Research Aggregation Table of Contents

Research Aggregation

Introduction

Writing my blog, that became the book, The Invisible War, it became apparent that I was reading news, adapting to it quickly and accepting it on the precautionary principle whereas much of the rest of the world was either not seeing it or discounting it and much of what I accepted as possibly true and built protocols for ended up being proven 8 weeks later in the West.  The difference was, that an 8-week body of evidence in the speed of a pandemic was a gruesome death toll well over 100,000 at the time of writing this (April 18, 2020) and millions of infected people. What this page serves to offer, in a raw form, are links to, when possible, source research material, or well-written magazine articles that informed me, the experts I listen to, or later, the mainstream media.  Considering this odd fact that rarely does one get an 8-week jump on breaking news, there may be some advantage to continue to update this page as things proceed, in the hopes of shortening the gap between what we can perceive on the periphery of our imagination, that first prickle of data, and the amount we need in order to act.  In wartime measures, we can not wait years for peer-reviewed studies, so we must act on good faith, good intuition, good intel, and a precautionary principle.

Updated: October 1, 2020, Jorah Kai Wood.

 

 

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COVID-19 Vaccine Tracker

Analysis of Measles-Mumps-Rubella (MMR) Titers of Recovered COVID-19 Patients

ABSTRACT

The measles-mumps-rubella (MMR) vaccine has been theorized to provide protection against coronavirus disease 2019 (COVID-19). Our aim was to determine whether any MMR IgG titers are inversely correlated with severity in recovered COVID-19 patients previously vaccinated with MMR II. We divided 80 subjects into two groups, comparing MMR titers to recent COVID-19 severity levels. The MMR II group consisted of 50 subjects who would primarily have MMR antibodies from the MMR II vaccine, and a comparison group of 30 subjects consisted of those who would primarily have MMR antibodies from sources other than MMR II, including prior measles, mumps, and/or rubella illnesses. There was a significant inverse correlation (rs = −0.71, P < 0.001) between mumps virus titers (mumps titers) and COVID-19 severity within the MMR II group. There were no significant correlations between mumps titers and severity in the comparison group, between mumps titers and age in the MMR II group, or between severity and measles or rubella titers in either group. Within the MMR II group, mumps titers of 134 to 300 arbitrary units (AU)/ml (n = 8) were found only in those who were functionally immune or asymptomatic; all with mild symptoms had mumps titers below 134 AU/ml (n = 17); all with moderate symptoms had mumps titers below 75 AU/ml (n = 11); all who had been hospitalized and had required oxygen had mumps titers below 32 AU/ml (n = 5). Our results demonstrate that there is a significant inverse correlation between mumps titers from MMR II and COVID-19 severity.

 

Vitamin D deficiency spikes COVID-19 risks

The Kids Are Not Alright: A Preliminary Report of Post-COVID Syndrome in University Students

ABSTRACT

Background Post-COVID syndrome is increasingly recognized by the medical community but has not been studied exclusively in young adults. This preliminary report investigates the prevalence and features of protracted symptoms in non-hospitalized university students who experienced mild-to-moderate acute illness.

Methods 148 students completed an online study to earn research credit for class. Data from COVID-19 positive participants with symptoms ≥28 days (N=22) were compared to those who fully recovered (N=21) and those not diagnosed with COVID-19 (N=58).

Results 51% of participants who contracted COVID-19 (N=43) experienced symptoms ≥28 days and were classified as having post-COVID syndrome; all but one (96%) were female. During acute illness the post-COVID group, compared to those who fully recovered, experienced significantly more chest pain (64% vs 14%; P=.002), fatigue (86% vs 48%; P=.009), fever (82% vs 48%; P=.02), olfactory impairment (82% vs 52%; P=.04), headaches (32% vs 5%; P<.05), and diarrhea (32% vs 5%; P<.05). Compared to those not diagnosed with COVID-19, the post-COVID syndrome group more frequently experienced exercise intolerance (43% vs. 0%; P<.001), dyspnea (43% vs. 0%; P<.001), chest pain (31% vs 7%; P=.002), olfactory impairment (19% vs 0%; P=.004), lymphadenopathy (19% vs 0%; P=.004), gustatory impairment (14% vs 0%; P=.02), and appetite loss (36% vs 14%; P=.02).

Interpretation Our results contradict the perception that this “yet to be defined” post-COVID syndrome predominantly affects middle-aged adults and suggest that exercise intolerance, dyspnea, chest pain, chemosensory impairment, lymphadenopathy, rhinitis, and appetite loss may differentiate post-COVID syndrome from general symptoms of pandemic, age, and academic related stress. These findings are also consistent with previous reports that females are more vulnerable to this post viral syndrome. Large-scale population-based studies are essential to discerning the magnitude and characterization of post-COVID syndrome in young adults as well as more diverse populations.

 

COVID-19: Attack Theory

Originally focussing on respiratory problems, doctors and researchers are now studying the many organs that can fail when attacked by COVID-19 and radical treatments that could be used to mitigate permanent organ damage, and save lives.

How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

Sciences COVID-19 reporting is supported by the Pulitzer Center.

On rounds in a 20-bed intensive care unit (ICU) one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped. All shared one thing, says Denson, a pulmonary and critical care physician at the Tulane University School of Medicine. “They are all COVID positive.”

As the number of confirmed cases of COVID-19 surges past 2.2 million globally and deaths surpass 150,000, clinicians and pathologists are struggling to understand the damage wrought by the coronavirus as it tears through the body. They are realizing that although the lungs are ground zero, its reach can extend to many organs including the heart and blood vessels, kidneys, gut, and brain.

“[The disease] can attack almost anything in the body with devastating consequences,” says cardiologist Harlan Krumholz of Yale University and Yale-New Haven Hospital, who is leading multiple efforts to gather clinical data on COVID-19. “Its ferocity is breathtaking and humbling.”

How does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toes

Sciences COVID-19 reporting is supported by the Pulitzer Center.

On rounds in a 20-bed intensive care unit (ICU) one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped. All shared one thing, says Denson, a pulmonary and critical care physician at the Tulane University School of Medicine. “They are all COVID positive.”

As the number of confirmed cases of COVID-19 surges past 2.2 million globally and deaths surpass 150,000, clinicians and pathologists are struggling to understand the damage wrought by the coronavirus as it tears through the body. They are realizing that although the lungs are ground zero, its reach can extend to many organs including the heart and blood vessels, kidneys, gut, and brain.

“[The disease] can attack almost anything in the body with devastating consequences,” says cardiologist Harlan Krumholz of Yale University and Yale-New Haven Hospital, who is leading multiple efforts to gather clinical data on COVID-19. “Its ferocity is breathtaking and humbling.”

