Tuesday, May 26, 2020

CMAAO CORONA FACTS and MYTH BUSTER 105 Covid in CMAAO countries


Covid in CMAAO countries vs Europe vs USA (Part 2)

CMAAO CORONA FACTS and MYTH BUSTER 105

Dr K K Aggarwal
President Confederation of Medical Associations of Asia and Oceania, HCFI, Past National President IMA, Chief Editor Medtalks


927: Minutes of Virtual Meeting of CMAAO NMAs


23rd May, 2020, Saturday
9.30am-10.30am

Participants

Member NMAs

Dr KK Aggarwal, President CMAAO
Dr Yeh Woei Chong, Singapore Chair CMAAO
Dr Kar Chai Koh, Malaysia, Vice Chair of Council
Dr Ravi Naidu, Past President CMAAO, Malaysia
Dr Rajan Sharma, National President IMA
Dr RV Asokan, Secretary General IMA
Dr Thirunavukarasu Rajoo, Hon. General Secretary, Malaysian Medical Association
Dr Alvin Yee-Shing Chan, Hong Kong
Dr Marie Uzawa Urabe, Japan
Dr Sajjad Qaisar, Pakistan
Dr Ashraf Nizami, Pakistan
Dr Deborah Cavalcanti, Brazil
Dr Marthanda Pillai, Member World Medical Council
Dr Md Jamaluddin Chowdhary, Bangladesh
Dr N Gnanabaskaran, President Malaysian Medical Association

Invitees

Dr Russell D’Souza, UNESCO Chair in Bioethics, Australia
Dr KK Kalra, Former CEO NABH
Dr Sanchita Sharma, Editor IJCP Group


  • Death rate is much lower in Asian countries compared to that in Europe and US. This low death rate is despite high population density.
  • In the US, death rate is higher in Black population. A reason for this can be that ACEIs do not work in this population. Could the level of ACE receptors be different in people from Asia vs Europe vs North US? We do not know.
  • Vaccine developed from a virus from US or Europe may not work in Asian population.
  • In an update, the CDC has said that person-to-person transmission is the primary and most important mode of transmission for COVID-19. Surface to human transmission is not the main way the virus spreads.
  • A latest study from Israel study says that 5% of population is responsible for the remaining 95% of cases.
  • Super-spreader is must to cause infection; in the absence of a super-spreader the infection will die out. If a super-spreader is present in closed space, the chances of transmission of infection are very high.
  • One reason for low mortality can be good ICU care. Good ICU care makes a difference in mortality by only 0.3-0.5%.
  • Another reason for low mortality is the availability of Airborne Infection Isolation (AII) rooms or negative pressure rooms.
  • Countries like Hong Kong, Singapore, South Korea have more number of AII rooms, which also serve as triage rooms and the patient is shifted to a Covid/non-Covid ward depending on the report, which is available within 3 hours in the triage room itself.
  • In countries like India who do not have AII rooms, the patient should be in a room which has an air purifier with at least 10 exchanges per hour.
  • The difference in clinical manifestations of the virus may influence mortality rates.  
o   It is a viral illness, so it is self-limiting disease in majority; antiviral drugs like remdesivir may work
o   It has bacterial activity as in some patients, high procalcitonin; antibiotics like doxycycline, azithromycin may be effective.
o   It has some HIV like properties, as there is lymphopenia (viruses usually cause lymphocytosis), decrease in CD4 cell count; such patients may respond to anti-HIV drugs.
o   It causes immuno-inflammation: Viral disorders do not cause immunoinflammation. But, increase in ESR, CRP, ferritin (acute phase reactants) is seen in Covid-19. Anti-inflammatory drugs (hydroxychloroquine) may be effective. Immunoinflammation is being seen much more in European countries than in Asian countries.
o   It causes thrombo-inflammation: Increase in d-dimer and fibrinogen; patient requires anticoagulation.
o   Silent hypoxia (walking dead phenomenon): Low oxygen but patient is conscious. Usually, people with hypoxia are drowsy, irritable. This was predominant in Italy. Their mortality improved when they stopped using ventilators.
o   Cytokine storm: ARDS
o   If we know the clinical pattern of patients in different countries, we can find out mortality and also identify a country-specific treatment. In the UK, multisystem immune inflammation is more with increased mortality. This is not seen in Asian countries.
  • Asian countries have lower mortality when compared to Europe and the US, but we do have a reasonable mortality rate and it may increase if we calculate accurately, register all cases and there is better investigation and reporting of cases. It may go up to 2.5-3% in Pakistan.
  • Other reasons can be: Asians already have high immunity; testing is not as aggressive as in Europe, US, the strain of the virus is not aggressive so mostly mild to moderate cases
  • Low mortality in Hong Kong may be attributed to: preventive measures (universal masking, people complying with the directives), local culture (no hugging/kissing), cases are in younger population and are imported, which are mild and lastly, well-prepared investment in ICU facilities and ventilators. Those who died had comorbidity like diabetes.
  • In Singapore, most cases are in migrants, who are young and therefore have mild infection.
  • The lower mortality in Malaysia is because of early interventions, the govt. has been preparing for the worst since March, and all persons who qualify for PUI (person under investigation) are screened and isolated based on the result.
  • Japan has 16,000 positive cases; 800 have died; mortality rate is 5%; Japan has limited PCR tests so this rate compared to the population is very low. Japan is carrying out genome analysis in 500 patients (from asymptomatic to patients with severe symptoms). HLA typing is on the way. High IgM level is related to the severity of disease. Some patients may have early detection of IgG. This may be related to previous infection with other coronavirus. Further research is needed.
  • India: Despite high numbers, the mortality rate is 3%. Experience of the European countries has helped us to lower mortality; also, there is genetic protection from the infection.

