Blacknarwhal
Let's Go Brandon!
Actually, you should just look at Georgia. They opened first, and it's been three weeks now.
CORONA Main Coronavirus thread
- Thread starter Heliobas Disciple
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Actually, you should just look at Georgia. They opened first, and it's been three weeks now.
Hummm.....
Posted for fair use.....
news.yahoo.com
How L.A. County became coronavirus epicenter: Slower shutdown, density, poverty among theories
Soumya Karlamangla, LA Times • May 23, 2020
In mid-March, as the specter of a society-upending pandemic grew, Los Angeles County emerged as something of a bright spot.
When Bay Area counties mandated on March 16 that all residents stay at home, officials said it didn’t make sense in L.A. County because far fewer cases of the coronavirus had been detected.
"We don’t have the same trajectory that they have up north," L.A. County Public Health Director Barbara Ferrer said that day when asked about a stay-at-home order.
Two months later, the situation has shifted dramatically. L.A. County now has the highest rate of deaths from COVID-19 in the state, and the second highest infection rate. On Friday, federal officials singled out Los Angeles because of its stubbornly high case counts of the coronavirus, despite precautions to slow the spread.
With so many factors at play, it is almost impossible to know which is the culprit, especially in the midst of an evolving outbreak, experts say.
Many epidemiologists pointed to densely packed neighborhoods with overcrowded housing, as well as high rates of poverty, homelessness and even pollution that could be fueling poor outcomes in L.A. County.
Another factor might be when local officials shut down. The Bay Area issued its stay-at-home order on March 16, followed by L.A. County three days later. Though earlier than the rest of the nation, the delay may have set the stage for L.A. County to succeed the Bay Area as California's center for COVID-19.
"The Bay Area probably figured it out sooner, and that's why the Bay Area looked like it was worse early on," said UCLA epidemiologist Dr. Timothy Brewer. "I think L.A. was a little bit behind S.F. and some of the surrounding areas in the Bay Area ... and now we're seeing the after effects of that."
L.A. County officials say that while deaths remain troublingly high, there are other indicators that the region is beginning to turn the corner. But understanding how things got so bad in the first place is going to take time.
"The way coronavirus is playing out in some sense is unique to the different cities and the different counties around the globe," said Amanda Daflos, chief innovation officer for the city of L.A. "We're monitoring everything very closely."
::
Compared with cities nationwide, Los Angeles' rate of COVID-19 cases and deaths has been relatively low. Approximately 2,000 people have died in L.A. County of COVID-19, while in New York City, which is roughly the same population size, the death toll has crossed 20,000.
But the region has emerged as an outlier within California. In L.A. County, 426 out of every 100,000 people have tested positive for COVID-19, compared with 270 in San Francisco. In L.A., 20 out of every 100,000 residents have died of COVID-19, compared with 4 in San Francisco.
"If you look at individual counties and cities, L.A. has been a hotbed," said UC Davis epidemiologist Bradley Pollock.
To try to make sense of these trends, data crunchers at the L.A. County Public Health Department recently ran some numbers, said chief science officer Dr. Paul Simon.
They looked into whether L.A. County's population was older than the rest of the state's. In Italy, an older-than-average population was believed to have contributed to that country's alarmingly high death rate. But the L.A. County analysis found that its population was not older than the rest of the state, and perhaps even skewed a little younger, Simon said.
Analysts also looked into whether the county’s residents were more likely to have diabetes, high blood pressure or obesity compared with the rest of the state, factors that could make them more likely to die from COVID-19. Again, they found no difference, he said.
“What does that leave us with?” Simon said. The answer has been a bit of a puzzle, he said.
One piece may be the delayed stay-at-home order.
Though it appeared in March that L.A. County had less coronavirus transmission than the Bay Area, experts say that it is now clear that there was likely widespread coronavirus transmission far before it was detected, especially in Los Angeles County, with its high number of incoming travelers.
So the idea that the Bay Area had more transmission than the rest of the state was simply an indicator of who detected it first, experts say. And catching those cases early may have actually helped the Bay Area because it prompted quick action and shifted public sentiment, experts say.
In San Francisco, fewer people were going out to restaurants and other public spaces as early as late February, far before such a change was seen in L.A., said UC San Francisco epidemiologist Dr. George Rutherford. Many tech companies in the Bay Area asked their employees to work from home even before those orders, something more difficult in Los Angeles County, where fewer people work in high-tech jobs, he said.
L.A. city, the largest within the county, ordered bars and restaurants to switch to take-out only on March 15, the day before Bay Area announced its shelter-at-home order. But the countywide stay-at-home mandate didn't come until three days after the Bay Area's, and the true effects were probably not felt for a few days after it was ordered, based on reports of people crowding beaches the weekend after the announcement ,Rutherford said.
"Functionally, it was probably like six days later, which could represent as many as 1.5 extra generations of viral spread, which makes a big difference," he said.
But Rutherford and other epidemiologists agreed that the delay does not account for the ongoing high rates of cases and deaths.
The city of L.A. did widely expand testing, now even for asymptomatic residents, which may be why case counts are not quickly falling despite the shutdowns, but that doesn't explain why the death rates are also higher, experts say.
The most common explanation cited was density: many people living close together, creating the perfect conditions for the coronavirus to spread. Data from other regions show the virus often transmits within households due to close, prolonged contact that facilitates its spread. Once the virus gets into those settings, it can spread widely, experts say.
"The county is 10 times more dense than the state as a whole," UCLA's Brewer said. "If you think about where we have seen very explosive outbreaks, they've tended to occur in places like meat-packing plants, skilled nursing facilities, assisted living homes — places where people are spending a fair amount of time together in close contact in enclosed environments."
L.A. County also has higher rates of poverty than all the Bay Area counties, as well as almost every urban county in the state. Poorer people are more likely to be homeless, and be unable to stay home when they are sick, have access to healthy foods and medical care, and more likely to live in polluted areas.
These factors have set the stage for outbreaks in L.A. County in the past, including typhus, hepatitis A and measles just in the last few years, said USC epidemiologist Dr. Neha Nanda.
Experts say their understanding of L.A. County's persistent outbreak will continue to develop in the coming months, though there are already some signs of hope.
Officials announced earlier this week that the transmission rate for the coronavirus had fallen lower than ever before. Prior to the stay-at-home orders in March, each person in L.A. County was likely infecting at least three other people. Now, that number has fallen below 1, a sign that the epidemic may begin to shrink.
But experts say that with infectious diseases, when a single case can turn into thousands, it is impossible to predict what will happen next. When it comes to L.A. County's outbreak, some factors are out of its control, said UCSF's Rutherford.
"It's also a matter of luck," he said.
Posted for fair use.....
How L.A. County became coronavirus epicenter: Slower shutdown, density, poverty among theories
Theories abound as to why L.A. County has the bulk of the state's confirmed coronavirus cases, but a clear explanation has been elusive.
How L.A. County became coronavirus epicenter: Slower shutdown, density, poverty among theories
Soumya Karlamangla, LA Times • May 23, 2020
In mid-March, as the specter of a society-upending pandemic grew, Los Angeles County emerged as something of a bright spot.
When Bay Area counties mandated on March 16 that all residents stay at home, officials said it didn’t make sense in L.A. County because far fewer cases of the coronavirus had been detected.
"We don’t have the same trajectory that they have up north," L.A. County Public Health Director Barbara Ferrer said that day when asked about a stay-at-home order.
Two months later, the situation has shifted dramatically. L.A. County now has the highest rate of deaths from COVID-19 in the state, and the second highest infection rate. On Friday, federal officials singled out Los Angeles because of its stubbornly high case counts of the coronavirus, despite precautions to slow the spread.
With so many factors at play, it is almost impossible to know which is the culprit, especially in the midst of an evolving outbreak, experts say.
Many epidemiologists pointed to densely packed neighborhoods with overcrowded housing, as well as high rates of poverty, homelessness and even pollution that could be fueling poor outcomes in L.A. County.
Another factor might be when local officials shut down. The Bay Area issued its stay-at-home order on March 16, followed by L.A. County three days later. Though earlier than the rest of the nation, the delay may have set the stage for L.A. County to succeed the Bay Area as California's center for COVID-19.
"The Bay Area probably figured it out sooner, and that's why the Bay Area looked like it was worse early on," said UCLA epidemiologist Dr. Timothy Brewer. "I think L.A. was a little bit behind S.F. and some of the surrounding areas in the Bay Area ... and now we're seeing the after effects of that."
L.A. County officials say that while deaths remain troublingly high, there are other indicators that the region is beginning to turn the corner. But understanding how things got so bad in the first place is going to take time.
"The way coronavirus is playing out in some sense is unique to the different cities and the different counties around the globe," said Amanda Daflos, chief innovation officer for the city of L.A. "We're monitoring everything very closely."
::
Compared with cities nationwide, Los Angeles' rate of COVID-19 cases and deaths has been relatively low. Approximately 2,000 people have died in L.A. County of COVID-19, while in New York City, which is roughly the same population size, the death toll has crossed 20,000.
But the region has emerged as an outlier within California. In L.A. County, 426 out of every 100,000 people have tested positive for COVID-19, compared with 270 in San Francisco. In L.A., 20 out of every 100,000 residents have died of COVID-19, compared with 4 in San Francisco.
"If you look at individual counties and cities, L.A. has been a hotbed," said UC Davis epidemiologist Bradley Pollock.
To try to make sense of these trends, data crunchers at the L.A. County Public Health Department recently ran some numbers, said chief science officer Dr. Paul Simon.
They looked into whether L.A. County's population was older than the rest of the state's. In Italy, an older-than-average population was believed to have contributed to that country's alarmingly high death rate. But the L.A. County analysis found that its population was not older than the rest of the state, and perhaps even skewed a little younger, Simon said.
Analysts also looked into whether the county’s residents were more likely to have diabetes, high blood pressure or obesity compared with the rest of the state, factors that could make them more likely to die from COVID-19. Again, they found no difference, he said.
“What does that leave us with?” Simon said. The answer has been a bit of a puzzle, he said.
One piece may be the delayed stay-at-home order.
Though it appeared in March that L.A. County had less coronavirus transmission than the Bay Area, experts say that it is now clear that there was likely widespread coronavirus transmission far before it was detected, especially in Los Angeles County, with its high number of incoming travelers.
So the idea that the Bay Area had more transmission than the rest of the state was simply an indicator of who detected it first, experts say. And catching those cases early may have actually helped the Bay Area because it prompted quick action and shifted public sentiment, experts say.
In San Francisco, fewer people were going out to restaurants and other public spaces as early as late February, far before such a change was seen in L.A., said UC San Francisco epidemiologist Dr. George Rutherford. Many tech companies in the Bay Area asked their employees to work from home even before those orders, something more difficult in Los Angeles County, where fewer people work in high-tech jobs, he said.
L.A. city, the largest within the county, ordered bars and restaurants to switch to take-out only on March 15, the day before Bay Area announced its shelter-at-home order. But the countywide stay-at-home mandate didn't come until three days after the Bay Area's, and the true effects were probably not felt for a few days after it was ordered, based on reports of people crowding beaches the weekend after the announcement ,Rutherford said.
"Functionally, it was probably like six days later, which could represent as many as 1.5 extra generations of viral spread, which makes a big difference," he said.
But Rutherford and other epidemiologists agreed that the delay does not account for the ongoing high rates of cases and deaths.
The city of L.A. did widely expand testing, now even for asymptomatic residents, which may be why case counts are not quickly falling despite the shutdowns, but that doesn't explain why the death rates are also higher, experts say.
The most common explanation cited was density: many people living close together, creating the perfect conditions for the coronavirus to spread. Data from other regions show the virus often transmits within households due to close, prolonged contact that facilitates its spread. Once the virus gets into those settings, it can spread widely, experts say.
"The county is 10 times more dense than the state as a whole," UCLA's Brewer said. "If you think about where we have seen very explosive outbreaks, they've tended to occur in places like meat-packing plants, skilled nursing facilities, assisted living homes — places where people are spending a fair amount of time together in close contact in enclosed environments."
L.A. County also has higher rates of poverty than all the Bay Area counties, as well as almost every urban county in the state. Poorer people are more likely to be homeless, and be unable to stay home when they are sick, have access to healthy foods and medical care, and more likely to live in polluted areas.
