March 22, 2021

Prior beliefs and evidence

Remember the bin lid?

Case C tested positive in MIQ at their day-12 test. They had a room next door to D and D’s child, E. D is the person who was initially thought to have been infected by touching a bin lid that C had also touched some 20 hours before.

There’s now a published paper by Jemma Geohegan and numerous co-workers, and Siouxsie Wiles has an explainer at the Spinoff:

Now we know that SARS-CoV-2 is airborne, a much more likely scenario is that case D was infected by exposure to airborne virus shed by case C. 

CCTV footage showed that C and D were never outside their MIQ rooms at the same time. But they both got their day 12 swabs taken on the same day. And these were taken from their doorways. C was tested first. Then there was a 50-second window between them closing their door and D opening theirs to be swabbed. It looks like having the hotel room doors open for as long as it took to be swabbed was enough to move airborne virus from C and their room into the enclosed and unventilated corridor and then on to D and into their room. From the genome sequencing, it looks like D then infected their child, E, and another household member, F. 

This might seem strange: we know there was a contaminated bin lid, and the opportunity for airborne* transmission was pretty marginal, so why are we concluding it was airborne*?

Back last year, scientists and public health people worked on the assumption that the Covid virus could spread via contaminated surfaces, because lots of microbes do and it’s a relatively easy fix.  Some of us went as far as washing individual tomatoes when we got them back from the supermarket.  It became clear fairly quickly that airborne*  transmission was important; there were some smoking-gun examples that couldn’t be explained any other way.  It took a lot longer to decide that contaminated surfaces were pretty much never important, because most cases that could have been surface transmission could also have been airborne* transmission. Still, there were no smoking-gun cases of transmission by contaminated surfaces, and you’d expect a few unless it was very rare.

As the numbers of active infections rose, it became harder to track down causes for any individual case.  Except, in New Zealand, it didn’t.  Since the end of the first outbreak we have had a very small number of cases, small enough that contact tracing and genome sequencing is possible for every person involved, plus the sort of hotel surveillance that’s unusual in the public sector outside prisons.  Here, it is possible to track most individual transmissions. So, the ‘bin lid’ case was interesting because it looked like an unambiguous case of transmission from a contaminated surface.

What we know now is that it wasn’t. That is, it wasn’t an unambiguous case of transmission from a contaminated surface; it could have been airborne*  transmission.  The ‘bin lid’ case

  • definitely isn’t the smoking gun for surface transmission that it first appeared
  • and so, based on everything else we know, probably was airborne*  transmission

It’s not that we have strong evidence for airborne*  transmission from the facts of this specific case, but we don’t have strong evidence against it, and other evidence definitely points that way.

 

 

* for some definition of the word, let’s not be dicks about it.

avatar

Thomas Lumley (@tslumley) is Professor of Biostatistics at the University of Auckland. His research interests include semiparametric models, survey sampling, statistical computing, foundations of statistics, and whatever methodological problems his medical collaborators come up with. He also blogs at Biased and Inefficient See all posts by Thomas Lumley »