You are absolutely phenomenal! I love your graphs and your explanations. And I realize that my next statement is not scientific but I believe that your daughters are absolutely blessed with the best💙
As for the potential April/May uptick, I’d love to hear your take on whether the rollout of Evusheld will affect that. My husband is now on the list to get it, and a friend who is a medical professional already got her first dose. They are both on ocrelizumab, so not the first “tier” of recipients, so I assume others who are more severely immuno-compromised are being treated now.
I swear, you read my mind with these post topics! I have been so worried about B.A.2 and needing some analysis. I would love to see a post, if possible, or even just a short comment, on your advice for those of us who are high-risk but not immunocompromised re: a second booster. I'm 6mo. out from mine and worrying that efficacy will wane as B.A.2 gains hold here and wondering if I should get another or wait until a more effective, pan-variant type vaccine is developed and/or until Fall when surges normally are worse. Any advice at all is SO appreciated.
my grandpa (94 yo) had the same exact question. i told him to hold off. the data coming out of the UK shows very strong protection with the first booster still. if you go off script, then it’s even harder to know what to do down the line as recommendations and data analysis will not align with your decision. i assume a second booster will be coming for 60+ but don’t know when. maybe next fall before the next winter surge?
Right now, I'm thinking the 2nd round of boosters for older patients, not immunocompromised, wi;; be at the 9-12 month interval. I think the new dosing interval for primary doses will help, though, and that a boost at 6 months after the longer-interval primary will see enhanced humeral immunity.
Thank you for this. The country/regional profile comparison is helpful. Because we have had a lull in your great general summaries while you were focusing on the excellent Long Covid series, I am not clear what your view is of the BA.2 variant . You said you think the rapid rise in cases is due to BA.2. Are you seeing evidence that it is more contagious than BA.1 ? or more lethal? Or is the rapid increase in cases due to behavioral or other factors? Hope you have time to address these questions in a future column. Know you cannot reply to all comments!!
I'm so thankful for these updates. Information I can trust out-of-the-box, without having to sift through multiple sources trying to figure it out for myself. I'm curious if you (Katelyn) or anyone here has thoughts on https://www.microcovid.org/. My wife is immunocompromised and she leans heavily on it for determining what feels safe for us. It seems sound enough, but I don't really know how to truly evaluate its methodology.
For consideration re:a COVID-19 spike due to war in Ukraine. Rather than considering the potential for spike due to displaced persons from Ukraine, despite their abysmal vaccination rate, consider the potential for spread by Russian forces who also have a poor vaccination uptake rate, but are also using vaccines of lower efficacy. As we see more intermingling of Russian and Ukrainian forces, I anticipate a spike in COVID.
One other thing... I've been tracking, on a near random basis while I write some code to automate this, minor upticks in R(t) despite decreasing cases. I'm concerned over this. I haven't seen any discussion, before yours, of a potential issue arising in the US. Most of the concern for Asia in the press is less factual and appears to be along the lines of "Oh, wow! In Hong Kong the virus didn't get the memo it was supposed to be finished!".
Thanks for the state of affairs, I look forward to these as a cliff notes of all the headlines I see throughout the week!! Quick Q: What is the source for the ~45% of Americans have caught Omicron? Or is it just adding up the daily cases each multiplied by the CDC variant proportion percentage estimates, I assume?
Thank you, Katelyn, for another clear concise summary of current conditions. You mentioned that "people are just not testing anymore". It would be helpful to hear your thoughts on the the ways in which increased availability of at-home testing (the results of which are usually not reported) has affected the use of PCR tests at public-health agency sites, and how that in turn impacts our ability to collect population-level data.
We may well be past the point where testing everyone periodically will be useful (I say this knowing the data geek in me really wants those data!) because, well, those data are now being ignored by most of the governments who employ public health professionals.
