View allAll Photos Tagged retesting
Hello, my lovelies.
It's been far too quiet around these parts. For that, I offer my sincerest apologies.
I've been trying to get back on track, but I've been thrown a little off-kilter the past few weeks. And, in some respects, the past few months.
My last post here was pre-scheduled. Which was handy, given I was sequestered (willingly!) in a friend's flat with her kitteh, Mia, and the slowest iMac known to woman (the last bit, not willingly!).
Unfortunately, that weekend also marked the beginning of a heatwave here in London.
Had I been home, the temperatures would have been higher than I'd have liked but manageable. However, in a first-floor flat with a curious kitteh, the windows could only be opened a small amount. When Mia wasn't hiding from the heat in a drawer under the bed, she was perched on the window openings cooling her tush.
Consequently, I spent most of the weekend lounging under a 10cm fan and keeping Mia company in her hatred of the heat.
The sun's emanations were too much for me to endure to see through my plan to visit some distinctive housing in the nearby neighbourhoods. Or to visit the Brockley and Ladywell Cemetery, as I had planned. Next time, Gadget, next time.
A busy but part-time week of work followed 'hot' on the heels of that.
I managed to sneak in some socialising outside my flat on Friday despite my ongoing health issues. Followed by a weekend of socialising inside my flat and hiding as much as possible from the heat.
The hottest day on record in the UK and the day preceding it blew out any plans I had for productivity outside my day job the following week.
It took most of the week to get my bedroom back down below 30 degrees, even at night. When it finally cooled almost enough, I celebrated by creating a Spotify playlist.
Health issues scuppered plans to walk the remaining section of the New River between Harringay Green Lanes Overground Station and Manor House/Finsbury Park with Scott and our cameras last Friday. At least we managed a pleasant afternoon of beers, ciders and conversation in place of that (with a detour to my GP's office).
On the positive side, at least I found out that day that the fatigue I've been feeling the past month or so wasn't just my imagination and or me being lazy. I'm vitamin D deficient and have low levels of vitamin B12 again. The former is being managed with some heavy-duty supplements. The latter requires retesting in six weeks. If still low, it will mean injections as I had back in 2007. Between now and then, I need to see if I can improve things from a dietary perspective to pump them back up a bit.
My other ongoing health issue hasn't been 100% diagnosed yet. I've been referred for further testing, but I have a new medication I started yesterday. That will hopefully manage the issues and get me back to photo walks and day trips soon enough. Fingers crossed.
Though, between dreams about the medication and my new bite guard, I've not had the best sleep the past few nights!
This is the first night I've managed to keep being creative after midnight for weeks. For someone who's a night owl and for whom this time is usually my most productive time, that has been beyond frustrating. I suspect this is because I took a long lunch today to nap for an hour and a half.
I hope to share more posts later in the day. And schedule new work for the weekend as I'll be away from home cat-sitting Lily, Sammy and Poppy from Thursday evening to Monday evening.
I'm also still working on my chapbook and other creative things. They're just taking far longer than I would have liked.
Thank you for your patience through all this.
I posted this early access for my Patreon patrons a few days ago.
Date registered: 22 September 1997
Tax due: 01 March 2019
MOT Expires: 25 September 2018
2017 MOT (retest) odometer: 45,969 miles
Taken mainly for the unusual colour, it's not something I'd pick but it does complement the shape well. Quite low mileage; on 55k as of last January, it's due a retest shortly.
Original Caption: Unhappy Motorist Learns That Her Car Has Failed the Test at an Auto Emission Inspection Station at Norwood, Ohio. All Hamilton County Light Duty, Spark Ignition Powered Motor Vehicles Must Be Tested Annually for Carbon Monoxide and Hydrocarbon Emissions Vehicles That Fail Are Issued 30-Day Temporary Stickers to Give Owners Time for Repairs and Retesting. Part of the Job of These Public Works Department Employees Is Patience and Public Relations with Customers 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15415
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Norwood (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557865
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
I was completely perplexed as to what this was, especially as it was wearing a Q plate. It appears to be a Jago Jeep, a kit car from a company based in Chichester built using bits of Ford Anglia. Showing 79k as of last September, it's due a retest in October.
Original Caption: Motorist Receives the Bad News That Her Car Has Failed the Test an Auto Emission Inspection Station in Norwood, Ohio. Since January, 1975, All Hamilton County Light Duty, Spark Ignition Powered Motor Vehicles Must Be Inspected Annually for Carbon Monoxide and Hydrocarbon Emissions. This Owner Will Be Issued a 30-Day Sticker to Allow Time for Repairs and Retesting. If a Car Does Not Have a Valid Sticker It Will Be Cited, and the Driver Will Have Seven Days to Have the Car Certified 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15413
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Norwood (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557863
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
Seen in Crawley, West Sussex.
T422 DCD
✓ Taxed - Tax due: 1 February 2020
✓ MOT Expires: 5 December 2019
Vehicle make: VAUXHALL
Date of first registration: 29 May 1999
Year of manufacture: 1999
Cylinder capacity (cc): 1199 cc
Fuel type: PETROL
Vehicle status: Tax not due
Vehicle colour: BLUE
Number of previous owners: 3
Current owner since April 2013
Mileage at last MOT: 166,484
Mileage since previous MOT: 9,854
Failed its MOT last year on 5 points with 9 advisories, all fixed for the retest.
I test-drove a Prius c today.
Similar to my experience test-driving the CR-Z in Dec. 2010, I feel mildly let down. Which is more a function of my high expectations than of anything seriously wrong with these cars (well, the CR-Z has a problem with rear visibility). But while test-driving the CR-Z confirmed my suspicion that it was not the car for me, test-driving the Prius c merely reined in slightly wishful thinking.
Going by the official specs, the Prius c has slightly more interior space than my 1996 Civic HX Coupe. While that might technically be the case for the passenger space, it's more than a little misleading with regards to cargo space (the numbers say the Prius c has 44% more, whereas a glance will tell you it has significantly less).
I say "technically" for the passenger space, because while I can believe the overall cabin dimensions, the front seats are spaced slightly farther apart than those of the Civic, paradoxically making it feel more cramped. My jacketed arm brushes against the door in the Prius c, but it just avoids doing so on the Civic, and this makes me feel crowded in the former.
Overall, though, the Prius c is surprisingly and sufficiently spacious and comfortable - especially in the rear seats, where the Prius c fits me like a glove but the Civic is someday going to cause me permanent spinal injury.
A more serious issue is the quality of the trim. Most aspects of the interior of the Prius c (esp. the "shifter" and the glove box) look and feel cheap. Both in terms of the look and feel of the plastics and their flimsiness. By comparison, my Civic (which at $14.4k was roughly in the same relative price range as the Prius c is now) uses softer, more substantial plastics with a still-basic but not particularly cheap look.
This cheapness extends to the speakers, especially those of the One trim. While I was only listening to FM (I need to retest with my iPod), that is all I have in my Civic too, and my Civic (even with the driver-side speaker broken) sounds like a live symphony orchestra compared to the One stereo. The Four-trim stereo sounded considerably clearer - although I was listening to an HD station in that case. Even that, though, was not on the same continent as my home theater system. Honestly, I don't know what a great car radio sounds like - the only ones I've heard are ghetto window rattlers and standard radios in cars so loud all attempts at fidelity are wasted.
But I'm probably making the car sound cheaper than it is. My guess is all of these components are adequate for most of the target audience for this car, and if they're not adequate, they'll soon be moddable. It's just that it's disappointing to get in a "Prius" and be aesthetically transported not to the future, but to 1989.
And that's where the wishful thinking came in. To expect the car to be the same quality and/or performance of a similarly-priced non-hybrid, but to then get all the hybrid goodness for free is unrealistic. Realistically, this is a Yaris Hybrid, and I should be happy to get a hybridized Yaris, with all of the original's entry-level trim, for only $4k or so more than the plain-Jane one. After all, my breakeven point on gas expenses alone, given the 198k miles my Civic will have by its sixteenth birthday and the $4/gallon average over the last year, is only a little over 7 years.
So, like for most other people considering the Prius c, it comes down to price/mileage ratio for me. I can't know with much certainty what mileage I would actually get with a Prius c, but I do know I get about 10% more than the EPA estimate for my Civic. If that means I can get 55 mpg in a c, I will be a happy camper. 45 mpg, though, and it's hard to see the point.
And of course that also depends on what I actually pay for a Prius c. All indicators point to demand exceeding supply right now. (In February, it was the third-best-selling new car in Japan, where 80% of production stays, and all Prius c's are made in Iwate, which is in the still-recovering tsunami disaster zone, but running overtime to try to keep up with Prius c demand.) The salesman today wouldn't even let us put a deposit down, they are so unsure of supply.
When more do become available, there are four trim levels to choose from. The One trim level is the base level, although one that is remarkably well equipped (well, remarkable if you're not used to Prius marketing). Still, I think I could justify the extra $950 to get to Two - if only for the cargo cover and better stereo and seat fabrics - although there are several other additions. Three and Four are thousands more than Two, so I'm not even considering them.
Finally, there's color. The Prius c comes in Toyota's usual assortment of shades of boring, Absolutely Red (they didn't have one, but they had a Yaris in that color, and it's pretty much what the name says), and the one I'm leaning towards: Habanero. Unfortunately, I have not seen it in person (and will not be purchasing a Prius c until I have), but the brochure and reviews show it to be a Day-Glo Orange. Not for me the years my mom spent trying to find her silver Camry in parking lots. I can see it now:
"Wanna see my brand new Prius c?"