Contact time: 10-30 minutes
  • If contact time is less than 10 minutes with precautions, the chances of transmission is very low
  • If a doctor is wearing a N95 mask and the contact time is less than 30 minutes, this is usually not a problem

Protocol of non-Covid clinic in Singapore

A patient who came to the clinic in the morning and tests positive in the evening, answer the following question:

Was the patient wearing a mask? If yes, then ask,

Was the doctor wearing a mask? If yes, then ask,

Was the surface decontaminated in the morning? If yes, then ask,

What was the contact time?

  • If less than 30 min: Monitor
  • If more than 30min: Quarantine

Covid-19 infection in children

  • 13% of children all over the world have Covid-19; mortality is 0.5% in children below 15 years of age.
  • Child to child transmission is rare; but, children can infect the elderly.
  • For children <2 years: no masking
  • For children >2 years: Country-specific guidelines for masking
  • European countries do not recommend masking for children; we do not have a guideline for Asian countries.

Chances of infection are highest when sitting face to face; chances of infection are lower when sitting side to side or face to side.

In schools and colleges, students sit facing front. So chances of infection very low; distance between students should be at least 6 feet. Students should go home immediately after school/college.









Monday, May 25, 2020



CMAAO CORONA FACTS and MYTH BUSTER 104 Immuno hyper inflammation

Dr K K Aggarwal

President Confederation of Medical Associations of Asia and Oceania, HCFI, Past National President IMA, Chief Editor Medtalks

926: IMA-CMAAO Webinar on “Update on Covid-19 -Immuno-hyper inflammation”

23rd May, 2020
4-5pm

Participants

Dr KK Aggarwal, President CMAAO
Dr Rajan Sharma, National President IMA
Dr RV Asokan, Honorary Secretary General IMA
Dr Ramesh K Dutta
Dr Jayakrishnan Alapet
Dr Sanchita Sharma

Faculty

Dr Rohini Handa
Senior Consultant Rheumatologist, Apollo Hospitals, New Delhi
Former Prof, Dept of Rheumatology, AIIMS, New Delhi

Excerpts

·        The Covid-19 virus is behaving differently in different people. Up to now, we have seen 7 different manifestations of the coronavirus.