In clinical medicine there's a trope that, if you don't want to find a fever, don't check a temperature. That's been the theme for the entire pandemic, in most venues after the original PCR test kit debacle with failed kits. Many states prioritized testing solely to individuals who met certain criteria, e.g., having traveled to an affected region, early on, or referred by a provider based on symptoms and clinical suspicion, or mandates from officials that patients remain symptomatic for some minimum period prior to testing (e.g., 5 days of symptoms before being ALLOWED to get a PCR test).
At home antigen and molecular tests are, as you note, usually not recorded or tracked. No rational tracking mechanism was ever developed nationwide, although some of the test manufacturers do have a way to self-report, and some few states, including Colorado, my new home, accept at-home test results, and track them, including them as a category in their state internal reports. And, in talking to their epidemiologists, they did this preemptively, with a plan, and it's been beneficial.
Personally, I'd love to see a national data collection project where we collect enough data to assure no one is spoofing or ballot-stuffing the system, but use relatively anonymized data from home testing to obtain a better sense of community spread. If coupled to community serology testing the data enhancement would allow us doing this analysis to have a much better understanding of the level of community exposure and spread.
Interesting question… The last forecast for Paxlovid availability didn’t look favorable for wide availability soon. I can’t offer conjecture on the second question now.
As an antiviral, paxlovid won’t affect testing unless it’s started before testing. We’ve already ruined the testing landscape, though. Positivity and absolute case numbers are nearly… or virtually meaningless.
Can you speak to the utility of sharing the percent of population with at least one dose of the vaccine? If we ultimately need three doses, is using one dose as a metric for reporting vaccine rates useful at all? I think it leads people to believe that one is better than none, even though one is still woefully short of protective.
First, it's a statistic we're used to using for multi-dose vaccines to give an idea of uptake. We can also see what the subsequent failure rate for completing the vaccination process, which tells the front-line practitioners if they need to pay more attention to getting people vaccinated.
Second, even a single dose will train the cellular immune system. Thus, while it takes a bit to activate compared to existing, circulating (neutralizing) antibodies, once the CD4 (helper) T-cell is sensitized it can help "coordinate" the work of the various components of the cellular immune system to address an infection.
So, noting the first-dose rate is useful in public health and clinical practice. And it's something we're used to doing.
Thanks, Gerry. I understand the utility of the rate for public health vaccine campaigns and the limited clinical use. I still don't understand the use of it for monitoring and reporting on outbreaks.
If I see a high magnitude transmission uptick with high single-dose uptake in a new outbreak, it's a rapid, surrogate indicator for me that we might be looking at something with the transmissivity, and ability to evade immunity, of omicron. It's just another data point, and a pretty good surrogate.
I'd also like to stop seeing people with two doses being called "fully vaccinated" by some. The US needs to do better to get boosted and keep up with vaccinations as needed.
That unfortunate label originated from when a boost dose wasn't anticipated. As with so many learning opportunities with the Pandemic, communications and clarity are important.
Thank you so much for the valuable information you are providing about the Corona virus and related issues. I find it very informative. Your writing and in-depth coverage of the subject matter is greatly appreciated.
For what it's worth, we're seeing those couple of months right now. The problem is, I predicted we'd have that last year in late September/early October, just before omicron was identified.
Since we're still not completely sure just why its transmission rate was so high... outside of the fact that it effectively evaded immunity acquired solely from infection, AND immunity derived from vaccination without boost that was more than 8 months past, that's an open question. The incidence curve for omicron looked a lot like that for an absolutely unprotected population widely exposed to an infectious process. Right now, however, while deaths are decreasing, that curve is prolonged in its downward trajectory.
I wonder if there is a push to start getting accurate data -
For Example the with verus From stats - such as:
Who died with - Who died from
Who is hospitalized with - Who is hospitalized from
The CDC released the 18 & under stats... that are vague again because it has deaths involving COVID -
Its hard enough to get accuracy with a vague denominator (so many with COVID are never tested and do not hit the books) but now we have a vague numerator.
I understand Katelyn's use of "With" vs "For" as a transmission surrogate, but when I start thinking clinically, it really doesn't matter in-hospital if you came in for respiratory failure due to COVID-19, or were found to have COVID-19 when admitted for your heart attack or ischemic bowel. SARS-CoV-2 is known to affect a large number of organs, and someone who's positive has to go into aerosol precautions, so it doesn't really matter.
