Talk:Transmissible spongiform encephalopathy

multi-stomach herbivore animals

Has there been any explanation of why Ruminant (multi-stomach herbivore animals) are over represented on the list of animals affected by Transmissible spongiform encephalopathy — Preceding unsigned comment added by 58.178.254.209 (talk) 10:24, 16 September 2018 (UTC)

Center for global food

The Center for Global Food Issues is a part of the remarkably right-wing Hudson Institute, hardly an NPV source.

narrowing the definition of transmissible

I understand that the "transmissible" in TSE stands for "transmissible between individuals". As such, some of the listed disease are not TSEs, even though they are caused by prions. Examples are [normal or spontaneous] CJD and FFI. These arise from spontaneous changes in protein conformation in individuals. It might be argued that they might be transmissable if infectious material was injected into the brain of another animal, but to my knowledge, this has not been done.

Does someone have source for the usage of transmissible in this context?

Is it indeed 'able to be transmitted'? if so, this could expanded upon.

Renaming

I agree with the comment above, and I think this page should be renamed to "Spongiform encephalopathy". For example, Fatal familial insomnia seems to be inherited. Are there any objections to this renaming? --Arcadian 20:20, 7 December 2005 (UTC)

While that name might be more correct, I think transmissible spongiform encephalopathy is the most commonly used name in medical literature (8885 vs. 1382 hits for a pubmed search), so I would say don't move it. (btw. all human TSEs can occur three ways: sporadically; as hereditary diseases; or through transmission from infected individuals) --WS 17:31, 17 December 2005 (UTC)

Result

It was requested that this article be renamed but there was no consensus for it to be moved. WhiteNight ^{T | @ | C} 21:22, 29 December 2005 (UTC)

[1]: Even if you're familiar with the subject or think you know what it literally means, one word encephalopathy covers a lot of territory. Spongiform might even be redundant for being typical, although I doubt it in the case of Parkinson's.

BTW, I made a large number of edits that you might have seen coming only if you had noticed my contributions to the page on prions under discussion [2]here or [3]here. 216.234.170.74 10:18, 31 July 2006 (UTC)

All TSEs are transmissible

What was your first clue?

I move that the redirect from Spongiform Encephalopathy to "Transmissible SE" be removed. Pathology where the case is not transmissible or infectious is bound to exist. Brewhaha@edmc.net 03:36, 21 March 2007 (UTC)

Prion peer review

I've nominated the prion article for peer review, any comments welcome here! --Purple 02:49, 11 March 2006 (UTC)

Alper's disease

If someone finds more information about Alper's disease, it would be nice to have it in Wikipedia. If Alper's disease really is a TSE, it would be remarkable. All other hereditary TSE:s are dominant mutations of the PrP gene. Alper's disease is caused by a resessive mutation of some other unknown gene.

Sources

[4]: I wonder how things have changed when Nature in this article on the protein-only hypothesis implies that In Vitro (with dead objects) is the standard for proof. It might be useful in leading to ex vivo (was alive) demonstration of the cause, and last time I read anything about it, that could be ingestion of incinerated remains of an affected host, something that probably precludes anything but elements as a cause. 216.234.170.74 16:17, 31 July 2006 (UTC)

Prion of bacterial disease?

Apparently prion hypothesis is not the only one to explain the condition. They may be responsible for a part of the cases, but some cases of the disease can be induced by Spiroplasma infection [5], thus prions have no role in them. Thus, the definition should be corrected to add bacteria as one of the possible infectious agents besides prions.--Oleksii0 (talk) 22:17, 10 February 2008 (UTC)

Requested move

On top of concerns listed before on this talk page, I think this name is now wholly incorrect; neither transmissibility nor sponge-like appearance are necessary features of prion diseases, which is by all measures the most correct term. The current title is increasingly being abandoned as a term. --Steven Fruitsmaak (Reply) 21:03, 14 January 2009 (UTC) Totally agree. I would not use the term TSE at all now as it is totally misleading. 82.46.212.111 (talk) 23:34, 17 July 2010 (UTC)

Quinine

On the quinine page it says this is used as a experimental treatment. —Preceding unsigned comment added by 92.239.38.135 (talk) 19:59, 5 August 2009 (UTC)

Article intention?

It seems to me that talking more about public health concerns is needed in this article. Most people curious about TSE's are either going to be looking for mad-cow or cannibalism related-answers. Finding a way within the guidelines to answer the question "If I eat one mad cow steak do I get prion disease?" or "If a serial killer eats a person do they get prion disease automatically?" in clearer, less indirect language would improve utility to the average end user, in my opinion. Khallus Maximus (talk) 21:08, 14 March 2012 (UTC)

Should this be split?

