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Dennis OConnor

The Coming Influenza Pandemic: Lessons From the Past for the Future | The Journal of th... - 0 views

jaoa.org/article.aspx

online-homeschool-covid research osteopathy

shared by Dennis OConnor on 19 Mar 20 - No Cached
  • in the case of a true pandemic, hospital capacity may well be overwhelmed, and healthcare workers may themselves become ill. 
  • However, the lessons learned within the osteopathic medical profession as a result of the 1917-1918 pandemic could prove useful once again if (or when) a new influenza pandemic occurs.
  • Time to roll up sleeves, vaccinate patients, and hone osteopathic manipulative skills
  • ...14 more annotations...
  • Obviously, the data collected shortly after the 1917-1918 pandemic must be treated cautiously.
  • In 1918, C.P. McConnell, DO,11 reported that the most effective treatment during the influenza pandemic was begun early in the onset of symptoms (within the first 24 hours) and consisted of carefully applied muscular relaxation and, most importantly, relaxation of the deep and extensive contractions of the deep spinal musculature and mobilization of the spine. These treatments would be repeated two or three times early in the course of the infection, along with traditional supportive measures such as hydration. During later influenza epidemics, such as the 1928-1929 and the 1936-1937 outbreaks, various lymphatic pump treatments and more attention to the cervical and upper thoracic regions were added to this recommended treatment protocol.12 These treatments, individualized to each patient's needs, were apparently the most commonly applied osteopathic medical procedures during the epidemics. 
  • action of these treatments were to diminish somatic inputs from contracted muscles
  • that had further stimulated the already overactive sympathetic system
  • hyperreactivity exacerbated the counterproductive and deadly immune respons
  • OMT) likely enhanced lymphatic drainage and encouraged appropriate immune response
  • we have no controlled data on the effects of OMT on the pandemic influenza
  • Noll et al13 demonstrated that OMT given to elderly patients with pneumonia decreases medication use and hospital stay
  • Whatever the mechanism, these beneficial outcomes have taught us a great deal about how the osteopathic medical profession might handle a coming pandemic.
  • treatments used back then can be used again and do not require patient hospitalization
  • methods can also be taught to family members
  • do not rely on the availability of potent, expensive, and often harmful (especially when one is in a weakened condition) medications.
  • treatments can be delivered by osteopathic medical students under the direction of a physician—a measure that would add significantly to the pool of trained healthcare providers available to assist the public in such an emergency.
  • OMT is meant to improve function, enabling the body itself to better
Dennis OConnor

Using influenza surveillance networks to estimate state-specific prevalence of SARS-CoV... - 0 views

stm.sciencemag.org/...scitranslmed.abc1126

data covid

shared by Dennis OConnor on 24 Jun 20 - No Cached
  • Dennis OConnor on 24 Jun 20
     
    "Abstract Detection of SARS-CoV-2 infections to date has relied heavily on RT-PCR testing. However, limited test availability, high false-negative rates, and the existence of asymptomatic or sub-clinical infections have resulted in an under-counting of the true prevalence of SARS-CoV-2. Here, we show how influenza-like illness (ILI) outpatient surveillance data can be used to estimate the prevalence of SARS-CoV-2. We found a surge of non-influenza ILI above the seasonal average in March 2020 and showed that this surge correlated with COVID-19 case counts across states. If 1/3 of patients infected with SARS-CoV-2 in the US sought care, this ILI surge would have corresponded to more than 8.7 million new SARS-CoV-2 infections across the US during the three-week period from March 8 to March 28, 2020. Combining excess ILI counts with the date of onset of community transmission in the US, we also show that the early epidemic in the US was unlikely to have been doubling slower than every 4 days. Together these results suggest a conceptual model for the COVID-19 epidemic in the US characterized by rapid spread across the US with over 80% infected patients remaining undetected. We emphasize the importance of testing these findings with seroprevalence data and discuss the broader potential to use syndromic surveillance for early detection and understanding of emerging infectious diseases."
Dennis OConnor

Osteopathy and Spainsh Influenza.pdf - 1 views

osteopathy influenza research

shared by Dennis OConnor on 19 Mar 20 - No Cached
  • Dennis OConnor on 19 Mar 20
     
    Dr. Michael Kurisu D.O. - This is an article that is well known in our Osteopathic community. Seems to be quite relevant in today's crisis. Although… there are several shortcomings to this article. - it was published over a century ago - it is a retrospective analysis - they did have or keep good public health data on infectivity and virulence and positive tests (We STILL DONT DO THIS!!!) - there is no documentation about what techniques used etc… Nonetheless… for an article that is over 100 years old, it IS a data point. And the data from back then shows that during Spanish influenza… the patients who saw a D.O. had a medical death rate that was 40X lower than the general population… Just another reason to have good D.Os around in the primary care workforce.
Dennis OConnor

