirus after returning home.

Within hours, Israel began closing the country to all South Korean travelers. Korean passengers flying on a Korean Air flight scheduled to land at Ben Gurion Airport at 7:30 p.m. Saturday would be barred entry into the country.

Health officials were working with the tourism ministry and travel agencies to book flights back to South Korea for the 1,700 South Korea tourists in Israel.
 
Re: conspiracy theory,

https://nypost.com/2020/02/22/dont-buy-chinas-story-the-coronavirus-may-have-leaked-from-a-lab/

Don't buy China's Story: ...


Lab-Made Coronavirus Triggers Debate

Lab-Made Coronavirus Triggers Debate


A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence. - PubMed - NCBI

A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence

"Shi ZL [4]
Author information
4 Key Labratory of Special Pathegens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China."
 
Regarding tylenol use discussed upthread, and liver involvement in the acute phase of disease-- elevated liver enzymes are one of the first indicators that the disease course will be severe. Most drugs (including ibuprofen) are metabolized by the liver, but acetominophen is a known "stressor" in regular or high doses.

This is a good overview-- will link a more technical article as well below.
Liver: Collateral damage
When a zoonotic coronavirus spreads from the respiratory system, your liver is often one downstream organ that suffers. Doctors have seen indications of liver injury with SARS, MERS, and COVID-19—often mild, though more severe cases have led to severe liver damage and even liver failure. So what’s happening?

“Once a virus gets into your bloodstream, they can swim to any part of your body,” Lok says. “The liver is a very vascular organ so [a coronavirus] can very easily get into your liver.”

Your liver works pretty hard to make sure your body can function properly. Its main job is to process your blood after it leaves the stomach, filtering out the toxins and creating nutrients your body can use. It also makes the bile that helps your small intestine break down fats. Your liver also contains enzymes, which speed up chemical reactions in the body.

In a normal body, Lok explains, liver cells are constantly dying off and releasing enzymes into your bloodstream. This resourceful organ then quickly regenerates new cells and carries on with its day. Because of that regeneration process, the liver can withstand a lot of injury.

When you have abnormally high levels of enzymes in your blood, though—as has been a common characteristic of patients suffering from SARS and MERS—it’s a warning sign. It might be a mild injury that the liver will quickly bounce back from or it could be something more severe—even liver failure.

Lok says scientists don’t completely understand how these respiratory viruses behave in the liver. The virus might be directly infecting the liver, replicating and killing off the cells itself. Or those cells might be collateral damage as your body’s immune response to the virus sets off a severe inflammatory reaction in the liver.

Either way, she notes that liver failure was never the sole cause of death for SARS patients. “By the time the liver fails,” she says, “oftentimes you’ll find that the patient not only has lung problems and liver problems but they may also have kidney problems. By then it becomes a systemic infection.”

Here’s what coronavirus does to the body

The pathological features of COVID-19 greatly resemble those seen in SARS and Middle Eastern respiratory syndrome (MERS) coronavirus infection.

In addition, the liver biopsy specimens of the patient with COVID-19 showed moderate microvascular steatosis and mild lobular and portal activity (figure 2C), indicating the injury could have been caused by either SARS-CoV-2 infection or drug-induced liver injury.

https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext
 
This is a very interesting article.

The graphic clinical record is very helpful.

https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext#fig2

This 50 year old male died of cardio/respiratory failure 14 days after the onset of cough and only 7 days after the onset of fever (although he had self-reported chills during the time he had a cough).

He also refused to go on a ventilator when he developed AARDS. The clinicians had to resort to HighFlowNasal Canula 02 therapy, which is not at all as effective in ventilation and oxygenation as intubation and mechanical ventilation.
 
Regarding tylenol use discussed upthread, and liver involvement in the acute phase of disease-- elevated liver enzymes are one of the first indicators that the disease course will be severe. Most drugs (including ibuprofen) are metabolized by the liver, but acetominophen is a known "stressor" in regular or high doses.

ttps://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext

Of note, his autopsy liver core samples show some inflammation, but at least in those samples, there is not apparent necrosis or cytolysis of hepatic tissue proper. The findings are pretty non-specific and don't imply fatal hepatocyte injury.

The lungs show hyaline membrane formation which is the hallmark of ARDS, along with the inflammation and edema, and the typical viral cytopathic effects. None of those features are at all specific for COVID-19 and this would be seen in many kinds of fatal viral pneumonias, including influenza, CMV, measles, etc.

(Hyaline membrane formation is also characteristic of Neonatal Respiratory Distress Syndrome seen in premature birth)
 
This is a very interesting article.