1.    It is a viral illness, so it is self-limiting disease; antiviral drugs are effective
2.    It has bacterial activity, procalcitonin is high in some persons; antibiotics like doxycycline, azithromycin may work.
3.    It has some HIV like properties, as there is lymphopenia (viruses usually cause lymphocytosis), decrease in CD4 cell count; anti-HIV drugs may be effective.
4.    It causes immuno-inflammation: rise in acute phase reactants (ESR, CRP, ferritin and platelet count). Hydroxychloroquine may work.
5.    It causes thrombo-inflammation: Increase in d-dimer and fibrinogen; anticoagulation may be important.
6.    Silent hypoxia (walking dead phenomenon): Hypoxia (oxygen 60-70%) without loss of consciousness.
7.    Cytokine storm and ARDS

·        The mortality in Europe is 10-12%, in US 6-7% and in India it is 3-4%. In Europe, we are seeing multisystem inflammatory disease in children with multiorgan involvement (Kawasaki like).
·        
A progressive in d-dimer levels with fall in leukocytic count is a sign of high mortality.

Inflammation is the protective response of the body to noxious stimuli resulting in containment of that insult at the site of injury, which can be cuts, innocuous injuries, infection, toxins etc.
Inflammation, in itself is not bad; it is the unchecked chronic inflammation, which creates problems.

Many diseases now have been identified to have inflammatory components e.g. bronchial asthma, atherosclerosis, obesity, rheumatoid arthritis.

Immunoinflammation is a subset of inflammation where the trigger is a dysregulated immune response. Immune-mediated inflammatory diseases are RA, SLE, systemic sclerosis, Sjogren, ANCA-associated vasculitides. The major trigger in these diseases is the aberrant immune response.



The host inflammatory response phase, which comes into play in some patients, is the major contributor of mortality.

·        Strictly speaking, in Covid-19, it is a hyperimmune response and not immunoinflammation.
·        In a dysfunctional immune response, the virus elicits a hyperimmune response, which is out of proportion to the inciting event in some people. This triggers a systemic cytokine storm, which is responsible for multiorgan failure and mortality.

·        In a healthy immune response, the virus is inactivated by the neutralizing antibodies. There is minimum inflammation and lung damage. This is how most people with viral infection, including Covid-19, recover.

·        But in a subset of people, the dysfunctional immune response goes on unchecked, called “hyperinflammation”, excessive infiltration of macrophages, monocytes and T cells, which leads to an inflammatory cascade, which triggers the cytokine storm, where a number of cytokines come into play leading to pulmonary edema, pneumonia and resulting in widespread inflammation and multiorgan damage.

·        Thrombo-inflammation is another manifestation of Covid-19, where there is interplay of coagulation and inflammation. The procoagulant pathway is triggered which produces microthrombi formation, seen in autopsy samples of Covid-19 patients who have succumbed to the disease.

·        The multiplicity of pathways is the reason why a variety of drugs are being tried.

·        Covid toes, thromboembolism, right heart involvement, Kawasaki-like multisystem inflammation have been seen, but without lung involvement (no ARDS and cytokine storm). So, there must be a separate pathway for hyperinflmmation other than cytokine crisis.  This means that hyperinflammation is only one part of the story; we have a long way to go before we understand the pathobiology of the infection and the pathogenetic mechanisms and the host response.
·        The stage at which the sample is collected will give different findings. This is a challenge.
·        Immuno-mediated inflammatory diseases like Rheumatoid, Sjogren’s, lupus, are no different from that encountered in the West. E.g. many people with history of joint pains, low levels of rheumatoid factor, no deformity are labeled as Rheumaotid, but they are actually Sjogren’s – no questions about dry eyes, dry mouth, caries are asked in these patients. We need to connect the dots.

·        Giant cell arteritis is extremely uncommon in India, Takayasu’s is more common.
·        In children, juvenile idiopathic arthritis (JIA), earlier known as juvenile rheumatoid arthritis, is the commonest type of immuno-inflammatory disease in children. But, it gets labeled as rheumatic fever in India.

