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CMAAO CORONA FACTS and MYTH
Author : Dr K Aggarwal , President CMAAO, HCFI, With input from Dr Monica Vasudev
India
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New Delhi, December 30, 2020 :
Children are more at risk of contracting the coronavirus at a social gathering than in a classroom or childcare setting, according to a study released by the University of Mississippi Medical Center and conducted in partnership with U.S. CDC featured in Dec. 18 Morbidity and Mortality Weekly Report.
Researchers surveyed patients younger than 18 who had tested positive for the virus in emergency departments and outpatient health facilities during September, October and November. Compared with children who tested negative, those who tested positive were more likely to have attended gatherings and have had visitors at home. Additionally, parents or guardians of children who were infected were less likely to report wearing masks at those gatherings.
Household contacts versus a contact at school appeared to be more important in a child’s risk for being infected. The report highlights what health professionals have seen “played out time and time again” during the pandemic.
There is some degree of immunity after the first dose of the COVID-19 vaccines, but it’s not optimal and we don’t know how long it will last. We do know definitively that immunity increases dramatically after the second dose and lasts considerably longer.
A “bridging study” in children will probably begin in mid-January to make sure that the COVID-19 vaccines’ efficacy and safety data are comparable to those of the successful adult vaccine trials. It’s not necessary to vaccinate children before we reopen schools.
April could be “open season” for the general public to start receiving COVID-19 vaccines in US. We could have “umbrella protection” across the country — establishing herd immunity — by the end of summer 2021.
Like all RNA viruses, this coronavirus has been mutating, and a new variant that has shown up in the United Kingdom may be more contagious. However, there is no evidence that it is more virulent or that current vaccines will not be effective against it.
A large study adds to evidence that people with type O or Rh−negative blood may be at slightly lower risk from the new coronavirus. Among 225,556 Canadians who were tested for the virus, the risk for a COVID-19 diagnosis was 12% lower and the risk for severe COVID-19 or death was 13% lower in people with blood group O versus those with A, AB, or B, researchers reported in Annals of Internal Medicine. People in any blood group who were Rh-negative were also somewhat protected, especially if they had O-negative blood.
People with type O blood, and those who are Rh negative, may have developed antibodies that can recognize some aspect of the new coronavirus and therefore might partly protect them against it.
SOURCE: https://bit.ly/2JhQvws Annals of Internal Medicine, online November 24, 2020.
COVID-19: Abnormal Clotting Common in More Severe Disease
Endothelial damage and subsequent clotting is common in severe and critical COVID-19 coronavirus, which may have implications for treatment. Clots in the small vessels of all organs, not only the lungs but also including the heart, the liver, and the kidney,” were described by Bin Cao, MD, of the National Clinical Research Center for Respiratory Diseases in Beijing. His group had reported March 11 in The Lancet that D-dimer levels over 1 μg/L at admission predicted an 18-fold increase in odds of dying before discharge among 191 COVID-19 patients seen at two hospitals in Wuhan, China. D-dimer, a fibrin degradation product indicating thrombosis, can exceed 70 or 80 μg/L.
Acute cardiac injury was reported in 12% of COVID-19 cases in a small case series in the Lancet cited by Cao. Another study suggested a rate of 7.2% among 138 patients from another hospital in Wuhan, noted Yundai Chen, MD, of the Chinese PLA General Hospital in Beijing, during the webinar. Comorbid cardiovascular disease is a distinct risk factor for COVID-19, associated with a mortality rate of up to 10.5% among more than 70,000 patients in one study. The virus can bind to the endothelial cells and may cause damage to the blood vessels especially the microcirculation of the small blood vessels,” which leads to platelet aggregation. It is not a myocardial infection, it is not a stroke, it is the clots all over the body. So you can imagine why the high D-dimer. It is because of the widespread of abnormal coagulation all over the body.
Along with endothelial shedding and thrombosis in vessels, autopsies showed inflammatory changes in the heart with fine interstitial mononuclear inflammatory infiltrates, but no viral inclusions in the heart,. Other potential mechanisms for the cardiac damage are hypoxia-induced myocardial injury, cardiac microvascular damage, and systemic inflammatory response syndrome. However, in the majority of mild and moderate cases, the only cardiac impact was some tachycardia and little higher troponin.
Chen pointed to the case of a COVID-19-infected man with apparent STEMI by ECG, troponin T over 10,000 ng/L, and CK-MB of 113 ng/L, but for whom coronary angiography showed no stenosis. After treatment with steroids, immunoglobulin, norepinephrine, diuretic, a vasodilator, and antibiotics, the man’s ejection fraction recovered from 27% to 66% and his enlarged heart normalized.
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