Tuesday, April 28, 2020

Herd immunity’ without a vaccine could mean 840,000 coronavirus deaths in California

Herd immunity’ without a vaccine could mean 840,000 coronavirus deaths in California

  • PUBLISHED:  | UPDATED: 
  • Categories:California NewsNews
Amid Gov. Gavin Newsom’s scenario of a post-sheltering world, there are two chilling words: herd immunity.
Tomorrow’s tableau — waiters with masks, distant desks, split-shift schools — will be the new normal, he told reporters in his Tuesday press briefing, “at least until we have herd immunity.”
The phrase came up again as he explained what’s ahead, as “we begin to transition into suppression, ultimately, on our way to herd immunity” and then a vaccine. He repeated it later, describing progress “towards herd immunity.”
What’s herd immunity? It’s when so many people have been infected and develop protective antibodies that a virus runs out of hosts. That’s likely what happened in the 1918-1919 flu pandemic, which killed 20 to 40 million people and then vanished.
What does “herd immunity” look like in the age of COVID-19? Without a vaccine, about 28 million infected Californians.
Based on current estimates, about 5 percent of infected people — or roughly 1.4 million Californians — would get severely ill. Of these, 840,000 could die, although there’s hope of holding that number down.
This bleak strategy may be the only way through a pandemic that is causing profound economic, social and education paralysis. A vaccine, which also could provide herd immunity, is 12 to 18 months away, with likely additional months needed to scale up manufacturing and distribution.
It’s also very scary. The governor’s promised “light at the end of the tunnel” could instead be the glaring halogens over an ICU bed.
As if in synchrony, on Tuesday scientists at Harvard’s prestigious Harvard T.H. Chan School of Public Health also conceded the inevitability of continued infections.
In a set of mathematical models published in the journal Science, they proposed a strategy of intermittent restrictions that would help us approach herd immunity as slowly as possible, so hospitals aren’t overwhelmed.
Rather than hiding from the virus, a goal is to spread out the number of infections at any one time, so fewer people die, they concluded.
“Several rounds of social distancing will be required to get us to ‘herd immunity’ in the absence of vaccination,” said Harvard epidemiologist and study co-author Dr. Marc Lipsitch.
This is the concept: If a large number of people — the “herd” — are immune, then a vulnerable person in the middle of the herd is unlikely to be exposed. Life goes on.
Based on early estimates of this virus’s infectiousness, we likely will need at least 70% of the population to be immune to have herd protection, according to Johns Hopkins School of Public Health epidemiologists Gypsyamber D’Souza and David Dowdy.
Why 70%? The more contagious the virus, the more people need to be vaccinated for herd immunity to work; contagious viruses are more likely to find that unprotected person in the herd. Immunity to measles is reached at 90-95%; for polio, it’s 80-85%.
Right now, we’re nowhere near that. It’s unclear exactly how far away we are, because COVID-19 antibody tests just now are coming online. Back in late February and early March, only two out of nearly 3,000 people with respiratory symptoms were later found to have had the virus, according to a Stanford study.
There’s a lot else we still don’t know. For instance, how many Californians would die with this strategy? We can only make estimates.  So far, the virus has killed 3% of Californians known to be infected. But the true death rate is almost certainly much lower, because many of those infected haven’t been tested. The vast majority of infected people – 80%, it is estimated – have only mild symptoms.
How much protection do antibodies confer on people who have recovered? The jury is still out on that.
When will new medicines blunt the impact of illness? We don’t know that, either.
Could we reach that magic 70% target by infecting just young people, segregating the sick and elders? Perhaps. But they’d pay a price. New data show that youth aren’t invincible; up to one-fifth of infected people ages 20-44 have been hospitalized — and 2%-4% required an ICU rescue.
The goal is to reach “herd immunity” without overshooting it, incurring unnecessary heartbreak, the Harvard experts said.
Dr. Sonia Angell, director of the California Department of Public Health, seems braced for this hard choice — and rather than denying it, is preparing.
“As we change interventions, as we make it possible for people to move around more freely, we do know that infections could increase,” she said Tuesday. “And indeed, there may be more demands on our hospitals. So it is essential that we ensure our ability to care for the sick.”
Diplomatically, she warned: “As we start to loosen up, there is the possibility for more movement of COVID-19. And we need to make sure that our hospitals are prepared. Some of the key questions we’ll be asking ourselves include, do we have adequate bed capacities, staff and supplies such as ventilators and masks?”
It would be easy to create herd immunity very quickly. Lifting all restrictions now would accelerate the process. It would also swamp our hospitals and fill our cemeteries.
A go-slow approach means that more of us will survive to join the herd. Studies show that death rates are highest — surpassing 10% — in Italy and Spain, where health systems were overwhelmed by a huge explosion of cases. In contrast, the death rate is 2.4% in Germany, 2.1% in South Korea and 0.5% in Iceland.
The goal is to infect the most while killing the least. That demands an exquisitely calibrated state strategy: counting each illness, then lifting or imposing very targeted restrictions to create smaller and better-managed outbreaks.
To reach herd immunity, “there’s no light switch here” of all-or-nothing restrictions, said Newsom. “It’s more like a dimmer … toggling back and forth.”