·        If there is deforming arthritis in a child, which is not getting better, and Echo is normal, rethink about rheumatic fever. Not all aches and pains in a child are rheumatic fever.

·        Could a virus be linked to autoimmune disorder? The trigger of autoimmunity is not known yet. But it has been believed for long that a virus could trigger an autoimmune disorder. The classical example is parvovirus, which was thought to cause arthritis and now there is Chikungunya. It is believed that Chikungunya may unmask latent autoimmune disorder.

·        Registry data has shown that rheumatoid arthritis patients, who are on a moderate immunosuppression, do not get Covid-19 more than their counterparts and behave similarly, unless they are taking high dose of steroids, or cyclophosphamide.

·        Joint manifestations are not a prominent feature of Covid-19 so far.

·        Pre-existing rheumatoid may flare up with viral infection. But, there is no specific data on Covid-19.

·        Monoclonal antibodies are derived from single cell line; these are biologics as they are derived from living cell systems. They target all three components of the inflammatory pathway: cytokines, receptor and the cell. MAbs target one process and not a large group of cytokines. We do not know yet which is the key cytokine.













Sunday, May 24, 2020

CMAAO CORONA FACTS and MYTH BUSTER 103 Remdesevir will be in India soon


CMAAO CORONA FACTS and MYTH BUSTER 103 Remdesevir will be in India soon

Dr K K Aggarwal
President Confederation of Medical Associations of Asia and Oceania, HCFI, Past National President IMA, Chief Editor Medtalks

With inputs from Dr Monica Vasudev

917:  For hospitalized patients with severe COVID-19, start remdesevir if available (Grade 1C).

918: Remdesivir for the Treatment of Covid-19 — Preliminary Report
A double-blind, randomized, placebo-controlled trial of intravenous remdesivir in adults hospitalized with Covid-19 with evidence of lower respiratory tract involvement. Patients were randomly assigned to receive either remdesivir (200 mg loading dose on day 1, followed by 100 mg daily for up to 9 additional days) or placebo for up to 10 days. The primary outcome was the time to recovery, defined by either discharge from the hospital or hospitalization for infection-control purposes only.

A total of 1063 patients underwent randomization. The data and safety monitoring board recommended early unblinding of the results on the basis of findings from an analysis that showed shortened time to recovery in the remdesivir group. Preliminary results from the 1059 patients (538 assigned to remdesivir and 521 to placebo) with data available after randomization indicated that those who received remdesivir had a median recovery time of 11 days (95% confidence interval [CI], 9 to 12), as compared with 15 days (95% CI, 13 to 19) in those who received placebo (rate ratio for recovery, 1.32; 95% CI, 1.12 to 1.55; P<0.001). The Kaplan-Meier estimates of mortality by 14 days were 7.1% with remdesivir and 11.9% with placebo (hazard ratio for death, 0.70; 95% CI, 0.47 to 1.04). Serious adverse events were reported for 114 of the 541 patients in the remdesivir group who underwent randomization (21.1%) and 141 of the 522 patients in the placebo group who underwent randomization (27.0%).
CONCLUSIONS: Remdesivir was superior to placebo in shortening the time to recovery in adults hospitalized with Covid-19 and evidence of lower respiratory tract infection. (Funded by the National Institute of Allergy and Infectious Diseases and others; New England Journal of Medicine].

919: In contrast, in a randomized trial from China of 237 patients with severe COVID-19, remdesivir and placebo had similar times to clinical improvement (median 21 versus 23 days) and mortality rates (14 versus 13 percent); however, confidence in the finding of no effect was reduced by use of concomitant therapies, differences in baseline comorbidities between the groups, and failure to meet the target enrollment [Wang Y, Zhang D, Du G, et al. Remdesivir in adults with severe COVID-19: A randomised, double-blind, placebo-controlled, multicentre trial. Lancet 2020.]


