Between Sand and Sky!

My feelings from space.

Sending healings and a bokeh of light

to our Alfie who is still very ill.

Today August 4th,2021 readmission to the clinic because he is in pain and can not eat. Ultrasound scan shows a lot of air in the abdomen. Will be put on an IV and nasogastric tube. To determine further blood tests for kidney functions.

Alf is not Alf anymore, luckily he had some weight reserves!

 

Oh sweet Alfie, please be strong 🙏 our dearest friend!

We are so sad, we don't want to lose you!

 

Unfortunately my lovely friend Alfie

has passed away ♱ on August 5th 2021

Goodbye my Heart♥

We miss you so much my darling!

 

p.p. done with Topaz.

Origin

 

Tora is a member of a race of magical ice people that live in the mountains of Norway. Her father, King Olafsdotter is the leader of these people.

 

When an engineer named Rod Schoendienst discovered the ice people, he made a pact with Tora's father that allowed her to leave their kingdom.

 

After Rod introduced Tora to Doctor Mist and the Global Guardians she joined the team as the second Ice maiden.

 

Soon after, she became close friends with Beatriz DaCosta, the superheroine known as Fire.

 

After the Global Guardians lost their U.N. funding, Tora and Beatriz applied for membership in a depleted Justice League International that was desperate for new members. Changing her name to Ice, Tora fought with the League for years.

 

Creation

 

The Global Guardians were created for an issue of the Superfriends where the Superfriends needed help to defuse bombs which had been planted around the world.

 

This created a team where each team had a hero from one specific country. The characters were generally portrayed stereotypically in terms of their association to the specific countries, thus the character from Norway, Ice Maiden, was given the ability to control ice.

 

Superfriends is considered non-canon though, so the characters first appearance in the DC universe came some time later.

 

After joining the Justice League, her name was changed along with Beatriz and is half of a play on words of a common phrase Fire and Ice (which is for instance the name of one of the best selling lipstick shades of all time.)

 

Character Evolution

 

The character was mostly one-dimensional throughout her early appearances. It was not until more female and more international characters were desired for Justice League International that her character was developed beyond a stock international character.

 

Her interaction with two characters really helped to define her character development. The first was with her best friend Fire, who was the unreserved exhibitionist, and Tora who was more reserved in her conduct and demeanor. The second would be with her on-again off-again romantic interest in Guy Gardner.

 

Relationship with Guy Gardner

 

Shortly, after joining the Justice League Tora found Guy Gardner rather sweet and charming and she ended up having a long on again off again relationship that got more complicated as it went on.

 

Ice first met Guy after he had suffered multiple concussions which caused Guy to have a really goody, goody personality. Before the character change Guy had been a short tempered, cocky, arrogant and a looking for a fight superhero.

 

His temper was so short he challenged other heroes regularly. He once got so ticked at Batman that he challenged to fight Batman without his Green Lantern ring. This ended up with the Batman knocking Guy out cold with only one punch, causing Guy to hit his head on the floor.

 

When Guy awoke he was very angry and swore revenge against Batman, but first he had to find his ring. He ended up finding it under the monitor station at the Justice League headquarters, but when a mouse appeared suddenly it startled him causing him to hit his head and black out again.

 

It was after this that Guy became the Goody, Goody that Tora met. Tora never knew Guy's personality before Guy's latest concussion so she just believed that was how Guy was. Ice ended up becoming attracted to Guy.

 

Unfortunately for her, Guy and Lobo got into a huge fight causing Guy to hit his head again and revert back to his old self. This version of Guy was not pleasing to Ice at all, but she knew that there was a sweeter side to him somewhere, and she already had strong feelings for him by that point.

 

Guy too was also very much in love with Ice, but he could never behave himself. Not even when he was around her. He even took her out to a strip club on one of their very first dates thinking that would be a good idea.

 

This awkwardness went on for a long while until Superman joined the Justice League. This is when things went really bad for their relationship. Ice started having feelings for Superman because he had a similar personality to Guy when he was being a goody, goody.

 

Major Story Arcs

 

Modern Age: New Earth

Justice League

 

The rest of the league didn't do much to help guy with his temper either. Booster Gold and Blue Beetle (Ted Kord) took much delight in pulling pranks on League members and Guy was one of their favorite targets.

 

One time in particular Ice told Guy that if she was going to go out on a date with him he had to be a perfect gentleman and keep his temper in check. He also had to take her where she wanted to go. Guy had such strong feelings for Ice that he agreed to both of her conditions.

 

Booster and Beetle couldn't pass up this chance to play a prank on Guy. They just had to get him to loose his temper. Ice wanted to go to the Ice Capades. Keeping to his promise Guy took Ice there despite of how embarrassing it was for him. This is where Beetle set their prank into motion.

 

They enlisted the help of Kilowog. Kilowog had been working for the league a while and proved himself to be quite a technological expert. He was asked to build a large and silly replica of Guy to be worn by a skater at the Ice Capades. They convinced Kilowog that Guy would like the attention and that it would be a great honor.

 

Things got really bad when Guy found out that Ice had a crush on Superman . This caused Guy to act even more irrational than he did in the past. He was never a fan of Superman in the first place, but when he felt that he had lost Ice to him he just didn't want to deal with it.

 

To make things worse Ice's best friend Fire hated the relationship between Ice and Guy because she felt Guy was no good for Ice. Fire felt like Ice's big sister and that she needed to look after her.

 

Eventually Hal Jordan returned to Earth and challenged Guy for the right to be the Green Lantern of Sector 2814. After a prolonged fight Hal eventually won and Guy was forced to surrender his ring.

 

Ice, despite everything that had happened (good and bad) with Guy was still rooting for him. She was upset when Guy left defeated.

 

Guy eventually came up with a way to regain his powers and after a grand adventure came into possession of Sinestro's Power Ring. Upon getting the ring Guy returned to rejoin the league, beat Superman to a pulp and win back Ice's heart. Not necessarily in that order.

 

Superman was dead set against Guy's readmission into the league and after a fight only consented when Batman intervened and told Superman that Guy was more dangerous outside the league where no one could keep an eye on him.

 

Shortly after Guy rejoined the JLA the monster that would become known as Doomsday appeared and began blazing a trail of destruction on his way to Metropolis. The Justice League of America arrived on the scene with Guy leading the charge only to be quickly dealt with. The remaining Leaguers put up a good fight but were all soundly beaten.

 

In the aftermath of the battle the Blue Beetle was comatose, Guy severely injured, Booster Gold was sidelined as his power suit was destroyed, Fire was powerless, Ice had a broken arm and Superman was dead.

 

Ice eventually took a leave of absence and returned to her people in the mountains of Norway. Ice's father was glad to have his daughter back and made plans for her to take over as Queen, much to her brother Ewald's disapproval.

 

Ewald later killed their father and claimed the throne for himself. Ewald was in league with the Overmaster, who had a grand scheme, that eventually brought the Justice League into the fight. In the resulting battle, Ice was forced to fight her brother to the death.

 

After the battle with her brother Ice revealed to her best friend that she had gained new powers. She pulled a metal rail up and bent it with great ease. She also demonstrated the ability to fly.

 

Around this time she and Guy appeared to come to an understand and the pair showed signs of rekindling their romance. Unfortunately there were different things in store for the couple.

 

The Death of Ice

 

During Guy's absence the Overmaster arrived with plans to destroy the Earth. With his henchmen, the Cadre, the Overmaster disrupted planetary communications and stopped all births and deaths throughout the planet.

 

The Overmaster brought Ice to his side after revealing that he was the hidden mastermind behind her brother. Ice captured her best friend and held her prisoner during this time.

 

Eventually Ice betrayed the Overmaster and rallied her teammates against him. The Overmaster then blasted Tora who apparently died.

 

Aftermath

 

The league she loved and the people she cared for all struggled with her death especially Guy and Fire. Guy and Fire finally resolved their issues.

 

After Ice's death a different girl wearing Tora's first costume shows up and tells Fire that she was the first Ice Maiden of the Global Guardians and her name is Sigrid Nanson.

 

Fire's initial reaction is disgust and she immediately attacks Ice Maiden whom she believe is an importer. Eventually cooler heads prevail and Fire comes to accept Ice Maiden.

 

Fire

 

Fire and Ice were not just best friends but they were also very close in a sister like relationship. Fire acted as the older more worldly, flirty and sultry older sister while Ice was more of a sweet, timid and naïve younger sister.

 

Fire expected the same kind of relationship with Ice Maiden that she had with Ice but she became even more protective because of the loss she felt for Ice and she could not bare to go through that pain again.

 

Ice Maiden on the other hand was not like Ice in her personality and was much more worldly and flirty than even Fire was.

 

Ice Maiden would end up being killed by Mist in a hollow death with no meaning or real reason other than to show power. Fire was not part of the team, it is not fully clear why.

 

Return of a Goddess

 

Sometime later, the Birds of Prey discovered Tora alive and in a Rocket Red exo-suit. They also find out about the Secret Six's involvement in their current mission.

 

Tora is awoken during the ensuing battle and proceeds to display the levels of power she had before her own death. Birds of Prey and the Secret Six alike are all targets of Ice's rage. It is only after Huntress slaps her and reminds her of Guy Gardner that Ice reverts to her wits.

 

It is revealed the villain Kerimov was responsible for her survival. He needed a Goddess to play on the Russian people's superstitions about an Ice Princesses.

 

Tora still felt somewhat loyal to Kerimov since he protected her from death. Her loyalty was proven moot as Deadshot dispatched Kerimov. Tora then left with the Birds of Prey.

 

Wanting to return to her normal life as much as possible, Tora met up with her best friend Bea at the Checkmate Compound. They caught up on old times and spoke of current ones.

 

While in Fire's care, Ice ventured out of the Checkmate compound on occasion to meet with other old friends (such as Blue Beetle and Booster Gold) and helped them with their current activities.

 

Most notably, Ice joined other heroes in the Sinestro Corps War. In the aftermath, she reunited with Guy Gardner. they have since begun their relationship anew.

 

Despite telling Guy that she wanted to take things slow, he proposed the idea of her moving to Oa to live with him. When she began to tell him that it wasn't such a good idea for her, he became angry thereby pushing Tora away.

 

She then departed back to Earth with one of the other Green Lanterns

 

Final Crisis

 

Fire and Thomas Jagger encountered Ice in Antarctica while on a mission. It is unknown how but Ice was "infected" with Darkseid's Anti-Life Equation.

 

She went on to "infect" both Fire and Thomas Jagger. They made their way into Checkmate's Antarctic base of operations and "infected" the rest of Checkmate, leaving only Mr. Terrific, Cheetah, and Snapper Carr un-"infected".

 

Blackest Night

 

Tora appears in a group of heroes that had succumbed to the Anti-Life Equation and come back. Later, she (along with other former members of Justice League International) are seen at the graveside of Ted Kord (the Blue Beetle) on a day dedicated to fallen super heroes.

 

Later, she is seen with other heroes of Earth trying to stop the newly resurrected citizens of Coast City. During the battle, Bruce Wayne is temporarily brought back as a Black Lantern.

 

This forms "emotional tethers" to the gathered heroes. Due to this "emotional tether" all of the heroes that had previously been affected by the Anti-Life equation and came back were transformed into Black Lanterns, Ice included.

 

While a Black Lantern, Ice faced off against the various heroes, most notably Guy Gardner. Their battle was not only one of strength and powers but also manipulation and bitter words.

 

Ice implied that he should end her life permanently because she hated dying and coming back and repeating the cycle seemingly endlessly. This unlocked Guy's compassion and he was able to stop her (for the time being).

 

Later still, when Black Hand's connection to the Black Lanterns was severed, Tora's time as a Black Lantern ended and she became a White Lantern. Free of the control of both the White and Black Lanterns, Ice has regained the land of the living.

 

Brightest Day

 

After the events of Blackest Night, Tora found herself reunited with various members of the Justice League International (Booster Gold, Fire, and Captain Atom). Responding to a distress call from Booster Gold's JLI Beacon, they found him lying in a pool of blood after facing Maxwell Lord.

 

Unfortunately for the four friends, Maxwell Lord used his vast telepathic abilities to wipe his very existence from the world's memories. Only the four were spared (for some unknown reason).

 

Fearful of what Maxwell may do, they attempt to persuade the various members of the Justice League and Checkmate that he is back and a bigger threat than before.

 

Each of them found that they were being discredited. Ice, herself, found that Maxwell had mentally concocted a story of Ice attempting to murder Guy Gardner while on a date. Feeling that there was nowhere to turn, the four teamed up again to take Maxwell down and restore their reputations.

 

While infiltrating one of Checkmate's bases of operations, Ice and the rest of the JLI encountered the Metal Men. During their encounter, Ice powered up to levels of power never seen of her before. After nearly killing Fire, Ice returned to normal. During this battle, Ice had memories return to her that were long buried. Soon after this, she joined the Global Guardians.

 

It is unclear as to whether or not these were true memories or more manipulations by Maxwell Lord. Her and her teammates had previously ventured to her homeland and met the magical Norse people. This investigation revealed several conflicts in Maxwell Lord's version of her origin.

 

After Captain Atom was shown killing Magog on live television (this was yet another manipulation of Maxwell Lord) Ice and the JLI battle Power Girl. During this battle with their friend, Power Girl's memories of Maxwell Lord returned and she promised to help spread the word and try to clear their names.

 

Most recently, the JLI were witness to Maxwell shooting the new Blue Beetle in the head, apparently killing him.

 

The Signal Masters

 

After the events of Flashpoint many heroes and team in the DC Universe where rebooted, one such team was the Justice League International.

 

Andre Briggs, a worker at the UN has finally gotten UN approval for a new Justice League. The team consists of August General in Iron, Rocket Red, Vixen, Godiva, Guy Gardner, Fire and Ice, and lead by Booster Gold.

 

Their first mission, which takes place mere minutes after everyone is introduced is to investigate some missing UN personnel in Peru. While there the team is attacked by a giant robot, and Ice is badly hurt. This causes the team to retreat and regroup. They learn that there are now four giant robots around the globe, so Booster splits the group into teams of two.

 

Ice and Rocket Red investigate a robot that appeared in Russia, there they discover a cavern underneath. They investigate but are ambushed by Mud-men and encased in rock.

 

They are then teleported back to Peru where they see the rest of the team trapped in the same rock. They then learn that Peraxxus, is responsible for the giant robots and plans on destroying the Earth and sell its resources. The team escape their rock cells but are no match for Peraxxus, and he leaves them for dead.

 

The team again regroups and attacks Peraxxus again but this time on his own ship. While the heavy hitters attack Peraxxus, Ice and Rocket Red hack into the ships navigation system and crash it into one of the giant robots, shutting them all down. This causes Peraxxus to retreat.

 

Ice is with the team when they are reintroduced and when the stage they are standing on is blown up by terrorists.

 

Powers and abilities

 

In addition to being a proficient hand-to-hand combatant, Ice can project in various forms quantities of ice and snow through her hands just enough to down an opponent. She can create platforms of ice upon which she can skate.

 

Before her initial demise, she was powered-up mysteriously (later revealed to be the result of the Overmaster). She was able to generate larger amounts of ice and snow, and gained super strength and the ability to fly.

 

After her return in Birds of Prey, Ice's powers seem incredibly destructive, expelling people from the building she's in as she awakens with bright white eyes, and conjuring a massive icy figure before her as well as controlling the weather to some degree, by causing the beginning of a blizzard far stronger than those known in that area.

 

⚡ Happy 🎯 Heroclix 💫 Friday! 👽

_____________________________

A year of the shows and performers of the Bijou Planks Theater.

 

Secret Identity: Tora Olafsdotter

 

Publisher: DC

 

First appearance: Justice League International #12 (April 1988)

 

Created by: Keith Giffen (writer)

J. M. DeMatteis (writer)

Kevin Maguire (artist)

The SLX wasn't the first single lens reflex from Rollei. Already at Photokina in 1966 the SL66 camera was presented.

However, while the SL66 was a mechanical camera, the new SLX presented at Photokina in 1974, was a totally electronic camera. No springs or feathers. An electric motor runs the camera and a new electrical shutter was build into all lenses.

This means that the camera is a "direct drive" camera not unlike what we know today from many modern electronic film cameras.

 

To make a fully electronic camera Rollei invented a new shutter with two linear motors build into the lens.

 

Constructing a leaf shutter capable of at least 1/500 sec. and with a big enough aperture wasn't easy but Rollei managed to construct a shutter with a diameter of 24mm and a maximum speed of 1/500 sec.

 

The lenses contains two linear motors; one for controlling the shutter and one for the aperture.

 

Later came an even faster shutter capable of 1/1000 sec. or a bigger diameter (34mm) for a larger maximum aperture.

 

This is my entrance in to Medium Format Film Photography, and my readmission to film photography. I played around with 35mm and a Pentax K1000 with black and white film, developed in the bathroom, many years back.

  

 

View On Black

 

Newsweek: Obama better represents Catholics than does the Pope

 

WSJ: Unemployment Up from 4.8% to currently 9.5% (20% in MI) and expected to rise

 

Obama flies pizza chef to Washington, DC from St. Louis to cater a party for him and his pals at White House.

 

Obama: "We are out of money"

 

Obama: "Its Working"

 

Facts: Government has nationalized AIG, Chrysler, GM, Citibank and has its eyes set on Health Care

 

This administration and congress has already outspent all previous 43 presidents combined

 

"Stimulus" is spent on bailing out failed social experiments and entitlement sinkholes by state governments controlled by "progressives"

 

House passes largest Tax Increase in the History of America - they aim to tax the air we breathe

 

Charitable donation levels and business investments down as tax levels increase

 

Obamas plan vacation at Martha's Vineyard

 

Obama promised unemployment would not exceed 8% - now its 9.5% and rising

 

Obama said it was mandatory that the 10 to 20 trillion dollar (with debt servicing) "stimulus" was passed right away or we are doomed - it was voted on and passed without those voting in the affirmative for it even reading it.

 

Once passed, the vast majority of the "stimulus" spending is deferred to 2010 which coincidentally is an election year for the politicians who voted for passage. An inference is that the only crisis was the socialists getting reelected after their policy of fascism failed to turn around the economy. A study of history will reveal their concern - no fascist/socialist enterprise has been successful at improving the quality of life for its citizens at any time in human history. No civilization has successfully taxed and spent its way out of a recession in the history of humanity.

 

Those who hold America's debt are frantically calling for a "world currency", knowing full well, that the certain forthcoming hyperinflation in America will significantly devalue the US Dollar and their investments will then be worth pennies on the dollar.

 

Now, Obama says that health care must be nationalized right away or we are doomed.

 

Now, Obama says that Sotomayor must be confirmed right away or we are doomed.

 

Now, Obama says that Cap and Trade (destroy and nationalize the energy sector) bill must be passed right away or we are doomed.

 

Now, Obama says that trillions of dollars of new taxes must be passed right away or we are doomed. These new taxes are on top of the trillions of dollars in new taxes that were already included in his "stimulus" bill and budget.

 

Is there a pattern? Does "we" refer to his constituents or perhaps himself and his political cronies?

 

No civilization has reversed a downward unemployment spiral by shrinking its private sector and growing its government bureaucracy.

 

The countries who have tried the fascist/socialist experiment are now moving back to more capitialistic free market policies - why? because shrinking their private sector and burdening it with increased government confiscatory/redistribution policies created misery in the form of unemployment, loss of individual freedom, lower quality of life and medical care rationing, shortages and misery.

 

Biden: We have to keep spending money to keep from going bankrupt.

 

Obama: We must pass nationalized health care so we can reduce costs. (We must do it now or we are doomed)

 

CBO Chief: Health Bills To Increase Federal Costs

 

White House wants more power to set Medicare rates

 

wiki.answers.com/Q/Name_and_explain_two_effects_of_price_...

 

When thinking about price controls, think of the supply and demand curves and remember that with a price control, it is impossible for a price to get into equilibrium. With that in mind, we can identify two problems that result from this.

 

1. A shortage/oversupply of the good. If there is a price ceiling, you have a shortage (a la gasoline during the price controls of the 70's.) If there is a floor, you have overproduction (a la ethanol. Which, granted, is subsidized, but that is effectively like a price floor). *Note* also consider the housing markets where rent control is present.

 

2. An inefficient allocation of resources. With ethanol being subsidized, we witnessed a massive increase in the price of corn. The market did not want this, and thus we saw an inefficient allocation of resources.

 

Should National Health Care pass in this country, I will not know where or when I will die, but I will know how - substandard medical care, denial of care, lack of r&d due to price controls and rationing emposed by the government - all based on decisions by bureaucrats, actuaries, accountants and political appointees who I do not know and who do not know me or my specific needs or wishes ... and more importantly do not care ... they care only about passing the next government audit cycle for cost control.

 

PLEASE STOP THIS TYRANNY

 

Analysis of Health Care Bill HR 3200 Print E-mail

Thursday, 06 August 2009 20:28

 

Below is a detailed, line by line, analysis of the Health Care bill (HR 3200) by CADC’s advisory board member, Mat Staver of the Liberty Council, and Dean of Liberty University School of Law.

 

Obama Health Care Plan Details

 

HR 3200 currently under consideration in the House of Representatives

 

*HC = "Health Care"

 

* Pg 22 of the HC Bill MANDATES the Government will audit the books of ALL EMPLOYERS that self insure!!

* Pg 29 lines 4-16 in the HC Bill - YOUR HEALTH CARE IS RATIONED!!!

* Pg 30 Sec 123 of HC Bill - THERE WILL BE A GOVERNMENT COMMITTEE that decides what treatments/benefits you get

* Pg 42 of HC Bill - The Health Choices Commissioner will choose your benefits for you. You have no choice!

* Pg 50 Section 152 in HC Bill - HC will be provided to ALL non-U.S. citizens, illegal or otherwise

* Pg 58 HC Bill – Government will have real-time access to individual’s finances and a National ID Health Care Card will be issued!

* Pg 59 HC Bill lines 21-24 Government will have direct access to your banks accounts for electronic funds transfer.

* Pg 65 Sec 164 is a payoff subsidized plan for retirees and their families in unions and community organizations (ACORN).

* Pg 72 Lines 8-14 Government is creating a Health Care Exchange to bring private health care plans under government control.

* Pg 84 Sec 203 HC Bill - Government mandates ALL benefit packages for private health care plans in the Exchange

* Pg 85 Line 7 HC Bill - Specs for of Benefit Levels for Plans = The government will ration your health care!

* Pg 91 Lines 4-7 HC Bill - Government mandates linguistic appropriate services.

* Pg 95 HC Bill Lines 8-18 The government will use groups i.e., ACORN & AmeriCorps to sign up individuals for government Health Care Plan

* Pg 85 Line 7 HC Bill - Specs of Ben Levels 4 Plans. #AARP members - Your health care WILL be rationed

* Pg 102 Lines 12-18 HC Bill - Medicaid Eligible Individual will be automatically enrolled in Medicaid. No choice.

* Pg 124 lines 24-25 HC No company can sue the government on price fixing. No "judicial review" against this government monopoly.

* Pg 127 Lines 1-16 HC Bill - Doctors/ #AMA - The government will tell YOU what you can make.

* Pg 145 Line 15-17 An employer MUST auto enroll employees into public option plan. NO CHOICE

* Pg 126 Lines 22-25 Employers MUST pay for health care for part-time employees AND their families.

* Pg 149 Lines 16-24 ANY Employer w/ payroll 400k and above who does not prov. pub opt. pays 8% tax on all payroll

* Pg 150 Lines 9-13 Businesses with payroll between 251k and 400k who do not provide public opt pays 2-6% tax on all payroll

* Pg 167 Lines 18-23 ANY individual who doesn’t have acceptable health care according to government will be taxed 2.5% of income.

* Pg 170 Lines 1-3 Any NONRESIDENT Alien is exempt from individual taxes (Americans will pay).

* Pg 195 Officers & employees of HC Administration (GOVT) will have access to ALL Americans' financial and personal records.

* Pg 203 Line 14-15 HC - "The tax imposed under this section shall not be treated as tax." Yes, it says that.

* Pg 239 Line 14-24 HC Bill Government will reduce physician services for Medicaid. Seniors, low income, poor affected.

* Pg 241 Line 6-8 HC Bill - Doctors, it does not matter what specialty you have, you’ll all be paid the same.

* Pg 253 Line 10-18 Government sets value of doctors' time, prof judg, etc. Literally value of humans.

* Pg 265 Sec 1131Government mandates and controls productivity for private health care industries.

* Pg 268 Sec 1141 Federal Government regulates rental and purchase of power-driven wheelchairs.

* Pg 272 SEC. 1145. Treatment of certain cancer hospitals – Cancer patients - welcome to rationing!

* Page 280 Sec 1151 The government will penalize hospitals for what government deems preventable readmissions. (Incentives for hospital to not treat and release.)

* Pg 298 Lines 9-11 Doctors that treat a patient during initial admission that results in a readmission-Government will penalize you.

* Pg 317 L 13-20 PROHIBITION on ownership/investment. Government tells Doctors what/how much they can own.

* Pg 317-318 lines 21-25, 1-3 PROHIBITION on expansion- Government is mandating hospitals cannot expand.

* pg 321 2-13 Hospitals have opportunity to apply for exception, BUT community input required. Can you say ACORN?!!

* Pg335 L 16-25 Pg 336-339 - Government mandates establishment of outcome based measures. Health Care the way they want. Rationing.

* Pg 341 Lines 3-9 Government has authority to disqualify Medicare Advantage Plans (Part B), HMOs, etc. Forcing people into Government plan.

* Pg 354 Sec 1177 - Government will RESTRICT enrollment of special needs people!

* Pg 379 Sec 1191 Government creates more bureaucracy – Tele-health Advisory Committee. Health care by phone/Internet?

* Pg 425 Lines 4-12 Government mandates Advance [Death] Care Planning Consultion. Think Senior Citizens end of life.

* Pg 425 Lines 17-19 Government will instruct and consult regarding living wills, durable powers of attorney. Mandatory!

* Pg 425 Lines 22-25, 426 Lines 1-3 Government provides approved list of end of life resources, guiding you in death.

* Pg 427 Lines 15-24 Government mandates program for orders for end of life. The government has a say in how your life ends.

* Pg 429 Lines 1-9 An "advanced care planning consult" will be used frequently as patient's health deteriorates.

* Pg 429 Lines 10-12 " advanced care consultation" may include an ORDER for end of life plans. AN ORDER from Government.

* Pg 429 Lines 13-25 - The government will specify which doctors can write an end of life order.

* PG 430 Lines 11-15 The government will decide what level of treatment you will have at end of life.

* Pg 469 - Community Based Home Medical Services=Non-profit orgs. Hello, ACORN Medical Services here!!?

* Pg 472 Lines 14-17 PAYMENT TO COMMUNITY-BASED ORG. 1 monthly payment to a community-based org. Like ACORN?

* Pg 489 Sec 1308 The government will cover Marriage and Family therapy. They will insert government into your marriage.

* Pg 494-498 Government will cover Mental Health Services including defining, creating, rationing those services.

* PG 502 Sec 1181 Center for Comparative Effectiveness Research Established. – Hello Big Brother – Literally.

* Pg 503 Lines 13-19 Government will build registries and data networks from YOUR electronic medical records.

* Pg 503 lines 21-25 Government may secure data directly from any department or agency of the U.S. who have any of your data.

* Pg 504 Lines 6-10 The "Center" will collect data both published and unpublished (that means public and your private info).

* PG 506 Lines 19-21 The Center will recommend policies that would allow for public access of data.

* PG 518 Lines 21-25 The Commission will have input from Health Care consumer reps – Can you say unions and ACORN?

* PG 524 18-22 Comparative Effectiveness Research Trust Fund set up. More taxes for ALL.

* PG 621 Lines 20-25 Government will define what quality means in health care. Since when does government know about quality?

* Pg 622 Lines 2-9 To pay for the Quality Standards, government will transfer money from other government Trust Funds. More Taxes.

* PG 624 "Quality" measures shall be designed to assess outcomes and functional status of patients.

* PG 624 "Quality" measures shall be designed to profile you including race, age, gender, place of residence, etc.

* Pg 628 Sec 1443 Government will give "Multi-Stake Holders" Pre-Rule Making input into Selection of "Quality" Measures.

* Pg 630 9-24/631 1-9 Those multi-stake holder groups include unions and groups like ACORN deciding health care quality.

* Pg 632 Lines 14-25 The Government may implement any "Quality measure" of health care services as they see fit.

* PG 633 14-25/ 634 1-9 The Secretary may issue non-endorsed "Quality Measures" for Physician Services and Dialysis Services.

* Pg 635 to 653 Physicians Payments Sunshine Provision – Government wants to shine sunlight on doctor but not government.

* Pg 654-659 Public Reporting on Health Care-Associated Infections – Looks okay.

* PG 660-671 Doctors in Residency – Government will tell you where your residency will be, thus where you’ll live.

* Pg 676-686 Government will regulate hospitals in EVERY aspect of residency programs, including teaching hospitals.

* Pg 686-700 Increased Funding to Fight Waste, Fraud, and Abuse. Do they mean like the government with an $18 million website?

* PGs 701-704 Sec 1619 If your part of health care plan isn’t in Government Health Care Exchange but you qualify for Federal aid, no payment.

* PG 705-709 SEC. 1128 If Secretary gets complaints (ACORN) on health care provider or supplier, government can do background check.

* PG 711 Lines 8-14 The Secretary has broad powers to deny health care providers/ suppliers admittance into Health Care Exchange. Your doctor could be thrown out of business.

* Pg 719-720 Sec 1637 ANY Doctor who orders durable medical equipment or home medical services MUST be enrolled in Medicare.

* PG 722 Sec 1639 Government MANDATES doctors must have face-to-face with patient to certify patient for Home Health Services.

* PG 724 23-25 PG 725 1-5 The same government certifications will apply to Medicaid and CHIP (your kids).

* PG 724 Lines 16-22 Government reserves right to apply face-to-face certification for patient to ANY other health care service.

* Pg 735 lines 16-25 For law enforcement, proposes the Secretary-HHS will give Attorney General access to ALL data.

* PG 740-757 Government sets guidelines for subsidizing the uninsured (That's your tax dollars people).

* Pg 757-762 Federal Government will shift burden of payments to Disproportionate Share Hospitals (DSH) to States. (Taxes)

* Pg 763 1-8 No DS/EA hospitals will be paid unless they provide services without regard to national origin.

* Pg 765 Sec 1711 Government will require Preventative Services including vaccines. (Choice?)

* Pg 768 Sec 1713 Government – Nurse Home Visitation Services (Hello union paybacks).

* Pg 769 11-14 Nurse Home Visit Services include economic self-sufficiency, employ adv, school-readiness.

* Pg 769 3-5 Nurse Home Visit Services - "increasing birth intervals between pregnancies." Government ABORTIONS anyone?

* Pg 770 SEC 1714 Federal Government mandates eligibility for State Family Planning Services. Abortion and State Sovereignty.

* Pg 789-797 Government will set, mandate drug prices, controlling which drugs brought to market. Bye innovation.

* Pgs 797-800 SEC. 1744 PAYMENTS for graduate medical education. The government will now control doctors’ educations.

* PG 801 Sec 1751 The government will decide which health care conditions will be paid. Can you say RATION!

* Pg 810 SEC. 1759. Billing Agents, clearinghouses, etc. req. to register. Government takes over private payment system.

* Pg 820-824 Sec 1801 Government will identify individuals ineligible for subsidies. Will access all personal financial information.

* Pg 824-829 SEC. 1802. Government sets up Comparative Effectiveness Research Trust Fund. Another tax black hole.

* PG 829-833 Government will impose a fee on ALL private health insurance plans including self-insured to pay for Trust Fund!

* PG 835 11-13 fees imposed by government for Trust Fund shall be treated as if they were taxes.

* Pg 838-840 Government will design and implement Home Visitation Program for families with young kids and families expecting kids.

* PG 844-845 This Home Visitation Program includes government coming into your house and telling you how to parent!!!

* Pg 859 Government will establish a Public Health Fund at a cost of $88,800,000,000. Yes that’s billion.

* Pg 865 The government will MANDATE the establishment of a National Health Service Corps.

* PG 865 to 876 The NHS Corps is a program where doctors perform mandatory health care for two years for part loan repayment.

* PG 876-892 The government takes over the education of our medical students and doctors.

* PG 898 The government will establish a Public Health Workforce Corps to ensure supply of public health prof.

* PG 898 The Public Health Workforce Corps shall consist of civilian employees of the U.S. as Secretary deems.

* PG 898 The Public Health Workforce Corps shall consist of officers of Regular and Reserve Corps of Service.

* PG 900 The Public Health Workforce Corps includes veterinarians.

* PG 901 The Public Health Workforce Corps WILL include commissioned Regular and Reserve Officers. HC Draft?

* PG 910 The government will develop, build, and run Public Health Training Centers.

* PG 913-914 Government starts a health care affirmative action program thru guise of diversity scholarships.

* PG 915 SEC. 2251. Government MANDDATES Cultural and linguistic competency training for health care professionals.

* Pg 932 The Government will establish Preventative and Wellness Trust fund- initial cost of $30,800,000,000 billion.

* PG 935 21-22 Government will identify specific goals & objectives for prevention & wellness activities. That means controlling YOU!!

* PG 936 Government will develop "Healthy People and National Public Health Performance Standards" Tell me what to eat?

* PG 942 Lines 22-25 More government? Offices of Surgeon General -Public Health Svc, Minority Health, Women’s Health

* PG 950- 980 BIG GOVERNMENT core pub health infrastructure including workforce capacity, lab systems, health info sys, etc.

* PG 993 Government will establish school based health clinics. Your kids won’t have a chance.

* PG 994 School Based Health Clinic will be integrated into the school environment. Say government brainwash!

* PG 1001 The government will establish a National Medical Device Registry. Will you be tracked?

 

bighugelabs.com/onblack.php?id=3719574887&size=large&...

 

Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The first case was identified in Wuhan, China, in December 2019. The disease has since spread worldwide, leading to an ongoing pandemic.

 

Symptoms of COVID-19 are variable, but often include fever, cough, fatigue, breathing difficulties, and loss of smell and taste. Symptoms begin one to fourteen days after exposure to the virus. Of those people who develop noticeable symptoms, most (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging), and 5% suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction). Older people are more likely to have severe symptoms. At least a third of the people who are infected with the virus remain asymptomatic and do not develop noticeable symptoms at any point in time, but they still can spread the disease.[ Around 20% of those people will remain asymptomatic throughout infection, and the rest will develop symptoms later on, becoming pre-symptomatic rather than asymptomatic and therefore having a higher risk of transmitting the virus to others. Some people continue to experience a range of effects—known as long COVID—for months after recovery, and damage to organs has been observed. Multi-year studies are underway to further investigate the long-term effects of the disease.

 

The virus that causes COVID-19 spreads mainly when an infected person is in close contact[a] with another person. Small droplets and aerosols containing the virus can spread from an infected person's nose and mouth as they breathe, cough, sneeze, sing, or speak. Other people are infected if the virus gets into their mouth, nose or eyes. The virus may also spread via contaminated surfaces, although this is not thought to be the main route of transmission. The exact route of transmission is rarely proven conclusively, but infection mainly happens when people are near each other for long enough. People who are infected can transmit the virus to another person up to two days before they themselves show symptoms, as can people who do not experience symptoms. People remain infectious for up to ten days after the onset of symptoms in moderate cases and up to 20 days in severe cases. Several testing methods have been developed to diagnose the disease. The standard diagnostic method is by detection of the virus' nucleic acid by real-time reverse transcription polymerase chain reaction (rRT-PCR), transcription-mediated amplification (TMA), or by reverse transcription loop-mediated isothermal amplification (RT-LAMP) from a nasopharyngeal swab.

 

Preventive measures include physical or social distancing, quarantining, ventilation of indoor spaces, covering coughs and sneezes, hand washing, and keeping unwashed hands away from the face. The use of face masks or coverings has been recommended in public settings to minimise the risk of transmissions. Several vaccines have been developed and several countries have initiated mass vaccination campaigns.

 

Although work is underway to develop drugs that inhibit the virus, the primary treatment is currently symptomatic. Management involves the treatment of symptoms, supportive care, isolation, and experimental measures.

 

SIGNS AND SYSTOMS

Symptoms of COVID-19 are variable, ranging from mild symptoms to severe illness. Common symptoms include headache, loss of smell and taste, nasal congestion and rhinorrhea, cough, muscle pain, sore throat, fever, diarrhea, and breathing difficulties. People with the same infection may have different symptoms, and their symptoms may change over time. Three common clusters of symptoms have been identified: one respiratory symptom cluster with cough, sputum, shortness of breath, and fever; a musculoskeletal symptom cluster with muscle and joint pain, headache, and fatigue; a cluster of digestive symptoms with abdominal pain, vomiting, and diarrhea. In people without prior ear, nose, and throat disorders, loss of taste combined with loss of smell is associated with COVID-19.

 

Most people (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging) and 5% of patients suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction). At least a third of the people who are infected with the virus do not develop noticeable symptoms at any point in time. These asymptomatic carriers tend not to get tested and can spread the disease. Other infected people will develop symptoms later, called "pre-symptomatic", or have very mild symptoms and can also spread the virus.

 

As is common with infections, there is a delay between the moment a person first becomes infected and the appearance of the first symptoms. The median delay for COVID-19 is four to five days. Most symptomatic people experience symptoms within two to seven days after exposure, and almost all will experience at least one symptom within 12 days.

Most people recover from the acute phase of the disease. However, some people continue to experience a range of effects for months after recovery—named long COVID—and damage to organs has been observed. Multi-year studies are underway to further investigate the long-term effects of the disease.

 

CAUSE

TRANSMISSION

Coronavirus disease 2019 (COVID-19) spreads from person to person mainly through the respiratory route after an infected person coughs, sneezes, sings, talks or breathes. A new infection occurs when virus-containing particles exhaled by an infected person, either respiratory droplets or aerosols, get into the mouth, nose, or eyes of other people who are in close contact with the infected person. During human-to-human transmission, an average 1000 infectious SARS-CoV-2 virions are thought to initiate a new infection.

 

The closer people interact, and the longer they interact, the more likely they are to transmit COVID-19. Closer distances can involve larger droplets (which fall to the ground) and aerosols, whereas longer distances only involve aerosols. Larger droplets can also turn into aerosols (known as droplet nuclei) through evaporation. The relative importance of the larger droplets and the aerosols is not clear as of November 2020; however, the virus is not known to spread between rooms over long distances such as through air ducts. Airborne transmission is able to particularly occur indoors, in high risk locations such as restaurants, choirs, gyms, nightclubs, offices, and religious venues, often when they are crowded or less ventilated. It also occurs in healthcare settings, often when aerosol-generating medical procedures are performed on COVID-19 patients.

 

Although it is considered possible there is no direct evidence of the virus being transmitted by skin to skin contact. A person could get COVID-19 indirectly by touching a contaminated surface or object before touching their own mouth, nose, or eyes, though this is not thought to be the main way the virus spreads. The virus is not known to spread through feces, urine, breast milk, food, wastewater, drinking water, or via animal disease vectors (although some animals can contract the virus from humans). It very rarely transmits from mother to baby during pregnancy.

 

Social distancing and the wearing of cloth face masks, surgical masks, respirators, or other face coverings are controls for droplet transmission. Transmission may be decreased indoors with well maintained heating and ventilation systems to maintain good air circulation and increase the use of outdoor air.

 

The number of people generally infected by one infected person varies. Coronavirus disease 2019 is more infectious than influenza, but less so than measles. It often spreads in clusters, where infections can be traced back to an index case or geographical location. There is a major role of "super-spreading events", where many people are infected by one person.

 

A person who is infected can transmit the virus to others up to two days before they themselves show symptoms, and even if symptoms never appear. People remain infectious in moderate cases for 7–12 days, and up to two weeks in severe cases. In October 2020, medical scientists reported evidence of reinfection in one person.

 

VIROLOGY

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel severe acute respiratory syndrome coronavirus. It was first isolated from three people with pneumonia connected to the cluster of acute respiratory illness cases in Wuhan. All structural features of the novel SARS-CoV-2 virus particle occur in related coronaviruses in nature.

 

Outside the human body, the virus is destroyed by household soap, which bursts its protective bubble.

 

SARS-CoV-2 is closely related to the original SARS-CoV. It is thought to have an animal (zoonotic) origin. Genetic analysis has revealed that the coronavirus genetically clusters with the genus Betacoronavirus, in subgenus Sarbecovirus (lineage B) together with two bat-derived strains. It is 96% identical at the whole genome level to other bat coronavirus samples (BatCov RaTG13). The structural proteins of SARS-CoV-2 include membrane glycoprotein (M), envelope protein (E), nucleocapsid protein (N), and the spike protein (S). The M protein of SARS-CoV-2 is about 98% similar to the M protein of bat SARS-CoV, maintains around 98% homology with pangolin SARS-CoV, and has 90% homology with the M protein of SARS-CoV; whereas, the similarity is only around 38% with the M protein of MERS-CoV. The structure of the M protein resembles the sugar transporter SemiSWEET.

 

The many thousands of SARS-CoV-2 variants are grouped into clades. Several different clade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR).

 

Several notable variants of SARS-CoV-2 emerged in late 2020. Cluster 5 emerged among minks and mink farmers in Denmark. After strict quarantines and a mink euthanasia campaign, it is believed to have been eradicated. The Variant of Concern 202012/01 (VOC 202012/01) is believed to have emerged in the United Kingdom in September. The 501Y.V2 Variant, which has the same N501Y mutation, arose independently in South Africa.

 

SARS-CoV-2 VARIANTS

Three known variants of SARS-CoV-2 are currently spreading among global populations as of January 2021 including the UK Variant (referred to as B.1.1.7) first found in London and Kent, a variant discovered in South Africa (referred to as 1.351), and a variant discovered in Brazil (referred to as P.1).

 

Using Whole Genome Sequencing, epidemiology and modelling suggest the new UK variant ‘VUI – 202012/01’ (the first Variant Under Investigation in December 2020) transmits more easily than other strains.

 

PATHOPHYSIOLOGY

COVID-19 can affect the upper respiratory tract (sinuses, nose, and throat) and the lower respiratory tract (windpipe and lungs). The lungs are the organs most affected by COVID-19 because the virus accesses host cells via the enzyme angiotensin-converting enzyme 2 (ACE2), which is most abundant in type II alveolar cells of the lungs. The virus uses a special surface glycoprotein called a "spike" (peplomer) to connect to ACE2 and enter the host cell. The density of ACE2 in each tissue correlates with the severity of the disease in that tissue and decreasing ACE2 activity might be protective, though another view is that increasing ACE2 using angiotensin II receptor blocker medications could be protective. As the alveolar disease progresses, respiratory failure might develop and death may follow.

 

Whether SARS-CoV-2 is able to invade the nervous system remains unknown. The virus is not detected in the CNS of the majority of COVID-19 people with neurological issues. However, SARS-CoV-2 has been detected at low levels in the brains of those who have died from COVID-19, but these results need to be confirmed. SARS-CoV-2 could cause respiratory failure through affecting the brain stem as other coronaviruses have been found to invade the CNS. While virus has been detected in cerebrospinal fluid of autopsies, the exact mechanism by which it invades the CNS remains unclear and may first involve invasion of peripheral nerves given the low levels of ACE2 in the brain. The virus may also enter the bloodstream from the lungs and cross the blood-brain barrier to gain access to the CNS, possibly within an infected white blood cell.

 

The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium as well as endothelial cells and enterocytes of the small intestine.

 

The virus can cause acute myocardial injury and chronic damage to the cardiovascular system. An acute cardiac injury was found in 12% of infected people admitted to the hospital in Wuhan, China, and is more frequent in severe disease. Rates of cardiovascular symptoms are high, owing to the systemic inflammatory response and immune system disorders during disease progression, but acute myocardial injuries may also be related to ACE2 receptors in the heart. ACE2 receptors are highly expressed in the heart and are involved in heart function. A high incidence of thrombosis and venous thromboembolism have been found people transferred to Intensive care unit (ICU) with COVID-19 infections, and may be related to poor prognosis. Blood vessel dysfunction and clot formation (as suggested by high D-dimer levels caused by blood clots) are thought to play a significant role in mortality, incidences of clots leading to pulmonary embolisms, and ischaemic events within the brain have been noted as complications leading to death in people infected with SARS-CoV-2. Infection appears to set off a chain of vasoconstrictive responses within the body, constriction of blood vessels within the pulmonary circulation has also been posited as a mechanism in which oxygenation decreases alongside the presentation of viral pneumonia. Furthermore, microvascular blood vessel damage has been reported in a small number of tissue samples of the brains – without detected SARS-CoV-2 – and the olfactory bulbs from those who have died from COVID-19.

 

Another common cause of death is complications related to the kidneys. Early reports show that up to 30% of hospitalized patients both in China and in New York have experienced some injury to their kidneys, including some persons with no previous kidney problems.

 

Autopsies of people who died of COVID-19 have found diffuse alveolar damage, and lymphocyte-containing inflammatory infiltrates within the lung.

 

IMMUNOPATHOLOGY

Although SARS-CoV-2 has a tropism for ACE2-expressing epithelial cells of the respiratory tract, people with severe COVID-19 have symptoms of systemic hyperinflammation. Clinical laboratory findings of elevated IL-2, IL-7, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-γ inducible protein 10 (IP-10), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1-α (MIP-1α), and tumour necrosis factor-α (TNF-α) indicative of cytokine release syndrome (CRS) suggest an underlying immunopathology.

 

Additionally, people with COVID-19 and acute respiratory distress syndrome (ARDS) have classical serum biomarkers of CRS, including elevated C-reactive protein (CRP), lactate dehydrogenase (LDH), D-dimer, and ferritin.

 

Systemic inflammation results in vasodilation, allowing inflammatory lymphocytic and monocytic infiltration of the lung and the heart. In particular, pathogenic GM-CSF-secreting T-cells were shown to correlate with the recruitment of inflammatory IL-6-secreting monocytes and severe lung pathology in people with COVID-19 . Lymphocytic infiltrates have also been reported at autopsy.