A medical worker tends to a covid-19 patient at an intensive care unit at Maimonides Medical Center in Brooklyn on April 1, 2020.

 

A medical worker tends to a covid-19 patient at an intensive care unit at Maimonides Medical Center in Brooklyn on April 1, 2020. (Jon Gerberg/The Washington Post)
April 15, 2020 at 7:00 p.m. GMT+8

The new coronavirus kills by inflaming and clogging the tiny air sacs in the lungs, choking off the body’s oxygen supply until it shuts down the organs essential for life.

But clinicians around the world are seeing evidence that suggests the virus also may be causing heart inflammation, acute kidney disease, neurological malfunction, blood clots, intestinal damage and liver problems. That development has complicated the treatment of the most severe cases of covid-19, the illness caused by the virus, and makes the course of recovery less certain, they said.

 

COVID-19 Strains and Mutations

Patient-derived mutations impact pathogenicity of SARS-CoV-2

Hangping Yao, Xiangyun Lu, Qiong Chen, Kaijin Xu, Yu Chen, Linfang Cheng, Fumin Liu, Zhigang Wu, Haibo Wu, Changzhong Jin, Min Zheng, Nanping Wu, Chao Jiang, Lanjuan Li

Dissemination in Media: 

SCIENTISTS: THE CORONAVIRUS HAS ALREADY MUTATED INTO 30+ STRAINS

ONE STRAIN, FOR EXAMPLE, APPEARED TO GENERATE 270 TIMES THE VIRAL LOAD.

New research suggests that SARS-CoV-2, the virus that causes COVID-19, could have already mutated into more than 30 separate strains.

The study found that different strains can generate vastly different levels of viral load as others, the South China Morning Post reports, making them far more dangerous.

One strain, for example, appeared to generate 270 times the viral load — meaning the infected person produces 270 times as much of the virus— than the least potent strain.

That makes it far harder to fight off infections and facilitates spread, hypothetically explaining why some cases of COVID-19 are significantly worse than others.

“Sars-CoV-2 has acquired mutations capable of substantially changing its pathogenicity,” Li Lanjuan, one of China’s most prolific epidemiologists and a researcher at Zhejiang University, wrote in the study, which was shared online in the preprint server MedRxiv on Sunday but hasn’t yet been vetted by the peer-review process or published in an academic journal.

In the research, Li isolated different strains and, under laboratory conditions, measured how quickly and effectively they could infect and kill off host cells.

The paper also traced different strains to outbreaks in different parts of the world, finding that the version of SARS-CoV-2 that spread across Europe and New York were far more efficient killers than the one that hit other parts of the U.S. such as Washington State.

“Drug and vaccine development, while urgent, need to take the impact of these accumulating mutations… into account to avoid potential pitfalls,” Li and her colleagues wrote.


Current Thinking on the Origins of COVID-19

 With all the rumors from bat soup, to bio-engineered, to a “5G connection”, newest science seems to show we still do not know much about the origins of COVID-19, but experts explain why it doesn’t, at least for now, matter: because it won’t change how we have to fight it, first and foremost. 

SARS-COV-2 was already spreading in France in late December 2019

Highlights

Covid-19 was already spreading in France in late December 2019, a month before the official first cases in the country.

Early community spreading changes our knowledge of covid-19 epidemic.

This new case changes our understanding of the epidemic and modeling studies should adjust to this new data.

Abstract

The COVID-19 epidemic is believed to have started in late January 2020 in France. We report here a case of a patient hospitalized in December 2019 in our intensive care, of our hospital in the north of Paris, for hemoptysis with no etiological diagnosis and for which RT-PCR was performed retrospectively on the stored respiratory sample which confirmed the diagnosis of COVID-19 infection. Based on this result, it appears that the COVID-19 epidemic started much earlier.

Science News
from research organizations

Science Daily: COVID-19: Genetic network analysis provides ‘snapshot’ of pandemic origins

Date:
April 9, 2020
Source:
University of Cambridge
Summary:
The first use of phylogenetic techniques shows the ‘ancestral’ virus genome closest to those in bats was not Wuhan’s predominant virus type. The study charts the ‘incipient supernova’ of COVID-19 through genetic mutations as it spread from China and Asia to Australia, Europe and North America. Researchers say their methods could be used to help identify undocumented infection sources.
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FULL STORY

Researchers from Cambridge, UK, and Germany have reconstructed the early “evolutionary paths” of COVID-19 in humans — as infection spread from Wuhan out to Europe and North America — using genetic network techniques.

By analysing the first 160 complete virus genomes to be sequenced from human patients, the scientists have mapped some of the original spread of the new coronavirus through its mutations, which creates different viral lineages.

“There are too many rapid mutations to neatly trace a COVID-19 family tree. We used a mathematical network algorithm to visualise all the plausible trees simultaneously,” said geneticist Dr Peter Forster, lead author from the University of Cambridge.

“These techniques are mostly known for mapping the movements of prehistoric human populations through DNA. We think this is the first time they have been used to trace the infection routes of a coronavirus like COVID-19.

Wuhan lab says there’s no way coronavirus originated there. Here’s the science.

This transmission electron microscopic image shows particles of SARS-CoV-2 isolated from the first U.S. case of COVID-19.

This transmission electron microscopic image shows particles of SARS-CoV-2 isolated from the first U.S. case of COVID-19.

An unprecedented amount of research has been focused solely on understanding the novel coronavirus that has taken nearly 150,000 lives across the globe. And while scientists have gotten to know some of the most intimate details of the virus called SARS-CoV-2, one question has evaded any definitive answers — Where did the virus come from? 

NEWSWEEK: CORONAVIRUS OUTBREAK MAY HAVE STARTED AS EARLY AS SEPTEMBER, SCIENTISTS SAY

Geneticist Peter Forster, from the U.K.’s University of Cambridge, is leading a research project to understand the historical processes that led to the COVID-19 pandemic. Ultimately, they hope to identify the first person who got the virus and served as the source for the initial outbreak. By analyzing networks, they have so far been able to chart the spread of the virus, including the genetic mutations, as it moved from China to Australia, Europe and the rest of the world.

Loss of Senses: Taste and Smell

An early warning symptom in some 60% of COVID-19 cases seems to be the loss of taste and smell. While the olfactory (smell) can be overwhelmed by any number of factors, losing your sense of taste is quite uncommon and is a good early warning sign you might have COVID-19. Anecdotally, these cases seem to indicate a more mild case of COVID-19 but should tip you off to self-isolate or quarantine immediately and amplify your social distancing procedures and protocols.