These factors have set the stage for outbreaks in L.A. County in the past, including typhus, hepatitis A and measles just in the last few years, said USC epidemiologist Dr. Neha Nanda.
Experts say their understanding of L.A. County's persistent outbreak will continue to develop in the coming months, though there are already some signs of hope.
Officials announced earlier this week that the transmission rate for the coronavirus had fallen lower than ever before. Prior to the stay-at-home orders in March, each person in L.A. County was likely infecting at least three other people. Now, that number has fallen below 1, a sign that the epidemic may begin to shrink.
But experts say that with infectious diseases, when a single case can turn into thousands, it is impossible to predict what will happen next. When it comes to L.A. County's outbreak, some factors are out of its control, said UCSF's Rutherford.
"It's also a matter of luck," he said.
marsh
On TB every waking moment
2:48 min
One America News NetworkReopening protests have made headlines nationwide for the way some demonstrators are treating reporters who choose to wear face masks. One America's Kyarra Harris explains.
jward
passin' thru
See How All 50 States Are Reopening
By Sarah Mervosh, Jasmine C. Lee, Lazaro Gamio and Nadja PopovichUpdated May 23, 2020
The United States has crossed an uneasy threshold, with all 50 states beginning to reopen in some way two months after the coronavirus thrust the country into lockdown. But there are substantial variations in how states are deciding to open up, with some forging far ahead of others.
Life in Georgia, which was among the first states to reopen many businesses in April, feels far different than in Illinois, which is one of three states and Washington, D.C., that are reopening in small ways but are still largely shut down. Several states are removing restrictions on beaches and pools going into Memorial Day weekend.
The lifting restrictions reflect the immense political and social pressures weighing on the nation’s governors to open up, even as epidemiologists remain cautious and warn of the potential for a second wave of cases.
Individual states info found at source
posted for fair use
See How All 50 States Are Reopening
By Sarah Mervosh, Jasmine C. Lee, Lazaro Gamio and Nadja PopovichUpdated May 23, 2020
The United States has crossed an uneasy threshold, with all 50 states beginning to reopen in some way two months after the coronavirus thrust the country into lockdown. But there are substantial variations in how states are deciding to open up, with some forging far ahead of others.
Life in Georgia, which was among the first states to reopen many businesses in April, feels far different than in Illinois, which is one of three states and Washington, D.C., that are reopening in small ways but are still largely shut down. Several states are removing restrictions on beaches and pools going into Memorial Day weekend.
The lifting restrictions reflect the immense political and social pressures weighing on the nation’s governors to open up, even as epidemiologists remain cautious and warn of the potential for a second wave of cases.
Individual states info found at source
posted for fair use
See How All 50 States Are Reopening
Weft and Warp
Senior Member
I'm not sure how you would do a search on the tablet, but on the PC, I searched my county by clicking and holding down the control button and then clicking the F key....to bring up a search bar. I then type in the county and scroll down through the results.
They're making it harder to find the data for each county. They used to report all the numbers on the LTCFs, even if it was one or two patients per place but now they have stopped reporting numbers if they are less than 5.
Last edited:
jward
passin' thru
Novel Coronavirus - Covid19
@PandemicCovid20
11m
Coronavirus: 'Baffling' observations from the front line -
View: https://twitter.com/PandemicCovid20/status/1264785934014447616?s=20
Article posted in it's entirety posted below:
@PandemicCovid20
11m
Coronavirus: 'Baffling' observations from the front line -
View: https://twitter.com/PandemicCovid20/status/1264785934014447616?s=20
Article posted in it's entirety posted below:
Heliobas Disciple
TB Fanatic
Time to get grapefruit juice back on the menu – Fruit Juice Focus
www.fruitjuicefocus.com
Time to get grapefruit juice back on the menu
Grapefruit juice could be the next big thing if marketers get it right suggests Caroline Whibley.
The health benefits of this wonder fruit really are encouraging.
It wasn’t long ago households regularly bought grapefruit for breakfast or drank the ‘tart’ grapefruit juice, and told themselves they were being healthy. In fact, back in the 30s the Grapefruit Diet, also called the Hollywood Diet, involved having grapefruit or grapefruit juice with every meal while cutting back on calories. People swore by it. Grapefruit has a long history with being associated with good health so where is it heading now?
‘In tests mice fed fatty foods
and juice gained 18%
less weight than others’
Lately the consumption of grapefruit juice has declined sharply, following the accidental discovery of the interaction between grapefruit juice and certain drugs, particularly statins, extensively prescribed as cholesterol reducers. Grapefruit juice was found to interfere with the absorption of the drugs in the small intestine, thus affecting their bioavailability and increasing their toxicity. Suddenly you find the juice on the no-no list of what not to consume from your doctor. However rather than spending a lifetime on statins surely we need to be teaching the public to consume food & drinks and health regimes that help them to keep a lower cholesterol – are statins a sticky plaster rather than really treating anything at all, and yes they benefit many, however . . .
Long term I think we all want to see more healthy remedies to our ills, so I’m pretty positive about grapefruit juice and think it’s one to watch out for, if we can get the marketing right this dynamo juice really has some excellent benefits according to organic associations, health specialists and the science arena . . .
Grapefruit juice helps reduce the effect of fatty food
According to scientists grapefruit juice really can help us lose weight. It is said drinking grapefruit juice when eating fatty food can help reduce weight put on by a fifth – now that is a nice statistic. They also say fruit juice could keep blood sugar levels under control. In tests mice fed fatty foods and juice gained 18% less weight than others. The research also suggested that grapefruit could be as good as prescription drugs at keeping blood sugar levels under control – a key part of managing diabetes. Professor Joseph Napoli, of the University of California, Berkeley, said: “We see all sorts of scams about nutrition.
But these results, based on controlled experiments, warrant further study of the potential health-promoting properties of grapefruit juice.” The British Dietetic Association said the fruit now needs to be thoroughly tested in humans to see if it could help with weight loss and stem the rise of obesity and diabetes.
Benefits
Grapefruit juice carries a range of health benefits, they are low in calories but are full of nutrients, and an excellent source of vitamins A and C.
Harvard Medical School states that grapefruit has a glycemic index of 25. This suggests that it does not significantly affect blood sugar and insulin levels. Many studies have suggested that increasing the consumption of plant foods such as grapefruit decreases the risk of obesity, diet, heart disease and overall mortality while. It is also said to promote a healthy complexion, increased energy, and lower overall weight.
Stroke
According to the American Heart Association, eating higher amounts of flavonoid may lower the risk of ischemic stroke for women. Flavonoids are compounds found in citrus fruits like oranges and grapefruit. The risk of ischemic stroke was 19% lower for those who consumed the highest amounts of citrus than for women who consumed the lowest amounts.
Blood pressure and heart health
The powerful nutrient combination of fiber, potassium, lycopene, vitamin C, and choline in grapefruit juice all help to maintain a healthy heart. In one study those who consumed 4069 milligrams (mg) of potassium per day had a 49% lower risk of death from ischemic heart disease compared with those who consumed less potassium. According to the United States Department of Agriculture (USDA) National Nutrient Database, one grapefruit with a 3-to-3.5-inch diameter contains 139 mg potassium. Grapefruit juice is an excellent option for helping to increase the daily intake of potassium. Increasing potassium intake is also important for lowering blood pressure because of its powerful vasodilation effects. Vasodilation widens the arteries. The DASH diet, designed to reduce blood pressure through dietary options, includes grapefruit as a recommended food.
Cancer
Grapefruit juice is a rich source of antioxidants, such as vitamin C. These can help combat the formation of free radicals known to cause cancer. Lycopene intake has been linked with a decreased risk of prostrate cancer in several studies.
Digestion & hydration
The Grapefruit , because of its water and fiber content, helps to prevent constipation and promote regularity for a healthy digestive tract. Grapefruit consists of 91% water. This makes it one of the most hydrating fruits available. Grapefruit juice is also full of electrolytes.
Skin
Grapefruit juice has been linked to healthy skin. However, caution is advised for people who spend a lot of time in the sun.
The antioxidant vitamin C can help to fight skin damage caused by the sun and pollution, reduce wrinkles, and improve overall skin texture when eaten in food or applied to the skin. Vitamin C plays a vital role in the formation of collagen , the main support system of the skin. Regular hydration and vitamin A are also crucial for healthy-looking skin. Grapefruit provides both of these.
Treat Influenza
Grapefruit juice is a valuable remedy for influenza since it helps minimize acidity in the system. The bitter properties arising from an essence called ‘naringin’ in grapefruits tone up the system and the digestive process. Naringin is also considered a flavonoid, which is a powerful antioxidant. Antioxidants have antiviral, antifungal, antibacterial, anti-cancer, and anti-inflammatory qualities, making them one of the most important lines of defense in the immune system, protecting against influenza as well as many other serious conditions.
Treat Malaria
The juice or grapefruit itself contains valuable and natural quinine, which is advantageous for the treatment of malaria. Quinine is an alkaloid with a long history of treating malaria, as well as lupus, arthritis and nocturnal leg cramps. It is not an easy component to find in many foods, so grapefruits are a beneficial and rare example. The quinine can be easily extracted from the fruits by boiling a quarter of grapefruit and straining the pulp.
Cure Fever
The pulp or the juice of grapefruit helps patients recover quickly from fever, and it reduces the burning sensation that occurs when the body reaches a high temperature. It is also known as a way to boost the immune system against cold and other common illnesses. Grapefruit juice, when combined with water, can quench thirst very quickly and keep you hydrated for longer. Most of these benefits come from the high content of vitamin C in grapefruits, which acts as a general immune system defense system and can help the body in fighting the fever.
Promote Sleep
A glass of grapefruit juice, if consumed before going to bed, can promote healthy sleep and alleviate the irritating symptoms and repercussions of insomnia. This is due to the presence of tryptophan in grapefruits, the chemical we often associate with becoming sleepy after big meals. The levels of tryptophan in grapefruit juice enable us to nod off peacefully.
Treat Urinary Disorders
Grapefruit juice is quite rich in potassium and vitamin C, so it is one of the best treatments for issues related to urination often caused by liver, kidney or heart problems. Furthermore, its high potassium content works as a vasodilator, meaning that blood vessels and arteries relax, thereby reducing blood pressure and lessening the risk of heart attack and stroke. Also, increased levels of potassium have been associated with higher cognitive function because of increased blood and oxygen flow to the brain!
STATS
- Revenue in the Grapefruit Juice segment amounts to US$276m in 2018. The market is expected to grow annually by 0.8% (CAGR 2018-2021).
- From an international perspective it is shown that most revenue is generated in the United States (US$314m in 2018).
- Sources: Science Direct, Medical News Today, Organicsfacts.net, Healthline.com, Mail Online, Statistica.com
One thing about grapefruit and grapefruit juice is that there are whole bunch of medications that warn not to eat it because it effects the medication so if you are on a prescription medication, check on google first to make sure it's not one of them.
HD
Heliobas Disciple
TB Fanatic
The beach is good because of the sunshine and Vitamin D, and also not so dangerous because the breeze will blow the airborne coronavirus away from your body until it settles in the sand. (studies posted somewhere on this thread). But you don't want to be crowded on to someone who could cough or sneeze on you. But if they're on a blanket 6 or more feet away from you, the beach is a good thing. I think they closed them because of the crowding and partying - unfortunately for the average family who was punished because of the spring breaker's typical behaviors. I have no issue with them being reopened if its done responsibly.
HD
Heliobas Disciple
TB Fanatic
I'm following your discussion on this and just wanted to add something, although not specifically about PA. It's not just deaths we have to worry about - it's long term issues of younger people who get the virus. So while the majority of deaths are those over 70, the ones who are going to be effected for a long time are the (previously) young and healthy.
HD
Heliobas Disciple
TB Fanatic
View: https://www.youtube.com/watch?v=yAo88FA6VYs
2:28 min
Dr. Fauci’s flip-flop: From extending shutdown to ‘irreparable damage’
•May 24, 2020
One America News Network
Once a strong proponent of furthering stay-at-home orders, Dr. Anthony Fauci made headlines this week by saying just the opposite. One America's Jenn Pelligrino has more from the White House.
I think he's flip flopping because he realizes he was pissing off Trump and he needs to be on Trump's good side to get his vaccine and his drug of choice Remdesivir pushed through by him. Me thinks he speaks with a forked tongue as a result. jmho, ymmv.