 

VIRAL AND HOST FACTORS

VIRUS PROTEINS

Multiple viral and host factors affect the pathogenesis of the virus. The S-protein, otherwise known as the spike protein, is the viral component that attaches to the host receptor via the ACE2 receptors. It includes two subunits: S1 and S2. S1 determines the virus host range and cellular tropism via the receptor binding domain. S2 mediates the membrane fusion of the virus to its potential cell host via the H1 and HR2, which are heptad repeat regions. Studies have shown that S1 domain induced IgG and IgA antibody levels at a much higher capacity. It is the focus spike proteins expression that are involved in many effective COVID-19 vaccines.

 

The M protein is the viral protein responsible for the transmembrane transport of nutrients. It is the cause of the bud release and the formation of the viral envelope. The N and E protein are accessory proteins that interfere with the host's immune response.

 

HOST FACTORS

Human angiotensin converting enzyme 2 (hACE2) is the host factor that SARS-COV2 virus targets causing COVID-19. Theoretically the usage of angiotensin receptor blockers (ARB) and ACE inhibitors upregulating ACE2 expression might increase morbidity with COVID-19, though animal data suggest some potential protective effect of ARB. However no clinical studies have proven susceptibility or outcomes. Until further data is available, guidelines and recommendations for hypertensive patients remain.

 

The virus' effect on ACE2 cell surfaces leads to leukocytic infiltration, increased blood vessel permeability, alveolar wall permeability, as well as decreased secretion of lung surfactants. These effects cause the majority of the respiratory symptoms. However, the aggravation of local inflammation causes a cytokine storm eventually leading to a systemic inflammatory response syndrome.

 

HOST CYTOKINE RESPONSE

The severity of the inflammation can be attributed to the severity of what is known as the cytokine storm. Levels of interleukin 1B, interferon-gamma, interferon-inducible protein 10, and monocyte chemoattractant protein 1 were all associated with COVID-19 disease severity. Treatment has been proposed to combat the cytokine storm as it remains to be one of the leading causes of morbidity and mortality in COVID-19 disease.

 

A cytokine storm is due to an acute hyperinflammatory response that is responsible for clinical illness in an array of diseases but in COVID-19, it is related to worse prognosis and increased fatality. The storm causes the acute respiratory distress syndrome, blood clotting events such as strokes, myocardial infarction, encephalitis, acute kidney injury, and vasculitis. The production of IL-1, IL-2, IL-6, TNF-alpha, and interferon-gamma, all crucial components of normal immune responses, inadvertently become the causes of a cytokine storm. The cells of the central nervous system, the microglia, neurons, and astrocytes, are also be involved in the release of pro-inflammatory cytokines affecting the nervous system, and effects of cytokine storms toward the CNS are not uncommon.

 

DIAGNOSIS

COVID-19 can provisionally be diagnosed on the basis of symptoms and confirmed using reverse transcription polymerase chain reaction (RT-PCR) or other nucleic acid testing of infected secretions. Along with laboratory testing, chest CT scans may be helpful to diagnose COVID-19 in individuals with a high clinical suspicion of infection. Detection of a past infection is possible with serological tests, which detect antibodies produced by the body in response to the infection.

 

VIRAL TESTING

The standard methods of testing for presence of SARS-CoV-2 are nucleic acid tests, which detects the presence of viral RNA fragments. As these tests detect RNA but not infectious virus, its "ability to determine duration of infectivity of patients is limited." The test is typically done on respiratory samples obtained by a nasopharyngeal swab; however, a nasal swab or sputum sample may also be used. Results are generally available within hours. The WHO has published several testing protocols for the disease.

 

A number of laboratories and companies have developed serological tests, which detect antibodies produced by the body in response to infection. Several have been evaluated by Public Health England and approved for use in the UK.

 

The University of Oxford's CEBM has pointed to mounting evidence that "a good proportion of 'new' mild cases and people re-testing positives after quarantine or discharge from hospital are not infectious, but are simply clearing harmless virus particles which their immune system has efficiently dealt with" and have called for "an international effort to standardize and periodically calibrate testing" On 7 September, the UK government issued "guidance for procedures to be implemented in laboratories to provide assurance of positive SARS-CoV-2 RNA results during periods of low prevalence, when there is a reduction in the predictive value of positive test results."

 

IMAGING

Chest CT scans may be helpful to diagnose COVID-19 in individuals with a high clinical suspicion of infection but are not recommended for routine screening. Bilateral multilobar ground-glass opacities with a peripheral, asymmetric, and posterior distribution are common in early infection. Subpleural dominance, crazy paving (lobular septal thickening with variable alveolar filling), and consolidation may appear as the disease progresses. Characteristic imaging features on chest radiographs and computed tomography (CT) of people who are symptomatic include asymmetric peripheral ground-glass opacities without pleural effusions.

 

Many groups have created COVID-19 datasets that include imagery such as the Italian Radiological Society which has compiled an international online database of imaging findings for confirmed cases. Due to overlap with other infections such as adenovirus, imaging without confirmation by rRT-PCR is of limited specificity in identifying COVID-19. A large study in China compared chest CT results to PCR and demonstrated that though imaging is less specific for the infection, it is faster and more sensitive.

Coding

In late 2019, the WHO assigned emergency ICD-10 disease codes U07.1 for deaths from lab-confirmed SARS-CoV-2 infection and U07.2 for deaths from clinically or epidemiologically diagnosed COVID-19 without lab-confirmed SARS-CoV-2 infection.

 

PATHOLOGY

The main pathological findings at autopsy are:

 

Macroscopy: pericarditis, lung consolidation and pulmonary oedema

Lung findings:

minor serous exudation, minor fibrin exudation

pulmonary oedema, pneumocyte hyperplasia, large atypical pneumocytes, interstitial inflammation with lymphocytic infiltration and multinucleated giant cell formation

diffuse alveolar damage (DAD) with diffuse alveolar exudates. DAD is the cause of acute respiratory distress syndrome (ARDS) and severe hypoxemia.

organisation of exudates in alveolar cavities and pulmonary interstitial fibrosis

plasmocytosis in BAL

Blood: disseminated intravascular coagulation (DIC); leukoerythroblastic reaction

Liver: microvesicular steatosis

 

PREVENTION

Preventive measures to reduce the chances of infection include staying at home, wearing a mask in public, avoiding crowded places, keeping distance from others, ventilating indoor spaces, washing hands with soap and water often and for at least 20 seconds, practising good respiratory hygiene, and avoiding touching the eyes, nose, or mouth with unwashed hands.

 

Those diagnosed with COVID-19 or who believe they may be infected are advised by the CDC to stay home except to get medical care, call ahead before visiting a healthcare provider, wear a face mask before entering the healthcare provider's office and when in any room or vehicle with another person, cover coughs and sneezes with a tissue, regularly wash hands with soap and water and avoid sharing personal household items.

 

The first COVID-19 vaccine was granted regulatory approval on 2 December by the UK medicines regulator MHRA. It was evaluated for emergency use authorization (EUA) status by the US FDA, and in several other countries. Initially, the US National Institutes of Health guidelines do not recommend any medication for prevention of COVID-19, before or after exposure to the SARS-CoV-2 virus, outside the setting of a clinical trial. Without a vaccine, other prophylactic measures, or effective treatments, a key part of managing COVID-19 is trying to decrease and delay the epidemic peak, known as "flattening the curve". This is done by slowing the infection rate to decrease the risk of health services being overwhelmed, allowing for better treatment of current cases, and delaying additional cases until effective treatments or a vaccine become available.

 

VACCINE

A COVID‑19 vaccine is a vaccine intended to provide acquired immunity against severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2), the virus causing coronavirus disease 2019 (COVID‑19). Prior to the COVID‑19 pandemic, there was an established body of knowledge about the structure and function of coronaviruses causing diseases like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), which enabled accelerated development of various vaccine technologies during early 2020. On 10 January 2020, the SARS-CoV-2 genetic sequence data was shared through GISAID, and by 19 March, the global pharmaceutical industry announced a major commitment to address COVID-19.

 

In Phase III trials, several COVID‑19 vaccines have demonstrated efficacy as high as 95% in preventing symptomatic COVID‑19 infections. As of March 2021, 12 vaccines were authorized by at least one national regulatory authority for public use: two RNA vaccines (the Pfizer–BioNTech vaccine and the Moderna vaccine), four conventional inactivated vaccines (BBIBP-CorV, CoronaVac, Covaxin, and CoviVac), four viral vector vaccines (Sputnik V, the Oxford–AstraZeneca vaccine, Convidicea, and the Johnson & Johnson vaccine), and two protein subunit vaccines (EpiVacCorona and RBD-Dimer). In total, as of March 2021, 308 vaccine candidates were in various stages of development, with 73 in clinical research, including 24 in Phase I trials, 33 in Phase I–II trials, and 16 in Phase III development.

Many countries have implemented phased distribution plans that prioritize those at highest risk of complications, such as the elderly, and those at high risk of exposure and transmission, such as healthcare workers. As of 17 March 2021, 400.22 million doses of COVID‑19 vaccine have been administered worldwide based on official reports from national health agencies. AstraZeneca-Oxford anticipates producing 3 billion doses in 2021, Pfizer-BioNTech 1.3 billion doses, and Sputnik V, Sinopharm, Sinovac, and Johnson & Johnson 1 billion doses each. Moderna targets producing 600 million doses and Convidicea 500 million doses in 2021. By December 2020, more than 10 billion vaccine doses had been preordered by countries, with about half of the doses purchased by high-income countries comprising 14% of the world's population.

 

SOCIAL DISTANCING

Social distancing (also known as physical distancing) includes infection control actions intended to slow the spread of the disease by minimising close contact between individuals. Methods include quarantines; travel restrictions; and the closing of schools, workplaces, stadiums, theatres, or shopping centres. Individuals may apply social distancing methods by staying at home, limiting travel, avoiding crowded areas, using no-contact greetings, and physically distancing themselves from others. Many governments are now mandating or recommending social distancing in regions affected by the outbreak.

 

Outbreaks have occurred in prisons due to crowding and an inability to enforce adequate social distancing. In the United States, the prisoner population is aging and many of them are at high risk for poor outcomes from COVID-19 due to high rates of coexisting heart and lung disease, and poor access to high-quality healthcare.

 

SELF-ISOLATION

Self-isolation at home has been recommended for those diagnosed with COVID-19 and those who suspect they have been infected. Health agencies have issued detailed instructions for proper self-isolation. Many governments have mandated or recommended self-quarantine for entire populations. The strongest self-quarantine instructions have been issued to those in high-risk groups. Those who may have been exposed to someone with COVID-19 and those who have recently travelled to a country or region with the widespread transmission have been advised to self-quarantine for 14 days from the time of last possible exposure.

Face masks and respiratory hygiene

 

The WHO and the US CDC recommend individuals wear non-medical face coverings in public settings where there is an increased risk of transmission and where social distancing measures are difficult to maintain. This recommendation is meant to reduce the spread of the disease by asymptomatic and pre-symptomatic individuals and is complementary to established preventive measures such as social distancing. Face coverings limit the volume and travel distance of expiratory droplets dispersed when talking, breathing, and coughing. A face covering without vents or holes will also filter out particles containing the virus from inhaled and exhaled air, reducing the chances of infection. But, if the mask include an exhalation valve, a wearer that is infected (maybe without having noticed that, and asymptomatic) would transmit the virus outwards through it, despite any certification they can have. So the masks with exhalation valve are not for the infected wearers, and are not reliable to stop the pandemic in a large scale. Many countries and local jurisdictions encourage or mandate the use of face masks or cloth face coverings by members of the public to limit the spread of the virus.

 

Masks are also strongly recommended for those who may have been infected and those taking care of someone who may have the disease. When not wearing a mask, the CDC recommends covering the mouth and nose with a tissue when coughing or sneezing and recommends using the inside of the elbow if no tissue is available. Proper hand hygiene after any cough or sneeze is encouraged. Healthcare professionals interacting directly with people who have COVID-19 are advised to use respirators at least as protective as NIOSH-certified N95 or equivalent, in addition to other personal protective equipment.

 

HAND-WASHING AND HYGIENE

Thorough hand hygiene after any cough or sneeze is required. The WHO also recommends that individuals wash hands often with soap and water for at least 20 seconds, especially after going to the toilet or when hands are visibly dirty, before eating and after blowing one's nose. The CDC recommends using an alcohol-based hand sanitiser with at least 60% alcohol, but only when soap and water are not readily available. For areas where commercial hand sanitisers are not readily available, the WHO provides two formulations for local production. In these formulations, the antimicrobial activity arises from ethanol or isopropanol. Hydrogen peroxide is used to help eliminate bacterial spores in the alcohol; it is "not an active substance for hand antisepsis". Glycerol is added as a humectant.

 

SURFACE CLEANING

After being expelled from the body, coronaviruses can survive on surfaces for hours to days. If a person touches the dirty surface, they may deposit the virus at the eyes, nose, or mouth where it can enter the body cause infection. Current evidence indicates that contact with infected surfaces is not the main driver of Covid-19, leading to recommendations for optimised disinfection procedures to avoid issues such as the increase of antimicrobial resistance through the use of inappropriate cleaning products and processes. Deep cleaning and other surface sanitation has been criticized as hygiene theater, giving a false sense of security against something primarily spread through the air.

 

The amount of time that the virus can survive depends significantly on the type of surface, the temperature, and the humidity. Coronaviruses die very quickly when exposed to the UV light in sunlight. Like other enveloped viruses, SARS-CoV-2 survives longest when the temperature is at room temperature or lower, and when the relative humidity is low (<50%).

 

On many surfaces, including as glass, some types of plastic, stainless steel, and skin, the virus can remain infective for several days indoors at room temperature, or even about a week under ideal conditions. On some surfaces, including cotton fabric and copper, the virus usually dies after a few hours. As a general rule of thumb, the virus dies faster on porous surfaces than on non-porous surfaces.

However, this rule is not absolute, and of the many surfaces tested, two with the longest survival times are N95 respirator masks and surgical masks, both of which are considered porous surfaces.

 

Surfaces may be decontaminated with 62–71 percent ethanol, 50–100 percent isopropanol, 0.1 percent sodium hypochlorite, 0.5 percent hydrogen peroxide, and 0.2–7.5 percent povidone-iodine. Other solutions, such as benzalkonium chloride and chlorhexidine gluconate, are less effective. Ultraviolet germicidal irradiation may also be used. The CDC recommends that if a COVID-19 case is suspected or confirmed at a facility such as an office or day care, all areas such as offices, bathrooms, common areas, shared electronic equipment like tablets, touch screens, keyboards, remote controls, and ATM machines used by the ill persons should be disinfected. A datasheet comprising the authorised substances to disinfection in the food industry (including suspension or surface tested, kind of surface, use dilution, disinfectant and inocuylum volumes) can be seen in the supplementary material of.

 

VENTILATION AND AIR FILTRATION

The WHO recommends ventilation and air filtration in public spaces to help clear out infectious aerosols.

 

HEALTHY DIET AND LIFESTYLE

The Harvard T.H. Chan School of Public Health recommends a healthy diet, being physically active, managing psychological stress, and getting enough sleep.

 

While there is no evidence that vitamin D is an effective treatment for COVID-19, there is limited evidence that vitamin D deficiency increases the risk of severe COVID-19 symptoms. This has led to recommendations for individuals with vitamin D deficiency to take vitamin D supplements as a way of mitigating the risk of COVID-19 and other health issues associated with a possible increase in deficiency due to social distancing.

 

TREATMENT

There is no specific, effective treatment or cure for coronavirus disease 2019 (COVID-19), the disease caused by the SARS-CoV-2 virus. Thus, the cornerstone of management of COVID-19 is supportive care, which includes treatment to relieve symptoms, fluid therapy, oxygen support and prone positioning as needed, and medications or devices to support other affected vital organs.

 

Most cases of COVID-19 are mild. In these, supportive care includes medication such as paracetamol or NSAIDs to relieve symptoms (fever, body aches, cough), proper intake of fluids, rest, and nasal breathing. Good personal hygiene and a healthy diet are also recommended. The U.S. Centers for Disease Control and Prevention (CDC) recommend that those who suspect they are carrying the virus isolate themselves at home and wear a face mask.

 

People with more severe cases may need treatment in hospital. In those with low oxygen levels, use of the glucocorticoid dexamethasone is strongly recommended, as it can reduce the risk of death. Noninvasive ventilation and, ultimately, admission to an intensive care unit for mechanical ventilation may be required to support breathing. Extracorporeal membrane oxygenation (ECMO) has been used to address the issue of respiratory failure, but its benefits are still under consideration.

Several experimental treatments are being actively studied in clinical trials. Others were thought to be promising early in the pandemic, such as hydroxychloroquine and lopinavir/ritonavir, but later research found them to be ineffective or even harmful. Despite ongoing research, there is still not enough high-quality evidence to recommend so-called early treatment. Nevertheless, in the United States, two monoclonal antibody-based therapies are available for early use in cases thought to be at high risk of progression to severe disease. The antiviral remdesivir is available in the U.S., Canada, Australia, and several other countries, with varying restrictions; however, it is not recommended for people needing mechanical ventilation, and is discouraged altogether by the World Health Organization (WHO), due to limited evidence of its efficacy.

 

PROGNOSIS

The severity of COVID-19 varies. The disease may take a mild course with few or no symptoms, resembling other common upper respiratory diseases such as the common cold. In 3–4% of cases (7.4% for those over age 65) symptoms are severe enough to cause hospitalization. Mild cases typically recover within two weeks, while those with severe or critical diseases may take three to six weeks to recover. Among those who have died, the time from symptom onset to death has ranged from two to eight weeks. The Italian Istituto Superiore di Sanità reported that the median time between the onset of symptoms and death was twelve days, with seven being hospitalised. However, people transferred to an ICU had a median time of ten days between hospitalisation and death. Prolonged prothrombin time and elevated C-reactive protein levels on admission to the hospital are associated with severe course of COVID-19 and with a transfer to ICU.

 

Some early studies suggest 10% to 20% of people with COVID-19 will experience symptoms lasting longer than a month.[191][192] A majority of those who were admitted to hospital with severe disease report long-term problems including fatigue and shortness of breath. On 30 October 2020 WHO chief Tedros Adhanom warned that "to a significant number of people, the COVID virus poses a range of serious long-term effects". He has described the vast spectrum of COVID-19 symptoms that fluctuate over time as "really concerning." They range from fatigue, a cough and shortness of breath, to inflammation and injury of major organs – including the lungs and heart, and also neurological and psychologic effects. Symptoms often overlap and can affect any system in the body. Infected people have reported cyclical bouts of fatigue, headaches, months of complete exhaustion, mood swings, and other symptoms. Tedros has concluded that therefore herd immunity is "morally unconscionable and unfeasible".

 

In terms of hospital readmissions about 9% of 106,000 individuals had to return for hospital treatment within 2 months of discharge. The average to readmit was 8 days since first hospital visit. There are several risk factors that have been identified as being a cause of multiple admissions to a hospital facility. Among these are advanced age (above 65 years of age) and presence of a chronic condition such as diabetes, COPD, heart failure or chronic kidney disease.

 

According to scientific reviews smokers are more likely to require intensive care or die compared to non-smokers, air pollution is similarly associated with risk factors, and pre-existing heart and lung diseases and also obesity contributes to an increased health risk of COVID-19.

 

It is also assumed that those that are immunocompromised are at higher risk of getting severely sick from SARS-CoV-2. One research that looked into the COVID-19 infections in hospitalized kidney transplant recipients found a mortality rate of 11%.

See also: Impact of the COVID-19 pandemic on children

 

Children make up a small proportion of reported cases, with about 1% of cases being under 10 years and 4% aged 10–19 years. They are likely to have milder symptoms and a lower chance of severe disease than adults. A European multinational study of hospitalized children published in The Lancet on 25 June 2020 found that about 8% of children admitted to a hospital needed intensive care. Four of those 582 children (0.7%) died, but the actual mortality rate could be "substantially lower" since milder cases that did not seek medical help were not included in the study.

 

Genetics also plays an important role in the ability to fight off the disease. For instance, those that do not produce detectable type I interferons or produce auto-antibodies against these may get much sicker from COVID-19. Genetic screening is able to detect interferon effector genes.

 

Pregnant women may be at higher risk of severe COVID-19 infection based on data from other similar viruses, like SARS and MERS, but data for COVID-19 is lacking.

 

COMPLICATIONS

Complications may include pneumonia, acute respiratory distress syndrome (ARDS), multi-organ failure, septic shock, and death. Cardiovascular complications may include heart failure, arrhythmias, heart inflammation, and blood clots. Approximately 20–30% of people who present with COVID-19 have elevated liver enzymes, reflecting liver injury.

 

Neurologic manifestations include seizure, stroke, encephalitis, and Guillain–Barré syndrome (which includes loss of motor functions). Following the infection, children may develop paediatric multisystem inflammatory syndrome, which has symptoms similar to Kawasaki disease, which can be fatal. In very rare cases, acute encephalopathy can occur, and it can be considered in those who have been diagnosed with COVID-19 and have an altered mental status.

 

LONGER-TERM EFFECTS

Some early studies suggest that that 10 to 20% of people with COVID-19 will experience symptoms lasting longer than a month. A majority of those who were admitted to hospital with severe disease report long-term problems, including fatigue and shortness of breath. About 5-10% of patients admitted to hospital progress to severe or critical disease, including pneumonia and acute respiratory failure.

 

By a variety of mechanisms, the lungs are the organs most affected in COVID-19.[228] The majority of CT scans performed show lung abnormalities in people tested after 28 days of illness.

 

People with advanced age, severe disease, prolonged ICU stays, or who smoke are more likely to have long lasting effects, including pulmonary fibrosis. Overall, approximately one third of those investigated after 4 weeks will have findings of pulmonary fibrosis or reduced lung function as measured by DLCO, even in people who are asymptomatic, but with the suggestion of continuing improvement with the passing of more time.

 

IMMUNITY

The immune response by humans to CoV-2 virus occurs as a combination of the cell-mediated immunity and antibody production, just as with most other infections. Since SARS-CoV-2 has been in the human population only since December 2019, it remains unknown if the immunity is long-lasting in people who recover from the disease. The presence of neutralizing antibodies in blood strongly correlates with protection from infection, but the level of neutralizing antibody declines with time. Those with asymptomatic or mild disease had undetectable levels of neutralizing antibody two months after infection. In another study, the level of neutralizing antibody fell 4-fold 1 to 4 months after the onset of symptoms. However, the lack of antibody in the blood does not mean antibody will not be rapidly produced upon reexposure to SARS-CoV-2. Memory B cells specific for the spike and nucleocapsid proteins of SARS-CoV-2 last for at least 6 months after appearance of symptoms. Nevertheless, 15 cases of reinfection with SARS-CoV-2 have been reported using stringent CDC criteria requiring identification of a different variant from the second infection. There are likely to be many more people who have been reinfected with the virus. Herd immunity will not eliminate the virus if reinfection is common. Some other coronaviruses circulating in people are capable of reinfection after roughly a year. Nonetheless, on 3 March 2021, scientists reported that a much more contagious Covid-19 variant, Lineage P.1, first detected in Japan, and subsequently found in Brazil, as well as in several places in the United States, may be associated with Covid-19 disease reinfection after recovery from an earlier Covid-19 infection.

 

MORTALITY

Several measures are commonly used to quantify mortality. These numbers vary by region and over time and are influenced by the volume of testing, healthcare system quality, treatment options, time since the initial outbreak, and population characteristics such as age, sex, and overall health. The mortality rate reflects the number of deaths within a specific demographic group divided by the population of that demographic group. Consequently, the mortality rate reflects the prevalence as well as the severity of the disease within a given population. Mortality rates are highly correlated to age, with relatively low rates for young people and relatively high rates among the elderly.

 

The case fatality rate (CFR) reflects the number of deaths divided by the number of diagnosed cases within a given time interval. Based on Johns Hopkins University statistics, the global death-to-case ratio is 2.2% (2,685,770/121,585,388) as of 18 March 2021. The number varies by region. The CFR may not reflect the true severity of the disease, because some infected individuals remain asymptomatic or experience only mild symptoms, and hence such infections may not be included in official case reports. Moreover, the CFR may vary markedly over time and across locations due to the availability of live virus tests.

 

INFECTION FATALITY RATE

A key metric in gauging the severity of COVID-19 is the infection fatality rate (IFR), also referred to as the infection fatality ratio or infection fatality risk. This metric is calculated by dividing the total number of deaths from the disease by the total number of infected individuals; hence, in contrast to the CFR, the IFR incorporates asymptomatic and undiagnosed infections as well as reported cases.

 

CURRENT ESTIMATES

A December 2020 systematic review and meta-analysis estimated that population IFR during the first wave of the pandemic was about 0.5% to 1% in many locations (including France, Netherlands, New Zealand, and Portugal), 1% to 2% in other locations (Australia, England, Lithuania, and Spain), and exceeded 2% in Italy. That study also found that most of these differences in IFR reflected corresponding differences in the age composition of the population and age-specific infection rates; in particular, the metaregression estimate of IFR is very low for children and younger adults (e.g., 0.002% at age 10 and 0.01% at age 25) but increases progressively to 0.4% at age 55, 1.4% at age 65, 4.6% at age 75, and 15% at age 85. These results were also highlighted in a December 2020 report issued by the WHO.

 

EARLIER ESTIMATES OF IFR

At an early stage of the pandemic, the World Health Organization reported estimates of IFR between 0.3% and 1%.[ On 2 July, The WHO's chief scientist reported that the average IFR estimate presented at a two-day WHO expert forum was about 0.6%. In August, the WHO found that studies incorporating data from broad serology testing in Europe showed IFR estimates converging at approximately 0.5–1%. Firm lower limits of IFRs have been established in a number of locations such as New York City and Bergamo in Italy since the IFR cannot be less than the population fatality rate. As of 10 July, in New York City, with a population of 8.4 million, 23,377 individuals (18,758 confirmed and 4,619 probable) have died with COVID-19 (0.3% of the population).Antibody testing in New York City suggested an IFR of ~0.9%,[258] and ~1.4%. In Bergamo province, 0.6% of the population has died. In September 2020 the U.S. Center for Disease Control & Prevention reported preliminary estimates of age-specific IFRs for public health planning purposes.

 

SEX DIFFERENCES

Early reviews of epidemiologic data showed gendered impact of the pandemic and a higher mortality rate in men in China and Italy. The Chinese Center for Disease Control and Prevention reported the death rate was 2.8% for men and 1.7% for women. Later reviews in June 2020 indicated that there is no significant difference in susceptibility or in CFR between genders. One review acknowledges the different mortality rates in Chinese men, suggesting that it may be attributable to lifestyle choices such as smoking and drinking alcohol rather than genetic factors. Sex-based immunological differences, lesser prevalence of smoking in women and men developing co-morbid conditions such as hypertension at a younger age than women could have contributed to the higher mortality in men. In Europe, 57% of the infected people were men and 72% of those died with COVID-19 were men. As of April 2020, the US government is not tracking sex-related data of COVID-19 infections. Research has shown that viral illnesses like Ebola, HIV, influenza and SARS affect men and women differently.

 

ETHNIC DIFFERENCES

In the US, a greater proportion of deaths due to COVID-19 have occurred among African Americans and other minority groups. Structural factors that prevent them from practicing social distancing include their concentration in crowded substandard housing and in "essential" occupations such as retail grocery workers, public transit employees, health-care workers and custodial staff. Greater prevalence of lacking health insurance and care and of underlying conditions such as diabetes, hypertension and heart disease also increase their risk of death. Similar issues affect Native American and Latino communities. According to a US health policy non-profit, 34% of American Indian and Alaska Native People (AIAN) non-elderly adults are at risk of serious illness compared to 21% of white non-elderly adults. The source attributes it to disproportionately high rates of many health conditions that may put them at higher risk as well as living conditions like lack of access to clean water. Leaders have called for efforts to research and address the disparities. In the U.K., a greater proportion of deaths due to COVID-19 have occurred in those of a Black, Asian, and other ethnic minority background. More severe impacts upon victims including the relative incidence of the necessity of hospitalization requirements, and vulnerability to the disease has been associated via DNA analysis to be expressed in genetic variants at chromosomal region 3, features that are associated with European Neanderthal heritage. That structure imposes greater risks that those affected will develop a more severe form of the disease. The findings are from Professor Svante Pääbo and researchers he leads at the Max Planck Institute for Evolutionary Anthropology and the Karolinska Institutet. This admixture of modern human and Neanderthal genes is estimated to have occurred roughly between 50,000 and 60,000 years ago in Southern Europe.

 

COMORBIDITIES

Most of those who die of COVID-19 have pre-existing (underlying) conditions, including hypertension, diabetes mellitus, and cardiovascular disease. According to March data from the United States, 89% of those hospitalised had preexisting conditions. The Italian Istituto Superiore di Sanità reported that out of 8.8% of deaths where medical charts were available, 96.1% of people had at least one comorbidity with the average person having 3.4 diseases. According to this report the most common comorbidities are hypertension (66% of deaths), type 2 diabetes (29.8% of deaths), Ischemic Heart Disease (27.6% of deaths), atrial fibrillation (23.1% of deaths) and chronic renal failure (20.2% of deaths).

 

Most critical respiratory comorbidities according to the CDC, are: moderate or severe asthma, pre-existing COPD, pulmonary fibrosis, cystic fibrosis. Evidence stemming from meta-analysis of several smaller research papers also suggests that smoking can be associated with worse outcomes. When someone with existing respiratory problems is infected with COVID-19, they might be at greater risk for severe symptoms. COVID-19 also poses a greater risk to people who misuse opioids and methamphetamines, insofar as their drug use may have caused lung damage.

 

In August 2020 the CDC issued a caution that tuberculosis infections could increase the risk of severe illness or death. The WHO recommended that people with respiratory symptoms be screened for both diseases, as testing positive for COVID-19 couldn't rule out co-infections. Some projections have estimated that reduced TB detection due to the pandemic could result in 6.3 million additional TB cases and 1.4 million TB related deaths by 2025.

 

NAME

During the initial outbreak in Wuhan, China, the virus and disease were commonly referred to as "coronavirus" and "Wuhan coronavirus", with the disease sometimes called "Wuhan pneumonia". In the past, many diseases have been named after geographical locations, such as the Spanish flu, Middle East Respiratory Syndrome, and Zika virus. In January 2020, the WHO recommended 2019-nCov and 2019-nCoV acute respiratory disease as interim names for the virus and disease per 2015 guidance and international guidelines against using geographical locations (e.g. Wuhan, China), animal species, or groups of people in disease and virus names in part to prevent social stigma. The official names COVID-19 and SARS-CoV-2 were issued by the WHO on 11 February 2020. Tedros Adhanom explained: CO for corona, VI for virus, D for disease and 19 for when the outbreak was first identified (31 December 2019). The WHO additionally uses "the COVID-19 virus" and "the virus responsible for COVID-19" in public communications.

 

HISTORY

The virus is thought to be natural and of an animal origin, through spillover infection. There are several theories about where the first case (the so-called patient zero) originated. Phylogenetics estimates that SARS-CoV-2 arose in October or November 2019. Evidence suggests that it descends from a coronavirus that infects wild bats, and spread to humans through an intermediary wildlife host.

 

The first known human infections were in Wuhan, Hubei, China. A study of the first 41 cases of confirmed COVID-19, published in January 2020 in The Lancet, reported the earliest date of onset of symptoms as 1 December 2019.Official publications from the WHO reported the earliest onset of symptoms as 8 December 2019. Human-to-human transmission was confirmed by the WHO and Chinese authorities by 20 January 2020. According to official Chinese sources, these were mostly linked to the Huanan Seafood Wholesale Market, which also sold live animals. In May 2020 George Gao, the director of the CDC, said animal samples collected from the seafood market had tested negative for the virus, indicating that the market was the site of an early superspreading event, but that it was not the site of the initial outbreak.[ Traces of the virus have been found in wastewater samples that were collected in Milan and Turin, Italy, on 18 December 2019.

 

By December 2019, the spread of infection was almost entirely driven by human-to-human transmission. The number of coronavirus cases in Hubei gradually increased, reaching 60 by 20 December, and at least 266 by 31 December. On 24 December, Wuhan Central Hospital sent a bronchoalveolar lavage fluid (BAL) sample from an unresolved clinical case to sequencing company Vision Medicals. On 27 and 28 December, Vision Medicals informed the Wuhan Central Hospital and the Chinese CDC of the results of the test, showing a new coronavirus. A pneumonia cluster of unknown cause was observed on 26 December and treated by the doctor Zhang Jixian in Hubei Provincial Hospital, who informed the Wuhan Jianghan CDC on 27 December. On 30 December, a test report addressed to Wuhan Central Hospital, from company CapitalBio Medlab, stated an erroneous positive result for SARS, causing a group of doctors at Wuhan Central Hospital to alert their colleagues and relevant hospital authorities of the result. The Wuhan Municipal Health Commission issued a notice to various medical institutions on "the treatment of pneumonia of unknown cause" that same evening. Eight of these doctors, including Li Wenliang (punished on 3 January), were later admonished by the police for spreading false rumours and another, Ai Fen, was reprimanded by her superiors for raising the alarm.

 

The Wuhan Municipal Health Commission made the first public announcement of a pneumonia outbreak of unknown cause on 31 December, confirming 27 cases—enough to trigger an investigation.

 

During the early stages of the outbreak, the number of cases doubled approximately every seven and a half days. In early and mid-January 2020, the virus spread to other Chinese provinces, helped by the Chinese New Year migration and Wuhan being a transport hub and major rail interchange. On 20 January, China reported nearly 140 new cases in one day, including two people in Beijing and one in Shenzhen. Later official data shows 6,174 people had already developed symptoms by then, and more may have been infected. A report in The Lancet on 24 January indicated human transmission, strongly recommended personal protective equipment for health workers, and said testing for the virus was essential due to its "pandemic potential". On 30 January, the WHO declared the coronavirus a Public Health Emergency of International Concern. By this time, the outbreak spread by a factor of 100 to 200 times.

 

Italy had its first confirmed cases on 31 January 2020, two tourists from China. As of 13 March 2020 the WHO considered Europe the active centre of the pandemic. Italy overtook China as the country with the most deaths on 19 March 2020. By 26 March the United States had overtaken China and Italy with the highest number of confirmed cases in the world. Research on coronavirus genomes indicates the majority of COVID-19 cases in New York came from European travellers, rather than directly from China or any other Asian country. Retesting of prior samples found a person in France who had the virus on 27 December 2019, and a person in the United States who died from the disease on 6 February 2020.

 

After 55 days without a locally transmitted case, Beijing reported a new COVID-19 case on 11 June 2020 which was followed by two more cases on 12 June. By 15 June there were 79 cases officially confirmed, most of them were people that went to Xinfadi Wholesale Market.

 

RT-PCR testing of untreated wastewater samples from Brazil and Italy have suggested detection of SARS-CoV-2 as early as November and December 2019, respectively, but the methods of such sewage studies have not been optimised, many have not been peer reviewed, details are often missing, and there is a risk of false positives due to contamination or if only one gene target is detected. A September 2020 review journal article said, "The possibility that the COVID-19 infection had already spread to Europe at the end of last year is now indicated by abundant, even if partially circumstantial, evidence", including pneumonia case numbers and radiology in France and Italy in November and December.

 

MISINFORMATION

After the initial outbreak of COVID-19, misinformation and disinformation regarding the origin, scale, prevention, treatment, and other aspects of the disease rapidly spread online.

 

In September 2020, the U.S. CDC published preliminary estimates of the risk of death by age groups in the United States, but those estimates were widely misreported and misunderstood.

 

OTHER ANIMALS

Humans appear to be capable of spreading the virus to some other animals, a type of disease transmission referred to as zooanthroponosis.

 

Some pets, especially cats and ferrets, can catch this virus from infected humans. Symptoms in cats include respiratory (such as a cough) and digestive symptoms. Cats can spread the virus to other cats, and may be able to spread the virus to humans, but cat-to-human transmission of SARS-CoV-2 has not been proven. Compared to cats, dogs are less susceptible to this infection. Behaviors which increase the risk of transmission include kissing, licking, and petting the animal.

 

The virus does not appear to be able to infect pigs, ducks, or chickens at all.[ Mice, rats, and rabbits, if they can be infected at all, are unlikely to be involved in spreading the virus.

 

Tigers and lions in zoos have become infected as a result of contact with infected humans. As expected, monkeys and great ape species such as orangutans can also be infected with the COVID-19 virus.

 

Minks, which are in the same family as ferrets, have been infected. Minks may be asymptomatic, and can also spread the virus to humans. Multiple countries have identified infected animals in mink farms. Denmark, a major producer of mink pelts, ordered the slaughter of all minks over fears of viral mutations. A vaccine for mink and other animals is being researched.

 

RESEARCH

International research on vaccines and medicines in COVID-19 is underway by government organisations, academic groups, and industry researchers. The CDC has classified it to require a BSL3 grade laboratory. There has been a great deal of COVID-19 research, involving accelerated research processes and publishing shortcuts to meet the global demand.

 

As of December 2020, hundreds of clinical trials have been undertaken, with research happening on every continent except Antarctica. As of November 2020, more than 200 possible treatments had been studied in humans so far.

Transmission and prevention research

Modelling research has been conducted with several objectives, including predictions of the dynamics of transmission, diagnosis and prognosis of infection, estimation of the impact of interventions, or allocation of resources. Modelling studies are mostly based on epidemiological models, estimating the number of infected people over time under given conditions. Several other types of models have been developed and used during the COVID-19 including computational fluid dynamics models to study the flow physics of COVID-19, retrofits of crowd movement models to study occupant exposure, mobility-data based models to investigate transmission, or the use of macroeconomic models to assess the economic impact of the pandemic. Further, conceptual frameworks from crisis management research have been applied to better understand the effects of COVID-19 on organizations worldwide.

 

TREATMENT-RELATED RESEARCH

Repurposed antiviral drugs make up most of the research into COVID-19 treatments. Other candidates in trials include vasodilators, corticosteroids, immune therapies, lipoic acid, bevacizumab, and recombinant angiotensin-converting enzyme 2.

 

In March 2020, the World Health Organization (WHO) initiated the Solidarity trial to assess the treatment effects of some promising drugs: an experimental drug called remdesivir; anti-malarial drugs chloroquine and hydroxychloroquine; two anti-HIV drugs, lopinavir/ritonavir; and interferon-beta. More than 300 active clinical trials were underway as of April 2020.

 

Research on the antimalarial drugs hydroxychloroquine and chloroquine showed that they were ineffective at best, and that they may reduce the antiviral activity of remdesivir. By May 2020, France, Italy, and Belgium had banned the use of hydroxychloroquine as a COVID-19 treatment.

 

In June, initial results from the randomised RECOVERY Trial in the United Kingdom showed that dexamethasone reduced mortality by one third for people who are critically ill on ventilators and one fifth for those receiving supplemental oxygen. Because this is a well-tested and widely available treatment, it was welcomed by the WHO, which is in the process of updating treatment guidelines to include dexamethasone and other steroids. Based on those preliminary results, dexamethasone treatment has been recommended by the NIH for patients with COVID-19 who are mechanically ventilated or who require supplemental oxygen but not in patients with COVID-19 who do not require supplemental oxygen.

 

In September 2020, the WHO released updated guidance on using corticosteroids for COVID-19. The WHO recommends systemic corticosteroids rather than no systemic corticosteroids for the treatment of people with severe and critical COVID-19 (strong recommendation, based on moderate certainty evidence). The WHO suggests not to use corticosteroids in the treatment of people with non-severe COVID-19 (conditional recommendation, based on low certainty evidence). The updated guidance was based on a meta-analysis of clinical trials of critically ill COVID-19 patients.

 

WIKIPEDIA

Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The first case was identified in Wuhan, China, in December 2019. The disease has since spread worldwide, leading to an ongoing pandemic.

 

Symptoms of COVID-19 are variable, but often include fever, cough, fatigue, breathing difficulties, and loss of smell and taste. Symptoms begin one to fourteen days after exposure to the virus. Of those people who develop noticeable symptoms, most (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging), and 5% suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction). Older people are more likely to have severe symptoms. At least a third of the people who are infected with the virus remain asymptomatic and do not develop noticeable symptoms at any point in time, but they still can spread the disease.[ Around 20% of those people will remain asymptomatic throughout infection, and the rest will develop symptoms later on, becoming pre-symptomatic rather than asymptomatic and therefore having a higher risk of transmitting the virus to others. Some people continue to experience a range of effects—known as long COVID—for months after recovery, and damage to organs has been observed. Multi-year studies are underway to further investigate the long-term effects of the disease.

 

The virus that causes COVID-19 spreads mainly when an infected person is in close contact[a] with another person. Small droplets and aerosols containing the virus can spread from an infected person's nose and mouth as they breathe, cough, sneeze, sing, or speak. Other people are infected if the virus gets into their mouth, nose or eyes. The virus may also spread via contaminated surfaces, although this is not thought to be the main route of transmission. The exact route of transmission is rarely proven conclusively, but infection mainly happens when people are near each other for long enough. People who are infected can transmit the virus to another person up to two days before they themselves show symptoms, as can people who do not experience symptoms. People remain infectious for up to ten days after the onset of symptoms in moderate cases and up to 20 days in severe cases. Several testing methods have been developed to diagnose the disease. The standard diagnostic method is by detection of the virus' nucleic acid by real-time reverse transcription polymerase chain reaction (rRT-PCR), transcription-mediated amplification (TMA), or by reverse transcription loop-mediated isothermal amplification (RT-LAMP) from a nasopharyngeal swab.

 

Preventive measures include physical or social distancing, quarantining, ventilation of indoor spaces, covering coughs and sneezes, hand washing, and keeping unwashed hands away from the face. The use of face masks or coverings has been recommended in public settings to minimise the risk of transmissions. Several vaccines have been developed and several countries have initiated mass vaccination campaigns.

 

Although work is underway to develop drugs that inhibit the virus, the primary treatment is currently symptomatic. Management involves the treatment of symptoms, supportive care, isolation, and experimental measures.

 

SIGNS AND SYSTOMS

Symptoms of COVID-19 are variable, ranging from mild symptoms to severe illness. Common symptoms include headache, loss of smell and taste, nasal congestion and rhinorrhea, cough, muscle pain, sore throat, fever, diarrhea, and breathing difficulties. People with the same infection may have different symptoms, and their symptoms may change over time. Three common clusters of symptoms have been identified: one respiratory symptom cluster with cough, sputum, shortness of breath, and fever; a musculoskeletal symptom cluster with muscle and joint pain, headache, and fatigue; a cluster of digestive symptoms with abdominal pain, vomiting, and diarrhea. In people without prior ear, nose, and throat disorders, loss of taste combined with loss of smell is associated with COVID-19.

 

Most people (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging) and 5% of patients suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction). At least a third of the people who are infected with the virus do not develop noticeable symptoms at any point in time. These asymptomatic carriers tend not to get tested and can spread the disease. Other infected people will develop symptoms later, called "pre-symptomatic", or have very mild symptoms and can also spread the virus.

 

As is common with infections, there is a delay between the moment a person first becomes infected and the appearance of the first symptoms. The median delay for COVID-19 is four to five days. Most symptomatic people experience symptoms within two to seven days after exposure, and almost all will experience at least one symptom within 12 days.

Most people recover from the acute phase of the disease. However, some people continue to experience a range of effects for months after recovery—named long COVID—and damage to organs has been observed. Multi-year studies are underway to further investigate the long-term effects of the disease.

 

CAUSE

TRANSMISSION

Coronavirus disease 2019 (COVID-19) spreads from person to person mainly through the respiratory route after an infected person coughs, sneezes, sings, talks or breathes. A new infection occurs when virus-containing particles exhaled by an infected person, either respiratory droplets or aerosols, get into the mouth, nose, or eyes of other people who are in close contact with the infected person. During human-to-human transmission, an average 1000 infectious SARS-CoV-2 virions are thought to initiate a new infection.

 

The closer people interact, and the longer they interact, the more likely they are to transmit COVID-19. Closer distances can involve larger droplets (which fall to the ground) and aerosols, whereas longer distances only involve aerosols. Larger droplets can also turn into aerosols (known as droplet nuclei) through evaporation. The relative importance of the larger droplets and the aerosols is not clear as of November 2020; however, the virus is not known to spread between rooms over long distances such as through air ducts. Airborne transmission is able to particularly occur indoors, in high risk locations such as restaurants, choirs, gyms, nightclubs, offices, and religious venues, often when they are crowded or less ventilated. It also occurs in healthcare settings, often when aerosol-generating medical procedures are performed on COVID-19 patients.

 

Although it is considered possible there is no direct evidence of the virus being transmitted by skin to skin contact. A person could get COVID-19 indirectly by touching a contaminated surface or object before touching their own mouth, nose, or eyes, though this is not thought to be the main way the virus spreads. The virus is not known to spread through feces, urine, breast milk, food, wastewater, drinking water, or via animal disease vectors (although some animals can contract the virus from humans). It very rarely transmits from mother to baby during pregnancy.

 

Social distancing and the wearing of cloth face masks, surgical masks, respirators, or other face coverings are controls for droplet transmission. Transmission may be decreased indoors with well maintained heating and ventilation systems to maintain good air circulation and increase the use of outdoor air.

 

The number of people generally infected by one infected person varies. Coronavirus disease 2019 is more infectious than influenza, but less so than measles. It often spreads in clusters, where infections can be traced back to an index case or geographical location. There is a major role of "super-spreading events", where many people are infected by one person.

 

A person who is infected can transmit the virus to others up to two days before they themselves show symptoms, and even if symptoms never appear. People remain infectious in moderate cases for 7–12 days, and up to two weeks in severe cases. In October 2020, medical scientists reported evidence of reinfection in one person.

 

VIROLOGY

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel severe acute respiratory syndrome coronavirus. It was first isolated from three people with pneumonia connected to the cluster of acute respiratory illness cases in Wuhan. All structural features of the novel SARS-CoV-2 virus particle occur in related coronaviruses in nature.

 

Outside the human body, the virus is destroyed by household soap, which bursts its protective bubble.