What The 1918 Flu Pandemic Can Tell Us About The COVID-19 Crisis : NPR - 0 views

www.npr.org/...l-us-about-the-covid-19-crisis

covid pandemic

shared by Dennis OConnor on 05 Aug 20 - No Cached
  • Dennis OConnor on 05 Aug 20
     
    "John Barry, author of the 2004 book, The Great Influenza, draws parallels between today's pandemic and the flu of 1918. In both cases, he says, "the outbreak was trivialized for a long time.""
Dennis OConnor

about - COVID HUMAN GENETIC EFFORT - 0 views

www.covidhge.com/about

genetics covid research SARS-CoV-2

shared by Dennis OConnor on 15 May 20 - No Cached
  • Dennis OConnor on 15 May 20
     
    Recommended by DeAunne Denmark, MD. Phd. : Summary of Our Work For many years, up to 25 years for some, members of the COVID Human Genetic Effort have studied the human genetic basis of life-threatening diseases striking previously healthy human beings in the course of primary infection by a variety of viruses, bacteria, fungi, or parasites. In particular, we and others have identified monogenic inborn errors of immunity (IEI) that selectively underlie life-threatening or lethal viral diseases in previously healthy children or adults, including various severe diseases caused by Epstein-Barr virus, herpes simplex virus encephalitis, varicella zoster virus encephalitis, fulminant hepatitis due to hepatitis A virus, lethal primary infection by cytomegalovirus, severe pneumonitis due to influenza virus or rhinovirus, beta-papillomavirus-driven skin cancer, human herpes virus 8-driven Kaposi sarcoma, and others (see references below).
Dennis OConnor

Harnessing wearable device data to improve state-level real-time surveillance of influe... - 0 views

www.thelancet.com/...fulltext

testing research data health tracking

shared by Dennis OConnor on 06 Apr 20 - No Cached
  • Dennis OConnor on 06 Apr 20
     
    "Jennifer M Radin, PhD Nathan E Wineinger, PhD Prof Eric J Topol, MD Steven R Steinhubl, MD"
Dennis OConnor

What We Know So Far About SARS-CoV-2 - The Atlantic - 0 views

www.theatlantic.com/...608338

covid research testing

shared by Dennis OConnor on 23 Mar 20 - No Cached
  • March 20, 2020
  • One of the few mercies during this crisis is that, by their nature, individual coronaviruses are easily destroyed.
  • These viruses don’t endure in the world. They need bodies.
  • ...30 more annotations...
  • To be clear, SARS-CoV-2 is not the flu. It causes a disease with different symptoms, spreads and kills more readily,
  • his family, the coronaviruses, includes just six other members that infect humans
  • OC43, HKU1, NL63, and 229E—have been gently annoying humans for more than a century, causing a third of common colds
  • MERS and SARS (or “SARS-classic,” as some virologists have started calling it)—both cause far more severe disease.
  • hy was this seventh coronavirus the one to go pandemic?
  • The structure of the virus provides some clues about its success. In shape, it’s essentially a spiky ball. Those spikes recognize and stick to a protein called ACE2
  • This is the first step to an infection
  • he exact contours of SARS-CoV-2’s spikes allow it to stick far more strongly to ACE2 than SARS-classic did
  • But in SARS-CoV-2, the bridge that connects the two halves can be easily cut by an enzyme called furin, which is made by human cells and—crucially—is found across many tissues. “This is probably important for some of the really unusual things we see in this virus,” says Kristian Andersen of Scripps Research Translational Institute.
  • SARS-CoV-2 seems to infect both upper and lower airways,
  • his double whammy could also conceivably explain why the virus can spread between people before symptoms show up
  • All of this is plausible but totally hypothetical; the virus was only discovered in January, and most of its biology is still a mystery.
  • The closest wild relative of SARS-CoV-2 is found in bats, which suggests it originated in a bat, then jumped to humans either directly or through another species.
  • Another coronavirus found in wild pangolins also resembles SARS-CoV-2
  • Indeed, why some coronaviruses are deadly and some are not is unclear. “There’s really no understanding at all of why SARS or SARS-CoV-2 are so bad but OC43 just gives you a runny nose,” Frieman says.
  • Once in the body, it likely attacks the ACE2-bearing cells that line our airways.
  • The immune system fights back and attacks the virus; this is what causes inflammation and fever
  • in extreme cases, the immune system goes berserk
  • These damaging overreactions are called cytokine storms.
  • they’re probably behind the most severe cases of COVID-19.
  • During a cytokine storm, the immune system isn’t just going berserk but is also generally off its game, attacking at will without hitting the right targets.
  • But why do some people with COVID-19 get incredibly sick, while others escape with mild or nonexistent symptoms
  • Age is a factor.
  • other factors—a person’s genes, the vagaries of their immune system, the amount of virus they’re exposed to, the other microbes in their bodies
  • “it’s a mystery why some people have mild disease, even within the same age group,”
  • Coronaviruses, much like influenza, tend to be winter viruses.
  • In the heat and humidity of summer, both trends reverse, and respiratory viruses struggle to get a foothold.
  • irus is tearing through a world of immunologically naive people, and that vulnerability is likely to swamp any seasonal variations.
  • And one recent modeling study concluded that “SARS-CoV-2 can proliferate at any time of year.
  • Unless people can slow the spread of the virus by sticking to physical-distancing recommendations, the summer alone won’t save us.
  • Dennis OConnor on 23 Mar 20
     