HD
Heliobas Disciple
TB Fanatic
I'm watching GA and FL. Both have had quiet days and then heavy days. Ups and downs. Of course a lot of that is a function of how many are tested. But it's not all a down trend by any means.
HD
Heliobas Disciple
TB Fanatic
So far, all models have been off, but since this is a positive one, I'll go ahead and post it anyway.
I commented on this before but I'll repeat in this context. I am holding out hope that because (I believe) this is a lab created virus, it may not have the resilency and hardiness of one that created itself naturally through a process of natural selection and fighting to stay alive as it jumped from species to species, that it does die out on its own, the sooner the better. (Of course, if it was lab created, what's to stop whoever created it, or benefitted from its release, to release version2 in the fall.) But overall this model is positive, so let's hope it's right.
www.soundhealthandlastingwealth.com
(fair use applies)
US coronavirus pandemic could be over as early as November, predictive model shows
The coronavirus pandemic in the United States could be over as early as mid-November, new modeling has shown.
Researchers at Singapore University of Technology and Design have created a complex model predicting the exact date the pandemic will end in the US, UK, and other countries around the world.
According to the data, the US is on track to be coronavirus-free by November 11, while the UK could see an earlier end date of September 30.
The model predicts the trajectory of the spread of the virus over time while tracking the actual number of new confirmed cases per day in a given country, as of May 12.
Predictive modeling by Singapore University of Technology and Design estimates the US coronavirus crisis could end by November 11
The US has the highest number of coronavirus cases in the world, topping 1.6million as of Saturday, and 95,979 deaths
However, researchers noted the predictions by nature are likely to be uncertain due to the complexity of the virus as well as other factors including the restrictions and testing protocols in place in a country.
In the US, changes in predictions were tracked over a one-week period and found to be relatively stable, suggesting a ‘long time to reach its theoretical ending’.
‘The estimated curves of USA for a week together, showing a high stability, while one might still want additional policies or actions to further shorten the tails of the curves,’ the report states.
The study also found predictive monitoring in early May showed the US – and second worst-hit country Brazil- could still suffer for the remainder of the year, without stricter restrictions or a vaccine.
For Italy, which once led the world in the number of coronavirus cases, could recover by October 24, according to modeling as of May 8.
However, scientists note the predictions are only estimates and subject to change depending various factors.
‘The model and data are inaccurate to the complex, evolving, and heterogeneous realities of different countries over time. Predictions are uncertain by nature,’ the report states.
‘Over-optimism based on some predictions is dangerous because it may loosen our disciplines and controls and cause the turnaround of the virus and infection, and must be avoided.’
As of Saturday, there are 1,600,937 confirmed cases of coronavirus in the US and 95,979 deaths.
It comes as all 50 states have begun gradually reopening and easing restrictions following months of lockdown.
But experts and health officials have since cautioned that easing restrictions too soon could lead to a spike in cases.
Earlier this month, director of the National Institute of Allergy and Infectious Diseases Dr. Anthony Fauci warned another wave of the virus was ‘inevitable’.
Dr Fauci said reopening cities and states too quickly could trigger an outbreak that would get out of control and turn the clock back on efforts to fight the coronavirus.
‘You will trigger an outbreak as you may not be able to control,’ he warned in his testimony before the Senate.
The model predicts the pandemic in the UK will be over by September 30
Even with widespread testing and social distancing measures, health authorities have warned there is no guarantee until a vaccine is developed.
In his testimony before the Senate Health, Education, Labor, and Pensions Committee, Fauci said scientists are already testing possible vaccines in a phase one clinical trial with an eye of going to phase two this summer.
‘If we are successful, we hope to know that in the late fall and early winter,’ he said.
He also said there were at least eight vaccines in clinical development.
He warned that with the testing could come negative consequences, including the death of patients.
‘I must warn that there is also the possibility of negative consequences where certain vaccines can actually enhance the negative effect of the infection,’ he said.
He also warned as states begin to reopen – thus pulling back on stay-at-home orders and social distancing – ‘you will see some cases reappear.’
‘There is no doubt even under the best of circumstances, when you pull back on mitigation, you will see some cases appear,’ Fauci warned, adding the U.S. must be prepared for ‘when the inevitable return of infections occurs.’
‘We will start to see little spikes that might turn into outbreaks,’ he noted.
I commented on this before but I'll repeat in this context. I am holding out hope that because (I believe) this is a lab created virus, it may not have the resilency and hardiness of one that created itself naturally through a process of natural selection and fighting to stay alive as it jumped from species to species, that it does die out on its own, the sooner the better. (Of course, if it was lab created, what's to stop whoever created it, or benefitted from its release, to release version2 in the fall.) But overall this model is positive, so let's hope it's right.
US coronavirus pandemic could be over as early as November, predictive model shows - Sound Health and Lasting Wealth
The coronavirus pandemic in the United States could be over as early as mid-November, new modeling has shown. Researchers at Singapore University of
www.soundhealthandlastingwealth.com
US coronavirus pandemic could be over as early as November, predictive model shows
The coronavirus pandemic in the United States could be over as early as mid-November, new modeling has shown.
Researchers at Singapore University of Technology and Design have created a complex model predicting the exact date the pandemic will end in the US, UK, and other countries around the world.
According to the data, the US is on track to be coronavirus-free by November 11, while the UK could see an earlier end date of September 30.
The model predicts the trajectory of the spread of the virus over time while tracking the actual number of new confirmed cases per day in a given country, as of May 12.
Predictive modeling by Singapore University of Technology and Design estimates the US coronavirus crisis could end by November 11
The US has the highest number of coronavirus cases in the world, topping 1.6million as of Saturday, and 95,979 deaths
However, researchers noted the predictions by nature are likely to be uncertain due to the complexity of the virus as well as other factors including the restrictions and testing protocols in place in a country.
In the US, changes in predictions were tracked over a one-week period and found to be relatively stable, suggesting a ‘long time to reach its theoretical ending’.
‘The estimated curves of USA for a week together, showing a high stability, while one might still want additional policies or actions to further shorten the tails of the curves,’ the report states.
The study also found predictive monitoring in early May showed the US – and second worst-hit country Brazil- could still suffer for the remainder of the year, without stricter restrictions or a vaccine.
For Italy, which once led the world in the number of coronavirus cases, could recover by October 24, according to modeling as of May 8.
However, scientists note the predictions are only estimates and subject to change depending various factors.
‘The model and data are inaccurate to the complex, evolving, and heterogeneous realities of different countries over time. Predictions are uncertain by nature,’ the report states.
‘Over-optimism based on some predictions is dangerous because it may loosen our disciplines and controls and cause the turnaround of the virus and infection, and must be avoided.’
As of Saturday, there are 1,600,937 confirmed cases of coronavirus in the US and 95,979 deaths.
It comes as all 50 states have begun gradually reopening and easing restrictions following months of lockdown.
But experts and health officials have since cautioned that easing restrictions too soon could lead to a spike in cases.
Earlier this month, director of the National Institute of Allergy and Infectious Diseases Dr. Anthony Fauci warned another wave of the virus was ‘inevitable’.
Dr Fauci said reopening cities and states too quickly could trigger an outbreak that would get out of control and turn the clock back on efforts to fight the coronavirus.
‘You will trigger an outbreak as you may not be able to control,’ he warned in his testimony before the Senate.
The model predicts the pandemic in the UK will be over by September 30
Even with widespread testing and social distancing measures, health authorities have warned there is no guarantee until a vaccine is developed.
In his testimony before the Senate Health, Education, Labor, and Pensions Committee, Fauci said scientists are already testing possible vaccines in a phase one clinical trial with an eye of going to phase two this summer.
‘If we are successful, we hope to know that in the late fall and early winter,’ he said.
He also said there were at least eight vaccines in clinical development.
He warned that with the testing could come negative consequences, including the death of patients.
‘I must warn that there is also the possibility of negative consequences where certain vaccines can actually enhance the negative effect of the infection,’ he said.
He also warned as states begin to reopen – thus pulling back on stay-at-home orders and social distancing – ‘you will see some cases reappear.’
‘There is no doubt even under the best of circumstances, when you pull back on mitigation, you will see some cases appear,’ Fauci warned, adding the U.S. must be prepared for ‘when the inevitable return of infections occurs.’
‘We will start to see little spikes that might turn into outbreaks,’ he noted.
Heliobas Disciple
TB Fanatic
Dodger Stadium is closed for now, so probably won't feel the effects. By the time they open, the factory should be open too. But what is going on with Smithfield? They must have horrendous working conditions if all their workers in so many different locations are getting ill. 
laist.com
(fair use applies)
There’s Been A COVID-19 Outbreak At Farmer John In Vernon
Updated May 21, 2020 5:54 PM | Published May 21, 2020 4:58 PM
Like other meatpacking facilities across the country, the Farmer John plant in Vernon — which manufactures the iconic Dodger Dog — has had an outbreak of COVID-19 cases.
At least 140 people who work for the Smithfield Foods-owned plant have tested positive over the past few months, according to Freddie Agyin, Director of the Health and Environmental Control Department in the City of Vernon.
He said they were first alerted to a cluster of six cases in the ham deboning department at the plant in mid-April.
When asked for comment, Smithfield said they’ve taken a number of steps to enhance worker safety, including installing plastic barriers, performing regular temperature checks, offering free virus testing, and distributing additional protective equipment, including masks and face shields.
However, some employees still feel unsafe and think the company should do more as the number of cases continues to grow.
Twenty-four additional cases were reported to Vernon’s Health and Environmental Control Department over the past week. It’s unclear if the rise in cases is due to additional testing or the virus continuing to spread amongst workers at the plant.
There’s Been A COVID-19 Outbreak At Farmer John In Vernon
The maker of Dodger Dogs is seeing a growing number of cases.
laist.com
There’s Been A COVID-19 Outbreak At Farmer John In Vernon
Updated May 21, 2020 5:54 PM | Published May 21, 2020 4:58 PM
Like other meatpacking facilities across the country, the Farmer John plant in Vernon — which manufactures the iconic Dodger Dog — has had an outbreak of COVID-19 cases.
At least 140 people who work for the Smithfield Foods-owned plant have tested positive over the past few months, according to Freddie Agyin, Director of the Health and Environmental Control Department in the City of Vernon.
He said they were first alerted to a cluster of six cases in the ham deboning department at the plant in mid-April.
When asked for comment, Smithfield said they’ve taken a number of steps to enhance worker safety, including installing plastic barriers, performing regular temperature checks, offering free virus testing, and distributing additional protective equipment, including masks and face shields.
However, some employees still feel unsafe and think the company should do more as the number of cases continues to grow.
Twenty-four additional cases were reported to Vernon’s Health and Environmental Control Department over the past week. It’s unclear if the rise in cases is due to additional testing or the virus continuing to spread amongst workers at the plant.
Heliobas Disciple
TB Fanatic
I ABSOLUTELY BELIEVE THIS TO BE TRUE. I've been saying it for months. This 'liberty' movement is paid for by Soros and company. Every day and night on my local news they have a different story of someone in a Trump hat or a Trump t-shirt screaming at someone about masks or shutdowns. They play the clip without comment, as if on script to just let it play and leave it be like that. My prediction: in the fall, they will show all these different clips of the "Trump deplorables" pushing for states to open up and the second wave hits and use it to effect the election outcome.
(fair use applies)
Nearly Half Of The Twitter Accounts Discussing ‘Reopening America’ May Be Bots
CMU Researchers Say Sophisticated, Orchestrated Bot Campaigns Aim To Sow Divide
Virginia Alvino Young
Wednesday, May 20, 2020
Scrolling through your Twitter feed, it may not be obvious when you come upon a bot account — something that is more likely to occur in the era of COVID-19. Carnegie Mellon University researchers have discovered that much of the discussion around the pandemic and stay-at-home orders is being fueled by misinformation campaigns that use convincing bots.
To analyze bot activity around the pandemic, CMU researchers since January have collected more than 200 million tweets discussing coronavirus or COVID-19. Of the top 50 influential retweeters, 82% are bots, they found. Of the top 1,000 retweeters, 62% are bots.
The monitoring of tweets is ongoing and collections from Facebook, Reddit and YouTube have been added to the research.
