“Infectious” means “transmissible between people”. As the name suggests, fatal familial insomnia is a genetic condition. (FFI and the others listed are also prion diseases—the prion just emerges on its own without a source prion and no part of the disease is contagious. This is an interesting trait of prions that could not happen with, say, a disease caused by a virus.)
Can someone catch FFI from coming into contact with the neural tissues of a patient with FFI?
I suspect it’s possible that FFI genes cause the patient’s body to create prions, but can those prions lead to illness in a person without the FFI gene? If yes, then FFI would still be “infectious” in some sense, I suppose.
Possibly if by “come in contact” we mean like ingesting or injecting or something. That’s the going theory for how the Kuru epidemic started—consumption of the brain of a person with sporadic (randomly-naturally-occuring) CJD. Fortunately cannibalism isn’t too common so this isn’t a usual means of transmission. I think if anything less intensive (say, skin or saliva contact) made CJD transmissible, we would know by now. See also brain contact with contaminated materials e.g. iatrogenic CJD, or Alzheimers which I mention briefly in this piece.
it’s possible that FFI genes cause the patient’s body to create prions,
I was thinking of iatrogenic transmissions, yeah (and prions have been a long term psychological fear of mine, too...so I perhaps crawled too much publicly available information about prions to be a normal person)
I wonder if there are any instances of FFI transmitted through the iatrogenic pathway, and whether it is possible to be distinguished from the typical CJD, and whether iatrogenic prions could become a significant issue for healthcare (more instances of prion diseases due to aging population could possibly mean more contaminated medical equipments, and the possible popularisation of brain-computer interface might give us some problems too) given the difficulty of sterilising prions.
Maybe the sample size is too small for us to know.
Can someone catch FFI from coming into contact with the neural tissues of a patient with FFI?
I suspect it’s possible that FFI genes cause the patient’s body to create prions, but can those prions lead to illness in a person without the FFI gene? If yes, then FFI would still be “infectious” in some sense, I suppose.
Possibly if by “come in contact” we mean like ingesting or injecting or something. That’s the going theory for how the Kuru epidemic started—consumption of the brain of a person with sporadic (randomly-naturally-occuring) CJD. Fortunately cannibalism isn’t too common so this isn’t a usual means of transmission. I think if anything less intensive (say, skin or saliva contact) made CJD transmissible, we would know by now. See also brain contact with contaminated materials e.g. iatrogenic CJD, or Alzheimers which I mention briefly in this piece.
Yep! That’s how it works. Real brutal.
I was thinking of iatrogenic transmissions, yeah (and prions have been a long term psychological fear of mine, too...so I perhaps crawled too much publicly available information about prions to be a normal person)
I wonder if there are any instances of FFI transmitted through the iatrogenic pathway, and whether it is possible to be distinguished from the typical CJD, and whether iatrogenic prions could become a significant issue for healthcare (more instances of prion diseases due to aging population could possibly mean more contaminated medical equipments, and the possible popularisation of brain-computer interface might give us some problems too) given the difficulty of sterilising prions.
Maybe the sample size is too small for us to know.