920:   Remdesivir is a novel nucleotide analogue that has activity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in vitro.

921: In the United States, the Food and Drug Administration (FDA) has issued an emergency use authorization for remdesivir for hospitalized children and adults with severe COVID-19 (SpO2 ≤94 percent on room air, requiring supplemental oxygen, mechanical ventilation, or extracorporeal membrane oxygenation [ECMO]).

922: The suggested adult dose is 200 mg intravenously on day 1 followed by 100 mg daily for 10 days total in patients on mechanical ventilation or ECMO and 5 days total in other patients (with extension to 10 days if there is no clinical improvement).

923: Remdesivir is not recommended in patients with an alanine aminotransferase ≥5 times the upper limit of normal (and should be discontinued if it rises above this level during treatment or if there are other signs of liver injury).

924: The pharmacokinetics of remdesivir in the setting of renal impairment are uncertain, and it is prepared in a cyclodextrin vehicle that accumulates in renal impairment and may be toxic; thus, remdesivir is not recommended in patients with an estimated glomerular filtration rate (eGFR) <30 mL/min per 1.73 m2 unless the potential benefit outweighs the potential risk.

925: Reported side effects include nausea, vomiting, and transaminase elevations. In a preliminary report from a trial of remdesevir among patients with severe COVID-19, grade 3 aminotransferase elevations occurred in 7 percent and led to drug discontinuation in 3 percent. Other adverse events described in patients who received remdesivir include worsening kidney injury, multiple organ failure, and worsened cardiopulmonary status


Saturday, May 23, 2020

CMAAO CORONA FACTS and MYTH BUSTER 102 Super Spreader

CMAAO CORONA FACTS and MYTH BUSTER 102 Super Spreader

Dr K K Aggarwal
President Confederation of Medical Associations of Asia and Oceania, HCFI, Past National President IMA, Chief Editor Medtalks
With inputs from Dr Monica Vasudev


916: Super-spreader a must for becoming a hot spot of Corona
Without a super spreader the cases in the Country may die out of its own

Superspreader, is a loosely defined term for people who infect a disproportionate large number of others, whether because of genetics, social habits or simply being in the wrong place at the wrong time.

Super-spreader is a feature of nearly every outbreak. Infact the primary case of every epidemic is a super spreader. China cases in Wuhan also might have started with a super spreader.

On average, each person infected with the new coronavirus is passing it on to between two and three other people. But this is only an average; some people will pass it on to nobody while others pass their infection on to far more.

In 2015, a super-spreading event led to 82 people being infected from a single hospital patient with Middle East respiratory syndrome (Mers). And in the Ebola epidemic in West Africa, most cases (61%) came from just a tiny handful of patients (3%).

Some just encounter far more people - either because of their job or where they live - and that means they can spread more of the disease, whether they themselves have symptoms. Others are "super-shedders", who release unusually large amounts of virus (or other bug) from their bodies, so anybody encountering them is more likely to become infected.

Hospitals treating SARS became a major centre of super-spreading because the sickest patients were also the most infectious and they encountered lots of healthcare workers.

It plays a big role at the beginning of any outbreak, when the virus is trying to get established. When it makes the jump into the first patient, the disease might fizzle out before it can cause a large outbreak. But if it can quickly find its way into a super-spreader, then it gives the outbreak a boost. The same rules apply when cases are imported into other countries.

"Typhoid Mary", Irish cook Mary Mallon (1869-1938), unknowingly passed on typhoid fever when she had no symptoms and ended up spending decades in exile and forced quarantine.

HIV person coinfected with STI becomes a super spreader. A heterosexual man co-infected with HIV, hepatitis C virus, and herpes simplex 2 virus has unusually high semen HIV RNA levels.

20/80 rule, a small percentage of individuals within any population control control most transmission events.