The graphic clinical record is very helpful.

https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(20)30076-X/fulltext#fig2

This 50 year old male died of cardio/respiratory failure 14 days after the onset of cough and only 7 days after the onset of fever (although he had self-reported chills during the time he had a cough).

He also refused to go on a ventilator when he developed AARDS. The clinicians had to resort to HighFlowNasal Canula 02 therapy, which is not at all as effective in ventilation and oxygenation as intubation and mechanical ventilation.

Ventilators in these cases are a response to the "work of breathing", more than "increasing oxygen diffusion at the cellular level". A ventilator alone can't fix or reverse what's going on at the cellular level in the alveoli in the disease process. The progression to respiratory failure and multi organ system dysfunction seems to happen pretty rapidly once the cytokine storm effects are clinically evident. (You can see these effects in Covid-19 patients in online pictures of vented patients with ventilator tubing full of secretions from the endotracheal tube all the way back to the ventilator machines.) It's likely he would not have survived even with ventilator care. Additionally, they tried steroids in his care, which I understand are agreed by most experts to be avoided in SARS type ARDS-- but I think it was all they had to try. He was already on the antiviral agents, among other meds for concomitant (opportunistic) bacterial pneumonia (the moxifloxacin).

For those with severe disease, who recover, most of them have a type of lung damage that is similar to emphysema. Sadly, if they are re-infected, the disease progression is often quite rapid and fatal.
 
Ventilators in these cases are a response to the "work of breathing", more than "increasing oxygen diffusion at the cellular level". A ventilator alone can't fix or reverse what's going on at the cellular level in the alveoli in the disease process. The progression to respiratory failure and multi organ system dysfunction seems to happen pretty rapidly once the cytokine storm effects are clinically evident. (You can see these effects in Covid-19 patients in online pictures of vented patients with ventilator tubing full of secretions from the endotracheal tube all the way back to the ventilator machines.) It's likely he would not have survived even with ventilator care. Additionally, they tried steroids in his care, which I understand are agreed by most experts to be avoided in SARS type ARDS-- but I think it was all they had to try. He was already on the antiviral agents, among other meds for concomitant (opportunistic) bacterial pneumonia (the moxifloxacin).

For those with severe disease, who recover, most of them have a type of lung damage that is similar to emphysema. Sadly, if they are re-infected, the disease progression is often quite rapid and fatal.

Yes, good point, but nasal cannula is just not going to be anywhere as efficient as a mechanical ventilator to present high levels of O2 to the alveoli.

And agree, they were aggressive in use of antivirals, antibiotics, and steroids, but the cytokine reaction storm is the difference between a simple bacterial pneumonia and this overwhelming and rapid respiratory failure.
 

Live chat now

The picture in Africa will start to clear soon as testing kits arrive
He suspects there are cases in Africa
Disease will take hold in poorer areas

Reduction in rates of infection in China
Despite Gross underestimate of figures

Chinese have taken draconian measures

Massive shutdown will reduce rate of spread
Giving us time to prepare

Epidemics have reached its natural peak in some areas

In a few weeks, rates the infection rate will go down in Wuhan.

Less people per day but over a longer period of time.

NK and Vietnam
'Informal trade', coming and going, from NK and Vietnam

Community based spread, the way the figures are going, it seems to be the case

Wrt Iran, official case numbers is a massive underestimate
His contacts in Iran, Doctors, report the disease conditions seem more severe in Iran
Viral myrocarditis?

Risk, Virus may have become more infectious and virulent
Not sure yet. Medical intervention, is a concern, where less medical attention is available.
 
Of note, his autopsy liver core samples show some inflammation, but at least in those samples, there is not apparent necrosis or cytolysis of hepatic tissue proper. The findings are pretty non-specific and don't imply fatal hepatocyte injury.

The lungs show hyaline membrane formation which is the hallmark of ARDS, along with the inflammation and edema, and the typical viral cytopathic effects. None of those features are at all specific for COVID-19 and this would be seen in many kinds of fatal viral pneumonias, including influenza, CMV, measles, etc.

(Hyaline membrane formation is also characteristic of Neonatal Respiratory Distress Syndrome seen in premature birth)

Agree. Unfortunately, there are not a lot of post mortem exams being done (or results shared with world experts) on the largest cohort of patients who have died, in China. We are still in the "gaining info" phase of this pathogen. Most of the severe cases in China were not autopsied, nor specimens preserved, prior to cremation, from what is in the news.