"We're seeing up to two times as much bot activity as we'd predicted based on previous natural disasters, crises and elections," said Kathleen Carley, a professor in the School of Computer Science’s Institute for Software Research and director of the Center for Computational Analysis of Social and Organizational Systems (CASOS) and Center for Informed Democracy & Social - Cybersecurity (IDeaS.)
Carley said multiple factors contribute to the surge. First, more individuals have time on their hands to create do-it-yourself bots. But the number of sophisticated groups that hire firms to run bot accounts also has increased. The nature of the pandemic matters, too. "Because it’s global, it’s being used by various countries and interest groups as an opportunity to meet political agendas," she said.
Carley's research team uses multiple methods to determine who is or isn't a bot. Artificial intelligence processes account information and looks at things such as the number of followers, frequency of tweeting and an account's mentions network.
"Tweeting more frequently than is humanly possible or appearing to be in one country and then another a few hours later is indicative of a bot," Carley said.
More than 100 types of inaccurate COVID-19 stories have been identified, such as those about potential cures. But bots are also dominating conversations about ending stay-at-home orders and "reopening America."
Many factors of the online discussions about “reopening America” suggest that bot activity is orchestrated. One indicator is the large number of bots, many of which are accounts that were recently created. Accounts that are possibly humans with bot assistants generate 66% of the tweets. Accounts that are definitely bots generate 34% of the tweets.
"When we see a whole bunch of tweets at the same time or back to back, it's like they're timed," Carley said. "We also look for use of the same exact hashtag, or messaging that appears to be copied and pasted from one bot to the next."
A subset of tweets about "reopening America" reference conspiracy theories, such as hospitals being filled with mannequins or the coronavirus being linked to 5G towers.
"Conspiracy theories increase polarization in groups. It’s what many misinformation campaigns aim to do," Carley said. "People have real concerns about health and the economy, and people are preying on that to create divides."
Carley said that spreading conspiracy theories leads to more extreme opinions, which can in turn lead to more extreme behavior and less rational thinking.
"Increased polarization will have a variety of real-world consequences, and play out in things like voting behavior and hostility towards ethnic groups," Carley said.
The research team cannot point to specific entities behind the orchestrated attempts to influence online conversations. "We do know that it looks like it's a propaganda machine, and it definitely matches the Russian and Chinese playbooks, but it would take a tremendous amount of resources to substantiate that," Carley said.
Carley adds that not enough is known to develop a counter measure. Blocked accounts can resurface, and the nature of the network is such that you can’t just attack at individual points.
But she said average users can do a lot to help protect themselves from bot influence. There is no guarantee, but closely examining an account can offer indications of a bot, such as sharing links with subtle typos, many tweets coming out very quickly, or a user name and profile image that don’t seem to match up.
"Even if someone appears to be from your community, if you don't know them personally, take a closer look, and always go to authoritative or trusted sources for information," Carley said. "Just be very vigilant."
(fair use applies)
Nearly Half Of The Twitter Accounts Discussing ‘Reopening America’ May Be Bots
CMU Researchers Say Sophisticated, Orchestrated Bot Campaigns Aim To Sow Divide
Virginia Alvino Young
Wednesday, May 20, 2020
Scrolling through your Twitter feed, it may not be obvious when you come upon a bot account — something that is more likely to occur in the era of COVID-19. Carnegie Mellon University researchers have discovered that much of the discussion around the pandemic and stay-at-home orders is being fueled by misinformation campaigns that use convincing bots.
To analyze bot activity around the pandemic, CMU researchers since January have collected more than 200 million tweets discussing coronavirus or COVID-19. Of the top 50 influential retweeters, 82% are bots, they found. Of the top 1,000 retweeters, 62% are bots.
The monitoring of tweets is ongoing and collections from Facebook, Reddit and YouTube have been added to the research.
"We're seeing up to two times as much bot activity as we'd predicted based on previous natural disasters, crises and elections," said Kathleen Carley, a professor in the School of Computer Science’s Institute for Software Research and director of the Center for Computational Analysis of Social and Organizational Systems (CASOS) and Center for Informed Democracy & Social - Cybersecurity (IDeaS.)
Carley said multiple factors contribute to the surge. First, more individuals have time on their hands to create do-it-yourself bots. But the number of sophisticated groups that hire firms to run bot accounts also has increased. The nature of the pandemic matters, too. "Because it’s global, it’s being used by various countries and interest groups as an opportunity to meet political agendas," she said.
Carley's research team uses multiple methods to determine who is or isn't a bot. Artificial intelligence processes account information and looks at things such as the number of followers, frequency of tweeting and an account's mentions network.
"Tweeting more frequently than is humanly possible or appearing to be in one country and then another a few hours later is indicative of a bot," Carley said.
More than 100 types of inaccurate COVID-19 stories have been identified, such as those about potential cures. But bots are also dominating conversations about ending stay-at-home orders and "reopening America."
Many factors of the online discussions about “reopening America” suggest that bot activity is orchestrated. One indicator is the large number of bots, many of which are accounts that were recently created. Accounts that are possibly humans with bot assistants generate 66% of the tweets. Accounts that are definitely bots generate 34% of the tweets.
"When we see a whole bunch of tweets at the same time or back to back, it's like they're timed," Carley said. "We also look for use of the same exact hashtag, or messaging that appears to be copied and pasted from one bot to the next."
A subset of tweets about "reopening America" reference conspiracy theories, such as hospitals being filled with mannequins or the coronavirus being linked to 5G towers.
"Conspiracy theories increase polarization in groups. It’s what many misinformation campaigns aim to do," Carley said. "People have real concerns about health and the economy, and people are preying on that to create divides."
Carley said that spreading conspiracy theories leads to more extreme opinions, which can in turn lead to more extreme behavior and less rational thinking.
"Increased polarization will have a variety of real-world consequences, and play out in things like voting behavior and hostility towards ethnic groups," Carley said.
The research team cannot point to specific entities behind the orchestrated attempts to influence online conversations. "We do know that it looks like it's a propaganda machine, and it definitely matches the Russian and Chinese playbooks, but it would take a tremendous amount of resources to substantiate that," Carley said.
Carley adds that not enough is known to develop a counter measure. Blocked accounts can resurface, and the nature of the network is such that you can’t just attack at individual points.
But she said average users can do a lot to help protect themselves from bot influence. There is no guarantee, but closely examining an account can offer indications of a bot, such as sharing links with subtle typos, many tweets coming out very quickly, or a user name and profile image that don’t seem to match up.
"Even if someone appears to be from your community, if you don't know them personally, take a closer look, and always go to authoritative or trusted sources for information," Carley said. "Just be very vigilant."
Wednesday November 4, 2020 to be more specificSo far, all models have been off, but since this is a positive one, I'll go ahead and post it anyway.
I commented on this before but I'll repeat in this context. I am holding out hope that because (I believe) this is a lab created virus, it may not have the resilency and hardiness of one that created itself naturally through a process of natural selection and fighting to stay alive as it jumped from species to species, that it does die out on its own, the sooner the better. (Of course, if it was lab created, what's to stop whoever created it, or benefitted from its release, to release version2 in the fall.) But overall this model is positive, so let's hope it's right.
(fair use applies)US coronavirus pandemic could be over as early as November, predictive model shows - Sound Health and Lasting Wealth
The coronavirus pandemic in the United States could be over as early as mid-November, new modeling has shown. Researchers at Singapore University of
US coronavirus pandemic could be over as early as November, predictive model shows
View attachment 198799
The coronavirus pandemic in the United States could be over as early as mid-November, new modeling has shown.
Researchers at Singapore University of Technology and Design have created a complex model predicting the exact date the pandemic will end in the US, UK, and other countries around the world.
According to the data, the US is on track to be coronavirus-free by November 11, while the UK could see an earlier end date of September 30.
The model predicts the trajectory of the spread of the virus over time while tracking the actual number of new confirmed cases per day in a given country, as of May 12.
Predictive modeling by Singapore University of Technology and Design estimates the US coronavirus crisis could end by November 11
The US has the highest number of coronavirus cases in the world, topping 1.6million as of Saturday, and 95,979 deaths
However, researchers noted the predictions by nature are likely to be uncertain due to the complexity of the virus as well as other factors including the restrictions and testing protocols in place in a country.
In the US, changes in predictions were tracked over a one-week period and found to be relatively stable, suggesting a ‘long time to reach its theoretical ending’.
‘The estimated curves of USA for a week together, showing a high stability, while one might still want additional policies or actions to further shorten the tails of the curves,’ the report states.
The study also found predictive monitoring in early May showed the US – and second worst-hit country Brazil- could still suffer for the remainder of the year, without stricter restrictions or a vaccine.
For Italy, which once led the world in the number of coronavirus cases, could recover by October 24, according to modeling as of May 8.
However, scientists note the predictions are only estimates and subject to change depending various factors.
‘The model and data are inaccurate to the complex, evolving, and heterogeneous realities of different countries over time. Predictions are uncertain by nature,’ the report states.
‘Over-optimism based on some predictions is dangerous because it may loosen our disciplines and controls and cause the turnaround of the virus and infection, and must be avoided.’
As of Saturday, there are 1,600,937 confirmed cases of coronavirus in the US and 95,979 deaths.
It comes as all 50 states have begun gradually reopening and easing restrictions following months of lockdown.
But experts and health officials have since cautioned that easing restrictions too soon could lead to a spike in cases.
Earlier this month, director of the National Institute of Allergy and Infectious Diseases Dr. Anthony Fauci warned another wave of the virus was ‘inevitable’.
Dr Fauci said reopening cities and states too quickly could trigger an outbreak that would get out of control and turn the clock back on efforts to fight the coronavirus.
‘You will trigger an outbreak as you may not be able to control,’ he warned in his testimony before the Senate.
The model predicts the pandemic in the UK will be over by September 30
Even with widespread testing and social distancing measures, health authorities have warned there is no guarantee until a vaccine is developed.
In his testimony before the Senate Health, Education, Labor, and Pensions Committee, Fauci said scientists are already testing possible vaccines in a phase one clinical trial with an eye of going to phase two this summer.
‘If we are successful, we hope to know that in the late fall and early winter,’ he said.
He also said there were at least eight vaccines in clinical development.
He warned that with the testing could come negative consequences, including the death of patients.
‘I must warn that there is also the possibility of negative consequences where certain vaccines can actually enhance the negative effect of the infection,’ he said.
He also warned as states begin to reopen – thus pulling back on stay-at-home orders and social distancing – ‘you will see some cases reappear.’
‘There is no doubt even under the best of circumstances, when you pull back on mitigation, you will see some cases appear,’ Fauci warned, adding the U.S. must be prepared for ‘when the inevitable return of infections occurs.’
‘We will start to see little spikes that might turn into outbreaks,’ he noted.
So far, all models have been off, but since this is a positive one, I'll go ahead and post it anyway.
I commented on this before but I'll repeat in this context. I am holding out hope that because (I believe) this is a lab created virus, it may not have the resilency and hardiness of one that created itself naturally through a process of natural selection and fighting to stay alive as it jumped from species to species, that it does die out on its own, the sooner the better. (Of course, if it was lab created, what's to stop whoever created it, or benefitted from its release, to release version2 in the fall.) But overall this model is positive, so let's hope it's right.
(fair use applies)US coronavirus pandemic could be over as early as November, predictive model shows - Sound Health and Lasting Wealth
The coronavirus pandemic in the United States could be over as early as mid-November, new modeling has shown. Researchers at Singapore University of
To be more specific, it will end on Wednesday, November 4, 2020
Vernon has a problem!Dodger Stadium is closed for now, so probably won't feel the effects. By the time they open, the factory should be open too. But what is going on with Smithfield? They must have horrendous working conditions if all their workers in so many different locations are getting ill.
(fair use applies)There’s Been A COVID-19 Outbreak At Farmer John In Vernon
The maker of Dodger Dogs is seeing a growing number of cases.
There’s Been A COVID-19 Outbreak At Farmer John In Vernon
Updated May 21, 2020 5:54 PM | Published May 21, 2020 4:58 PM
Like other meatpacking facilities across the country, the Farmer John plant in Vernon — which manufactures the iconic Dodger Dog — has had an outbreak of COVID-19 cases.
At least 140 people who work for the Smithfield Foods-owned plant have tested positive over the past few months, according to Freddie Agyin, Director of the Health and Environmental Control Department in the City of Vernon.