Loss of smell and taste validated as COVID-19 symptoms in patients with high recovery rate

Study suggests clinicians should include sensory impairment as standard screening measure

Date:
April 13, 2020
Source:
University of California – San Diego
Summary:
Researchers have published the first empirical findings that strongly associate sensory loss and COVID-19, the respiratory disease caused by the novel coronavirus.

Loss of smell and taste has been anecdotally linked to COVID-19 infections. In a study published April 12, 2020 in the journal International Forum of Allergy & Rhinology, researchers at UC San Diego Health report the first empirical findings that strongly associate sensory loss with COVID-19, the respiratory disease caused by the novel coronavirus.

“Based on our study, if you have smell and taste loss, you are more than 10 times more likely to have COVID-19 infection than other causes of infection. The most common first sign of a COVID-19 infection remains fever, but fatigue and loss of smell and taste follow as other very common initial symptoms,” said Carol Yan, MD, an otolaryngologist and head and neck surgeon at UC San Diego Health. “We know COVID-19 is an extremely contagious virus. This study supports the need to be aware of smell and taste loss as early signs of COVID-19.”

ARTICLE

Does Loss of Smell Require COVID-19 Precautions?

APR 12, 2020 | KENNETH BENDER, PHARMD, MA

The loss of smell or taste could occur with coronavirus disease 2019 (COVID-19) in absence of other symptoms, according to case reports in the US and abroad. This could heighten the risk of exposure for unknowing contacts and add to presenting conditions that could warrant testing for the novel coronavirus.

A report from Norway described that the daughter-in-law of an elderly patient with COVID-19 experienced loss of smell approximately 1 week after she had been in close contact with him, before his hospitalization. Her husband also developed loss of taste shortly after. Both individuals subsequently tested positive for SARS-CoV-2 RNA without developing other symptoms, and both experienced return of these senses after approximately 10 and 16 days, respectively.

“National and international health authorities should consider whether isolated disturbances of smell and/or taste are a sufficient basis for testing for COVID-19 and/or isolation to limit spread of the infection,” the report concluded.

In a report from France, a patient with loss of smell who subsequently tested positive for the virus was found on CT scan with confirming MRI to have bilateral inflammatory obstruction of the olfactory clefts, with no anomalies of the olfactory bulbs and tracts.

This obstructive inflammation of olfactory clefts, the report indicated, “severely impaired the olfactory function by preventing odorant molecules from reaching the olfactory epithelium.”


CDC Releases New Data on Children & COVID-19

By and large, children seem to receive relatively mild symptoms or no symptoms at all. This is a blessing for parents but means children pose a large risk as asymptomatic or pre-symptomatic carriers so social distancing and impeccable hygiene are important to protect your families. Updated April 18, 2020 Jorah Kai Wood.

Immune Response and Immunology Re: COVID-19

‘No evidence’ of virus immunity in recovered patients – WHO

There is currently no evidence to support the belief that people who have recovered from coronavirus then have immunity, the World Health Organization has said.

Senior WHO epidemiologists warned despite the hopes governments across the world have piled on antibody tests, there is no proof those who have been infected cannot be infected again.

Many tests being developed are pinprick blood tests similar to widely used instant HIV tests and measure for raised levels of the antibodies the body uses to fight the virus.

Speaking at a press conference in Geneva, Dr Maria van Kerkhove said: “There are a lot of countries that are suggesting using rapid diagnostic serological tests to be able to capture what they think will be a measure of immunity.

“Right now, we have no evidence that the use of a serological test can show that an individual has immunity or is protected from reinfection.”

Science on Face Masks for Everyone

April 10, 2020: After 8 weeks of fighting the CDC recommendations that the general public should not wear face masks in public when doing critical shopping trips or emergency work, most experts have revised their guidelines and suggested that, while their PPE stocks are not sufficient to supply everyone with an N95 mask or respirator, even DIY face masks can significantly reduce the amount of respiratory droplets a sick or asymptomatic carrier may expel into the air. This is not a trifling matter, since M.I.T. published a study that shows a sneeze in a congested, unventilated area could travel 10 meters less than a second, so someone in the middle of a bus could infect most people on that bus and contaminate most of the seats and handrails in a moment. If that person had been wearing a surgical mask or even a bandana, 99.99% of their respiratory droplets would have been caught in the mask, not contaminating the bus surfaces or becoming aerosolized and infecting the other passengers.  Since 30%+ (maybe as high as half) of cases are asymptomatic, meaning that unlike SARS, we can not simply isolate the symptomatic people, we must all assume we can be carriers, to break the exponential curve of infection. Face masks for all in public has been demonstrated to work in many countries and must be used in every country. Here is the science, presented in a handful of data-driven and evocative video presentations. Updated: April 18, 2020 Jorah Kai Wood.

HEALTH

The case for mandatory mask-wearing in Canada

Opinion: Countries that adopted universal masking saw their mortality rates go down within a couple of weeks. That should be all the proof we need.

 Dr. Joe Vipond is an emergency room physician, and a clinical assistant professor at the University of Calgary.  

As the death statistics continue to grow higher in Canada and around the world, there are corners where the curve has been flattened immensely. And the thing those jurisdictions have in common is universal mandatory masking.

An amazing but little-discussed fact: no country which has imposed mandatory masking has been overwhelmed by the pandemic. Moreover, in Asian countries, that policy has had far less economic impact than the lengthy lockdowns imposed by Western nations.

But there has been great resistance outside of Asia to making non-medical, homemade masks mandatory, with no end of excuses why requiring face-coverings for all people in public settings couldn’t possibly work here. “It’s cultural,” we’re told (non-Asians would just never accept masks). Or “there is no possible way we could teach people to wear them safely” (despite the fact that we seem to successfully be able to teach people to drive cars). Or “the evidence is weak” (when in fact the evidence is growing stronger every day). Masks, we are told, are no substitute for physical distancing (although plenty of countries have instituted physical distancing without successfully bending the curve).

Masks for all? The science says yes.

Confused about mask wearing? Sure, it’s complicated. But not as complicated as some people imply. We’ve been looking at the science (see our papers Face Masks Against COVID-19: An Evidence Review — with 84 references! — and Face masks for the public during the covid-19 crisis). Here’s a summary of the different streams of evidence, and our take on what it all means.

CDC: Use of Cloth Face Coverings to Help Slow the Spread of COVID-19

Business Insider: Using blue shop towels in homemade face masks can filter particles 2x to 3x better than cotton, 3 clothing designers discover after testing dozens of fabrics. Polyester hydro knit towels are readily available at hardware and automotive stores.