Similarly, the question of cause of death doesn't really matter when you consider the excess deaths numbers we're seeing both for the US and worldwide.
Well -I agree with you if that is the CAUSE of death or the CAUSE of hospitalization.
Where do you find the excess death numbers? That is interesting. Have 1m more Americans died in the past 2 years? This website shows an increase in the increase death rate of Americans since 2012.
Are you suggesting that a child with a broken legs be listed as in ER with COVID if the test was positive?
Same with deaths - Do you think a motorcycle accident should be a COVID death if they test positive?
As for a heart attack being classified as a COVID hospitalization should depend on the patient not the broad stroke of a brush called COVID. Some cardiac patients actually died before COVID. That actually seems irresponsible if you are using that broad stroke.
Why would you want to do that vs find the real cause of death from the treating physician?
In general terms, we have seen a marked increase in both the US and world death rate beyond expected numbers. Some of these can be directly attributable to COVID-19 and the direct disease processes. OTHERS, however, are a result of delaying care and medical/surgical procedures because of the epidemic. Overall, however, the excess death toll is almost certainly a result of the pandemic and how various medical systems in different countries handled things.
COVID deaths have been handled and reported differently around the world as you'll see in the cited articles. Some countries require autopsy findings associated directly with COVID-19 (e.g., Russia) before the cause of death can be attributed to COVID. I am personally aware of states and counties that would not allocate testing to coroners' offices but then required positive test results to attribute the cause of death to COVID.
Something you're missing is that an incidental finding of COVID immediately changes the procedural management of a patient presenting for another reason. Your child with a broken limb and a positive COVID test would have to be placed in isolation and appropriate precautions taken. On the other hand, a multitrauma patient, e.g., motorcycle patient with incidental COVID would almost certainly not be tested unless they'd survived long enough to be transferred to ICU, where an incoming test would dictate which room they could go into, and how they've got to be cared for, for the safety of other patients and staff.
Heart attacks and strokes are a completely different kettle of fish, because disseminated COVID has significant effect on clotting and directly on blood vessels. As for being irresponsible for painting with a broad brush, I'd say my research in cardiovascular medicine and surgery, if somewhat dated, allows me to have an opinion. Colleagues with whom I've spoken to, as well as published research, have started concluding that SARS-CoV-2 has a great affinity for vascular tissue. As mentioned above, the predisposition of patients with moderate or severe COVID symptoms toward increased clotting in the microvasculature and larger vessels, including otherwise unexpected clotting the cerebral vasculature was the reason d-dimer assays were common early; the reduction in their use now is simply because ALL COVID patients with moderate to severe disease have markedly elevated d-dimer levels; most hospitalized patients are anticoagulated based on general protocol. To reduce the risk of cardiovascular events.
In general, a death certificate has a list of precipitating causes. Think of this as a differential diagnosis of the cause of death, and often it's a lot like the prototypical differential diagnosis we work with when we first see the patient, although your differential is often fluid in the course of care of a really complicated ICU patient as new issues arise. It's not a case of not wanting to know what killed the patient, but a list of what the most likely causes were. If the patient is sent for autopsy, that "differential" can be modified and the pathologist is responsible for the cause of death.
You are absolutely phenomenal! I love your graphs and your explanations. And I realize that my next statement is not scientific but I believe that your daughters are absolutely blessed with the best💙
As for the potential April/May uptick, I’d love to hear your take on whether the rollout of Evusheld will affect that. My husband is now on the list to get it, and a friend who is a medical professional already got her first dose. They are both on ocrelizumab, so not the first “tier” of recipients, so I assume others who are more severely immuno-compromised are being treated now.
Also also interested in this. My wife is trying to see if she can qualify. She does not currently qualify through Rheumatology.
All depends on what she might be on in terms of biologicals. The guidelines are pretty specific.
Also interested in this. I'm not up to speed (yet) on Evusheld, so while I'm gathering data, I'd love to see solid, authoritative information.