He said they were first alerted to a cluster of six cases in the ham deboning department at the plant in mid-April.
When asked for comment, Smithfield said they’ve taken a number of steps to enhance worker safety, including installing plastic barriers, performing regular temperature checks, offering free virus testing, and distributing additional protective equipment, including masks and face shields.
However, some employees still feel unsafe and think the company should do more as the number of cases continues to grow.
Twenty-four additional cases were reported to Vernon’s Health and Environmental Control Department over the past week. It’s unclear if the rise in cases is due to additional testing or the virus continuing to spread amongst workers at the plant.
Coronavirus outbreaks hits Farmer John, 8 other plants in Vernon
Coronavirus outbreaks hits Farmer John and other food processing plants in Vernon.
www.latimes.com
By LAURA NEWBERRYSTAFF WRITER
MAY 24, 2020
5:17 PM
Outbreaks of COVID-19 have struck nine industrial facilities in Vernon, including five meatpacking plants, Los Angeles County health officials said Sunday.
The largest outbreak occurred at the Smithfield Foods-owned Farmer John plant — producer of the beloved Dodger Dog — where 153 of 1,837 employees tested positive for COVID-19 between March and May, the Department of Public Health said.
The other eight facilities with outbreaks are CLW Foods (meat), Vie De France Yamazaki (baked goods), California Farms Meat (meat), Takaokaya USA (green tea), F. Gavina & Sons (coffee), Golden West Trading (meat), Overhill Farms (frozen food), and Rose & Shore (deli meat and prepared foods).
Between five and 24 employees at each of the facilities tested positive, county data show, although it wasn’t clear when those numbers were last updated. By the county’s standards, an outbreak has occurred when five or more workers have contracted the novel coronavirus.
Though Vernon has just a few dozen residents and is almost exclusively industrial, workers who have contracted the virus in the city just south of Los Angeles could spread it in their own communities, the county warned. On Sunday, health officials reported 940 new cases of the novel coronavirus and 14 related deaths countywide.
More at the link
Heliobas Disciple
TB Fanatic
Heliobas Disciple
TB Fanatic
I wonder what's going on there. A cluster that turned into a hot spot (?). Are they using public transportation to get to work? Is that how it's spreading between plants?
HD
Meat plants and nursing homes have very tight air systems, imo. Little outside air or sunlight. I know legionella is a bacteria but can't help but see some correlation..... uneducated opinion here...
Since all of those businesses are food-related, my guess would be a delivery person introduced the virus. And yes, I suspect they do use public transpo.
naegling62
Veteran Member
And don't forget Alabama...up..up and away!
Last month Kroger stores had a problem; I wondered if it was delivery person in this case, too. The employees were being encouraged to wear masks at that time.
Kroger employees test positive for COVID-19 at 9 Kentuckiana stores
Apr 22, 2020
LOUISVILLE, Ky. (WDRB) -- Employees of at least nine Kroger stores throughout Kentucky and Indiana have tested positive for COVID-19. A Kroger spokesperson says at least 13 employees have tested positive at stores around Kentuckiana.
Kroger spokesperson Erin Grant said most of those employees have already returned to work. Grant could not say when the employees last worked at the stores, but said Kroger has not had a confirmed case in more than a week.
Stores where employees have tested positive include:
12450 La Grange Rd.- Louisville, KY
12611 Taylorsville Rd.- Louisville, KY
200 New Albany Plaza- New Albany, IN
1670 Starlite Dr.- Owensboro, KY
2630 Frederica St.- Owensboro, KY
1600 Leestown Rd., Ste 150- Lexington, KY
704 Euclid Ave.- Lexington, KY
399 Campbellsville Bypass- Campbellsville, KY
Jay C- 1541 E Tipton St.- Seymour, IN
Once an employee tests positive, Grant said Kroger works closely with state and local health experts, and follows all sanitation and cleaning procedures. Kroger is following guidance from local, state and federal agencies, including the CDC and other health organizations. Stores are also deep cleaned and sanitized. Grant did not give specifics on which stores have been deep cleaned, but did say even with suspected cases not confirmed with a test, additional cleaning is done in an abundance of caution.
Kroger is asking all associates to monitor their health and take their temperature at home before coming to work. If they experience symptoms like a fever, Grant said Kroger is encouraging employees to contact their health care provider and stay home.
Grant says Kroger also is encouraging all associates to wear masks, and the company provides fresh masks at the beginning of each shift. Currently the company is working to supply the hardest hit areas with enough masks to mandate this among associates.
www.wdrb.com
Kroger employees test positive for COVID-19 at 9 Kentuckiana stores
Apr 22, 2020
LOUISVILLE, Ky. (WDRB) -- Employees of at least nine Kroger stores throughout Kentucky and Indiana have tested positive for COVID-19. A Kroger spokesperson says at least 13 employees have tested positive at stores around Kentuckiana.
Kroger spokesperson Erin Grant said most of those employees have already returned to work. Grant could not say when the employees last worked at the stores, but said Kroger has not had a confirmed case in more than a week.
Stores where employees have tested positive include:
12450 La Grange Rd.- Louisville, KY
12611 Taylorsville Rd.- Louisville, KY
200 New Albany Plaza- New Albany, IN
1670 Starlite Dr.- Owensboro, KY
2630 Frederica St.- Owensboro, KY
1600 Leestown Rd., Ste 150- Lexington, KY
704 Euclid Ave.- Lexington, KY
399 Campbellsville Bypass- Campbellsville, KY
Jay C- 1541 E Tipton St.- Seymour, IN
Once an employee tests positive, Grant said Kroger works closely with state and local health experts, and follows all sanitation and cleaning procedures. Kroger is following guidance from local, state and federal agencies, including the CDC and other health organizations. Stores are also deep cleaned and sanitized. Grant did not give specifics on which stores have been deep cleaned, but did say even with suspected cases not confirmed with a test, additional cleaning is done in an abundance of caution.
Kroger is asking all associates to monitor their health and take their temperature at home before coming to work. If they experience symptoms like a fever, Grant said Kroger is encouraging employees to contact their health care provider and stay home.
Grant says Kroger also is encouraging all associates to wear masks, and the company provides fresh masks at the beginning of each shift. Currently the company is working to supply the hardest hit areas with enough masks to mandate this among associates.
Kroger employees test positive for COVID-19 at 9 Kentuckiana stores
Stores include two Krogers in Louisville, one in New Albany and the Jay-C in Seymour, Indiana.
Zagdid
Veteran Member
I can't imagine any predictive modeling that would drop a curve on data in that manner taking into account the significant variables presented by the building contagion in South America and Mexico that will eventually flow into the southwestern US. Then I saw the source. Singapore? Really?So far, all models have been off, but since this is a positive one, I'll go ahead and post it anyway.
I commented on this before but I'll repeat in this context. I am holding out hope that because (I believe) this is a lab created virus, it may not have the resilency and hardiness of one that created itself naturally through a process of natural selection and fighting to stay alive as it jumped from species to species, that it does die out on its own, the sooner the better. (Of course, if it was lab created, what's to stop whoever created it, or benefitted from its release, to release version2 in the fall.) But overall this model is positive, so let's hope it's right.
(fair use applies)US coronavirus pandemic could be over as early as November, predictive model shows - Sound Health and Lasting Wealth
The coronavirus pandemic in the United States could be over as early as mid-November, new modeling has shown. Researchers at Singapore University of
US coronavirus pandemic could be over as early as November, predictive model shows
View attachment 198799
The coronavirus pandemic in the United States could be over as early as mid-November, new modeling has shown.
Researchers at Singapore University of Technology and Design have created a complex model predicting the exact date the pandemic will end in the US, UK, and other countries around the world.
According to the data, the US is on track to be coronavirus-free by November 11, while the UK could see an earlier end date of September 30.
The model predicts the trajectory of the spread of the virus over time while tracking the actual number of new confirmed cases per day in a given country, as of May 12.
Predictive modeling by Singapore University of Technology and Design estimates the US coronavirus crisis could end by November 11
The US has the highest number of coronavirus cases in the world, topping 1.6million as of Saturday, and 95,979 deaths
However, researchers noted the predictions by nature are likely to be uncertain due to the complexity of the virus as well as other factors including the restrictions and testing protocols in place in a country.
In the US, changes in predictions were tracked over a one-week period and found to be relatively stable, suggesting a ‘long time to reach its theoretical ending’.
‘The estimated curves of USA for a week together, showing a high stability, while one might still want additional policies or actions to further shorten the tails of the curves,’ the report states.
The study also found predictive monitoring in early May showed the US – and second worst-hit country Brazil- could still suffer for the remainder of the year, without stricter restrictions or a vaccine.
For Italy, which once led the world in the number of coronavirus cases, could recover by October 24, according to modeling as of May 8.
However, scientists note the predictions are only estimates and subject to change depending various factors.
‘The model and data are inaccurate to the complex, evolving, and heterogeneous realities of different countries over time. Predictions are uncertain by nature,’ the report states.
‘Over-optimism based on some predictions is dangerous because it may loosen our disciplines and controls and cause the turnaround of the virus and infection, and must be avoided.’
As of Saturday, there are 1,600,937 confirmed cases of coronavirus in the US and 95,979 deaths.
It comes as all 50 states have begun gradually reopening and easing restrictions following months of lockdown.
But experts and health officials have since cautioned that easing restrictions too soon could lead to a spike in cases.
Earlier this month, director of the National Institute of Allergy and Infectious Diseases Dr. Anthony Fauci warned another wave of the virus was ‘inevitable’.
Dr Fauci said reopening cities and states too quickly could trigger an outbreak that would get out of control and turn the clock back on efforts to fight the coronavirus.
‘You will trigger an outbreak as you may not be able to control,’ he warned in his testimony before the Senate.
The model predicts the pandemic in the UK will be over by September 30
Even with widespread testing and social distancing measures, health authorities have warned there is no guarantee until a vaccine is developed.
In his testimony before the Senate Health, Education, Labor, and Pensions Committee, Fauci said scientists are already testing possible vaccines in a phase one clinical trial with an eye of going to phase two this summer.
‘If we are successful, we hope to know that in the late fall and early winter,’ he said.
He also said there were at least eight vaccines in clinical development.
He warned that with the testing could come negative consequences, including the death of patients.
‘I must warn that there is also the possibility of negative consequences where certain vaccines can actually enhance the negative effect of the infection,’ he said.
He also warned as states begin to reopen – thus pulling back on stay-at-home orders and social distancing – ‘you will see some cases reappear.’
‘There is no doubt even under the best of circumstances, when you pull back on mitigation, you will see some cases appear,’ Fauci warned, adding the U.S. must be prepared for ‘when the inevitable return of infections occurs.’
‘We will start to see little spikes that might turn into outbreaks,’ he noted.
Indiana
Regenstrief has added Recovered to their dashboard. Here are the case definitions:
Recovered = Estimated number/ratio of people who have recovered from Covid-19, defined as:
Distinct individuals with a Covid-19 test >21 days ago who have not been hospitalized
PLUS
Distinct patients with Covid-19 test who have been hospitalized and were discharged and have had at least 7 days to recover
MINUS
Total number of deaths due to Covid-19 as reported by the state of Indiana
Active = Estimated number/ration of individuals tested positive for Covid-19 who are still infected and not yet recovered (i.e. either within 21 days of positive test or still hospitalized.)
Deceased = Individuals tested positive for Covid-19 who have died (all deaths as documented by state of Indiana)
As of yesterday the state dashboard has 31,367 positives and 1824 deaths. Here are Regenstrief numbers:
Recovered: 18,075 (58%)
Active: 11,302 (36%)
Deceased: 1824 (6%)
I also included the length of hospitalization numbers in the screen cap below
Regenstrief has added Recovered to their dashboard. Here are the case definitions:
Recovered = Estimated number/ratio of people who have recovered from Covid-19, defined as:
Distinct individuals with a Covid-19 test >21 days ago who have not been hospitalized
PLUS
Distinct patients with Covid-19 test who have been hospitalized and were discharged and have had at least 7 days to recover
MINUS
Total number of deaths due to Covid-19 as reported by the state of Indiana
Active = Estimated number/ration of individuals tested positive for Covid-19 who are still infected and not yet recovered (i.e. either within 21 days of positive test or still hospitalized.)
