>The risk of cow->human BSE transmission is infinitesimal.
I don't think your sources support this conclusion.
bovine spongiform encephalopathy (BSE) rarely passes the species barrier, but it is difficult, if not impossible to estimate what the rate is in the absence of mitigations.
There are a plethora of unknowns that make it very difficult to check transmission rate.
Transmission is rare, but this could be impacted by lots of factors. There were hundreds of thousands of cows in the UK, but there were also testing and culling programs to try to prevent them from entering the food supply. There were also regulations on which parts of the cows could be used for human consumption.
Last but not least, there are huge uncertainties around the diagnosis rate of mad cow in humans.
For example, a 2013 study (1) found that 1 in 2000 people in the UK now have Creutzfeldt-Jakob disease.
Based on this, it could be possible that transmission rates are very high if a human were to eat mad cow nervous tissue.
This study is looking at the appendix, not any brain tissue. Without considering symptoms, it's possible that altered PrP expression and/or folding in the appendix does not cause vCJD or result from exposure to PrP(Sc).
Also, these antibodies are not very selective for a given confirmation. Idk how this made it into the BMJ because standard in the PrP field is a protease resistance assay given the issues with Ab specificity.
This article is from the UK National Centre for Infectious Disease Surveillance and Control and is cited by by the NHS and widely in the literature.
I am not an expert in the field, but it seems relevant to consider latent or asymptomatic PrP expression when assessing how often it crosses the species barrier.
I don't think your sources support this conclusion. bovine spongiform encephalopathy (BSE) rarely passes the species barrier, but it is difficult, if not impossible to estimate what the rate is in the absence of mitigations.