The article in confusing from the start: "Transmissible spongiform encephalopathies (TSEs), also known as prion diseases" - prion diseases are a subset of TSEs, but even this page mentions the existence of TSEs that are not prion diseases. This means most of the article is about prion diseases, except for a couple of sentences about non-prion TSEs that just adds confusion, especially when a substantial section exists about the cause of the disease, implying a controversy that doesn't exist. That prion diseases is caused by prions is no longer controversial, but TSEs don't necessarily have anything to do with prions, and conflating the two is not really helpful. I'd suggest moving most of this article to Prion Diseases, which seems to be the more common term, and leave information on this page about other causes, and obviously linking to prion disease as a subset of TSEs. Don't know if anyone has any problems with this, or any knowledge on how to do it? If anyone still even edits this page? its a little out of date, which I'll try to help do something about Jasonisme (talk) 14:12, 19 October 2012 (UTC)

"Transmissible TSE" is redundant

"Transmissible Transmissible Spongiform Encephalopathy" is redundant, and the acronym should either be expanded when clarification is needed, or simply kept as an acronym. — Preceding unsigned comment added by Dredsina (talk • contribs) 23:28, 23 May 2014 (UTC)

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Last bullet under Protein hypothesis makes no sense

The last bullet under the protein hypothesis talks about inoculation with PrPSc. The abstract only refers to serum PrPSc staying elevated. There is no talk of inoculation. 40.134.106.218 (talk) 21:06, 9 March 2017 (UTC)

I clarified this point. Ruslik_Zero 14:10, 11 March 2017 (UTC)

Revision of Epidemiology Section

Transmissible spongiform encephalopathies are very rare but can reach epidemic proportions. It is very hard to map the spread of the disease due to the difficulty of identifying individual strains of the prions. This means that, if animals at one farm begin to show the disease after an outbreak on a nearby farm, it is very difficult to determine whether it is the same strain affecting both herds—suggesting transmission—or if the second outbreak came from a completely different source.

CWD (chronic wasting disease) is a prion disease of North America in deer and elk. The first case was identified as a fatal wasting syndrome in 1960s, then recognized as a TSE in 1978. Surveillance studies showed the endemic of CWD in free-ranging deer and elk in northeastern Colorado, southeastern Wyoming and western Nebraska. It was also realized that CWD may have been present in free-ranging animals of a proportion decades before the initial recognition. In the United States the discovery of CWD raised concerns about the transmission of this prion disease to humans, many apparent cases of CJD were suspected transmission of CWD, however the evidence was lacking and not convincing.

Another form of TSE is BSE (bovine spongiform encephalopathy) or known as “mad cow disease”. In the 1980s and 1990 BSE spread in cattle at an epidemic rate, this occurred because the cattle was fed processed remains of other cattle. You can say that prions may be a way that nature tells us not to be cannibals. Then our consumption of these cattle created a outbreak of the human form CJD. There was a dramatic decline in BSE when feeding bans (infectious parts of cattle in the animal feed) were in place. The total estimated number of cattle infected was approximately 750,000 between 1980 and 1996. The exact source of the outbreak is not fully understood. In North America on May 20, 2003 there was the first BSE case confirmed, the source could not be clearly identified but rendered cohorts of 1993 proposed imported BSE cow may have been the source. In the United States the USDA created safeguards to minimize the risk of BSE in human exposure.

Classic Creutzfeldt-Jakob disease (CJD) was discovered in 1920. It occurs sporadically over the world but is very rare. It affects about one person per million each year. Typically, the cause is unknown for these cases. It has been found to be passed on genetically in some cases. 250 patients got the disease through iatrogenic transmission (from use of contaminated surgical equipment). This was before equipment sterilization was required in 1976 and there have been no other iatrogenic cases since then. In order to prevent the spread of infection, the World Health Organization created a guide to tell health care workers what to do when CJD appears and how to dispose of contaminated equipment.The Centers for Disease Control and Prevention (CDC) have been keeping surveillance on CJD cases, particularly by looking at death certificate information.

Variant Creutzfeldt-Jakob disease (vCJD) was discovered in 1996 in England. There is strong evidence to suggest that vCJD was caused by the same prion as bovine spongiform encephalopathy. 231 total cases of vCJD have been reported since it was first discovered. These cases have been found in a total of 12 countries with 178 in the United Kingdom, 27 in France, 5 in Spain, 4 in Ireland, 4 in the United States, 3 in the Netherlands, 3 in Italy, 2 in Portugal, 2 in Canada, and one in Japan, Saudi Arabia, and Taiwan.