The two brands they tested were ToolBox’s shop towel and ZEP’s industrial blue towel. Interestingly, Scott’s pro shop towels, which are also made with a hydro knit fabric, didn’t work as well, Schempf said.

 

Homemade masks can stop the spread of COVID-19 and save lives#Masks4

All the scientific evidence and global consensus is clear: homemade masks can stop the spread of COVID-19. Take action now to save lives and restore the global economy!

How To Make A Mask

Request Mandatory Mask Laws

Papers about effectiveness of basic masks #masks4all

Curated by Jeremy Howard and the fast.ai community. Summaries by Reshama Shaikh. Additional help from Frederik Questier. The papers below have been used to create a video, and a newspaper article, summarizing the utility of basic masks. In summary: everyone should wear masks, which they should make themselves using t-shirts and/or paper towels, whenever they go out in public. I’ve also made a little summary on Twitter of the video, and a summary of the article.

We ended up, somewhat accidentally, finding that we’d created a campaign after we made this literature summary! So now you’ll find lots of information about masks, including how to make your own, at Masks4All.co.

Paper Summaries

Assessment of Fabric Masks as Alternatives to Standard Surgical Masks in Terms of Particle Filtration Efficiency

Amy V Mueller, Loretta A Fernandez

Abstract

In response to the critical shortage of medical masks resulting from the COVID-19 pandemic, large portions of the population are mobilizing to produce cloth masks using locally-sourced fabrics, however the efficacy of these masks as a means of protecting the wearer from airborne particles carrying virus is not well known. Further, existing protocols are designed for testing the fit and performance N95 respirators and tight-fitting facemasks rather than the relatively more loose-fitting surgical mask style most cloth masks follow. In this study tools and methods typically used to assess tight-fitting facemasks were modified to assess the efficacy of community-produced fabric and commercially-produced surgical masks in terms of protecting the wearer from airborne particles that may be carrying virus. Two TSI PortaCount (model 8028) instruments were operated concurrently to collect particle counts (particles/cm^3) in size range 0.02 to >1 um from ambient air and air just inside the breathing zone of the mask (1 measurement per second, evaluation period of 1 minute per test). Percent particle removal was determined for ten home-made, fabric masks of different designs, with and without filter layers, as well as three commercially-produced surgical-type masks. N95 masks were used to validate the method, and a 3M model 1826 surgical mask was used as a baseline for comparison of other masks of this style. Home-made masks worn as designed always had lower particle removal rates than the 3M masks, achieving between 38% and 96% of this baseline. As has been previously observed by Cooper et al. (1983), adding a layer of nylon stocking over the masks minimized the flow of air around the edges of the masks and improved particle filtration efficiency for all masks, including all commercial products tested. Use of a nylon stocking overlayer brought the particle filtration efficiency for five of the ten fabric masks above the 3M surgical mask baseline. This rapid testing method (<2 hours per mask design) provides a holistic evaluation of mask particle removal efficacy (material, design, and fit), and use of this method for testing a wider range of mask materials and designs will provide the public and health care providers with information needed to optimize health protection given resources at hand.

Adding A Nylon Stocking Layer Could Boost Protection From Cloth Masks, Study Finds

Surface Contamination

FYI: This is meant as a guide for your safety. If you must reuse masks, as many of us do, use and store them with care. Here is a method for storing masks for reuse that does not risk touching and surface contamination spread.

Social Distancing

Does it work? Yes. Why? Well, because of science. Let’s look at some of the interesting studies and articles that explain why social distancing reduces pandemic spread.

April 13, 2020

UW team illustrates the adverse impact of visiting ‘just one friend’ during COVID-19 lockdown

UW News

After weeks of social distancing during the COVID-19 pandemic, people of all ages may be asking: What could be the harm of visiting just one friend?

Unfortunately, it could potentially undo the goal of social distancing, which is to give the COVID-19 virus fewer opportunities to spread. According to a website set up by researchers at the University of Washington, easing the social distancing rules so that each household could have contact with just one or two others would reconnect most households in a community, providing conduits through which the COVID-19 virus could spread.

2 meters enough for social distancing? MIT researcher says droplets carrying coronavirus can travel up to 8 meters

2 meters enough for social distancing? MIT researcher says droplets carrying coronavirus can travel up to 8 meters

 

Multiphase Turbulent Gas Cloud From a Human Sneeze. Credit: JAMA (2020). DOI: 10.1001/jama.2020.4756

The novel coronavirus has prompted social distancing measures around the world. One researcher believes what’s being done isn’t enough.

Lydia Bourouiba, an associate professor at MIT, has researched the dynamics of exhalations (coughs and sneezes, for instance) for years at The Fluid Dynamics of Disease Transmission Laboratory and found exhalations cause gaseous clouds that can travel up to 27 feet (8.2 meters).

COVID-19 Prevention: How To Practice Social Distancing In A Family Of 5 Or More?

Coronavirus (COVID-19) prevention: Doctors say that one must practice social distancing in not just the community, but also inside their homes. Stay at a distance of at least three feet from each other. If anyone in the house is experiencing symptoms, then s/he should stay in a separate room.

COVID-19 Prevention: How To Practice Social Distancing In A Family Of 5 Or More?

COVID-19 prevention: Social distancing within the family is important for the prevention of coronavirus

Modeling the effect of mitigation during the Covid-19 pandemic

Dataset

 posted on  by Astrid Chevance

This file contains articles of the collection “COVID-19 SARS COV-2 prepreints from medRxiv” related to the evaluation of the effect of mitigation (from social distancing on to complete lockdown) using modeling techniques (SEIR, etc).

Asymptomatic Transmission

Early science out of China at the end of January, 2020 showed asymptomatic transmission was possible. Germany confirmed this by early February. Despite this, in much of Europe and North America, no precautionary principles and protocols were taken. In fact, Canada’s top health officer, Dr. Theresa Tam recently lamented that Ontario were so confident in their SARS protocols from 2003-2004 that they underestimated COVID-19 transmission and were slow to revise their protocols. It is clear to all now, that asymptomatic carriers are a huge vector for the exponential growth and spread of the pandemic, so here is this science behind that. Last updated April 18, 2020 Jorah Kai Wood.

Presumed Asymptomatic Carrier Transmission of COVID-19.

Bai Y1, Yao L2, Wei T3, Tian F4, Jin DY5, Chen L1, Wang M1.

The COVID-19 Pandemic in the USA Clinical Update

JAMA. Published online April 6, 2020. doi:10.1001/jama.2020.5788

COVID-19: Respiratory or Airborne?