"Sure. Which one is your... oh."
P.S. I haven't discussed performance yet, because there's not much to discuss. It's a dedicated hybrid car, but even slower than other hybrid cars. It seems fast enough to keep up with traffic though. You can maybe split hairs about whether it is more fun to drive than a Prius Liftback or Honda Insight - and maybe it is noticeably more fun to drive than those - but none of these could possibly approach the sportiness of my Civic - which is a ludicrous statement right there because my Civic is a far, far cry from sporty.
P.P.S. Before you protest that this Prius c discussion has nothing to do with the lovely Volvo P220 above, consider:
- The Amazon is also a five-door car.
- In sports trim, the 2238-lb. Amazon made only 85 hp (also from a little four-banger), yielding a slightly worse power-to-weight ratio than the ~2500-lb., 99-hp Prius c.
- While the Amazon is obviously longer than a Prius c, it is only about as long as a Honda Insight, with a wheelbase only 4 cm longer than either of those modern cars.
- As befits a Volvo, the Amazon was the first car with three-point safety belts. But only on the front seats: like many 2012 models, the Prius c has five three-point safety belts, nine airbags, ABS, traction control, stability control, electronic brake-force distribution, brake assist, etc.
Original Caption: Red Light of the Exhaust Analyzer Indicates That This Car Failed the Test at the Auto Emission Inspection Station at Norwood Ohio. A Red Light Will Glow If Either the Carbon Monoxide Or Hydrocarbon Emissions Are Above the Maximum Limits for a Particular Model Year. The Car Owner Will Be Given a 30-Day Sticker to Have His Auto Repaired and Be Returned for Retesting. If the Vehicle Is Not Certified Within That Time, It Can Be Ticketed by the Police 09/1975
U.S. National Archives’ Local Identifier: 412-DA-15400
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Norwood (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557850
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
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
heaven and hell to the longdistance lover
Bronica EC, Nikkor PC 2.8/75; Kodak slide film,
retesting the Componon-S as reproduction lens, dusting the D1x sensor
Initial Contact
I was not prepared for what I saw, when I answered a call from a local farmer about a stray dog they found sleeping in their barn after a particularly cold winter night. I have seen pictures of emaciated dogs, but to actually see one in front of me felt like I was stabbed in the heart. I had not even stepped out of the car when I knew we had to take care of her. And if there had been any doubt, it would have all disappeared when this friendly dog, who had every right to hate or fear people, came right up and leaned into me to be comforted.
The dog before us was a purebred Rottweiler. Pictures do not begin to capture her degree of emaciation. Her entire rib cage is visible and when stroking her side it feels like a washboard to the touch. Other parts of her anatomy that should be protected by body fat also protrude. She has no muscle tone to speak of.
There is scar tissue and soars on all of her feet and up her legs. Her bum has huge symmetrical pressure soars, resembling the back-end of a baboon.
First Night
There was a lot of fussing over Phoenix upon her arrival at Keshet. Not to mention the throwing around of suitable names for her. She ate - a lot. She drank - a lot. She was given fresh bedding and chew toys. But, although a little weary, she was mostly interested in the attention she was getting. Starvation, clearly wasn’t restricted to food, but also to companionship. Nonetheless, when she was left to be on her own, she quickly lay down to sleep.
Visit To The Vet
For her own welfare and the safety of the other residents, it was important for Phoenix to see the vet as soon as possible. So that is exactly what we did the following day. Having absolutely no history on Phoenix, the visit was to include a complete work-up.
That Phoenix was a Rottweiler and severely malnourished was determined immediately. Further to a physical exam the following was also determined:
- She is guestimated to be around 5 years old.
- There is evidence that she has had puppies and likely remains unaltered.
- Her ears are like elephant skin indicating chronic yeast infections.
- The pressure soars on her bum are classic from being thin and being housed on hard flooring.
- There is chronic scar tissue on all of her legs, especially the front legs, as a result of cellulitis (skin infection caused by bacteria).
- There is significant swelling in the front right carpus (wrist).
Phoenix tested a strong positive for whipworm for which she is being treated. Given the evidence that she has been rummaging through garbage (i.e. McDonalds Catsup packaging and portion of a plastic bag in her poop), she was also given a shot to treat her against all tapeworms. She got 4 additional pokes: Rabies, Bordetella, DHPP and blood draw.
Then came the results of the blood work. To the naked eye, it seemed there was no active infection. But the elevated white blood cell count says otherwise. For this, Phoenix has been started on a course of anti-biotics. But worst of all, Phoenix tested a strong positive for heartworm.
Following her visit to the vet, I realized how lucky we were to have gotten to Phoenix when we did.
Course of Action
We know that Phoenix is emaciated, full of parasites and has heartworm. Her body is fighting infection. When severe malnutrition is involved, it is conceivable that the skin will suffer and there will be infections. This would explain the condition of her ears and legs.
As already mentioned, deworming and treatment for infection is underway. Before Phoenix can undergo any invasive treatment or surgery, she has to be a healthy weight. Heartworm needs to be treated before she can be spayed. It will take 4 months after she has been treated before we can retest for heartworm. And only then, assuming she tests negative, will we be able to spay her.
The chronic scar tissue and bed soars did not happen overnight. The extent of the soars also suggests she has had to sit upright for extended periods of time. We can only assume that even in her “better days”, she was neglected. It would not be far fetched to think that she was a puppy factory.
But the truth is, we will never know where Phoenix came from, how long she had been fending for herself or for how long she has been infected with heartworm. What we do know, is that Phoenix’s rise from the ashes to begin her new life starts here and now.
And for this we reach out for your help.
No amount is too small.
Sponsorships towards Phoenix’s road to recovery can be made through PayPal at:
ChipIn: keshet.chipin.com/phoenix-road-to-recovery
Website: moodofthenation.net/client/24/donate_choose/
You can also mail a check directly to:
Keshet
PO Box 41
Carlsbad Springs, Ontario
K0A 1K0 Canada
Thank you in advance for your support.
*****************************
Phoenix's Story, Part 2 - On The Road To Recovery: www.flickr.com/photos/keshet_rescue/8386320068/in/photost...
Phoenix's Story, Part 3 - Temporary Setback: www.flickr.com/photos/keshet_rescue/8403306949/in/photost...
©2011 Susan Ogden-All Rights Reserved Images Thruthelookingglass
Texture: Kim Klassen
I love to smile....and i do, most all of the time. I am wearing a very bright smile again today....the weather is behaving more like spring and summer combined, with mild temps and plentiful sunshine (altho today there is a threat of showers...but it IS still very mild) I am pretty sure mom nature will get us back....altho this might just be her apology for the 6 inches of snow and 6 days of no power i endured in October when she miscalculated fall and winter on her calendar! i like to keep a positive attitude, and am not above a teeny bit of butt kissing if she keeps the temps this warm for say, another 4 to 6 months before turning the heat on in ernest!
Warm temps and warm smile! Yep, love them both....and besides, smiles most of the time confound a lot of people, and that is a little “hobby” of mine....those kind of people NEED something to ponder and i am simply delighted to provide fodder for that!
Happy Bokeh Wednesday! i took this on my hour walk through the woods that i chose as my me time this past Sunday, before heading back to my duties of taking care of my daughter and Lileigh Grace. Tomorrow is recheck and retest day for my daughter...i will be here with them, for the next day or two and then they will be staying with me at home while the addition (lileigh grace’s new bedroom) begins....if all works out ok, i will be back in the classroom next week, and home each day by the time Lileigh gets up from her nap to take over again. Kaileigh’s good friend works for my husband in the office at home and will give them lunch and get Lileigh in for her nap. We should know after the test results come back, how long this will continue....but suffice it to say, i am in for the duration....the goal is to keep the new little bun in the oven until it is fully baked!! It is truly torture to my daughter to have to stay in bed, other than bathroom needs and a quick shower. Lileigh’s birthday party is next Saturday and she is determined to decorate the ELMO cupcakes! We’ll see how that goes....i may be getting a crash course in cake decorating this week!
HAPPY HUMP DAY for all who celebrate!! ;)
ET GOX vent system retest - STS-2. LETF.
Image from NASA, originally appeared on this site: science.ksc.nasa.gov/gallery/photos/
Reposted by San Diego Air and Space Museum
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
Adding to my album for my 'new' lens. KONICA HEXANON AR 50mm F1.4. Was a bit disappointed with the sharpness of this lens in this image. So will need to revisit this location again to retest. Was a relatively expensive lens and from what I've seen so far, my much more affordable Pentax 55mm f1.8 lens is definitely sharper.
I don't often use Olive Oil in soapmaking (I know, gasp!) and it's been years since I soaped this simple holy trinity formula that is so popular in soapmaking. All it took was this little reminder why: scant lather and a slimey feeling.
To keep everything fair, all samples were soaped between January 1, 2012 and January 7, 2012, so this bar has some age on it. I'll definitely be retesting again in several months.
At this point the car is still not running. You can see that the rubber bellows between the air flow regulator and the intake manifold is still off. That must mean that I was still trouble shooting the fuel injection system.
Below are the details of my efforts to troubleshoot the CI system after I'd gotten the new fuel tank, sender unit, and fuel lines in. Thanks very much to Bruce Young and Art Benstein of Brickboard.com.....I would have scrapped the project at this point if it hadn't been for their advice and patience.