Monday, April 27, 2020





APRIL 27, 2020

High-dose chloroquine diphosphate not recommended for severe COVID-19, link between SARS-CoV-2 viral load in sputum and risk of COVID-19 progression

By Denise Baez
NEW YORK -- April 27, 2020 -- In today’s DG Alert, we cover the effect of high versus low doses of chloroquine diphosphate as adjunctive therapy for patients hospitalised with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and the link between SARS-CoV-2 viral load in sputum with risk of coronavirus disease 2019 (COVID-19) progression. 
Preliminary findings of a randomised study published in JAMA Network Open suggest that high doses of chloroquine diphosphate should not be used in critically ill patients with COVID-19 because of its potential safety hazards, especially when taken concurrently with azithromycin and oseltamivir. 
“In this phase 2b randomised clinical trial of 81 patients with COVID-19, an unplanned interim analysis recommended by an independent data safety and monitoring board found that a higher dosage of chloroquine diphosphate for 10 days was associated with more toxic effects and lethality, particularly affecting QTc interval prolongation,” wrote Mayla Gabriela Silva Borba, MD, Fundação de Medicina Tropical Dr Heitor Vieira Dourado, Manaus, Brazil, and colleagues. 
The authors noted that the limited sample size did not allow the study to show any benefit overall regarding treatment efficacy. The findings do not apply to patients with mild disease.
In the study, patients (mean age, 51.1 years; 75.3% were male) were randomised to receive chloroquine diphosphate 600 mg twice daily for 10 days (n = 41) or chloroquine diphosphate 450 mg twice daily on day 1 and once daily for 4 days (n = 40). All patients also received intravenous ceftriaxone 1 g twice daily for 7 days plus azithromycin 500 mg once daily for 5 days starting on day 0. 
Lethality until day 13 -- the primary endpoint -- was 39.0% in the high-dose group (16/41) and 15.0% in the low-dose group (6/40). Viral RNA was detected in 77.5% (31/40) of patients in the low-dose group and in 75.6% (31/41) of patients in high-dose group. 
Of the patients receiving high-dose chloroquine diphosphate, 18.9% experienced QTc interval >500 milliseconds compared with 11.1% of patients receiving low-dose chloroquine diphosphate. 
Two patients in the high-dose group experienced ventricular tachycardia before death, without torsade de pointes. This severe type of arrhythmia is usually facilitated when QTc interval is prolonged. 
“In a unique pandemic situation, health professionals have to choose between offering medical assistance and generating and reporting reliable data -- dichotomy that compromises the ability to generate high-quality evidence for clinical management,” the authors wrote. “However, global recommendations for COVID-19 are being made based on unpowered studies, and because of the chaotic urgency of the situation, drugs are being prescribed in a compassionate manner given the severity of the disease. Chloroquine diphosphate is a safe drug, used for more than 70 years to treat malaria. However, in the context of patients with severe COVID-19, our study raises enough red flags to stop the use of a high-dosage regimen because the risks of toxic effects overcame the benefits.”
Another study, published in Critical Care, found a positive association between sputum viral load and disease severity as well as risk of progression.
Xia Yu, MD, the First Affiliated Hospital, Hangzhou, China, and colleagues compared the baseline viral loads between 30 patients with severe COVID-19 and 62 patients with mild to moderate disease who were admitted from January 19, 2020, to March 19, 2020, at the First Affiliated Hospital of Zhejiang University. 
Patients with severe disease had significantly lower cycle threshold (Ct) values than patients with mild or moderate cases at admission (25 vs 28; P = 0.017), suggesting a higher viral load in the lower respiratory tract. 
Of the patients with mild to moderate COVID-19, 11 became severe during hospitalisation. Higher viral load was observed in sputum specimens from these patients compared with patients who did not become severely ill during hospitalisation (24 vs 29; P = 0.008). 
The Ct values of reverse transcriptase-polymerase chain reaction assays negatively correlated with the probability of progression to severe type in all the patients presenting with mild or moderate disease at admission.
“We found that the viral load of the sputum specimen in the lower respiratory tract tested at baseline is closely related to the severity of COVID-19,” the authors wrote. “More importantly, patients with a higher baseline viral load are more likely to become severe. This finding apparently justifies the concept that early antiviral treatment, if effective, would reduce the risk of progression and thereby the mortality, which has been demonstrated in influenza. In our study, sputum specimens were used, instead of nasopharyngeal and oropharyngeal swabs because it has been shown that samples from lower respiratory tract generally contain a higher level of viral load than nasopharyngeal and oropharyngeal swabs and acquiring swabs is uncomfortable for patients.”
SOURCE: JAMA Network Open, Critical Care