 

SARS-CoV-2 is closely related to the original SARS-CoV. It is thought to have an animal (zoonotic) origin. Genetic analysis has revealed that the coronavirus genetically clusters with the genus Betacoronavirus, in subgenus Sarbecovirus (lineage B) together with two bat-derived strains. It is 96% identical at the whole genome level to other bat coronavirus samples (BatCov RaTG13). The structural proteins of SARS-CoV-2 include membrane glycoprotein (M), envelope protein (E), nucleocapsid protein (N), and the spike protein (S). The M protein of SARS-CoV-2 is about 98% similar to the M protein of bat SARS-CoV, maintains around 98% homology with pangolin SARS-CoV, and has 90% homology with the M protein of SARS-CoV; whereas, the similarity is only around 38% with the M protein of MERS-CoV. The structure of the M protein resembles the sugar transporter SemiSWEET.

 

The many thousands of SARS-CoV-2 variants are grouped into clades. Several different clade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR).

 

Several notable variants of SARS-CoV-2 emerged in late 2020. Cluster 5 emerged among minks and mink farmers in Denmark. After strict quarantines and a mink euthanasia campaign, it is believed to have been eradicated. The Variant of Concern 202012/01 (VOC 202012/01) is believed to have emerged in the United Kingdom in September. The 501Y.V2 Variant, which has the same N501Y mutation, arose independently in South Africa.

 

SARS-CoV-2 VARIANTS

Three known variants of SARS-CoV-2 are currently spreading among global populations as of January 2021 including the UK Variant (referred to as B.1.1.7) first found in London and Kent, a variant discovered in South Africa (referred to as 1.351), and a variant discovered in Brazil (referred to as P.1).

 

Using Whole Genome Sequencing, epidemiology and modelling suggest the new UK variant ‘VUI – 202012/01’ (the first Variant Under Investigation in December 2020) transmits more easily than other strains.

 

PATHOPHYSIOLOGY

COVID-19 can affect the upper respiratory tract (sinuses, nose, and throat) and the lower respiratory tract (windpipe and lungs). The lungs are the organs most affected by COVID-19 because the virus accesses host cells via the enzyme angiotensin-converting enzyme 2 (ACE2), which is most abundant in type II alveolar cells of the lungs. The virus uses a special surface glycoprotein called a "spike" (peplomer) to connect to ACE2 and enter the host cell. The density of ACE2 in each tissue correlates with the severity of the disease in that tissue and decreasing ACE2 activity might be protective, though another view is that increasing ACE2 using angiotensin II receptor blocker medications could be protective. As the alveolar disease progresses, respiratory failure might develop and death may follow.

 

Whether SARS-CoV-2 is able to invade the nervous system remains unknown. The virus is not detected in the CNS of the majority of COVID-19 people with neurological issues. However, SARS-CoV-2 has been detected at low levels in the brains of those who have died from COVID-19, but these results need to be confirmed. SARS-CoV-2 could cause respiratory failure through affecting the brain stem as other coronaviruses have been found to invade the CNS. While virus has been detected in cerebrospinal fluid of autopsies, the exact mechanism by which it invades the CNS remains unclear and may first involve invasion of peripheral nerves given the low levels of ACE2 in the brain. The virus may also enter the bloodstream from the lungs and cross the blood-brain barrier to gain access to the CNS, possibly within an infected white blood cell.

 

The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium as well as endothelial cells and enterocytes of the small intestine.

 

The virus can cause acute myocardial injury and chronic damage to the cardiovascular system. An acute cardiac injury was found in 12% of infected people admitted to the hospital in Wuhan, China, and is more frequent in severe disease. Rates of cardiovascular symptoms are high, owing to the systemic inflammatory response and immune system disorders during disease progression, but acute myocardial injuries may also be related to ACE2 receptors in the heart. ACE2 receptors are highly expressed in the heart and are involved in heart function. A high incidence of thrombosis and venous thromboembolism have been found people transferred to Intensive care unit (ICU) with COVID-19 infections, and may be related to poor prognosis. Blood vessel dysfunction and clot formation (as suggested by high D-dimer levels caused by blood clots) are thought to play a significant role in mortality, incidences of clots leading to pulmonary embolisms, and ischaemic events within the brain have been noted as complications leading to death in people infected with SARS-CoV-2. Infection appears to set off a chain of vasoconstrictive responses within the body, constriction of blood vessels within the pulmonary circulation has also been posited as a mechanism in which oxygenation decreases alongside the presentation of viral pneumonia. Furthermore, microvascular blood vessel damage has been reported in a small number of tissue samples of the brains – without detected SARS-CoV-2 – and the olfactory bulbs from those who have died from COVID-19.

 

Another common cause of death is complications related to the kidneys. Early reports show that up to 30% of hospitalized patients both in China and in New York have experienced some injury to their kidneys, including some persons with no previous kidney problems.

 

Autopsies of people who died of COVID-19 have found diffuse alveolar damage, and lymphocyte-containing inflammatory infiltrates within the lung.

 

IMMUNOPATHOLOGY

Although SARS-CoV-2 has a tropism for ACE2-expressing epithelial cells of the respiratory tract, people with severe COVID-19 have symptoms of systemic hyperinflammation. Clinical laboratory findings of elevated IL-2, IL-7, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-γ inducible protein 10 (IP-10), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1-α (MIP-1α), and tumour necrosis factor-α (TNF-α) indicative of cytokine release syndrome (CRS) suggest an underlying immunopathology.

 

Additionally, people with COVID-19 and acute respiratory distress syndrome (ARDS) have classical serum biomarkers of CRS, including elevated C-reactive protein (CRP), lactate dehydrogenase (LDH), D-dimer, and ferritin.

 

Systemic inflammation results in vasodilation, allowing inflammatory lymphocytic and monocytic infiltration of the lung and the heart. In particular, pathogenic GM-CSF-secreting T-cells were shown to correlate with the recruitment of inflammatory IL-6-secreting monocytes and severe lung pathology in people with COVID-19 . Lymphocytic infiltrates have also been reported at autopsy.

 

VIRAL AND HOST FACTORS

VIRUS PROTEINS

Multiple viral and host factors affect the pathogenesis of the virus. The S-protein, otherwise known as the spike protein, is the viral component that attaches to the host receptor via the ACE2 receptors. It includes two subunits: S1 and S2. S1 determines the virus host range and cellular tropism via the receptor binding domain. S2 mediates the membrane fusion of the virus to its potential cell host via the H1 and HR2, which are heptad repeat regions. Studies have shown that S1 domain induced IgG and IgA antibody levels at a much higher capacity. It is the focus spike proteins expression that are involved in many effective COVID-19 vaccines.

 

The M protein is the viral protein responsible for the transmembrane transport of nutrients. It is the cause of the bud release and the formation of the viral envelope. The N and E protein are accessory proteins that interfere with the host's immune response.

 

HOST FACTORS

Human angiotensin converting enzyme 2 (hACE2) is the host factor that SARS-COV2 virus targets causing COVID-19. Theoretically the usage of angiotensin receptor blockers (ARB) and ACE inhibitors upregulating ACE2 expression might increase morbidity with COVID-19, though animal data suggest some potential protective effect of ARB. However no clinical studies have proven susceptibility or outcomes. Until further data is available, guidelines and recommendations for hypertensive patients remain.

 

The virus' effect on ACE2 cell surfaces leads to leukocytic infiltration, increased blood vessel permeability, alveolar wall permeability, as well as decreased secretion of lung surfactants. These effects cause the majority of the respiratory symptoms. However, the aggravation of local inflammation causes a cytokine storm eventually leading to a systemic inflammatory response syndrome.

 

HOST CYTOKINE RESPONSE

The severity of the inflammation can be attributed to the severity of what is known as the cytokine storm. Levels of interleukin 1B, interferon-gamma, interferon-inducible protein 10, and monocyte chemoattractant protein 1 were all associated with COVID-19 disease severity. Treatment has been proposed to combat the cytokine storm as it remains to be one of the leading causes of morbidity and mortality in COVID-19 disease.

 

A cytokine storm is due to an acute hyperinflammatory response that is responsible for clinical illness in an array of diseases but in COVID-19, it is related to worse prognosis and increased fatality. The storm causes the acute respiratory distress syndrome, blood clotting events such as strokes, myocardial infarction, encephalitis, acute kidney injury, and vasculitis. The production of IL-1, IL-2, IL-6, TNF-alpha, and interferon-gamma, all crucial components of normal immune responses, inadvertently become the causes of a cytokine storm. The cells of the central nervous system, the microglia, neurons, and astrocytes, are also be involved in the release of pro-inflammatory cytokines affecting the nervous system, and effects of cytokine storms toward the CNS are not uncommon.

 

DIAGNOSIS

COVID-19 can provisionally be diagnosed on the basis of symptoms and confirmed using reverse transcription polymerase chain reaction (RT-PCR) or other nucleic acid testing of infected secretions. Along with laboratory testing, chest CT scans may be helpful to diagnose COVID-19 in individuals with a high clinical suspicion of infection. Detection of a past infection is possible with serological tests, which detect antibodies produced by the body in response to the infection.

 

VIRAL TESTING

The standard methods of testing for presence of SARS-CoV-2 are nucleic acid tests, which detects the presence of viral RNA fragments. As these tests detect RNA but not infectious virus, its "ability to determine duration of infectivity of patients is limited." The test is typically done on respiratory samples obtained by a nasopharyngeal swab; however, a nasal swab or sputum sample may also be used. Results are generally available within hours. The WHO has published several testing protocols for the disease.

 

A number of laboratories and companies have developed serological tests, which detect antibodies produced by the body in response to infection. Several have been evaluated by Public Health England and approved for use in the UK.

 

The University of Oxford's CEBM has pointed to mounting evidence that "a good proportion of 'new' mild cases and people re-testing positives after quarantine or discharge from hospital are not infectious, but are simply clearing harmless virus particles which their immune system has efficiently dealt with" and have called for "an international effort to standardize and periodically calibrate testing" On 7 September, the UK government issued "guidance for procedures to be implemented in laboratories to provide assurance of positive SARS-CoV-2 RNA results during periods of low prevalence, when there is a reduction in the predictive value of positive test results."

 

IMAGING

Chest CT scans may be helpful to diagnose COVID-19 in individuals with a high clinical suspicion of infection but are not recommended for routine screening. Bilateral multilobar ground-glass opacities with a peripheral, asymmetric, and posterior distribution are common in early infection. Subpleural dominance, crazy paving (lobular septal thickening with variable alveolar filling), and consolidation may appear as the disease progresses. Characteristic imaging features on chest radiographs and computed tomography (CT) of people who are symptomatic include asymmetric peripheral ground-glass opacities without pleural effusions.

 

Many groups have created COVID-19 datasets that include imagery such as the Italian Radiological Society which has compiled an international online database of imaging findings for confirmed cases. Due to overlap with other infections such as adenovirus, imaging without confirmation by rRT-PCR is of limited specificity in identifying COVID-19. A large study in China compared chest CT results to PCR and demonstrated that though imaging is less specific for the infection, it is faster and more sensitive.

Coding

In late 2019, the WHO assigned emergency ICD-10 disease codes U07.1 for deaths from lab-confirmed SARS-CoV-2 infection and U07.2 for deaths from clinically or epidemiologically diagnosed COVID-19 without lab-confirmed SARS-CoV-2 infection.

 

PATHOLOGY

The main pathological findings at autopsy are:

 

Macroscopy: pericarditis, lung consolidation and pulmonary oedema

Lung findings:

minor serous exudation, minor fibrin exudation

pulmonary oedema, pneumocyte hyperplasia, large atypical pneumocytes, interstitial inflammation with lymphocytic infiltration and multinucleated giant cell formation

diffuse alveolar damage (DAD) with diffuse alveolar exudates. DAD is the cause of acute respiratory distress syndrome (ARDS) and severe hypoxemia.

organisation of exudates in alveolar cavities and pulmonary interstitial fibrosis

plasmocytosis in BAL

Blood: disseminated intravascular coagulation (DIC); leukoerythroblastic reaction

Liver: microvesicular steatosis

 

PREVENTION

Preventive measures to reduce the chances of infection include staying at home, wearing a mask in public, avoiding crowded places, keeping distance from others, ventilating indoor spaces, washing hands with soap and water often and for at least 20 seconds, practising good respiratory hygiene, and avoiding touching the eyes, nose, or mouth with unwashed hands.

 

Those diagnosed with COVID-19 or who believe they may be infected are advised by the CDC to stay home except to get medical care, call ahead before visiting a healthcare provider, wear a face mask before entering the healthcare provider's office and when in any room or vehicle with another person, cover coughs and sneezes with a tissue, regularly wash hands with soap and water and avoid sharing personal household items.

 

The first COVID-19 vaccine was granted regulatory approval on 2 December by the UK medicines regulator MHRA. It was evaluated for emergency use authorization (EUA) status by the US FDA, and in several other countries. Initially, the US National Institutes of Health guidelines do not recommend any medication for prevention of COVID-19, before or after exposure to the SARS-CoV-2 virus, outside the setting of a clinical trial. Without a vaccine, other prophylactic measures, or effective treatments, a key part of managing COVID-19 is trying to decrease and delay the epidemic peak, known as "flattening the curve". This is done by slowing the infection rate to decrease the risk of health services being overwhelmed, allowing for better treatment of current cases, and delaying additional cases until effective treatments or a vaccine become available.

 

VACCINE

A COVID‑19 vaccine is a vaccine intended to provide acquired immunity against severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2), the virus causing coronavirus disease 2019 (COVID‑19). Prior to the COVID‑19 pandemic, there was an established body of knowledge about the structure and function of coronaviruses causing diseases like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), which enabled accelerated development of various vaccine technologies during early 2020. On 10 January 2020, the SARS-CoV-2 genetic sequence data was shared through GISAID, and by 19 March, the global pharmaceutical industry announced a major commitment to address COVID-19.

 

In Phase III trials, several COVID‑19 vaccines have demonstrated efficacy as high as 95% in preventing symptomatic COVID‑19 infections. As of March 2021, 12 vaccines were authorized by at least one national regulatory authority for public use: two RNA vaccines (the Pfizer–BioNTech vaccine and the Moderna vaccine), four conventional inactivated vaccines (BBIBP-CorV, CoronaVac, Covaxin, and CoviVac), four viral vector vaccines (Sputnik V, the Oxford–AstraZeneca vaccine, Convidicea, and the Johnson & Johnson vaccine), and two protein subunit vaccines (EpiVacCorona and RBD-Dimer). In total, as of March 2021, 308 vaccine candidates were in various stages of development, with 73 in clinical research, including 24 in Phase I trials, 33 in Phase I–II trials, and 16 in Phase III development.

Many countries have implemented phased distribution plans that prioritize those at highest risk of complications, such as the elderly, and those at high risk of exposure and transmission, such as healthcare workers. As of 17 March 2021, 400.22 million doses of COVID‑19 vaccine have been administered worldwide based on official reports from national health agencies. AstraZeneca-Oxford anticipates producing 3 billion doses in 2021, Pfizer-BioNTech 1.3 billion doses, and Sputnik V, Sinopharm, Sinovac, and Johnson & Johnson 1 billion doses each. Moderna targets producing 600 million doses and Convidicea 500 million doses in 2021. By December 2020, more than 10 billion vaccine doses had been preordered by countries, with about half of the doses purchased by high-income countries comprising 14% of the world's population.

 

SOCIAL DISTANCING

Social distancing (also known as physical distancing) includes infection control actions intended to slow the spread of the disease by minimising close contact between individuals. Methods include quarantines; travel restrictions; and the closing of schools, workplaces, stadiums, theatres, or shopping centres. Individuals may apply social distancing methods by staying at home, limiting travel, avoiding crowded areas, using no-contact greetings, and physically distancing themselves from others. Many governments are now mandating or recommending social distancing in regions affected by the outbreak.

 

Outbreaks have occurred in prisons due to crowding and an inability to enforce adequate social distancing. In the United States, the prisoner population is aging and many of them are at high risk for poor outcomes from COVID-19 due to high rates of coexisting heart and lung disease, and poor access to high-quality healthcare.

 

SELF-ISOLATION

Self-isolation at home has been recommended for those diagnosed with COVID-19 and those who suspect they have been infected. Health agencies have issued detailed instructions for proper self-isolation. Many governments have mandated or recommended self-quarantine for entire populations. The strongest self-quarantine instructions have been issued to those in high-risk groups. Those who may have been exposed to someone with COVID-19 and those who have recently travelled to a country or region with the widespread transmission have been advised to self-quarantine for 14 days from the time of last possible exposure.

Face masks and respiratory hygiene

 

The WHO and the US CDC recommend individuals wear non-medical face coverings in public settings where there is an increased risk of transmission and where social distancing measures are difficult to maintain. This recommendation is meant to reduce the spread of the disease by asymptomatic and pre-symptomatic individuals and is complementary to established preventive measures such as social distancing. Face coverings limit the volume and travel distance of expiratory droplets dispersed when talking, breathing, and coughing. A face covering without vents or holes will also filter out particles containing the virus from inhaled and exhaled air, reducing the chances of infection. But, if the mask include an exhalation valve, a wearer that is infected (maybe without having noticed that, and asymptomatic) would transmit the virus outwards through it, despite any certification they can have. So the masks with exhalation valve are not for the infected wearers, and are not reliable to stop the pandemic in a large scale. Many countries and local jurisdictions encourage or mandate the use of face masks or cloth face coverings by members of the public to limit the spread of the virus.

 

Masks are also strongly recommended for those who may have been infected and those taking care of someone who may have the disease. When not wearing a mask, the CDC recommends covering the mouth and nose with a tissue when coughing or sneezing and recommends using the inside of the elbow if no tissue is available. Proper hand hygiene after any cough or sneeze is encouraged. Healthcare professionals interacting directly with people who have COVID-19 are advised to use respirators at least as protective as NIOSH-certified N95 or equivalent, in addition to other personal protective equipment.

 

HAND-WASHING AND HYGIENE

Thorough hand hygiene after any cough or sneeze is required. The WHO also recommends that individuals wash hands often with soap and water for at least 20 seconds, especially after going to the toilet or when hands are visibly dirty, before eating and after blowing one's nose. The CDC recommends using an alcohol-based hand sanitiser with at least 60% alcohol, but only when soap and water are not readily available. For areas where commercial hand sanitisers are not readily available, the WHO provides two formulations for local production. In these formulations, the antimicrobial activity arises from ethanol or isopropanol. Hydrogen peroxide is used to help eliminate bacterial spores in the alcohol; it is "not an active substance for hand antisepsis". Glycerol is added as a humectant.

 

SURFACE CLEANING

After being expelled from the body, coronaviruses can survive on surfaces for hours to days. If a person touches the dirty surface, they may deposit the virus at the eyes, nose, or mouth where it can enter the body cause infection. Current evidence indicates that contact with infected surfaces is not the main driver of Covid-19, leading to recommendations for optimised disinfection procedures to avoid issues such as the increase of antimicrobial resistance through the use of inappropriate cleaning products and processes. Deep cleaning and other surface sanitation has been criticized as hygiene theater, giving a false sense of security against something primarily spread through the air.

 

The amount of time that the virus can survive depends significantly on the type of surface, the temperature, and the humidity. Coronaviruses die very quickly when exposed to the UV light in sunlight. Like other enveloped viruses, SARS-CoV-2 survives longest when the temperature is at room temperature or lower, and when the relative humidity is low (<50%).

 

On many surfaces, including as glass, some types of plastic, stainless steel, and skin, the virus can remain infective for several days indoors at room temperature, or even about a week under ideal conditions. On some surfaces, including cotton fabric and copper, the virus usually dies after a few hours. As a general rule of thumb, the virus dies faster on porous surfaces than on non-porous surfaces.

However, this rule is not absolute, and of the many surfaces tested, two with the longest survival times are N95 respirator masks and surgical masks, both of which are considered porous surfaces.

 

Surfaces may be decontaminated with 62–71 percent ethanol, 50–100 percent isopropanol, 0.1 percent sodium hypochlorite, 0.5 percent hydrogen peroxide, and 0.2–7.5 percent povidone-iodine. Other solutions, such as benzalkonium chloride and chlorhexidine gluconate, are less effective. Ultraviolet germicidal irradiation may also be used. The CDC recommends that if a COVID-19 case is suspected or confirmed at a facility such as an office or day care, all areas such as offices, bathrooms, common areas, shared electronic equipment like tablets, touch screens, keyboards, remote controls, and ATM machines used by the ill persons should be disinfected. A datasheet comprising the authorised substances to disinfection in the food industry (including suspension or surface tested, kind of surface, use dilution, disinfectant and inocuylum volumes) can be seen in the supplementary material of.

 

VENTILATION AND AIR FILTRATION

The WHO recommends ventilation and air filtration in public spaces to help clear out infectious aerosols.

 

HEALTHY DIET AND LIFESTYLE

The Harvard T.H. Chan School of Public Health recommends a healthy diet, being physically active, managing psychological stress, and getting enough sleep.

 

While there is no evidence that vitamin D is an effective treatment for COVID-19, there is limited evidence that vitamin D deficiency increases the risk of severe COVID-19 symptoms. This has led to recommendations for individuals with vitamin D deficiency to take vitamin D supplements as a way of mitigating the risk of COVID-19 and other health issues associated with a possible increase in deficiency due to social distancing.

 

TREATMENT

There is no specific, effective treatment or cure for coronavirus disease 2019 (COVID-19), the disease caused by the SARS-CoV-2 virus. Thus, the cornerstone of management of COVID-19 is supportive care, which includes treatment to relieve symptoms, fluid therapy, oxygen support and prone positioning as needed, and medications or devices to support other affected vital organs.

 

Most cases of COVID-19 are mild. In these, supportive care includes medication such as paracetamol or NSAIDs to relieve symptoms (fever, body aches, cough), proper intake of fluids, rest, and nasal breathing. Good personal hygiene and a healthy diet are also recommended. The U.S. Centers for Disease Control and Prevention (CDC) recommend that those who suspect they are carrying the virus isolate themselves at home and wear a face mask.

 

People with more severe cases may need treatment in hospital. In those with low oxygen levels, use of the glucocorticoid dexamethasone is strongly recommended, as it can reduce the risk of death. Noninvasive ventilation and, ultimately, admission to an intensive care unit for mechanical ventilation may be required to support breathing. Extracorporeal membrane oxygenation (ECMO) has been used to address the issue of respiratory failure, but its benefits are still under consideration.

Several experimental treatments are being actively studied in clinical trials. Others were thought to be promising early in the pandemic, such as hydroxychloroquine and lopinavir/ritonavir, but later research found them to be ineffective or even harmful. Despite ongoing research, there is still not enough high-quality evidence to recommend so-called early treatment. Nevertheless, in the United States, two monoclonal antibody-based therapies are available for early use in cases thought to be at high risk of progression to severe disease. The antiviral remdesivir is available in the U.S., Canada, Australia, and several other countries, with varying restrictions; however, it is not recommended for people needing mechanical ventilation, and is discouraged altogether by the World Health Organization (WHO), due to limited evidence of its efficacy.

 

PROGNOSIS

The severity of COVID-19 varies. The disease may take a mild course with few or no symptoms, resembling other common upper respiratory diseases such as the common cold. In 3–4% of cases (7.4% for those over age 65) symptoms are severe enough to cause hospitalization. Mild cases typically recover within two weeks, while those with severe or critical diseases may take three to six weeks to recover. Among those who have died, the time from symptom onset to death has ranged from two to eight weeks. The Italian Istituto Superiore di Sanità reported that the median time between the onset of symptoms and death was twelve days, with seven being hospitalised. However, people transferred to an ICU had a median time of ten days between hospitalisation and death. Prolonged prothrombin time and elevated C-reactive protein levels on admission to the hospital are associated with severe course of COVID-19 and with a transfer to ICU.

 

Some early studies suggest 10% to 20% of people with COVID-19 will experience symptoms lasting longer than a month.[191][192] A majority of those who were admitted to hospital with severe disease report long-term problems including fatigue and shortness of breath. On 30 October 2020 WHO chief Tedros Adhanom warned that "to a significant number of people, the COVID virus poses a range of serious long-term effects". He has described the vast spectrum of COVID-19 symptoms that fluctuate over time as "really concerning." They range from fatigue, a cough and shortness of breath, to inflammation and injury of major organs – including the lungs and heart, and also neurological and psychologic effects. Symptoms often overlap and can affect any system in the body. Infected people have reported cyclical bouts of fatigue, headaches, months of complete exhaustion, mood swings, and other symptoms. Tedros has concluded that therefore herd immunity is "morally unconscionable and unfeasible".

 

In terms of hospital readmissions about 9% of 106,000 individuals had to return for hospital treatment within 2 months of discharge. The average to readmit was 8 days since first hospital visit. There are several risk factors that have been identified as being a cause of multiple admissions to a hospital facility. Among these are advanced age (above 65 years of age) and presence of a chronic condition such as diabetes, COPD, heart failure or chronic kidney disease.

 

According to scientific reviews smokers are more likely to require intensive care or die compared to non-smokers, air pollution is similarly associated with risk factors, and pre-existing heart and lung diseases and also obesity contributes to an increased health risk of COVID-19.

 

It is also assumed that those that are immunocompromised are at higher risk of getting severely sick from SARS-CoV-2. One research that looked into the COVID-19 infections in hospitalized kidney transplant recipients found a mortality rate of 11%.

See also: Impact of the COVID-19 pandemic on children

 

Children make up a small proportion of reported cases, with about 1% of cases being under 10 years and 4% aged 10–19 years. They are likely to have milder symptoms and a lower chance of severe disease than adults. A European multinational study of hospitalized children published in The Lancet on 25 June 2020 found that about 8% of children admitted to a hospital needed intensive care. Four of those 582 children (0.7%) died, but the actual mortality rate could be "substantially lower" since milder cases that did not seek medical help were not included in the study.

 

Genetics also plays an important role in the ability to fight off the disease. For instance, those that do not produce detectable type I interferons or produce auto-antibodies against these may get much sicker from COVID-19. Genetic screening is able to detect interferon effector genes.

 

Pregnant women may be at higher risk of severe COVID-19 infection based on data from other similar viruses, like SARS and MERS, but data for COVID-19 is lacking.

 

COMPLICATIONS

Complications may include pneumonia, acute respiratory distress syndrome (ARDS), multi-organ failure, septic shock, and death. Cardiovascular complications may include heart failure, arrhythmias, heart inflammation, and blood clots. Approximately 20–30% of people who present with COVID-19 have elevated liver enzymes, reflecting liver injury.

 

Neurologic manifestations include seizure, stroke, encephalitis, and Guillain–Barré syndrome (which includes loss of motor functions). Following the infection, children may develop paediatric multisystem inflammatory syndrome, which has symptoms similar to Kawasaki disease, which can be fatal. In very rare cases, acute encephalopathy can occur, and it can be considered in those who have been diagnosed with COVID-19 and have an altered mental status.

 

LONGER-TERM EFFECTS

Some early studies suggest that that 10 to 20% of people with COVID-19 will experience symptoms lasting longer than a month. A majority of those who were admitted to hospital with severe disease report long-term problems, including fatigue and shortness of breath. About 5-10% of patients admitted to hospital progress to severe or critical disease, including pneumonia and acute respiratory failure.

 

By a variety of mechanisms, the lungs are the organs most affected in COVID-19.[228] The majority of CT scans performed show lung abnormalities in people tested after 28 days of illness.

 

People with advanced age, severe disease, prolonged ICU stays, or who smoke are more likely to have long lasting effects, including pulmonary fibrosis. Overall, approximately one third of those investigated after 4 weeks will have findings of pulmonary fibrosis or reduced lung function as measured by DLCO, even in people who are asymptomatic, but with the suggestion of continuing improvement with the passing of more time.

 

IMMUNITY

The immune response by humans to CoV-2 virus occurs as a combination of the cell-mediated immunity and antibody production, just as with most other infections. Since SARS-CoV-2 has been in the human population only since December 2019, it remains unknown if the immunity is long-lasting in people who recover from the disease. The presence of neutralizing antibodies in blood strongly correlates with protection from infection, but the level of neutralizing antibody declines with time. Those with asymptomatic or mild disease had undetectable levels of neutralizing antibody two months after infection. In another study, the level of neutralizing antibody fell 4-fold 1 to 4 months after the onset of symptoms. However, the lack of antibody in the blood does not mean antibody will not be rapidly produced upon reexposure to SARS-CoV-2. Memory B cells specific for the spike and nucleocapsid proteins of SARS-CoV-2 last for at least 6 months after appearance of symptoms. Nevertheless, 15 cases of reinfection with SARS-CoV-2 have been reported using stringent CDC criteria requiring identification of a different variant from the second infection. There are likely to be many more people who have been reinfected with the virus. Herd immunity will not eliminate the virus if reinfection is common. Some other coronaviruses circulating in people are capable of reinfection after roughly a year. Nonetheless, on 3 March 2021, scientists reported that a much more contagious Covid-19 variant, Lineage P.1, first detected in Japan, and subsequently found in Brazil, as well as in several places in the United States, may be associated with Covid-19 disease reinfection after recovery from an earlier Covid-19 infection.

 

MORTALITY

Several measures are commonly used to quantify mortality. These numbers vary by region and over time and are influenced by the volume of testing, healthcare system quality, treatment options, time since the initial outbreak, and population characteristics such as age, sex, and overall health. The mortality rate reflects the number of deaths within a specific demographic group divided by the population of that demographic group. Consequently, the mortality rate reflects the prevalence as well as the severity of the disease within a given population. Mortality rates are highly correlated to age, with relatively low rates for young people and relatively high rates among the elderly.

 

The case fatality rate (CFR) reflects the number of deaths divided by the number of diagnosed cases within a given time interval. Based on Johns Hopkins University statistics, the global death-to-case ratio is 2.2% (2,685,770/121,585,388) as of 18 March 2021. The number varies by region. The CFR may not reflect the true severity of the disease, because some infected individuals remain asymptomatic or experience only mild symptoms, and hence such infections may not be included in official case reports. Moreover, the CFR may vary markedly over time and across locations due to the availability of live virus tests.

 

INFECTION FATALITY RATE

A key metric in gauging the severity of COVID-19 is the infection fatality rate (IFR), also referred to as the infection fatality ratio or infection fatality risk. This metric is calculated by dividing the total number of deaths from the disease by the total number of infected individuals; hence, in contrast to the CFR, the IFR incorporates asymptomatic and undiagnosed infections as well as reported cases.

 

CURRENT ESTIMATES

A December 2020 systematic review and meta-analysis estimated that population IFR during the first wave of the pandemic was about 0.5% to 1% in many locations (including France, Netherlands, New Zealand, and Portugal), 1% to 2% in other locations (Australia, England, Lithuania, and Spain), and exceeded 2% in Italy. That study also found that most of these differences in IFR reflected corresponding differences in the age composition of the population and age-specific infection rates; in particular, the metaregression estimate of IFR is very low for children and younger adults (e.g., 0.002% at age 10 and 0.01% at age 25) but increases progressively to 0.4% at age 55, 1.4% at age 65, 4.6% at age 75, and 15% at age 85. These results were also highlighted in a December 2020 report issued by the WHO.

 

EARLIER ESTIMATES OF IFR

At an early stage of the pandemic, the World Health Organization reported estimates of IFR between 0.3% and 1%.[ On 2 July, The WHO's chief scientist reported that the average IFR estimate presented at a two-day WHO expert forum was about 0.6%. In August, the WHO found that studies incorporating data from broad serology testing in Europe showed IFR estimates converging at approximately 0.5–1%. Firm lower limits of IFRs have been established in a number of locations such as New York City and Bergamo in Italy since the IFR cannot be less than the population fatality rate. As of 10 July, in New York City, with a population of 8.4 million, 23,377 individuals (18,758 confirmed and 4,619 probable) have died with COVID-19 (0.3% of the population).Antibody testing in New York City suggested an IFR of ~0.9%,[258] and ~1.4%. In Bergamo province, 0.6% of the population has died. In September 2020 the U.S. Center for Disease Control & Prevention reported preliminary estimates of age-specific IFRs for public health planning purposes.

 

SEX DIFFERENCES

Early reviews of epidemiologic data showed gendered impact of the pandemic and a higher mortality rate in men in China and Italy. The Chinese Center for Disease Control and Prevention reported the death rate was 2.8% for men and 1.7% for women. Later reviews in June 2020 indicated that there is no significant difference in susceptibility or in CFR between genders. One review acknowledges the different mortality rates in Chinese men, suggesting that it may be attributable to lifestyle choices such as smoking and drinking alcohol rather than genetic factors. Sex-based immunological differences, lesser prevalence of smoking in women and men developing co-morbid conditions such as hypertension at a younger age than women could have contributed to the higher mortality in men. In Europe, 57% of the infected people were men and 72% of those died with COVID-19 were men. As of April 2020, the US government is not tracking sex-related data of COVID-19 infections. Research has shown that viral illnesses like Ebola, HIV, influenza and SARS affect men and women differently.

 

ETHNIC DIFFERENCES

In the US, a greater proportion of deaths due to COVID-19 have occurred among African Americans and other minority groups. Structural factors that prevent them from practicing social distancing include their concentration in crowded substandard housing and in "essential" occupations such as retail grocery workers, public transit employees, health-care workers and custodial staff. Greater prevalence of lacking health insurance and care and of underlying conditions such as diabetes, hypertension and heart disease also increase their risk of death. Similar issues affect Native American and Latino communities. According to a US health policy non-profit, 34% of American Indian and Alaska Native People (AIAN) non-elderly adults are at risk of serious illness compared to 21% of white non-elderly adults. The source attributes it to disproportionately high rates of many health conditions that may put them at higher risk as well as living conditions like lack of access to clean water. Leaders have called for efforts to research and address the disparities. In the U.K., a greater proportion of deaths due to COVID-19 have occurred in those of a Black, Asian, and other ethnic minority background. More severe impacts upon victims including the relative incidence of the necessity of hospitalization requirements, and vulnerability to the disease has been associated via DNA analysis to be expressed in genetic variants at chromosomal region 3, features that are associated with European Neanderthal heritage. That structure imposes greater risks that those affected will develop a more severe form of the disease. The findings are from Professor Svante Pääbo and researchers he leads at the Max Planck Institute for Evolutionary Anthropology and the Karolinska Institutet. This admixture of modern human and Neanderthal genes is estimated to have occurred roughly between 50,000 and 60,000 years ago in Southern Europe.

 

COMORBIDITIES

Most of those who die of COVID-19 have pre-existing (underlying) conditions, including hypertension, diabetes mellitus, and cardiovascular disease. According to March data from the United States, 89% of those hospitalised had preexisting conditions. The Italian Istituto Superiore di Sanità reported that out of 8.8% of deaths where medical charts were available, 96.1% of people had at least one comorbidity with the average person having 3.4 diseases. According to this report the most common comorbidities are hypertension (66% of deaths), type 2 diabetes (29.8% of deaths), Ischemic Heart Disease (27.6% of deaths), atrial fibrillation (23.1% of deaths) and chronic renal failure (20.2% of deaths).

 

Most critical respiratory comorbidities according to the CDC, are: moderate or severe asthma, pre-existing COPD, pulmonary fibrosis, cystic fibrosis. Evidence stemming from meta-analysis of several smaller research papers also suggests that smoking can be associated with worse outcomes. When someone with existing respiratory problems is infected with COVID-19, they might be at greater risk for severe symptoms. COVID-19 also poses a greater risk to people who misuse opioids and methamphetamines, insofar as their drug use may have caused lung damage.

 

In August 2020 the CDC issued a caution that tuberculosis infections could increase the risk of severe illness or death. The WHO recommended that people with respiratory symptoms be screened for both diseases, as testing positive for COVID-19 couldn't rule out co-infections. Some projections have estimated that reduced TB detection due to the pandemic could result in 6.3 million additional TB cases and 1.4 million TB related deaths by 2025.

 

NAME

During the initial outbreak in Wuhan, China, the virus and disease were commonly referred to as "coronavirus" and "Wuhan coronavirus", with the disease sometimes called "Wuhan pneumonia". In the past, many diseases have been named after geographical locations, such as the Spanish flu, Middle East Respiratory Syndrome, and Zika virus. In January 2020, the WHO recommended 2019-nCov and 2019-nCoV acute respiratory disease as interim names for the virus and disease per 2015 guidance and international guidelines against using geographical locations (e.g. Wuhan, China), animal species, or groups of people in disease and virus names in part to prevent social stigma. The official names COVID-19 and SARS-CoV-2 were issued by the WHO on 11 February 2020. Tedros Adhanom explained: CO for corona, VI for virus, D for disease and 19 for when the outbreak was first identified (31 December 2019). The WHO additionally uses "the COVID-19 virus" and "the virus responsible for COVID-19" in public communications.

 

HISTORY

The virus is thought to be natural and of an animal origin, through spillover infection. There are several theories about where the first case (the so-called patient zero) originated. Phylogenetics estimates that SARS-CoV-2 arose in October or November 2019. Evidence suggests that it descends from a coronavirus that infects wild bats, and spread to humans through an intermediary wildlife host.

 

The first known human infections were in Wuhan, Hubei, China. A study of the first 41 cases of confirmed COVID-19, published in January 2020 in The Lancet, reported the earliest date of onset of symptoms as 1 December 2019.Official publications from the WHO reported the earliest onset of symptoms as 8 December 2019. Human-to-human transmission was confirmed by the WHO and Chinese authorities by 20 January 2020. According to official Chinese sources, these were mostly linked to the Huanan Seafood Wholesale Market, which also sold live animals. In May 2020 George Gao, the director of the CDC, said animal samples collected from the seafood market had tested negative for the virus, indicating that the market was the site of an early superspreading event, but that it was not the site of the initial outbreak.[ Traces of the virus have been found in wastewater samples that were collected in Milan and Turin, Italy, on 18 December 2019.

 

By December 2019, the spread of infection was almost entirely driven by human-to-human transmission. The number of coronavirus cases in Hubei gradually increased, reaching 60 by 20 December, and at least 266 by 31 December. On 24 December, Wuhan Central Hospital sent a bronchoalveolar lavage fluid (BAL) sample from an unresolved clinical case to sequencing company Vision Medicals. On 27 and 28 December, Vision Medicals informed the Wuhan Central Hospital and the Chinese CDC of the results of the test, showing a new coronavirus. A pneumonia cluster of unknown cause was observed on 26 December and treated by the doctor Zhang Jixian in Hubei Provincial Hospital, who informed the Wuhan Jianghan CDC on 27 December. On 30 December, a test report addressed to Wuhan Central Hospital, from company CapitalBio Medlab, stated an erroneous positive result for SARS, causing a group of doctors at Wuhan Central Hospital to alert their colleagues and relevant hospital authorities of the result. The Wuhan Municipal Health Commission issued a notice to various medical institutions on "the treatment of pneumonia of unknown cause" that same evening. Eight of these doctors, including Li Wenliang (punished on 3 January), were later admonished by the police for spreading false rumours and another, Ai Fen, was reprimanded by her superiors for raising the alarm.

 

The Wuhan Municipal Health Commission made the first public announcement of a pneumonia outbreak of unknown cause on 31 December, confirming 27 cases—enough to trigger an investigation.

 

During the early stages of the outbreak, the number of cases doubled approximately every seven and a half days. In early and mid-January 2020, the virus spread to other Chinese provinces, helped by the Chinese New Year migration and Wuhan being a transport hub and major rail interchange. On 20 January, China reported nearly 140 new cases in one day, including two people in Beijing and one in Shenzhen. Later official data shows 6,174 people had already developed symptoms by then, and more may have been infected. A report in The Lancet on 24 January indicated human transmission, strongly recommended personal protective equipment for health workers, and said testing for the virus was essential due to its "pandemic potential". On 30 January, the WHO declared the coronavirus a Public Health Emergency of International Concern. By this time, the outbreak spread by a factor of 100 to 200 times.

 

Italy had its first confirmed cases on 31 January 2020, two tourists from China. As of 13 March 2020 the WHO considered Europe the active centre of the pandemic. Italy overtook China as the country with the most deaths on 19 March 2020. By 26 March the United States had overtaken China and Italy with the highest number of confirmed cases in the world. Research on coronavirus genomes indicates the majority of COVID-19 cases in New York came from European travellers, rather than directly from China or any other Asian country. Retesting of prior samples found a person in France who had the virus on 27 December 2019, and a person in the United States who died from the disease on 6 February 2020.

 

After 55 days without a locally transmitted case, Beijing reported a new COVID-19 case on 11 June 2020 which was followed by two more cases on 12 June. By 15 June there were 79 cases officially confirmed, most of them were people that went to Xinfadi Wholesale Market.

 

RT-PCR testing of untreated wastewater samples from Brazil and Italy have suggested detection of SARS-CoV-2 as early as November and December 2019, respectively, but the methods of such sewage studies have not been optimised, many have not been peer reviewed, details are often missing, and there is a risk of false positives due to contamination or if only one gene target is detected. A September 2020 review journal article said, "The possibility that the COVID-19 infection had already spread to Europe at the end of last year is now indicated by abundant, even if partially circumstantial, evidence", including pneumonia case numbers and radiology in France and Italy in November and December.

 

MISINFORMATION

After the initial outbreak of COVID-19, misinformation and disinformation regarding the origin, scale, prevention, treatment, and other aspects of the disease rapidly spread online.

 

In September 2020, the U.S. CDC published preliminary estimates of the risk of death by age groups in the United States, but those estimates were widely misreported and misunderstood.

 

OTHER ANIMALS

Humans appear to be capable of spreading the virus to some other animals, a type of disease transmission referred to as zooanthroponosis.

 

Some pets, especially cats and ferrets, can catch this virus from infected humans. Symptoms in cats include respiratory (such as a cough) and digestive symptoms. Cats can spread the virus to other cats, and may be able to spread the virus to humans, but cat-to-human transmission of SARS-CoV-2 has not been proven. Compared to cats, dogs are less susceptible to this infection. Behaviors which increase the risk of transmission include kissing, licking, and petting the animal.

 

The virus does not appear to be able to infect pigs, ducks, or chickens at all.[ Mice, rats, and rabbits, if they can be infected at all, are unlikely to be involved in spreading the virus.

 

Tigers and lions in zoos have become infected as a result of contact with infected humans. As expected, monkeys and great ape species such as orangutans can also be infected with the COVID-19 virus.

 

Minks, which are in the same family as ferrets, have been infected. Minks may be asymptomatic, and can also spread the virus to humans. Multiple countries have identified infected animals in mink farms. Denmark, a major producer of mink pelts, ordered the slaughter of all minks over fears of viral mutations. A vaccine for mink and other animals is being researched.

 

RESEARCH

International research on vaccines and medicines in COVID-19 is underway by government organisations, academic groups, and industry researchers. The CDC has classified it to require a BSL3 grade laboratory. There has been a great deal of COVID-19 research, involving accelerated research processes and publishing shortcuts to meet the global demand.

 

As of December 2020, hundreds of clinical trials have been undertaken, with research happening on every continent except Antarctica. As of November 2020, more than 200 possible treatments had been studied in humans so far.

Transmission and prevention research

Modelling research has been conducted with several objectives, including predictions of the dynamics of transmission, diagnosis and prognosis of infection, estimation of the impact of interventions, or allocation of resources. Modelling studies are mostly based on epidemiological models, estimating the number of infected people over time under given conditions. Several other types of models have been developed and used during the COVID-19 including computational fluid dynamics models to study the flow physics of COVID-19, retrofits of crowd movement models to study occupant exposure, mobility-data based models to investigate transmission, or the use of macroeconomic models to assess the economic impact of the pandemic. Further, conceptual frameworks from crisis management research have been applied to better understand the effects of COVID-19 on organizations worldwide.

 

TREATMENT-RELATED RESEARCH

Repurposed antiviral drugs make up most of the research into COVID-19 treatments. Other candidates in trials include vasodilators, corticosteroids, immune therapies, lipoic acid, bevacizumab, and recombinant angiotensin-converting enzyme 2.

 

In March 2020, the World Health Organization (WHO) initiated the Solidarity trial to assess the treatment effects of some promising drugs: an experimental drug called remdesivir; anti-malarial drugs chloroquine and hydroxychloroquine; two anti-HIV drugs, lopinavir/ritonavir; and interferon-beta. More than 300 active clinical trials were underway as of April 2020.

 

Research on the antimalarial drugs hydroxychloroquine and chloroquine showed that they were ineffective at best, and that they may reduce the antiviral activity of remdesivir. By May 2020, France, Italy, and Belgium had banned the use of hydroxychloroquine as a COVID-19 treatment.

 

In June, initial results from the randomised RECOVERY Trial in the United Kingdom showed that dexamethasone reduced mortality by one third for people who are critically ill on ventilators and one fifth for those receiving supplemental oxygen. Because this is a well-tested and widely available treatment, it was welcomed by the WHO, which is in the process of updating treatment guidelines to include dexamethasone and other steroids. Based on those preliminary results, dexamethasone treatment has been recommended by the NIH for patients with COVID-19 who are mechanically ventilated or who require supplemental oxygen but not in patients with COVID-19 who do not require supplemental oxygen.

 

In September 2020, the WHO released updated guidance on using corticosteroids for COVID-19. The WHO recommends systemic corticosteroids rather than no systemic corticosteroids for the treatment of people with severe and critical COVID-19 (strong recommendation, based on moderate certainty evidence). The WHO suggests not to use corticosteroids in the treatment of people with non-severe COVID-19 (conditional recommendation, based on low certainty evidence). The updated guidance was based on a meta-analysis of clinical trials of critically ill COVID-19 patients.

 

WIKIPEDIA

Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The first case was identified in Wuhan, China, in December 2019. The disease has since spread worldwide, leading to an ongoing pandemic.

 

Symptoms of COVID-19 are variable, but often include fever, cough, fatigue, breathing difficulties, and loss of smell and taste. Symptoms begin one to fourteen days after exposure to the virus. Of those people who develop noticeable symptoms, most (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging), and 5% suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction). Older people are more likely to have severe symptoms. At least a third of the people who are infected with the virus remain asymptomatic and do not develop noticeable symptoms at any point in time, but they still can spread the disease.[ Around 20% of those people will remain asymptomatic throughout infection, and the rest will develop symptoms later on, becoming pre-symptomatic rather than asymptomatic and therefore having a higher risk of transmitting the virus to others. Some people continue to experience a range of effects—known as long COVID—for months after recovery, and damage to organs has been observed. Multi-year studies are underway to further investigate the long-term effects of the disease.