A study from Israel has found that so-called super spreaders in Israel have been unusually potent: While, with many viruses, 20 percent of patients are often responsible for 80 percent of cases, the Israeli coronavirus data showed that only five percent of patients were responsible for spreading the disease to 80 percent of those ultimately infected. uper

Example after example have shown the microbe’s affinity for density. The virus has spread easily in nursing homes, prisons, cruise ships and meatpacking plants — places where many people are living or working in proximity. A recent CDC report described how a choir practice in Washington state in March became a super-spreader event when one sick person infected as many as 52 others.

Distinguishing between those who are more infectious and those less infectious could make an enormous difference in the ease and speed with which an outbreak is contained. If the infected person is a super-spreader, contact tracing is especially important. But if the infected person is the opposite of a super-spreader, someone who for whatever reason does not transmit the virus, contact tracing can be a wasted effort.

There has to be a link between people in order to transmit an infection. A link is necessary but not sufficient and the second factor is how infectious a person is.

It can be easy to misattribute multiple infections to an individual — possibly exposing the person to public attack — when the spread has nothing to do with the person’s infectiousness. If you are the first person in a crowded room to get infected and if this is an easily spread disease, you will look like a superspreader. Anyone in that room could have had the same impact. You were just the first in line.

Superspreading events may involve people with symptoms that linger but who are not sick enough to stay home.

Or they could involve infected people who shed an unusual amount of virus — a poorly studied factor that might be due to variations in the amount of virus in the aerosol droplets from a patient’s cough or the amount of infectious virus in feces.

No matter what the cause, public health measures, like avoiding crowds, and cough hygiene, can prevent a superspreading event.

Medical history is replete with stories of superspreading in outbreaks of parasitic disease, tuberculosis, measles and other illness. There is Mary Mallon, a cook better known as Typhoid Mary, who spread typhoid fever to more than 50 people in the early years of the twentieth century. She herself was not ill but was asymptomatic — silently infected with typhoid.

1. China first case looks like was a super spreader
2. The cases in Diamond Princess ship was a case of super spreader focal outbreak
3. The lady in South Korea cult church was a super spreader. There were 28 cases of the coronavirus in South Korea on Feb. 13. Four days had passed without a new confirmed infection. President Moon Jae-in predicted that the outbreak would “disappear before long,” while the prime minister assured people that it was OK not to wear surgical masks outdoors. They probably missed the super spreader possibility. The virus had been rapidly spreading at the time through a large, ​secretive ​church in Daegu, with the presence of a super spreader, where it has since mushroomed into the largest epidemic of the coronavirus outside China, with 1,766 cases, including 13 deaths. Now the president is facing a political backlash over his response as the number of cases continues to climb — 505 new infections on Thursday alone. ​
 4. Iran outbreak is possibly from a super spreader


Possibilities of finding super spreaders

1.     Person with lower respiratory corona illness

2.     Person with coronas pneumonia

3.     Critically ill or terminal corona infected patients

4.     Immunocompromised persons with corona infection

5.     Person who have not suffered from any other corona illness in past with non-virulent strains

6.     Rapidly developing corona illness with very short incubation period

7.     Direct exposure to a super spreader compared to secondary or tertiary cases

8.     Co-infection with another pathogen

9.     Delayed identification and hospital admission of a super spreader


Summary
1.     Low grade transmission: Through a spreader
2.     High grade transmission: through a super spreader, usually will end up with community spread.

Virus ‘does not spread easily’ from contaminated surfaces or animals, revised CDC website states



The coronavirus primarily spreads from person to person and not easily from a contaminated surface.

The revised guidance now states, in headline-size type, “The virus spreads easily between people.” It also notes that the coronavirus, which causes the disease covid-19, “is spreading very easily and sustainably between people.”

The CDC made another key change to its website, clarifying what sources are not major risks. Under the new heading “The virus does not spread easily in other ways,” the agency explains that touching contaminated objects or surfaces does not appear to be a significant mode of transmission. The same is true for exposure to infected animals.