Deceased = Individuals tested positive for Covid-19 who have died (all deaths as documented by state of Indiana)
As of yesterday the state dashboard has 31,367 positives and 1824 deaths. Here are Regenstrief numbers:
Recovered: 18,075 (58%)
Active: 11,302 (36%)
Deceased: 1824 (6%)
I also included the length of hospitalization numbers in the screen cap below
Zagdid
Veteran Member
6-Year-Old Tests Positive For Coronavirus, Complicating South Korea's School Reopening Plans
South Korea closes 10 kindergartens and five elementary schools after a 6-year-old boy tests positive for the novel coronavirus.
www.forbes.com
6-Year-Old Tests Positive For Coronavirus, Complicating South Korea's School Reopening Plans
BREAKING|May 25, 2020,12:19pm EDT
Tommy BeerForbes Staff
Just two days before South Korea planned to move to “phase two” of its school reopening timeline — in which lower grades of elementary schools could resume classes— a 6-year-old kindergarten student in Seoul tested positive for Covid-19, resulting in school closures and revealing the complicated task for governments trying to reopen economies while the virus is still spreading.
KEY FACTS
In the first phase of South Korea's reopening plan, a number of schools opened up on May 20 and the second phase is set to begin on Wednesday.
According to South Korea’s Yonhap News Agency, the 6-year-old is believed to have contracted the virus from his art teacher at Young Rembrandts, a private art school in Magok of Gangseo on the south side of the Han River.
The teacher tested positive Sunday and taught 35 students at the institute and had contact with three other teachers there; the teachers all wore masks, according to the Seoul Metropolitan Office of Education.
Ten nearby kindergartens and five elementary schools will remain closed for two days for disinfection and other precautionary measures.
According to the news report, "the education office is mulling whether to have the boy's kindergarten offer online classes to prevent the potential spread of the virus. A decision on other affected schools will be determined based on the test results."
(online kindergarten - good luck with that!)
bw
Fringe Ranger
Pandas have to eat constantly because they eat bamboo, which no other animal wants. Instead of fighting for better resources, they took the loser's path. Probably a lesson there somewhere.
parsonswife
Veteran Member
Excellent article. Thankyou
marsh
On TB every waking moment
They work shoulder to shoulder in a line - no distancingDodger Stadium is closed for now, so probably won't feel the effects. By the time they open, the factory should be open too. But what is going on with Smithfield? They must have horrendous working conditions if all their workers in so many different locations are getting ill.
(fair use applies)There’s Been A COVID-19 Outbreak At Farmer John In Vernon
The maker of Dodger Dogs is seeing a growing number of cases.
There’s Been A COVID-19 Outbreak At Farmer John In Vernon
Updated May 21, 2020 5:54 PM | Published May 21, 2020 4:58 PM
Like other meatpacking facilities across the country, the Farmer John plant in Vernon — which manufactures the iconic Dodger Dog — has had an outbreak of COVID-19 cases.
At least 140 people who work for the Smithfield Foods-owned plant have tested positive over the past few months, according to Freddie Agyin, Director of the Health and Environmental Control Department in the City of Vernon.
He said they were first alerted to a cluster of six cases in the ham deboning department at the plant in mid-April.
When asked for comment, Smithfield said they’ve taken a number of steps to enhance worker safety, including installing plastic barriers, performing regular temperature checks, offering free virus testing, and distributing additional protective equipment, including masks and face shields.
However, some employees still feel unsafe and think the company should do more as the number of cases continues to grow.
Twenty-four additional cases were reported to Vernon’s Health and Environmental Control Department over the past week. It’s unclear if the rise in cases is due to additional testing or the virus continuing to spread amongst workers at the plant.
marsh
On TB every waking moment
I believe I read that many live in dorm like housing and commute in a bus or van together.
HHS chief suggests workers are to blame for COVID outbreaks at meatpacking plants
Health and Human Services (HHS) Secretary Alex Azar reportedly suggested that the social habits and living conditions of workers at meatpacking plants were the reason for recent COVID-19 outbreaks …
thehill.com
HHS chief suggests workers are to blame for COVID outbreaks at meatpacking plants
BY RAFAEL BERNAL - 05/07/20 12:01 PM EDT 193
37,854
© Getty Images
Health and Human Services (HHS) Secretary Alex Azar reportedly suggested that the social habits and living conditions of workers at meatpacking plants were the reason for recent COVID-19 outbreaks at processing facilities.
Azar made the remarks on an April 28 call with lawmakers, when he referenced the "home and social" conditions of the workers, Politico reported Thursday, citing three people on the call.
"He was essentially turning it around, blaming the victim and implying that their lifestyle was the problem," Rep. Ann Kuster (D-N.H.), who was on the call, told the publication. "Their theory of the case is that they are not becoming infected in the meat processing plant, they're becoming infected because of the way they live in their home."
When reached for comment, Michael Caputo, the HHS assistant secretary for public affairs, told The Hill that Azar "simply made the point that many public health officials have made: in addition to the meat packing plants themselves, many workers at certain remote and rural meatpacking facilities have living conditions that involve multifamily and congregate living, which have been conducive to rapid spread of the disease. This is nothing more than a statement of the obvious."
Still, Azar's remarks reflect a position that has shown signs of taking hold among some meat processing company executives and GOP leaders.
South Dakota Gov. Kristi Noem (R) told Fox News last month that an outbreak at the Smithfield Foods pork processing facility in her state did not happen at the plant, but rather where workers live.
"We believe that 99 percent of what's going on today wasn't happening inside the facility. It was more at home, where these employees were going home and spreading some of the virus. Because a lot of these folks that work at this plant live in the same community, same building, sometimes in the same apartment," said Noem.
“Living circumstances in certain cultures are different than they are with your traditional American family,” a Smithfield spokeswoman told BuzzFeed News in an article published April 20.
Keira Lombardo, executive vice president of corporate affairs and compliance at Smithfield, told The Hill on Thursday that the article was "in no way, shape or form representative of our position on this topic."
Lombardo instead pointed to an April 24 announcement by Smithfield that said the company is "proud of the multi-culturalism on display every day throughout many of our facilities, including in Sioux Falls. Our employees are our strength. They come from all over the world and speak dozens of languages and dialects. Our position is this: We cannot fight this virus by finger-pointing."
Democrats have cited the outbreaks in their criticism of the Trump administration's coronavirus response.
Former Vice President Joe Biden, the presumptive Democratic presidential nominee, said on a video conference call Monday that he would tighten safety conditions at meatpacking plants, and that workers should get hazard pay during the pandemic.
Biden also implied that the source of contagion for workers is at the plants, not at home.
"They're afraid to go to work," said Biden. "[They're afraid of] what they might be bringing back and spreading to people they love and adore."
Biden added that the Trump administration has designated meatpacking and other food supply workers as essential, then treated them "as disposable."
"It's quite frankly inhumane and immoral," he said.
Outbreaks have hit plants in other states as well.
The Iowa Department of Public Health reported on Tuesday that 730 workers at a Tyson Foods pork processing plant in Perry had contracted the virus, representing 58 percent of its staff, according to local news reports. The department also noted that more than 1,600 workers at four meatpacking plants across the state had suffered infections.
Rep. Jesús García (D-Ill.) last week blamed meatpacking companies for the spread of the deadly virus among workers. He also lashed out at those pointing the finger at cultural circumstances.
"I find those remarks to be reprehensible, nothing short of racism," said García. "It seeks to blame the victims of the tough working conditions, dangerous working conditions, that people in the meatpacking industry endure."
"Because companies did not take measures to observe social distancing practices is why you've had a rapid spread of the virus," he added.
Updated at 3:33 p.m.
Last edited:
marsh
On TB every waking moment
5:37 min
Hilton: There won’t be economic recovery unless we reopen schools now
•May 25, 2020
Fox News
If children can't go to school, parents can't go to work.
_______________________________
6:34 min
‘The Next Revolution’ examines strength of American spirit amid coronavirus crisis
•May 25, 2020
Fox News
It's not just government plans and vaccines that will fuel recovery.
marsh
On TB every waking moment
19:55 min
Coronavirus Pandemic Update 75: COVID-19 Lung Autopsies - New Data
•May 25, 2020
MedCram - Medical Lectures Explained CLEARLY
COVID-19 Update 75 with Roger Seheult, MD. All coronavirus updates available free at our website https://www.medcram.com/courses/coron...
A new article from the New England Journal of Medicine details observations of endothelial damage and thrombosis in lung autopsies of patients who had COVID-19. This report supports the hypothesis that Dr. Seheult has illustrated over the past few weeks.
Dr. Seheult also discusses the re-opening of the largest county in California and reviews a recent article published in Nature about how T-cells found in COVID-19 patients is a favorable sign for long-term immunity. (This video was recorded on May 25, 2020)
------------------------------ Links referenced in this video: Johns Hopkins Tracker - https://coronavirus.jhu.edu/map.html Worldometer https://www.worldometers.info/coronav... Washington Post - https://www.washingtonpost.com/health... Science - https://www.sciencemag.org/news/2020/... NEJM - https://www.nejm.org/doi/full/10.1056... National Geographic - https://www.nationalgeographic.com/sc... Bronchoscopy - https://medlineplus.gov/ency/article/... -------------------------------------------
marsh
On TB every waking moment
(Article referenced in MedCram)
Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19
Abstract
BACKGROUND
Progressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19.
METHODS
We examined 7 lungs obtained during autopsy from patients who died from Covid-19 and compared them with 7 lungs obtained during autopsy from patients who died from acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection and 10 age-matched, uninfected control lungs.
The lungs were studied with the use of seven-color immunohistochemical analysis, micro–computed tomographic imaging, scanning electron microscopy, corrosion casting, and direct multiplexed measurement of gene expression.
RESULTS
In patients who died from Covid-19–associated or influenza-associated respiratory failure, the histologic pattern in the peripheral lung was diffuse alveolar damage with perivascular T-cell infiltration. The lungs from patients with Covid-19 also showed distinctive vascular features, consisting of severe endothelial injury associated with the presence of intracellular virus and disrupted cell membranes. Histologic analysis of pulmonary vessels in patients with Covid-19 showed widespread thrombosis with microangiopathy. Alveolar capillary microthrombi were 9 times as prevalent in patients with Covid-19 as in patients with influenza (P<0.001). In lungs from patients with Covid-19, the amount of new vessel growth — predominantly through a mechanism of intussusceptive angiogenesis — was 2.7 times as high as that in the lungs from patients with influenza (P<0.001).
CONCLUSIONS
In our small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection.
The universality and clinical implications of our observations require further research to define. (Funded by the National Institutes of Health and others.)
Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in humans is associated with a broad spectrum of clinical respiratory syndromes, ranging from mild upper airway symptoms to progressive life-threatening viral pneumonia.1,2 Clinically, patients with severe coronavirus disease 2019 (Covid-19) have labored breathing and progressive hypoxemia and often receive mechanical ventilatory support. Radiographically, peripheral lung ground-glass opacities on computed tomographic (CT) imaging of the chest fulfill the Berlin criteria for acute respiratory distress syndrome (ARDS).3,4 Histologically, the hallmark of the early phase of ARDS is diffuse alveolar damage with edema, hemorrhage, and intraalveolar fibrin deposition, as described by Katzenstein et al.5 Diffuse alveolar damage is a nonspecific finding, since it may have noninfectious or infectious causes, including Middle East respiratory syndrome coronavirus (MERS-CoV),6 SARS-CoV,7SARS-CoV-2,8-10 and influenza viruses.11
Among the distinctive features of Covid-19 are the vascular changes associated with the disease. With respect to diffuse alveolar damage in SARS-CoV7 and SARS-CoV-2 infection,8,12 the formation of fibrin thrombi has been observed anecdotally but not studied systematically. Clinically, many patients have elevated d-dimer levels, as well as cutaneous changes in their extremities suggesting thrombotic microangiopathy.13 Diffuse intravascular coagulation and large-vessel thrombosis have been linked to multisystem organ failure.14-16 Peripheral pulmonary vascular changes are less well characterized; however, vasculopathy in the gas-exchange networks, depending on its effect on the matching of ventilation and perfusion that results, could potentially contribute to hypoxemia and the effects of posture (e.g., prone positioning) on oxygenation.17
Despite previous experience with SARS-CoV18 and early experience with SARS-CoV-2, the morphologic and molecular changes associated with these infections in the peripheral lung are not well documented. Here, we examine the morphologic and molecular features of lungs obtained during autopsy from patients who died from Covid-19, as compared with those of lungs from patients who died from influenza and age-matched, uninfected control lungs.