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I'm working on a 1977 242DL that has been in outside storage (non running) since December 1999. It was my daily driver prior to that.
To date I have replaced
-fuel tank
-fuel sender unit, internal pump & sock filter
-Fuel lines to external pump
-Fuel lines from tank and accumulator to engine bay
-The external pump is original and operates, but is noisy and I haven't made any attempt to determine if it is operating to spec.
-Accumulator is original
After completing the work above, I tried to start the car today and got only several backfires and one explosive detonation in the engine compartment. While very stimulating and offering the exciting prospect that the patient can, with expenditure of sufficient time and money be brought back to life, it was ultimately disappointing.
Next I went to the factory manuals and started through the complete checkout of the CI system. I confirmed that the cold start injector is firing for the appropriate length of time and then shutting off.
I pulled the bellows off the air mass meter and it (the bellows) was in good condition. I put the ignition to the accessory position so the fuel pumps were running and moved the venturi plate upwards but didn't hear the injectors cut on or off.
In the course of monkeying around with the air mass meter I noticed raw fuel smell in the engine bay and noticed a pool of fuel around the number two injector. I took this injector off and put the ignition in accessory (with the venturi plate in the rest position) and the injector immediately opened and sprayed continuously. Checked the remaining three injectors and another one also sprays when the ignition is in accessory, but it cuts on after a several second delay. One of the remaining two injectors gets wet and drips after ten seconds or so and the other one stays dry.
My questions:
-does fuel flow through an injector with the venturi plate in the rest position definitely mean that the fuel distributor is bad (as the factory manual indicates)?
-Why would one injector start spraying immediately, another after a several second delay, and a third only get wet and drip after an even longer delay?
-If this condition is due to the plunger hanging up in the fuel distributor because of varnish or oxidation, is there any hope of cleaning it? Haynes says that nothing can be done, Bentley indicates that it can be carefully cleaned with raw fuel and put back together.
-If I need to replace it, does anyone have recommendations on any of the replacement options? RockAuto.com has everything from a Bosch unit ($800 or so, and out of the question), to under $200 for a rebuilt unit that their photo makes look pretty gloppy and suspect. I'm assuming that a salvaged distributor would be just as much at risk of being useless and could set me back a good deal of time in finding that out.
-Am I totally off target in suspecting the distributor and is there something else I should be looking to eliminate first.
Thanks very much in advance!
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"-does fuel flow through an injector with the venturi plate in the rest position definitely mean that the fuel distributor is bad (as the factory manual indicates)?"
• Not necessarily, in your case. I could be that the control plunger is gummed up and not following the airflow (not "venturi") plate down to the rest position. Or someone may have been playing with the 3mm hex setscrew adjustment on the airflow plate, and turned it way too far clockwise.
"-Why would one injector start spraying immediately, another after a several second delay, and a third only get wet and drip after an even longer delay?"
• Is this with the airflow plate at rest, as above? If so, that should be corrected before you try to diagnose individual line/injector flow. Given the history, contamination in the FD or injectors is possible.
Once the plunger question is answered or known to be OK, an initial setting procedure for the 3mm setscrew will also test for roughly even flow from each of the 4 FD ports.
"-If this condition is due to the plunger hanging up in the fuel distributor because of varnish or oxidation, is there any hope of cleaning it? Haynes says that nothing can be done, Bentley indicates that it can be carefully cleaned with raw fuel and put back together."
• The plunger can be removed by taking the fuel lines off the FD, then taking the FD off the airflow meter (see Bentley 240-14 Fig. 24 for your type). Holding the FD in both hands, with a large socket on the underside where the plunger will (hopefully) come out, smack the FD w/socket down on a hard surface. It might take 2 or 3 smacks, but the plunger should come out. Clean with something like lacquer thinner, then rinse with gas and replace it in the FD. Use very light oil instead of gas for storage.
Don't try to swap in a plunger from another FD. Each plunger has only one unique home.
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I removed the fuel distributor this morning and tried to free up the piston from the cylinder using the technique you recommended, but it is gummed in there tight. After about a dozen smacks onto a granite slab it moved only about 2-3mm and wouldn't come out any further. I used a shop towel and some plier to try to gently pull it out, but nothing. The little bit that is showing is covered in sticky varnish.
Can you recommend any procedure to get it out of the cylinder, or should I just start hunting for rebuilts?
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My first thought is to gently tap it back in a little, and set it facing up where you can keep dribbling acetone or lacquer thinner on it for several minutes.
After that, try the "smacking" again, just enough to get some movement. Then add solvent and tap it back in. Repeat the sequence several times — hoping to gain a little more range of movement each time.
I have a few old FD's that I bench tested several years ago and packed away.
What is the bosch # on yours?
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I guess that great minds think alike; I went back to the barn after I posted the last message and did exactly what you suggested, but using the magical WD-40. After about another dozen smacks or so I was able to free up the plunger. There was a ring of varnish near the end of it (just beyond the conical part). I cleaned that off with WD-40 and am going to leave it for a few days (due to travel) and will clean everything off with fresh gas and start reassembling it on Saturday.
Some more questions for you:
-Do I need to be concerned that smacking the unit to free the plunger will have caused any damage to the unit?
-Is fuel pressure used to somehow return the plunger to the rest/downward position? My plunger is moving pretty freely now, but when holding it with the plunger downwards I have to jiggle it a bit for the plunger to drop out of the bottom.
-When I reassemble it, must I use new copper washers around all of the banjo fittings, or is it ok to re-use the old ones?
The model number of my FD is 0438 100 005.
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I don't think WD40 has much residual lubricant, but probably OK for short term.
Some more questions for you:
-Do I need to be concerned that smacking the unit to free the plunger will have caused any damage to the unit?
* I doubt it, having done it a few times with no problems.
-Is fuel pressure used to somehow return the plunger to the rest/downward position? My plunger is moving pretty freely now, but when holding it with the plunger downwards I have to jiggle it a bit for the plunger to drop out of the bottom.
• Yes, a "Control Pressure" is bled off in the FD and applied to the top of the plunger. It acts as a counter force and "damper" to the airflow plate's upward movement. The CP also influences the amount of fuel to the injectors for a given rise in the airflow plate. And since the CP can be varied by the CP Regulator (based on temperature), it also allows varying plunger rise for a given airflow, and thus "fine tunes" the mixture around the "coarser" 3mm plate adjustment.**
-When I reassemble it, must I use new copper washers around all of the banjo fittings, or is it ok to re-use the old ones?
• I usually reuse them, snugging first, then tighter if needed, and have a collection of old ones to pick from. I do have the bosch numbers for all sizes but have never took the time to find a supplier.
** Most of what I know about K-Jet came from a Bentley book I strongly recommend. It covers all Bosch FI systems, is very well written, and only costs about $25. It's called "Bosch Fuel Injection & Engine Management" Bentley stock number GFIB.
I just searched on bentley book gfib and and this was at the top. $22.95
Yes, I have an 005 FD.
And am adding a poor picture of the tiny filter that should be at the bottom of each injector port. You might want to pick them out with a jeweler's screwdriver to see if they stopped any crud from the FD.
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I can't thank you enough for the quick replies and the advice. I do have the Bosch book (collected a bunch of stuff before starting this project), but didn't think to go back to it after I started tracing the faults using the factory manuals. I'll pull it out this week and start reading through it now that I've got some hand's on experience (when I first looked through it it was pretty intimidating).
Since this area is such a bear to access, should I do anything with the fuel pressure regulator while I've got it in plain sight? I have no reason to suspect there's a problem with it at this point, but given that everything in the fuel system from back to front so far has been problematic, I'm wondering if I'll get the jillion things that connect to the intake manifold back together only to find that I have to yank it out again.
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Don't be intimidated by that book. Your part (now) is less than 1/5th of it.
"Since this area is such a bear to access, should I do anything with the fuel pressure regulator while I've got it in plain sight?"
Nothing to do until it's hooked up and you can put the pressure gauge on it. That'll be fun the first time or two. And btw, on the K-jet it's called a Control Pressure Regulator (CPR), or in most Bosch books, the Warm Up Regulator (WUR).
I like WUR best because that's when it's most active — low pressure when cold, letting the plunger come up farther for a rich mixture, then higher pressure when warm for the leaned-out running mixture.
You will have to take the larger fitting off and interpose the pressure gauge hose, using fittings supplied with the Gauge. It get's easier, believe me.
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I'll see if I can pull out the little filters and clean them up while I'm at it and will forego any monkeying with the WUR until my JC Whitney CIS pressure test kit arrives and I can scope everything out.
In terms of mechanical function, I should be able to leave the intake manifold off while performing all of the pressure testing, right? I sure hope so!
I also hope that it gets easier from here on out. I figured it would be hard to get the car started after its extended hibernation, but this has caused me to go way, way, way beyond my comfort zone. Until now my greatest mechanical achievements have been the replacement of easily accessible components like water pumps, radiators, master cylinders, brake pads, and stuff like that.
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In terms of mechanical function, I should be able to leave the intake manifold off while performing all of the pressure testing, right? I sure hope so!
Yes, you can run the pump for pressure testing by jumpering fuses 5 and 7 (left side contacts, for normal current flow), or jumpering at the relay plug, 30 (Red) to 87 (W/R). I have a long jumper made up, with a switch at the underhood end.
The battery should be charged (or at least not run way down) for pressure tests.
The actual testing should take only 3-4 minutes to know what you have. See Bentley 240-6 for approximate Control Pressure, depending on ambient.