Friday, May 22, 2020

CMAAO CORONA FACTS and MYTH BUSTER 101 Mantra, Alphabets and Speech


CMAAO CORONA FACTS and MYTH BUSTER 101 Mantra, Alphabets and Speech

Dr K K Aggarwal
President Confederation of Medical Associations of Asia and Oceania, HCFI, Past National President IMA, Chief Editor Medtalks
With inputs from Dr Monica Vasudev, Ashok Chakradhar and Preti Prajapati


893:  Speech May Spread COVID-19

Yes, Normal human speech emits droplets capable of carrying the novel coronavirus (SARS-CoV-2) that causes COVID-19. The droplets lingered in the air for up to 14 minutes and this reinforces the importance of masking.

894: Talking, shouting, talking loudly, singing, coughing and sneezing all can transmit the infection. [Valentyn Stadnytskyi, from the National Institute of Diabetes and Digestive and Kidney Diseases, and colleagues in May 13 in PNAS.]


895: Previous research showed these droplets can contain respiratory pathogens such as Mycobacterium tuberculosisinfluenza viruses, and measles virus. Could they also carry SARS-CoV-2?

896: Method: To measure the size of droplets emitted through speech, they used an intense sheet of laser to visualize bursts of speech droplets produced when subjects said the words "stay healthy." The method is particularly sensitive in detecting speech droplets with diameters of less than 30 μm, which could remain airborne for longer than the larger droplets that have typically been the subject of research.

897: One minute of loud speaking generates at least 1000 droplets capable of carrying virions — units of the virus that can cause infection. The droplets remained airborne for 8 to 14 minutes, long enough for someone to inhale them and become infected.

898: Droplet nuclei averaged 12 to 21 μm in diameter when first emitted and 4 μm after drying in the air, and that a 10-μm droplet has a 0.37% probability of containing at least one virion.

899: The study does build on previous research, notably a study of hospitals in Wuhan, China, that showed RNA from the virus could be found in droplets as small as 0.25 μm. Yuan Liu, from State Key Laboratory of Virology, Wuhan University, China, and colleagues published their findings online April 27 in the journal Nature. They also did not measure virions.

900: On the other hand, a laboratory study led by the National Institute of Allergy and Infectious Diseases (NIAID) showed that virions persisted in aerosols created by artificial means for hours, with a median half-life of 1.1 to 1.2 hours. NIAID researchers Neeltje van Doremalen, PhD, and Trenton Bushmaker, BSc, along with colleagues published their findings online April 19 in the New England Journal of Medicine. Their study did not measure the size of droplet needed to carry a virion.

901: A study by Chicago researchers finding that tightly woven cloth masks — cotton, natural silk and chiffon — can filter more than half of particles ranging from 10 nm to 6.0 μm if they fit well. But a poor fit can decrease their efficiency by more than 60%.

902:  A bad mask might be worse than none at all if it gives the wearer false confidence

903: Even a mask that provides partial protection can significantly reduce exposure.

904: The higher the dose the worse the case. We all want to get the kind of SARS-CoV-2 that causes mild symptoms."

 

905: What are alphabets

        Kwarga:         ka             kha     ga    gha           nga   (throat)
        Chavarga:     Cha           Chha   Ja     Jha           nga    (Palate)
        Tavarga         ta              Tha    da     dha           na      (tongue)
        Tvarga           ta              tha    da     dha           na      (dental)
        Pavarga         pa             pha    ba     bha           ma     (lips)


906: What are alpa prana
        Alphabets of akshar which uses little breath and little force ( aspirate) are less likely to spread the infection.
        Source: Ayugma vargayamaga yanascalpasavah smrtah or अयुग्मा वर्गयमगा यणश्चाल्पासवः स्मृताः which means the vowels, semivowels, nasals and the letters (1 and 3) क् च् ट् त् प् ग् ज् ड् द् ब् (k c ṭ t p g j ḍ d b).
        Source: Alpaprāṇa (अल्पप्राण) have little power or strength, having short breath, asthmatic; °णश्च क्रियासु भवति (ṇaśca kriyāsu bhavati) Suśr. (-ṇaḥ) 1 slight breathing or weak aspiration.
906: What are maha prana

