The Eyes are the windows to Our Souls, and a Potential Pathway for the TSE Prion disease, what if?
O17 Evaluation of iatrogenic risk of CJD transmission associated with corneal transplantation
Douet JY. (1), Cassard H. (1), Huor A. (1), Lacroux C. (1), Haïk S. (2), Lugan S. (1), Tillier C. (1), Aron N. (1), Ironside J.W. (3), Andreoletti O. (1) (1) UMR INRA-ENVT 1225, Ecole Nationale Vétérinaire de Toulouse, France. (2) Université Pierre et Marie Curie, UMR-S 1127, CNRS UMR 722, Institut du Cerveau et de la Moelle Epinière, G.H. Pitié-Salpêtrière, Paris, France. (3) National CJD Research and Surveillance Unit Centre for Clinical Brain Sciences, University of Edinburgh, UK.
Sporadic Creutzfeldt–Jakob disease (sCJD) has been documented to be accidentally transmitted by contaminated corneal transplants. To date, only one case is considered as definite, while 5 other suspect cases are classified as probable or possible. However, the specific transmission risk associated with this widely-performed transplantation procedure has never been studied.
In this study, bioassays in transgenic mice expressing the human PrP confirmed the presence of infectivity in the cornea of 2 sCJD patients. Infectivity was also detected in other ocular tissues (optic nerve, retina, vitreous body, choroid and lacrymal gland) from one of these patients. Based on these results, we investigated the presence of infectivity in the cornea of different TSE animal models. In conventional mice (RML strain) as well as in sheep (PG127 scrapie), infectivity could only be detected in the corneas collected at the late stage of the disease incubation phase. In parallel to these experiments, corneas collected at different stages of the incubation period in infected mice and sheep were grafted into healthy recipients.
Our results showed that corneas collected during the late asymptomatic phase or in affected animals were able to transmit TSE infectivity. Importantly, after the death of the recipients (up to 2.5 years after surgery) infectivity could still be detected in the grafted cornea.
These data confirm the potential for sCJD transmission by corneal grafts. They also provide crucial data for the assessing the TSE transmission risk associated with various other ophthalmologic procedures.
Prion Conference 2018 Abstract source reference O17 Evaluation of iatrogenic risk of CJD transmission associated with corneal transplantation
Prion Seeds Distribute throughout the Eyes of Sporadic Creutzfeldt-Jakob Disease Patients
Christina D. Orrù, Katrin Soldau, Christian Cordano, Jorge Llibre-Guerra, Ari J. Green, Henry Sanchez, Bradley R. Groveman, Steven D. Edland, Jiri G. Safar, Jonathan H. Lin, Byron Caughey,Michael D. Geschwind, Christina J. Sigurdson Reed B. Wickner, Editor DOI: 10.1128/mBio.02095-18
ABSTRACT
Sporadic Creutzfeldt-Jakob disease (sCJD) is the most common prion disease in humans and has been iatrogenically transmitted through corneal graft transplantation. Approximately 40% of sCJD patients develop visual or oculomotor symptoms and may seek ophthalmological consultation. Here we used the highly sensitive real-time quaking-induced conversion (RT-QuIC) assay to measure postmortem prion seeding activities in cornea, lens, ocular fluid, retina, choroid, sclera, optic nerve, and extraocular muscle in the largest series of sCJD patient eyes studied by any assay to date. We detected prion seeding activity in 100% of sCJD eyes, representing three common sCJD subtypes, with levels varying by up to 4 log-fold among individuals. The retina consistently showed the highest seed levels, which in some cases were only slightly lower than brain. Within the retina, prion deposits were detected by immunohistochemistry (IHC) in the retinal outer plexiform layer in most sCJD cases, and in some eyes the inner plexiform layer, consistent with synaptic prion deposition. Prions were not detected by IHC in any other eye region. With RT-QuIC, prion seed levels generally declined in eye tissues with increased distance from the brain, and yet all corneas had prion seeds detectable. Prion seeds were also present in the optic nerve, extraocular muscle, choroid, lens, vitreous, and sclera. Collectively, these results reveal that sCJD patients accumulate prion seeds throughout the eye, indicating the potential diagnostic utility as well as a possible biohazard.
IMPORTANCE Cases of iatrogenic prion disease have been reported from corneal transplants, yet the distribution and levels of prions throughout the eye remain unknown. This study probes the occurrence, level, and distribution of prions in the eyes of patients with sporadic Creutzfeldt-Jakob disease (sCJD). We tested the largest series of prion-infected eyes reported to date using an ultrasensitive technique to establish the prion seed levels in eight regions of the eye. All 11 cases had detectable prion seeds in the eye, and in some cases, the seed levels in the retina approached those in brain. In most cases, prion deposits could also be seen by immunohistochemical staining of retinal tissue; other ocular tissues were negative. Our results have implications for estimating the risk for iatrogenic transmission of sCJD as well as for the development of antemortem diagnostic tests for prion diseases.