 

The virus that causes COVID-19 spreads mainly when an infected person is in close contact[a] with another person. Small droplets and aerosols containing the virus can spread from an infected person's nose and mouth as they breathe, cough, sneeze, sing, or speak. Other people are infected if the virus gets into their mouth, nose or eyes. The virus may also spread via contaminated surfaces, although this is not thought to be the main route of transmission. The exact route of transmission is rarely proven conclusively, but infection mainly happens when people are near each other for long enough. People who are infected can transmit the virus to another person up to two days before they themselves show symptoms, as can people who do not experience symptoms. People remain infectious for up to ten days after the onset of symptoms in moderate cases and up to 20 days in severe cases. Several testing methods have been developed to diagnose the disease. The standard diagnostic method is by detection of the virus' nucleic acid by real-time reverse transcription polymerase chain reaction (rRT-PCR), transcription-mediated amplification (TMA), or by reverse transcription loop-mediated isothermal amplification (RT-LAMP) from a nasopharyngeal swab.

 

Preventive measures include physical or social distancing, quarantining, ventilation of indoor spaces, covering coughs and sneezes, hand washing, and keeping unwashed hands away from the face. The use of face masks or coverings has been recommended in public settings to minimise the risk of transmissions. Several vaccines have been developed and several countries have initiated mass vaccination campaigns.

 

Although work is underway to develop drugs that inhibit the virus, the primary treatment is currently symptomatic. Management involves the treatment of symptoms, supportive care, isolation, and experimental measures.

 

SIGNS AND SYSTOMS

Symptoms of COVID-19 are variable, ranging from mild symptoms to severe illness. Common symptoms include headache, loss of smell and taste, nasal congestion and rhinorrhea, cough, muscle pain, sore throat, fever, diarrhea, and breathing difficulties. People with the same infection may have different symptoms, and their symptoms may change over time. Three common clusters of symptoms have been identified: one respiratory symptom cluster with cough, sputum, shortness of breath, and fever; a musculoskeletal symptom cluster with muscle and joint pain, headache, and fatigue; a cluster of digestive symptoms with abdominal pain, vomiting, and diarrhea. In people without prior ear, nose, and throat disorders, loss of taste combined with loss of smell is associated with COVID-19.

 

Most people (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging) and 5% of patients suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction). At least a third of the people who are infected with the virus do not develop noticeable symptoms at any point in time. These asymptomatic carriers tend not to get tested and can spread the disease. Other infected people will develop symptoms later, called "pre-symptomatic", or have very mild symptoms and can also spread the virus.

 

As is common with infections, there is a delay between the moment a person first becomes infected and the appearance of the first symptoms. The median delay for COVID-19 is four to five days. Most symptomatic people experience symptoms within two to seven days after exposure, and almost all will experience at least one symptom within 12 days.

Most people recover from the acute phase of the disease. However, some people continue to experience a range of effects for months after recovery—named long COVID—and damage to organs has been observed. Multi-year studies are underway to further investigate the long-term effects of the disease.

 

CAUSE

TRANSMISSION

Coronavirus disease 2019 (COVID-19) spreads from person to person mainly through the respiratory route after an infected person coughs, sneezes, sings, talks or breathes. A new infection occurs when virus-containing particles exhaled by an infected person, either respiratory droplets or aerosols, get into the mouth, nose, or eyes of other people who are in close contact with the infected person. During human-to-human transmission, an average 1000 infectious SARS-CoV-2 virions are thought to initiate a new infection.

 

The closer people interact, and the longer they interact, the more likely they are to transmit COVID-19. Closer distances can involve larger droplets (which fall to the ground) and aerosols, whereas longer distances only involve aerosols. Larger droplets can also turn into aerosols (known as droplet nuclei) through evaporation. The relative importance of the larger droplets and the aerosols is not clear as of November 2020; however, the virus is not known to spread between rooms over long distances such as through air ducts. Airborne transmission is able to particularly occur indoors, in high risk locations such as restaurants, choirs, gyms, nightclubs, offices, and religious venues, often when they are crowded or less ventilated. It also occurs in healthcare settings, often when aerosol-generating medical procedures are performed on COVID-19 patients.

 

Although it is considered possible there is no direct evidence of the virus being transmitted by skin to skin contact. A person could get COVID-19 indirectly by touching a contaminated surface or object before touching their own mouth, nose, or eyes, though this is not thought to be the main way the virus spreads. The virus is not known to spread through feces, urine, breast milk, food, wastewater, drinking water, or via animal disease vectors (although some animals can contract the virus from humans). It very rarely transmits from mother to baby during pregnancy.

 

Social distancing and the wearing of cloth face masks, surgical masks, respirators, or other face coverings are controls for droplet transmission. Transmission may be decreased indoors with well maintained heating and ventilation systems to maintain good air circulation and increase the use of outdoor air.

 

The number of people generally infected by one infected person varies. Coronavirus disease 2019 is more infectious than influenza, but less so than measles. It often spreads in clusters, where infections can be traced back to an index case or geographical location. There is a major role of "super-spreading events", where many people are infected by one person.

 

A person who is infected can transmit the virus to others up to two days before they themselves show symptoms, and even if symptoms never appear. People remain infectious in moderate cases for 7–12 days, and up to two weeks in severe cases. In October 2020, medical scientists reported evidence of reinfection in one person.

 

VIROLOGY

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel severe acute respiratory syndrome coronavirus. It was first isolated from three people with pneumonia connected to the cluster of acute respiratory illness cases in Wuhan. All structural features of the novel SARS-CoV-2 virus particle occur in related coronaviruses in nature.

 

Outside the human body, the virus is destroyed by household soap, which bursts its protective bubble.

 

SARS-CoV-2 is closely related to the original SARS-CoV. It is thought to have an animal (zoonotic) origin. Genetic analysis has revealed that the coronavirus genetically clusters with the genus Betacoronavirus, in subgenus Sarbecovirus (lineage B) together with two bat-derived strains. It is 96% identical at the whole genome level to other bat coronavirus samples (BatCov RaTG13). The structural proteins of SARS-CoV-2 include membrane glycoprotein (M), envelope protein (E), nucleocapsid protein (N), and the spike protein (S). The M protein of SARS-CoV-2 is about 98% similar to the M protein of bat SARS-CoV, maintains around 98% homology with pangolin SARS-CoV, and has 90% homology with the M protein of SARS-CoV; whereas, the similarity is only around 38% with the M protein of MERS-CoV. The structure of the M protein resembles the sugar transporter SemiSWEET.

 

The many thousands of SARS-CoV-2 variants are grouped into clades. Several different clade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR).

 

Several notable variants of SARS-CoV-2 emerged in late 2020. Cluster 5 emerged among minks and mink farmers in Denmark. After strict quarantines and a mink euthanasia campaign, it is believed to have been eradicated. The Variant of Concern 202012/01 (VOC 202012/01) is believed to have emerged in the United Kingdom in September. The 501Y.V2 Variant, which has the same N501Y mutation, arose independently in South Africa.

 

SARS-CoV-2 VARIANTS

Three known variants of SARS-CoV-2 are currently spreading among global populations as of January 2021 including the UK Variant (referred to as B.1.1.7) first found in London and Kent, a variant discovered in South Africa (referred to as 1.351), and a variant discovered in Brazil (referred to as P.1).

 

Using Whole Genome Sequencing, epidemiology and modelling suggest the new UK variant ‘VUI – 202012/01’ (the first Variant Under Investigation in December 2020) transmits more easily than other strains.

 

PATHOPHYSIOLOGY

COVID-19 can affect the upper respiratory tract (sinuses, nose, and throat) and the lower respiratory tract (windpipe and lungs). The lungs are the organs most affected by COVID-19 because the virus accesses host cells via the enzyme angiotensin-converting enzyme 2 (ACE2), which is most abundant in type II alveolar cells of the lungs. The virus uses a special surface glycoprotein called a "spike" (peplomer) to connect to ACE2 and enter the host cell. The density of ACE2 in each tissue correlates with the severity of the disease in that tissue and decreasing ACE2 activity might be protective, though another view is that increasing ACE2 using angiotensin II receptor blocker medications could be protective. As the alveolar disease progresses, respiratory failure might develop and death may follow.

 

Whether SARS-CoV-2 is able to invade the nervous system remains unknown. The virus is not detected in the CNS of the majority of COVID-19 people with neurological issues. However, SARS-CoV-2 has been detected at low levels in the brains of those who have died from COVID-19, but these results need to be confirmed. SARS-CoV-2 could cause respiratory failure through affecting the brain stem as other coronaviruses have been found to invade the CNS. While virus has been detected in cerebrospinal fluid of autopsies, the exact mechanism by which it invades the CNS remains unclear and may first involve invasion of peripheral nerves given the low levels of ACE2 in the brain. The virus may also enter the bloodstream from the lungs and cross the blood-brain barrier to gain access to the CNS, possibly within an infected white blood cell.

 

The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium as well as endothelial cells and enterocytes of the small intestine.

 

The virus can cause acute myocardial injury and chronic damage to the cardiovascular system. An acute cardiac injury was found in 12% of infected people admitted to the hospital in Wuhan, China, and is more frequent in severe disease. Rates of cardiovascular symptoms are high, owing to the systemic inflammatory response and immune system disorders during disease progression, but acute myocardial injuries may also be related to ACE2 receptors in the heart. ACE2 receptors are highly expressed in the heart and are involved in heart function. A high incidence of thrombosis and venous thromboembolism have been found people transferred to Intensive care unit (ICU) with COVID-19 infections, and may be related to poor prognosis. Blood vessel dysfunction and clot formation (as suggested by high D-dimer levels caused by blood clots) are thought to play a significant role in mortality, incidences of clots leading to pulmonary embolisms, and ischaemic events within the brain have been noted as complications leading to death in people infected with SARS-CoV-2. Infection appears to set off a chain of vasoconstrictive responses within the body, constriction of blood vessels within the pulmonary circulation has also been posited as a mechanism in which oxygenation decreases alongside the presentation of viral pneumonia. Furthermore, microvascular blood vessel damage has been reported in a small number of tissue samples of the brains – without detected SARS-CoV-2 – and the olfactory bulbs from those who have died from COVID-19.

 

Another common cause of death is complications related to the kidneys. Early reports show that up to 30% of hospitalized patients both in China and in New York have experienced some injury to their kidneys, including some persons with no previous kidney problems.

 

Autopsies of people who died of COVID-19 have found diffuse alveolar damage, and lymphocyte-containing inflammatory infiltrates within the lung.

 

IMMUNOPATHOLOGY

Although SARS-CoV-2 has a tropism for ACE2-expressing epithelial cells of the respiratory tract, people with severe COVID-19 have symptoms of systemic hyperinflammation. Clinical laboratory findings of elevated IL-2, IL-7, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-γ inducible protein 10 (IP-10), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1-α (MIP-1α), and tumour necrosis factor-α (TNF-α) indicative of cytokine release syndrome (CRS) suggest an underlying immunopathology.

 

Additionally, people with COVID-19 and acute respiratory distress syndrome (ARDS) have classical serum biomarkers of CRS, including elevated C-reactive protein (CRP), lactate dehydrogenase (LDH), D-dimer, and ferritin.

 

Systemic inflammation results in vasodilation, allowing inflammatory lymphocytic and monocytic infiltration of the lung and the heart. In particular, pathogenic GM-CSF-secreting T-cells were shown to correlate with the recruitment of inflammatory IL-6-secreting monocytes and severe lung pathology in people with COVID-19 . Lymphocytic infiltrates have also been reported at autopsy.

 

VIRAL AND HOST FACTORS

VIRUS PROTEINS

Multiple viral and host factors affect the pathogenesis of the virus. The S-protein, otherwise known as the spike protein, is the viral component that attaches to the host receptor via the ACE2 receptors. It includes two subunits: S1 and S2. S1 determines the virus host range and cellular tropism via the receptor binding domain. S2 mediates the membrane fusion of the virus to its potential cell host via the H1 and HR2, which are heptad repeat regions. Studies have shown that S1 domain induced IgG and IgA antibody levels at a much higher capacity. It is the focus spike proteins expression that are involved in many effective COVID-19 vaccines.

 

The M protein is the viral protein responsible for the transmembrane transport of nutrients. It is the cause of the bud release and the formation of the viral envelope. The N and E protein are accessory proteins that interfere with the host's immune response.

 

HOST FACTORS

Human angiotensin converting enzyme 2 (hACE2) is the host factor that SARS-COV2 virus targets causing COVID-19. Theoretically the usage of angiotensin receptor blockers (ARB) and ACE inhibitors upregulating ACE2 expression might increase morbidity with COVID-19, though animal data suggest some potential protective effect of ARB. However no clinical studies have proven susceptibility or outcomes. Until further data is available, guidelines and recommendations for hypertensive patients remain.

 

The virus' effect on ACE2 cell surfaces leads to leukocytic infiltration, increased blood vessel permeability, alveolar wall permeability, as well as decreased secretion of lung surfactants. These effects cause the majority of the respiratory symptoms. However, the aggravation of local inflammation causes a cytokine storm eventually leading to a systemic inflammatory response syndrome.

 

HOST CYTOKINE RESPONSE

The severity of the inflammation can be attributed to the severity of what is known as the cytokine storm. Levels of interleukin 1B, interferon-gamma, interferon-inducible protein 10, and monocyte chemoattractant protein 1 were all associated with COVID-19 disease severity. Treatment has been proposed to combat the cytokine storm as it remains to be one of the leading causes of morbidity and mortality in COVID-19 disease.

 

A cytokine storm is due to an acute hyperinflammatory response that is responsible for clinical illness in an array of diseases but in COVID-19, it is related to worse prognosis and increased fatality. The storm causes the acute respiratory distress syndrome, blood clotting events such as strokes, myocardial infarction, encephalitis, acute kidney injury, and vasculitis. The production of IL-1, IL-2, IL-6, TNF-alpha, and interferon-gamma, all crucial components of normal immune responses, inadvertently become the causes of a cytokine storm. The cells of the central nervous system, the microglia, neurons, and astrocytes, are also be involved in the release of pro-inflammatory cytokines affecting the nervous system, and effects of cytokine storms toward the CNS are not uncommon.

 

DIAGNOSIS

COVID-19 can provisionally be diagnosed on the basis of symptoms and confirmed using reverse transcription polymerase chain reaction (RT-PCR) or other nucleic acid testing of infected secretions. Along with laboratory testing, chest CT scans may be helpful to diagnose COVID-19 in individuals with a high clinical suspicion of infection. Detection of a past infection is possible with serological tests, which detect antibodies produced by the body in response to the infection.

 

VIRAL TESTING

The standard methods of testing for presence of SARS-CoV-2 are nucleic acid tests, which detects the presence of viral RNA fragments. As these tests detect RNA but not infectious virus, its "ability to determine duration of infectivity of patients is limited." The test is typically done on respiratory samples obtained by a nasopharyngeal swab; however, a nasal swab or sputum sample may also be used. Results are generally available within hours. The WHO has published several testing protocols for the disease.

 

A number of laboratories and companies have developed serological tests, which detect antibodies produced by the body in response to infection. Several have been evaluated by Public Health England and approved for use in the UK.

 

The University of Oxford's CEBM has pointed to mounting evidence that "a good proportion of 'new' mild cases and people re-testing positives after quarantine or discharge from hospital are not infectious, but are simply clearing harmless virus particles which their immune system has efficiently dealt with" and have called for "an international effort to standardize and periodically calibrate testing" On 7 September, the UK government issued "guidance for procedures to be implemented in laboratories to provide assurance of positive SARS-CoV-2 RNA results during periods of low prevalence, when there is a reduction in the predictive value of positive test results."

 

IMAGING

Chest CT scans may be helpful to diagnose COVID-19 in individuals with a high clinical suspicion of infection but are not recommended for routine screening. Bilateral multilobar ground-glass opacities with a peripheral, asymmetric, and posterior distribution are common in early infection. Subpleural dominance, crazy paving (lobular septal thickening with variable alveolar filling), and consolidation may appear as the disease progresses. Characteristic imaging features on chest radiographs and computed tomography (CT) of people who are symptomatic include asymmetric peripheral ground-glass opacities without pleural effusions.

 

Many groups have created COVID-19 datasets that include imagery such as the Italian Radiological Society which has compiled an international online database of imaging findings for confirmed cases. Due to overlap with other infections such as adenovirus, imaging without confirmation by rRT-PCR is of limited specificity in identifying COVID-19. A large study in China compared chest CT results to PCR and demonstrated that though imaging is less specific for the infection, it is faster and more sensitive.

Coding

In late 2019, the WHO assigned emergency ICD-10 disease codes U07.1 for deaths from lab-confirmed SARS-CoV-2 infection and U07.2 for deaths from clinically or epidemiologically diagnosed COVID-19 without lab-confirmed SARS-CoV-2 infection.

 

PATHOLOGY

The main pathological findings at autopsy are:

 

Macroscopy: pericarditis, lung consolidation and pulmonary oedema

Lung findings:

minor serous exudation, minor fibrin exudation

pulmonary oedema, pneumocyte hyperplasia, large atypical pneumocytes, interstitial inflammation with lymphocytic infiltration and multinucleated giant cell formation

diffuse alveolar damage (DAD) with diffuse alveolar exudates. DAD is the cause of acute respiratory distress syndrome (ARDS) and severe hypoxemia.

organisation of exudates in alveolar cavities and pulmonary interstitial fibrosis

plasmocytosis in BAL

Blood: disseminated intravascular coagulation (DIC); leukoerythroblastic reaction

Liver: microvesicular steatosis

 

PREVENTION

Preventive measures to reduce the chances of infection include staying at home, wearing a mask in public, avoiding crowded places, keeping distance from others, ventilating indoor spaces, washing hands with soap and water often and for at least 20 seconds, practising good respiratory hygiene, and avoiding touching the eyes, nose, or mouth with unwashed hands.

 

Those diagnosed with COVID-19 or who believe they may be infected are advised by the CDC to stay home except to get medical care, call ahead before visiting a healthcare provider, wear a face mask before entering the healthcare provider's office and when in any room or vehicle with another person, cover coughs and sneezes with a tissue, regularly wash hands with soap and water and avoid sharing personal household items.

 

The first COVID-19 vaccine was granted regulatory approval on 2 December by the UK medicines regulator MHRA. It was evaluated for emergency use authorization (EUA) status by the US FDA, and in several other countries. Initially, the US National Institutes of Health guidelines do not recommend any medication for prevention of COVID-19, before or after exposure to the SARS-CoV-2 virus, outside the setting of a clinical trial. Without a vaccine, other prophylactic measures, or effective treatments, a key part of managing COVID-19 is trying to decrease and delay the epidemic peak, known as "flattening the curve". This is done by slowing the infection rate to decrease the risk of health services being overwhelmed, allowing for better treatment of current cases, and delaying additional cases until effective treatments or a vaccine become available.

 

VACCINE

A COVID‑19 vaccine is a vaccine intended to provide acquired immunity against severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2), the virus causing coronavirus disease 2019 (COVID‑19). Prior to the COVID‑19 pandemic, there was an established body of knowledge about the structure and function of coronaviruses causing diseases like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), which enabled accelerated development of various vaccine technologies during early 2020. On 10 January 2020, the SARS-CoV-2 genetic sequence data was shared through GISAID, and by 19 March, the global pharmaceutical industry announced a major commitment to address COVID-19.

 

In Phase III trials, several COVID‑19 vaccines have demonstrated efficacy as high as 95% in preventing symptomatic COVID‑19 infections. As of March 2021, 12 vaccines were authorized by at least one national regulatory authority for public use: two RNA vaccines (the Pfizer–BioNTech vaccine and the Moderna vaccine), four conventional inactivated vaccines (BBIBP-CorV, CoronaVac, Covaxin, and CoviVac), four viral vector vaccines (Sputnik V, the Oxford–AstraZeneca vaccine, Convidicea, and the Johnson & Johnson vaccine), and two protein subunit vaccines (EpiVacCorona and RBD-Dimer). In total, as of March 2021, 308 vaccine candidates were in various stages of development, with 73 in clinical research, including 24 in Phase I trials, 33 in Phase I–II trials, and 16 in Phase III development.

Many countries have implemented phased distribution plans that prioritize those at highest risk of complications, such as the elderly, and those at high risk of exposure and transmission, such as healthcare workers. As of 17 March 2021, 400.22 million doses of COVID‑19 vaccine have been administered worldwide based on official reports from national health agencies. AstraZeneca-Oxford anticipates producing 3 billion doses in 2021, Pfizer-BioNTech 1.3 billion doses, and Sputnik V, Sinopharm, Sinovac, and Johnson & Johnson 1 billion doses each. Moderna targets producing 600 million doses and Convidicea 500 million doses in 2021. By December 2020, more than 10 billion vaccine doses had been preordered by countries, with about half of the doses purchased by high-income countries comprising 14% of the world's population.

 

SOCIAL DISTANCING

Social distancing (also known as physical distancing) includes infection control actions intended to slow the spread of the disease by minimising close contact between individuals. Methods include quarantines; travel restrictions; and the closing of schools, workplaces, stadiums, theatres, or shopping centres. Individuals may apply social distancing methods by staying at home, limiting travel, avoiding crowded areas, using no-contact greetings, and physically distancing themselves from others. Many governments are now mandating or recommending social distancing in regions affected by the outbreak.

 

Outbreaks have occurred in prisons due to crowding and an inability to enforce adequate social distancing. In the United States, the prisoner population is aging and many of them are at high risk for poor outcomes from COVID-19 due to high rates of coexisting heart and lung disease, and poor access to high-quality healthcare.

 

SELF-ISOLATION

Self-isolation at home has been recommended for those diagnosed with COVID-19 and those who suspect they have been infected. Health agencies have issued detailed instructions for proper self-isolation. Many governments have mandated or recommended self-quarantine for entire populations. The strongest self-quarantine instructions have been issued to those in high-risk groups. Those who may have been exposed to someone with COVID-19 and those who have recently travelled to a country or region with the widespread transmission have been advised to self-quarantine for 14 days from the time of last possible exposure.

Face masks and respiratory hygiene

 

The WHO and the US CDC recommend individuals wear non-medical face coverings in public settings where there is an increased risk of transmission and where social distancing measures are difficult to maintain. This recommendation is meant to reduce the spread of the disease by asymptomatic and pre-symptomatic individuals and is complementary to established preventive measures such as social distancing. Face coverings limit the volume and travel distance of expiratory droplets dispersed when talking, breathing, and coughing. A face covering without vents or holes will also filter out particles containing the virus from inhaled and exhaled air, reducing the chances of infection. But, if the mask include an exhalation valve, a wearer that is infected (maybe without having noticed that, and asymptomatic) would transmit the virus outwards through it, despite any certification they can have. So the masks with exhalation valve are not for the infected wearers, and are not reliable to stop the pandemic in a large scale. Many countries and local jurisdictions encourage or mandate the use of face masks or cloth face coverings by members of the public to limit the spread of the virus.

 

Masks are also strongly recommended for those who may have been infected and those taking care of someone who may have the disease. When not wearing a mask, the CDC recommends covering the mouth and nose with a tissue when coughing or sneezing and recommends using the inside of the elbow if no tissue is available. Proper hand hygiene after any cough or sneeze is encouraged. Healthcare professionals interacting directly with people who have COVID-19 are advised to use respirators at least as protective as NIOSH-certified N95 or equivalent, in addition to other personal protective equipment.

 

HAND-WASHING AND HYGIENE

Thorough hand hygiene after any cough or sneeze is required. The WHO also recommends that individuals wash hands often with soap and water for at least 20 seconds, especially after going to the toilet or when hands are visibly dirty, before eating and after blowing one's nose. The CDC recommends using an alcohol-based hand sanitiser with at least 60% alcohol, but only when soap and water are not readily available. For areas where commercial hand sanitisers are not readily available, the WHO provides two formulations for local production. In these formulations, the antimicrobial activity arises from ethanol or isopropanol. Hydrogen peroxide is used to help eliminate bacterial spores in the alcohol; it is "not an active substance for hand antisepsis". Glycerol is added as a humectant.

 

SURFACE CLEANING

After being expelled from the body, coronaviruses can survive on surfaces for hours to days. If a person touches the dirty surface, they may deposit the virus at the eyes, nose, or mouth where it can enter the body cause infection. Current evidence indicates that contact with infected surfaces is not the main driver of Covid-19, leading to recommendations for optimised disinfection procedures to avoid issues such as the increase of antimicrobial resistance through the use of inappropriate cleaning products and processes. Deep cleaning and other surface sanitation has been criticized as hygiene theater, giving a false sense of security against something primarily spread through the air.

 

The amount of time that the virus can survive depends significantly on the type of surface, the temperature, and the humidity. Coronaviruses die very quickly when exposed to the UV light in sunlight. Like other enveloped viruses, SARS-CoV-2 survives longest when the temperature is at room temperature or lower, and when the relative humidity is low (<50%).

 

On many surfaces, including as glass, some types of plastic, stainless steel, and skin, the virus can remain infective for several days indoors at room temperature, or even about a week under ideal conditions. On some surfaces, including cotton fabric and copper, the virus usually dies after a few hours. As a general rule of thumb, the virus dies faster on porous surfaces than on non-porous surfaces.

However, this rule is not absolute, and of the many surfaces tested, two with the longest survival times are N95 respirator masks and surgical masks, both of which are considered porous surfaces.

 

Surfaces may be decontaminated with 62–71 percent ethanol, 50–100 percent isopropanol, 0.1 percent sodium hypochlorite, 0.5 percent hydrogen peroxide, and 0.2–7.5 percent povidone-iodine. Other solutions, such as benzalkonium chloride and chlorhexidine gluconate, are less effective. Ultraviolet germicidal irradiation may also be used. The CDC recommends that if a COVID-19 case is suspected or confirmed at a facility such as an office or day care, all areas such as offices, bathrooms, common areas, shared electronic equipment like tablets, touch screens, keyboards, remote controls, and ATM machines used by the ill persons should be disinfected. A datasheet comprising the authorised substances to disinfection in the food industry (including suspension or surface tested, kind of surface, use dilution, disinfectant and inocuylum volumes) can be seen in the supplementary material of.

 

VENTILATION AND AIR FILTRATION

The WHO recommends ventilation and air filtration in public spaces to help clear out infectious aerosols.

 

HEALTHY DIET AND LIFESTYLE

The Harvard T.H. Chan School of Public Health recommends a healthy diet, being physically active, managing psychological stress, and getting enough sleep.

 

While there is no evidence that vitamin D is an effective treatment for COVID-19, there is limited evidence that vitamin D deficiency increases the risk of severe COVID-19 symptoms. This has led to recommendations for individuals with vitamin D deficiency to take vitamin D supplements as a way of mitigating the risk of COVID-19 and other health issues associated with a possible increase in deficiency due to social distancing.

 

TREATMENT

There is no specific, effective treatment or cure for coronavirus disease 2019 (COVID-19), the disease caused by the SARS-CoV-2 virus. Thus, the cornerstone of management of COVID-19 is supportive care, which includes treatment to relieve symptoms, fluid therapy, oxygen support and prone positioning as needed, and medications or devices to support other affected vital organs.

 

Most cases of COVID-19 are mild. In these, supportive care includes medication such as paracetamol or NSAIDs to relieve symptoms (fever, body aches, cough), proper intake of fluids, rest, and nasal breathing. Good personal hygiene and a healthy diet are also recommended. The U.S. Centers for Disease Control and Prevention (CDC) recommend that those who suspect they are carrying the virus isolate themselves at home and wear a face mask.

 

People with more severe cases may need treatment in hospital. In those with low oxygen levels, use of the glucocorticoid dexamethasone is strongly recommended, as it can reduce the risk of death. Noninvasive ventilation and, ultimately, admission to an intensive care unit for mechanical ventilation may be required to support breathing. Extracorporeal membrane oxygenation (ECMO) has been used to address the issue of respiratory failure, but its benefits are still under consideration.

Several experimental treatments are being actively studied in clinical trials. Others were thought to be promising early in the pandemic, such as hydroxychloroquine and lopinavir/ritonavir, but later research found them to be ineffective or even harmful. Despite ongoing research, there is still not enough high-quality evidence to recommend so-called early treatment. Nevertheless, in the United States, two monoclonal antibody-based therapies are available for early use in cases thought to be at high risk of progression to severe disease. The antiviral remdesivir is available in the U.S., Canada, Australia, and several other countries, with varying restrictions; however, it is not recommended for people needing mechanical ventilation, and is discouraged altogether by the World Health Organization (WHO), due to limited evidence of its efficacy.

 

PROGNOSIS

The severity of COVID-19 varies. The disease may take a mild course with few or no symptoms, resembling other common upper respiratory diseases such as the common cold. In 3–4% of cases (7.4% for those over age 65) symptoms are severe enough to cause hospitalization. Mild cases typically recover within two weeks, while those with severe or critical diseases may take three to six weeks to recover. Among those who have died, the time from symptom onset to death has ranged from two to eight weeks. The Italian Istituto Superiore di Sanità reported that the median time between the onset of symptoms and death was twelve days, with seven being hospitalised. However, people transferred to an ICU had a median time of ten days between hospitalisation and death. Prolonged prothrombin time and elevated C-reactive protein levels on admission to the hospital are associated with severe course of COVID-19 and with a transfer to ICU.

 

Some early studies suggest 10% to 20% of people with COVID-19 will experience symptoms lasting longer than a month.[191][192] A majority of those who were admitted to hospital with severe disease report long-term problems including fatigue and shortness of breath. On 30 October 2020 WHO chief Tedros Adhanom warned that "to a significant number of people, the COVID virus poses a range of serious long-term effects". He has described the vast spectrum of COVID-19 symptoms that fluctuate over time as "really concerning." They range from fatigue, a cough and shortness of breath, to inflammation and injury of major organs – including the lungs and heart, and also neurological and psychologic effects. Symptoms often overlap and can affect any system in the body. Infected people have reported cyclical bouts of fatigue, headaches, months of complete exhaustion, mood swings, and other symptoms. Tedros has concluded that therefore herd immunity is "morally unconscionable and unfeasible".

 

In terms of hospital readmissions about 9% of 106,000 individuals had to return for hospital treatment within 2 months of discharge. The average to readmit was 8 days since first hospital visit. There are several risk factors that have been identified as being a cause of multiple admissions to a hospital facility. Among these are advanced age (above 65 years of age) and presence of a chronic condition such as diabetes, COPD, heart failure or chronic kidney disease.

 

According to scientific reviews smokers are more likely to require intensive care or die compared to non-smokers, air pollution is similarly associated with risk factors, and pre-existing heart and lung diseases and also obesity contributes to an increased health risk of COVID-19.

 

It is also assumed that those that are immunocompromised are at higher risk of getting severely sick from SARS-CoV-2. One research that looked into the COVID-19 infections in hospitalized kidney transplant recipients found a mortality rate of 11%.

See also: Impact of the COVID-19 pandemic on children

 

Children make up a small proportion of reported cases, with about 1% of cases being under 10 years and 4% aged 10–19 years. They are likely to have milder symptoms and a lower chance of severe disease than adults. A European multinational study of hospitalized children published in The Lancet on 25 June 2020 found that about 8% of children admitted to a hospital needed intensive care. Four of those 582 children (0.7%) died, but the actual mortality rate could be "substantially lower" since milder cases that did not seek medical help were not included in the study.

 

Genetics also plays an important role in the ability to fight off the disease. For instance, those that do not produce detectable type I interferons or produce auto-antibodies against these may get much sicker from COVID-19. Genetic screening is able to detect interferon effector genes.

 

Pregnant women may be at higher risk of severe COVID-19 infection based on data from other similar viruses, like SARS and MERS, but data for COVID-19 is lacking.

 

COMPLICATIONS

Complications may include pneumonia, acute respiratory distress syndrome (ARDS), multi-organ failure, septic shock, and death. Cardiovascular complications may include heart failure, arrhythmias, heart inflammation, and blood clots. Approximately 20–30% of people who present with COVID-19 have elevated liver enzymes, reflecting liver injury.

 

Neurologic manifestations include seizure, stroke, encephalitis, and Guillain–Barré syndrome (which includes loss of motor functions). Following the infection, children may develop paediatric multisystem inflammatory syndrome, which has symptoms similar to Kawasaki disease, which can be fatal. In very rare cases, acute encephalopathy can occur, and it can be considered in those who have been diagnosed with COVID-19 and have an altered mental status.

 

LONGER-TERM EFFECTS

Some early studies suggest that that 10 to 20% of people with COVID-19 will experience symptoms lasting longer than a month. A majority of those who were admitted to hospital with severe disease report long-term problems, including fatigue and shortness of breath. About 5-10% of patients admitted to hospital progress to severe or critical disease, including pneumonia and acute respiratory failure.

 

By a variety of mechanisms, the lungs are the organs most affected in COVID-19.[228] The majority of CT scans performed show lung abnormalities in people tested after 28 days of illness.

 

People with advanced age, severe disease, prolonged ICU stays, or who smoke are more likely to have long lasting effects, including pulmonary fibrosis. Overall, approximately one third of those investigated after 4 weeks will have findings of pulmonary fibrosis or reduced lung function as measured by DLCO, even in people who are asymptomatic, but with the suggestion of continuing improvement with the passing of more time.

 

IMMUNITY

The immune response by humans to CoV-2 virus occurs as a combination of the cell-mediated immunity and antibody production, just as with most other infections. Since SARS-CoV-2 has been in the human population only since December 2019, it remains unknown if the immunity is long-lasting in people who recover from the disease. The presence of neutralizing antibodies in blood strongly correlates with protection from infection, but the level of neutralizing antibody declines with time. Those with asymptomatic or mild disease had undetectable levels of neutralizing antibody two months after infection. In another study, the level of neutralizing antibody fell 4-fold 1 to 4 months after the onset of symptoms. However, the lack of antibody in the blood does not mean antibody will not be rapidly produced upon reexposure to SARS-CoV-2. Memory B cells specific for the spike and nucleocapsid proteins of SARS-CoV-2 last for at least 6 months after appearance of symptoms. Nevertheless, 15 cases of reinfection with SARS-CoV-2 have been reported using stringent CDC criteria requiring identification of a different variant from the second infection. There are likely to be many more people who have been reinfected with the virus. Herd immunity will not eliminate the virus if reinfection is common. Some other coronaviruses circulating in people are capable of reinfection after roughly a year. Nonetheless, on 3 March 2021, scientists reported that a much more contagious Covid-19 variant, Lineage P.1, first detected in Japan, and subsequently found in Brazil, as well as in several places in the United States, may be associated with Covid-19 disease reinfection after recovery from an earlier Covid-19 infection.

 

MORTALITY

Several measures are commonly used to quantify mortality. These numbers vary by region and over time and are influenced by the volume of testing, healthcare system quality, treatment options, time since the initial outbreak, and population characteristics such as age, sex, and overall health. The mortality rate reflects the number of deaths within a specific demographic group divided by the population of that demographic group. Consequently, the mortality rate reflects the prevalence as well as the severity of the disease within a given population. Mortality rates are highly correlated to age, with relatively low rates for young people and relatively high rates among the elderly.

 

The case fatality rate (CFR) reflects the number of deaths divided by the number of diagnosed cases within a given time interval. Based on Johns Hopkins University statistics, the global death-to-case ratio is 2.2% (2,685,770/121,585,388) as of 18 March 2021. The number varies by region. The CFR may not reflect the true severity of the disease, because some infected individuals remain asymptomatic or experience only mild symptoms, and hence such infections may not be included in official case reports. Moreover, the CFR may vary markedly over time and across locations due to the availability of live virus tests.

 

INFECTION FATALITY RATE

A key metric in gauging the severity of COVID-19 is the infection fatality rate (IFR), also referred to as the infection fatality ratio or infection fatality risk. This metric is calculated by dividing the total number of deaths from the disease by the total number of infected individuals; hence, in contrast to the CFR, the IFR incorporates asymptomatic and undiagnosed infections as well as reported cases.

 

CURRENT ESTIMATES

A December 2020 systematic review and meta-analysis estimated that population IFR during the first wave of the pandemic was about 0.5% to 1% in many locations (including France, Netherlands, New Zealand, and Portugal), 1% to 2% in other locations (Australia, England, Lithuania, and Spain), and exceeded 2% in Italy. That study also found that most of these differences in IFR reflected corresponding differences in the age composition of the population and age-specific infection rates; in particular, the metaregression estimate of IFR is very low for children and younger adults (e.g., 0.002% at age 10 and 0.01% at age 25) but increases progressively to 0.4% at age 55, 1.4% at age 65, 4.6% at age 75, and 15% at age 85. These results were also highlighted in a December 2020 report issued by the WHO.

 

EARLIER ESTIMATES OF IFR

At an early stage of the pandemic, the World Health Organization reported estimates of IFR between 0.3% and 1%.[ On 2 July, The WHO's chief scientist reported that the average IFR estimate presented at a two-day WHO expert forum was about 0.6%. In August, the WHO found that studies incorporating data from broad serology testing in Europe showed IFR estimates converging at approximately 0.5–1%. Firm lower limits of IFRs have been established in a number of locations such as New York City and Bergamo in Italy since the IFR cannot be less than the population fatality rate. As of 10 July, in New York City, with a population of 8.4 million, 23,377 individuals (18,758 confirmed and 4,619 probable) have died with COVID-19 (0.3% of the population).Antibody testing in New York City suggested an IFR of ~0.9%,[258] and ~1.4%. In Bergamo province, 0.6% of the population has died. In September 2020 the U.S. Center for Disease Control & Prevention reported preliminary estimates of age-specific IFRs for public health planning purposes.

 

SEX DIFFERENCES

Early reviews of epidemiologic data showed gendered impact of the pandemic and a higher mortality rate in men in China and Italy. The Chinese Center for Disease Control and Prevention reported the death rate was 2.8% for men and 1.7% for women. Later reviews in June 2020 indicated that there is no significant difference in susceptibility or in CFR between genders. One review acknowledges the different mortality rates in Chinese men, suggesting that it may be attributable to lifestyle choices such as smoking and drinking alcohol rather than genetic factors. Sex-based immunological differences, lesser prevalence of smoking in women and men developing co-morbid conditions such as hypertension at a younger age than women could have contributed to the higher mortality in men. In Europe, 57% of the infected people were men and 72% of those died with COVID-19 were men. As of April 2020, the US government is not tracking sex-related data of COVID-19 infections. Research has shown that viral illnesses like Ebola, HIV, influenza and SARS affect men and women differently.

 

ETHNIC DIFFERENCES

In the US, a greater proportion of deaths due to COVID-19 have occurred among African Americans and other minority groups. Structural factors that prevent them from practicing social distancing include their concentration in crowded substandard housing and in "essential" occupations such as retail grocery workers, public transit employees, health-care workers and custodial staff. Greater prevalence of lacking health insurance and care and of underlying conditions such as diabetes, hypertension and heart disease also increase their risk of death. Similar issues affect Native American and Latino communities. According to a US health policy non-profit, 34% of American Indian and Alaska Native People (AIAN) non-elderly adults are at risk of serious illness compared to 21% of white non-elderly adults. The source attributes it to disproportionately high rates of many health conditions that may put them at higher risk as well as living conditions like lack of access to clean water. Leaders have called for efforts to research and address the disparities. In the U.K., a greater proportion of deaths due to COVID-19 have occurred in those of a Black, Asian, and other ethnic minority background. More severe impacts upon victims including the relative incidence of the necessity of hospitalization requirements, and vulnerability to the disease has been associated via DNA analysis to be expressed in genetic variants at chromosomal region 3, features that are associated with European Neanderthal heritage. That structure imposes greater risks that those affected will develop a more severe form of the disease. The findings are from Professor Svante Pääbo and researchers he leads at the Max Planck Institute for Evolutionary Anthropology and the Karolinska Institutet. This admixture of modern human and Neanderthal genes is estimated to have occurred roughly between 50,000 and 60,000 years ago in Southern Europe.

 

COMORBIDITIES

Most of those who die of COVID-19 have pre-existing (underlying) conditions, including hypertension, diabetes mellitus, and cardiovascular disease. According to March data from the United States, 89% of those hospitalised had preexisting conditions. The Italian Istituto Superiore di Sanità reported that out of 8.8% of deaths where medical charts were available, 96.1% of people had at least one comorbidity with the average person having 3.4 diseases. According to this report the most common comorbidities are hypertension (66% of deaths), type 2 diabetes (29.8% of deaths), Ischemic Heart Disease (27.6% of deaths), atrial fibrillation (23.1% of deaths) and chronic renal failure (20.2% of deaths).

 

Most critical respiratory comorbidities according to the CDC, are: moderate or severe asthma, pre-existing COPD, pulmonary fibrosis, cystic fibrosis. Evidence stemming from meta-analysis of several smaller research papers also suggests that smoking can be associated with worse outcomes. When someone with existing respiratory problems is infected with COVID-19, they might be at greater risk for severe symptoms. COVID-19 also poses a greater risk to people who misuse opioids and methamphetamines, insofar as their drug use may have caused lung damage.

 

In August 2020 the CDC issued a caution that tuberculosis infections could increase the risk of severe illness or death. The WHO recommended that people with respiratory symptoms be screened for both diseases, as testing positive for COVID-19 couldn't rule out co-infections. Some projections have estimated that reduced TB detection due to the pandemic could result in 6.3 million additional TB cases and 1.4 million TB related deaths by 2025.

 

NAME

During the initial outbreak in Wuhan, China, the virus and disease were commonly referred to as "coronavirus" and "Wuhan coronavirus", with the disease sometimes called "Wuhan pneumonia". In the past, many diseases have been named after geographical locations, such as the Spanish flu, Middle East Respiratory Syndrome, and Zika virus. In January 2020, the WHO recommended 2019-nCov and 2019-nCoV acute respiratory disease as interim names for the virus and disease per 2015 guidance and international guidelines against using geographical locations (e.g. Wuhan, China), animal species, or groups of people in disease and virus names in part to prevent social stigma. The official names COVID-19 and SARS-CoV-2 were issued by the WHO on 11 February 2020. Tedros Adhanom explained: CO for corona, VI for virus, D for disease and 19 for when the outbreak was first identified (31 December 2019). The WHO additionally uses "the COVID-19 virus" and "the virus responsible for COVID-19" in public communications.

 

HISTORY

The virus is thought to be natural and of an animal origin, through spillover infection. There are several theories about where the first case (the so-called patient zero) originated. Phylogenetics estimates that SARS-CoV-2 arose in October or November 2019. Evidence suggests that it descends from a coronavirus that infects wild bats, and spread to humans through an intermediary wildlife host.

 

The first known human infections were in Wuhan, Hubei, China. A study of the first 41 cases of confirmed COVID-19, published in January 2020 in The Lancet, reported the earliest date of onset of symptoms as 1 December 2019.Official publications from the WHO reported the earliest onset of symptoms as 8 December 2019. Human-to-human transmission was confirmed by the WHO and Chinese authorities by 20 January 2020. According to official Chinese sources, these were mostly linked to the Huanan Seafood Wholesale Market, which also sold live animals. In May 2020 George Gao, the director of the CDC, said animal samples collected from the seafood market had tested negative for the virus, indicating that the market was the site of an early superspreading event, but that it was not the site of the initial outbreak.[ Traces of the virus have been found in wastewater samples that were collected in Milan and Turin, Italy, on 18 December 2019.

 

By December 2019, the spread of infection was almost entirely driven by human-to-human transmission. The number of coronavirus cases in Hubei gradually increased, reaching 60 by 20 December, and at least 266 by 31 December. On 24 December, Wuhan Central Hospital sent a bronchoalveolar lavage fluid (BAL) sample from an unresolved clinical case to sequencing company Vision Medicals. On 27 and 28 December, Vision Medicals informed the Wuhan Central Hospital and the Chinese CDC of the results of the test, showing a new coronavirus. A pneumonia cluster of unknown cause was observed on 26 December and treated by the doctor Zhang Jixian in Hubei Provincial Hospital, who informed the Wuhan Jianghan CDC on 27 December. On 30 December, a test report addressed to Wuhan Central Hospital, from company CapitalBio Medlab, stated an erroneous positive result for SARS, causing a group of doctors at Wuhan Central Hospital to alert their colleagues and relevant hospital authorities of the result. The Wuhan Municipal Health Commission issued a notice to various medical institutions on "the treatment of pneumonia of unknown cause" that same evening. Eight of these doctors, including Li Wenliang (punished on 3 January), were later admonished by the police for spreading false rumours and another, Ai Fen, was reprimanded by her superiors for raising the alarm.

 

The Wuhan Municipal Health Commission made the first public announcement of a pneumonia outbreak of unknown cause on 31 December, confirming 27 cases—enough to trigger an investigation.

 

During the early stages of the outbreak, the number of cases doubled approximately every seven and a half days. In early and mid-January 2020, the virus spread to other Chinese provinces, helped by the Chinese New Year migration and Wuhan being a transport hub and major rail interchange. On 20 January, China reported nearly 140 new cases in one day, including two people in Beijing and one in Shenzhen. Later official data shows 6,174 people had already developed symptoms by then, and more may have been infected. A report in The Lancet on 24 January indicated human transmission, strongly recommended personal protective equipment for health workers, and said testing for the virus was essential due to its "pandemic potential". On 30 January, the WHO declared the coronavirus a Public Health Emergency of International Concern. By this time, the outbreak spread by a factor of 100 to 200 times.

 

Italy had its first confirmed cases on 31 January 2020, two tourists from China. As of 13 March 2020 the WHO considered Europe the active centre of the pandemic. Italy overtook China as the country with the most deaths on 19 March 2020. By 26 March the United States had overtaken China and Italy with the highest number of confirmed cases in the world. Research on coronavirus genomes indicates the majority of COVID-19 cases in New York came from European travellers, rather than directly from China or any other Asian country. Retesting of prior samples found a person in France who had the virus on 27 December 2019, and a person in the United States who died from the disease on 6 February 2020.

 

After 55 days without a locally transmitted case, Beijing reported a new COVID-19 case on 11 June 2020 which was followed by two more cases on 12 June. By 15 June there were 79 cases officially confirmed, most of them were people that went to Xinfadi Wholesale Market.

