Well, I can tell you this: 17 years ago, your grandmother was NOT suspected of Mad Cow Disease. It didn’t exist, as far as we know.
Personally, I strongly dislike the term “Mad Cow Disease” - unless, of course, you’re a cow. Cows can get a prion disease called Bovine Spongiform Encephalopathy. Sheep can get a priion disease called scrapie. Humans can get a prion disease called Cruetzfield-Jacob.
This is not just a picky issue of terminology. People have always gotten Cruetzfield-Jacob. It’s just a unlucky refolding of an essential brain protein. Some peopl are more prone to it (e.g. they may have a variant of the protein that refolds slightly more easily), but it’s till just pure luck: one of the godzillion copies of the protein may refold itself, and it in turn may catalyze other copies to refold (that’s what is so special about this one refolding of this one protein) and those proteins can built up until the cell they’re in sickens and bursts…
…or dozens, maybe hundreds, of copies of the protein my refold themselves, but due to luck and circumstance, the refolding either doesn’t spread, or causes so little damage before you die that neither you nor an autopsy will ever spot it.
It’s hard to say exactly what the incidence of CJD is, because it can take decades to develop in the early stages, and the older you are, the longer you’ve had to get an unlucky refolding. The symptoms of CJD are similar to other age-related brain diseases so the diagnosis can be tricky or obscured by the co-existence of some more common brain disease, like Alzheimers. A rough guess might be one in a million. That would mean that there were 200-300 cases of CJD 17 years ago, and none of them came from cows (as far as we know) Even today, essentially none of the hundreds of cases every year has anything to do with cows, as far as we know
Your brain produces the susceptible protein. It can refold on its own. Even if you were ‘infected’ (a completely inaccurate word) by a cow, it would be your own self-manufactured proteins that cause and spread the disease. A cow prion just helps the first refolding.
It just so happens that I was doing lab research in aging and dementias (including what were then incorrectly called ‘slow virus diseases’) back in the 80s, and though the prion hypothesis was bouncing around, the evidence for transmission between species was fairly weak, and the hard evidence evidence of transmission from cow to man was not just anecdotes and guesswork, it was guesswork about anecdotes. We didn’t have a test. We didn’t know what we were looking for, and there was (is, and may always be) no way to know if the first refolding was accidental or induced.
So basically, at worst, they might have suspected CJD - one of hundreds of such cases every year. They would never have said it was caused by cows, and even if you got CJD today, it would probably be self-induced. The only test would have been an autopsy, which would have been more to rule out other disease, and even if a diagnosis were made - whhat would the CDC do with a report of a self-caused disease that’s almost always more analogous to a random mutation than a “Communicable Disease” (which is what the Center for Communicable Diseases studies)
Though I always like the information gained from autopsies, I really don’t know what I could have done with a confirmed diagnosis that my deceased patient had a nongenetic disease that spontaneously arises once in a million people.
Today, of course, we know it can be transmitted to man, but the bottom line is: even if I report a confirmed case of teh “new variant” [nvCJD] and the CDC sent a team to investigate, it wouldn’t help anyone. We could only guess if it was an exposure or spontaneous. We couldn’t trace it to a given hamburger or cow, and it’d be years too late for anyone who would have been exposed the same way.
I’ve glossed over a lot of molecular biology and new advances to try to cover the basic principles in simple language (and it’s not my field anymore, anyway). Corrections and additions are, as always, eagerly welcomed.