        Alphabets of akshar which uses more breath and more  force ( aspirate) are more likely to spread the infection.
         Maha Prana: they are letters 2,4 and sibilants  sh shh s h,

अल्पप्राण व्यंजन

ऐसे व्यंजन जिनको बोलने में कम समय लगता है और बोलते समय मुख से कम वायु निकलती है उन्हें अल्पप्राण व्यंजन (Alppran) कहते हैं। इनकी संख्या 20 होती है।
                 







इसमें
वर्ग का पहला, तीसरा, पाँचवा अक्षर
वर्ग का पहला, तीसरा, पाँचवा अक्षर
वर्ग का पहला, तीसरा, पाँचवा अक्षर
वर्ग का पहला, तीसरा, पाँचवा अक्षर
वर्ग का पहला, तीसरा, पाँचवा अक्षर
चारों अन्तस्थ व्यंजन -
एक उच्छिप्त व्यंजन

महाप्राण व्यंजन

ऐसे व्यंजन जिनको बोलने में अधिक प्रत्यन करना पड़ता है और बोलते समय मुख से अधिक वायु निकलती है। उन्हें महाप्राण व्यंजन (Mahapran) कहते हैं। इनकी संख्या 15 होती है।









इसमें
वर्ण का दूसरा, चौथा अक्षर
वर्ण का दूसरा, चौथा अक्षर
वर्ण का दूसरा, चौथा अक्षर
वर्ण का दूसरा, चौथा अक्षर
वर्ण का दूसरा, चौथा अक्षर
चारों उष्म व्यंजन -
एक उच्छिप्त व्यंजन
                   
                   

906: Ushma sounds which can reduce the size of the droplet

907: अघोष Aghosh: 1,2, sh shh s श  Non-Vibratory

908: सघोष  Saghosh: 3,4,5, ',, , व्  'ह’ Vibratory

909: Bengali do not differentiate between three sibilants

910: Tamils have no Mahapranas

911:  Combination of maha prana, ushma, and vibratory will be most dangerous: श ह,  घ,  झ,  ढ,  ध, भ

912: स्टे हेल्दी has 2 sibilants or ushma sounds and will spread the infection far ahead then AUM

913:  काव्य गुण मुख्य रूप से तीन प्रकार के होते हैं -     1. माधुर्य     2. ओज    3. प्रसाद
1.
माधुर्य गुण : किसी काव्य को पढने या सुनने से ह्रदय में जहाँ मधुरता का संचार होता है , वहाँ माधुर्य गुण होता है यह गुण विशेष रूप से श्रृंगार, शांत, एवं करुण रस में पाया जाता है
(
) माधुर्य गुण युक्त काव्य में कानों को प्रिय लगने वाले मृदु वर्णों का प्रयोग होता है जैसे - ,, , , , , , , , , .... आदि ( वर्ग को छोडकर)
(
इसमें कठोर एवं संयुक्ताक्षर वाले वर्णों का प्रयोग नहीं किया जाता
(
) आनुनासिक वर्णों की अधिकता |
(
) अल्प समास या समास का अभाव

2. ओज गुण : ओज का शाब्दिक अर्थ है तेज, प्रताप या दीप्ति |

 जिस काव्य को पढने या सुनने से ह्रदय में ओज, उमंग और उत्साह का संचार होता है, उसे ओज गुण प्रधान काव्य कहा जाता हैं
यह गुण मुख्य रूप से वीर, वीभत्स, रौद्र और भयानक रस में पाया जाता है
(इस प्रकार के काव्य में कठोर संयुक्ताक्षर वाले वर्णों का प्रयोग होता है
(
)   इसमें संयुक्त वर्ण '' के संयोगयुक्त , , , , का प्राचुर्य होता है |
(
समासाधिक्य और कठोर वर्णों की प्रधानता होती है।

3. प्रसाद गुण 

 प्रसाद का शाब्दिकार्थ है - निर्मलता , प्रसन्नता