Originally thought to be a respiratory droplet disease, new studies show SARS-COV-2 particles can travel on airflow inside closed areas for hours, or remain in clouds in an infectious state in offices or pass through ventilation systems, increasing the necessity for NPI’s and all people to wear masks in non-green-zone areas.

JAMA Insights
March 26, 2020

Turbulent Gas Clouds and Respiratory Pathogen EmissionsPotential Implications for Reducing Transmission of COVID-19

WHO: Modes of transmission of virus causing COVID-19: implications for IPC precaution recommendations

Scientific brief

29 March 2020

The COVID-19 Coronavirus May Travel in Aerosols

Several studies have indicated that SARS-CoV-2 might be spread through air, but not all experts are convinced.

Amy Schleunes

Amy Schleunes
Apr 3, 2020

You may be able to spread coronavirus just by breathing, new report finds

Science’s COVID-19 reporting is supported by the Pulitzer Center.  The National Academy of Sciences (NAS) has given a boost to an unsettling idea: that the novel coronavirus can spread through the air—not just through the large droplets emitted in a cough or sneeze. Though current studies aren’t conclusive, “the results of available studies are consistent with aerosolization of virus from normal breathing,” Harvey Fineberg, who heads a standing committee on Emerging Infectious Diseases and 21st Century Health Threats, wrote in a 1 April letter to Kelvin Droegemeier, head of the White House Office of Science and Technology Policy.

Air, Surface Environmental, and Personal Protective Equipment Contamination by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) From a Symptomatic Patient

New England Journal of Medicine: Aerosol and Surface Stability of SARS-CoV-2 as Compared with SARS-CoV-1

A novel human coronavirus that is now named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (formerly called HCoV-19) emerged in Wuhan, China, in late 2019 and is now causing a pandemic.1 We analyzed the aerosol and surface stability of SARS-CoV-2 and compared it with SARS-CoV-1, the most closely related human coronavirus.2

We evaluated the stability of SARS-CoV-2 and SARS-CoV-1 in aerosols and on various surfaces and estimated their decay rates using a Bayesian regression model (see the Methods section in the Supplementary Appendix, available with the full text of this letter at NEJM.org). SARS-CoV-2 nCoV-WA1-2020 (MN985325.1) and SARS-CoV-1 Tor2 (AY274119.3) were the strains used. Aerosols (<5 μm) containing SARS-CoV-2 (105.25 50% tissue-culture infectious dose [TCID50] per milliliter) or SARS-CoV-1 (106.75-7.00 TCID50 per milliliter) were generated with the use of a three-jet Collison nebulizer and fed into a Goldberg drum to create an aerosolized environment. The inoculum resulted in cycle-threshold values between 20 and 22, similar to those observed in samples obtained from the upper and lower respiratory tract in humans.

Can HEPA Air Purifiers Capture the Coronavirus?

  • We have included new research that suggests the virus that causes COVID-19 may be transmitted through the air.

The virus that causes COVID-19 is approximately 0.125 micron (125 nanometers) in diameter. It falls squarely within the particle-size range that HEPA filters capture with extraordinary efficiency: 0.01 micron (10 nanometers) and above. Many media outlets have incorrectly stated that HEPA filters don’t filter below 0.3 micron and therefore could not capture airborne coronaviruses. That is flat wrong. (This NASA study of HEPA filtration is quite technical, but the graph on page 7 and the preceding paragraph do a good job of explaining why HEPA filters are actually most efficient—almost 100 percent at 0.01 micron—at capturing ultrafine particles below the 0.3-micron HEPA test standard.)

Hemoglobin Attack Theory Re: COVID-19

Is the coronavirus (COVID-19) a lung disease that causes blood problems, or a blood disease that causes lung problems? The newest science suggests there are many things about COVID-19 we still don’t understand.

MUST READ! Research Reveals That COVID-19 Attacks Hemoglobin In Red Blood Cells, Rendering It Incapable Of Transporting Oxygen. Current Medical Protocols Could All Be Wrong!

Source: COVID-19 Research  Apr 09, 2020  8 days ago
COVID-19 Research: Findings from a new study released by Chinese researchers , Dr  Wenzhong Liu from Sichuan University and Dr Hualan Li from Yibin University has revealed that the Sars-CoV-2 coronavirus attacks hemoglobin in the the red blood cells through a series of cellular actions, that ultimately renders the red blood cells incapable of transporting oxygen. https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173

COVID-19: Thrombosis and Hemoglobin

The Novel Coronavirus 2019, was first reported on in Wuhan, China in late December 2019.  The outbreak was declared a public health emergency of international concern in January 2020 and on March 11th, 2020, the outbreak was declared a global pandemic.  The spread of this virus is now global with lots of media attention.  The virus has been named SARS-CoV-2 and the disease it causes has become known as coronavirus disease 2019 (COVID-19).  This new outbreak has been producing lots of hysteria and false truths being spread, however the data surrounding the biology, epidemiology, and clinical characteristics are growing daily, making this a moving target.  This post will serve as a summary of thrombosis and hemoglobin in regard to COVID-19.

Could red blood cells hold the secret to treating COVID-19?


One of the most severe complications of the coronavirus is called Acute Respiratory Distress Syndrome. It generally results when fluid accumulates in the lungs and oxygen can’t cross it, so patients can’t breathe. (Pixabay)

 

COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism

The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory infection caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus. In this study, conserved domain analysis, homology modeling, and molecular docking were used to compare the biological roles of certain proteins of the novel coronavirus. The results showed the ORF8 and surface glycoprotein could bind to the porphyrin, respectively. At the same time, orf1ab, ORF10, and ORF3a proteins could coordinate attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin. The attack will cause less and less hemoglobin that can carry oxygen and carbon dioxide. The lung cells have extremely intense poisoning and inflammatory due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images. The mechanism also interfered with the normal heme anabolic pathway of the human body, is expected to result in human disease. According to the validation analysis of these finds, chloroquine could prevent orf1ab, ORF3a, and ORF10 to attack the heme to form the porphyrin, and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent, effectively relieve the symptoms of respiratory distress. Since the ability of chloroquine to inhibit structural proteins is not particularly obvious, the therapeutic effect on different people may be different. Favipiravir could inhibit the envelope protein and ORF7a protein bind to porphyrin, prevent the virus from entering host cells, and catching free porphyrins. This paper is only for academic discussion, the correctness needs to be confirmed by other laboratories. Due to the side effects and allergic reactions of drugs such as chloroquine, please consult a qualified doctor for treatment details, and do not take the medicine yourself.