I swear, you read my mind with these post topics! I have been so worried about B.A.2 and needing some analysis. I would love to see a post, if possible, or even just a short comment, on your advice for those of us who are high-risk but not immunocompromised re: a second booster. I'm 6mo. out from mine and worrying that efficacy will wane as B.A.2 gains hold here and wondering if I should get another or wait until a more effective, pan-variant type vaccine is developed and/or until Fall when surges normally are worse. Any advice at all is SO appreciated.
my grandpa (94 yo) had the same exact question. i told him to hold off. the data coming out of the UK shows very strong protection with the first booster still. if you go off script, then it’s even harder to know what to do down the line as recommendations and data analysis will not align with your decision. i assume a second booster will be coming for 60+ but don’t know when. maybe next fall before the next winter surge?
THANK YOU. Your advice really means so much.
Right now, I'm thinking the 2nd round of boosters for older patients, not immunocompromised, wi;; be at the 9-12 month interval. I think the new dosing interval for primary doses will help, though, and that a boost at 6 months after the longer-interval primary will see enhanced humeral immunity.
I really appreciate you breaking down this information into understandable terms, thank you so much, you are doing good work!
Thank you for this. The country/regional profile comparison is helpful. Because we have had a lull in your great general summaries while you were focusing on the excellent Long Covid series, I am not clear what your view is of the BA.2 variant . You said you think the rapid rise in cases is due to BA.2. Are you seeing evidence that it is more contagious than BA.1 ? or more lethal? Or is the rapid increase in cases due to behavioral or other factors? Hope you have time to address these questions in a future column. Know you cannot reply to all comments!!
I'm so thankful for these updates. Information I can trust out-of-the-box, without having to sift through multiple sources trying to figure it out for myself. I'm curious if you (Katelyn) or anyone here has thoughts on https://www.microcovid.org/. My wife is immunocompromised and she leans heavily on it for determining what feels safe for us. It seems sound enough, but I don't really know how to truly evaluate its methodology.
For consideration re:a COVID-19 spike due to war in Ukraine. Rather than considering the potential for spike due to displaced persons from Ukraine, despite their abysmal vaccination rate, consider the potential for spread by Russian forces who also have a poor vaccination uptake rate, but are also using vaccines of lower efficacy. As we see more intermingling of Russian and Ukrainian forces, I anticipate a spike in COVID.
One other thing... I've been tracking, on a near random basis while I write some code to automate this, minor upticks in R(t) despite decreasing cases. I'm concerned over this. I haven't seen any discussion, before yours, of a potential issue arising in the US. Most of the concern for Asia in the press is less factual and appears to be along the lines of "Oh, wow! In Hong Kong the virus didn't get the memo it was supposed to be finished!".
We so appreciate your expertise and your outreach. Thank you!
Thanks for the state of affairs, I look forward to these as a cliff notes of all the headlines I see throughout the week!! Quick Q: What is the source for the ~45% of Americans have caught Omicron? Or is it just adding up the daily cases each multiplied by the CDC variant proportion percentage estimates, I assume?
Thank you, Katelyn, for another clear concise summary of current conditions. You mentioned that "people are just not testing anymore". It would be helpful to hear your thoughts on the the ways in which increased availability of at-home testing (the results of which are usually not reported) has affected the use of PCR tests at public-health agency sites, and how that in turn impacts our ability to collect population-level data.
We may well be past the point where testing everyone periodically will be useful (I say this knowing the data geek in me really wants those data!) because, well, those data are now being ignored by most of the governments who employ public health professionals.
In clinical medicine there's a trope that, if you don't want to find a fever, don't check a temperature. That's been the theme for the entire pandemic, in most venues after the original PCR test kit debacle with failed kits. Many states prioritized testing solely to individuals who met certain criteria, e.g., having traveled to an affected region, early on, or referred by a provider based on symptoms and clinical suspicion, or mandates from officials that patients remain symptomatic for some minimum period prior to testing (e.g., 5 days of symptoms before being ALLOWED to get a PCR test).
