1/ "We identified high loads of #monkeypox virus DNA by qPCR in 35 (85%) of 41 saliva samples. Infectious monkeypox virus was recovered from 22 (67%) of 33 saliva samples positive for monkeypox virus DNA."
2/ Detection of viral DNA in various samples is not equal to transmission. We often say that culturable virus is a proxy for transmission potential, but even this doesn't mean transmission routes from those specimens are inherently effective ones.
3/ We saw this epidemiologically play out during the current #monkeypox outbreak. We did not see major spillover outside of MSM sexual networks. If there was substantial droplet transmission, transmission patterns would likely have looked different than they did.
4/ We are monitoring mpox virus in immunocompromised cases, especially as it relates to viral mutations (publication on this hopefully soon). And this is important for surveillance purposes in case any transmission enhancing mutations were to arise that could make certain
5/ transmission routes more viable. But for now, important to reflect on the outbreak we did see, and why some of the hypotheses about potential transmission routes did not actually play out that way.
This. In these mask RCTs, what’s rarely accounted for & hard to determine is when transmission happened. If it happens mostly when masks are off & that is happening way more than you account for in your analysis, you likely have significant misclassification of exposure bias.
2/ This doesn’t mean masks don’t work. What it might mean is that masks aren’t worn at all times they need to be in order for them to work. So pragmatically an intervention may need to increase compliance at specific high risk times when they are being removed.
3/ And when I use the word "work" here, it is really not a binary. The trial would be set up with an estimated effect size of the intervention. You are looking to detect that effect. That estimate is based on people complying with the intervention. But compliance is complex here
1/ Also, the move recently has been away from screening asymptomatic patients who are being admitted to the hospital. This will reduce burden on hospital/labs to process tons of samples, many which will be negative. It will miss some cases who are incubating + infectious
2/ I appreciate costs/benefits of this. On one hand, missed cases could transmit to staff who may be wearing surgical masks (still some protection but less than N95). For shared rooms, more concerning (see our paper) so would definitely screen prior
3/ In times of low community incidence, screening all asymptomatic may put strain on lab capacity for small benefit. If symptomatic or in shared rooms, would definitely advocate for testing in this scenario though as outlined above. Benefit of hospital is you can identify quickly
1/ I was asked yesterday by @mehdirhasan about the ‘with v for’ argument on #covid19 hospitalizations/deaths which has been used by some to argue that hospitals are over-counting @MSNBC
2/ One of the arguments is that we have 'over-screened' because many infections aren't leading to 2020-21 pneumonia syndromes. Or, that screening can/does sometimes pick up persistent positive on rtPCR representing old infections
3/ This is true to an extent. But the other side of this is that screening during times where there is high level of community spread still helps identify cases who would likely benefit from antivirals. And, to reduce spread to other hospitalized patients and staff.
CDC has public facing data on excess deaths during the pandemic— they specifically highlight that it’s still likely an undercount given covid-related complications aren’t always accounted for in the reporting.
2/ Many of us who have worked on primary teams in the hospital during the pandemic have filled out death certificates. We put thought into this when referring to the primary cause of death as well as contributing causes.
3/ It’s true that covid19 as a clinical syndrome has presented differently over time. In the beginning we saw mostly covid19 pneumonia. Over time, we have seen the clinical syndrome change as more have been vaccinated & have survived prior infections.
Many postmortems of the first years of the pandemic clearly point to social inequities as the biggest driver of rapid pathogen transmission. What have we done to change this for the next time we are dealing w a highly transmissible pandemic-prone pathogen?
2/ We were able to stop covid19 transmission in 2020…with enough money and resources, the NBA did this, creating a literal bubble to allow their business to continue as frontline workers couldn’t even get proper PPE to protect themselves and families from dying. Think about it
3/ We now are watching a struggle between advocates who are pushing for public health institutions in this country to do more & others who are tasked with protecting the status quo. There’s no way forward until we fix the major fault lines that allowed covid19 to hit us this hard
Anecdotes and/or personal experiences play an outsized role in how people see or understand diseases. This is a problem in epidemics. The fallacy that covid wasn’t a significant problem & mitigation efforts are overblown because you personally had mild disease is case in point.
2/ This is especially a problem in highly contagious diseases spread person-person, in which people may have ways of reducing spread but may lack motivation to do so because they don’t personally feel threatened. This exploits vulnerabilities in our lack of social cohesion.
3/ Depending on the altruism of others unfortunately isn’t a great strategy, especially when mortality rate & hospitalization rate are sig different depending on age, comorbidities etc & society has been structured to favor those above a certain threshold of means & privileges