And I just remembered, the jumpering I gave you above will run the pumps, but it won't put voltage on the WUR heater (to put the WUR thru its cold-to-warm transition). For that you must jumper at the relay plug, so that 87 (R/Y) AND 87b (Blue) both get voltage from 30(R). Then you test for about 2 minutes to get the warm WUR pressure value. The Bentley/Bosch book has more on this I think.
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Spent a good portion of the day reassembling the fuel lines and pressure testing. Here's the rundown:
-Cleaned all banjo fittings and dried with compressed air.
-blew out all fuel lines to injectors liberally with compressed air.
-mounted new Bosch injectors and injector seals to lines
-mounted fuel distributor to air metering unit and reattached all fuel lines
-charged battery fully
-turned on fuel pump and lifted sensor plate on air metering unit and listened for buzz of injectors. No buzzing. Repeated with same result.
-attached CI pressure testing rig between control pressure regulator and fuel distributor as specified in factory manual 2(23) operation B14. Turned on fuel pump, opened test valve, and bled test rig. Pressure observed was approx 42 psi vice the 65-77 it should be.
-Checked for fuel leaks and noted none in engine compartment or elsewhere. There was some very slow dripping of a banjo fitting where it connected to the test rig, but I dismissed that as a possible cause of the low pressure reading.
-I'm going to continue going through the tests for low pressure as specified in manual 2(23) beginning with operation B54. I'd appreciate your thoughts on the most likely cause for the low pressure.
--Internal fuel pump is from salvaged car, but pump and sending unit it is mounted on appear (quite literally) nearly new and I believe they were NOS (the sending unit definitely is Volvo).
--External/main pump is the original and runs, but is very noisy.
--Accumulator is original, no leaks noted
--All fuel lines from the tank to the engine compartment are new (braided stainless)
--Pressure regulator valve on the fuel distributor has not been monkeyed with. I removed, inspected, and cleaned it in fresh gasoline as specified in the factory manuals. I didn't remove the shims and was extremely careful not to lose any when dis-assembling it (i.e. I'm sure it is set up as it was before the car stopped running).
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That's a nice, well-detailed outline of your testing, but it would help to know your location, or more specifically the ambient temperature. I base this on that 47psi reading, wondering you might actually be seeing Control pressure? That could happen if (a) the gauge valve was open by mistake (rather than closed) and (b) the CPR/WUR plug had not been disconnected at the start, thus allowing allowing the Control pressure to rise to a warm level (just a couple of minutes will do it).
The fact that I don't have your Volvo manual to refer to also hampers things a bit. But you also have the Bentley-Bosch book (I'll call it B-B), so I'll comment based on that. Here's the testing sequence I'd suggest:
1) Starting with a COLD engine/system, be prepared to monitor battery for an 11.5V minimum during testing.
2) B-B, 6-17, last paragraph. Disconnect plugs at CPR and Aux Air Valve (AAV).
3) B-B, 6-12/13. Do the "Delivery Test" to be sure the pump can deliver the volume needed (whatever your book says -- my guess 850cc in 30 seconds). Then read 4.2 "Fuel Pressure Flowthrough" and do "Testing Control Pressure Throughflow as described (160 to 240cc in 60 seconds). If that's not right, it can bias the CP high or low.
4) B-B, 6-17-19. Now do the Pressure tests as described, starting with "System" (line) pressure. I assume your book has the cold-to-warm Control Pressure chart that's right for your CPR.
Comments on your test results:
-turned on fuel pump and lifted sensor plate on air metering unit and listened for buzz of injectors. No buzzing. Repeated with same result.
• Maybe air needs to be bled out of FD?
-I'm going to continue going through the tests for low pressure as specified in manual 2(23) beginning with operation B54. I'd appreciate your thoughts on the most likely cause for the low pressure.
• Again, be sure it's not Control pressure, and that the delivery volume is OK before trying to raise the system pressure.
NOTE: I'm guessing you are using the Ignition key to control the pump on/off, which is possible if the airflow safety contacts are missing the 2-pin plug that puts them in the circuit. That plug should be nearby to the airflow meter—a White and a Black wire I think. Plugging that in and out would save you from going back and forth to the key.
That's all I can think of for now. In the meantime I'll see if I can scare up a PDF of that manual you are using, so we'll be "on the same page".
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Gotcha on the factory manuals; I'll try to work from the Bentley manual from now on (or at least describe the factory manual test procedures fully) so we have a common frame of reference. Also, I'm located in southern NH, and the ambient temp during testing yesterday was about 45F and today it was about 30F.
I did not disconnect the WUR wiring, so that might have biased the test results (factory manual doesn't reference that, or if it did, I missed it).
However, got some more data for you based on some tinkering this afternoon, and it may shed some more light on the issue (which I'm beginning to think is the main fuel pump that sat on the dormant car for the last 10 years).
-I figured that I might as well eliminate the possibility that the low pressure was due to a bad in-tank fuel pump since the manual's next three steps were related to checking its function (amperage draw, audible signs of operation, etc.), and since I had previously ordered an aftermarket in-tank pump from FCP Groton. I removed the fuel sending unit and swapped the pumps and put everything back together, checked for leaks, and then performed the same pressure test as described yesterday (also with the WUR wiring connected). THis time the pressure was down 2 psi to 40, so I assume that eliminated the possibility that the in-tank pump is the culprit (though the aftermarket and old pump are/were really, really loud, much louder than I remember when the car used to be on the road).
-The next step in the factory manual is to test the fuel delivery volume by disconnecting the return line in the engine compartment and running the pump for 30 seconds and measuring the fuel delivered. Proper delivery volume for a 77 B21F is supposed to be a minimum of .8 liters. I ran the test twice and measured .150 liters. I'm assuming at this point that the problem must be the main fuel pump, and am about the order a rebuilt OEM unit from FCP Groton...should I or would it be better to hold off?
-Also, when I ran the fuel volume delivery test above, I happened to notice that the test gauge was reading 30 psi (even after the pump stopped running and before I reconnected the return line), which I thought was kind of odd since the system was open on the return side. Or is there a check valve in the WUR that would account for this?? Guess maybe it's time to start delving into the Bentley Bosch CI book.
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"-Also, when I ran the fuel volume delivery test above, I happened to notice that the test gauge was reading 30 psi (even after the pump stopped running and before I reconnected the return line), which I thought was kind of odd since the system was open on the return side."
I've also experienced that "hang on" pressure at the end. Enough so that I figured it was normal, but never took time to dig into the reason for it. It would slowly drop off when I cyled the gauge valve back and forth. And you might have reason to question that new tank pump, because Art Benstein recently got one with reversed polarity at the terminals, which made it a sucker. He may jump in here with more details.
I don't have anything to add at this point except that I feel it's important to first establish that (1) the pump can deliver the specified volume and (2) the FD "flow-thru" volume to the CPR is within the 160 to 240cc range described in the B-B book page 6-12. And that all these preliminary tests (up until measuring the warm Control pressure) be done with the CPR heater unplugged.
I'm an early riser, so I'm turning the lamp down about now. If anything comes to me in a dream I'll be back in the AM. Double check the use of that gauge valve, as it's quite possible that 47psi you saw was really Control (not System) pressure, and was influenced by CPR warm-up due to heater being plugged in for a couple of minutes.
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I'm stumped, making no apparent progress, and getting increasingly confused and frustrated. Here are the results of the tests that I ran this morning:
-Environmental conditions/battery charge: 55 degrees F/12.77 volts
-Bosch-Bentley (B-B)6-17. Discovered that I had installed the pressure test rig backwards for last weekend's tests and remedied this. Bled system and moved valve open/closed for 10 second intervals several times as per B-B to ensure no air in system. Read system pressure and got reading of 38 psi. WUR power was disconnected and when I switched the valve to check control pressure, reading was identical.
-Got distracted referring to various manuals and noted factory manual tests to ensure correct electrical function of WUR. Checked the voltage of connector for WUR as well as ground and WUR continuity. All checked out normal (11.86 volts at connection with fuel pumps running and battery indicating 12.16 volts. WUR resistance measured at 20.2 ohms, factory manual indicates normal range to be 20-30 ohms).
-Figured there might be reversed polarity of the FCP Groton fuel pump as reported in Art's post from last week and removed the line feeding the main fuel pump and turned pumps on and got no fuel flow coming from tank. Removed in tank pump and was preparing to test function outside of tank to see whether it was sucking or pumping and found that it was now inoperable (I had swapped it in for what looked like a very new but used probably Bosch (("Made in the UK")) in tank pump that had been mounted on the salvaged fuel sending unit I bought). No clue why...it had been operating last weekend when I installed it (at that time I disconnected juice to main pump and could hear the in-tank pump buzzing away). I ran test leads from the FCP Groton pump to a battery and it was/is dead as a doornail.
-Re-installed the used in-tank pump referenced above and tested its function. Pumped goodly volume of fuel to line feeding main pump. Assumed that this would now result in a system pressure reading closer to the normal range of 65 psi.
-Went back to pressure testing and bled pressure gauge as per B-B and then took system reading again. Down to 30 psi now!?!?!?!? Same pressure showed when I switched valve to read control pressure?!?!?!?
-Performed fuel pump test on the main (external) pump as per B-B 4 11-12. There were 12.02 volts at the connector. Tested ground continuity by running a test lead from the ground screw in the trunk where all the fuel pumps ground to the negative terminal of the main pump wiring harness and got reading of 0.2 ohms. Ran test lead to ground in engine compartment to main pump harness negative terminal and got reading of 0.2 ohms.
