a really bad flu

Flu: The Story of the Great Influenza Pandemic of 1918 and the Search for the Virus That Caused It

…Alfred Crosby, puzzling over the epidemic’s impact, went to the Reader’s Guide to Periodical Literature from 1919 to 1921 and counted the column inches devoted to the influenza epidemic as compared with other topics. There were, he wrote, 13 inches citing articles on baseball, 20 inches on Bolshevism, and 47 on Prohibition. Just 8 inches of citations referred to the flu.

Crosby looked at a recent edition of the Encyclopaedia Britannica. The 1918 flu got three sentences. He looked at a recent edition of the Encyclopedia Americana. One sentence was devoted to the flu, and it said that the epidemic killed 21 million people. “That was a gross understatement,” Crosby says. But even so, he remarks, “21 million people? One sentence? Hello?”

…In asking why, Crosby proposes a combination of factors that, he said, acting together accounted for the world’s collective amnesia. For one, he argues, In asking why, Crosby proposes a combination of factors that, he said, acting together accounted for the world’s collective amnesia. For one, he argues, argues, the epidemic simply was so dreadful and so rolled up in people’s minds with the horrors of the war that most people did not want to think about it or write about it once the terrible year of 1918 was over. The flu blended into the general nightmare of World War I, an unprecedented event that introduced trench warfare, submarines, the bloody battles of the Somme and Verdun, and the horrors of chemical warfare.

The sickness preyed on the young and healthy. One day you are fine, strong, and invulnerable. You might be busy at work in your office. Or maybe you are knitting a scarf for the brave troops fighting the war to end all wars. Or maybe you are a soldier reporting for basic training, your first time away from home and family. You might notice a dull headache. Your eyes might start to burn. You start to shiver and you will take to your bed, curling up in a ball. But no amount of blankets can keep you warm. You fall into a restless sleep, dreaming the distorted nightmares of delirium as your fever climbs. And when you drift out of sleep, into a sort of semi-consciousness, your muscles will ache and your head will throb and you will somehow know that, step by step, as your body feebly cries out “no,” you are moving steadily toward death. It may take a few days, it may take a few hours, but there is nothing that can stop the disease’s progress. Doctors and nurses have learned to spot the signs. Your face turns a dark brownish purple. You start to cough up blood. Your feet turn black. Finally, as the end nears, you frantically gasp for breath. A blood-tinged saliva bubbles out of your mouth. You die—by drowning, actually—as your lungs fill with a reddish fluid.

And when a doctor does an autopsy, he will observe your lungs lying heavy and sodden in your chest, engorged with a thin bloody liquid, useless, like slabs of liver. They called the plague of 1918 influenza, but it was like no influenza ever seen before. It was more like a biblical prophecy come true, something from Revelations that predicted that first the world was to be struck by war, then famine, and then, with the breaking of the fourth seal of the scroll foretelling the future, the appearance of a horse, “deathly pale, and its rider was called Plague, and Hades followed at its heels.”

Alveolar phase of COVID-19

COVID-19 can be divided into three clinical stages, and one can speculate that these stages correlate with where the infection resides. For the asymptomatic phase, the infection mostly resides in the nose, where it elicits a minimal innate immune response. For the mildly symptomatic phase, the infection is mostly in the pseudostratified epithelium of the larger airways and is accompanied by a more vigorous innate immune response. In the conducting airways, the epithelium can recover from the infection, because the keratin 5 basal cells are spared and they are the progenitor cells for the bronchial epithelium. There may be more severe disease in the bronchioles, where the club cells are likely infected. The devastating third phase is in the gas exchange units of the lung, where ACE2-expressing alveolar type II cells and perhaps type I cells are infected.

The first phase of the disease is in the nose. Here the virus likely infects ciliated and secretory cells, replicates, but apparently does not induce a vigorous innate immune response.

The second phase of COVID-19 takes place along the conducting airways, the bronchi and bronchioles. The virus infects ciliated cells as the disease progresses deeper into the lung. SARS-CoV-1 infects ciliated but not mucus cells in air-liquid interface cultures.

The third phase of the disease is the lethal phase, as the infection spreads into the gas exchange portion of the lung and infects alveolar type II cells.

Gastrointestinal aspects of COVID

Prevalence of Gastrointestinal Symptoms and Fecal Viral Shedding in Patients With Coronavirus Disease 2019

These findings suggest that patients with SARS-CoV-2 infection can present with gastrointestinal symptoms with possible fecal-oral route of transmission due to the presence of viral RNA in stool.

These findings suggest that that 12% of patients with COVID-19 will manifest GI symptoms; however, SAR-CoV-2 shedding was observed in 40.5% of patients with confirmed SARS-CoV-2 infection. This highlights the need to better understand what measures are needed to prevent further spread of this highly contagious pathogen.