 

RT-PCR testing of untreated wastewater samples from Brazil and Italy have suggested detection of SARS-CoV-2 as early as November and December 2019, respectively, but the methods of such sewage studies have not been optimised, many have not been peer reviewed, details are often missing, and there is a risk of false positives due to contamination or if only one gene target is detected. A September 2020 review journal article said, "The possibility that the COVID-19 infection had already spread to Europe at the end of last year is now indicated by abundant, even if partially circumstantial, evidence", including pneumonia case numbers and radiology in France and Italy in November and December.

 

MISINFORMATION

After the initial outbreak of COVID-19, misinformation and disinformation regarding the origin, scale, prevention, treatment, and other aspects of the disease rapidly spread online.

 

In September 2020, the U.S. CDC published preliminary estimates of the risk of death by age groups in the United States, but those estimates were widely misreported and misunderstood.

 

OTHER ANIMALS

Humans appear to be capable of spreading the virus to some other animals, a type of disease transmission referred to as zooanthroponosis.

 

Some pets, especially cats and ferrets, can catch this virus from infected humans. Symptoms in cats include respiratory (such as a cough) and digestive symptoms. Cats can spread the virus to other cats, and may be able to spread the virus to humans, but cat-to-human transmission of SARS-CoV-2 has not been proven. Compared to cats, dogs are less susceptible to this infection. Behaviors which increase the risk of transmission include kissing, licking, and petting the animal.

 

The virus does not appear to be able to infect pigs, ducks, or chickens at all.[ Mice, rats, and rabbits, if they can be infected at all, are unlikely to be involved in spreading the virus.

 

Tigers and lions in zoos have become infected as a result of contact with infected humans. As expected, monkeys and great ape species such as orangutans can also be infected with the COVID-19 virus.

 

Minks, which are in the same family as ferrets, have been infected. Minks may be asymptomatic, and can also spread the virus to humans. Multiple countries have identified infected animals in mink farms. Denmark, a major producer of mink pelts, ordered the slaughter of all minks over fears of viral mutations. A vaccine for mink and other animals is being researched.

 

RESEARCH

International research on vaccines and medicines in COVID-19 is underway by government organisations, academic groups, and industry researchers. The CDC has classified it to require a BSL3 grade laboratory. There has been a great deal of COVID-19 research, involving accelerated research processes and publishing shortcuts to meet the global demand.

 

As of December 2020, hundreds of clinical trials have been undertaken, with research happening on every continent except Antarctica. As of November 2020, more than 200 possible treatments had been studied in humans so far.

Transmission and prevention research

Modelling research has been conducted with several objectives, including predictions of the dynamics of transmission, diagnosis and prognosis of infection, estimation of the impact of interventions, or allocation of resources. Modelling studies are mostly based on epidemiological models, estimating the number of infected people over time under given conditions. Several other types of models have been developed and used during the COVID-19 including computational fluid dynamics models to study the flow physics of COVID-19, retrofits of crowd movement models to study occupant exposure, mobility-data based models to investigate transmission, or the use of macroeconomic models to assess the economic impact of the pandemic. Further, conceptual frameworks from crisis management research have been applied to better understand the effects of COVID-19 on organizations worldwide.

 

TREATMENT-RELATED RESEARCH

Repurposed antiviral drugs make up most of the research into COVID-19 treatments. Other candidates in trials include vasodilators, corticosteroids, immune therapies, lipoic acid, bevacizumab, and recombinant angiotensin-converting enzyme 2.

 

In March 2020, the World Health Organization (WHO) initiated the Solidarity trial to assess the treatment effects of some promising drugs: an experimental drug called remdesivir; anti-malarial drugs chloroquine and hydroxychloroquine; two anti-HIV drugs, lopinavir/ritonavir; and interferon-beta. More than 300 active clinical trials were underway as of April 2020.

 

Research on the antimalarial drugs hydroxychloroquine and chloroquine showed that they were ineffective at best, and that they may reduce the antiviral activity of remdesivir. By May 2020, France, Italy, and Belgium had banned the use of hydroxychloroquine as a COVID-19 treatment.

 

In June, initial results from the randomised RECOVERY Trial in the United Kingdom showed that dexamethasone reduced mortality by one third for people who are critically ill on ventilators and one fifth for those receiving supplemental oxygen. Because this is a well-tested and widely available treatment, it was welcomed by the WHO, which is in the process of updating treatment guidelines to include dexamethasone and other steroids. Based on those preliminary results, dexamethasone treatment has been recommended by the NIH for patients with COVID-19 who are mechanically ventilated or who require supplemental oxygen but not in patients with COVID-19 who do not require supplemental oxygen.

 

In September 2020, the WHO released updated guidance on using corticosteroids for COVID-19. The WHO recommends systemic corticosteroids rather than no systemic corticosteroids for the treatment of people with severe and critical COVID-19 (strong recommendation, based on moderate certainty evidence). The WHO suggests not to use corticosteroids in the treatment of people with non-severe COVID-19 (conditional recommendation, based on low certainty evidence). The updated guidance was based on a meta-analysis of clinical trials of critically ill COVID-19 patients.

 

WIKIPEDIA

Psychological resilience is defined as an individual's ability to successfully adapt to life tasks in the face of social disadvantage or other highly adverse conditions.Adversity and stress can come in the shape of family or relationship problems, health problems, or workplace and financial worries, among others. Resilience is the ability to bounce back from a negative experience with "competent functioning". Resilience is not a rare ability; in reality, it is found in the average individual and it can be learned and developed by virtually anyone. Resilience is a process, rather than a trait to be had. It is a process of individuation through a structured system with gradual discovery of personal and unique abilities. A common misconception is that resilient people are free from negative emotions or thoughts, and remain optimistic in most or all situations. To the contrary, resilient individuals have, through time, developed proper coping techniques that allow them to effectively and relatively easily navigate around or through crises. In other words, people who demonstrate resilience are people with optimistic attitudes and positive emotionality; they are, in practice, able to effectively counter negative emotions with positive emotions. Compare the pressures you face in a typical week with a few years ago: have they increased? Now think about the years ahead: are the pressures likely to keep growing? If you’re answering 'yes', this could be a good time to review and renew your strategies for resilience. Alan Heeks has many years’ experience of exploring how people can raise their wellbeing and resilience through contact with nature.Resilience is generally thought of as a "positive adaptation" after a stressful or adverse situation. When a person is "bombarded by daily stress, it disrupts their internal and external sense of balance, presenting challenges as well as opportunities." Resilience is the integrated adaptation of physical, mental and spiritual aspects in a set of "good or bad" circumstances, a coherent sense of self that is able to maintain normative developmental tasks that occur at various stages of life. The Children's Institute of the University of Rochester explains that "resilience research is focused on studying those who engage in life with hope and humor despite devastating losses". It is important to note that resilience is not only about overcoming a deeply stressful situation, but also coming out of the said situation with "competent functioning". Resiliency allows a person to rebound from adversity as a strengthened and more resourceful person. “One of the themes that emerges from these groups is that people feel increasingly depleted by everyday life and work, and it’s getting worse.

"There are many reasons for this, including the many hours spent with smartphones and screens, which mean that they are constantly overloaded with too much information, and alarming news from across the globe. Medical School quotes many research studies showing how long hours in front of screens put people in a continual state of alert, which makes it hard for them both to concentrate, and also to relax. An example of what we can learn from nature is composting: in woods, as in organic farms and gardens, the major source of future growth is waste, dead matter which can be transformed into nutrition for future growth.Resilience is generally thought of as a "positive adaptation" after a stressful or adverse situation.[8] When a person is "bombarded by daily stress, it disrupts their internal and external sense of balance, presenting challenges as well as opportunities." Resilience is the integrated adaptation of physical, mental and spiritual aspects in a set of "good or bad" circumstances, a coherent sense of self that is able to maintain normative developmental tasks that occur at various stages of life. The Children's Institute of the University of Rochester explains that "resilience research is focused on studying those who engage in life with hope and humor despite devastating losses". It is important to note that resilience is not only about overcoming a deeply stressful situation, but also coming out of the said situation with "competent functioning". Resiliency allows a person to rebound from adversity as a strengthened and more resourceful person. You could do the same: imagine recycling negative feelings and anxious thoughts, and using their energy to give you insights and growth. Another theme which emerges for some people at the wood is their concerns for the state of the world, climate change, and damage to the environment. Many people feel helpless about such problems, and simply stuff their worries down. Alan said: “I find that these deep, denied worries affect a lot of people, and sap their energy and resilience. We offer a range of processes, such as composting and deep ecology, to help people face these anxieties, and find a more positive outlook.” The way to positive change for the state of our world begins with dreams. He points out that dreams, in the sense of inspiring visions, and myths, in the sense of prevailing beliefs, have a huge influence in our world. It believes that the wisdom of Gaia, planet earth, can team up with the inventiveness of humans, to find solutions even to the current threats. The mega-crisis represents a mega-opportunity. You could look at it as a chance for humans to grow dramatically in resilience, and in their connection with Nature. We have to dare to dream: if we can at least carry a vision of the future we hope for, it starts to gather momentum.” He provides organic growth approaches for people and their work that help to build resilience. Jane has many years’ experience of working with mindfulness, deep ecology and other approaches to wellbeing, and is part of the Wisdom Tree team.Resilience is generally thought of as a "positive adaptation" after a stressful or adverse situation.[8] When a person is "bombarded by daily stress, it disrupts their internal and external sense of balance, presenting challenges as well as opportunities." Resilience is the integrated adaptation of physical, mental and spiritual aspects in a set of "good or bad" circumstances, a coherent sense of self that is able to maintain normative developmental tasks that occur at various stages of life.The Children's Institute of the University of Rochester explains that "resilience research is focused on studying those who engage in life with hope and humor despite devastating losses". It is important to note that resilience is not only about overcoming a deeply stressful situation, but also coming out of the said situation with "competent functioning". Resiliency allows a person to rebound from adversity as a strengthened and more resourceful person.Three notable bases for resilience, self-confidence, self-esteem and self-concept, all have roots in three different nervous systems—respectively, the somatic nervous system, the autonomic nervous system and the central nervous system. An emerging field in the study of resilience is the neurobiological basis of resilience to stress. For example, neuropeptide Y (NPY) and 5-Dehydroepiandrosterone (5-DHEA) are thought to limit the stress response by reducing sympathetic nervous system activation and protecting the brain from the potentially harmful effects of chronically elevated cortisol levels respectively. In addition, the relationship between social support and stress resilience is thought to be mediated by the oxytocin system's impact on the hypothalamic-pituitary-adrenal axis. "Resilience, conceptualized as a positive bio-psychological adaptation, has proven to be a useful theoretical context for understanding variables for predicting long-term health and well-being".There is some limited research that, like trauma, resilience is epigenetic—that is, it may be inherited—but the science behind this finding is preliminary.Studies show that there are several factors which develop and sustain a person's resilience: The ability to make realistic plans and being capable of taking the steps necessary to follow through with them

Confidence in one’s strengths and abilities

Communication and problem-solving skills

The ability to manage strong impulses and feelings

Resilience is negatively correlated with personality traits of neuroticism and negative emotionality, which represents tendencies to see and react to the world as threatening, problematic, and distressing, and to view oneself as vulnerable. Positive correlations stands with personality traits of openness and positive emotionality, that represents tendencies to engage and confront the world with confidence in success and a fair value to self-directedness.There is significant research found in scientific literature on the relationship between positive emotions and resilience. Studies show that maintaining positive emotions whilst facing adversity promote flexibility in thinking and problem solving. Positive emotions serve an important function in their ability to help an individual recover from stressful experiences and encounters. That being said, maintaining a positive emotionality aids in counteracting the physiological effects of negative emotions. It also facilitates adaptive coping, builds enduring social resources, and increases personal well-being. Formation of conscious perception and monitoring one's own socioemotional factors is considered as a stablity aspect of positive emotions.[citation needed] This is not to say that positive emotions are merely a by-product of resilience, but rather that feeling positive emotions during stressful experiences may have adaptive benefits in the coping process of the individual. Empirical evidence for this prediction arises from research on resilient individuals who have a propensity for coping strategies that concretely elicit positive emotions, such as benefit-finding and cognitive reappraisal, humor, optimism, and goal-directed problem-focused coping. Individuals who tend to approach problems with these methods of coping may strengthen their resistance to stress by allocating more access to these positive emotional resources.Social support from caring adults encouraged resilience among participants by providing them with access to conventional activities.Positive emotions not only have physical outcomes but also physiological ones. Some physiological outcomes caused by humor include improvements in immune system functioning and increases in levels of salivary immunoglobulin A, a vital system antibody, which serves as the body’s first line of defense in respiratory illnesses. Moreover, other health outcomes include faster injury recovery rate and lower readmission rates to hospitals for the elderly, and reductions in a patient’s stay in the hospital, among many other benefits. A study was done on positive emotions in trait-resilient individuals and the cardiovascular recovery rate following negative emotions felt by those individuals. The results of the study showed that trait-resilient individuals experiencing positive emotions had an acceleration in the speed in rebounding from cardiovascular activation initially generated by negative emotional arousal, i.e. heart rate and the like.A study was conducted among high achieving professionals who seek challenging situations that require resilience. Research has examined 13 high achievers from various professions, all of whom had experienced challenges in the workplace and negative life events over the course of their careers but who had also been recognized for their great achievements in their respective fields. Participants were interviewed about everyday life in the workplace as well as their experiences with resilience and thriving. The study found six main predictors of resilience: positive and proactive personality, experience and learning, sense of control, flexibility and adaptability, balance and perspective, and perceived social support. High achievers were also found to engage in many activities unrelated to their work such as engaging in hobbies, exercising, and organizing meetups with friends and loved ones. Several factors are found to modify the negative effects of adverse life situations. Many studies show that the primary factor is to have relationships that provide care and support, create love and trust, and offer encouragement, both within and outside the family. Additional factors are also associated with resilience, like the capacity to make realistic plans, having self-confidence and a positive self image,developing communications skills, and the capacity to manage strong feelings and impulses. Temperamental and constitutional disposition is considered as a major factor in resilience. It is one of the necessary precursors of resilience along with warmth in family cohesion and accessibility of prosocial support systems. There are three kinds of temperamental systems that play part in resilience, they are the appetitive system, defensive system and attentional system. Another protective factor is related to moderating the negative effects of environmental hazards or a stressful situation in order to direct vulnerable individuals to optimistic paths, such as external social support. More specifically a 1995 study distinguished three contexts for protective factors:personal attributes, including outgoing, bright, and positive self-concepts; the family, such as having close bonds with at least one family member or an emotionally stable parent; and the community, such as receiving support or counsel from peers. Furthermore, a study of the elderly in Zurich, Switzerland, illuminated the role humor plays as a coping mechanism to maintain a state of happiness in the face of age-related adversity. Besides the above distinction on resilience, research has also been devoted to discovering the individual differences in resilience. Self-esteem, ego-control, and ego-resiliency are related to behavioral adaptation. For example, maltreated children who feel good about themselves may process risk situations differently by attributing different reasons to the environments they experience and, thereby, avoid producing negative internalized self-perceptions. Ego-control is "the threshold or operating characteristics of an individual with regard to the expression or containment"[49] of their impulses, feelings, and desires. Ego-resilience refers to "dynamic capacity, to modify his or her model level of ego-control, in either direction, as a function of the demand characteristics of the environmental context"Maltreated children who experienced some risk factors (e.g., single parenting, limited maternal education, or family unemployment), showed lower ego-resilience and intelligence than nonmaltreated children. Furthermore, maltreated children are more likely than nonmaltreated children to demonstrate disruptive-aggressive, withdraw, and internalized behavior problems. Finally, ego-resiliency, and positive self-esteem were predictors of competent adaptation in the maltreated children. Demographic information (e.g., gender) and resources (e.g., social support) are also used to predict resilience. Examining people's adaptation after disaster showed women were associated with less likelihood of resilience than men. Also, individuals who were less involved in affinity groups and organisations showed less resilience.

Certain aspects of religions and spirituality may, hypothetically, promote or hinder certain psychological virtues that increase resilience. Research has not established connection between spirituality and resilience. According to the 4th edition of Psychology of Religion by Hood, et al., the "study of positive psychology is a relatively new development...there has not yet been much direct empirical research looking specifically at the association of religion and ordinary strengths and virtues".In a review of the literature on the relationship between religiosity/spirituality and PTSD, amongst the significant findings, about half of the studies showed a positive relationship and half showed a negative relationship between measures of religiosity/spirituality and resilience. The United States Army has received criticism for promoting spirituality in its new [Comprehensive Soldier Fitness] program as a way to prevent PTSD, due to the lack of conclusive supporting data. In military studies it has been found that resilience is also dependent on group support: unit cohesion and morale is the best predictor of combat resiliency within a unit or organization. Resilience is highly correlated to peer support and group cohesion. Units with high cohesion tend to experience a lower rate of psychological breakdowns than units with low cohesion and morale. High cohesion and morale enhance adaptive stress reactions.

 

en.wikipedia.org/wiki/Psychological_resilience

Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The first case was identified in Wuhan, China, in December 2019. The disease has since spread worldwide, leading to an ongoing pandemic.

 

Symptoms of COVID-19 are variable, but often include fever, cough, fatigue, breathing difficulties, and loss of smell and taste. Symptoms begin one to fourteen days after exposure to the virus. Of those people who develop noticeable symptoms, most (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging), and 5% suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction). Older people are more likely to have severe symptoms. At least a third of the people who are infected with the virus remain asymptomatic and do not develop noticeable symptoms at any point in time, but they still can spread the disease.[ Around 20% of those people will remain asymptomatic throughout infection, and the rest will develop symptoms later on, becoming pre-symptomatic rather than asymptomatic and therefore having a higher risk of transmitting the virus to others. Some people continue to experience a range of effects—known as long COVID—for months after recovery, and damage to organs has been observed. Multi-year studies are underway to further investigate the long-term effects of the disease.

 

The virus that causes COVID-19 spreads mainly when an infected person is in close contact[a] with another person. Small droplets and aerosols containing the virus can spread from an infected person's nose and mouth as they breathe, cough, sneeze, sing, or speak. Other people are infected if the virus gets into their mouth, nose or eyes. The virus may also spread via contaminated surfaces, although this is not thought to be the main route of transmission. The exact route of transmission is rarely proven conclusively, but infection mainly happens when people are near each other for long enough. People who are infected can transmit the virus to another person up to two days before they themselves show symptoms, as can people who do not experience symptoms. People remain infectious for up to ten days after the onset of symptoms in moderate cases and up to 20 days in severe cases. Several testing methods have been developed to diagnose the disease. The standard diagnostic method is by detection of the virus' nucleic acid by real-time reverse transcription polymerase chain reaction (rRT-PCR), transcription-mediated amplification (TMA), or by reverse transcription loop-mediated isothermal amplification (RT-LAMP) from a nasopharyngeal swab.

 

Preventive measures include physical or social distancing, quarantining, ventilation of indoor spaces, covering coughs and sneezes, hand washing, and keeping unwashed hands away from the face. The use of face masks or coverings has been recommended in public settings to minimise the risk of transmissions. Several vaccines have been developed and several countries have initiated mass vaccination campaigns.

 

Although work is underway to develop drugs that inhibit the virus, the primary treatment is currently symptomatic. Management involves the treatment of symptoms, supportive care, isolation, and experimental measures.

 

SIGNS AND SYSTOMS

Symptoms of COVID-19 are variable, ranging from mild symptoms to severe illness. Common symptoms include headache, loss of smell and taste, nasal congestion and rhinorrhea, cough, muscle pain, sore throat, fever, diarrhea, and breathing difficulties. People with the same infection may have different symptoms, and their symptoms may change over time. Three common clusters of symptoms have been identified: one respiratory symptom cluster with cough, sputum, shortness of breath, and fever; a musculoskeletal symptom cluster with muscle and joint pain, headache, and fatigue; a cluster of digestive symptoms with abdominal pain, vomiting, and diarrhea. In people without prior ear, nose, and throat disorders, loss of taste combined with loss of smell is associated with COVID-19.

 

Most people (81%) develop mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging) and 5% of patients suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction). At least a third of the people who are infected with the virus do not develop noticeable symptoms at any point in time. These asymptomatic carriers tend not to get tested and can spread the disease. Other infected people will develop symptoms later, called "pre-symptomatic", or have very mild symptoms and can also spread the virus.

 

As is common with infections, there is a delay between the moment a person first becomes infected and the appearance of the first symptoms. The median delay for COVID-19 is four to five days. Most symptomatic people experience symptoms within two to seven days after exposure, and almost all will experience at least one symptom within 12 days.

Most people recover from the acute phase of the disease. However, some people continue to experience a range of effects for months after recovery—named long COVID—and damage to organs has been observed. Multi-year studies are underway to further investigate the long-term effects of the disease.

 

CAUSE

TRANSMISSION

Coronavirus disease 2019 (COVID-19) spreads from person to person mainly through the respiratory route after an infected person coughs, sneezes, sings, talks or breathes. A new infection occurs when virus-containing particles exhaled by an infected person, either respiratory droplets or aerosols, get into the mouth, nose, or eyes of other people who are in close contact with the infected person. During human-to-human transmission, an average 1000 infectious SARS-CoV-2 virions are thought to initiate a new infection.

 

The closer people interact, and the longer they interact, the more likely they are to transmit COVID-19. Closer distances can involve larger droplets (which fall to the ground) and aerosols, whereas longer distances only involve aerosols. Larger droplets can also turn into aerosols (known as droplet nuclei) through evaporation. The relative importance of the larger droplets and the aerosols is not clear as of November 2020; however, the virus is not known to spread between rooms over long distances such as through air ducts. Airborne transmission is able to particularly occur indoors, in high risk locations such as restaurants, choirs, gyms, nightclubs, offices, and religious venues, often when they are crowded or less ventilated. It also occurs in healthcare settings, often when aerosol-generating medical procedures are performed on COVID-19 patients.

 

Although it is considered possible there is no direct evidence of the virus being transmitted by skin to skin contact. A person could get COVID-19 indirectly by touching a contaminated surface or object before touching their own mouth, nose, or eyes, though this is not thought to be the main way the virus spreads. The virus is not known to spread through feces, urine, breast milk, food, wastewater, drinking water, or via animal disease vectors (although some animals can contract the virus from humans). It very rarely transmits from mother to baby during pregnancy.

 

Social distancing and the wearing of cloth face masks, surgical masks, respirators, or other face coverings are controls for droplet transmission. Transmission may be decreased indoors with well maintained heating and ventilation systems to maintain good air circulation and increase the use of outdoor air.

 

The number of people generally infected by one infected person varies. Coronavirus disease 2019 is more infectious than influenza, but less so than measles. It often spreads in clusters, where infections can be traced back to an index case or geographical location. There is a major role of "super-spreading events", where many people are infected by one person.

 

A person who is infected can transmit the virus to others up to two days before they themselves show symptoms, and even if symptoms never appear. People remain infectious in moderate cases for 7–12 days, and up to two weeks in severe cases. In October 2020, medical scientists reported evidence of reinfection in one person.

 

VIROLOGY

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel severe acute respiratory syndrome coronavirus. It was first isolated from three people with pneumonia connected to the cluster of acute respiratory illness cases in Wuhan. All structural features of the novel SARS-CoV-2 virus particle occur in related coronaviruses in nature.

 

Outside the human body, the virus is destroyed by household soap, which bursts its protective bubble.

 

SARS-CoV-2 is closely related to the original SARS-CoV. It is thought to have an animal (zoonotic) origin. Genetic analysis has revealed that the coronavirus genetically clusters with the genus Betacoronavirus, in subgenus Sarbecovirus (lineage B) together with two bat-derived strains. It is 96% identical at the whole genome level to other bat coronavirus samples (BatCov RaTG13). The structural proteins of SARS-CoV-2 include membrane glycoprotein (M), envelope protein (E), nucleocapsid protein (N), and the spike protein (S). The M protein of SARS-CoV-2 is about 98% similar to the M protein of bat SARS-CoV, maintains around 98% homology with pangolin SARS-CoV, and has 90% homology with the M protein of SARS-CoV; whereas, the similarity is only around 38% with the M protein of MERS-CoV. The structure of the M protein resembles the sugar transporter SemiSWEET.

 

The many thousands of SARS-CoV-2 variants are grouped into clades. Several different clade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR).

 

Several notable variants of SARS-CoV-2 emerged in late 2020. Cluster 5 emerged among minks and mink farmers in Denmark. After strict quarantines and a mink euthanasia campaign, it is believed to have been eradicated. The Variant of Concern 202012/01 (VOC 202012/01) is believed to have emerged in the United Kingdom in September. The 501Y.V2 Variant, which has the same N501Y mutation, arose independently in South Africa.

 

SARS-CoV-2 VARIANTS

Three known variants of SARS-CoV-2 are currently spreading among global populations as of January 2021 including the UK Variant (referred to as B.1.1.7) first found in London and Kent, a variant discovered in South Africa (referred to as 1.351), and a variant discovered in Brazil (referred to as P.1).

 

Using Whole Genome Sequencing, epidemiology and modelling suggest the new UK variant ‘VUI – 202012/01’ (the first Variant Under Investigation in December 2020) transmits more easily than other strains.

 

PATHOPHYSIOLOGY

COVID-19 can affect the upper respiratory tract (sinuses, nose, and throat) and the lower respiratory tract (windpipe and lungs). The lungs are the organs most affected by COVID-19 because the virus accesses host cells via the enzyme angiotensin-converting enzyme 2 (ACE2), which is most abundant in type II alveolar cells of the lungs. The virus uses a special surface glycoprotein called a "spike" (peplomer) to connect to ACE2 and enter the host cell. The density of ACE2 in each tissue correlates with the severity of the disease in that tissue and decreasing ACE2 activity might be protective, though another view is that increasing ACE2 using angiotensin II receptor blocker medications could be protective. As the alveolar disease progresses, respiratory failure might develop and death may follow.

 

Whether SARS-CoV-2 is able to invade the nervous system remains unknown. The virus is not detected in the CNS of the majority of COVID-19 people with neurological issues. However, SARS-CoV-2 has been detected at low levels in the brains of those who have died from COVID-19, but these results need to be confirmed. SARS-CoV-2 could cause respiratory failure through affecting the brain stem as other coronaviruses have been found to invade the CNS. While virus has been detected in cerebrospinal fluid of autopsies, the exact mechanism by which it invades the CNS remains unclear and may first involve invasion of peripheral nerves given the low levels of ACE2 in the brain. The virus may also enter the bloodstream from the lungs and cross the blood-brain barrier to gain access to the CNS, possibly within an infected white blood cell.

 

The virus also affects gastrointestinal organs as ACE2 is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium as well as endothelial cells and enterocytes of the small intestine.

 

The virus can cause acute myocardial injury and chronic damage to the cardiovascular system. An acute cardiac injury was found in 12% of infected people admitted to the hospital in Wuhan, China, and is more frequent in severe disease. Rates of cardiovascular symptoms are high, owing to the systemic inflammatory response and immune system disorders during disease progression, but acute myocardial injuries may also be related to ACE2 receptors in the heart. ACE2 receptors are highly expressed in the heart and are involved in heart function. A high incidence of thrombosis and venous thromboembolism have been found people transferred to Intensive care unit (ICU) with COVID-19 infections, and may be related to poor prognosis. Blood vessel dysfunction and clot formation (as suggested by high D-dimer levels caused by blood clots) are thought to play a significant role in mortality, incidences of clots leading to pulmonary embolisms, and ischaemic events within the brain have been noted as complications leading to death in people infected with SARS-CoV-2. Infection appears to set off a chain of vasoconstrictive responses within the body, constriction of blood vessels within the pulmonary circulation has also been posited as a mechanism in which oxygenation decreases alongside the presentation of viral pneumonia. Furthermore, microvascular blood vessel damage has been reported in a small number of tissue samples of the brains – without detected SARS-CoV-2 – and the olfactory bulbs from those who have died from COVID-19.

 

Another common cause of death is complications related to the kidneys. Early reports show that up to 30% of hospitalized patients both in China and in New York have experienced some injury to their kidneys, including some persons with no previous kidney problems.

 

Autopsies of people who died of COVID-19 have found diffuse alveolar damage, and lymphocyte-containing inflammatory infiltrates within the lung.

 

IMMUNOPATHOLOGY

Although SARS-CoV-2 has a tropism for ACE2-expressing epithelial cells of the respiratory tract, people with severe COVID-19 have symptoms of systemic hyperinflammation. Clinical laboratory findings of elevated IL-2, IL-7, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-γ inducible protein 10 (IP-10), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 1-α (MIP-1α), and tumour necrosis factor-α (TNF-α) indicative of cytokine release syndrome (CRS) suggest an underlying immunopathology.

 

Additionally, people with COVID-19 and acute respiratory distress syndrome (ARDS) have classical serum biomarkers of CRS, including elevated C-reactive protein (CRP), lactate dehydrogenase (LDH), D-dimer, and ferritin.

 

Systemic inflammation results in vasodilation, allowing inflammatory lymphocytic and monocytic infiltration of the lung and the heart. In particular, pathogenic GM-CSF-secreting T-cells were shown to correlate with the recruitment of inflammatory IL-6-secreting monocytes and severe lung pathology in people with COVID-19 . Lymphocytic infiltrates have also been reported at autopsy.

 

VIRAL AND HOST FACTORS

VIRUS PROTEINS

Multiple viral and host factors affect the pathogenesis of the virus. The S-protein, otherwise known as the spike protein, is the viral component that attaches to the host receptor via the ACE2 receptors. It includes two subunits: S1 and S2. S1 determines the virus host range and cellular tropism via the receptor binding domain. S2 mediates the membrane fusion of the virus to its potential cell host via the H1 and HR2, which are heptad repeat regions. Studies have shown that S1 domain induced IgG and IgA antibody levels at a much higher capacity. It is the focus spike proteins expression that are involved in many effective COVID-19 vaccines.

 

The M protein is the viral protein responsible for the transmembrane transport of nutrients. It is the cause of the bud release and the formation of the viral envelope. The N and E protein are accessory proteins that interfere with the host's immune response.

 

HOST FACTORS

Human angiotensin converting enzyme 2 (hACE2) is the host factor that SARS-COV2 virus targets causing COVID-19. Theoretically the usage of angiotensin receptor blockers (ARB) and ACE inhibitors upregulating ACE2 expression might increase morbidity with COVID-19, though animal data suggest some potential protective effect of ARB. However no clinical studies have proven susceptibility or outcomes. Until further data is available, guidelines and recommendations for hypertensive patients remain.

 

The virus' effect on ACE2 cell surfaces leads to leukocytic infiltration, increased blood vessel permeability, alveolar wall permeability, as well as decreased secretion of lung surfactants. These effects cause the majority of the respiratory symptoms. However, the aggravation of local inflammation causes a cytokine storm eventually leading to a systemic inflammatory response syndrome.

 

HOST CYTOKINE RESPONSE

The severity of the inflammation can be attributed to the severity of what is known as the cytokine storm. Levels of interleukin 1B, interferon-gamma, interferon-inducible protein 10, and monocyte chemoattractant protein 1 were all associated with COVID-19 disease severity. Treatment has been proposed to combat the cytokine storm as it remains to be one of the leading causes of morbidity and mortality in COVID-19 disease.

 

A cytokine storm is due to an acute hyperinflammatory response that is responsible for clinical illness in an array of diseases but in COVID-19, it is related to worse prognosis and increased fatality. The storm causes the acute respiratory distress syndrome, blood clotting events such as strokes, myocardial infarction, encephalitis, acute kidney injury, and vasculitis. The production of IL-1, IL-2, IL-6, TNF-alpha, and interferon-gamma, all crucial components of normal immune responses, inadvertently become the causes of a cytokine storm. The cells of the central nervous system, the microglia, neurons, and astrocytes, are also be involved in the release of pro-inflammatory cytokines affecting the nervous system, and effects of cytokine storms toward the CNS are not uncommon.

 

DIAGNOSIS

COVID-19 can provisionally be diagnosed on the basis of symptoms and confirmed using reverse transcription polymerase chain reaction (RT-PCR) or other nucleic acid testing of infected secretions. Along with laboratory testing, chest CT scans may be helpful to diagnose COVID-19 in individuals with a high clinical suspicion of infection. Detection of a past infection is possible with serological tests, which detect antibodies produced by the body in response to the infection.

 

VIRAL TESTING

The standard methods of testing for presence of SARS-CoV-2 are nucleic acid tests, which detects the presence of viral RNA fragments. As these tests detect RNA but not infectious virus, its "ability to determine duration of infectivity of patients is limited." The test is typically done on respiratory samples obtained by a nasopharyngeal swab; however, a nasal swab or sputum sample may also be used. Results are generally available within hours. The WHO has published several testing protocols for the disease.

 

A number of laboratories and companies have developed serological tests, which detect antibodies produced by the body in response to infection. Several have been evaluated by Public Health England and approved for use in the UK.

 

The University of Oxford's CEBM has pointed to mounting evidence that "a good proportion of 'new' mild cases and people re-testing positives after quarantine or discharge from hospital are not infectious, but are simply clearing harmless virus particles which their immune system has efficiently dealt with" and have called for "an international effort to standardize and periodically calibrate testing" On 7 September, the UK government issued "guidance for procedures to be implemented in laboratories to provide assurance of positive SARS-CoV-2 RNA results during periods of low prevalence, when there is a reduction in the predictive value of positive test results."

 

IMAGING

Chest CT scans may be helpful to diagnose COVID-19 in individuals with a high clinical suspicion of infection but are not recommended for routine screening. Bilateral multilobar ground-glass opacities with a peripheral, asymmetric, and posterior distribution are common in early infection. Subpleural dominance, crazy paving (lobular septal thickening with variable alveolar filling), and consolidation may appear as the disease progresses. Characteristic imaging features on chest radiographs and computed tomography (CT) of people who are symptomatic include asymmetric peripheral ground-glass opacities without pleural effusions.

 

Many groups have created COVID-19 datasets that include imagery such as the Italian Radiological Society which has compiled an international online database of imaging findings for confirmed cases. Due to overlap with other infections such as adenovirus, imaging without confirmation by rRT-PCR is of limited specificity in identifying COVID-19. A large study in China compared chest CT results to PCR and demonstrated that though imaging is less specific for the infection, it is faster and more sensitive.

Coding

In late 2019, the WHO assigned emergency ICD-10 disease codes U07.1 for deaths from lab-confirmed SARS-CoV-2 infection and U07.2 for deaths from clinically or epidemiologically diagnosed COVID-19 without lab-confirmed SARS-CoV-2 infection.

 

PATHOLOGY

The main pathological findings at autopsy are:

 

Macroscopy: pericarditis, lung consolidation and pulmonary oedema

Lung findings:

minor serous exudation, minor fibrin exudation

pulmonary oedema, pneumocyte hyperplasia, large atypical pneumocytes, interstitial inflammation with lymphocytic infiltration and multinucleated giant cell formation

diffuse alveolar damage (DAD) with diffuse alveolar exudates. DAD is the cause of acute respiratory distress syndrome (ARDS) and severe hypoxemia.

organisation of exudates in alveolar cavities and pulmonary interstitial fibrosis

plasmocytosis in BAL

Blood: disseminated intravascular coagulation (DIC); leukoerythroblastic reaction

Liver: microvesicular steatosis

 

PREVENTION

Preventive measures to reduce the chances of infection include staying at home, wearing a mask in public, avoiding crowded places, keeping distance from others, ventilating indoor spaces, washing hands with soap and water often and for at least 20 seconds, practising good respiratory hygiene, and avoiding touching the eyes, nose, or mouth with unwashed hands.

 

Those diagnosed with COVID-19 or who believe they may be infected are advised by the CDC to stay home except to get medical care, call ahead before visiting a healthcare provider, wear a face mask before entering the healthcare provider's office and when in any room or vehicle with another person, cover coughs and sneezes with a tissue, regularly wash hands with soap and water and avoid sharing personal household items.

 

The first COVID-19 vaccine was granted regulatory approval on 2 December by the UK medicines regulator MHRA. It was evaluated for emergency use authorization (EUA) status by the US FDA, and in several other countries. Initially, the US National Institutes of Health guidelines do not recommend any medication for prevention of COVID-19, before or after exposure to the SARS-CoV-2 virus, outside the setting of a clinical trial. Without a vaccine, other prophylactic measures, or effective treatments, a key part of managing COVID-19 is trying to decrease and delay the epidemic peak, known as "flattening the curve". This is done by slowing the infection rate to decrease the risk of health services being overwhelmed, allowing for better treatment of current cases, and delaying additional cases until effective treatments or a vaccine become available.

 

VACCINE

A COVID‑19 vaccine is a vaccine intended to provide acquired immunity against severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2), the virus causing coronavirus disease 2019 (COVID‑19). Prior to the COVID‑19 pandemic, there was an established body of knowledge about the structure and function of coronaviruses causing diseases like severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), which enabled accelerated development of various vaccine technologies during early 2020. On 10 January 2020, the SARS-CoV-2 genetic sequence data was shared through GISAID, and by 19 March, the global pharmaceutical industry announced a major commitment to address COVID-19.

 

In Phase III trials, several COVID‑19 vaccines have demonstrated efficacy as high as 95% in preventing symptomatic COVID‑19 infections. As of March 2021, 12 vaccines were authorized by at least one national regulatory authority for public use: two RNA vaccines (the Pfizer–BioNTech vaccine and the Moderna vaccine), four conventional inactivated vaccines (BBIBP-CorV, CoronaVac, Covaxin, and CoviVac), four viral vector vaccines (Sputnik V, the Oxford–AstraZeneca vaccine, Convidicea, and the Johnson & Johnson vaccine), and two protein subunit vaccines (EpiVacCorona and RBD-Dimer). In total, as of March 2021, 308 vaccine candidates were in various stages of development, with 73 in clinical research, including 24 in Phase I trials, 33 in Phase I–II trials, and 16 in Phase III development.

Many countries have implemented phased distribution plans that prioritize those at highest risk of complications, such as the elderly, and those at high risk of exposure and transmission, such as healthcare workers. As of 17 March 2021, 400.22 million doses of COVID‑19 vaccine have been administered worldwide based on official reports from national health agencies. AstraZeneca-Oxford anticipates producing 3 billion doses in 2021, Pfizer-BioNTech 1.3 billion doses, and Sputnik V, Sinopharm, Sinovac, and Johnson & Johnson 1 billion doses each. Moderna targets producing 600 million doses and Convidicea 500 million doses in 2021. By December 2020, more than 10 billion vaccine doses had been preordered by countries, with about half of the doses purchased by high-income countries comprising 14% of the world's population.

 

SOCIAL DISTANCING

Social distancing (also known as physical distancing) includes infection control actions intended to slow the spread of the disease by minimising close contact between individuals. Methods include quarantines; travel restrictions; and the closing of schools, workplaces, stadiums, theatres, or shopping centres. Individuals may apply social distancing methods by staying at home, limiting travel, avoiding crowded areas, using no-contact greetings, and physically distancing themselves from others. Many governments are now mandating or recommending social distancing in regions affected by the outbreak.

 

Outbreaks have occurred in prisons due to crowding and an inability to enforce adequate social distancing. In the United States, the prisoner population is aging and many of them are at high risk for poor outcomes from COVID-19 due to high rates of coexisting heart and lung disease, and poor access to high-quality healthcare.

 

SELF-ISOLATION

Self-isolation at home has been recommended for those diagnosed with COVID-19 and those who suspect they have been infected. Health agencies have issued detailed instructions for proper self-isolation. Many governments have mandated or recommended self-quarantine for entire populations. The strongest self-quarantine instructions have been issued to those in high-risk groups. Those who may have been exposed to someone with COVID-19 and those who have recently travelled to a country or region with the widespread transmission have been advised to self-quarantine for 14 days from the time of last possible exposure.

Face masks and respiratory hygiene

 

The WHO and the US CDC recommend individuals wear non-medical face coverings in public settings where there is an increased risk of transmission and where social distancing measures are difficult to maintain. This recommendation is meant to reduce the spread of the disease by asymptomatic and pre-symptomatic individuals and is complementary to established preventive measures such as social distancing. Face coverings limit the volume and travel distance of expiratory droplets dispersed when talking, breathing, and coughing. A face covering without vents or holes will also filter out particles containing the virus from inhaled and exhaled air, reducing the chances of infection. But, if the mask include an exhalation valve, a wearer that is infected (maybe without having noticed that, and asymptomatic) would transmit the virus outwards through it, despite any certification they can have. So the masks with exhalation valve are not for the infected wearers, and are not reliable to stop the pandemic in a large scale. Many countries and local jurisdictions encourage or mandate the use of face masks or cloth face coverings by members of the public to limit the spread of the virus.

 

Masks are also strongly recommended for those who may have been infected and those taking care of someone who may have the disease. When not wearing a mask, the CDC recommends covering the mouth and nose with a tissue when coughing or sneezing and recommends using the inside of the elbow if no tissue is available. Proper hand hygiene after any cough or sneeze is encouraged. Healthcare professionals interacting directly with people who have COVID-19 are advised to use respirators at least as protective as NIOSH-certified N95 or equivalent, in addition to other personal protective equipment.

 

HAND-WASHING AND HYGIENE

Thorough hand hygiene after any cough or sneeze is required. The WHO also recommends that individuals wash hands often with soap and water for at least 20 seconds, especially after going to the toilet or when hands are visibly dirty, before eating and after blowing one's nose. The CDC recommends using an alcohol-based hand sanitiser with at least 60% alcohol, but only when soap and water are not readily available. For areas where commercial hand sanitisers are not readily available, the WHO provides two formulations for local production. In these formulations, the antimicrobial activity arises from ethanol or isopropanol. Hydrogen peroxide is used to help eliminate bacterial spores in the alcohol; it is "not an active substance for hand antisepsis". Glycerol is added as a humectant.

 

SURFACE CLEANING

After being expelled from the body, coronaviruses can survive on surfaces for hours to days. If a person touches the dirty surface, they may deposit the virus at the eyes, nose, or mouth where it can enter the body cause infection. Current evidence indicates that contact with infected surfaces is not the main driver of Covid-19, leading to recommendations for optimised disinfection procedures to avoid issues such as the increase of antimicrobial resistance through the use of inappropriate cleaning products and processes. Deep cleaning and other surface sanitation has been criticized as hygiene theater, giving a false sense of security against something primarily spread through the air.

 

The amount of time that the virus can survive depends significantly on the type of surface, the temperature, and the humidity. Coronaviruses die very quickly when exposed to the UV light in sunlight. Like other enveloped viruses, SARS-CoV-2 survives longest when the temperature is at room temperature or lower, and when the relative humidity is low (<50%).

 

On many surfaces, including as glass, some types of plastic, stainless steel, and skin, the virus can remain infective for several days indoors at room temperature, or even about a week under ideal conditions. On some surfaces, including cotton fabric and copper, the virus usually dies after a few hours. As a general rule of thumb, the virus dies faster on porous surfaces than on non-porous surfaces.

However, this rule is not absolute, and of the many surfaces tested, two with the longest survival times are N95 respirator masks and surgical masks, both of which are considered porous surfaces.

 

Surfaces may be decontaminated with 62–71 percent ethanol, 50–100 percent isopropanol, 0.1 percent sodium hypochlorite, 0.5 percent hydrogen peroxide, and 0.2–7.5 percent povidone-iodine. Other solutions, such as benzalkonium chloride and chlorhexidine gluconate, are less effective. Ultraviolet germicidal irradiation may also be used. The CDC recommends that if a COVID-19 case is suspected or confirmed at a facility such as an office or day care, all areas such as offices, bathrooms, common areas, shared electronic equipment like tablets, touch screens, keyboards, remote controls, and ATM machines used by the ill persons should be disinfected. A datasheet comprising the authorised substances to disinfection in the food industry (including suspension or surface tested, kind of surface, use dilution, disinfectant and inocuylum volumes) can be seen in the supplementary material of.

 

VENTILATION AND AIR FILTRATION

The WHO recommends ventilation and air filtration in public spaces to help clear out infectious aerosols.

 

HEALTHY DIET AND LIFESTYLE

The Harvard T.H. Chan School of Public Health recommends a healthy diet, being physically active, managing psychological stress, and getting enough sleep.

 

While there is no evidence that vitamin D is an effective treatment for COVID-19, there is limited evidence that vitamin D deficiency increases the risk of severe COVID-19 symptoms. This has led to recommendations for individuals with vitamin D deficiency to take vitamin D supplements as a way of mitigating the risk of COVID-19 and other health issues associated with a possible increase in deficiency due to social distancing.

 

TREATMENT

There is no specific, effective treatment or cure for coronavirus disease 2019 (COVID-19), the disease caused by the SARS-CoV-2 virus. Thus, the cornerstone of management of COVID-19 is supportive care, which includes treatment to relieve symptoms, fluid therapy, oxygen support and prone positioning as needed, and medications or devices to support other affected vital organs.

 

Most cases of COVID-19 are mild. In these, supportive care includes medication such as paracetamol or NSAIDs to relieve symptoms (fever, body aches, cough), proper intake of fluids, rest, and nasal breathing. Good personal hygiene and a healthy diet are also recommended. The U.S. Centers for Disease Control and Prevention (CDC) recommend that those who suspect they are carrying the virus isolate themselves at home and wear a face mask.

 

People with more severe cases may need treatment in hospital. In those with low oxygen levels, use of the glucocorticoid dexamethasone is strongly recommended, as it can reduce the risk of death. Noninvasive ventilation and, ultimately, admission to an intensive care unit for mechanical ventilation may be required to support breathing. Extracorporeal membrane oxygenation (ECMO) has been used to address the issue of respiratory failure, but its benefits are still under consideration.

Several experimental treatments are being actively studied in clinical trials. Others were thought to be promising early in the pandemic, such as hydroxychloroquine and lopinavir/ritonavir, but later research found them to be ineffective or even harmful. Despite ongoing research, there is still not enough high-quality evidence to recommend so-called early treatment. Nevertheless, in the United States, two monoclonal antibody-based therapies are available for early use in cases thought to be at high risk of progression to severe disease. The antiviral remdesivir is available in the U.S., Canada, Australia, and several other countries, with varying restrictions; however, it is not recommended for people needing mechanical ventilation, and is discouraged altogether by the World Health Organization (WHO), due to limited evidence of its efficacy.