-Performed fuel volume test again (WUR wiring disconnected)and with pressure test rig connected. No fuel coming out of return line. Tried again with WUR wiring connected with same result. Removed test rig and both of the return lines (from WUR to return side of fuel distributor and the large one from the return side of the FD). Blew out both return lines with compressed air.
-Re-installed all fuel lines (fuel pressure test gauge removed), leaving the return line near the fuel filter open for fuel volume test and powered up pumps again; no fuel flow on return side.
What does all of this mean?
-Based on the low system pressure readout and what I assume is adequate voltage running to main pump and good ground to main pump, I'm inclined to think that the main pump is bad (again, it sat on the car, dormant and outside for about 10 years).
-But then again, there's obviously something wrong elsewhere as well, since I'm now getting no fuel on the return side of the system. Could the WUR be mechanically fried so that no fuel is returning? I also don't see how a bad WUR could lead to incorrect system pressure readings (obviously it's isolated from the system being tested when the pressure test valve is closed so as to read system pressure). Last weekend when I did the fuel volume test (with WUR connected to power) I had .15 litres of fuel after 30 seconds of operation. How could anything that I did in the tests above have altered the result?
-Could the FD be bad? When I re-installed it the plunger was moving freely. Today with pressure in the system I lifted the air flow sensor plate and noted steady resistance while lifting (assume that's normal since there is pressure on the top of the plunger). When I let the sensor plate fall down it "bounces" slightly as it should, and after a fraction of a second I can hear the FD plunger come to rest on the control arm (or whatever it's called).
Any help you can provide would be very welcome; beginning to wonder if this project is beyond my abilities.
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Cheer up, I see you making progress. I still get that gauge mixed up with infrequent usage. After one reading (paragraphs please! ;-), it looks like a delivery problem causing the low 38psi pressure. And I think the WUR might be the same because the pressure wasn't high enough (or ambient temp low enough) for the WUR's "bleed off" return to produce a different Control Pressure value.
"Re-installed the used in-tank pump referenced above and tested its function. Pumped goodly volume of fuel to line feeding main pump."
• Off hand, I'm not aware of a " goodly volume" Tank pump spec. But the Main pump spec (Bentley 230-3 and 4) is 1 liter in 30 seconds. And since that 1 liter has to come from the Tank pump, that's about what I'd expect from that little sucker pumper too.
"Assumed that this would now result in a system pressure reading closer to the normal range of 65 psi.
• Me too. But not until we've proven that the Tank pump can deliver what the Main pump needs. BTW, how is the battery holding up? I think the Bosch book wants 11.5V minimum. That's while pumping, not a static reading. So that's a consideration.
"Performed fuel pump test on the main (external) pump as per B-B 4 11-12. There were 12.02 volts at the connector."
• B-B 4 is "pulsed injection" (LH) Theory. The values may be close, but best to stay in B-B 6, Continuous Injection Maintenance. And I wonder what that 12.02V dropped to with pump running?
... more coming as long as I can edit in (~2 hour window). Just wanted you to know I'm here and still reading...
EDIT follow on...
"-Re-installed all fuel lines (fuel pressure test gauge removed), leaving the return line near the fuel filter open for fuel volume test and powered up pumps again; no fuel flow on return side.
-Based on the low system pressure readout and what I assume is adequate voltage running to main pump and good ground to main pump, I'm inclined to think that the main pump is bad (again, it sat on the car, dormant and outside for about 10 years)."
• Yes, the Main pump is subject to speculation, given it's history. But without knowing the "working" battery voltage and the "measured" Tank pump delivery volume, all we can do is speculate at this point.
"-But then again, there's obviously something wrong elsewhere as well, since I'm now getting no fuel on the return side of the system."
• Agreed. That's a mystery here too, for now. Art?
"Could the WUR be mechanically fried so that no fuel is returning?"
• No, that's not how it works. The Main return is (should be) from the FD. The WUR return line just taps in at that point.
"Last weekend when I did the fuel volume test (with WUR connected to power) I had .15 litres of fuel after 30 seconds of operation. How could anything that I did in the tests above have altered the result?"
• Hard to speculate here. Having the WUR (heater) powered was not right at that time, but that's not a volume delivery factor that I can see. Since then, the Tank pump that was used is now dead, and an unproven used one is in it's place.
"...beginning to wonder if this project is beyond my abilities"
• Not from where I see things. Tomorrow is another day. And maybe Art will chime in.
EDIT #2
Glad Art mentioned that his sender was mis-wired, not the pump. I meant to run that fact by you, since your sender is also new. I'd suggest you verify that yours is NOT like the bad one Art recently got, as shown below.
(Although I sorta hope it is, since that seems to be where we're stuck.)
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Thanks for the additional suggestions. Based on the test results today, I am assuming that the problem (or one of the problems) is the main fuel pump. Here's what I came up with:
Charged the battery last night and tested it before I began work today; it was 13.27 volts at rest. Ambient temp in the barn is about 55 degrees.
Removed the line from the in-tank pump at the main pump and ran the pump for 30 seconds. It delivered a little over a litre of gas.
Removed the fuel line between the main pump and the filter (I ran stainless braided line and there's a junction above the rear axle) and did the same volume test and got the same result (a little more than a litre in 30 secs).
Connected the pressure test rig to the fuel line between the main pump and filter (would have done it after the filter, but 30 minutes of searching thru various nipples and bushings at the local hardware store didn't yield any combination that I could work to make a connection there) and fired both of the pumps and bled the test lines. Result: 41 psi. This is a bit higher than yesterday, but I'm guessing the difference might be due to the higher voltage to the pumps because of the just-charged battery.
Tested operating voltage at the main pump and got a reading of 11.62 volts.
Where do you recommend that I go from here? Is it time to pull the trigger on a new main pump? If so, can you recommend a source for the OEM type for this year (honking big Bosch thing)? I see that FCP Groton has rebuilts in its offering...heard anything about them? If I replace the main pump should I also go ahead and get a new accumulator, or should I continue to use the original since it isn't leaking? If I can avoid replacing it that would be my preference.
-------------------------
Unless Art sees something else, the main pump does look bad. I have an old one on my test bench rig (below) that I just tested at a wavering 62-65 psi, running a kerosene techron mix with 13.4 volts from a charger-assisted battery. First time run in months, and with too-thin, jury-rigged wiring.
----------------------
I swapped out the fuel pump this morning and then tested the system and control pressures and fuel delivery volume. I've still got a problem somewhere and based on the factory manuals the WUR seems most likely:
-Battery at 12.5 volts at beginning of testing
-Temperature 50 degrees
-System pressure: a wavering 62-64 which I figure should be close enough to the minimal threshold of 65 (is it?)
-Control pressure: identical reading to system pressure. WUR was disconnected from power at all times
-Fuel delivery volume: .5 liters in 30 seconds (factory manual says it should be at least .8). I've got a brand new aftermarket fuel filter on the car and the only gas that's been run through it is new gas fed from a new tank through new fuel lines. Should I be concerned about this at this point, or fix the control pressure first and then retest for volume??
-I also performed the control pressure throughflow test (B-B 6-12 para 4.2) twice and got the same result (200cc delivered in exactly 60 seconds). Since B-B says that 150cc to 240cc range indicates FD is OK, does this now mean that the WUR is certainly bad?
I referred to the factory manuals for troubleshooting in case of control pressure being too high and it is pretty straight-forward: blow out the return lines (which I did last weekend) and if the pressure doesn't test within specs, then retest with a new WUR.
Do you have any alternative recommendations?
--------------------
"-System pressure: a wavering 62-64 which I figure should be close enough to the minimal threshold of 65 (is it?)"
• The wavering pressure isn't ideal, but it should work. For how long is another question.
-Control pressure: identical reading to system pressure. WUR was disconnected from power at all times.
I referred to the factory manuals for troubleshooting in case of control pressure being too high and it is pretty straight-forward: blow out the return lines (which I did last weekend) and if the pressure doesn't test within specs, then retest with a new WUR."
I've got the same problem with the WUR on my test rig. You could try taking it apart, hoping to eliminate whatever is blocking the return internally. That sometimes works, but mine has been apart 3 times and will pass 20±psi air, but not a drop of fuel. I didn't think to try a reverse flush. That maybe worth a try if you can rig something.
You might start another thread looking for ideas and/or a used WUR. I got rid of my spares last year but don't remember who got them.
-------------------
FCP Groton has rebuilt WURs for the 76-77 for $68.83, which seems like a ridiculously low price (www.fcpgroton.com/product-exec/product_id/5313/nm/1976_19...).
I'm going to take the old one out tomorrow and rip it apart and see what I can do with it; if I can't figure anything out I'm going to order the FCP reman one so that I can swap it out this week.
---------------
The rebuilt WUR arrived and I couldn't wait to see if I was finally through with this pressure testing hoo-hah, so I put it in, hooked up the test gauge, plopped in the newly-recharged battery, fired up the pumps, bled the air out of the system, and have an entirely new, unwelcome, and unexpected result:
-System pressure: where it previously held steady at a jittery 62-64 psi, it's now oscillating wildly between a high of 42 psi and a low around 26 or so. It slowly builds up to 42 and then the drops suddenly back down and starts building up again. Did the main pump suddenly decide to go keerflooie, or could it be the check valve all of a sudden!?!?