COVID-19 Disease: ORF8 and Surface Glycoprotein Inhibit Heme Metabolism by Binding to Porphyrin

Preprint · March 2020with 17,711 Reads DOI: 10.26434/chemrxiv.11938173

Abstract
The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory infection caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus. Due to the limits of the existing experimental tools, many protein roles of novel coronavirus including ORF8 are still unclear. Therefore, in the current scene of an emergency epidemic, it is of high scientific significance to predict the biological role of viral proteins through bioinformatics methods. In this study, conserved domain analysis, homology modeling, and molecular docking were used to compare the biological roles of certain proteins of the novel coronavirus. The results showed the ORF8 and surface glycoprotein could bind to the porphyrin, respectively, while orf1ab, ORF10 and ORF3a proteins could coordinately attack heme to dissociate the iron to form the porphyrin. The mechanism seriously interfered with the normal heme anabolic pathway of the human body, being expected to result in human disease. According to the validation analysis of these finds, Chloroquine could prevent orf1ab, ORF3a and ORF10 to attack the heme to form the porphyrin, and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent. Therefore, this research is of high value to contemporary biological experiments, disease prevention and clinical treatment.

COVID-19 – causing death by cutting off oxygen and oxidation of the lungs?

Coronavirus

Steve’s post that linked to a piece on Medium I would now label as cutting edge – the first time I had seen the angle that COVID-19’s real attack is to free up the iron ion located within the heme molecule that binds oxygen into the heme (e.g., hemoglobin) within your red blood cells.  No oxygen mean hypoxia – oxygen starvation like what jet fighter pilots get when their O2 machines fail or hikers get when above 10,000 foot climbs. Except you’re in a hospital bed and no amount of air pressure from a ventilator pumping O2 into your lungs can fix. Which, sad to say, is useless – the ventilator pressure hurts the aveoli sacs in your lungs (that actually do the gas transfer of O2 in and CO2 out) and there’s nothing in your blood stream to pick up that O2 anyways.

New research study reveals that COVID-19 attacks hemoglobin in red blood cells, rendering it incapable of transporting oxygen. Are we using a false medical paradigm to treat a new disease?

We’ve been covering the deadly coronavirus since December 2019 when the virus began in Wuhan, China. Our focus has primarily been on trying to identify the true origin of the virus. Over the past few weeks, however, our coverage has shifted to the treatment of the virus using the three drug regimen of Hydroxychloroquine, Zinc Sulfate and Azithromycin after the renowned French Dr. Didier Raoult published results of his first treatment of COVID-19 patients in France.

According to the National Institute of Health (NIH), the full genome sequencing of SARS-CoV-2 was isolated from putative the 2019 novel coronavirus disease (COVID-19) patients in Korea, by cell culture back in January. However, we don’t fully know how COVID virus attack human cell. In as much as we want people to be cured from this horrible disease, we think this information is vital to providing the right treatment to COVID-19 patients. Yes, the three drug regimen may be showing some positive results, but they are not conclusive until they can be demonstrated in clinical trials. For now, these drugs are proving the much needed relief to coronavirus patients.

Vitamin D on Prevention and Treatment of COVID-19

Vitamin D on Prevention and Treatment of COVID-19 (COVITD-19)

Brief Summary:
The new outbreak of the SARS-CoV-2 coronavirus is causing an important pandemic affecting a large number of people all-over the world. Vitamin D is a hormone precursor produced by our own body with the help of sunlight which has an important role on adaptive immunity and cellular differentiation, maturation and proliferation of several immune cells. Reduced levels of vitamin D in calves were positioned as the main cause of bovine coronavirus infection in the past. Therefore, it seems plausible that the use of vitamin D as a nutritional ergogenic aid could be a potential intervention to fight against COVID-19 infected patients which remain asymptomatic or which have non-severe and severe symptoms. This study aims to investigate whether the use of vitamin D as an immune modulator agent induces significant improvements of health status and outcomes in non-severe symptomatic patients infected with COVID-19 as well as preventing COVID-19 health deterioration. We hypothesize that vitamin D will significantly improve hard endpoints related to COVID-19 deleterious consequences compared with a usual care control group.

 

Modulation of the Immune Response to Respiratory Viruses by Vitamin D

Abstract

Background: Vitamin D deficiency has been shown to be independently associated with increased risk of viral acute respiratory infection (ARI) in a number of observational studies, and meta-analysis of clinical trials of vitamin D supplementation for prevention of ARI has demonstrated protective effects. Several cellular studies have investigated the effects of vitamin D metabolites on immune responses to respiratory viruses, but syntheses of these reports are lacking. Scope: In this article, we review the literature reporting results of in vitro experiments investigating immunomodulatory actions of vitamin D metabolites in human respiratory epithelial cells infected with respiratory viruses. Key findings: Vitamin D metabolites do not consistently influence replication or clearance of rhinovirus, respiratory syncytial virus (RSV) or influenza A virus in human respiratory epithelial cell culture, although they do modulate expression and secretion of type 1 interferon, chemokines including CXCL8 and CXCL10 and pro-inflammatory cytokines, such as TNF and IL-6. Future research: More studies are needed to clarify the effects of vitamin D metabolites on respiratory virus-induced expression of cell surface markers mediating viral entry and bacterial adhesion to respiratory epithelial cells.

Keywords: vitamin D, respiratory viruses, antiviral immunity

The Canada Connection: Quercetin & COVID-19

Potential Treatments (antivirals, antibodies, etc):

Efficacy and safety of current therapeutic options for COVID-19 – lessons to be learnt from SARS and MERS epidemic: A systematic review and meta-analysis.

Zhong H, Wang Y, Zhang ZL, et al.  Pharmacol Res. 2020 Apr 30:104872. doi: 10.1016/j.phrs.2020.104872.