 

PROGNOSIS

The severity of COVID-19 varies. The disease may take a mild course with few or no symptoms, resembling other common upper respiratory diseases such as the common cold. In 3–4% of cases (7.4% for those over age 65) symptoms are severe enough to cause hospitalization. Mild cases typically recover within two weeks, while those with severe or critical diseases may take three to six weeks to recover. Among those who have died, the time from symptom onset to death has ranged from two to eight weeks. The Italian Istituto Superiore di Sanità reported that the median time between the onset of symptoms and death was twelve days, with seven being hospitalised. However, people transferred to an ICU had a median time of ten days between hospitalisation and death. Prolonged prothrombin time and elevated C-reactive protein levels on admission to the hospital are associated with severe course of COVID-19 and with a transfer to ICU.

 

Some early studies suggest 10% to 20% of people with COVID-19 will experience symptoms lasting longer than a month.[191][192] A majority of those who were admitted to hospital with severe disease report long-term problems including fatigue and shortness of breath. On 30 October 2020 WHO chief Tedros Adhanom warned that "to a significant number of people, the COVID virus poses a range of serious long-term effects". He has described the vast spectrum of COVID-19 symptoms that fluctuate over time as "really concerning." They range from fatigue, a cough and shortness of breath, to inflammation and injury of major organs – including the lungs and heart, and also neurological and psychologic effects. Symptoms often overlap and can affect any system in the body. Infected people have reported cyclical bouts of fatigue, headaches, months of complete exhaustion, mood swings, and other symptoms. Tedros has concluded that therefore herd immunity is "morally unconscionable and unfeasible".

 

In terms of hospital readmissions about 9% of 106,000 individuals had to return for hospital treatment within 2 months of discharge. The average to readmit was 8 days since first hospital visit. There are several risk factors that have been identified as being a cause of multiple admissions to a hospital facility. Among these are advanced age (above 65 years of age) and presence of a chronic condition such as diabetes, COPD, heart failure or chronic kidney disease.

 

According to scientific reviews smokers are more likely to require intensive care or die compared to non-smokers, air pollution is similarly associated with risk factors, and pre-existing heart and lung diseases and also obesity contributes to an increased health risk of COVID-19.

 

It is also assumed that those that are immunocompromised are at higher risk of getting severely sick from SARS-CoV-2. One research that looked into the COVID-19 infections in hospitalized kidney transplant recipients found a mortality rate of 11%.

See also: Impact of the COVID-19 pandemic on children

 

Children make up a small proportion of reported cases, with about 1% of cases being under 10 years and 4% aged 10–19 years. They are likely to have milder symptoms and a lower chance of severe disease than adults. A European multinational study of hospitalized children published in The Lancet on 25 June 2020 found that about 8% of children admitted to a hospital needed intensive care. Four of those 582 children (0.7%) died, but the actual mortality rate could be "substantially lower" since milder cases that did not seek medical help were not included in the study.

 

Genetics also plays an important role in the ability to fight off the disease. For instance, those that do not produce detectable type I interferons or produce auto-antibodies against these may get much sicker from COVID-19. Genetic screening is able to detect interferon effector genes.

 

Pregnant women may be at higher risk of severe COVID-19 infection based on data from other similar viruses, like SARS and MERS, but data for COVID-19 is lacking.

 

COMPLICATIONS

Complications may include pneumonia, acute respiratory distress syndrome (ARDS), multi-organ failure, septic shock, and death. Cardiovascular complications may include heart failure, arrhythmias, heart inflammation, and blood clots. Approximately 20–30% of people who present with COVID-19 have elevated liver enzymes, reflecting liver injury.

 

Neurologic manifestations include seizure, stroke, encephalitis, and Guillain–Barré syndrome (which includes loss of motor functions). Following the infection, children may develop paediatric multisystem inflammatory syndrome, which has symptoms similar to Kawasaki disease, which can be fatal. In very rare cases, acute encephalopathy can occur, and it can be considered in those who have been diagnosed with COVID-19 and have an altered mental status.

 

LONGER-TERM EFFECTS

Some early studies suggest that that 10 to 20% of people with COVID-19 will experience symptoms lasting longer than a month. A majority of those who were admitted to hospital with severe disease report long-term problems, including fatigue and shortness of breath. About 5-10% of patients admitted to hospital progress to severe or critical disease, including pneumonia and acute respiratory failure.

 

By a variety of mechanisms, the lungs are the organs most affected in COVID-19.[228] The majority of CT scans performed show lung abnormalities in people tested after 28 days of illness.

 

People with advanced age, severe disease, prolonged ICU stays, or who smoke are more likely to have long lasting effects, including pulmonary fibrosis. Overall, approximately one third of those investigated after 4 weeks will have findings of pulmonary fibrosis or reduced lung function as measured by DLCO, even in people who are asymptomatic, but with the suggestion of continuing improvement with the passing of more time.

 

IMMUNITY

The immune response by humans to CoV-2 virus occurs as a combination of the cell-mediated immunity and antibody production, just as with most other infections. Since SARS-CoV-2 has been in the human population only since December 2019, it remains unknown if the immunity is long-lasting in people who recover from the disease. The presence of neutralizing antibodies in blood strongly correlates with protection from infection, but the level of neutralizing antibody declines with time. Those with asymptomatic or mild disease had undetectable levels of neutralizing antibody two months after infection. In another study, the level of neutralizing antibody fell 4-fold 1 to 4 months after the onset of symptoms. However, the lack of antibody in the blood does not mean antibody will not be rapidly produced upon reexposure to SARS-CoV-2. Memory B cells specific for the spike and nucleocapsid proteins of SARS-CoV-2 last for at least 6 months after appearance of symptoms. Nevertheless, 15 cases of reinfection with SARS-CoV-2 have been reported using stringent CDC criteria requiring identification of a different variant from the second infection. There are likely to be many more people who have been reinfected with the virus. Herd immunity will not eliminate the virus if reinfection is common. Some other coronaviruses circulating in people are capable of reinfection after roughly a year. Nonetheless, on 3 March 2021, scientists reported that a much more contagious Covid-19 variant, Lineage P.1, first detected in Japan, and subsequently found in Brazil, as well as in several places in the United States, may be associated with Covid-19 disease reinfection after recovery from an earlier Covid-19 infection.

 

MORTALITY

Several measures are commonly used to quantify mortality. These numbers vary by region and over time and are influenced by the volume of testing, healthcare system quality, treatment options, time since the initial outbreak, and population characteristics such as age, sex, and overall health. The mortality rate reflects the number of deaths within a specific demographic group divided by the population of that demographic group. Consequently, the mortality rate reflects the prevalence as well as the severity of the disease within a given population. Mortality rates are highly correlated to age, with relatively low rates for young people and relatively high rates among the elderly.

 

The case fatality rate (CFR) reflects the number of deaths divided by the number of diagnosed cases within a given time interval. Based on Johns Hopkins University statistics, the global death-to-case ratio is 2.2% (2,685,770/121,585,388) as of 18 March 2021. The number varies by region. The CFR may not reflect the true severity of the disease, because some infected individuals remain asymptomatic or experience only mild symptoms, and hence such infections may not be included in official case reports. Moreover, the CFR may vary markedly over time and across locations due to the availability of live virus tests.

 

INFECTION FATALITY RATE

A key metric in gauging the severity of COVID-19 is the infection fatality rate (IFR), also referred to as the infection fatality ratio or infection fatality risk. This metric is calculated by dividing the total number of deaths from the disease by the total number of infected individuals; hence, in contrast to the CFR, the IFR incorporates asymptomatic and undiagnosed infections as well as reported cases.

 

CURRENT ESTIMATES

A December 2020 systematic review and meta-analysis estimated that population IFR during the first wave of the pandemic was about 0.5% to 1% in many locations (including France, Netherlands, New Zealand, and Portugal), 1% to 2% in other locations (Australia, England, Lithuania, and Spain), and exceeded 2% in Italy. That study also found that most of these differences in IFR reflected corresponding differences in the age composition of the population and age-specific infection rates; in particular, the metaregression estimate of IFR is very low for children and younger adults (e.g., 0.002% at age 10 and 0.01% at age 25) but increases progressively to 0.4% at age 55, 1.4% at age 65, 4.6% at age 75, and 15% at age 85. These results were also highlighted in a December 2020 report issued by the WHO.

 

EARLIER ESTIMATES OF IFR

At an early stage of the pandemic, the World Health Organization reported estimates of IFR between 0.3% and 1%.[ On 2 July, The WHO's chief scientist reported that the average IFR estimate presented at a two-day WHO expert forum was about 0.6%. In August, the WHO found that studies incorporating data from broad serology testing in Europe showed IFR estimates converging at approximately 0.5–1%. Firm lower limits of IFRs have been established in a number of locations such as New York City and Bergamo in Italy since the IFR cannot be less than the population fatality rate. As of 10 July, in New York City, with a population of 8.4 million, 23,377 individuals (18,758 confirmed and 4,619 probable) have died with COVID-19 (0.3% of the population).Antibody testing in New York City suggested an IFR of ~0.9%,[258] and ~1.4%. In Bergamo province, 0.6% of the population has died. In September 2020 the U.S. Center for Disease Control & Prevention reported preliminary estimates of age-specific IFRs for public health planning purposes.

 

SEX DIFFERENCES

Early reviews of epidemiologic data showed gendered impact of the pandemic and a higher mortality rate in men in China and Italy. The Chinese Center for Disease Control and Prevention reported the death rate was 2.8% for men and 1.7% for women. Later reviews in June 2020 indicated that there is no significant difference in susceptibility or in CFR between genders. One review acknowledges the different mortality rates in Chinese men, suggesting that it may be attributable to lifestyle choices such as smoking and drinking alcohol rather than genetic factors. Sex-based immunological differences, lesser prevalence of smoking in women and men developing co-morbid conditions such as hypertension at a younger age than women could have contributed to the higher mortality in men. In Europe, 57% of the infected people were men and 72% of those died with COVID-19 were men. As of April 2020, the US government is not tracking sex-related data of COVID-19 infections. Research has shown that viral illnesses like Ebola, HIV, influenza and SARS affect men and women differently.

 

ETHNIC DIFFERENCES

In the US, a greater proportion of deaths due to COVID-19 have occurred among African Americans and other minority groups. Structural factors that prevent them from practicing social distancing include their concentration in crowded substandard housing and in "essential" occupations such as retail grocery workers, public transit employees, health-care workers and custodial staff. Greater prevalence of lacking health insurance and care and of underlying conditions such as diabetes, hypertension and heart disease also increase their risk of death. Similar issues affect Native American and Latino communities. According to a US health policy non-profit, 34% of American Indian and Alaska Native People (AIAN) non-elderly adults are at risk of serious illness compared to 21% of white non-elderly adults. The source attributes it to disproportionately high rates of many health conditions that may put them at higher risk as well as living conditions like lack of access to clean water. Leaders have called for efforts to research and address the disparities. In the U.K., a greater proportion of deaths due to COVID-19 have occurred in those of a Black, Asian, and other ethnic minority background. More severe impacts upon victims including the relative incidence of the necessity of hospitalization requirements, and vulnerability to the disease has been associated via DNA analysis to be expressed in genetic variants at chromosomal region 3, features that are associated with European Neanderthal heritage. That structure imposes greater risks that those affected will develop a more severe form of the disease. The findings are from Professor Svante Pääbo and researchers he leads at the Max Planck Institute for Evolutionary Anthropology and the Karolinska Institutet. This admixture of modern human and Neanderthal genes is estimated to have occurred roughly between 50,000 and 60,000 years ago in Southern Europe.

 

COMORBIDITIES

Most of those who die of COVID-19 have pre-existing (underlying) conditions, including hypertension, diabetes mellitus, and cardiovascular disease. According to March data from the United States, 89% of those hospitalised had preexisting conditions. The Italian Istituto Superiore di Sanità reported that out of 8.8% of deaths where medical charts were available, 96.1% of people had at least one comorbidity with the average person having 3.4 diseases. According to this report the most common comorbidities are hypertension (66% of deaths), type 2 diabetes (29.8% of deaths), Ischemic Heart Disease (27.6% of deaths), atrial fibrillation (23.1% of deaths) and chronic renal failure (20.2% of deaths).

 

Most critical respiratory comorbidities according to the CDC, are: moderate or severe asthma, pre-existing COPD, pulmonary fibrosis, cystic fibrosis. Evidence stemming from meta-analysis of several smaller research papers also suggests that smoking can be associated with worse outcomes. When someone with existing respiratory problems is infected with COVID-19, they might be at greater risk for severe symptoms. COVID-19 also poses a greater risk to people who misuse opioids and methamphetamines, insofar as their drug use may have caused lung damage.

 

In August 2020 the CDC issued a caution that tuberculosis infections could increase the risk of severe illness or death. The WHO recommended that people with respiratory symptoms be screened for both diseases, as testing positive for COVID-19 couldn't rule out co-infections. Some projections have estimated that reduced TB detection due to the pandemic could result in 6.3 million additional TB cases and 1.4 million TB related deaths by 2025.

 

NAME

During the initial outbreak in Wuhan, China, the virus and disease were commonly referred to as "coronavirus" and "Wuhan coronavirus", with the disease sometimes called "Wuhan pneumonia". In the past, many diseases have been named after geographical locations, such as the Spanish flu, Middle East Respiratory Syndrome, and Zika virus. In January 2020, the WHO recommended 2019-nCov and 2019-nCoV acute respiratory disease as interim names for the virus and disease per 2015 guidance and international guidelines against using geographical locations (e.g. Wuhan, China), animal species, or groups of people in disease and virus names in part to prevent social stigma. The official names COVID-19 and SARS-CoV-2 were issued by the WHO on 11 February 2020. Tedros Adhanom explained: CO for corona, VI for virus, D for disease and 19 for when the outbreak was first identified (31 December 2019). The WHO additionally uses "the COVID-19 virus" and "the virus responsible for COVID-19" in public communications.

 

HISTORY

The virus is thought to be natural and of an animal origin, through spillover infection. There are several theories about where the first case (the so-called patient zero) originated. Phylogenetics estimates that SARS-CoV-2 arose in October or November 2019. Evidence suggests that it descends from a coronavirus that infects wild bats, and spread to humans through an intermediary wildlife host.

 

The first known human infections were in Wuhan, Hubei, China. A study of the first 41 cases of confirmed COVID-19, published in January 2020 in The Lancet, reported the earliest date of onset of symptoms as 1 December 2019.Official publications from the WHO reported the earliest onset of symptoms as 8 December 2019. Human-to-human transmission was confirmed by the WHO and Chinese authorities by 20 January 2020. According to official Chinese sources, these were mostly linked to the Huanan Seafood Wholesale Market, which also sold live animals. In May 2020 George Gao, the director of the CDC, said animal samples collected from the seafood market had tested negative for the virus, indicating that the market was the site of an early superspreading event, but that it was not the site of the initial outbreak.[ Traces of the virus have been found in wastewater samples that were collected in Milan and Turin, Italy, on 18 December 2019.

 

By December 2019, the spread of infection was almost entirely driven by human-to-human transmission. The number of coronavirus cases in Hubei gradually increased, reaching 60 by 20 December, and at least 266 by 31 December. On 24 December, Wuhan Central Hospital sent a bronchoalveolar lavage fluid (BAL) sample from an unresolved clinical case to sequencing company Vision Medicals. On 27 and 28 December, Vision Medicals informed the Wuhan Central Hospital and the Chinese CDC of the results of the test, showing a new coronavirus. A pneumonia cluster of unknown cause was observed on 26 December and treated by the doctor Zhang Jixian in Hubei Provincial Hospital, who informed the Wuhan Jianghan CDC on 27 December. On 30 December, a test report addressed to Wuhan Central Hospital, from company CapitalBio Medlab, stated an erroneous positive result for SARS, causing a group of doctors at Wuhan Central Hospital to alert their colleagues and relevant hospital authorities of the result. The Wuhan Municipal Health Commission issued a notice to various medical institutions on "the treatment of pneumonia of unknown cause" that same evening. Eight of these doctors, including Li Wenliang (punished on 3 January), were later admonished by the police for spreading false rumours and another, Ai Fen, was reprimanded by her superiors for raising the alarm.

 

The Wuhan Municipal Health Commission made the first public announcement of a pneumonia outbreak of unknown cause on 31 December, confirming 27 cases—enough to trigger an investigation.

 

During the early stages of the outbreak, the number of cases doubled approximately every seven and a half days. In early and mid-January 2020, the virus spread to other Chinese provinces, helped by the Chinese New Year migration and Wuhan being a transport hub and major rail interchange. On 20 January, China reported nearly 140 new cases in one day, including two people in Beijing and one in Shenzhen. Later official data shows 6,174 people had already developed symptoms by then, and more may have been infected. A report in The Lancet on 24 January indicated human transmission, strongly recommended personal protective equipment for health workers, and said testing for the virus was essential due to its "pandemic potential". On 30 January, the WHO declared the coronavirus a Public Health Emergency of International Concern. By this time, the outbreak spread by a factor of 100 to 200 times.

 

Italy had its first confirmed cases on 31 January 2020, two tourists from China. As of 13 March 2020 the WHO considered Europe the active centre of the pandemic. Italy overtook China as the country with the most deaths on 19 March 2020. By 26 March the United States had overtaken China and Italy with the highest number of confirmed cases in the world. Research on coronavirus genomes indicates the majority of COVID-19 cases in New York came from European travellers, rather than directly from China or any other Asian country. Retesting of prior samples found a person in France who had the virus on 27 December 2019, and a person in the United States who died from the disease on 6 February 2020.

 

After 55 days without a locally transmitted case, Beijing reported a new COVID-19 case on 11 June 2020 which was followed by two more cases on 12 June. By 15 June there were 79 cases officially confirmed, most of them were people that went to Xinfadi Wholesale Market.

 

RT-PCR testing of untreated wastewater samples from Brazil and Italy have suggested detection of SARS-CoV-2 as early as November and December 2019, respectively, but the methods of such sewage studies have not been optimised, many have not been peer reviewed, details are often missing, and there is a risk of false positives due to contamination or if only one gene target is detected. A September 2020 review journal article said, "The possibility that the COVID-19 infection had already spread to Europe at the end of last year is now indicated by abundant, even if partially circumstantial, evidence", including pneumonia case numbers and radiology in France and Italy in November and December.

 

MISINFORMATION

After the initial outbreak of COVID-19, misinformation and disinformation regarding the origin, scale, prevention, treatment, and other aspects of the disease rapidly spread online.

 

In September 2020, the U.S. CDC published preliminary estimates of the risk of death by age groups in the United States, but those estimates were widely misreported and misunderstood.

 

OTHER ANIMALS

Humans appear to be capable of spreading the virus to some other animals, a type of disease transmission referred to as zooanthroponosis.

 

Some pets, especially cats and ferrets, can catch this virus from infected humans. Symptoms in cats include respiratory (such as a cough) and digestive symptoms. Cats can spread the virus to other cats, and may be able to spread the virus to humans, but cat-to-human transmission of SARS-CoV-2 has not been proven. Compared to cats, dogs are less susceptible to this infection. Behaviors which increase the risk of transmission include kissing, licking, and petting the animal.

 

The virus does not appear to be able to infect pigs, ducks, or chickens at all.[ Mice, rats, and rabbits, if they can be infected at all, are unlikely to be involved in spreading the virus.

 

Tigers and lions in zoos have become infected as a result of contact with infected humans. As expected, monkeys and great ape species such as orangutans can also be infected with the COVID-19 virus.

 

Minks, which are in the same family as ferrets, have been infected. Minks may be asymptomatic, and can also spread the virus to humans. Multiple countries have identified infected animals in mink farms. Denmark, a major producer of mink pelts, ordered the slaughter of all minks over fears of viral mutations. A vaccine for mink and other animals is being researched.

 

RESEARCH

International research on vaccines and medicines in COVID-19 is underway by government organisations, academic groups, and industry researchers. The CDC has classified it to require a BSL3 grade laboratory. There has been a great deal of COVID-19 research, involving accelerated research processes and publishing shortcuts to meet the global demand.

 

As of December 2020, hundreds of clinical trials have been undertaken, with research happening on every continent except Antarctica. As of November 2020, more than 200 possible treatments had been studied in humans so far.

Transmission and prevention research

Modelling research has been conducted with several objectives, including predictions of the dynamics of transmission, diagnosis and prognosis of infection, estimation of the impact of interventions, or allocation of resources. Modelling studies are mostly based on epidemiological models, estimating the number of infected people over time under given conditions. Several other types of models have been developed and used during the COVID-19 including computational fluid dynamics models to study the flow physics of COVID-19, retrofits of crowd movement models to study occupant exposure, mobility-data based models to investigate transmission, or the use of macroeconomic models to assess the economic impact of the pandemic. Further, conceptual frameworks from crisis management research have been applied to better understand the effects of COVID-19 on organizations worldwide.

 

TREATMENT-RELATED RESEARCH

Repurposed antiviral drugs make up most of the research into COVID-19 treatments. Other candidates in trials include vasodilators, corticosteroids, immune therapies, lipoic acid, bevacizumab, and recombinant angiotensin-converting enzyme 2.

 

In March 2020, the World Health Organization (WHO) initiated the Solidarity trial to assess the treatment effects of some promising drugs: an experimental drug called remdesivir; anti-malarial drugs chloroquine and hydroxychloroquine; two anti-HIV drugs, lopinavir/ritonavir; and interferon-beta. More than 300 active clinical trials were underway as of April 2020.

 

Research on the antimalarial drugs hydroxychloroquine and chloroquine showed that they were ineffective at best, and that they may reduce the antiviral activity of remdesivir. By May 2020, France, Italy, and Belgium had banned the use of hydroxychloroquine as a COVID-19 treatment.

 

In June, initial results from the randomised RECOVERY Trial in the United Kingdom showed that dexamethasone reduced mortality by one third for people who are critically ill on ventilators and one fifth for those receiving supplemental oxygen. Because this is a well-tested and widely available treatment, it was welcomed by the WHO, which is in the process of updating treatment guidelines to include dexamethasone and other steroids. Based on those preliminary results, dexamethasone treatment has been recommended by the NIH for patients with COVID-19 who are mechanically ventilated or who require supplemental oxygen but not in patients with COVID-19 who do not require supplemental oxygen.

 

In September 2020, the WHO released updated guidance on using corticosteroids for COVID-19. The WHO recommends systemic corticosteroids rather than no systemic corticosteroids for the treatment of people with severe and critical COVID-19 (strong recommendation, based on moderate certainty evidence). The WHO suggests not to use corticosteroids in the treatment of people with non-severe COVID-19 (conditional recommendation, based on low certainty evidence). The updated guidance was based on a meta-analysis of clinical trials of critically ill COVID-19 patients.

 

WIKIPEDIA

A group of Australian Police officers pass a statue of a Mob of Kangaroos outside the Council House, St Georges Terrace, Perth City, Western Australia. (CHOGAM meeting 2011)

 

(The Commonwealth - news)

Commonwealth leaders meeting in Perth, Australia, have welcomed the interest shown by the Government of South Sudan in joining the Commonwealth.

Commonwealth Heads of Government met in Perth, Australia, from 28 to 30 October 2011, under the theme ‘Building National Resilience, Building Global Resilience’. Reflecting on the unique nature of the Commonwealth, a voluntary association which brings together 54 developing and developed nations from six continents, Heads reaffirmed their commitment to the values and principles of the Commonwealth and agreed to a series of actions to maintain the Commonwealth’s relevance, to ensure its effectiveness in responding to contemporary global challenges and to build resilient societies and economies. Given the significant challenges facing the global economy, Heads emphasised the importance of the international community working cooperatively to secure a sustainable global recovery. Heads highlighted the importance of a strong response to these challenges to provide the necessary confidence to global markets.

Heads welcomed the report of the Eminent Persons Group, ‘A Commonwealth of the People: Time for Urgent Reform’, and thanked members of the Group for their outstanding work. They agreed that the report provided a strong basis to revitalise the Commonwealth and its institutions and ensure its continued relevance to member states and their people – today and in the future.

To this end, Heads agreed to the following:

1. Reform of the Commonwealth to ensure that it is a more effective institution, responsive to members’ needs, and capable of tackling the significant global challenges of the 21st century.

This includes:

a) the reform of the Commonwealth Ministerial Action Group (CMAG);

b) consideration of the Eminent Persons Group (EPG) recommendations on reform;

c) strengthening the management and delivery of Commonwealth programmes, including through regular review of their efficiency, effectiveness and results, against measurable indicators;

d) to this end, focusing delivery of practical assistance to members through greater prioritisation and alignment of programmes to members’ priorities on the basis of Commonwealth comparative advantage and, where necessary, retiring programmes that do not meet these criteria; and

e) undertaking associated reform of the Commonwealth Secretariat and ensuring the adequacy of resources and their appropriate use to enable it to deliver on its agreed mandates.

2. To actively promote, uphold, preserve and defend the fundamental values, principles and aspirations of the Commonwealth. Heads agreed to do this by:

a) agreeing to the recommendations of CMAG to strengthen the role of CMAG, in order to enable the Group to deal with the full range of serious or persistent violations of Commonwealth values;

b) resolving that the composition of CMAG for the next biennium should be as follows: Australia, Bangladesh, Canada, Jamaica, Maldives, Sierra Leone, Tanzania, Trinidad and Tobago and Vanuatu.

c) agreeing that there should be a "Charter of the Commonwealth", as proposed by the Eminent Persons Group, embodying the principles contained in previous declarations, drawn together in a single, consolidated document that is not legally binding.

d) Heads will agree to a text for the Charter in 2012, following a process of national consultations, consideration by a Task Force of Ministers drawn from all geographical groupings of the Commonwealth, and a full meeting of Foreign Ministers in New York in September;

e) tasking the Secretary-General and CMAG to further evaluate relevant options relating to the EPG's proposal for a Commissioner for Democracy, the Rule of Law and Human Rights and to report back to Foreign Ministers at their September meeting in New York;

f) noting that the EPG's recommendations relating to CMAG were consistent with the CMAG reforms adopted by Heads at this meeting;

g) responding to the remaining EPG recommendations as follows

i. adopting without reservation 30 recommendations;

ii. adopting, subject to consideration of financial implications, 12 further recommendations;

iii. asking the Task Force of Ministers (para 2(d) above) to provide more detailed advice on 43 other recommendations to Foreign Ministers at their September meeting in New York, as a basis for further decision by Heads; and

iv. deeming 11 recommendations inappropriate for adoption.

h) strengthening the newly established Commonwealth Network of Election Management Bodies as well as election monitoring, and supporting capacity building for professional election administrators;

i) urging the interim government of Fiji to restore democracy without further delay, to respect human rights, and to uphold the rule of law, and reaffirming that the Commonwealth should continue to remain engaged with Fiji and support efforts towards that end;

j) urging members to consider becoming parties to all major international human rights instruments; to implement fully the rights and freedoms set out in the Universal Declaration of Human Rights and the Vienna Declaration and Programme of Action, as well as those human rights treaties to which they are a party; to uphold these rights and freedoms; to share best practice and lessons learned, including from the United Nations Universal Periodic Review process; and to continue to support the work of National Human Rights Institutions; and

k) promoting tolerance, respect, understanding and religious freedom which, inter alia, are essential to the development of free and democratic societies.

 

3. Revitalising the Commonwealth’s development priorities to ensure it effectively articulates and meets the development needs of member states today and in the future. To this end, Heads:

a) agreed the Perth Declaration on Food Security Principles;

b) reflected on the multiple development challenges confronting small states in the global economy as a result of their inherent vulnerabilities, and agreed that this is having an adverse impact on their sustainable development and growth prospects; and in this context:

i. welcomed and endorsed the outcomes of the first Global Biennial Conference of Small States held in 2010;

ii. endorsed the outcomes of the Commonwealth and Developing Small States meeting, which stressed in relation to Commonwealth and developing small states, Least Developed Countries (LDCs) and Small Island Developing States (SIDS): the importance of taking urgent action on climate change and sustainable development, particularly through the G20, the UN climate change conference in Durban, and Rio+20; the need to work towards legally binding outcomes under the UN Framework Convention on Climate Change (UNFCCC) capable of avoiding dangerous climate change; the need for enhanced action on adaptation and transparent and accessible climate finance to support developing small states; the need for practical outcomes at Rio+20 on the 'blue economy' to ensure the sustainable management of our oceans as the basis for livelihoods, food security and economic development; and for Commonwealth G20 members to reflect these concerns and perspectives at the upcoming G20 summit;

iii. agreed that vulnerability to climate change is widespread and particularly affects small states. The Commonwealth has an important role to play in advancing the climate change priorities of Commonwealth small and vulnerable states as well as fostering mutual collaboration among Commonwealth countries in order to address such priorities;

iv. agreed to assist small and climate vulnerable states develop their capacity to respond in a timely and effective way to disasters and to build their national disaster response capabilities;

v. welcomed the establishment of the Commonwealth Office for Small States in Geneva and urged further support for it;

vi. considered the substantive work that the Commonwealth has done on the issue of small states, including on SIDS, and called for this expertise to be shared with other international institutions, such as the UN, which are involved in the implementation of the Mauritius Strategy and the Barbados Programme of Action;

c) recalled the Port of Spain Climate Change Consensus and noted the undisputed threat that climate change poses to the security, prosperity and economic and social development of the people, as well as the impact it has in terms of deepening poverty and affecting the attainment of the Millennium Development Goals (MDGs), and reaffirmed their commitment to work towards a shared vision for long-term cooperative action to achieve the objective of the UNFCCC, addressing mitigation, adaptation, finance, technology development and transfer, and capacity building in a balanced, integrated and comprehensive manner; in this context:

i. committed to advocate for these actions at the UNFCCC conference in Durban and beyond, for legally binding outcomes;

ii. committed to work together to build climate resilience and to facilitate the efficient mobilisation of funding for urgent and effective mitigation, adaptation and capacity building, prioritising the most vulnerable developing countries, including small island developing states; and recognised the importance of markets in maximising global emission reductions at the least possible cost, and the promotion of technology transfer to these countries;

iii. recognising the existential impact of climate change on coastal and island communities, emphasised the great importance of building national resilience to ameliorate local climate change-induced population displacement, as well as the imperative to reach strong and effective solutions to reduce global emissions and enhance multilateral, regional and bilateral cooperation on adaptation;

iv. committed to practical action in line with the Lake Victoria Commonwealth Climate Change Action Plan, including efforts to facilitate immediate access to climate change finance and technology transfer, especially for mitigation and adaptation;

d) agreed to focus on practical and ambitious outcomes at the UN Conference on Sustainable Development (Rio+20) in June 2012 to address the challenges facing this and future generations, including with a view to expediting implementation of the outcomes of the Global Conference on Sustainable Development of Small Island Developing States; in this regard:

i. committed to advocate urgent action at Rio+20 to assist developing states to build resilience through sustainable development, in particular by taking steps to transition towards green growth trajectories and to strengthen institutional frameworks for achieving this transition. Rio+20 should deliver an outcome which allows progress to be measured in a meaningful way. The value of natural resources should be given due consideration in economic decision-making;

ii. agreed to explore options for sharing best practice on resource management and promote initiatives to provide access to monitoring, research, education and training, and technical and policy expertise;

iii. welcomed the briefing they received on the emerging conclusions of the UN Secretary-General’s High-level Panel on Global Sustainability;

iv. recognised the need to preserve the policy space of countries to frame their own national strategies to prioritise according to their national circumstances;

v. supported and upheld the role and place of local government, in partnership with the private sector, for promoting strategies for localism, sustainable development and economic growth, and supported the implementation of the Cardiff Consensus for Local Economic Development in the Commonwealth;

vi. recognised the valuable role clean and renewable energy will play in a sustainable future and the importance of promoting the implementation of green technology;

vii. recognised the importance of energy security through improved efficiency measures and the promotion of clean and affordable energy, including renewable energy;

viii. recognised also the need for sustainable management of oceans for livelihoods, food security and economic development;

ix. emphasised that poverty eradication and the provision of universal access to energy for all remain important priorities and that the green economy is a pathway to achieve these objectives on the basis of the Rio Principles of Sustainable Development;

e) agreed to promote more effective natural resource management through greater transparency and better governance, and taking account of the values of natural capital in decision-making, build on the Commonwealth’s longstanding practical contributions to member governments in this area. To that end:

i. agreed to build capacity in and share best practice on resource management, and welcomed members’ initiatives to provide access to research, education and training, and technical and policy expertise;

ii. welcomed the Extractive Industries Transparency Initiative principles and encouraged Commonwealth countries to consider supporting or implementing them;

iii. committed to combating the illegal exploitation of natural resources, including through supporting the Lusaka Declaration of the International Conference of the Great Lakes Region;

f) agreed to promote inclusive education and to accelerate efforts to achieve quality universal primary education, in line with the MDGs and Education For All goals. They further agreed to:

i. help children attain basic levels of literacy and numeracy by strengthening international mechanisms and cooperation, including through new technologies;

ii. create opportunities for skills development and quality secondary and higher education;

iii. call for a successful completion of the first replenishment of the Global Partnership for Education in Copenhagen in November 2011;

g) committed to universal access to health care, and services to improve maternal and reproductive health, supporting access to safe, affordable and quality medicines, and support for all Commonwealth people by accelerating the implementation of international conventions and eradicating disease by improving domestic health strategies and immunisation systems. Heads agreed to do this by:

i. accelerating action and financial support to eradicate polio including by improving routine immunisation systems;

ii. accelerating implementation of the Political Declaration of the UN High-Level Meeting on the Prevention and Control of Non-Communicable Diseases and the World Health Organization Framework Convention on Tobacco Control;

iii. committing to accelerating action to implement the objectives outlined in the 2011 UN Political Declaration on AIDS;

iv. recognising that malaria is one of the leading causes of death and a major obstacle to the achievement of sustainable development and poverty alleviation, agreeing to work proactively with key stakeholders and partners towards accelerated implementation of strategies to reduce malarial morbidity and mortality in member countries;

v. addressing malnutrition, measles, acute respiratory infections and diarrhoea as leading causes of death for children under five, as well as prevalent diseases such as tuberculosis and rotavirus, including through proven international mechanisms such as the GAVI Alliance;

h) committed to maximise the economic and social benefits of migration to improve the resilience and prosperity of Commonwealth members, whilst addressing the challenges posed by irregular migration which undermines legal migration policies. They:

i. called for stronger international cooperation to manage migration effectively in countries of origin, transit and destination, in order to bolster migration’s positive effects and to enhance safety nets for migrants;

ii. called for cooperation in the fight against irregular migration, including in particular the readmission of own nationals staying irregularly in other states, in accordance with bilateral agreements and international obligations;

iii. in this context, articulated the link between migration and development, affirming the importance of adopting migration strategies that would reduce the cost of migration, and create incentives for diaspora communities to invest their financial resources and expertise in the development of their countries of origin;

iv. noted and encouraged participation in the Global Forum on Migration and Development, which Mauritius will host in 2012;

i) agreed to work together, provide financial support to, and make the policy and institutional changes needed to accelerate achieving the MDGs; and:

i. directed the Commonwealth Secretariat to assist members in having their priorities reflected at the special event to be organised by the President of the Sixty-Eighth session of the UN General Assembly to take stock of efforts made towards achieving the MDGs;

j) called for renewed international commitment to the principles of aid effectiveness to achieve the MDGs by 2015, more imperative than ever in the current challenging global economic and financial environment and, in this regard, noted with appreciation the Commonwealth Statement on Accelerating Development with More Effective Aid, and expressed their desire to achieve a successful outcome at the Fourth High-Level Forum in Busan;

k) welcomed the launch of the Commonwealth Connects portal as a contemporary platform for networking, building partnerships and strengthening the Commonwealth’s values and effectiveness, and encouraged its use; and

l) reiterated their support for the Commonwealth Connects programme which is encouraging greater effort from member countries to harness the benefits provided by technology, through promoting strategic partnerships, building ICT capacity and sharing ICT expertise; encouraged member countries to contribute to the Commonwealth Connects Special Fund; and requested the Secretariat’s continued support for the programme.

 

4. Working together and with global partners to secure the global economic recovery and ensure a stronger, more sustainable and balanced global economic system that will benefit all Commonwealth countries, by:

a) committing to avoid trade protectionism and advocating the importance of an open, transparent and rules-based multilateral trading system as a driver of global growth and to support development, and in this context:

i. congratulated the thirteen Commonwealth countries that have agreed to formal negotiations to create an African Free Trade Area, covering 26 countries from the Cape to Cairo, by 2014;

b) committing also to support regional economic integration, enhancing market access and building the capacity of LDCs, land-locked developing states, and other small and vulnerable economies, including SIDS, to participate in and benefit from the global trading and economic system and to further encourage pan-Commonwealth trade;

c) reaffirming their commitment to pursuing development-oriented and ambitious results in the World Trade Organization (WTO) Doha Development Round, but noting with grave concern the impasse in current negotiations and calling upon WTO members to make substantive progress at the Eighth WTO Ministerial Conference in December 2011 for an early conclusion of the Doha Round, they:

i. reaffirmed the role of the World Trade Organization in making rules which keep pace with demands generated by global economic shifts, help police protectionist measures, and contribute to a sustainable global economic recovery;

ii. urged the international community to accelerate efforts to enhance market access for LDCs, land-locked developing states and SIDS at the forthcoming WTO Ministerial Conference;

iii. urged support for an anti-protectionist pledge at the forthcoming WTO Ministerial Conference;

iv. considered innovative approaches to drive forward trade liberalisation and to strengthen the multilateral rules-based trading system;

v. further reaffirmed the importance of sustained and predictable Aid for Trade in strengthening the capacity of developing country members, in particular small and vulnerable economies, to become more competitive and better able to capture opportunities created by more open regional and global markets. To this end, Heads called for continued support for Aid for Trade and improved disbursement procedures at the forthcoming WTO Ministerial Conference;

d) urging the G20 to take the necessary steps to address current economic instability and to take concrete steps to put open trade, jobs, social protection and economic development at the heart of the recovery. This will provide the necessary confidence to global markets and ensure a more stable global economic environment. In support of this, Commonwealth countries:

i. committed to take all necessary steps to support the global economic recovery;

ii. supported ongoing high-level political engagement with the G20 chair and, in this context, welcomed the interaction of the Secretaries-General of the Commonwealth and La Francophonie with the Chair of the G20, as initiated in 2010;

iii. agreed that Commonwealth G20 members would undertake to convey Commonwealth members’ perspectives and priority concerns to the G20 Summit in Cannes, France;

iv. agreed to launch an annual officials-level Commonwealth meeting on the G20 development agenda, building on the Commonwealth’s current contributions to the G20 Development Working Group; and

e) agreeing to reduce the cost of remittance transfers by removing barriers to remitting and encouraging greater competition in the transfer market, by endorsing the World Bank’s General Principles for International Remittance Services

i. in line with this, Commonwealth countries committed to implement practical measures at the national level to reduce the cost of remittances.

 

5. Improving gender equality and the empowerment of women in the Commonwealth by:

a) supporting national programmes to this effect, including initiatives to eliminate gender-based violence, intensifying efforts to promote women’s decision-making roles at all levels, and continuing to improve advocacy for women’s leadership and the empowerment of women as leaders;

b) implementing international instruments and agreements on women’s rights, including the Convention on the Elimination of All Forms of Discrimination Against Women (CEDAW), the Beijing Declaration and Platform for Action, the Commonwealth’s Plan of Action for Gender Equality 2005-2015, and the ‘Joint Statement on Advancing Women’s Political Participation’[2] and UN Security Council Resolutions (UNSCRs) 1325, 1888 and 1889;[3]

c) applauding the work of the Commonwealth Secretariat in promoting the significance of the 2011 Commonwealth Day Theme “Women as Agents of Change" and the centrality of gender equality and the empowerment of women to achieving the MDGs;

d) directing the Commonwealth Secretariat to institutionalise the principles of gender mainstreaming, as enshrined in the Commonwealth Plan of Action; and to provide recommendations to Heads, through the Tenth Commonwealth Women’s Affairs Ministers Meeting (WAMM) on steps that need to be taken to mainstream gender equality across all Commonwealth work; and to make real progress on implementation of the Plan of Action;

e) supporting the call made by Ministers at the Ninth WAMM held in Bridgetown, Barbados in June 2010, for a more effective response from all actors in the global community to the disproportionately negative impact of the current international and national economic crises on women; and

f) giving due consideration to the domestic legislation of member countries, the Commonwealth may address the issue of early and forced marriage, and consider actions to support the rights of women and children and to share its best practices to promote the implementation of measures to tackle early and forced marriage.

 

6. Providing a greater voice and more effective role for youth in the Commonwealth, who represent over 50 per cent of the Commonwealth population, by:

a) directing the Commonwealth Secretariat to undertake an assessment of the Commonwealth’s progress on the Plan of Action for Youth Empowerment, to be submitted with recommendations to Heads, through the Commonwealth Youth Ministers Meeting in 2012, on steps that need to be taken to improve youth engagement and empowerment;

b) enhancing communication with youth, collecting and sharing good practices, and ensuring the voice of youth is represented in Commonwealth actions at the national and international level; and

c) recognising the important role of government, the private sector and technical and vocational training institutions in addressing youth unemployment and the vital importance of sport in assisting young people to stay healthy, contribute to society and develop into leaders of their communities.

 

7. Maintaining their commitment to a stable and secure national and international environment, as a foundation for sustainable growth and resilience for Commonwealth countries and the broader international community. Heads committed to improve international security by:

a) unequivocally preventing the use of their territories for the support, incitement to violence or commission of terrorist acts, implementing the necessary legal framework for the suppression of terrorist financing, and preventing the raising and use of funds by terrorists, terrorist front organisations, and transnational terrorist organisations;

b) accelerating efforts to conclude negotiations on a Comprehensive Convention on International Terrorism;

c) accelerating efforts to combat piracy in a manner consistent with international law and to strengthen maritime security, including through enhancing the capacity of coastal states;

d) urging the international community to recognise that the menace of piracy in the Indian Ocean cannot be effectively tackled in the absence of political stability and security in Somalia; urging concerted efforts towards strengthening the Transitional Federal Government and other state institutions, including the security sector; encouraging the international community to mobilise additional funding for AMISOM, as appropriate; and encouraging global support in combating piracy and terrorism, including through enhanced maritime security;

e) encouraging states to continue supporting the Contact Group on Piracy off the Coast of Somalia in its coordination of international counter-piracy efforts;

f) combating proliferation and trafficking of illicit small arms and light weapons;

g) embracing moderation as an important value to overcome all forms of extremism, as called for in the ‘Global Movement of the Moderates’;

h) encouraging participation in the 2012 Diplomatic Conference to negotiate on the basis of consensus an effective Arms Trade Treaty which is of broad universal acceptance;

i) improving legislation and capacity in tackling cyber crime and other cyber space security threats, including through the Commonwealth Internet Governance Forum’s Cyber Crime Initiative;

j) affirming support for the Biological and Toxin Weapons Convention and its Seventh Review Conference in December 2011; and

k) continuing to tackle the root causes of conflict, including through the promotion of democracy, development and strong legitimate institutions.

 

8. Combating people smuggling and human trafficking by clamping down on illicit criminal organisations and bringing the perpetrators of these crimes to justice, while protecting and supporting the victims of trafficking. Heads committed to:

a) fight people-smuggling as part of their broader efforts to maintain border integrity and manage migration, including through enhancing border security and regional cooperation;

b) put in place the necessary legal and administrative framework to address the challenge of human trafficking; and affirmed their commitment to the principle of solidarity and cooperation between states with regard to the identification, assistance and protection of victims of trafficking; and

c) comply with all obligations arising under international law and urged all countries to become parties to and implement the UN Convention against Transnational Organised Crime and the Protocols thereto, in particular the Protocol to Prevent, Suppress and Punish Trafficking in Persons, Especially Women and Children, and the Protocol Against the Smuggling of Migrants by Land, Sea and Air.

 

9. To promote the future of the Commonwealth through the strong and important voice of its people by:

a) welcoming the contribution made by inter-governmental, associated and other Commonwealth organisations, including the Commonwealth Foundation, Commonwealth of Learning, Commonwealth Parliamentary Association, Commonwealth Business Council, Commonwealth Local Government Forum and the Commonwealth Association of Public Administration and Management;

b) urging Commonwealth organisations and civil society to enhance Commonwealth networks and partnerships with a view to achieving the fundamental values and aspirations of the Commonwealth;

c) relaunching the Commonwealth Foundation in 2012, while retaining its fundamental intergovernmental nature and maintaining its accountability to member states, with a revised mandate and Memorandum of Understanding so that it can more effectively deliver the objectives of strengthening and mobilising civil society in support of Commonwealth principles and priorities; and

d) welcoming the outcomes of the Commonwealth People’s Forum, Business Forum, and Youth Forum.

 

10. To reaffirm previous CHOGM Communiqués on Cyprus and express full support for the sovereignty, independence, territorial integrity and unity of the Republic of Cyprus and the efforts of the leaders of the two communities, under the auspices of the UN Secretary-General’s Good Offices Mission, to bring about a comprehensive Cyprus settlement, based on the UN Charter and the relevant UNSCRs for a State of Cyprus with a single sovereignty, single international personality and a single citizenship, in a bicommunal, bizonal federation with political equality as described in the relevant UNSCRs. Heads called for the implementation of UNSCRs, in particular 365 (1974), 541 (1983), 550 (1984), and 1251 (1999) and reiterated their support for the full respect of the human rights of all Cypriots and for the accounting for all missing persons. To extend their full support and solidarity to the Republic of Cyprus in the exercise of its sovereign rights under international law, including the United Nations Convention on the Law of the Sea, to explore and exploit the natural resources in its Exclusive Economic Zone.

 

11. To note recent developments in the ongoing efforts of Belize to seek a just, peaceful and definitive resolution to Guatemala’s territorial claims. Heads noted that, due to the electoral campaigns scheduled in both Belize and Guatemala in the coming months, it was envisaged that the earliest date for the referenda required to submit the matter to the International Court of Justice (ICJ) would be in late 2013. Heads expressed a high level of confidence that the dispute could be resolved through the judicial procedure of the ICJ, and urged the support and financial assistance of the international community for this process. Heads further expressed satisfaction with the ongoing Confidence Building Measures supported by the Organization of American States, which had contributed immensely to stability in the adjacent border areas of Belize and Guatemala. They noted with concern the environmental problems being faced by Belize in its national parks along its adjacent areas with Guatemala due to the increasing encroachments by Guatemalan citizens for illegal logging. Heads reiterated their firm support for the territorial integrity, security and sovereignty of Belize, and mandated the Secretary-General to continue to convene the Commonwealth Ministerial Committee on Belize whenever necessary.