This raises the question of inadvertent human-to-human transmission via the fecal route despite public health emphasis on droplet transmission and precautions for contact with respiratory secretions. Hence, additional information and understanding the involvement of the digestive system in transmission of COVID-19 during this pandemic would be useful.

COVID-19 and the gastrointestinal tract: more than meets the eye

In about 50% of COVID-19 cases, the presence of SARS-CoV-2 in faecal samples and detection of SARS-CoV-2 in intestinal mucosa of infected patients suggest that enteric symptoms could be caused by invasion of ACE2 expressing enterocytes and the GI tract may be an alternative route of infection. In over half of the patients, faecal samples remained positive for SARS-CoV2 RNA for a mean of 11 days after clearance of respiratory tract samples.

Coronavirus SARS-CoV-2 infects cells of the intestine

https://www.sciencedaily.com/releases/2020/05/200504091438.htm

Researchers from the Hubrecht Institute in Utrecht, Erasmus MC University Medical Center Rotterdam, and Maastricht University in the Netherlands have found that the coronavirus SARS-CoV-2, which causes COVID-19, can infect cells of the intestine and multiply there.

Asymptomatic Spread Revisited

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…On June 7, Dr. Maria Van Kerkhove, head of the WHO’s emerging diseases and zoonosis unit, told a press conference that from the known research, asymptomatic spread was “very rare.” “From the data we have, it still seems to be rare that an asymptomatic person actually transmits onward to a secondary individual.” She added for emphasis: “It’s very rare.”


Post-lockdown SARS-CoV-2 nucleic acid screening in nearly ten million residents of Wuhan, China

…In summary, the detection rate of asymptomatic positive cases in the post-lockdown Wuhan was very low (0.303/10,000), and there was no evidence that the identified asymptomatic positive cases were infectious. These findings enabled decision makers to adjust prevention and control strategies in the post-lockdown period. Further studies are required to fully evaluate the impacts and cost-effectiveness of the citywide screening of SARS-CoV-2 infections on population’s health, health behaviours, economy, and society.

What's the Frequency?

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Description of the problem: WHO has received user feedback on an elevated risk for false SARS-CoV-2 results when testing specimens using RT-PCR reagents on open systems.  

As with any diagnostic procedure, the positive and negative predictive values for the product in a given testing population are important to note. As the positivity rate for SARS-CoV-2 decreases, the positive predictive value also decreases. This means that the probability that a person who has a positive result (SARS-CoV-2 detected) is truly infected with SARS-CoV-2 decreases as positivity rate decreases, irrespective of the assay specificity. Therefore, healthcare providers are encouraged to take into consideration testing results along with clinical signs and symptoms, confirmed status of any contacts, etc.

But, What’s the Frequency?!!!

What number of Amplification Cycles being used in the PCR tests?

Mathematics of Testing

Marshall Project (digesting the numbers)

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…One in every five state and federal prisoners in the United States has tested positive for the coronavirus, a rate more than four times as high as the general population.

…As the pandemic enters its tenth month—and as the first Americans begin to receive a long-awaited COVID-19 vaccine—at least 275,000 prisoners have been infected, more than 1,700 have died and the spread of the virus behind bars shows no sign of slowing.

(Without information on rate of influx or release, will assume steady-state. -rws)

Deriving from the above:

numeric type
1,375,000Total Population
275,000Infections
1,700Deaths
20%Infection Ratio
0.62%Death/Infection Ratio
0.12%Death/ Prison Population Ratio

Separately….

Counts of COVID-19 cases and presumed or confirmed deaths among prisoners were collected daily by the UCLA Law COVID-19 Behind Bars Data Project from March 31, 2020, to June 6, 2020.

Novel coronavirus disease 2019 (COVID-19) represents a challenge to prisons because of close confinement, limited access to personal protective equipment, and elevated burden of cardiac and respiratory conditions that exacerbate COVID-19 risk among prisoners…. systematic data are lacking

The COVID-19 case rate for prisoners was 5.5 times higher than the US population case rate of 587 per 100 000. The crude COVID-19 death rate in prisons was 39 deaths per 100,000 prisoners, which was higher than the US population rate of 29 deaths per 100,000.

[As is age and morbidity data is not detailed, would require deeper analysis to interpret a 5.5 times higher case rate but only a 1.3 times higher death rate. Additionally, it would seem appropriate to consider this data in the context of historical general prison health/death figures. -rws]

Mortality in State and Federal Prisons, 2001-2016 – Statistical Tables

In 2016, a total of 4,117 state and federal prisoners died in publicly or privately operated prisons.

From 2015 to 2016, deaths in state prisons increased from 296 to 303 deaths per 100,000 state prisoners. [~ 0.30%]

From 2015 to 2016, deaths in federal prisons decreased for the first time since 2012, from 283 to 252 deaths per 100,000 federal prisoners. [~ 0.25%]

Illness-related deaths made up 86% of deaths in state prisons in 2016, with more than half of those being due to cancer (30% of all deaths) or heart disease (28%).