Abstract

The rapidly progressing of coronavirus disease 2019 (COVID-19) pandemic has become a global concern. This meta-analysis aimed at evaluating the efficacy and safety of current option of therapies for severe acute respiratory syndrome (SARS), Middle Eastern respiratory syndrome (MERS) besides COVID-19, in an attempt to identify promising therapy for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infected patients. We searched PubMed, EMBASE, Cochrane Library, China National Knowledge Infrastructure (CNKI), China Science and Technology Journal Database (VIP), and WANFANG DATA for randomized controlled trials (RCTs), prospective cohort, and retrospective cohort studies that evaluated therapies (hydroxychloroquine, lopinavir/ritonavir-based therapy, and ribavirin-based therapy, etc.) for SARS, MERS, and COVID-19. The primary outcomes were mortality, virological eradication and clinical improvement, and secondary outcomes were improvement of symptoms and chest radiography results, incidence of acute respiratory disease syndrome (ARDS), utilization of mechanical ventilation, and adverse events (AEs). Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random-effects models, and the quality of evidence was appraised using GRADEpro. Eighteen articles (5 RCTs, 2 prospective cohort studies, and 11 retrospective cohort studies) involving 4,941 patients were included. Compared with control treatment, anti-coronary virus interventions significantly reduced mortality (RR 0.65, 95% CI 0.44-0.96; I2 = 81.3%), remarkably ameliorate clinical improvement (RR 1.52, 95% CI 1.05-2.19) and radiographical improvement (RR 1.62, 95% CI 1.11-2.36, I2 = 11.0 %), without manifesting clear effect on virological eradication, incidence of ARDS, intubation, and AEs. Subgroup analyses demonstrated that the combination of ribavirin and corticosteroids remarkably decreased mortality (RR 0.43, 95% CI 0.27-0.68). The lopinavir/ritonavir-based combination showed superior virological eradication and radiographical improvement with reduced rate of ARDS. Likewise, hydroxychloroquine improved radiographical result. For safety, ribavirin could induce more bradycardia, anemia and transaminitis. Meanwhile, hydroxychloroquine could increase AEs rate especially diarrhea. Overall, the quality of evidence on most outcomes were very low. In conclusion, although we could not draw a clear conclusion for the recommendation of potential therapies for COVID-19 considering the very low quality of evidence and wide heterogeneity of interventions and indications, our results may help clinicians to comprehensively understand the advantages and drawbacks of each anti-coronavirus agents on efficacy and safety profiles. Lopinavir/ritonavir combinations might observe better virological eradication capability than other anti-coronavirus agents. Conversely, ribavirin might cause more safety concerns especially bradycardia. Thus, large RCTs objectively assessing the efficacy of antiviral therapies for SARS-CoV-2 infections should be conducted with high priority.

Convalescent plasma transfusion for the treatment of COVID-19: Systematic review.

Rajendran K, Narayanasamy K, Rangarajan J, et al.  J Med Virol. 2020 May 1. doi: 10.1002/jmv.25961.

Abstract

BACKGROUND: The recent emergence of COVID-19 pandemic has reassessed the usefulness of historic convalescent plasma transfusion (CPT). This review was conducted to evaluate the effectiveness of CPT therapy in COVID-19 patients based on the publications reported till date. To our knowledge, this is the first systematic review on convalescent plasma on clinically relevant outcomes in individuals with COVID-19.

METHODS: PubMed, EMBASE and Medline databases were searched upto 19 April 2020. All records were screened as per the protocol eligibility criteria.

RESULTS: We included 5 studies reporting CPT to COVID-19 patients. The main findings from available data are as follows: (1) Convalescent plasma may reduce mortality in critically ill patients (2) Increase in neutralizing antibody titers and disappearance of SARS-CoV-2 RNA was observed in almost all the patients after CPT therapy (3) Beneficial effect on clinical symptoms after administration of convalescent plasma.

CONCLUSIONS: Based on the limited scientific data, CPT therapy in COVID-19 patient appears safe, clinically effective and reduces mortality. Well-designed large multi center clinical trial studies should be conducted urgently to establish the efficacy of CPT to COVID-19 patients. This article is protected by copyright. All rights reserved.

Antiviral therapy in management of COVID-19: a systematic review on current evidence 

Yousefifard M, Zali A, Mohamed Ali K, et al. 

Arch Acad Emerg Med. 2020 Apr 6;8(1):e45. eCollection 2020.Abstract

Background: The purpose of the current systematic review is to evaluate the efficacy of antiviral therapies in treatment of COVID-19. In addition, clinical trials on the efficacy of antiviral therapies in the management of Severe Acute Respiratory Syndrome coronavirus (SARS-Cov) or Middle East Respiratory Syndrome coronavirus (MERS-CoV) have also been reviewed, in order to identify potential treatment options for COVID-19.

Method: An extensive search was performed in Medline, Embase, Scopus, Web of Science and CENTRAL databases until the end of March 15, 2020. Two independent researchers performed the screening, and finally the related studies were included.

Results: Only one clinical trial on the efficacy of antiviral therapy in management of COVID-19 was found. The results depicted that adding Lopinavir-Ritonavir to the standard treatment regimen of patients with severe COVID-19 has no benefits. Moreover, 21 case-series and case-report studies reported the prescription of antiviral agents in COVID-19, none of which can be used to determine the efficacy of antiviral therapies in confronting COVID-19. In addition, no clinical trials were found to be performed on the efficacy of antiviral agents in the management of SARS-CoV and MERS-CoV.

Conclusion: The current evidence impede researchers from proposing an appropriate antiviral therapy against COVID-19, making the current situation a serious concern for international organizations such as World Health Organization (WHO). In the time of the current pandemic and future epidemics, organizations such as WHO should pursue more proactive actions and plan well-designed clinical trials so that their results can be used in managing future epidemics.

Neutralizing antibody responses to SARS-CoV-2 in a COVID-19 recovered patient cohort and their implications

Fan Wu, Aojie Wang, Mei Liu, Qimin Wang, Jun Chen, Shuai Xia, Yun Ling, Yuling Zhang, Jingna Xun, Lu Lu, Shibo Jiang, Hongzhou Lu, Yumei Wen, Jinghe Huang

Abstract

Background The COVID-19 pandemic caused by SARS-CoV-2 coronavirus threatens global public health. Currently, neutralizing antibodies (NAbs) versus this virus are expected to correlate with recovery and protection of this disease. However, the characteristics of these antibodies have not been well studied in association with the clinical manifestations in patients. Methods Plasma collected from 175 COVID-19 recovered patients with mild symptoms were screened using a safe and sensitive pseudotyped-lentiviral-vector-based neutralization assay. Spike-binding antibody in plasma were determined by ELISA using RBD, S1, and S2 proteins of SARS-CoV-2. The levels and the time course of SARS-CoV-2-specific NAbs and the spike-binding antibodies were monitored at the same time. Findings SARS-CoV-2 NAbs were unable to cross-reactive with SARS-CoV virus. SARS-CoV-2-specific NAbs were detected in patients from day 10-15 after the onset of the disease and remained thereafter. The titers of NAb among these patients correlated with the spike-binding antibodies targeting S1, RBD, and S2 regions. The titers of NAbs were variable in different patients. Elderly and middle-age patients had significantly higher plasma NAb titers (P<0.0001) and spike-binding antibodies (P=0.0003) than young patients. Notably, among these patients, there were ten patients whose NAb titers were under the detectable level of our assay (ID50: < 40); while in contrast, two patients, showed very high titers of NAb, with ID50 :15989 and 21567 respectively. The NAb titers were positive correlated with plasma CRP levels but negative correlated with the lymphocyte counts of patients at the time of admission, indicating an association between humoral response and cellular immune response. Interpretation The variations of SARS-CoV-2 specific NAbs in recovered COVID-19 patients may raise the concern about the role of NAbs on disease progression. The correlation of NAb titers with age, lymphocyte counts, and blood CRP levels suggested that the interplay between virus and host immune response in coronavirus infections should be further explored for the development of effective vaccine against SARS-CoV-2 virus. Furthermore, titration of NAb is helpful prior to the use of convalescent plasma for prevention or treatment. Funding Ministry of Science and Technology of China, National Natural Science Foundation of China, Shanghai Municipal Health Commission, and Chinese Academy of Medical Sciences

