Apr 7, 2020,05:34pm EDT
The COVID-19 Coronavirus Disease May Be Twice As Contagious As We Thought

A single person with COVID-19 may be more likely to infect up to 5 or 6 other people, rather than 2 or 3, suggests a new study of Chinese data from the CDC. It’s not clear if this higher number applies only to the cases in China or if it will be similar in other countries.

If the higher number does remain true elsewhere, it means that more people in a population need to be immune from the disease—either from having already had it or from a vaccine—to stop it from circulating.

The new study, published in the Emerging Infectious Diseases journal, shifts the R0 for COVID-19 from about 2.2 to about 5.7. With the lower number, only 55% of a population needs to be immune from COVID-19 to stop its spread through herd immunity. Herd immunity refers to enough of a population being immune to a disease that the disease cannot travel through it.
But if more people get infected from a single person with COVID-19, then more people need to be protected from the disease to stop it from continuing to spread. With an R0 of 5.7, approximately 82% of the population needs to be immune to reach herd immunity and stop the disease from spreading easily through the population, the researchers concluded.

Bacterial Pneumonia Caused Most Deaths in 1918 Influenza Pandemic. ... The pneumonia was caused when bacteria that normally inhabit the nose and throat invaded the lungs along a pathway created when the virus destroyed the cells that line the bronchial tubes and lungs

From Publishers Weekly
In 1918, a plague swept across the world virtually without warning, killing healthy young adults as well as vulnerable infants and the elderly. Hospitals and morgues were quickly overwhelmed; in Philadelphia, 4,597 people died in one week alone and bodies piled up on the streets to be carted off to mass graves. But this was not the dreaded Black Death-it was "only influenza." In this sweeping history, Barry (Rising Tide) explores how the deadly confluence of biology (a swiftly mutating flu virus that can pass between animals and humans) and politics (President Wilson's all-out war effort in WWI) created conditions in which the virus thrived, killing more than 50 million worldwide and perhaps as many as 100 million in just a year. Overcrowded military camps and wide-ranging troop deployments allowed the highly contagious flu to spread quickly; transport ships became "floating caskets." Yet the U.S. government refused to shift priorities away from the war and, in effect, ignored the crisis. Shortages of doctors and nurses hurt military and civilian populations alike, and the ineptitude of public health officials exacerbated the death toll. In Philadelphia, the hardest-hit municipality in the U.S., "the entire city government had done nothing" to either contain the disease or assist afflicted families. Instead, official lies and misinformation, Barry argues, created a climate of "fear... [that] threatened to break the society apart." Barry captures the sense of panic and despair that overwhelmed stricken communities and hits hard at those who failed to use their power to protect the public good. He also describes the work of the dedicated researchers who rushed to find the cause of the disease and create vaccines. Flu shots are widely available today because of their heroic efforts, yet we remain vulnerable to a virus that can mutate to a deadly strain without warning. Society's ability to survive another devastating flu pandemic, Barry argues, is as much a political question as a medical one.

Svartalf wrote:There's one thing I wonder about. So they say that chloroquin and hydroxychloroquin seem to have antiviral properties... all right.

But I hear repeatedly that to combat coronavirus, the drug has to be combined with the antibiotic azithromycin. I just don't get why.
I mean, I've been hearing for years, maybe decades that antibiotics are useless against viral diseases... so why use that one to boost chloroquin's efficiency? I know that antibiotics are sometimes given to viral patients to prevent or combat bacterial surinfection, but I've not heard of this being the reason, especially since azithromycin is not often a first intent treatment.

anybody has data on the matter?

It is interesting to note that 6 patients were prescribed azithromycin “to prevent bacterial super-infection” and the investigators found that viral eradication was numerically superior in this subgroup (6 of 6, 100%) compared with those who received hydroxychloroquine alone (8 of 14, 57%). The authors concluded that azithromycin “reinforced” the SARS-CoV-2 viral load achieved by hydroxychloroquine. Although these data are intriguing, certain limitations to this data set must be acknowledged. First, although viral eradication is an important endpoint, the authors did not report clinical outcomes in these patients. Second, the cohort initially contained 26 hydroxychloroquine patients, but 6 of them were removed from the analysis due to early cessation of hydroxychloroquine therapy including 3 PCR-positive patients who were transferred to the intensive care unit (ICU), 1 PCR-negative patient who passed away, and 1 PCR-positive patient who discontinued hydroxychloroquine due to nausea. Finally, the hydroxychloroquine monotherapy arm included patients with significantly higher viral loads, represented by lower cycle threshold (CT) values than those who received combination therapy. If the hydroxychloroquine monotherapy patients with CT values <23 are separated from those with CT values ≥23, there is a notable discordance in viral eradication rates (1 of 5, 20% vs 7 of 9, 78%), with this latter number approaching the 6 of 6 demonstrated with hydroxychloroquine and azithromycin combination therapy in which all patients had CT values ≥23. Given this finding, the small numbers in this study, the lack of clinical outcomes presented, the potential for additive toxicity with hydroxychloroquine and azithromycin, and the desperate need to practice good antimicrobial stewardship during the COVID-19 pandemic, we would caution clinicians against using these data to support combination therapy.

- Canada's 12 deaths per million

TRACKING COVID-19 IN THE U.S.
Positive cases: 469,285 (1,429.7 per 1 mil people)
Deaths: 16,772 (51.1 per 1 mil people)

Keep It Real wrote:
Needless to say I deleted what misinformation I could which I'd propagated online RE the air-travel boom being the main culprit, as much as I'd have "liked" that to be the case.

Spearthrower wrote:

Keep It Real wrote:
Needless to say I deleted what misinformation I could which I'd propagated online RE the air-travel boom being the main culprit, as much as I'd have "liked" that to be the case.

That, if you don't mind me saying, is actually insightful, self-aware, and the kind of thinking that a shit tonne more people need to grasp; sorting acceptable facts according to previously held treasured ideas is self-limiting.

- More than two-thirds of severely ill COVID-19 patients saw their condition improve after treatment with remdesivir, an experimental drug being developed by Gilead Sciences Inc. (GILD.O), according to new data based on patient observation.

The analysis, published on Friday by the New England Journal of Medicine, does not detail what other treatments the 61 hospitalized patients were given and data on eight of them were not included — in one case because of a dosing error.

The paper’s author called the findings “hopeful,” but cautioned that it is difficult to interpret the results since they do not include comparison to a control group, as would be the case in a randomized clinical trial. In addition, the patient numbers were small, the details being disclosed are limited, and the follow-up time was relatively short.