-Control pressure: temperature in the barn is about an even 40 degrees and the temp of the WUR is probably a bit below that. I got a control pressure reading of about 12 which seems to be OK (the factory manuals only chart pressure down to about 50 degrees, but if I extrapolate downwards this would seem to be in the right range.
------------------------
How about removing and "gutting" the check valve (for now)?
It's only meant to aid warm starts (minimize chance of vapor lock), and the accumulator usually holds residual pressure OK.
-------------------------
ust to help anyone who might be crazy enough to wade this far down the thread, I identified the problem with the pulsating (peaking at 42 psi then dropping to the 20s and building slowly back up). The low pressure line from the in-tank pump to the main pump was kinked.
Unkinked the line and had steady system pressure at about 64 psi.
The rebuilt WUR is bad, though; it's delivering a constant control pressure of 12 psi, regardless of ambient temp and also regardless of how long it is connected to power.
----------------------------
In regard to the reversed polarity, it was an aftermarket sender assembly that was wired wrong at the factory. The pump itself was OK. Bogging, crawls up hill (long post) Check out the reply from Afton Crafton. Pure BTDT.
But that brings up a concern I had earlier - that the noise, coupled with low pressure and volume, may lead you to replace a very reliable (and expensive) component, the main pump, simply because it is not being fed enough fuel (like in my case) or enough electricity.
Paul, if you're set on doing it, at least do a volume test at the main pump inlet - testing the volume of the tank pump. In order to provide close to a liter from the main pump, it must be given the same amount or more. Also, be sure the main pump is getting full battery voltage.
Here's a link to the notes I made on measuring pressure, done on a 79. Using the K-jet Fuel Pressure Test Kit
----------------------------
Thanks very much for the link to the post on the bad wiring on FCP aftermarket in-tank pumps. I'm holding off on buying any new components until I run the volume tests at the tank as you suggest, and until I run the pressure tests properly. I'll report back results next weekend. Thanks again for your advice!
------------------------
Managed to carve out some quality time with the car today and got those relay numbers for you. They are 0332 209 158 (this replaced the original 0332 204 110, and I confirmed the new application by calling two separate dealers before procuring the part), and 0332 015 006 (replaced the original relay with the same part number).
Also, the info I gave you about pumps running when the ignition was in the "I" position was faulty; I looked at the ignition key cylinder today and the pumps run when the key is in the "II" position. Not sure if this makes the issue any less troublesome, as the engine is obviously not running in this position either.
Unfortunately my pressure test kit won't arrive until the middle of next week, so I consoled myself by doing a thorough cleaning of the fuel distributor, to include the pressure regulating piston (operations E37 and E38 in the factory manual), and blew the entire unit out with pressurized air before storing it in a zip lock baggie until the test kit comes in and I reassemble everything.
I also decided to spring for a new set of injectors so that I don't have to kick myself down the road for not doing so when I had things broken down to this level. The originals were 0437 502 007s and I decided to pocure them locally (though they were available much cheaper online at FCP Groton). The local Bosch distributor advised that Bosch had been replacing the 007s with an 015 (which corresponded to the application info online at FCP Groton and RockAuto.com), and when they went to order that they were told that 0437 502 024 is the new application. I'm leery about all of the part number swapping....but guess that goes with the territory on an old clunker.
---------------------
Those relay numbers look OK but they've sure evolved thru several changes since the original pair of 0 332 204 110's. I think some of it came with the introduction of the added "lift pump" in the tank. Was yours so retrofitted?
Just be sure to use the 158 as the "Main" relay (grey wire on 30), with the 006 (grey on 86) feeding the pump (pumps?).
-----
Based on your recommendations I'm going to remove the FD and check/clean the plunger next. The car was running when it went dormant, and I'm certain that the hex setscrew adjustment on the airflow plate.
I'll post results here once I get that sorted (hopefully tomorrow since it's a holiday).
------------------
Original Caption: Hamilton County Auto Emission Inspection Station in the Village of Newtown, Ohio. Formerly Was Operated as an Auto Dealership. Arrows Efficiently Direct Traffic through the Testing Lane. All Light Duty, Spark Ignition Powered Motor Vehicles Registered in Hamilton County Must Be Inspected on an Annual Basis for Carbon Monoxide and Hydrocarbon Emissions. If a Vehicle Fails the Test, Its Owner Is Given a 30-Day Temporary Sticker to Allow Time for Repairs and Retesting 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15376
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Newtown (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557826
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
The purpose of the visit at Ensignbus was to get a MOT retest on our DT29 G29 TGW. She waits a slot into the testing area as a down Eurostar rushes past. Friday 8th September 2023. DSCN56935.
Barring any calamity DT29's next outing will be at the Metrobus garage open and running day on Saturday 23rd September.
Dennis Dart - Carlyle Dartline 8.5m.
Seen in Reigate, Surrey.
Sierra has been off the road for 27 years!
D585 TGO
✗ Untaxed - Tax due: 1 April 1997
MOT - No details held by DVLA
Vehicle make FORD
Date of first registration June 1987
Year of manufacture 1987
Cylinder capacity 1993 cc
Fuel type PETROL
Export marker No
Vehicle status Untaxed
Vehicle colour RED
_____________________________________
R35 BOA (700RPG until Mar 2004)
✗ Untaxed - Tax due: 1 November 2019
✗ MOT Expired: 2 November 2020
Vehicle make ASTON MARTIN
Date of first registration 22 April 1998
Year of manufacture 1998
Cylinder capacity 3239 cc
Fuel typePETROL
Export marker No
Vehicle status Untaxed
Vehicle colour GREEN
Current owner since April 2004
Mileage at last MOT: 54,305
Last MOT expired (after 6 month Covid extension) without retest.
Original Caption: Employee Waiting for Business at the Hamilton County Auto Emission Inspection Station at Newtown, Ohio. The Building Formerly Housed an Auto Dealership. All Light Duty, Spark Ignition Powered Motor Vehicles Registered in the County Must Be Inspected on an Annual Basis for Carbon Monoxide and Hydrocarbon Emissions. If a Vehicle Fails the Test, Its Owner Is Given a 30-Day Temporary Sticker to Allow Time for Repairs and Retesting 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15377
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Newtown (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557827
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
Joanne Mei
Lead Research Chemist, Newborn Screening Quality Assurance Program
Centers for Disease Control and Prevention
I work in the newborn screening quality assurance program. We help state newborn screening laboratories make sure that their newborn screening tests are of the highest quality. We prepare blood samples that look like newborn baby samples for more than 50 disorders. We send those samples to state public health labs to test. The state labs do not know which disorders are supposed to be detected. The labs test each sample and send us their results. If they miss a sample, we help them figure out why. Because of this testing, doctors and families can be assured that the labs are providing accurate results.
Working on newborn screening is challenging because we are looking for a few affected babies among most who are healthy. Newborn screening casts a wide net in order to find those few babies. If a baby has a positive result, retesting is important to find out if the baby does have the condition. If so, it’s important for parents to know quickly so the baby can be treated early.
When I had my daughter, I was working in newborn screening. I had to explain newborn screening to my OB-GYN! There was no information at my doctor’s office. I had to ask the pediatrician about my daughter’s newborn screening results. I think most parents only find out about their child’s results if there’s a problem.
I feel it’s important for pregnant women to talk to their doctor about newborn screening so that they know that the tests will be done, and they can ask for the results.
Learn more about newborn screening:
www.cdc.gov/features/ScreeningNewborns/ www.cdc.gov/spanish/especialesCDC/PruebasRecienNacidos/
www.cdc.gov/ncbddd/pediatricgenetics/newborn_screening.html
www.cdc.gov/ncbddd/pediatricgenetics/CCHDscreening.html
www.cdc.gov/labstandards/nsqap.html
It's been a long while since I looked at how my previous cars are getting on, so thought I'd do an update. There have been a few changes lately and also a surprising discovery in one case.
First up, the BMW E90 which I sold in 2017. Not surprisingly it's still going and was on 88k in March when it failed its MOT on a couple of minor items, before passing the retest.
Seen here near Lancaster in November 2012.
Original Caption: A Car Owner Reviews the Results of His Car's Inspection with an Employee of the Hamilton County Auto Emission Inspection Station at Newtown, Ohio. The Exhaust Analyzer Gives Readings for Carbon Monoxide and Hydrocarbon Emissions. If a Vehicle Fails the Test, the Owner Is Given a 30-Day Temporary Sticker to Allow Time for Repairs and Retesting. All Light Duty, Spark Ignition Powered Motor Vehicles in the County Must Be Certified Annually 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15385
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Newtown (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557835
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
Original Caption: Motorist Engages in a Lengthy Confrontation with Public Works Employees of an Auto Emission Inspection Station in Norwood Ohio. He Was Unconvinced That His Station Wagon Was Not Maintained Well Enough to Pass the Exhaust Analyzer Test for Carbon Monoxide Emission. His Vehicle Did Pass the Hydrocarbons Portion of the Test. The Motorist Was Issued a 30-Day Sticker to Give Him Time to Have Repairs Made and Allow for Retesting. 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15406
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Norwood (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557856
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
Original Caption: Norwood, Ohio, Auto Emission Inspection Station, Part of a Hamilton County System in Which All Light Duty, Spark Ignition Powered Motor Vehicles Must Be Certified Annually. Vehicles Are Attached to an Exhaust Analyzer That Gives Readings for Carbon Monoxide and Hydrocarbon Emissions. If a Vehicle Fails the Test, the Owner Is Given a 30-Day Temporary Sticker to Allow Time for Repairs and Retesting. Officials Report 250,000 Vehicles Registered in Norwood and Cincinnati 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15386
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Norwood (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557836
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
Ahead of a retest to renew my rating to fly on instruments I few an instrument approach to Cardiff Airport.