 

12. Having received a report on Guyana-Venezuela relations, to express their satisfaction that the relations between the two countries continued to grow and deepen. Heads noted that the Foreign Ministers of Guyana and Venezuela had met recently in Trinidad and Tobago to address the concerns of the Government of Venezuela over Guyana’s submission of a claim to an extended continental shelf to the Commission on the Limits of the Continental Shelf. Heads expressed the view that the current climate in the relations between Guyana and Venezuela was conducive to the realisation of the mandate of the UN Good Offices Process. Heads reaffirmed their unequivocal support for the maintenance and safeguarding of Guyana’s territorial integrity and sovereignty.

 

13. To welcome the interest shown by the Government of South Sudan in joining the Commonwealth, and to request the Commonwealth Secretariat to pursue the established procedures in this regard.

 

14. To look forward to the conditions being created for the return of Zimbabwe to the Commonwealth and continue to encourage the parties to implement the Global Political Agreement faithfully and effectively.

 

15. To congratulate the Head of the Commonwealth on her Diamond Jubilee in 2012. Heads welcomed proposed Commonwealth initiatives to mark this historic occasion, in particular the establishment of a Queen Elizabeth Diamond Jubilee Trust, which would be funded by private donations and voluntary contributions from governments. This will support charitable projects and organisations across the Commonwealth, focusing on areas such as tackling curable diseases, the promotion of all forms of education and culture and other Commonwealth priorities.

 

16. To reappoint Mr Kamalesh Sharma as Commonwealth Secretary-General for a further four-year term commencing April 2012.

 

17. Finally, to reaffirm their decisions to meet next in Sri Lanka in 2013 and thereafter in Mauritius in 2015, as well as to welcome the offer by Malaysia to host the 2019 CHOGM.

 

Perth

Australia

30 October 2011

 

[1] One member, Fiji, is currently suspended.

[2] From the ‘Women’s Political Participation – Making Gender Equality in Politics a Reality’ high-level event during the 66th Session of the UN General Assembly in New York.

[3] UNSCRs 1325, 1888 and 1889 are each titled ‘Women and peace and security’.

Introduction

 

It was very sad news indeed last Sunday to hear of the death of David R Smith, former Provost and Convenor. Our sympathies go to David’s wife and family.

 

As many of you will know, Margot Russell arranged for me to meet with David at the start of the Dalkeith Burns Monument Campaign – a meeting that helped a great deal with the research on the monument and its history. Indeed, it was a paper of David’s published in 1980 that helped inspire that campaign at the outset. He was a great support and inspiration to me with the work that followed and, despite his deteriorating health, he wrote to me on a number of occasions with further information and photographs. On the day before the unveiling of the restored and repositioned Burns fountain, he called me and offered he some last-minute and very welcome advice and encouragement. I will always be grateful to him for that.

 

From the start of the Burns Campaign through to the subsequent establishment of Dalkeith: Historic Town, it is actually David’s work on the town’s history that we return to time and time again. Without David, much of Dalkeith’s history would have gone untold and, in many ways, the Dalkeith: Historic Town page stands as a tribute to him and his work.

However, from what I know, David’s life seems in large part characterised by a devotion to Dalkeith and its people. On that point, I am pleased to record his story on this page. In what follows, I have recorded the highlights of his life, as he himself recorded them in biographical notes which Margot has passed to me. To these notes, I have added some detail from my own research on his life and career. I think you’ll see that, like Dalkeith, he had a full, fascinating and rich history.

David R Smith, thank you for all that you’ve given to the town in so many different ways.

 

Some Biographical Details

He was born in a farm cottage at Borthwick Mains on 11 April 1930 but lived in Dalkeith from infancy. He was educated at Dalkeith High School. After school, he took up employment as an office boy in a leading Edinburgh firm of Charted Accountants and was soon to be promoted into the audit staff. Between 1948 and 1950, he did National Service in the Royal Air Force. In 1950, he joined the internal audit staff of the Regional Hospital Board where he remained until 1958. From there, he was employed by the National Coal Board; firstly, in the Finance Department and then with the Marketing Department where he had special responsibilities for the promotion of good relations with local authorities.

  

Political Development

 

At school, David took a keen interest in the Second World War. This led to an interest in politics. During the 1945 election campaign he attended mass rallies in Edinburgh addressed by leading Labour politicians. He assisted in the North Midlothian Labour committee rooms. At 16 years of age, he joined the Labour Party. By the age of 20, he was chairman of the Dalkeith branch. At this time, David could be found sitting in the public benches of meetings of the Town Council. Unexpectedly, a vacancy on the council occurred in 1951 when Baillie A K Wilson resigned for health reasons. David was asked to accept it. It was the custom to fill vacancies by co-option at this time but David insisted that there be an election. It was the first by-election in the history of the town and he went on to win it in February 1952. At just 21 years, he had become the youngest councillor in Scotland. He was appointed the chairman of the Health Committee and played a leading part in the closure of insanitary lodging houses as well as a sub-standard slaughter-house.

 

Outwith the Council, he joined the Leith section of the Labour League of Youth and took part in political debates and social events. A keen intellect, he had interests in biology, philosophy and astronomy but also contributed to Socialist periodicals and was on the Editorial Board of a left-wing newspaper. His awareness of global politics was sharp and in 1951 he was reported to have “floored his opponent” in a public debate on the Khrushchev ‘anti-Stalin’ disclosures.

On the Council, he had a number of key positions before 1965 when he became the Provost. He served in that capacity until 1975 when the re-organisation of local government took place. He was then appointed the Convenor of the Midlothian District Council, a position he held for six years.

 

During his time as Provost, the town made remarkable progress. The municipal housing programme was very much expanded with an improvement in the quality, the shopping centre was transformed to present new opportunities, new social facilities such as a community centre, library and arts centre were introduced and many community organisations were established. The Saltire Society awarded the town the title of being the most lively small burgh in Scotland. Before the new shopping centre was opened, the centre of the town was congested with unfit and derelict properties.

 

County Council Conflict & Labour Party Expulsion

 

In 1959, David and a colleague on the Town Council were expelled from the Labour Party for publicly condemning the Council’s policy for the placing of building contracts. They alleged that a particular building form was being favoured in dubious circumstances. The two councillors called for a public inquiry and a police investigation. Despite great pressure, they refused to withdraw their allegations and were willing to face a libel charge if need be. As it turned out, their campaign spread into other areas as it became clear that in many parts of Scotland the contractor was using irregular methods for the gaining of contracts.

 

In Dalkeith, the expulsions caused a major upheaval in the ranks of Labour. There was a mass resignation from the local branch which led to the formation of the Dalkeith Independent Labour Party. The official branch of the Party was reformed by the Scottish Office of Labour and the local elections over the following few years were fought between the two parties. The local electorate gave overwhelming support to the rebels. Official Labour came to recognise that there was no future for it without the re-admission of the Independents. The expelled councillors had stated at the outset that they would seek a return to the Labour Party but on no account would they retreat from their allegations. They contended that persons in high places obstructed the efforts to investigate.

 

The position was different in the North-East of England where similar contracts arrangements were in operations involving the same builder. The Ministry of Housing intervened to cancel a contract. A few years later the Chairman of the Dundee Housing Committee went to prison for accepting bribes from the contractor - the subject of the Dalkeith allegations – who was heavily fined and the Lord Provost was placed under suspicion. Arising from findings arising from a Royal Commission into the standards of public life, the authorities became much more inclined to probe into questionable building practices. The Dalkeith allegations were ahead of their time.

 

Following readmission to the Labour Party, David entered into new fields. He became the Chairman of the Midlothian Constituency Labour Party – a position which he occupied for a few years. He also moved up the ladder as a member of the County Council. He was one of five members that the Town Council had on the County Council. He had entered the County Council to better conduct his campaign against suspect building contracts. He forced open debates with the result that a number of the other councillors began to realise that there was something not right with contract arrangements. After his rehabilitation he became the Chairman of the Planning Committee. Working closely with the more progressive officers, he urged the Committee to make full use of its powers. Until then it had been mainly a negative force, confining its operations to dealing with planning applications from outside parties. It now began to exercise a programme for change. A Country Park at Almondell was designated, and a lesser one at Roslin. Walks were created along the Union Canal and disused railway lines were put to a similar purpose. The Chairman of the Planning Committee insisted that the Committee members try them out themselves before expecting the public to use them. As Chairman, he also provided a lead in creating conservation areas in some of the older communities. Before the County Council was abolished in 1975, he was elected by his colleagues as Vice-Convenor of that body.

 

Potential Parliamentary Candidate

In 1966, delegates of the Midlothian Constituency Labour party met to adopt a parliamentary candidate. There were six nominees, including David. The successful candidate, Alex Eadie, had been sponsored by the Scottish Miners’ Union which had considerable voting power amongst the delegates. David came a close second.

 

Work with Other Public Bodies

 

After becoming a town councillor, David was the means of setting up a Dalkeith Old People’s Welfare Committee with the primary object of building a centre for the exclusive use of the elderly. It was achieved within a new medical centre.

He was keen to promote an interest in the arts and thought that a building for that purpose should be erected. After the provision had been made, he played a leafing part in the formation of a lively Arts Guild.

 

He was a member of the Lothian Building Trust which saved a row of cottages on London Road from destruction.

He was also a founder-member of the St Nicholas Apse Trust which raised funds to enhance and protect part of the structure of the old parish church.

He was invited to serve on the Dalkeith Business Renewal Trust which assisted in the renovation of properties in the town’s conservation area.

 

For a period, he was Chairman of Voluntary Action which gave support to groups operating in the voluntary sector. A success story was its operation of the Woodburn Day Care Centre.

 

For some years he was also a Chairman of Midlothian Local Health Council which reviewed the quality and adequacy of local NHS services.

 

David was also a strong advocate of independent working-class education and was the driving force behind the formation of the Esk Valley branch of the Workers Education Association and was its chairman for the duration of its existence. The body ran a wide range of subjects such as foreign policy, economic issues, painting, music, the practice of government, the conservation of the countryside and threats to the environment.

 

In keeping with his thoughts on independent education, he became a Governor of Newbattle Abbey College and remained one for over 20 years, completing his service as chairman of the Finance Committee. He experienced the decision of the Secretary of State to withdraw funding, plunging the College into a critical situation. The Board was compelled to introduce many new ways to finance a continuation of study courses, made more difficult by the need to protect a building of outstanding historic importance. The College resumed its role with a new team of management personnel. In addition to his position as Governor, David did much to reveal the history of the building, giving many lectures to visitors.

 

Twinning

 

In 1960, the Town Council concluded a friendship agreement with Jarnac, a town in France. David supported the twinning arrangement from the outset and joined a Committee that was set up in order to further its aim of harmony between nations. As Provost in 1965, he presided over a ceremony to officially open Jarnac Court in the centre of Dalkeith. He took an active part in many subsequent activities.

 

The success of twinning between towns inspired in Midlothian County Council to consider the possibility of a similar union with counties in Europe. In due course, a charter of friendship was signed with a county of Germany and one in Hungary. As a means of promoting cultural exchanges, a Midlothian Twinning Association was formed. As chairman of the association for a number of years, David development many for the success of the partnerships, the principal one being the Festival of Friendship which every two years brought together the three counties in a display of music, dance and sport. In recognition of his personal contribution, Jarnac made him a Freeman of the town and the Hungarian county presented him with a special honour.

 

Dalkeith History Society

 

David founded the Dalkeith History Society in 1973 after enlisting the support of the Town Council. It was thought that the identity of the town would be weakened by its integration into a wider framework of local government. A Society would help to preserve Dalkeith’s historic background and character. The Council gave a substantial grant to the Society to encourage local research. A great deal has been done by the Society to justify its terms of reference.

 

In addition to municipal affairs, David devoted the bulk of his time to the research of the burgh’s past. Much of the Buccleuch papers had never been touched until David examined them. This enabled him to write various booklets on aspects of local history. He also produced numerous articles for the local newspaper and delivered lectures to local groups. In 2019, a selection of his articles originally published in the Advertiser was published entitled Dalkeith – Aspects of this history of a Scottish burgh.

 

Other Political Activities

 

David’s political involvement was not just confined to local government. In 1953, a freely elected government in British Guiana was overthrown by the British Government for wanting to nationalise the sugar industry. There was much protest and David became secretary of an Edinburgh Committee to present the facts. It arranged a public meeting which was addressed by the deposed Prime Minister and there was a large public attendance.

 

He was secretary of the Edinburgh branch of the Union of Democratic Control, a body set-up in the First World War to expose secret diplomacy and to campaign for an ethical foreign policy.

 

He was chairman of the Edinburgh branch of the Movement for Colonial Freedom which condemned colonial repression and injustice.

 

He was an active member of the Campaign for Nuclear Disarmament and Chairman of the Midlothian Peace Committee.

 

He also took part in the Anti-apartheid Group.

 

Honours

 

In 1976, Prime Minister James Callaghan proposed to David that he recommend him for an Order of the British Empire (OBE). David politely refused the offer. While agreeing that there be a method of recognising service, he did not approve of the current system. Nor did he want to be associated with any empire.

 

In 1996, he accepted a decision of Midlothian District Council that he, like Nelson Mandela shortly before, became a Freeman of Midlothian.

 

Family

 

David developed a keen interest in the Hungarian Revolution in 1956. That year, he met refugees who came to Middleton Camp after the country’s revolt against the government. One of the refugees was a young girl called Kornelia. Two years later, he was able to enter the country as a tourist although the visit was tightly organised. At some risk, he visited Kornelia’s parents. There he met Edit who was later to become his wife. He made return visits which resulted in marriage in 1961. It was very difficult to get all the consents from the Hungarian government, some of the residents thinking it impossible. Much effort had its success. Edit and David have a son and a daughter.

 

IF YOU ARE INTERESTED IN DALKEITH HISTORY AND WOULD LIKE TO JOIN A NEW FACEBOOK PAGE WHICH CELEBRATES IT, PLEASE FOLLOW THE LINK.

 

www.facebook.com/groups/398465947021162/?fref=ts

    

Howard University professors and students hold a press conference at Douglass Hall June 28, 1967 following their dismissal from the university for political activities during the spring semester.

 

From left to right: professor Andress Taylor, law student JeRoyd Greene and student leader Anthony Gittens.

 

As the names trickled out of the school, the total dismissals grew to five faculty members, including noted black liberation advocate Dr. Nathan Hare. Another three students were suspended from school for a year.

 

The administration was reacting to a March 21, 1967 planned speech by Selective Service Director Lewis Hershey at Crampton Auditorium where he was shouted down by students opposed to the Vietnam War.

 

As the school moved to discipline four involved in the Hershey demonstration, student protests only grew, climaxing in a boycott of classes May 10, 1967 that was upwards of 90 percent effective according to some observers.

 

The student demands included no discipline against the four, the rescinding of a university policy restricting demonstrations, a university guarantee of no reprisals against students or faculty for political activity, abolishing the senior comprehensive exams and compulsory Reserve Officer Training Corp (ROTC) be abolished.

 

The school met with student leaders following the boycott and, according to student leaders, agreed to many of the demands, including that of no reprisals.

 

Nevertheless, the administration went ahead with discipline.

 

The action would only bring more intensive student protests including a walkout of President James Nabrit’s fall opening speech, a disruption of Charter Day in March 1968 and a four-day seizure of virtually all campus buildings following more threats of discipline for the Charter Day protests.

 

Protests would continue in 1969 with boycotts of the medical and law schools.

 

Those dismissed in 1967 filed suit in court.

 

During the discovery phase, it was learned that Howard undertook a secret investigation of “disruptive” students, compiled dossiers on them and took disciplinary measures against them without the ability of the students or professors to defend themselves against the university.

 

Two associate deans, Carl E. Anderson and James L. Carey compiled the information and forwarded it to Dr. Armour J. Blackburn, dean of students.

 

Greene’s name was at the top of the list of those expelled. The charge against him was “Mr. Charles Rush and Dean Blackburn heard Mr. Greene refer to Dr Nabrit as an ‘Old Uncle Tom who shuffles downtown with hat in hand to seek funds.’”

 

Some of the students who received warnings included Robin Gregory “To be watched carefully. Record to be flagged in case she applies to some other school or college at the university.”

 

Another, James Porter, had an entry, “Flag record. If he applies for readmission his case is to be considered at that time. Take a good hard look at it.”

 

For Beatrice Patton, “Dean Blackburn, in consultation with Dean Calhoun, will decide whether the student needs psychiatric care, and whether she should be warned or watched.”

 

Two lists were compiled: the first of “hard core” student activists alleged to be the ringleaders of “disruptive” demonstrations and other students who bore “watching.”

 

The names on the lists came from professors, security guards and two student informers.

 

At a May 19, 1967 meeting of 32 university personnel, a list of 56 students was made and forwarded to a 15-person academic discipline committee headed by Stanton Wormley, academic vice president at Howard.

 

On June 20th, the committee met, without calling any of the students or professors cited nor giving them any opportunity to present exculpatory evidence, and meted out discipline ranging from expulsion to “warnings.”

 

The students won a quick 2-1 U.S. Court of Appeals decision September 23, 1967 that ordered their reinstatement for the academic year until a “final determination” was made. The students won their case on the school’s failure to give a fair hearing on specific charges.

 

The school appealed the decision but reinstated the students in the interim.

 

The professors’ case, none of whom were tenured, took longer. However on June 18, 1969 the U.S. Court of Appeals ruled that dismissals were invalid and that the professors were entitled to collect damages from the university.

 

The 13-page opinion noted that Howard’s faculty handbook “makes it clear, in writing what the appellants knew to be true in practice: a faculty member, if not finally informed by April 15 that his contract was not be renewed, had legitimate reason to believe that he could rely on returning to Howard the following semester.” .

 

The opinion also dismissed as moot the students’ appeal since Howard had reinstated them, but ordered the school to expunge from their records all reference to the disciplinary action.

 

Of those pictured, Taylor took work as an English professor at the University of the District of Columbia after his termination where he stayed for 30 years. He won awards for his prison rehabilitation program whose participants had a recidivist rate of less than 10 percent. Taylor died in 2005.

 

Gittens was one of the leaders of the 1968 student strike and occupation on campus and also went on to join the faculty at UDC where he established the Black Film Institute.

 

Greene would become a crusading civil rights attorney in the Richmond, Va. area later changing his name first to JeRoyd X Greene and then to Sa’ad El-Amin.

 

He once represented former D.C. Mayor Marion Barry over a prison transfer issue while Barry was incarcerated. He was cited several times for contempt of court for his zealous representation of defendants.

 

He was elected to the Richmond City Council and served from 1998-2003, but resigned when he pleaded guilty to mis-representing a client and spent nearly three years in prison. Now 80 years old in 2020, he remains active in Richmond social justice issues.

 

For more information and related images, see flic.kr/s/aHskadsfh7

 

Photo by Schmick. The image is courtesy of the D.C. Public Library Washington Star Collection © Washington Post.

 

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South Africa's nine-wicket win in Melbourne sealed their first Test series win in Australia. Cricinfo spoke to four players who were part of the teams that beat Australia 3-1 and 4-0 in consecutive series, both at home, in 1966-67 and 1969-70.

    

Mike Procter, scored 226 runs at 25.11 and took 41 wickets at 15.02 in seven of the nine Tests

 

I might have been one of the only few to have witnessed both of South Africa's series victories over Australia. This victory will rank as one of the greatest sporting moments in South African history. The two Test matches South Africa won have been incredible. It just showed the tremendous character of the team because in both the Tests there was no way they could win the game and they ended up winning both matches very comfortably.

 

Chasing 414 [in Perth] was a monumental effort and winning by six wickets was incredible. And then when South Africa were seven down for 180-odd on the second day, there was only going be one result at the MCG. And the team changed that round and won by nine wickets. Absolutely incredible.

 

I know this team will be measured against the 1970s' side. Back then, we won every game pretty comfortably and there were no major problems. In these two Tests South Africa were almost staring at defeat on the second or third day and they turned that around and won convincingly. After the victory I told Graeme 'you must be very, very proud'. He is a very tough guy, highly respected and the team would do anything for him. The way the bowlers handled the situation in the second innings in Perth and Melbourne was very special and very disciplined and the batters came to the fore, too. It was just amazing.

 

Ali Bacher, was captain during South Africa's 4-0 whitewash in 1969-70

 

The one moment I, and all South Africans, will always cherish is JP Duminy's 160-odd. His second Test match, we are into our tail at 180 for 7, playing at the famous MCG in front of a huge crowd, huge pressure, and the youngster plays like he has been around for ten years. His inspirational performance in the midst of some very fine performances by our guys will be remembered for years to come.

 

This is history in the making. How good is the South African team? Certainly after our return to international cricket, the two best teams we had in Test cricket was the one led by the late Hansie Cronje in the late 1990s and this current one. But the records will show this team is better. They started by beating Pakistan in Pakistan, beat England in England, drew with India in India and now Australia in Australia - there can be no question they are the No. 1 in world cricket today.

 

Peter Pollock, scored 257 runs at 32.12 and took 27 wickets at 26.96 in the two series

 

When I was in Australia in September I told the media that for the first time after readmission a South African cricket team would arrive believing that they could beat the Aussies. Jacques Kallis said during the Perth Test when South Africa were not in a good position, that they could still win the Test. For a team to be a good cricket team, you need some players who are bit above the rest. We have certain cricketers who are really good cricketers.

 

The potential of young guys like [Dale] Steyn, [AB] de Villiers, Duminy is really big and they are going to be more than just ordinary Test players. That is what makes the difference at the highest level - I am not talking about playing Test matches, I am talking about winning Test matches. We also have to acknowledge the Australian side was pretty poor and they have not done well of late. We have won the rugby World Cup twice and that was huge, but we are country that is going through transition so every time we do something good we really hang on to it. This series victory is one of the better moments of South African sport , no question about it.

 

Barry Richards, scored 508 runs at 72.57 in 1969-70, during which he played the only four Tests of his career

 

Obviously I'm very proud of the victory. It is a great thing to do it in Australia. Our side was scheduled to tour Australia in 1971 and we would have defeated them easily but it is great that Graeme Smith has done it. He has shown a lot of maturity as a skipper and as a player he really has come to the fore. He has led by example and he has kept a cool head all the way through. I hope this victory now encourages a lot of people to take up the game in South Africa. Obviously with Duminy coming through it is a real plus for South Africa.

 

Comparing the side I played and the present South African one is like comparing Ben Hogan to Tiger Woods. You just can't do that. They are so far apart: the bats are different, the size of the fields were bigger in the old days and the wickets were little bit friendly towards the bowlers in the old days.

 

Nagraj Gollapudi is an assistant editor at Cricinfo

This is the oldest building on the campus of the University of Texas Medical Branch (UTMB) in Galveston, the oldest medical school in Texas. They call the building 'Old Red' for fairly obvious reasons. It is named for Ashbel Smith, who was a physician and Yale graduate who came to Texas in 1837. After the Texas Revolution Smith served as surgeon general of the Republic of Texas and as a minister plenipotentiary to both Britain and France. During the Civil War he commanded Confederate soldiers at the Battles of Shiloh, Corinth, and Vicksburg. Later, after Texas' readmission to the Union, he served in the Texas legislature and as the first president of the University of Texas Board of Regents. He also helped found UTMB. Now, *that* was a career.

In a stunning reversal, India achieved their first Test win in South Africa, and what some observers thought was their best-ever away win. Their hero was Sreesanth, the wild and wacky seamer from Kerala playing only his sixth Test, who started South Africa's collapse for 84 in their first innings with a maiden five-for. There was no eccentricity in Sreesanth's actual delivery, which arrived with pace, aggression and a vertical seam. He ended the game with eight for 99, the match award, and a fine of 20% of his match fee for giving Amla an unnecessary send-off after claiming his wicket for the second time.

 

Dravid's decision to bat first was almost recklessly brave, given that the start was delayed by 90 minutes because of dampness in the pitch. It was a baking hot and sunny morning, just as it had been for the three previous days, which was why Chris Scott, the head groundsman, had decided to water the pitch the previous evening, to prevent it from cracking prematurely. But he overdid it. The result was a hard pitch with a wet top, and so much seaming bounce that South Africa's bowlers didn't know what to do with it. The defiant first-day batting of Dravid and Tendulkar required every iota of their skill and experience, and their runs were worth double, at least. Ganguly's emotionally charged return after a year as a Test outcast resulted in an innings of huge heart and determination, during which he was peppered with bouncers, most of which he played with survival instincts rather than cricketing ones. But, when Ntini pitched one up, Ganguly slogged him over midwicket for six.

 

Their combined application meant that 205 for nine was competitive, and then last man Vikram Singh belted an amusing 29 to help boost the final total. Those watching realised that 249 was a good score, but no one knew quite how good. They soon found out. The South Africans had banged it in short, but Sreesanth pitched it up, full and straight, and was rewarded with five of the first seven wickets - two lbw, two caught at second slip, one bowled. At that stage, South Africa were 45 for seven, and the sense of disbelief, even among the Indians, was palpable. A slog from Nel helped raise the score to 84, but it made little difference to the level of shame felt by South Africa, whose total was their lowest, not just since readmission in 1991-92, but since England twice skittled them for 72 in 1956-57.

 

Twenty wickets tumbled on the second day, but as the pitch eased a little India had started to build on what had become a formidable lead. Laxman displayed the temperament of a scholar, ignoring the inevitable snorters which still came his way. Quietly grateful when these missed his bat or the stumps, he tucked singles away on the leg side and regarded each of his dozen fours as a great bonus in an innings of 73 as valuable as many centuries. He finally edged Ntini to slip, but the lead was then approaching the eventual 401, and the game was well beyond South Africa, whose only moment of satisfaction had come when Pollock's classic late away-swinger had Dravid caught behind. It made him the tenth bowler - but the first South African - to take 400 wickets in Test cricket.

 

Sreesanth again flattened the top order, taking three of the first four wickets, before Prince delayed the inevitable with an obdurate 97 from 223 balls. Pollock enjoyed the attacking fields, spanking a quick 40, but Dravid had another ace up his sleeve, one with more than 500 wickets to his name - and a spinner, too, something South Africa did not have. Kumble bought Pollock's wicket by tossing a couple of inviting deliveries up in the air and then castling him with a quicker one, before spoiling Prince's chance of a century by bowling him too, around his legs trying a sweep.

 

If there had been 20 stumps available as souvenirs, they wouldn't have been enough for India when the match ended. The party was long and loud. Bullied abroad for so long, India had fought back in triumph, and had done so by playing the bullies at their own game in their own back yard.

The curse is finally lifted, and the identity of the man who has delivered South Africa's first series win in England for 43 years comes as no surprise whatsoever. Graeme Smith's irrepressible willpower was first demonstrated to the English public way back in 2003, when - as the most mature 22-year-old imaginable - he scored back-to-back double-centuries, at Edgbaston then at Lord's, to announce a new chapter in his country's sporting history.

  

Today, however, he finally closed that chapter and looked forward to the next, after producing the innings that he declared, without equivocation, as his greatest yet. "I've had some really meaningful innings in my life, and the double-hundreds here last time have to go down among my greatest achievements," he said. "But ever since readmission, we have really strived for victory in England and have always been disappointed. It's bigger than just us, this victory, and so I have to say it's my best."

  

The importance of a South African victory in England cannot be overstated. When the coach, Mickey Arthur, declared on Friday evening that his side was "desperate" to win, he was speaking not only for the eleven men on the field, but those back home in South Africa who recognised that, almost two decades on from their readmission to international cricket, the time was nigh for closure. For Smith, it was as if he had set his agenda on his maiden tour five years ago, and was now ready to cement his ambitions.

  

"If you taken the whole bigger picture," said Smith, "of all the players who've come before us, those who've come here and given it their all and had the disappointment, as well as the many who haven't had the opportunity in the many years past, as well as the fans back home who can imagine what it's like. For us this was bigger than a cricket game, it was a huge moment and something we're really proud of."

  

South Africa's transformation since apartheid has been a long and often traumatic process, and the country's cricketing misfortunes have often been seen as a part of the healing. But under Smith the team has achieved a rare unity and consistency that, for the first time ever, has transcended racial politics. Their current series record reads seven wins and a draw in India, a run that ranks among the very best of all time.

  

What is more, it has been delivered by a team that can no longer be accused of tokenism. From Ashwell Prince to Hashim Amla, via the fading but unyielding Makhaya Ntini, and all the way to the young white stars, AB de Villiers, Dale Steyn and Morne Morkel - all have been worthy members of a team whose next major assignment is a mouthwatering trip to Australia in December, where further ghosts await exorcism. It would have been unjust for them to fail, especially when you consider the turbulance that afflicted the England camp after their rout at Headingley.

        

But ever since readmission, we have really strived for victory in England and have always been disappointed. It's bigger than just us, this victory, and so I have to say it's my best -

Graeme Smith on South Africa's achievement

    

And yet, for all the magnificence of the current South African team, their efforts would have come to nought had it not been for their imperturbable captain. The day began as the previous one had finished, with England in the ascendancy, stretching their lead through the efforts of Paul Collingwood and Ryan Sidebottom and then, after a relatively calm opening stand of 65, instigating a chaotic collapse of four wickets for 28 runs.

   

Neil McKenzie and a steamed-up Jacques Kallis failed to pick Andrew Flintoff's full length against the problematic pavilion sightscreen, and as the Edgbaston crowd erupted in recognition of the moment, Smith feared that the "hot-headedness" that can characterise South African sporting teams was about to come to the fore once again.

  

Not that he was afflicted by the same emotions, however. Far from it. "I couldn't control that," he said. "I was just hoping that the right-handers could start picking up those low full-tosses. For me it was just about a real focus on my own game. Bat and hope someone could bat with me, because I knew if we could get a decent total on the board we could get close, England might get desperate and try a few things, and give us a few free deliveries."

  

In the final analysis, that is precisely what happened, as the combative Mark Boucher emerged to exorcise his own demons from the 1998 Test series, not to mention the World Cup semi-final on this very ground one year later. But there was nothing free about the runs that Smith accumulated. It was fitting that his final score was 154 not out, because there cannot have been a more brilliant and meaningful matchwinning century scored in England since Graham Gooch took down the West Indians at Headingley in 1991.

  

Like Gooch 17 years ago, Smith batted through a barrage and, until Boucher's late role, found only token support from his colleagues. And symbolically he too batted on into the gloaming when others might have called it quits and returned to complete the job in the morning. Instead, he claimed the extra half-hour on the stroke of seven o'clock, and hurtled to victory in five further overs.

  

"I knew we had England tired because their seamers had bowled a lot of overs," he said. "The new ball was at the back of my mind - if we'd lost a wicket we had a bit of a tail - but eventually I thought: 'Let's go for it. We've got England on the ropes, so let's back ourselves.'"

 

And to think Smith might not even have taken part in this match. He pulled out of training on the eve of the game after suffering a back complaint while batting against Bangladesh A, and admitted afterwards that the problem had never entirely gone away. "It's been a bit sore, but I'm thankful I got on the field," he said. "I've been on a few painkillers, but at the moment there's a lot of adrenalin so I'm not feeling any pain."

  

Victory is always the best painkiller, but in South Africa's case, it extends beyond the fitness of their captain. The capitulations of 1994, 1998 and 2003 can at last be forgotten, and by blotting the date "1965" out of their record-books, the final link with the apartheid era has been severed. South Africa are a team going forward at high speed, and for their captain, the journey has never been so pleasant.

 

Andrew Miller

William Woods Holden was North Carolina’s first popularly elected republican governor, elected in 1868, following the state’s readmission to the Union in 1867. He replaced Raleigh’s sitting Board of Commissioners with Republican appointees, including two African Americans. Gov. Holden’s suppression of the Ku Klux Klan in 1870 led to his impeachment trial in 1871.

 

digital.ncdcr.gov/cdm/compoundobject/collection/p249901co...

(pp.12, 180)

 

From the Barden Collection, State Archives of North Carolina.

Hi there!

Is that time of the year again, and Noveny is looking for new faces to join our blogger team! Please read carefully the rules before applying since the break of these would end up with your suspension and probably no-readmission.

Good luck to everyone!

 

maps.secondlife.com/secondlife/Orchard%20Heights/184/40/1663

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No Guts, No Glory: Tackling Healthcare Headon: Hospital readmissions is one of biggest challenges in healthcare, for the patient of course and also for the hospitals. With the new Medicare 30-day policy, new practices are dire to comply. Enter the tech innovators who are tackling this challenge head-on.What if you could continue to see your doctor without having to physically go back to the hospital? And what if reliable (and non-intrusive) monitoring could help detect when you need help most? Now that would surely cut costs and improve outcome. Hear directly from the innovators making this vision a reality—from reducing hospital readmissions to preventing complications and re-occurrance.

 

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The Digital Health Summit, www.digitalhealthsummit.com , produced by Living in Digital Times, convenes one of the broadest spectrum audiences which makes it a can’t miss event. Everyone from medical providers, policy makers, buyers, payers, investors, developers, leading consumer electronics companies, innovators driving the marketplace and all the other industries starting to cross-pollinate into digital health including the automotive, fitness and gaming industries.

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The Poet Goes Floppy

Methiant y Bardd

 

He:

Lovely one with slinky waist,

Royal and slender, do your worst:

Precious ladyship, I cast

My love upon you, by Christ!

Once, you granted permission;

What chance of readmission?

 

She:

How will you gain, with wheyish face?

You must pledge to make no fuss.

 

He:

By your legs – yes, I’ve seen them –

I’d be silent between them.

 

She:

Put your knees between my legs:

Beguile a girl with what she likes.

 

He:

What, haughty girl, will I do?

My wily tool won’t rise for you.

 

She:

What happened to your words?

Deeds fail you. All men are duds.

 

He:

My lust’s a husk - winds winnow -

My words blew out the window.

 

She:

Curse the ladies and the girls

You have known – he who beguiles

His way between my white thighs,

Gets me hot and barely thaws!

Take your tool which mopes and flops,

And lie down with fleas and lice!

 

He:

Sleep alone with your wild arse

For company, with Christ’s curse!

 

Poem by Dafydd ap Gwilym, paraphrased by Giles Watson, 2011. A travelling poet and musician would have needed some bawdy material in his repertoire, and there seems to be little reason for doubting Dafydd’s authorship here. Even though it has been argued that the poem was written by a woman, there are plenty of unquestionably canonical poems which demonstrate Dafydd’s own self-irony, and in the mediaeval manuscripts, Dafydd’s is the only name associated with it.

19 dec 1899 liz in padded room

 

11868 Elizabeth Chatterton Chorlton

19 Dec 1899

Married

children 12 (8 now living)

Church of England

Well nourished

9s 7lb

Recurrent Mania

Tonic - Moral - Employment

19th June 1900

Discharged “Recovered” Readmission

10s 1lb

Has a wild, excited appearance, is under restraint in padded

room, says her father’s soul is in the room with her, that

she hears voices calling to her through the wall and sees people

looking at her, says her mother who is dead has got her soul

 

Religious Mania

Ill-health

During last lactation an abcess formed in leg

- went to Hospital about May - returned in

Sept - seemed going wrong then

  

John Burke died at the hospital yesterday while chloroform, was being administered for the purpose of undergoing an operation.

paperspast.natlib.govt.nz/newspapers/THS19020114.2.23

 

DEATH UNDER CHLOROFORM.

A man named John Burke died yesterday afternoon at the hospital, while under chloroform. The deceased, who was a married man, was a labourer, aged 45, and had lived in Victoria-street West. In November last he was admitted to the hospital suffering from stricture. On December 12 an operation was performed by Dr. Scott. While under treatment deceased, in defiance of advice, left the institution, and the result was that he had to apply for readmission, and on January 8 last he was successfully operated upon by Dr. Scott, chloroform being administered by Dr. Teague, the house physician. Yesterday, at about half-past twelve deceased was again prepared for chloroforming by Dr. Teague, in order that a catheter might be used upon him. An attempt was made to use the instrument, but it was not successful. At about a-quarter to five yesterday Dr. Collins, the medical superintendent, instructed Dr. Teague to again give the patient chloroform, and he did —using Flockhart's best chloroform, with an ordinary, mask. About a couple of minutes after the chloroforming was started (and before the catheter could be used) the deceased all at once showed signs of collapse. Every possible means was immediately taken to stimulate the heart's action, and Burke showed signs of recovery, but suddenly the heart failed absolutely. Deceased was very carefully examined by Dr. Teague upon this and the former occasions, prior to administering the anaesthetic, and the heart was found to be sound in every instance. It was absolutely necessary to use the catheter, and deceased refused to allow it to be done without an anaesthetic, owing to the pain he suffered. An inquest will be held by Mr. Thomas Gresham, city coroner, at the hospital at nine o'clock this morning.

paperspast.natlib.govt.nz/newspapers/NZH19020114.2.20

 

DEATH UNDER CHLOROFORM.

HOSPITAL STAFF EXONORATED.

The adjourned inquest touching the death of John Burke, who died at the Auckland Hospital on Monday evening, January 13, while under chloroform, took place to-day.

Dr Collins, senior medical superintendent, deposed that deceased waa first admitted to the hospital on September 7th, and left the hospital without permission on the 24th September. He became very bad and was sent again by a medical man on November 8th. He was then in a very bad condition. He was operated upon for urethral stricture by Dr. Scott on December 11th, Dr. Teague administering chloroform. Shortly afterwards he left the hospital without orders. He was absent from the hospital until his re-admission. He was operated upon again by Dr. Scott on January 8th for the same complaint, and again on the 13th inst. Deceased was compelled to return to the hospital because the stricture had become impassable. The operation on January 8th was quite successful, and the patient was well two days after. On the 11th inst. it became necessary to remove the catheter, which had been tied into the bladder. On the 13th it was again a matter of urgency to re-introduce the catheter, as the stricture was quite impassable. He had refused to take ether both on the 8th and 13th of January, as he said it choked him. He had consented to the use of chloroform, and would not allow any operation to be performed without it. The chloroform was administered to him in his bed at about half-past four on the evening of the 13th by Dr. Teague, whom witness had requested to administer the chloroform. After sixty drops had been administered on the skin of the mask deceased suddenly collapsed. The mask used was Skinner's mask, the use of which, according to "Anaesthetics and Their Administration," a publication brought quite up-to-date, had been attended by only two fatalities out of a total of 210 deaths under chloroform, which was the lowest percentage of fatalities out of the different methods of administration. He submitted statistics showing that during the past five years there had been 3500 administrations of chloroform at the hospital, and only three deaths, giving an average of one death in 1166 administrations. At St. Bartholomew's Hospital during the years 1876-1896 there were 58,787 administrations, of which 30,871 were chloroform. The deaths under chloroform were one in 1470. At the operation when the patient collapsed Dr. Teague called witness' attention to his condition. Efforts were immediately made to restore respiration, but deceased gave only a few gasps and then the action of the heart failed completely. The condition of the kidneys would be sufficient to account for death. There was no method of administration of chloroform absolutely safe. The chloroform used was the best procurable. About two and a half minutes after the application of the mask a sudden gush of urine through the wound took place. The chloroform mask was immediately removed from the patient. In his opinion the sudden evacuation of the bladder contributed largely to the collapse of the

Dr. William George Scott stated that he was senior operating surgeon at the hospital. He had operated on deceased on December 11 and January 8. From time to time, when he had wanted to operate upon deceased, he had been debarred from doing so by deceased's state of health, and his condition would not admit of the operation being performed, although it was urgent. On several occasions he was compelled to postpone operation until a more favourable opportunity. At the first operation in December the administration of ether was commenced by Dr. Teague, but deceased gradually showed signs of resistance, and finally jumped off the table. As the use of ether was impossible, it was necessary to use chloroform, but the patient still struggled so violently that it was only with great difficulty that anaesthesia was completed. At the second operation chloroform was administered by Dr. Teague, but the patient still struggled. On this occasion something in the condition of the patient caused him to ask if there was any trouble with regard to anaesthesia. Dr. Teague answered that there had been a little difficulty in breathing, but the patient was all right now. Ether had a tendency to induce a dangerous condition of the kidneys, and consequently chloroform was preferable and was safer as an anaesthetic for an operation in connection with the kidneys and bladder. He had been present on many occasions when Dr. Teague had administered ether and chloroform, and he was convinced that he did so in a careful and skilful manner. He confirmed the evidence of Dr. Collins with regard to the operation on January 8. On Sunday last he visited the patient with a view to the reintroduction of the catheter, but the condition of the patient was not favourable. He advised that the catheter be re-introduced on the following day. From the condition of the bladder and kidneys, which he had seen after the post mortem, he considered the administration of an anaesthetic exceedingly hazardous, although the operation was absolutely necessary. The responsibility rested entirely with the administrator of the anaesthetic, and not with the operator. He agreed with Dr. Collins that the sudden evacuation of the bladder by a large quantity would cause death, and in this case it undoubtedly contributed to the collapse of the patient.

Dr. T. Hope-Lewis deposed to making a post-mortem examination of the body of John Burke. He found several old scars on the body, and an incision about two inches long on the perineum. The kidneys were affected with a chronic inflammatory disease, and the walls of the bladder were thickened to ten times the normal thickness. There was also a tight stricture of the urethra. He considered the cause of death was poisoning by urea and chloroform. The case was one of absolute necessity, and the use of chloroform was absolutely necessary. The man would have died had the operation not been performed, and the evacuation of the bladder caused his collapse. The condition of the various organs tended to indicate that the patient had suffered from syphilis.

After a short retirement the jury returned a verdict "That John Burke died during the administration of chloroform for the relief of stricture, death being accelerated by urine poisoning, caused by the diseased state of the kidneys and bladder, and are of opinion that the medical staff of the hospital took all possible precaution, and acted with perfect skill."

paperspast.natlib.govt.nz/newspapers/AS19020116.2.11

  

Plot 32: John Burke (45) 13/1/1902 – Labourer – Urea & chloroform poisoning – at Hospital (R.C.)

 

Anglican divisions M and N are what is known as ‘Potters Fields’, they were used to bury some of the people whose families were unable to afford burial costs, were institutionalised or unidentified at the time of burial. These plots were common graves with many having several individuals interred in each. They were narrower and closer together and, because they were not paid for, permanent grave markers were not permitted to be erected.

 

It is now no longer known where either Anglican Division M or N starts let alone the rows or individual plots which have now been protected by ghost gums, native trees & flax.

 

However it is believed that Division M starts closest to Eucalyptus Ave & that single rows were used for both areas.

Moderator:Dr. Alan Stein, VP Healthcare Technology, HP Software Hewlett-Packard

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No Guts, No Glory: Tackling Healthcare Headon: Hospital readmissions is one of biggest challenges in healthcare, for the patient of course and also for the hospitals. With the new Medicare 30-day policy, new practices are dire to comply. Enter the tech innovators who are tackling this challenge head-on.What if you could continue to see your doctor without having to physically go back to the hospital? And what if reliable (and non-intrusive) monitoring could help detect when you need help most? Now that would surely cut costs and improve outcome. Hear directly from the innovators making this vision a reality—from reducing hospital readmissions to preventing complications and re-occurrance.

 

Thank you to our sponsor: WebMD www.webmd.com

Follow: www.twitter.com/webmd

 

The Digital Health Summit, www.digitalhealthsummit.com , produced by Living in Digital Times, convenes one of the broadest spectrum audiences which makes it a can’t miss event. Everyone from medical providers, policy makers, buyers, payers, investors, developers, leading consumer electronics companies, innovators driving the marketplace and all the other industries starting to cross-pollinate into digital health including the automotive, fitness and gaming industries.

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Senator Martin Looney visited the Atwater Senior Center in New Haven to discuss a proposed bill which will guarantee that caregivers are given follow-up care instructions when a patient is discharged from the hospital to improve in-home care and reduce costly hospital readmissions. The #CAREAct has been successfully passed in other states and Senator Looney hopes to see it passed in Connecticut this year. (February 13, 2015)

Senator Cathy Osten talks to constituents during a visit to the Norwich Senior Center where she discussed a proposed bill which will guarantee that caregivers are given follow-up care instructions when a patient is discharged from the hospital to improve in-home care and reduce costly hospital readmissions. The #CAREAct has been successfully passed in other states and Senator Osten hopes to see it passed in Connecticut this year. (February 12, 2015)

Senator Cathy Osten talks to constituents during a visit to the Norwich Senior Center where she discussed a proposed bill which will guarantee that caregivers are given follow-up care instructions when a patient is discharged from the hospital to improve in-home care and reduce costly hospital readmissions. The #CAREAct has been successfully passed in other states and Senator Osten hopes to see it passed in Connecticut this year. (February 12, 2015)

One way for hospitals

to reduce readmission

rates is by partnering

with organizations

like Meals on Wheels

America that provide

home-delivered meals

to food-insecure

seniors.

I will never return to Universal!

 

This was taken at Universal Islands of Adventure on 12/28/2011. This was the worst theme park experience I have had.

 

We arrived about 10 minutes after the park opened, we rode the hulk (5 minute line) then Fearfall (20 minute line). We then headed to the Harry Potter section that was already over capacity and jam packed. So we watched a stunt show and a Dr. Seuss show. Coming out of Dr. Seuss, we ended up in this crowd, so we left the park for an early lunch and were then denied readmission to the park, even though we each had $85 tickets, because the park was at capacity.

 

The park is also obnoxious; like Disney, they have express lines, unlike Disney which allows everyone limited access to express lines, Universal sells an express line ticket for $256 per.. us schmucks that got the $85 ticket wait. All lines this day were 2 hours or more by 9:30. What a rip off, but at least Universal personnel was there in line with you, ready to sell you bottles of water at $3 each.

 

Look carefully at this crowd, we were completely dead locked for at least 15 minutes -- nobody moved either direction until security came and made people near the back ends (out of site in this picture) turn the other direction. I have been to Time Square on new years eve, this was worse! Young children (and their parents were literally freaking out).

 

It was Christmas Week, we expected crowds, and we got them: here, at Disney & Sea World. But Universal was the only place like this: selling $85 tickets to you (we had a party of six) and then not allowing you to reenter the park after an early lunch.

 

Shouldn't they stop selling tickets when the park reaches capacity rather than stop letting ticketed customers enter the park?