Saturday, April 25, 2020

America, you are welcome!

Please be appreciative and supportive of every one in health carING !

Friday, April 24, 2020

Diagnosis, prevention, and treatment of thromboembolic complications in COVID-19

APRIL 24, 2020

Diagnosis, prevention, and treatment of thromboembolic complications in COVID-19

By Denise Baez
NEW YORK -- April 24, 2020 - A special reportpublished in the journal Radiology outlines prevention, diagnosis and treatment of venous thromboembolism (VTE) in patients with coronavirus disease 2019 (COVID-19). 
Based on recent reports that demonstrated a strong association between elevated D-dimer levels and poor prognosis, concerns about thrombotic complications in patients with COVID-19 have arisen. The National Institute for Public Health of the Netherlands asked a group of radiology and vascular medicine experts to provide guidance for the imaging workup and treatment of these important complications. Their report summarises evidence for thromboembolic disease and potential diagnostic and preventive actions that can be taken.
“Worldwide, COVID-19 is being treated as a primary pulmonary disease,” said Edwin J.R. van Beek, MD, Queens Medical Research Institute, the University of Edinburgh, Edinburgh, United Kingdom. “From the analysis of all available current medical, laboratory, and imaging data on COVID-19, it became clear that symptoms and diagnostic tests could not be explained by impaired pulmonary ventilation alone.”
Recent observations suggest that respiratory failure in COVID-19 is not driven by the development of acute respiratory distress syndrome alone, but that microvascular thrombotic processes may play a role. This may have important consequences for the diagnostic and therapeutic management of these patients. There is a strong association between D-dimer levels, disease progression, and chest CT features suggesting venous thrombosis. In addition, various studies in patients with COVID-19 have shown a very strong association between increased D-dimer levels and severe disease/poor prognosis.
The authors stressed that careful attention needs to be paid to the initial diagnosis and treatment of the prothrombotic and thrombotic state that can occur in a substantial percentage of patients with COVID-19.
“Imaging and pathological investigations confirmed the COVID-19 syndrome is a thrombo-inflammatory process that initially affects lung perfusion, but consecutively affects all organs of the body,” said Dr. van Beek. “This highly thrombotic syndrome leads to macro-thrombosis and embolism. Therefore, strict thrombosis prophylaxis, close laboratory monitoring, and appropriate imaging monitoring, with early anticoagulant therapy in case of suspected venous thromboembolism, are indicated.”
Recommendations for diagnostic and therapeutic management, which vary based on patient symptoms and risk profiles, include prophylactic-dose heparin, chest CT, CT pulmonary angiography, and routine D-dimer testing.
“COVID-19 is more than a lung infection,” said Dr. van Beek. “It affects the vasculature of the lungs and other organs and has a high thrombosis risk with acute life-threatening events that require adequate treatment with anticoagulants based on laboratory monitoring with appropriate imaging tests as required.”
SOURCE: Radiological Society of North America