Biopsy samples from a 50-year-old Beijing man who died from his infection found that lung, liver, and heart tissue showed pathologic features similar to severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome coronavirus (MERS-CoV) infection, a team from China reported today in The Lancet Respiratory Medicine. It wasn't clear if the changes in liver tissue were drug-induced or from the COVID-19 virus. Overactivation of T cells may have accounted for severe immune injury, the authors noted. And they didn't observe any obvious histologic changes in heart tissue.

China COVID-19 cases rise, as do worries over Diamond Princess risk
 
Agree. Unfortunately, there are not a lot of post mortem exams being done (or results shared with world experts) on the largest cohort of patients who have died, in China. We are still in the "gaining info" phase of this pathogen. Most of the severe cases in China were not autopsied, nor specimens preserved, prior to cremation, from what is in the news.



China COVID-19 cases rise, as do worries over Diamond Princess risk

I see the use of postmortem "biopsies" being used in a more widespread fashion to avoid the risk of a full open autopsy. Presumable pre-morbid CT or other imaging has defined the organs most affected, and systems that don't need extensive examination. Very simple to get large core samples of most all organs.
 
Yes, good point, but nasal cannula is just not going to be anywhere as efficient as a mechanical ventilator to present high levels of O2 to the alveoli.

And agree, they were aggressive in use of antivirals, antibiotics, and steroids, but the cytokine reaction storm is the difference between a simple bacterial pneumonia and this overwhelming and rapid respiratory failure.

Agree- a nc in this case was likely not much more effective for him than room air. But the article says he refused intubation and vent care, FWIW.

One more thing to remember is that we have no idea what the past medical history of this patient was prior to his fatal course with Covid-19. As most adult males are heavy smokers in Beijing (and all of China) from their teenage years, he likely had some clinically significant lung disease prior to this illness, as he was over 50.

I was just in China a few months ago, and hadn't been there since before 2015 when they implemented the "no indoor smoking" rules country wide. It was much more pleasant to be in restaurants, but the overall smoking rate in the country does not seem to have changed at all. (To my observation, anyway.) Many, many (most!) people over age 40 have a baseline chronic productive cough, too (air pollution, etc.). But interestingly, the childhood asthma rate there is not anywhere close to that of the U.S., even with their poor air quality and heavy smoking.
 
Crazy? thought about how coronavirus might travel to Iran from China or anywhere- without direct person to person contact...
Could the virus droplets be rising into the atmosphere, "riding" in the smog, moving along and released?
Obviously complete speculation, imo.

Neat real-time pollution map..
AirVisual Earth - 3D Real-time Air pollution map

Watch air pollution flow across the planet in real time | Science | AAAS
''China’s air is notoriously toxic: Each year, it contributes to the premature deaths of some 1.6 million people. Concerned about how such pollution was affecting his family, Beijing-based data scientist Yann Boquillod founded AirVisual Earth, an online air pollution map that uses data from satellites and more than 8000 monitoring stations to display global air pollution in real time. The AirVisual Earth interactive maps prevailing wind patterns and shows color-coded concentrations of PM2.5—airborne particulate matter less than 2.5 microns in diameter that can penetrate deep into the lungs. Users can zoom in, tilt, and spin the globe for better viewing''
rbbm

Airvisual map is cool.
 
I see the use of postmortem "biopsies" being used in a more widespread fashion to avoid the risk of a full open autopsy. Presumable pre-morbid CT or other imaging has defined the organs most affected, and systems that don't need extensive examination. Very simple to get large core samples of most all organs.

Yes, if China will share the results in aggregate, and "if" they are treating each severe case with some standardization across all facilities, which I doubt. And "if" they are truly keeping the detail and quality of medical records comparable to western standards, which I also sincerely doubt. They are in crisis mode, rotating medical professionals in as fast as they can find and mobilize them. Continuity of care and standard algorithms for care are not likely a priority at this time. I think the med pros are doing the best they can with what they have, for as many as they can.
 
Today's WHO situation report is out.

New info for studies within it.

https://www.who.int/docs/default-so...0222-sitrep-33-covid-19.pdf?sfvrsn=c9585c8f_2

Dr. Campbell's live Q&A still going on 90 minutes later. (He had to reboot as froze up 30 minutes in). He's talking now how even in his hospital he has 9 (I think) rooms for critical folks needing support, and numbers projected if/when comes they would not have resources. (They would need 500 beds for JUST the CRITICAL patients if they had 100,000 infections)


ETA and as was noted above, only 10 hospitals in US with proper airborne biocontrol rooms

ETA2 Within the sit rep, it has link with Dr. Pedros in Africa re COVID-19 earlier today. That apparently replaced the Geneva presser.
 
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