There were individual Jews living in England in Roman and Anglo-Saxon times (80-1066 A.D.), but not an organized community. When William the Conqueror arrived in England in 1066, he encouraged Jewish merchants and artisans from northern France to move to England. The Jews came mostly from France with some from Germany, Italy and Spain, seeking prosperity and a haven from anti-Semitism. Serving as special representatives of the king, these Jews worked as moneylenders and coin dealers. Over the course of a generation, Jews established communities in London, York, Bristol, Canterbury and other major cities. They generally lived in segregated areas by themselves.

 

The first recorded mention of Jews in Canterbury was in 1160. By 1200 Canterbury Jewry is the third most important in England. The Jews are on good terms with both town and clergy. Jews live in the commercial heart of the city, principally in present day Jewry lane, White Horse Lane, Stour Street, High Street, and Best Lane. They own around 20 houses. Other Jews are known to live out in the surrounding villages. The Jews of Canterbury were never so numerous as those of London, York, Lincoln, Cambridge, and other cities, but they were evidently an influential section of the community during the greater part of the twelfth and thirteenth centuries. In 1206 the Jewish community is estimated to number some 100 Jews - a large Jewry for the time. The community appears to have flourished in the 1240’s but for some reason by 1255 the Jewish community declines to the rank of the eighth most important Jewry in the country, and in 1261 the Jews suffer a pogrom at the hands of clergy and laity during the rebellion of Barons led by Simon de Montfort, Earl of Leicester. No lives are lost but many are violently assaulted. In 1264 Gilbert de Clare, Earl of Gloucester, one of the rebellious barons, captures Canterbury and sacks the Jewish quarter. The object is to destroy records of debt, Jews are violently assaulted some may have been killed.

 

During the Barons Wars of 1263, the Jews were seen as instruments of royal oppression and between 1263 and 1266, one Jewish community after another was ransacked and many of its inhabitants killed. In 1265, the Crown started dealing with Italian bankers, minimizing their dependence on the Jews for financial services. In 1269, the Crown further restricted Jewish rights. Jews were not allowed to hold land and Jewish children could not inherit their parent’s money. When a Jew died, his money reverted to the government.

 

In 1275, Edward I issued the Jewish Affairs Bill, forbidding the Jews of England to loan money on interest. They could earn a living as tradesmen or farmers, but were ineligible for membership in tradesmen guilds or tenure as a farmer. The Jews became poor and the king could no longer collect taxes from them. In 1278, many were arrested and hanged for secretly continuing their money lending. Six Canterbury Jews were executed in London on charges of coin clipping, and their properties were confiscated. The rest were temporarily incarcerated in the castle, and various of their goods and chattels were illegally seized by local people.

By 1284 tax returns show there are now only 34 Jews living in Canterbury aged 12 years and above. In 1290, shortly after money lending was made heretical and illegal in England, Edward I expelled the Jews from England, making England the first European country to do so. Most Jews fled to continental Europe, settling mostly in France and Germany, although some managed to remain in England by hiding their identity and religion. The Jewish exile from England lasted 350 years.

 

Historians disagree as to the exact date of the official readmission of Jews to England as well as to whether or not it was Oliver Cromwell who granted it. Cromwell came to power in 1649. The re-establishment of the Jews in England was a gradual process, one which took many years. In 1698, the Act for Suppressing Blasphemy granted recognition to the legality of practicing Judaism in England. Some time in the early 1700’s Jews return to live in Canterbury, but they are forced to reside and worship outside of the ancient city limits. In 1730 a new Jewish congregation is formed, and worship is established in a temporary building in the St Dunstan's area of the city. However, by the dawn of the twentieth century there are only 12 Jews left in the city.

 

There is no longer an operating Synagogue in Canterbury

  

Senate President Pro Tempore Martin Looney was joined by other legislators, advocates and caregivers to show support for a proposed bill which will guarantee that caregivers are given follow-up care instructions when a patient is discharged from the hospital to improve in-home care and reduce costly hospital readmissions. (February 10, 2015)

Fighting may have ended but migration continues. Despite increasingly strict EU policies on immigration, the “western dream” still exerts a powerful force of attraction on the people of the Balkans. In recent years there has been an increase in the number of migrants being forcibly repatriated, under readmission agreements signed by all the west Balkan countries with the EU.

 

For any form of publication, please include the link to this page:

www.grida.no/resources/6865

 

This photo has been graciously provided to be used in the GRID-Arendal resources library by: Philippe Rekacewicz, Stephane Kluser, Matthias Beilstein, Ieva Rucevska, Cecile Marin, Otto Simonett

Moderator:Dr. Alan Stein, VP Healthcare Technology, HP Software Hewlett-Packard

Website: bit.ly/HP_DHS

Twitter: @hpnews

Company LinkedIn: bit.ly/HP_Lknd_DHS

Facebook: bit.ly/HP_fb_DHS

 

Speaker: John Bojanowski, President, Honeywell HomMed

Website: bit.ly/Honeywell_DHS

Company Twitter: @HoneywellHomMed

Company LinkedIn: bit.ly/HoneywellLknd_DHS

 

Speaker: Randy Parker President and Chief Executive Officer (Founder) MDLIVE, Inc

Website: bit.ly/MDLive_DHS

Twitter: @MDLIVEInc

Company LinkedIn: bit.ly/MDLiveLknd_DHS

LinkedIn: bit.ly/RParker_DHS

Facebook: bit.ly/MDLiveFB_DHS

 

Speaker: David Ip, Senior Digital Product Manager, Anthem Blue Cross Blue Shield

Website: bit.ly/Anthem_DHS

Twitter: @HealthJoinIn

Facebook: bit.ly/AnthemFB_DHS

 

No Guts, No Glory: Tackling Healthcare Headon: Hospital readmissions is one of biggest challenges in healthcare, for the patient of course and also for the hospitals. With the new Medicare 30-day policy, new practices are dire to comply. Enter the tech innovators who are tackling this challenge head-on.What if you could continue to see your doctor without having to physically go back to the hospital? And what if reliable (and non-intrusive) monitoring could help detect when you need help most? Now that would surely cut costs and improve outcome. Hear directly from the innovators making this vision a reality—from reducing hospital readmissions to preventing complications and re-occurrance.

 

Thank you to our sponsor: WebMD www.webmd.com

Follow: www.twitter.com/webmd

 

The Digital Health Summit, www.digitalhealthsummit.com , produced by Living in Digital Times, convenes one of the broadest spectrum audiences which makes it a can’t miss event. Everyone from medical providers, policy makers, buyers, payers, investors, developers, leading consumer electronics companies, innovators driving the marketplace and all the other industries starting to cross-pollinate into digital health including the automotive, fitness and gaming industries.

Official Hashtag: #DigitalHealthCES

 

Twitter: www.twitter.com/dhsummit

Hashtags: #digitalhealthces #webmdces #ces2015

Blog & Videos: www.digitalhealthsummit.com/blog

Photos: www.flickr.com/digitalhealthsummit

 

Conference Producer: Jill Gilbert, @GilbertGuide

Photos by: Asa Mathat www.asamathat.com

Senator Joe Crisco joined with AARP volunteers at the Joseph Doyle Senior Center in Ansonia to discuss a proposed bill which will guarantee that caregivers are given follow-up care instructions when a patient is discharged from the hospital to improve in-home care and reduce costly hospital readmissions. The #CAREAct has been successfully passed in other states and Senator Crisco hopes to see it passed in Connecticut this year. (February 12, 2015)

Senator Joe Crisco talks with AARP advocate Pat Gerckens of Derby during a visit to the Joseph Doyle Senior Center in Ansonia to discuss a proposed bill which will guarantee that caregivers are given follow-up care instructions when a patient is discharged from the hospital to improve in-home care and reduce costly hospital readmissions. The #CAREAct has been successfully passed in other states and Senator Crisco hopes to see it passed in Connecticut this year. (February 12, 2015)

William Woods Holden was North Carolina’s first popularly elected republican governor, elected in 1868, following the state’s readmission to the Union in 1867. He replaced Raleigh’s sitting Board of Commissioners with Republican appointees, including two African Americans. Gov. Holden’s suppression of the Ku Klux Klan in 1870 led to his impeachment trial in 1871.

 

Photo by Albert Barden. From the Albert Barden Collection, State Archives of North Carolina, Raleigh, NC.

This is the label we had embroidered at Barbara's Embroidery - San Francisco (call or email for appointment as she has limited hours) for Melody Chan Doss' Fashionista Crazy Quilt we took to the Santa Clara Convention Center on October 15, 2013 to hang and be juried in the Pacific International Quilt Festival 2013. This was white thread embroidery on black cotton material. The unedited label also includes an address. The PIQF ran for four days in Santa Clara from Oct 17 - Oct 20, 2013. Hope you get a chance to attend. Tickets good for readmission.

As you can read, Melody dedicated this quilt to her mother - who toiled as a seamstress in workshop conditions to contribute to the raising of her three children - and to Mrs Lucy Spector who founded Britex fabrics in San Francisco with her husband Martin and who inspired a sense of fashion in Melody.

Australia v South Africa, Tri-Nations Series, Suncorp Stadium 17.7.99 Brisbane

Result Australia won 32 - 6

 

The contest between The Wallabies and The Springboks is one of the major rivalries in rugby union.

The team's first meeting was on 8 July 1933 at Newlands in Cape Town in the first of 5 tests on the 1933 Wallabies tour. The test was won 17-3 by South Africa who also won that first series 3-2.

South Africa has a better than 57% winning record against Australia, and before the era of sporting boycotts, dominated the early encounters up to 1971. Since South African rugby's readmission in 1992, however, the head-to-head record is quite even, with Australia holding the slight edge.

Both sides have exhibited a considerable home advantage, with South Africa winning more than 75% of matches played in South Africa, and Australia winning more than 60% of matches played in Australia…

Rugby World Cup

Australia and South Africa have met three times in the Rugby World Cup. In 1995 they were drawn in the same pool and host nation South Africa won 27-18, going on to win the cup. In 1999 Australia knocked South Africa out of the competition in a semi-final at Twickenham, winning 27-21. In 2011, Australia again knocked South Africa out of the competition, in a quarter-final at Westpac Stadium in Wellington, winning 11-9.

Wikipedia

 

Moderator:Dr. Alan Stein, VP Healthcare Technology, HP Software Hewlett-Packard

Website: bit.ly/HP_DHS

Twitter: @hpnews

Company LinkedIn: bit.ly/HP_Lknd_DHS

Facebook: bit.ly/HP_fb_DHS

 

Speaker: John Bojanowski, President, Honeywell HomMed

Website: bit.ly/Honeywell_DHS

Company Twitter: @HoneywellHomMed

Company LinkedIn: bit.ly/HoneywellLknd_DHS

 

Speaker: Randy Parker President and Chief Executive Officer (Founder) MDLIVE, Inc

Website: bit.ly/MDLive_DHS

Twitter: @MDLIVEInc

Company LinkedIn: bit.ly/MDLiveLknd_DHS

LinkedIn: bit.ly/RParker_DHS

Facebook: bit.ly/MDLiveFB_DHS

 

Speaker: David Ip, Senior Digital Product Manager, Anthem Blue Cross Blue Shield

Website: bit.ly/Anthem_DHS

Twitter: @HealthJoinIn

Facebook: bit.ly/AnthemFB_DHS

 

No Guts, No Glory: Tackling Healthcare Headon: Hospital readmissions is one of biggest challenges in healthcare, for the patient of course and also for the hospitals. With the new Medicare 30-day policy, new practices are dire to comply. Enter the tech innovators who are tackling this challenge head-on.What if you could continue to see your doctor without having to physically go back to the hospital? And what if reliable (and non-intrusive) monitoring could help detect when you need help most? Now that would surely cut costs and improve outcome. Hear directly from the innovators making this vision a reality—from reducing hospital readmissions to preventing complications and re-occurrance.

 

Thank you to our sponsor: WebMD www.webmd.com

Follow: www.twitter.com/webmd

 

The Digital Health Summit, www.digitalhealthsummit.com , produced by Living in Digital Times, convenes one of the broadest spectrum audiences which makes it a can’t miss event. Everyone from medical providers, policy makers, buyers, payers, investors, developers, leading consumer electronics companies, innovators driving the marketplace and all the other industries starting to cross-pollinate into digital health including the automotive, fitness and gaming industries.

Official Hashtag: #DigitalHealthCES

 

Twitter: www.twitter.com/dhsummit

Hashtags: #digitalhealthces #webmdces #ces2015

Blog & Videos: www.digitalhealthsummit.com/blog

Photos: www.flickr.com/digitalhealthsummit

 

Conference Producer: Jill Gilbert, @GilbertGuide

Photos by: Asa Mathat www.asamathat.com

"Para William, Walmir e Barroso, mortos na greve de novembro de 1988. A homenagem de seus companheiros."

 

(To William, Walmir and Barroso, assassinated during the strike in November 1988. Homage from your workmates.)

 

During the second night of the strike from 7 to 23 November 1988 at the National Steel Mill (CSN), the streets of Volta Redonda's city centre and its residential streets showed scenes of war with sniper bullets and soldiers in tanks all over. People spent the night flat on their bellies in the houses. The end of dictatorship in Brazil was not very far behind yet and it felt like it could come back any time soon. Thanks to the president of that time, José Sarney, the army was allowed to try to take over the steel mill in the night of 9th of November. They injured many people and killed three of them:

William Fernandes Leite, 22 years old;

Valmir Freitas Monteiro, 27 years old;

Carlos Augusto Barroso, 19 years.

 

In the end, the workers won the negotiations with the enterprise and obtained what they had striked for: readmission of colleagues, shortening the work shift by 2 hours and a salary increase.

 

Soldiers were sent in the night of 1st to 2nd of May 1989, just after the inauguration of the monument, to destroy the monument with a bomb. That is why it looks so brittle. Oscar Niemeyer, who designed the monument, decided that the marks of this attack should stay to remember the second attempt to workers and citizens rights.

The windows of the houses in a diameter of a 1km were broken.

Photo from the William Wynn Mood photo album, Wofford College Archives, Spartanburg, SC

Photo dated Aug. 15, 1872

Rev. Walsh was licensed to preach in 1827 and admitted to the South Carolina Conference in 1830. He located in 1837 and was readmitted in 1849. During that period, he was in charge of the Marion Academy. On his readmission he served churches for 3 years, then became president of Carolinas Female College in North Carolina, where he served until 1860. He returned to local churches in 1860 and continued until his death in 1867.

Moderator:Dr. Alan Stein, VP Healthcare Technology, HP Software Hewlett-Packard

Website: bit.ly/HP_DHS

Twitter: @hpnews

Company LinkedIn: bit.ly/HP_Lknd_DHS

Facebook: bit.ly/HP_fb_DHS

 

Speaker: John Bojanowski, President, Honeywell HomMed

Website: bit.ly/Honeywell_DHS

Company Twitter: @HoneywellHomMed

Company LinkedIn: bit.ly/HoneywellLknd_DHS

 

Speaker: Randy Parker President and Chief Executive Officer (Founder) MDLIVE, Inc

Website: bit.ly/MDLive_DHS

Twitter: @MDLIVEInc

Company LinkedIn: bit.ly/MDLiveLknd_DHS

LinkedIn: bit.ly/RParker_DHS

Facebook: bit.ly/MDLiveFB_DHS

 

Speaker: David Ip, Senior Digital Product Manager, Anthem Blue Cross Blue Shield

Website: bit.ly/Anthem_DHS

Twitter: @HealthJoinIn

Facebook: bit.ly/AnthemFB_DHS

 

No Guts, No Glory: Tackling Healthcare Headon: Hospital readmissions is one of biggest challenges in healthcare, for the patient of course and also for the hospitals. With the new Medicare 30-day policy, new practices are dire to comply. Enter the tech innovators who are tackling this challenge head-on.What if you could continue to see your doctor without having to physically go back to the hospital? And what if reliable (and non-intrusive) monitoring could help detect when you need help most? Now that would surely cut costs and improve outcome. Hear directly from the innovators making this vision a reality—from reducing hospital readmissions to preventing complications and re-occurrance.

 

Thank you to our sponsor: WebMD www.webmd.com

Follow: www.twitter.com/webmd

 

The Digital Health Summit, www.digitalhealthsummit.com , produced by Living in Digital Times, convenes one of the broadest spectrum audiences which makes it a can’t miss event. Everyone from medical providers, policy makers, buyers, payers, investors, developers, leading consumer electronics companies, innovators driving the marketplace and all the other industries starting to cross-pollinate into digital health including the automotive, fitness and gaming industries.

Official Hashtag: #DigitalHealthCES

 

Twitter: www.twitter.com/dhsummit

Hashtags: #digitalhealthces #webmdces #ces2015

Blog & Videos: www.digitalhealthsummit.com/blog

Photos: www.flickr.com/digitalhealthsummit

 

Conference Producer: Jill Gilbert, @GilbertGuide

Photos by: Asa Mathat www.asamathat.com

Moderator:Dr. Alan Stein, VP Healthcare Technology, HP Software Hewlett-Packard

Website: bit.ly/HP_DHS

Twitter: @hpnews

Company LinkedIn: bit.ly/HP_Lknd_DHS

Facebook: bit.ly/HP_fb_DHS

 

Speaker: John Bojanowski, President, Honeywell HomMed

Website: bit.ly/Honeywell_DHS

Company Twitter: @HoneywellHomMed

Company LinkedIn: bit.ly/HoneywellLknd_DHS

 

Speaker: Randy Parker President and Chief Executive Officer (Founder) MDLIVE, Inc

Website: bit.ly/MDLive_DHS

Twitter: @MDLIVEInc

Company LinkedIn: bit.ly/MDLiveLknd_DHS

LinkedIn: bit.ly/RParker_DHS

Facebook: bit.ly/MDLiveFB_DHS

 

Speaker: David Ip, Senior Digital Product Manager, Anthem Blue Cross Blue Shield

Website: bit.ly/Anthem_DHS

Twitter: @HealthJoinIn

Facebook: bit.ly/AnthemFB_DHS

 

No Guts, No Glory: Tackling Healthcare Headon: Hospital readmissions is one of biggest challenges in healthcare, for the patient of course and also for the hospitals. With the new Medicare 30-day policy, new practices are dire to comply. Enter the tech innovators who are tackling this challenge head-on.What if you could continue to see your doctor without having to physically go back to the hospital? And what if reliable (and non-intrusive) monitoring could help detect when you need help most? Now that would surely cut costs and improve outcome. Hear directly from the innovators making this vision a reality—from reducing hospital readmissions to preventing complications and re-occurrance.

 

Thank you to our sponsor: WebMD www.webmd.com

Follow: www.twitter.com/webmd

 

The Digital Health Summit, www.digitalhealthsummit.com , produced by Living in Digital Times, convenes one of the broadest spectrum audiences which makes it a can’t miss event. Everyone from medical providers, policy makers, buyers, payers, investors, developers, leading consumer electronics companies, innovators driving the marketplace and all the other industries starting to cross-pollinate into digital health including the automotive, fitness and gaming industries.

Official Hashtag: #DigitalHealthCES

 

Twitter: www.twitter.com/dhsummit

Hashtags: #digitalhealthces #webmdces #ces2015

Blog & Videos: www.digitalhealthsummit.com/blog

Photos: www.flickr.com/digitalhealthsummit

 

Conference Producer: Jill Gilbert, @GilbertGuide

Photos by: Asa Mathat www.asamathat.com

Moderator:Dr. Alan Stein, VP Healthcare Technology, HP Software Hewlett-Packard

Website: bit.ly/HP_DHS

Twitter: @hpnews

Company LinkedIn: bit.ly/HP_Lknd_DHS

Facebook: bit.ly/HP_fb_DHS

 

Speaker: John Bojanowski, President, Honeywell HomMed

Website: bit.ly/Honeywell_DHS

Company Twitter: @HoneywellHomMed

Company LinkedIn: bit.ly/HoneywellLknd_DHS

 

Speaker: Randy Parker President and Chief Executive Officer (Founder) MDLIVE, Inc

Website: bit.ly/MDLive_DHS

Twitter: @MDLIVEInc

Company LinkedIn: bit.ly/MDLiveLknd_DHS

LinkedIn: bit.ly/RParker_DHS

Facebook: bit.ly/MDLiveFB_DHS

 

Speaker: David Ip, Senior Digital Product Manager, Anthem Blue Cross Blue Shield

Website: bit.ly/Anthem_DHS

Twitter: @HealthJoinIn

Facebook: bit.ly/AnthemFB_DHS

 

No Guts, No Glory: Tackling Healthcare Headon: Hospital readmissions is one of biggest challenges in healthcare, for the patient of course and also for the hospitals. With the new Medicare 30-day policy, new practices are dire to comply. Enter the tech innovators who are tackling this challenge head-on.What if you could continue to see your doctor without having to physically go back to the hospital? And what if reliable (and non-intrusive) monitoring could help detect when you need help most? Now that would surely cut costs and improve outcome. Hear directly from the innovators making this vision a reality—from reducing hospital readmissions to preventing complications and re-occurrance.

 

Thank you to our sponsor: WebMD www.webmd.com

Follow: www.twitter.com/webmd

 

The Digital Health Summit, www.digitalhealthsummit.com , produced by Living in Digital Times, convenes one of the broadest spectrum audiences which makes it a can’t miss event. Everyone from medical providers, policy makers, buyers, payers, investors, developers, leading consumer electronics companies, innovators driving the marketplace and all the other industries starting to cross-pollinate into digital health including the automotive, fitness and gaming industries.

Official Hashtag: #DigitalHealthCES

 

Twitter: www.twitter.com/dhsummit

Hashtags: #digitalhealthces #webmdces #ces2015

Blog & Videos: www.digitalhealthsummit.com/blog

Photos: www.flickr.com/digitalhealthsummit

 

Conference Producer: Jill Gilbert, @GilbertGuide

Photos by: Asa Mathat www.asamathat.com

Moderator:Dr. Alan Stein, VP Healthcare Technology, HP Software Hewlett-Packard

Website: bit.ly/HP_DHS

Twitter: @hpnews

Company LinkedIn: bit.ly/HP_Lknd_DHS

Facebook: bit.ly/HP_fb_DHS

 

Speaker: John Bojanowski, President, Honeywell HomMed

Website: bit.ly/Honeywell_DHS

Company Twitter: @HoneywellHomMed

Company LinkedIn: bit.ly/HoneywellLknd_DHS

 

Speaker: Randy Parker President and Chief Executive Officer (Founder) MDLIVE, Inc

Website: bit.ly/MDLive_DHS

Twitter: @MDLIVEInc

Company LinkedIn: bit.ly/MDLiveLknd_DHS

LinkedIn: bit.ly/RParker_DHS

Facebook: bit.ly/MDLiveFB_DHS

 

Speaker: David Ip, Senior Digital Product Manager, Anthem Blue Cross Blue Shield

Website: bit.ly/Anthem_DHS

Twitter: @HealthJoinIn

Facebook: bit.ly/AnthemFB_DHS

 

No Guts, No Glory: Tackling Healthcare Headon: Hospital readmissions is one of biggest challenges in healthcare, for the patient of course and also for the hospitals. With the new Medicare 30-day policy, new practices are dire to comply. Enter the tech innovators who are tackling this challenge head-on.What if you could continue to see your doctor without having to physically go back to the hospital? And what if reliable (and non-intrusive) monitoring could help detect when you need help most? Now that would surely cut costs and improve outcome. Hear directly from the innovators making this vision a reality—from reducing hospital readmissions to preventing complications and re-occurrance.

 

Thank you to our sponsor: WebMD www.webmd.com

Follow: www.twitter.com/webmd

 

The Digital Health Summit, www.digitalhealthsummit.com , produced by Living in Digital Times, convenes one of the broadest spectrum audiences which makes it a can’t miss event. Everyone from medical providers, policy makers, buyers, payers, investors, developers, leading consumer electronics companies, innovators driving the marketplace and all the other industries starting to cross-pollinate into digital health including the automotive, fitness and gaming industries.

Official Hashtag: #DigitalHealthCES

 

Twitter: www.twitter.com/dhsummit

Hashtags: #digitalhealthces #webmdces #ces2015

Blog & Videos: www.digitalhealthsummit.com/blog

Photos: www.flickr.com/digitalhealthsummit

 

Conference Producer: Jill Gilbert, @GilbertGuide

Photos by: Asa Mathat www.asamathat.com

TUESDAY, MAY 22, 2012 - This is the 2012 SSM Leadership Conference, "It's a New World", at the Ritz-Carlton Hotel in St. Louis, Mo.

 

Within a pilot unit at SSM DePaul Health Center, an opportunity exists to re-design the care, coordination of care, and care transition utilizing the IPC group of hospitalist physicians. The goal of this redesign would be to improve patient satisfaction and prepare SSM-Health Care St. Louis for the new Centers for Medicare and Medicaid Services (CMS) regulation for admissions. Beginning this fall, inpatient prospective payment system hospitals with higher-than-expected readmission rates will experience decreased Medicare payments for all Medicare discharges. Performance evaluation will be based on the 30-day readmission measures for heart attack, heart failure, and pneumonia. Additional reductions in reimbursement for higher-than-expected readmissions will follow through 2015, and additional conditions will be added as well. An opportunity exists to reduce readmission rates to avoid any financial penalties, as well as to improve patient outcomes and satisfaction.

 

Michelle Meyer, Team Leader, 5 South

Sarada Sripada, MD, IPC Hospitalist

Richard Covert, MD, Physician Advisor, 5th Floor

Brenda Peterson, Executive Director, SSM Health Care – St. Louis Case Management, Social Services, Clinical Documentation

Suzanne Jones, Staff CSN 5 South

Felicita Moran, Staff LPN 5 South

  

©Photo by Jerry Naunheim Jr.

     

Adelbert Ames (October 31, 1835 – April 12, 1933) was an American sailor, soldier, and politician. He served with distinction as a Union Army general during the American Civil War.

 

As a Radical Republican and a Carpetbagger, he was military governor, Senator and civilian governor in Reconstruction-era Mississippi.

 

In 1898 he served as a United States Army general during the Spanish-American War.

 

Ames was the last general officer of the American Civil War from either side of the conflict to die, dying at age 97 in 1933.

 

Ames was born in 1835 in the town of Rockland, located in Knox County, Maine. He was the son of a sea captain named Jesse Ames. Adelbert Ames also grew up to be a sailor, becoming a mate on a clipper ship, and also served briefly as a merchant seaman on his own father's ship.

 

On July 1, 1856, he entered the United States Military Academy at West Point, and was still there when the American Civil War began in 1861.

 

Ames graduated from the United States Military Academy on May 6, 1861, standing fifth in his class of 45. On that same date he was commissioned a second lieutenant in the 2nd U.S. Artillery. Eight days later he was promoted to first lieutenant and was assigned to the 5th U.S. Artillery. During the First Battle of Bull Run that July, Ames was badly wounded in the right thigh but refused to leave his guns. He was brevetted to the rank of major on July 21 for his actions during Bull Run. In 1893 Ames would also receive the Medal of Honor for his performance there.

 

Returning to duty the following spring, Ames was part of the defenses of Washington, D.C.. He then fought in the Peninsula Campaign, and saw action at the Battle of Yorktown from April 5 to May 4, the Battle of Gaines' Mill on June 27, and the Battle of Malvern Hill that July.

 

Although Ames was becoming an excellent artillery officer, he realized that significant promotions would be available only in the infantry. He returned to Maine and politicked to receive a commission as a regimental commander of infantry and was assigned to command the 20th Maine Volunteer Infantry Regiment on August 20, 1862. The 20th Maine fought in the Maryland Campaign, but saw little action at the Battle of Antietam on September 17, while in a reserve capacity. During the Union defeat at the Battle of Fredericksburg that winter, Ames led his regiment in one of the last charges on December 13 against Marye's Heights. During the Chancellorsville Campaign in May 1863, Ames volunteered as an aide-de-camp to Maj. Gen. George G. Meade, commander of the V Corps.

 

Ames assumed brigade command in the XI Corps of the Army of the Potomac, relinquishing his command of the 20th Maine to Lt. Col. Joshua L. Chamberlain, who would soon lead the regiment to fame in the Battle of Gettysburg that July.

 

While his own experience at Gettysburg did not achieve the renown of Chamberlain's, Ames performed well under difficult circumstances. During the massive assault by Confederate Lt. Gen. Richard S. Ewell on July 1, 1863, Ames's division commander, Brig. Gen. Francis C. Barlow, moved his division well in front of other elements of the XI Corps to a slight rise that is now known as Barlow's Knoll. This salient position was quickly overrun, and Barlow was wounded and captured. Ames took command of the division and led it in retreat through the streets of Gettysburg to a position on Cemetery Hill. On July 2, the second day of battle, Ames's battered division bore the brunt of the assault on East Cemetery Hill by Maj. Gen. Jubal A. Early, but was able to hold the critical position with help from surrounding units. At one point Ames himself took part in the hand-to-hand fighting. After the battle, the men of the 20th Maine presented Ames with their battle flag as a token of their esteem.

 

In 1864, Ames's division, now part of the X Corps of the Army of the James, served under Maj. Gen. Benjamin Franklin Butler in the Bermuda Hundred Campaign and the Siege of Petersburg.

 

In the future, he would become Butler's son-in-law.

 

That winter, the division was reassigned to the XXIV Corps and sent to North Carolina. He led the successful assault in the Second Battle of Fort Fisher (commanding the 2nd Division, XXIV Corps), accompanying his men into the formidable coastal fortress as most of his staff were shot down by Confederate snipers.

 

In 1868, Ames was appointed by Congress to be provisional Governor of Mississippi. His command soon extended to the Fourth Military District, which consisted of Mississippi and Arkansas.

 

During his administration, he took several steps to advance the rights of freed slaves, appointing the first black office-holders in state history. White supremacist violence was prevalent in the state, one of the last to comply with Reconstruction, but a general election was held during his tenure in 1869 and the legislature convened at the beginning of the following year.

 

The Mississippi Legislature elected Ames to the U.S. Senate after the readmission of Mississippi to the Union; he served from February 24, 1870 to January 10, 1874, as a Republican.

 

In Washington, Ames met and married Blanche Butler, daughter of his former commander, and now U.S. Representative, Benjamin Butler, on July 21, 1870. They had six children including Adelbert Ames Jr. and Butler Ames. As a Senator, Ames became a talented public speaker.

 

Upon being elected governor of Mississippi, he resigned his seat to assume his duties. As a Carpetbagger, Ames battled James Lusk Alcorn—a former Confederate general and now a Scalawag—for control of the Republican party, which comprised mostly black voters. Their struggle ripped apart the party. In 1873 they both sought a decision by running for governor. Ames was supported by the Radicals and most African Americans, while Alcorn won the votes of conservative whites and most of the scalawags. Ames won by a vote of 69,870 to 50,490. A riot broke out in Vicksburg in December 1874 that started a series of reprisals against many Republican supporters, the vast majority of them black.

 

There was factionalism within the Democratic Party between the Regulars and New Departures, but as the state election of 1875 approached, the Democrats united and brought out the "Mississippi Plan" which called for the systematic organization of all whites to defeat the Republicans. Armed attacks by the Red Shirts and White League on Republican activists proliferated, and Governor Ames appealed to the federal government for assistance, which was refused.

 

That November, Democrats gained firm control of both houses of the legislature. Ames requested the intervention of the U.S. Congress since he believed that the election was full of voter intimidation and fraud. The state legislature, convening in 1876, drew up articles of impeachment against him and all statewide officials. He resigned a few months after the legislature agreed to drop the articles against him.

 

After leaving office, Ames settled briefly in Northfield, Minnesota, where he joined his father and brother in their flour-milling business.

 

During his residence there, in September 1876, Jesse James and his gang of former Confederate guerrillas raided the town's bank, largely because of Ames's (and controversial Maj. Gen. Benjamin Butler's) investment in it, but failed in their attempt to rob it.

 

Ames next headed to New York City, then later settled in Tewksbury, Massachusetts as an executive in a flour mill, along with other business interests in the nearby city of Lowell.

 

In 1898, he was appointed brigadier general of volunteers in the Spanish-American War and fought in Cuba.

 

Several years afterward, he retired from business pursuits in Lowell but continued in real-estate and entertainment projects in Atlantic City, New Jersey, and Florida. Ames corresponded extensively with the historian James Wilford Garner during this period; Garner's dissertation viewed Reconstruction as "unwise," but absolved Ames of personal corruption.

 

Ames died in 1933 at the age of 97 in his winter home, located in Ormond Beach, Florida, next to the former Southern plantation which had been seized by his friend John D. Rockefeller.

 

At the time of his death, Ames was the last surviving general who had served in the Civil War.

 

Ames is buried in the Hildreth family cemetery—the family of his mother-in-law, Sarah Hildreth Butler—behind the main cemetery (also known as Hildreth Cemetery) on Hildreth Street in Lowell. Buried with him are his wife Blanche Butler Ames, their six children, and the spouses of his son Butler and his daughter Edith.

Born c. 1462/1464

 

Died 14th July 1514

 

"Of Westmorland origins, he was a nephew of Bishop Thomas Langton of Winchester, represented the continuation of Langton's influence and teaching, and succeeded him in many of his appointments, not least as provost of The Queen's College in the University of Oxford. Towards the end of the reign of King Henry VII he was successively Master of the Rolls, a Privy Counsellor, Dean of Windsor and Bishop of Durham. Becoming Archbishop of York (and therefore Primate of England) in 1508, he was sent as procurator of King Henry VIII to the papal court of Pope Julius II, where he was active in the diplomatic affairs leading to Henry's war with France, and took part in the election of Julius's successor Pope Leo X. He was murdered by poisoning in Italy in 1514, and was succeeded as Archbishop of York by Thomas Wolsey. Christopher Bainbridge was born in Hilton, Westmorland (then in the parish of St Michael Bongate, in Appleby) to an established local family with roots in Bainbridge, North Yorkshire. He was said to have been fifty years old at his death and must therefore have been born about 1464. A son of Reginald Bainbridge and Isobel Langton, he was a nephew and protégé of Thomas Langton of Appleby, Bishop of Winchester, a relationship formative in his ecclesiastical career. Hilton is due east of Appleby, on the eastern margin of the Vale of Eden where it rises into the Pennines.

 

It is supposed that Christopher received part of his education at The Queen's College, Oxford although there is no surviving record of this. His uncle Langton had been a student of the college, and returned to it in 1487 as Provost, a post to which Bainbridge himself succeeded. He also studied law at Ferrara and Bologna. He was granted an indult in 1479 which allowed him to hold church benefices while still un-ordained and under the age of 16, and another in 1482 that allowed him to hold more than one benefice concurrently. His cousin Robert Langton "the pilgrim" (died 1524) was educated at Queen's College Oxford and there proceeded D.C.L. in 1501.

 

The appointment of Thomas Langton to the see of Salisbury left a vacancy for Bainbridge's presentation to the church of Pembridge, Herefordshire on 28 April 1485. He held the prebend of South Grantham (Lincolnshire) in the Salisbury diocese until February 1485/86, when he exchanged it for that of Chardstock, Dorset, and two months later received the prebend of Horton, Dorset, which he held until 1508. He was described as magister, or scientist, by 1486.

 

In the early 1490s he was named a chamberlain of the English Hospice in Rome and rented one of its houses. At Bologna he was admitted DCL in 1492; he was in Rome between 1492 and 1494. Having received the prebend of North Kelsey, Lincolnshire (in Lincoln cathedral) in 1495/96, which he held until 1500, he succeeded Thomas Langton as Provost of Queen's College in 1496. Langton was elected Archbishop of Canterbury but died in January 1500/01 before he could be installed. His will appointed Christopher Bainbridge one of his executors, and Bainbridge was one of three who swore to administer at probate in 1501. He may therefore have participated in the establishment of Langton's tomb and chantry in the chapel of St Birinus at Winchester Cathedral, and was certainly involved in setting up his chantry in Bongate, Appleby.

 

By 1497 he had become chaplain to king Henry VII, and in 1501 was named archdeacon of Surrey in the diocese of Winchester. Having been presented to the prebend of Strensall, North Riding of Yorkshire, in the cathedral of York in September 1503, in December of that year he became dean of York. He was appointed Master of the Rolls in 1504, and was incorporated at Lincoln's Inn on 20 January 1505: in the same year, being admitted to the Privy Council, he became Dean of St. George's Chapel, Windsor. He was appointed Bishop of Durham on 27 August 1507.

 

Archbishop of York and Cardinal

 

Bainbridge was translated to York on 22 September 1508 (a sign of the favour he enjoyed at court), where his kinsman Dr Henry Machell, Doctor of both Laws in the University of Cambridge, became Commissary (holding the prebend of North Newbald), and Robert Langton his Treasurer (with the prebend of Weighton both of them were admitted to the York Guild of Corpus Christi in 1510. Bainbridge attended the coronation of King Henry VIII on 23 June 1509, and on 24 September Henry appointed him to be his personal Orator, Procurator, Agent, Factor, Negotiator and Special Nuncio to the Roman Curia of Pope Julius II. In this mission, which occupied the remainder of his life, Bainbridge took with him a train including Richard Pace, who had studied in Oxford and in Padua as a protégé of Thomas Langton's, and held Bainbridge in great admiration.

 

Just at this time Julius had taken alarm at the invasion of Italy by Louis XII of France, and the support of England was therefore of great importance. It is said that Bainbridge, who was to support the cause of the Venetians, sent letters urging Henry to intervene against France, to provide a pretext to close the war in Italy and reignite it in France. The French historian Aubéry accuses Bainbridge of cunning and artifice, and of mixing his personal ambition to become a cardinal with the interests of his royal master. Julius left Rome to relieve Bologna, and was nearly taken prisoner in the war. A group of pro-French cardinals summoned a council in opposition to him at Pisa, which Julius opposed by calling another council at Rome, the Fifth Lateran Council, in the course of which he created (in March 1511) several new Cardinals, of whom Bainbridge was one, with the title of "Cardinal of St. Praxed's" or Santa Prassede.

 

Aubéry repeats what was said by Paride de' Grassi in his Life of Julius II concerning two occasions on which Bainbridge acted surprisingly while in Rome. On the first occasion, while he was still only Archbishop of York, he was required to make a speech of thanks before the Pope and the Sacred College, when the pope had bestowed upon King Henry the Golden Rose, a special token of Papal affection. Bainbridge had hardly begun his speech when he suddenly said nothing more by way of thanks or explanation, and left the conclave amidst much confusion.

 

A very similar thing happened a few days after his promotion as Cardinal, when it fell to him to pay a ceremonial visit to the Dean of the Sacred College and to make a speech of thanks and acknowledgement on behalf of himself and all the others who had been appointed Cardinals. De' Grassi, the Master of Ceremonies, had instructed him to make his speech under four simple points, first to magnify the dignity of Cardinal, second to lessen the merits of himself and his fellows, third to extol the beneficence of the Pope, and to conclude with thanks and the submission of their humble service. He went clean against these instructions and again cut his speech short. Bainbridge no doubt remembered that in accepting the sees of Durham and of York, he had renounced everything prejudicial to the king in the papal bulls, and had given his fealty to the king.

 

Bainbridge was immediately sent with an army to lay siege to Ferrara, but the creation of the Holy League relieved the papacy of some pressure by involving Spain against the French forces. In recognition of England's part in this formation Pope Julius granted the spiritual and temporal command of the castle and domain of Vetralla to Bainbridge (as representing the English crown) in 1511, and in 1512 the Cardinal had a marble sculpture incorporating his own arms and the English royal arms installed upon the grand stair of the palazzo comunale of Vetralla. Pope Julius II was succeeded on his death by Pope Leo X (Giovanni de' Medici), who was elected with the support of the della Rovere cardinals. Bainbridge took part in the 1513 papal conclave, where at the first scrutiny he himself received two votes, and gave his own vote to Fabrizio del Carretto, Grand Master of the Knights Hospitaller.

 

Pope Leo was initially willing to grant the title of Christianissimus Rex (Most Christian King) to Henry, after Francis had automatically forfeited the title by waging war on the Pope. Bainbridge's letter of September 1513 to King Henry concerning this, and the accompanying communication from Cardinal Marco Vigerio della Rovere, Bishop of Senigallia and Bishop of Palestrina, survive and provide a sample of his diplomatic style. However, Henry's making peace with France in 1514 probably ended these hopes.

 

Bainbridge obtained other Italian benefices, both at Vicenza and in the administration of San Giovanni Battista at Treviso: and by bull of 29 November 1513 he became Cardinal protector of the Cistercian Order. He and Matthäus Schiner, Bishop of Sion, had held out against Pope Leo's decision to rehabilitate the schismatic churchmen of the Council of Pisa (1511), the colleagues of Cardinal Federico Sanseverino and Bernardino López de Carvajal, and refused to attend the ceremony of their readmission.

 

The Liber Pontificalis of Archbishop Bainbridge, which is the latest surviving example of the Old English rite, and contains musical notation, was edited for the Surtees Society.

 

Death

 

Bainbridge died on 14 July 1514, having been poisoned by a priest, Rinaldo de Modena, who acted as his steward or bursar, in revenge for a blow which the cardinal, a man of violent temper, had given him. Rinaldo was imprisoned and confessed to the crime. He also implicated Silvester de Giglis, then Bishop of Worcester, as the instigator of the plot. De Giglis was the resident English ambassador at Rome, and regarded Bainbridge as a threat to his position: he also had sufficient power and influence to make Rinaldo retract his confession and have him killed in prison.[36] Richard Pace and John Clerk, the cardinal's executors, were eager to prosecute De Giglis, but he maintained that the priest was a madman whom he had dismissed from his own service some years before in England, and his defence was accepted as sufficient.

 

Christopher Bainbridge left two wills, one of them (on his becoming Archbishop) in English dated 21 September 1509, which is kept in the muniments of Queen's College, and one in Latin. Correspondence of Richard Pace with Thomas Wolsey concerning the late Cardinal's affairs survives. According to this, Richard Pace was the principal executor for the Cardinal's affairs in Italy, assisted by William Burbank, and that both were associated with John Wythers in the administration of the Cardinal's estate in England: but Wythers had no part in the Italian estate.

 

Monument

 

Bainbridge was buried in the chapel of St Thomas of Canterbury at the English hospice in Rome, which later became the Venerable English College. His tomb is there represented by a white marble monument with a full-length recumbent effigy, supported by two lions. The Latin epitaph reads:

 

"Christophoro Archiepiscopo Eboracensi S. Praxedis Presbytero Cardinali Angliae A Ivlio II Pontifice Maximo Ob Egregiam Operam S.R. Ecclesiae Præstitam Dvm Svi Regni Legatvs Esset Assvmpto Qvam Mox Domi Et Foris Castris Pontificiis Præfectvs Tvtatvs Est."

 

(In Memory of Christopher, Archbishop of York, and Cardinal Priest of St. Praxede; created by Pope Julius II, for the eminent services done by him to the Holy Roman Church, during his embassy from his own nation, and afterwards defending the same, both at home and abroad, as Legate of the Papal army.)

 

The effigy is likely to have formed the basis of the painted portrait of Bainbridge (at The Queen's College, Oxford), which was made as an idealized representation during the 19th century by G. Francisi and is not a genuine Renaissance portrait.

 

Heraldry

 

The Vetralla monument provides a contemporary display of the quartering arms of Cardinal Bainbridge, showing (for Bainbridge), 1 & 4: Azure, two battle axes in pale argent, on a chief or two mullets gules pierced of the field, and (for ?[51]), 2 & 3: Argent a squirrel sejant gules. These arms also appear on the British Museum candle-snuffer attributed to Bainbridge, in both cases surmounted by the cardinal's hat. The arms are also displayed in Ripon Minster.

 

The Langton and Bainbridge chantry at Bongate, Appleby

Bainbridge left "Baldington" Manor (Toot Baldon), Oxfordshire to Queen's College, making provision for a chantry to be maintained by the college for himself and for Thomas Langton, and for the souls of their parents, in the church of St Michael in Bongate at Appleby. This was effectively the re-foundation of a chantry established by Thomas Langton at Bongate, intended to continue for 100 years, the maintenance of which Langton entrusted to his sister and brother-in-law, Roland and Elizabeth Machell (the Machell family had their seat at Crackenthorpe, in the same parish). Langton's executors, among them John Wythers and Christopher Bainbridge, used the surplus of his estate to purchase the manor of Helton Bacon, or Beacon (so-named for the beacon of Hilton Fell). The settlements of Hilton and Langton, now in Murton, were both formerly in St Michael Bongate. The manor was acquired in two moieties, each of which included lands and houses in Bongate. One moiety, to which a dwelling called Bongate Hall and many acres of meadow and pasture belonged, was sold by the executors to Roland Machell on trust that he would apply the rents and revenues to the chantry; and similarly the other moiety was in the hands of Christopher Bainbridge (whose parents were still living at Hilton), for the same uses.

 

At Bainbridge's death in 1514 the Langton chantry at Bongate was effectively incorporated with his own, and endowed with his bequest of Toot Baldon, to be managed by Queen's College. Roland Machell was still living, but died around 1520, when the Bongate Hall moiety passed into the hands of his son and heir Edmond Machell. The other Hilton moiety, in the tenure of Reginald Bainbridge, came into the hands of Thomas Bainbridge, Christopher's brother. Langton's executor John Wythers continued to seek redress for the revenues and arrearages from both parts of the manor, and sold the Hilton moiety in 1524 to the Revd Edward Hilton of Bletchingdon in Oxfordshire, who made a conveyance to John Pantre, Provost (1515-1541) of Queen's College. Edmond Machell also died, 2 February 1521/22, holding the Bongate Hall moiety, though Thomas Bainbridge also held those deeds. Edmond's widow Alice remarried to Nicholas Rudd and claimed the moiety for herself and as the inheritance of her son John Machell, who at the age of 18 in November 1527 was found by Edmond Machell's inquisition post mortem, then held, to be his father's heir. Cardinal Wolsey ordered Rudd to accept the decision of the Duke of Richmond's council in this matter, but in November 1527 Rudd had ignored three summonses and was believed to have gone to London.

 

The records of Queen's College show that the Bongate chantry under the Bainbridge endowment remained active until the Dissolution, and pensions were still being paid to proxies into the 1570s. Robert Langton established the free school at Bongate."

 

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