Methods
PATIENT SELECTION AND WORKFLOW
We analyzed pulmonary autopsy specimens from seven patients who died from respiratory failure caused by SARS-CoV-2 infection and compared them with lungs from seven patients who died from pneumonia caused by influenza A virus subtype H1N1 (A[H1N1]) — a strain associated with the 1918 and 2009 influenza pandemics. The lungs from patients with influenza were archived tissue from the 2009 pandemic and were chosen for the best possible match with respect to age, sex, and disease severity from among the autopsies performed at the Hannover Medical School. Ten lungs that had been donated but not used for transplantation served as uninfected control specimens. The Covid-19 group consisted of lungs from two female and five male patients with mean (±SD) ages of 68±9.2 years and 80±11.5 years, respectively (clinical data are provided in Table S1A in the Supplementary Appendix, available with the full text of this article at NEJM.org). The influenza group consisted of lungs from two female and five male patients with mean ages of 62.5±4.9 years and 55.4±10.9 years, respectively. Five of the uninfected lungs were from female donors (mean age, 68.2±6.9 years), and five were from male donors (mean age, 79.2±3.3 years) (clinical data are provided in Table S1B). The study was approved by and conducted according to requirements of the ethics committees at the Hannover Medical School and the University of Leuven. There was no commercial support for this study.
All lungs were comprehensively analyzed with the use of microCT, histopathological, and multiplexed immunohistochemical analysis, transmission and scanning electron microscopy, corrosion casting, and direct multiplexed gene-expression analysis, as described in detail in the Methods section of the Supplementary Appendix.
STATISTICAL ANALYSIS
All comparisons of numeric variables (including those in the gene-expression analysis) were conducted with Student’s t-test familywise error rates due to multiplicity set at 0.05 with the use of the Benjamini–Hochberg method of controlling false discovery rates. Original P values are reported only for the tests that met the criteria for false discovery rates. All confidence intervals have been calculated on the basis of the t-distribution, as well. Additional details are provided in the Methods section of the Supplementary Appendix.
Results
GROSS EXAMINATION
The mean (±SE) weight of the lungs from patients with proven influenza pneumonia was significantly higher than that from patients with proven Covid-19 (2404±560 g vs. 1681±49 g; P=0.04). The mean weight of the uninfected control lungs (1045±91 g) was significantly lower than those in the influenza group (P=0.003) and the Covid-19 group (P<0.001).
ANGIOCENTRIC INFLAMMATION
Figure 1.
Lymphocytic Inflammation in a Lung from a Patient Who Died from Covid-19.
All lung specimens from the Covid-19 group had diffuse alveolar damage with necrosis of alveolar lining cells, pneumocyte type 2 hyperplasia, and linear intraalveolar fibrin deposition (Figure 1). In four of seven cases, the changes were focal, with only mild interstitial edema. The remaining three cases had homogeneous fibrin deposits and marked interstitial edema with early intraalveolar organization. The specimens in the influenza group had florid diffuse alveolar damage with massive interstitial edema and extensive fibrin deposition in all cases. In addition, three specimens in the influenza group had focal organizing and resorptive inflammation (Fig. S2). These changes were reflected in the much higher weight of the lungs from patients with influenza.
Immunohistochemical analysis of angiotensin-converting enzyme 2 (ACE2) expression, measured as mean (±SD) relative counts of ACE2-positive cells per field of view, in uninfected control lungs showed scarce expression of ACE2 in alveolar epithelial cells (0.053±0.03) and capillary endothelial cells (0.066±0.03). In lungs from patients with Covid-19 and lungs from patients with influenza, the relative counts of ACE2-positive cells per field of view were 0.25±0.14 and 0.35±0.15, respectively, for alveolar epithelial cells and 0.49±0.28 and 0.55±0.11, respectively, for endothelial cells. Furthermore, ACE2-positive lymphocytes were not seen in perivascular tissue or in the alveoli of the control lungs but were present in the lungs in the Covid-19 group and the influenza group (relative counts of 0.22±0.18 and 0.15±0.09, respectively). (Details of counting are provided in Table S2.)
In the lungs from patients with Covid-19 and patients with influenza, similar mean (±SD) numbers of CD3-positive T cells were found within a 200-μm radius of precapillary and postcapillary vessel walls in 20 fields of examination per patient (26.2±13.1 for Covid-19 and 14.8±10.8 for influenza). With the same field size used for examination, CD4-positive T cells were more numerous in lungs from patients with Covid-19 than in lungs from patients with influenza (13.6±6.0 vs. 5.8±2.5, P=0.04), whereas CD8-positive T cells were less numerous (5.3±4.3 vs. 11.6±4.9, P=0.008). Neutrophils (CD15 positive) were significantly less numerous adjacent to the alveolar epithelial lining in the Covid-19 group than in the influenza group (0.4±0.5 vs. 4.8±5.2, P=0.002).
A multiplexed analysis of inflammation-related gene expression examining 249 genes from the nCounter Inflammation Panel (NanoString Technologies) revealed similarities and differences between the specimens in the Covid-19 group and those in the influenza group. A total of 79 inflammation-related genes were differentially regulated only in specimens from patients with Covid-19, whereas 2 genes were differentially regulated only in specimens from patients with influenza; a shared expression pattern was found for 7 genes (Fig. S1).
THROMBOSIS AND MICROANGIOPATHY
Figure 2.
Microthrombi in the Interalveolar Septa of a Lung from a Patient Who Died from Covid-19.
The pulmonary vasculature of the lungs in the Covid-19 group and the influenza group was analyzed with hematoxylin–eosin, trichrome, and immunohistochemical staining (as described in the Methods section of the Supplementary Appendix). Analysis of precapillary vessels showed that in four of the seven lungs from patients with Covid-19 and four of the seven lungs from the patients with influenza, thrombi were consistently present in pulmonary arteries with a diameter of 1 mm to 2 mm, without complete luminal obstruction (Figs. S3 and S5). Fibrin thrombi of the alveolar capillaries could be seen in all the lungs from both groups of patients (Figure 2). Alveolar capillary microthrombi were 9 times as prevalent in patients with Covid-19 as in patients with influenza (mean [±SD] number of distinct thrombi per square centimeter of vascular lumen area, 159±73 and 16±16, respectively; P=0.002). Intravascular thrombi in postcapillary venules of less than 1 mm diameter were seen in lower numbers in the lungs from patients with Covid-19 than in those from patients with influenza (12±14 vs. 35±16, P=0.02). Two lungs in the Covid-19 group had involvement of all segments of the vasculature, as compared with four of the lungs in the influenza group; in three of the lungs in the Covid-19 group and three of the lungs in the influenza group, combined capillary and venous thrombi were found without arterial thrombi.
The histologic findings were supported by three-dimensional microCT of the pulmonary specimens: the lungs from patients with Covid-19 and from patients with influenza showed nearly total occlusions of precapillary and postcapillary vessels.
(see link for rest of article)
Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19
Abstract
BACKGROUND
Progressive respiratory failure is the primary cause of death in the coronavirus disease 2019 (Covid-19) pandemic. Despite widespread interest in the pathophysiology of the disease, relatively little is known about the associated morphologic and molecular changes in the peripheral lung of patients who die from Covid-19.
METHODS
We examined 7 lungs obtained during autopsy from patients who died from Covid-19 and compared them with 7 lungs obtained during autopsy from patients who died from acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection and 10 age-matched, uninfected control lungs.
The lungs were studied with the use of seven-color immunohistochemical analysis, micro–computed tomographic imaging, scanning electron microscopy, corrosion casting, and direct multiplexed measurement of gene expression.
RESULTS
In patients who died from Covid-19–associated or influenza-associated respiratory failure, the histologic pattern in the peripheral lung was diffuse alveolar damage with perivascular T-cell infiltration. The lungs from patients with Covid-19 also showed distinctive vascular features, consisting of severe endothelial injury associated with the presence of intracellular virus and disrupted cell membranes. Histologic analysis of pulmonary vessels in patients with Covid-19 showed widespread thrombosis with microangiopathy. Alveolar capillary microthrombi were 9 times as prevalent in patients with Covid-19 as in patients with influenza (P<0.001). In lungs from patients with Covid-19, the amount of new vessel growth — predominantly through a mechanism of intussusceptive angiogenesis — was 2.7 times as high as that in the lungs from patients with influenza (P<0.001).
CONCLUSIONS
In our small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection.
The universality and clinical implications of our observations require further research to define. (Funded by the National Institutes of Health and others.)
Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in humans is associated with a broad spectrum of clinical respiratory syndromes, ranging from mild upper airway symptoms to progressive life-threatening viral pneumonia.1,2 Clinically, patients with severe coronavirus disease 2019 (Covid-19) have labored breathing and progressive hypoxemia and often receive mechanical ventilatory support. Radiographically, peripheral lung ground-glass opacities on computed tomographic (CT) imaging of the chest fulfill the Berlin criteria for acute respiratory distress syndrome (ARDS).3,4 Histologically, the hallmark of the early phase of ARDS is diffuse alveolar damage with edema, hemorrhage, and intraalveolar fibrin deposition, as described by Katzenstein et al.5 Diffuse alveolar damage is a nonspecific finding, since it may have noninfectious or infectious causes, including Middle East respiratory syndrome coronavirus (MERS-CoV),6 SARS-CoV,7SARS-CoV-2,8-10 and influenza viruses.11
Among the distinctive features of Covid-19 are the vascular changes associated with the disease. With respect to diffuse alveolar damage in SARS-CoV7 and SARS-CoV-2 infection,8,12 the formation of fibrin thrombi has been observed anecdotally but not studied systematically. Clinically, many patients have elevated d-dimer levels, as well as cutaneous changes in their extremities suggesting thrombotic microangiopathy.13 Diffuse intravascular coagulation and large-vessel thrombosis have been linked to multisystem organ failure.14-16 Peripheral pulmonary vascular changes are less well characterized; however, vasculopathy in the gas-exchange networks, depending on its effect on the matching of ventilation and perfusion that results, could potentially contribute to hypoxemia and the effects of posture (e.g., prone positioning) on oxygenation.17
Despite previous experience with SARS-CoV18 and early experience with SARS-CoV-2, the morphologic and molecular changes associated with these infections in the peripheral lung are not well documented. Here, we examine the morphologic and molecular features of lungs obtained during autopsy from patients who died from Covid-19, as compared with those of lungs from patients who died from influenza and age-matched, uninfected control lungs.
Methods
PATIENT SELECTION AND WORKFLOW
We analyzed pulmonary autopsy specimens from seven patients who died from respiratory failure caused by SARS-CoV-2 infection and compared them with lungs from seven patients who died from pneumonia caused by influenza A virus subtype H1N1 (A[H1N1]) — a strain associated with the 1918 and 2009 influenza pandemics. The lungs from patients with influenza were archived tissue from the 2009 pandemic and were chosen for the best possible match with respect to age, sex, and disease severity from among the autopsies performed at the Hannover Medical School. Ten lungs that had been donated but not used for transplantation served as uninfected control specimens. The Covid-19 group consisted of lungs from two female and five male patients with mean (±SD) ages of 68±9.2 years and 80±11.5 years, respectively (clinical data are provided in Table S1A in the Supplementary Appendix, available with the full text of this article at NEJM.org). The influenza group consisted of lungs from two female and five male patients with mean ages of 62.5±4.9 years and 55.4±10.9 years, respectively. Five of the uninfected lungs were from female donors (mean age, 68.2±6.9 years), and five were from male donors (mean age, 79.2±3.3 years) (clinical data are provided in Table S1B). The study was approved by and conducted according to requirements of the ethics committees at the Hannover Medical School and the University of Leuven. There was no commercial support for this study.
All lungs were comprehensively analyzed with the use of microCT, histopathological, and multiplexed immunohistochemical analysis, transmission and scanning electron microscopy, corrosion casting, and direct multiplexed gene-expression analysis, as described in detail in the Methods section of the Supplementary Appendix.