This image is from a video, we are very short final to land on runway 12
Sigma 10-20mm f/3.5-6. It's been years since I used the 20D with the 10-20mm. It's suitable for indoor and outdoor events with flash or no flash. As well as long exposure for places like the museums and not bad for landscapes; depending on the mood you're looking for, preferably favorited for a dark distant portrait on a dark landscape... or bright.
20D is a moody camera if you know how to use it, and they are also cheaper now and a little heavier.
Exam week is just about to start.
I have a retest to do tomorrow morning, darn you Julius Caesar!
and I have reviews due tomorrow as well.
oh goodness.
PLUS i have a concert to attend to tomorrow night :D
12/12/10
Original Caption: Closeup of a Motorist Who Has Just Gotten Out of His Station Wagon to Look at the Exhaust Analyzer Which Gives Readings on Carbon Monoxide and Hydrocarbon Emissions From His Vehicle. He Has Driven Into an Auto Emission Inspection Station at Norwood Ohio, to Receive a Yearly Inspection. the Glowing Red Light Indicates His Vehicle Has Failed the Carbon Monoxide Portion of the Test. a 30-Day Sticker Will Allow Him Time for Repairs and Retesting. (See Pictures #15405 and 06) 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15404
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Norwood (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557854
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
Original Caption: Hamilton County Auto Emission Inspection Station Sign in the Village of Newtown, Ohio. Since January 1, 1975, All Light Duty, Spark Ignition Powered Motor Vehicles Must Be Certified Annually for Carbon Monoxide and Hydrocarbon Emissions If Registered Within the County. If a Vehicle Fails the Test, Its Owner Is Given a 30-Day Temporary Sticker to Allow Time for Repairs and Retesting 08/1975
U.S. National Archives’ Local Identifier: 412-DA-15374
Photographer: Eiler, Lyntha Scott, 1946-
Subjects:
Newtown (Hamilton county, Ohio, United States) inhabited place
Environmental Protection Agency
Project DOCUMERICA
Persistent URL: arcweb.archives.gov/arc/action/ExternalIdSearch?id=557824
Repository: Still Picture Records Section, Special Media Archives Services Division (NWCS-S), National Archives at College Park, 8601 Adelphi Road, College Park, MD, 20740-6001.
For information about ordering reproductions of photographs held by the Still Picture Unit, visit: www.archives.gov/research/order/still-pictures.html
Reproductions may be ordered via an independent vendor. NARA maintains a list of vendors at www.archives.gov/research/order/vendors-photos-maps-dc.html
Access Restrictions: Unrestricted
Use Restrictions: Unrestricted
Not a car that I am familiar with, it's never been to my work before, and I don't recall seeing it in the local area before either, though it does have a local registration.
In for an MOT, which it failed on a few items, couple of tyres and a suspension ball joint being the worst of it I think. It got collected soon after these (slightly rushed) photos, and hopefully I will see it again when it comes back for either a retest or for us to do the work. It appeared to be quite a tidy car under the dirt, so I'd hate to see it scrapped.
Also of note here is the registration on the Astra Van. I don't know what it means or if it is particularly valuable, but it is a very tidy van owned by an amusement arcade.
NBC NEWS：
www.nbcnews.com/health/health-news/what-taiwan-can-teach-...
What Taiwan can teach the world on fighting the coronavirus
Analysis: Taiwan put lessons it learned during the 2003 SARS outbreak to good use, and this time its government and people were prepared.
TAIPEI, Taiwan — As countries around the world grapple with the coronavirus, Taiwan may offer valuable lessons on how to curb its spread.
The island is just 81 miles and a short flight away from mainland China, where COVID-19 is believed to have originated in the city of Wuhan. As the outbreak took hold in January, many Taiwanese business people and their families based in China were returning to celebrate the Lunar New Year, and up to 2,000 Chinese tourists a day visited the island, potentially bringing the virus with them.
And yet, Taiwan has had only 47 cases of COVID-19 and one death as of Tuesday — far fewer than China’s 80,754 cases and 3,136 deaths, a stark contrast even when taking into account the enormous population difference: Taiwan’s 23 million to China’s 1.4 billion. Taiwan’s numbers are also much lower than neighboring countries such as South Korea, which has had more than 7,500 cases, and Japan, with 530. It’s also faring better than countries much farther away from China, such as Italy, with more than 9,000 cases, and the United States, which has over 700.
Of the 100-plus countries and territories affected, Taiwan has the lowest incidence rate per capita — around 1 in every 500,000 people — for a place that is located so close to China and with so much travel to and from.
What lessons can Taiwan teach the world so other countries can stem the spread of the virus?
Image: Schoolchildren use plastic dividers at a school in Taiwan.
Schoolchildren use plastic dividers at a school in Taiwan.Courtesy of the Da Jia Elementary School
Be alert and proactive
Partly because it’s near China and speaks the same language, Taiwan learned early that a “severe pneumonia” was spreading in Wuhan. But it was the proactive measures the island took that helped it avert a major outbreak.
On Dec. 31, the same day China notified the World Health Organization that it had several cases of an unknown pneumonia, Taiwan’s Centers for Disease Control immediately ordered inspections of passengers arriving on flights from Wuhan.
And despite poor relations with Beijing, Taiwan asked and received permission to send a team of experts to the mainland on a fact-finding mission Jan. 12.
“They didn’t let us see what they didn’t want us to see, but our experts sensed the situation was not optimistic,” government spokesperson Kolas Yotaka told NBC News.
Shortly after the team returned, Taiwan began requiring hospitals to test for and report cases. That helped the government identify those infected, trace their contacts and isolate everyone involved, preventing the virus from spreading to the community.
All this happened long before Taiwan confirmed its first case Jan. 21 and the rest of the world became alarmed.
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News
10 ways the coronavirus is making people change their daily lives
Set up a command center
Equally important, Taiwan's CDC activated the Central Epidemic Command Center relatively early on Jan. 20 and that allowed it to quickly roll out a series of epidemic control measures, according to Stanford Health Policy’s Jason Wang, a pediatrics professor who also has a doctorate in policy analysis.
“Taiwan has rapidly produced and implemented a list of at least 124 action items in the past five weeks — that’s three to four per day — to protect public health,” Wang said in an email. “The policies and actions go beyond border control because they recognized that that’s not enough.”
Headed by Health Minister Chen Shih-chung, the command center not only investigates confirmed and suspected cases, it also works with ministries and local governments to coordinate the response across Taiwan, including allocating funds, mobilizing personnel and advising on the disinfection of schools.
Take quick and decisive action
Taiwan also took tough action early. On Jan. 26, five days after it confirmed its first case, Taiwan banned arrivals from Wuhan, earlier than any other country.
Not long after, it did the same for flights from all but a handful of Chinese cities, and only Taiwanese people were allowed to fly in.
Use technology to detect and track cases
After securing its borders, Taiwan used technology to fight the virus. Temperature monitors were already set up at airports after the 2003 SARS outbreak to detect anyone with a fever, a symptom of coronavirus.
Passengers can also scan a QR code and report their travel history and health symptoms online. That data is then given directly to Taiwan’s CDC.
Those coming from badly affected areas are put under mandatory 14-day home quarantine, even if they are not sick, and are tracked using location sharing on their mobile phone. Absconding can lead to heavy fines.
That also goes for not reporting symptoms.
One man who didn’t tell the authorities he had symptoms after he returned from Wuhan and went to a dance club the next day was fined $10,000.
Taiwan’s concert hall gets a deep clean after musician tests positive for coronavirus
March 9, 202000:43
The authorities in Taiwan also quickly determine whom the confirmed cases had been in contact with, and then test them, and put them in home quarantine.
“They also proactively find new cases by retesting those who tested negative,” Wang said.
Ensure availability of supplies
To ensure a steady supply of masks, the government quickly banned manufacturers from exporting them, implemented a rationing system and set the price at just 16 cents each.
It also set up new production lines and dispatched soldiers to staff factories, significantly increasing production.
These masks are the tools for residents in Taiwan’s densely populated cities to protect themselves; they made them feel safe and not panic.
Educate the public
The government also asked television and radio stations to broadcast hourly public service announcements on how the virus is spread, the importance of washing hands properly, and when to wear a mask.
“We think only when information is transparent, and people have sufficient medical knowledge, will their fear be reduced,” Kolas, the government spokeswoman, said.
Residents learned that most patients had mild or no symptoms, so the death rate could be lower than what was reported. They also understood that a person’s travel history or contact with infected individuals determined their risk level, not their nationality or race. That understanding helped reduce discrimination.
Get public buy-in
The public’s cooperation with the government’s recommended measures was crucial to prevent the spread of the virus, including among students, school principal Tu Chen-yang said.
“More than 95 percent of our parents take their child’s temperature at home and report it to the school before the children arrive,” Tu said. “Regardless of what the government does, people have to take responsibility for their own health.”
Bank building manager Nature Lin echoed such views, as he checked the temperature of employees arriving for work,on a detection camera set up in the lobby.
“We were already stocking up on alcohol disinfectants and temperature guns during the holiday,” he said.