Hydroxychloroquine misinformation makes way for political disinformation

Antiviral Therapy in Management of COVID-19: A Systematic Review on Current Evidence

Affiliations 
    • PMID: 32309809

 

Abstract

Background: The purpose of the current systematic review is to evaluate the efficacy of antiviral therapies in treatment of COVID-19. In addition, clinical trials on the efficacy of antiviral therapies in the management of Severe Acute Respiratory Syndrome coronavirus (SARS-Cov) or Middle East Respiratory Syndrome coronavirus (MERS-CoV) have also been reviewed, in order to identify potential treatment options for COVID-19.

Method: An extensive search was performed in Medline, Embase, Scopus, Web of Science and CENTRAL databases until the end of March 15, 2020. Two independent researchers performed the screening, and finally the related studies were included.

Results: Only one clinical trial on the efficacy of antiviral therapy in management of COVID-19 was found. The results depicted that adding Lopinavir-Ritonavir to the standard treatment regimen of patients with severe COVID-19 has no benefits. Moreover, 21 case-series and case-report studies reported the prescription of antiviral agents in COVID-19, none of which can be used to determine the efficacy of antiviral therapies in confronting COVID-19. In addition, no clinical trials were found to be performed on the efficacy of antiviral agents in the management of SARS-CoV and MERS-CoV.

Conclusion: The current evidence impede researchers from proposing an appropriate antiviral therapy against COVID-19, making the current situation a serious concern for international organizations such as World Health Organization (WHO). In the time of the current pandemic and future epidemics, organizations such as WHO should pursue more proactive actions and plan well-designed clinical trials so that their results can be used in managing future epidemics.

Keywords: Antiviral Therapy; COVID-19; Treatment.

To Ventilate or Not to Ventilate?

Special Report: As virus advances, doctors rethink rush to ventilate

Silvia Aloisi, Deena Beasley, Gabriella Borter, Thomas Escritt and Kate Kelland

A CT scan picture shows lungs of 48-year-old coronavirus disease (COVID-19) patient Andre Bergmann, in this screen grab released on April 14, 2020 by the Bethanien Hospital lung clinic in Moers, Germany. HOSPITAL BETHANIEN MOERS/THOMAS VOSHAAR/Handout via
REUTERS
Thomas Voshaar, head doctor of the Lung Clinic at the Bethanien Hospital in Moers, Germany poses in this undated handout picture. Bethanien Hospital/Handout via
REUTERS
BERLIN (Reuters) – When he was diagnosed with COVID-19, Andre Bergmann knew exactly where he wanted to be treated: the Bethanien hospital lung clinic in Moers, near his home in northwestern Germany.

The clinic is known for its reluctance to put patients with breathing difficulties on mechanical ventilators – the kind that involve tubes down the throat.

The 48-year-old physician, father of two and aspiring triathlete worried that an invasive ventilator would be harmful. But soon after entering the clinic, Bergmann said, he struggled to breathe even with an oxygen mask, and felt so sick the ventilator seemed inevitable.

Even so, his doctors never put him on a machine that would breathe for him. A week later, he was well enough to go home.

Felines & COVID-19

Tigers (and other cats) can catch the coronavirus

What cat-adoring people should know

Malayan tiger cub in its enclosure at the Bronx Zoo. It’s unclear whether this is one of the tigers that was exposed to the novel coronavirus. 

Photo by Andrew Lichtenstein / Corbis via Getty Images

When I heard that a tiger at the Bronx Zoo tested positive for COVID-19, I started to worry about my own little lion, a tabby cat with asthma. I’ve sequestered myself away from friends and family, but could my company be unwittingly putting my cat at risk? While there have been some cases of animals contracting COVID-19, it’s rare — and there are precautions that pet owners can take if they’re worried about their furry family members.

Coronaviruses are zoonotic, which means that they can be passed between animals and humans. In New York City, the virus apparently jumped from an asymptomatic human to three lions and four tigers, including four-year-old tiger Nadia, that tested positive for the virus. The zoo says it expects all of the animals to make full recoveries.

The Real Reason Veterinarians Gave a Tiger a Covid-19 Test

It’s hard for humans in New York City to get a test for the coronavirus. So when a Bronx Zoo tiger tested positive for Covid-19, it invited some questions.

a tiger in the bronx zoo

Earlier this month, a tiger at the Bronx Zoo (not necessarily this tiger), tested positive for the coronavirus. PHOTOGRAPH: JAMES DEVANEY/GETTY IMAGES

NADIA HAD A cough. A dry cough, to be specific, and it wasn’t just her. The 4-year-old Malayan tiger lives in an exhibit in the Bronx Zoo with her sister, Azul, who had also started coughing at the end of March. Altogether, seven of the zoo’s big cats appeared ill, two Amur tigers and three African lions in addition to Nadia and Azul. They neglected their meals. They wheezed. And they worried their keepers. Fears over the spread of the coronavirus had already led the zoo to close its doors to the public starting in mid-March. Once Nadia and the other cats began showing symptoms, the remaining staff wanted to find the source of their malaise.

“Nadia was not coming around and was getting a little worse, so we anesthetized her in order to treat her,” Bronx Zoo veterinarian Paul Calle says. “We did x-rays and ultrasounds. We did blood work. We ran lots of tests, panels for normal domestic cat infectious diseases.” Although the Covid-19 pandemic had hit humans living in areas around the zoo hard, it wasn’t initially assumed to be the likely culprit. After all, no animal in the United States had been known to catch the disease. It wasn’t even clear a tiger could contract it. But with so many cases in the city, the team decided to test for SARS-Cov-2, the coronavirus that causes Covid-19, just to be sure.