STATISTICAL ANALYSIS
All comparisons of numeric variables (including those in the gene-expression analysis) were conducted with Student’s t-test familywise error rates due to multiplicity set at 0.05 with the use of the Benjamini–Hochberg method of controlling false discovery rates. Original P values are reported only for the tests that met the criteria for false discovery rates. All confidence intervals have been calculated on the basis of the t-distribution, as well. Additional details are provided in the Methods section of the Supplementary Appendix.
Results
GROSS EXAMINATION
The mean (±SE) weight of the lungs from patients with proven influenza pneumonia was significantly higher than that from patients with proven Covid-19 (2404±560 g vs. 1681±49 g; P=0.04). The mean weight of the uninfected control lungs (1045±91 g) was significantly lower than those in the influenza group (P=0.003) and the Covid-19 group (P<0.001).
ANGIOCENTRIC INFLAMMATION
Figure 1.
All lung specimens from the Covid-19 group had diffuse alveolar damage with necrosis of alveolar lining cells, pneumocyte type 2 hyperplasia, and linear intraalveolar fibrin deposition (Figure 1). In four of seven cases, the changes were focal, with only mild interstitial edema. The remaining three cases had homogeneous fibrin deposits and marked interstitial edema with early intraalveolar organization. The specimens in the influenza group had florid diffuse alveolar damage with massive interstitial edema and extensive fibrin deposition in all cases. In addition, three specimens in the influenza group had focal organizing and resorptive inflammation (Fig. S2). These changes were reflected in the much higher weight of the lungs from patients with influenza.
Immunohistochemical analysis of angiotensin-converting enzyme 2 (ACE2) expression, measured as mean (±SD) relative counts of ACE2-positive cells per field of view, in uninfected control lungs showed scarce expression of ACE2 in alveolar epithelial cells (0.053±0.03) and capillary endothelial cells (0.066±0.03). In lungs from patients with Covid-19 and lungs from patients with influenza, the relative counts of ACE2-positive cells per field of view were 0.25±0.14 and 0.35±0.15, respectively, for alveolar epithelial cells and 0.49±0.28 and 0.55±0.11, respectively, for endothelial cells. Furthermore, ACE2-positive lymphocytes were not seen in perivascular tissue or in the alveoli of the control lungs but were present in the lungs in the Covid-19 group and the influenza group (relative counts of 0.22±0.18 and 0.15±0.09, respectively). (Details of counting are provided in Table S2.)
In the lungs from patients with Covid-19 and patients with influenza, similar mean (±SD) numbers of CD3-positive T cells were found within a 200-μm radius of precapillary and postcapillary vessel walls in 20 fields of examination per patient (26.2±13.1 for Covid-19 and 14.8±10.8 for influenza). With the same field size used for examination, CD4-positive T cells were more numerous in lungs from patients with Covid-19 than in lungs from patients with influenza (13.6±6.0 vs. 5.8±2.5, P=0.04), whereas CD8-positive T cells were less numerous (5.3±4.3 vs. 11.6±4.9, P=0.008). Neutrophils (CD15 positive) were significantly less numerous adjacent to the alveolar epithelial lining in the Covid-19 group than in the influenza group (0.4±0.5 vs. 4.8±5.2, P=0.002).
A multiplexed analysis of inflammation-related gene expression examining 249 genes from the nCounter Inflammation Panel (NanoString Technologies) revealed similarities and differences between the specimens in the Covid-19 group and those in the influenza group. A total of 79 inflammation-related genes were differentially regulated only in specimens from patients with Covid-19, whereas 2 genes were differentially regulated only in specimens from patients with influenza; a shared expression pattern was found for 7 genes (Fig. S1).
THROMBOSIS AND MICROANGIOPATHY
Figure 2.
The pulmonary vasculature of the lungs in the Covid-19 group and the influenza group was analyzed with hematoxylin–eosin, trichrome, and immunohistochemical staining (as described in the Methods section of the Supplementary Appendix). Analysis of precapillary vessels showed that in four of the seven lungs from patients with Covid-19 and four of the seven lungs from the patients with influenza, thrombi were consistently present in pulmonary arteries with a diameter of 1 mm to 2 mm, without complete luminal obstruction (Figs. S3 and S5). Fibrin thrombi of the alveolar capillaries could be seen in all the lungs from both groups of patients (Figure 2). Alveolar capillary microthrombi were 9 times as prevalent in patients with Covid-19 as in patients with influenza (mean [±SD] number of distinct thrombi per square centimeter of vascular lumen area, 159±73 and 16±16, respectively; P=0.002). Intravascular thrombi in postcapillary venules of less than 1 mm diameter were seen in lower numbers in the lungs from patients with Covid-19 than in those from patients with influenza (12±14 vs. 35±16, P=0.02). Two lungs in the Covid-19 group had involvement of all segments of the vasculature, as compared with four of the lungs in the influenza group; in three of the lungs in the Covid-19 group and three of the lungs in the influenza group, combined capillary and venous thrombi were found without arterial thrombi.
The histologic findings were supported by three-dimensional microCT of the pulmonary specimens: the lungs from patients with Covid-19 and from patients with influenza showed nearly total occlusions of precapillary and postcapillary vessels.
(see link for rest of article)
marsh
On TB every waking moment
Science | AAAS
www.sciencemag.org
T cells found in COVID-19 patients ‘bode well’ for long-term immunity
By Mitch LeslieMay. 14, 2020 , 9:00 PM
Science’s COVID-19 reporting is supported by the Pulitzer Center.
Immune warriors known as T cells help us fight some viruses, but their importance for battling SARS-CoV-2, the virus that causes COVID-19, has been unclear. Now, two studies reveal infected people harbor T cells that target the virus—and may help them recover. Both studies also found some people never infected with SARS-CoV-2 have these cellular defenses, most likely because they were previously infected with other coronaviruses.
“This is encouraging data,” says virologist Angela Rasmussen of Columbia University. Although the studies don’t clarify whether people who clear a SARS-CoV-2 infection can ward off the virus in the future, both identified strong T cell responses to it, which “bodes well for the development of long-term protective immunity,” Rasmussen says. The findings could also help researchers create better vaccines.
The more than 100 COVID-19 vaccines in development mainly focus on another immune response: antibodies. These proteins are made by B cells and ideally latch onto SARS-CoV-2 and prevent it from entering cells. T cells, in contrast, thwart infections in two different ways. Helper T cells spur B cells and other immune defenders into action, whereas killer T cells target and destroy infected cells. The severity of disease can depend on the strength of these T cell responses.
Using bioinformatics tools, a team led by Shane Crotty and Alessandro Sette, immunologists at the La Jolla Institute for Immunology, predicted which viral protein pieces would provoke the most powerful T cell responses. They then exposed immune cells from 10 patients who had recovered from mild cases of COVID-19 to these viral snippets.
All of the patients carried helper T cells that recognized the SARS-CoV-2 spike protein, which enables the virus to infiltrate our cells. They also harbored helper T cells that react to other SARS-CoV-2 proteins. And the team detected virus-specific killer T cells in 70% of the subjects, they report today in Cell. “The immune system sees this virus and mounts an effective immune response,” Sette says.
The results jibe with those of a study posted as a preprint on medRxiv on 22 April by immunologist Andreas Thiel of the Charité University Hospital in Berlin and colleagues. They identified helper T cells targeting the spike protein in 15 out of 18 patients hospitalized with COVID-19.
The teams also asked whether people who haven’t been infected with SARS-CoV-2 also produce cells that combat it. Thiel and colleagues analyzed blood from 68 uninfected people and found that 34% hosted helper T cells that recognized SARS-CoV-2. The La Jolla team detected this crossreactivity in about half of stored blood samples collected between 2015 and 2018, well before the current pandemic began. The researchers think these cells were likely triggered by past infection with one of the four human coronaviruses that cause colds; proteins in these viruses resemble those of SARS-CoV-2.
The results suggest “one reason that a large chunk of the population may be able to deal with the virus is that we may have some small residual immunity from our exposure to common cold viruses,” says viral immunologist Steven Varga of the University of Iowa. However, neither of the studies attempted to establish that people with crossreactivity don’t become as ill from COVID-19.
Before these studies, researchers didn’t know whether T cells played a role in eliminating SARS-CoV-2, or even whether they could provoke a dangerous immune system overreaction. “These papers are really helpful because they start to define the T cell component of the immune response,” Rasmussen says. But she and other scientists caution that the results do not mean that people who have recovered from COVID-19 are protected from reinfection.
To spark production of antibodies, vaccines against the virus need to stimulate helper T cells, Crotty notes. “It is encouraging that we are seeing good helper T cell responses against SARS-CoV-2 in COVID-19 cases,” he says. The results have other significant implications for vaccine design, says molecular virologist Rachel Graham of the University of North Carolina, Chapel Hill. Most vaccines under development aim to elicit an immune response against spike, but the La Jolla group’s study determined that T cells reacted to several viral proteins, suggesting vaccines that sic the immune system on these proteins as well could be more effective. “It is important to not just concentrate on one protein,” Graham says.
marsh
On TB every waking moment
22:23 min
Scientific evidence for mask wearing
•May 21, 2020
Dr. John Campbell
Masks and hamsters https://www.foxnews.com/health/wearin...
https://fightcovid19.hku.hk/hku-hamst... https://jamanetwork.com/journals/jama...
Hong Kong Rate transmission through respiratory droplets or airborne particles dropped up to 75% using masks. Public mask wearing effectiveness, huge,” (Dr. Yuen Kwok-yung) Transmission can be reduced by 50 percent, especially when masks are worn by infected people Universal masking = 80% will significantly flatten the curve https://www.who.int/news-room/q-a-det...
Linda Bourouiba JAMA Sneeze (10-30 m/s), 7 – 8 m or 23-26 feet Cough 5 - 6 metres or 19 feet, Breath 2 metres or 7 feet Masks, droplets come out of the side, reduces range Background Dichotomous classification between large vs small droplets, or droplets vs aerosol Arbitrary droplet diameter cutoffs, from 5 to 10 μm Host-to-host transmission as droplets or aerosol routes Rapid international spread of COVID-19, using arbitrary droplet size cutoffs may not be accurate Possibly contributing to the ineffectiveness of some procedures used to limit the spread of respiratory disease.
Recent work Exhalations, sneezes, and coughs, mucosalivary droplets Multiphase turbulent gas cloud Continuum of droplet sizes Droplets can survive for minutes in clouds Payload of pathogen-bearing droplets A hot and moist gas cloud Ambient environment (temperature, humidity, and airflow) Residues or droplet nuclei that may stay suspended in the air for hours Ambient environment (temperature, humidity, and airflow). China (2020), COVID-19 found in ventilation systems in hospital rooms of infected patients Implications World Health Organization recommendations 3-foot (1-m) Centers for Disease Control, 6-foot (2-m) separation. May underestimate the distance Mask efficacy as source control depends on the ability of the mask to trap or alter the high-momentum gas cloud emission with its pathogenic payload.
https://www.youtube.com/watch?v=XJMlcKbFOEI
marsh
On TB every waking moment
3:46 min
Despite COVID-19 risks, Americans swarm beaches across the country
•May 25, 2020
CBS This Morning
As Americans celebrate the first big holiday weekend of the summer, many appear to ignore the COVID-19 social distancing guidelines in pools, parks and river shorelines. Don Dahler reports.
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4:16 min
Beaches, churches crowded amid COVID-19 spike in 8 states l GMA
•May 25, 2020
Good Morning America
Eight states are still reporting increases in new COVID-19 cases as beaches, pools and churches in many states were crowded over the Memorial Day weekend.
[COMMENT: I think some are just saying - If I am going to get it, let's get it over with so I can get on with my life.]
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marsh
On TB every waking moment
27:28 min
New York Gov. Andrew Cuomo Holds Coronavirus Briefing | NBC News
•Streamed live 6 hours ago
NBC News
Watch coronavirus livestream coverage of the outbreak as COVID-19 spreads, impacting markets and daily life across the U.S. and abroad.
marsh
On TB every waking moment
15:51 min
How Will Coronavirus Change Dating?
•May 24, 2020
CNBC
With a highly contagious virus and mandatory stay-at-home orders around the country, dating app downloads are seeing record numbers. Many singles are turning to online dating in order to find love under lockdown—or to simply beat the loneliness of self-isolation.