At home antigen and molecular tests are, as you note, usually not recorded or tracked. No rational tracking mechanism was ever developed nationwide, although some of the test manufacturers do have a way to self-report, and some few states, including Colorado, my new home, accept at-home test results, and track them, including them as a category in their state internal reports. And, in talking to their epidemiologists, they did this preemptively, with a plan, and it's been beneficial.
Personally, I'd love to see a national data collection project where we collect enough data to assure no one is spoofing or ballot-stuffing the system, but use relatively anonymized data from home testing to obtain a better sense of community spread. If coupled to community serology testing the data enhancement would allow us doing this analysis to have a much better understanding of the level of community exposure and spread.
What will happen to testing if
a) Paxlovid becomes much more widely available
And
b) We discover that Paxlovid is effective for a staggeringly large class of viruses
Interesting question… The last forecast for Paxlovid availability didn’t look favorable for wide availability soon. I can’t offer conjecture on the second question now.
Oh, not asking you to weigh in on whether either of those things are likely to happen. What if they do, at some undetermined time?
As an antiviral, paxlovid won’t affect testing unless it’s started before testing. We’ve already ruined the testing landscape, though. Positivity and absolute case numbers are nearly… or virtually meaningless.
Can you speak to the utility of sharing the percent of population with at least one dose of the vaccine? If we ultimately need three doses, is using one dose as a metric for reporting vaccine rates useful at all? I think it leads people to believe that one is better than none, even though one is still woefully short of protective.
First, it's a statistic we're used to using for multi-dose vaccines to give an idea of uptake. We can also see what the subsequent failure rate for completing the vaccination process, which tells the front-line practitioners if they need to pay more attention to getting people vaccinated.
Second, even a single dose will train the cellular immune system. Thus, while it takes a bit to activate compared to existing, circulating (neutralizing) antibodies, once the CD4 (helper) T-cell is sensitized it can help "coordinate" the work of the various components of the cellular immune system to address an infection.
So, noting the first-dose rate is useful in public health and clinical practice. And it's something we're used to doing.
Thanks, Gerry. I understand the utility of the rate for public health vaccine campaigns and the limited clinical use. I still don't understand the use of it for monitoring and reporting on outbreaks.
If I see a high magnitude transmission uptick with high single-dose uptake in a new outbreak, it's a rapid, surrogate indicator for me that we might be looking at something with the transmissivity, and ability to evade immunity, of omicron. It's just another data point, and a pretty good surrogate.
I'd also like to stop seeing people with two doses being called "fully vaccinated" by some. The US needs to do better to get boosted and keep up with vaccinations as needed.
That unfortunate label originated from when a boost dose wasn't anticipated. As with so many learning opportunities with the Pandemic, communications and clarity are important.
Thank you so much for the valuable information you are providing about the Corona virus and related issues. I find it very informative. Your writing and in-depth coverage of the subject matter is greatly appreciated.
Julie Nathanson
A couple months of relative freedom, at least. Good. Make hay while the sun shines.
For what it's worth, we're seeing those couple of months right now. The problem is, I predicted we'd have that last year in late September/early October, just before omicron was identified.
I don't think anybody had crazy high transmissable Omicron on their 2021 dance card. Can a new variant top it by as much? Hopefully not!
Since we're still not completely sure just why its transmission rate was so high... outside of the fact that it effectively evaded immunity acquired solely from infection, AND immunity derived from vaccination without boost that was more than 8 months past, that's an open question. The incidence curve for omicron looked a lot like that for an absolutely unprotected population widely exposed to an infectious process. Right now, however, while deaths are decreasing, that curve is prolonged in its downward trajectory.
Obligatory masking went in Ireland on Feb 28th and the cases have been going up and up. It does feel like an own-goal.
Another great one from you!
Great info yet again.
I wonder if there is a push to start getting accurate data -
For Example the with verus From stats - such as:
Who died with - Who died from
Who is hospitalized with - Who is hospitalized from
The CDC released the 18 & under stats... that are vague again because it has deaths involving COVID -
Its hard enough to get accuracy with a vague denominator (so many with COVID are never tested and do not hit the books) but now we have a vague numerator.