    Dr. Michael Kurisu D.O.: We've known about SARS-CoV-2 for only three months, but scientists can make some educated guesses about where it came from and why it's behaving in such an extreme way.
Dennis OConnor

In the coronavirus pandemic, we're making decisions without reliable data - 4 views

www.statnews.com/...ecisions-without-reliable-data

covid testing research pandemic data

shared by Dennis OConnor on 19 Mar 20 - No Cached
  • A fiasco in the making? As the coronavirus pandemic takes hold, we are making decisions without reliable data
  • This evidence fiasco creates tremendous uncertainty about the risk of dying from Covid-19.
  • As most health systems have limited testing capacity, selection bias may even worsen in the near future.
  • ...8 more annotations...
  • The one situation where an entire, closed population was tested was the Diamond Princess cruise ship and its quarantine passengers. The case fatality rate there was 1.0%, but this was a largely elderly population, in which the death rate from Covid-19 is much higher.
  • Projecting the Diamond Princess mortality rate onto the age structure of the U.S. population, the death rate among people infected with Covid-19 would be 0.125%. But since this estimate is based on extremely thin data — there were just seven deaths among the 700 infected passengers and crew — the real death rate could stretch from five times lower (0.025%) to five times higher (0.625%).
  • Although successful surveillance systems have long existed for influenza, the disease is confirmed by a laboratory in a tiny minority of cases.
  • Some worry that the 68 deaths from Covid-19 in the U.S. as of March 1610 will increase exponentially to 680, 6,800, 68,000, 680,000 … along with similar catastrophic patterns around the globe. Is that a realistic scenario, or bad science fiction? How can we tell at what point such a curve might stop?
  • In the absence of data, prepare-for-the-worst reasoning leads to extreme measures of social distancing and lockdowns.
  • This has been the perspective behind the different stance of the United Kingdom keeping schools open12, at least until as I write this. In the absence of data on the real course of the epidemic, we don’t know whether this perspective was brilliant or catastrophic.
  • One of the bottom lines is that we don’t know how long social distancing measures and lockdowns can be maintained without major consequences to the economy, society, and mental health.
  • At a minimum, we need unbiased prevalence and incidence data for the evolving infectious load to guide decision-making.
  • Dennis OConnor on 19 Mar 20
     
    Dr. Michael Kurisu D.O. "My take is this article is written by a very credible source. John P.A. Ioannidis is from Stanford and great resource. Makes argument that we are basing a LOT of our decisions on faulty or NO data ! Its fascinating to me that there has been less than 10,000 deaths globally and we have had SO MUCH DISRUPTION in the economy. I definitely feel we should be tracking the amount of deaths that are going to occur from people that will be pushed into poverty as well as the number of people being denied access to medical care right now. Yes… with COVID19, it CAN get much worse…. But maybe not… we don't know yet. This article actually increased my morale and put me on track to help GET MORE DATA. Then we can make informed decisions. And then TRACK ALL THE DATA moving forward.
  • Dennis OConnor on 19 Mar 20
     
    DeAunne Denmark, MD, PhD, "Excellent piece spelling out the pervasive and critical issues due to abysmal lack/tardiness in US testing, especially of large populations where initial outbreaks occurred, for those both visibly sick and not. And most importantly, healthcare workers. We cannot even begin to estimate CFR, much less develop reliable projection models, without valid data on everybody who is carrying. "The most valuable piece of information for answering those questions would be to know the current prevalence of the infection in a random sample of a population and to repeat this exercise at regular time intervals to estimate the incidence of new infections."
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