Mp2332 (talk) 05:55, 9 November 2017 (UTC)Mp2332

"Transmissible spongiform encephalopathies are very rare but can reach epidemic proportions." seems self-contradictory. Expand/explain? --D Anthony Patriarche (talk) 05:01, 7 June 2018 (UTC)

I suppose it means "it rarely arises" compared to how often you get zoonotic viruses. Something like that. Artoria2e5 🌉 10:48, 19 January 2022 (UTC)

References

added information about treatment for it

limited to only human treatment. could be expanded upon for others. NorthernStares (talk) 17:18, 17 July 2024 (UTC)

I need help

It would seem that this page has improved somewhat. I see there is now a section for "Viral hypothesis". As we examine how to give voice to "minority views" in science, I am left wondering which peer-reviewed papers can be considered admissible as evidence to the great public forum of Wikipedia, when there are so many papers in this world. As someone who is personally unconvinced that TSEs are possible without an informational molecule, I struggle when considering edits to be made to this page, as I fear subscribers to prion hypothesis will quickly revert them. The prion hypothesis, a somewhat sci-fi idea, is easy to summarize quickly, because it has no evidentiary basis, no complete mathematical formulation, and no accurate chemical model. Thus, its format is perfect for the short summary style articles of Wikipedia. The prion hypothesis is subterfuge, and very little of the actual literature on TSEs actually deals with their cause. Essentially, proponents of the prion hypothesis are pointing at brain homogenate and saying "Well, obviously this is just one protein". There is no scientific paper that you can read that will contradict the statement I have just made. Opposition views to the prion hypothesis, having less funding, are still nascent. As science progresses, I am sure eventually we will get to the bottom of this and the truth will come out. As of yet, I struggle with how to move forward to improve this Wikipedia page. I am left to wonder how long science will continue down this fruitless path of protein misfolding. Anyone who cares about this, if you're out there, let's get a dialog going. An informational molecule is involved in these diseases. It's just what I believe and I would love to talk to anyone about making this page better for everyone. IanJedd (talk) 11:34, 14 August 2024 (UTC)

I'm not educated enough on this topic to say much about any of the information you talked about however before you make any edits to this page I encourage you to read over the manual of style for medical pages as well as how to identify reliable medical sources. When editing medical pages there are a couple policies that are enforced, the main ones to look out for are avoiding primary sources, assessing evidence quality, and using independant sources. I also recomend you check out Wikipedia:Neutral point of view#Due and undue weight. CursedWithTheAbilityToDoTheMath (talk) 17:09, 14 August 2024 (UTC)

Thanks for your reply. I was wondering if you could look at something for me. The second sentence of this article says "According to the most widespread hypothesis, they are transmitted by prions, though some other data suggest an involvement of a Spiroplasma infection."

and it links to this source. https://www.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.47159-0

How would Wikipedia's "avoiding primary sources" policy apply to this source?

Would it meet the requirements of the policy or not? Why?

I'm asking because I genuinely am not sure. IanJedd (talk) 09:34, 16 August 2024 (UTC)

When assessing a source I usually go through several steps. First I check if the source itself is reliable. The easiest way to do this is to use the usercript User:Headbomb/unreliable. It does appear that the source used comes from a reputable publisher so it passes that check. Then I look at what type of study it is, in this case the source is adone with animals which means its low on the heriechy of evidence. Lastly I look at how the source is used in the article. In this case the study is used to show that there is other theories behind TSEs which is appropraite usage. My only concern with it would be that usually these types of things are best left out of the lead due to Wikipedia:Neutral_point_of_view#Due_and_undue_weight and therefore an arguement could be made to remove the second half of that sentence and just leave it as "According to the most widespread hypothesis, they are transmitted by prions". I'm glad that you read through the policies and guidlines and are taking intrest in making sure they are being followed as many dont. CursedWithTheAbilityToDoTheMath (talk) 09:49, 16 August 2024 (UTC)

Looking for sources

Hi there, I was wondering if anyone could find some sources for me to help verify some of this information. Under the "Cause" section, under genetics.

"Mutations in the PRNP gene cause prion disease. Familial forms of prion disease are caused by inherited mutations in the PRNP gene."

And further down.

"Point mutations in this gene cause cells to produce an abnormal form of the prion protein, known as PrPSc"

Please, do you know of any scientific papers to support these claims?

Especially this last one. Is there a scientific paper that says this? IanJedd (talk) 09:53, 16 August 2024 (UTC)

Generally when trying to find sources for unsourced claims I will google a couple key terms and see what I can find. For example, for the claim "Mutations in the PRNP gene cause prion disease. Familial forms of prion disease are caused by inherited mutations in the PRNP gene." I would search "PRNP gene mutations prion disease". In this case I was able to find this article that may help you: Bernardi, Livia; Bruni, Amalia C. (2019-07-23). "Mutations in Prion Protein Gene: Pathogenic Mechanisms in C-Terminal vs. N-Terminal Domain, a Review". International Journal of Molecular Sciences. 20 (14). MDPI AG: 3606. doi:10.3390/ijms20143606. ISSN 1422-0067. as well as this article: Kroll, François; Dimitriadis, Athanasios; Campbell, Tracy; Darwent, Lee; Collinge, John; Mead, Simon; Vire, Emmanuelle (2022-05-18). "Prion protein gene mutation detection using long-read Nanopore sequencing". Scientific Reports. 12 (1). Springer Science and Business Media LLC. doi:10.1038/s41598-022-12130-7. ISSN 2045-2322. CursedWithTheAbilityToDoTheMath (talk) 10:00, 16 August 2024 (UTC)