I understand Katelyn's use of "With" vs "For" as a transmission surrogate, but when I start thinking clinically, it really doesn't matter in-hospital if you came in for respiratory failure due to COVID-19, or were found to have COVID-19 when admitted for your heart attack or ischemic bowel. SARS-CoV-2 is known to affect a large number of organs, and someone who's positive has to go into aerosol precautions, so it doesn't really matter.
Similarly, the question of cause of death doesn't really matter when you consider the excess deaths numbers we're seeing both for the US and worldwide.
Well -I agree with you if that is the CAUSE of death or the CAUSE of hospitalization.
Where do you find the excess death numbers? That is interesting. Have 1m more Americans died in the past 2 years? This website shows an increase in the increase death rate of Americans since 2012.
Are you suggesting that a child with a broken legs be listed as in ER with COVID if the test was positive?
Same with deaths - Do you think a motorcycle accident should be a COVID death if they test positive?
As for a heart attack being classified as a COVID hospitalization should depend on the patient not the broad stroke of a brush called COVID. Some cardiac patients actually died before COVID. That actually seems irresponsible if you are using that broad stroke.
Why would you want to do that vs find the real cause of death from the treating physician?
https://www.macrotrends.net/countries/USA/united-states/death-rate
Excess mortality stats:
https://journals.sagepub.com/doi/full/10.1177/0141076820956802
https://www.cdc.gov/nchs/nvss/vsrr/covid19/excess_deaths.htm
https://www.nature.com/articles/d41586-022-00104-8
In general terms, we have seen a marked increase in both the US and world death rate beyond expected numbers. Some of these can be directly attributable to COVID-19 and the direct disease processes. OTHERS, however, are a result of delaying care and medical/surgical procedures because of the epidemic. Overall, however, the excess death toll is almost certainly a result of the pandemic and how various medical systems in different countries handled things.
COVID deaths have been handled and reported differently around the world as you'll see in the cited articles. Some countries require autopsy findings associated directly with COVID-19 (e.g., Russia) before the cause of death can be attributed to COVID. I am personally aware of states and counties that would not allocate testing to coroners' offices but then required positive test results to attribute the cause of death to COVID.
Something you're missing is that an incidental finding of COVID immediately changes the procedural management of a patient presenting for another reason. Your child with a broken limb and a positive COVID test would have to be placed in isolation and appropriate precautions taken. On the other hand, a multitrauma patient, e.g., motorcycle patient with incidental COVID would almost certainly not be tested unless they'd survived long enough to be transferred to ICU, where an incoming test would dictate which room they could go into, and how they've got to be cared for, for the safety of other patients and staff.
Heart attacks and strokes are a completely different kettle of fish, because disseminated COVID has significant effect on clotting and directly on blood vessels. As for being irresponsible for painting with a broad brush, I'd say my research in cardiovascular medicine and surgery, if somewhat dated, allows me to have an opinion. Colleagues with whom I've spoken to, as well as published research, have started concluding that SARS-CoV-2 has a great affinity for vascular tissue. As mentioned above, the predisposition of patients with moderate or severe COVID symptoms toward increased clotting in the microvasculature and larger vessels, including otherwise unexpected clotting the cerebral vasculature was the reason d-dimer assays were common early; the reduction in their use now is simply because ALL COVID patients with moderate to severe disease have markedly elevated d-dimer levels; most hospitalized patients are anticoagulated based on general protocol. To reduce the risk of cardiovascular events.
In general, a death certificate has a list of precipitating causes. Think of this as a differential diagnosis of the cause of death, and often it's a lot like the prototypical differential diagnosis we work with when we first see the patient, although your differential is often fluid in the course of care of a really complicated ICU patient as new issues arise. It's not a case of not wanting to know what killed the patient, but a list of what the most likely causes were. If the patient is sent for autopsy, that "differential" can be modified and the pathologist is responsible for the cause of death.