Monkey Pox info

[BumRushDaShow]

18. What are you talking about?

Read my original post again.

You were talking about saying covid wasn't spread throw air, and now we're talking about mask mandates today?

And you didn't read the rest of why I used that as an example. I will repeat it again -

In reality, what epidemiologists and others need to do is MONITOR how this latest viral outbreak is manifesting (just like they are monitoring the so-called "mysterious" Hepatitis outbreak in young children), and not make hasty, rash and loudly conclusionary statements that end up turning out to be wrong.

This is why the public continues to be confused and distrustful of the scientific and Public Health community.

When the statement you quoted was made, we had weeks worth of data on covid.

This is absolutely incorrect.

As I noted earlier, there were YEARS worth of data associated with SARS CoV-1, which was the predecessor to the current "SARS CoV-2 (why the hell do you think the virus that is associated with COVID-19 is called "SARS CoV-2" or maybe you didn't know that? ). Here is one such paper -

Evidence of Airborne Transmission of the Severe Acute Respiratory Syndrome Virus
List of authors.

Ignatius T.S. Yu, M.B., B.S., M.P.H., Yuguo Li, Ph.D., Tze Wai Wong, M.B., B.S., Wilson Tam, M.Phil., Andy T. Chan, Ph.D., Joseph H.W. Lee, Ph.D., Dennis Y.C. Leung, Ph.D., and Tommy Ho, B.Sc.


April 22, 2004
N Engl J Med 2004; 350:1731-1739
DOI: 10.1056/NEJMoa032867


Abstract


Background

There is uncertainty about the mode of transmission of the severe acute respiratory syndrome (SARS) virus. We analyzed the temporal and spatial distributions of cases in a large community outbreak of SARS in Hong Kong and examined the correlation of these data with the three-dimensional spread of a virus-laden aerosol plume that was modeled using studies of airflow dynamics.
Methods

We determined the distribution of the initial 187 cases of SARS in the Amoy Gardens housing complex in 2003 according to the date of onset and location of residence. We then studied the association between the location (building, floor, and direction the apartment unit faced) and the probability of infection using logistic regression. The spread of the airborne, virus-laden aerosols generated by the index patient was modeled with the use of airflow-dynamics studies, including studies performed with the use of computational fluid-dynamics and multizone modeling.
Results

The curves of the epidemic suggested a common source of the outbreak. All but 5 patients lived in seven buildings (A to G), and the index patient and more than half the other patients with SARS (99 patients) lived in building E. Residents of the floors at the middle and upper levels in building E were at a significantly higher risk than residents on lower floors; this finding is consistent with a rising plume of contaminated warm air in the air shaft generated from a middle-level apartment unit. The risks for the different units matched the virus concentrations predicted with the use of multizone modeling. The distribution of risk in buildings B, C, and D corresponded well with the three-dimensional spread of virus-laden aerosols predicted with the use of computational fluid-dynamics modeling.

Conclusions

Airborne spread of the virus appears to explain this large community outbreak of SARS, and future efforts at prevention and control must take into consideration the potential for airborne spread of this virus. Hong Kong was the hardest-hit area during the worldwide epidemic of infection with the severe acute respiratory syndrome (SARS) virus in 2003, with the highest incidence rate (1755 cases in a population of 6.7 million) and a high case fatality rate of 17 percent (299 deaths).1 In fact, the infection in Hong Kong was believed to be the source of the spread of the disease to many other countries.2 A series of case clusters that occurred during the epidemic in Hong Kong2-6 suggested that environmental factors might have been involved in the spread of the virus.

(snip)

https://www.nejm.org/doi/full/10.1056/nejmoa032867

CDC has a timeline of discovery of it - https://www.cdc.gov/museum/timeline/covid19.html

On January 22, 2020 when W.H.O. met, they refused to call it a "pandemic".

They met a little over a week later and STILL didn't call it a pandemic (although they had evidence it was spreading). Meanwhile the U.S. had started gearing up.

A few more weeks later, W.H.O. names the "disease" caused by SARS CoV-2 "COVID-19" but STILL hadn't declared it a "pandemic".

It wasn't until March 11, 2020 when it was declared "a pandemic".

The point of this is that "scientists", the "medical community" (including researchers in both types of fields and I happen to be a retired chemist by the way), and Public Health officials, tend to "tunnel vision" their interpretations of the SAME data based on their "expertises" and when doing so, have essentially botched the response to this COVID-19 pandemic.

And given that same "tunnel vision" exists for many other diseases - particularly viral ones that are often difficult to treat, one should not go along the same path when dealing with "sudden outbreaks" (like Monkey Pox) in this COVID-19 environment, where odd mutations can and have happened to make something "more transmissible".

And an example of a swing and a miss was the last "outbreak" of a bird flu (not associated with the current one) that lead to an expectation of and preparation for an avian flu pandemic that lead to a miss of what eventually became a swine flu pandemic instead.

As it is, the ultimate illustration of "disagreements", in a somewhat related subject given the vaccine to be used for the Monkey Pox outbreak, was the earlier "declaration" that "smallpox was eradicated", and the subsequent years of debate that ensued over the past couple decades about destroying the last of the smallpox samples.

Point being that the unfortunate aspect of a natural discord within a scientific and medical community, can exasperate the manner of dealing with pathogens that impact humans.