Practically every office building, school and community sports center check temperatures and prevent anyone with a fever from entering. Apartment buildings also place hand sanitizer inside or outside elevators.
Image: Commuters travel on the subway in Taiwan.
Commuters travel on the subway in Taiwan.Cindy Sui / NBC News
Learn from experience
Taiwan was able to put the lessons it learned during the SARS outbreak in 2003 to good use. That epidemic ended up killing 73 people and hurting the economy.
This time, Taiwan's government and people were prepared, and that readiness has helped push up President Tsai Ing-wen’s approval rating.
Last but not the least, Kolas said that she believes the country’s health insurance system, which covers 99 percent of the population, has been crucial to fighting the spread of the outbreak.
“Taiwan’s health insurance lets everyone not be afraid to go to the hospital. If you suspect you have coronavirus, you won’t have to worry that you can’t afford the hospital visit to get tested,” she said.
“You can get a free test, and if you’re forced to be isolated, during the 14 days, we pay for your food, lodging and medical care,” Kolas said. “So no one would avoid seeing the doctor because they can’t pay for health care.”
An unusual choice for a daily driver; the G-Wagen is still available to buy new despite the shape being practically unchanged since the 1970s. It has a timeless air of quality to it; in that it wouldn't look out of place in any scenario no matter how rough or how stately and that's a rare thing in motoring.
I can't imagine the 5.0 V8 is very economical, but it's still with the owner who bought it new nearly 15 years ago so they've clearly had their money's worth. It's also got very low mileage indeed; it only covers a tiny amount each year and in May last year (it's due a retest on June 7th) it was only on just over 22,500 miles.
Magnifique vendredi soir passé en compagnie de mon pote Greg a Verossaz!
J'en ai profité pour faire un filé d'étoile composé de 44 pose longue de 4min ! (12mm f/7.1 ISO 100 240sec)
Je suis asser content du résultat, mais a retester un jours ou ce ne sera pas la pleine lune :D
A great smog shop if you live in the Berkley, Richmond, Albany, Pinole, Solano or El Cerrito area.
Francisco was able to give me some tips to make sure my old Honda Civic passed the test.
Read my review of Smog Express Richmond on Yelp.
NBC NEWS：
www.nbcnews.com/health/health-news/what-taiwan-can-teach-...
What Taiwan can teach the world on fighting the coronavirus
Analysis: Taiwan put lessons it learned during the 2003 SARS outbreak to good use, and this time its government and people were prepared.
TAIPEI, Taiwan — As countries around the world grapple with the coronavirus, Taiwan may offer valuable lessons on how to curb its spread.
The island is just 81 miles and a short flight away from mainland China, where COVID-19 is believed to have originated in the city of Wuhan. As the outbreak took hold in January, many Taiwanese business people and their families based in China were returning to celebrate the Lunar New Year, and up to 2,000 Chinese tourists a day visited the island, potentially bringing the virus with them.
And yet, Taiwan has had only 47 cases of COVID-19 and one death as of Tuesday — far fewer than China’s 80,754 cases and 3,136 deaths, a stark contrast even when taking into account the enormous population difference: Taiwan’s 23 million to China’s 1.4 billion. Taiwan’s numbers are also much lower than neighboring countries such as South Korea, which has had more than 7,500 cases, and Japan, with 530. It’s also faring better than countries much farther away from China, such as Italy, with more than 9,000 cases, and the United States, which has over 700.
Of the 100-plus countries and territories affected, Taiwan has the lowest incidence rate per capita — around 1 in every 500,000 people — for a place that is located so close to China and with so much travel to and from.
What lessons can Taiwan teach the world so other countries can stem the spread of the virus?
Image: Schoolchildren use plastic dividers at a school in Taiwan.
Schoolchildren use plastic dividers at a school in Taiwan.Courtesy of the Da Jia Elementary School
Be alert and proactive
Partly because it’s near China and speaks the same language, Taiwan learned early that a “severe pneumonia” was spreading in Wuhan. But it was the proactive measures the island took that helped it avert a major outbreak.
On Dec. 31, the same day China notified the World Health Organization that it had several cases of an unknown pneumonia, Taiwan’s Centers for Disease Control immediately ordered inspections of passengers arriving on flights from Wuhan.
And despite poor relations with Beijing, Taiwan asked and received permission to send a team of experts to the mainland on a fact-finding mission Jan. 12.
“They didn’t let us see what they didn’t want us to see, but our experts sensed the situation was not optimistic,” government spokesperson Kolas Yotaka told NBC News.
Shortly after the team returned, Taiwan began requiring hospitals to test for and report cases. That helped the government identify those infected, trace their contacts and isolate everyone involved, preventing the virus from spreading to the community.
All this happened long before Taiwan confirmed its first case Jan. 21 and the rest of the world became alarmed.
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Set up a command center
Equally important, Taiwan's CDC activated the Central Epidemic Command Center relatively early on Jan. 20 and that allowed it to quickly roll out a series of epidemic control measures, according to Stanford Health Policy’s Jason Wang, a pediatrics professor who also has a doctorate in policy analysis.
“Taiwan has rapidly produced and implemented a list of at least 124 action items in the past five weeks — that’s three to four per day — to protect public health,” Wang said in an email. “The policies and actions go beyond border control because they recognized that that’s not enough.”
Headed by Health Minister Chen Shih-chung, the command center not only investigates confirmed and suspected cases, it also works with ministries and local governments to coordinate the response across Taiwan, including allocating funds, mobilizing personnel and advising on the disinfection of schools.
Take quick and decisive action
Taiwan also took tough action early. On Jan. 26, five days after it confirmed its first case, Taiwan banned arrivals from Wuhan, earlier than any other country.
Not long after, it did the same for flights from all but a handful of Chinese cities, and only Taiwanese people were allowed to fly in.
Use technology to detect and track cases
After securing its borders, Taiwan used technology to fight the virus. Temperature monitors were already set up at airports after the 2003 SARS outbreak to detect anyone with a fever, a symptom of coronavirus.
Passengers can also scan a QR code and report their travel history and health symptoms online. That data is then given directly to Taiwan’s CDC.
Those coming from badly affected areas are put under mandatory 14-day home quarantine, even if they are not sick, and are tracked using location sharing on their mobile phone. Absconding can lead to heavy fines.
That also goes for not reporting symptoms.
One man who didn’t tell the authorities he had symptoms after he returned from Wuhan and went to a dance club the next day was fined $10,000.
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The authorities in Taiwan also quickly determine whom the confirmed cases had been in contact with, and then test them, and put them in home quarantine.
“They also proactively find new cases by retesting those who tested negative,” Wang said.
Ensure availability of supplies
To ensure a steady supply of masks, the government quickly banned manufacturers from exporting them, implemented a rationing system and set the price at just 16 cents each.
It also set up new production lines and dispatched soldiers to staff factories, significantly increasing production.
These masks are the tools for residents in Taiwan’s densely populated cities to protect themselves; they made them feel safe and not panic.
Educate the public
The government also asked television and radio stations to broadcast hourly public service announcements on how the virus is spread, the importance of washing hands properly, and when to wear a mask.
“We think only when information is transparent, and people have sufficient medical knowledge, will their fear be reduced,” Kolas, the government spokeswoman, said.
Residents learned that most patients had mild or no symptoms, so the death rate could be lower than what was reported. They also understood that a person’s travel history or contact with infected individuals determined their risk level, not their nationality or race. That understanding helped reduce discrimination.
Get public buy-in
The public’s cooperation with the government’s recommended measures was crucial to prevent the spread of the virus, including among students, school principal Tu Chen-yang said.
“More than 95 percent of our parents take their child’s temperature at home and report it to the school before the children arrive,” Tu said. “Regardless of what the government does, people have to take responsibility for their own health.”
Bank building manager Nature Lin echoed such views, as he checked the temperature of employees arriving for work,on a detection camera set up in the lobby.
“We were already stocking up on alcohol disinfectants and temperature guns during the holiday,” he said.
Practically every office building, school and community sports center check temperatures and prevent anyone with a fever from entering. Apartment buildings also place hand sanitizer inside or outside elevators.
Image: Commuters travel on the subway in Taiwan.
Commuters travel on the subway in Taiwan.Cindy Sui / NBC News
Learn from experience
Taiwan was able to put the lessons it learned during the SARS outbreak in 2003 to good use. That epidemic ended up killing 73 people and hurting the economy.
This time, Taiwan's government and people were prepared, and that readiness has helped push up President Tsai Ing-wen’s approval rating.
Last but not the least, Kolas said that she believes the country’s health insurance system, which covers 99 percent of the population, has been crucial to fighting the spread of the outbreak.
“Taiwan’s health insurance lets everyone not be afraid to go to the hospital. If you suspect you have coronavirus, you won’t have to worry that you can’t afford the hospital visit to get tested,” she said.
“You can get a free test, and if you’re forced to be isolated, during the 14 days, we pay for your food, lodging and medical care,” Kolas said. “So no one would avoid seeing the doctor because they can’t pay for health care.”
I've recently had to bang my new car in for an MOT as it was very soon to expire.
Fortunately it did really well, failing only on a load of blown bulbs and a dodgy handbrake.
Unfortunately fixing the handbrake was a pig. The caliper pins needed removing and copper greasing, and the two handbrake cables replacing.
The cables were a bloody pig, and involved lifting the carpet which is always a pain in the arse.
I just need to sort out the retest now and I should be home and dry. :)