INTRODUCTION
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DISCUSSION We detected high prion seed levels in 100% of sCJD patient eyes from three common subtypes and two mixed subtypes, MM1/MV1, VV2, MV2, MM1-2, and MV1-2, using the exceptionally sensitive and quantitative RT-QuIC technique. In more than half the cases, prion seeding activities in retina were remarkably high and approached levels in brain, consistent with efficient prion conversion in neural tissue. The VV2 subtype showed the highest prion seeding activities in the retina and visible deposits in the inner and outer plexiform layers (46). In all other subtypes, retinal prion seeding activities were at least 0.5-log lower; however, prion deposits were consistently visible by IHC in the outer plexiform layer. Ironside and colleagues also reported prion immunolabeling in the plexiform layers from a VV2 patient and an MM1 sCJD patient, with more widespread deposition in the VV2 case as seen here (15, 32). We found that strong prion immunolabeling in the retina correlated with high prion seeding activity.
In all sCJD cases, prion seeding activity accumulated in other (nonretinal) ocular tissues, specifically the choroid, sclera, optic nerve, and cornea, as well as extraocular muscles, lens, and vitreous of most eyes. We noted that high prion seed levels in the optic nerve correlated with high seed levels in the retina, but not in the cornea. Surprisingly, all corneas contained low to moderate prion seeding activity, and levels did not vary substantially among the patients. These differences may reflect prion entry by multiple cranial nerves transporting PrPSc, as prions may be spreading from prion-infected brain into the retina by retrograde axonal transport in the optic nerve (47–50). Prions may be accumulating in the abundant small nerves within the cornea, originating from cranial nerves V and VII.
Our findings support the World Health Organization classification of eye components as having high prion infectivity and have implications for patient safety. As the early-disease phase of sCJD often includes visual symptoms (27–29), patients with sCJD will often have diagnostic assessments performed by an ophthalmologist, potentially contaminating instruments. Experimental models have shown that prions spread from brain to the retina in mice by 60% of the incubation period, prior to the onset of clinical disease (51). Although in humans it is not yet clear when prions accumulate in the eye, the finding of prion seeding activity in all sCJD eyes bolsters recommendations for single-use instruments or other decontamination procedures to prevent iatrogenic prion transmission. Cadaveric corneas have been a source of iatrogenic prion transmission, and grafts are commonly performed (35). With the increased frequency of corneal grafting worldwide, optimizing biosynthetic substitutes would be a justified research priority and is currently under development in multiple laboratories (54, 55).
In all sCJD patient eyes examined, PrPSc aggregates were highly visible in the posterior retina, an accessible CNS window that could potentially be exploited for the early diagnosis of prion disease. For example, an electroretinogram is an antemortem, noninvasive diagnostic tool that may reveal early electrical abnormalities, particularly considering the prion deposits in synaptic plexi. Because other protein aggregates such as amyloid-β, α-synuclein, and tau may also spread from brain to retina, it would also be important to continue to evaluate eyes from patients having more common neurodegenerative diseases, such as Alzheimer’s disease, synucleinopathies, and tauopathies, particularly in light of recent findings showing the prion-like spread of protein aggregates through the CNS (56–59).
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KEYWORDS Creutzfeldt-Jakob disease, RT-QuIC, eye, prion
''Cadaveric corneas have been a source of iatrogenic prion transmission, and grafts are commonly performed (35). With the increased frequency of corneal grafting worldwide, optimizing biosynthetic substitutes would be a justified research priority and is currently under development in multiple laboratories (54, 55). In all sCJD patient eyes examined, PrPSc aggregates were highly visible in the posterior retina, an accessible CNS window that could potentially be exploited for the early diagnosis of prion disease. For example, an electroretinogram is an antemortem, noninvasive diagnostic tool that may reveal early electrical abnormalities, particularly considering the prion deposits in synaptic plexi. Because other protein aggregates such as amyloid-synuclein, and tau may also spread from brain to retina, it would also be important to continue to evaluate eyes from patients having more common neurodegenerative diseases, such as Alzheimer’s disease, synucleinopathies, and tauopathies, particularly in light of recent findings showing the prion-like spread of protein aggregates through the CNS (56–59).''
1999 Subject: RE-The Eyes Have It (cjd) and they could be stealing them from your loved one... "pay back time"
Date: Sat, 16 Sep 2000 10:04:26 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
Greetings List Members,
I hate to keep kicking a madcow, but this still is very disturbing to me. Not only for the recipient of the cornea's, but as well, for the people whom would be operated on, using the same tools that were used to put those stolen cornea's in the recipient with. No history of this donor or his family (re-ffi), or anything would be known, using stolen organs and or tissue's. I just think this is not only wrong, but very dangerous to a great many other people, as this is one of the most infectious tissues of TSE's. It seems that this practice of stealing organ/tissue happens more than we think. Anyway, the family of the victim which had their cornea's stolen, are now suing. In the example I used with my Mother, if 3 months before, she would have been in a catastrophic accident (car wreck, whatever), no autopsy (for whatever reason), no family (for whatever reason), she lay in the morgue, and after 4 hours, they come steal the cornea's, lot of people could have been infected, just because of lack of medical history of donor/family. It may be hypothetical, but very real. We need to stop the spread of this disease.
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
===========================================
Previous story--
Cadaver corneal transplants -- without family permission...
Cadaver corneal transplants -- without family permission Houston, Texas channel 11 news 28 Nov 99
Reported by Terry S. Singeltary Sr.son of CJD victim
"It was a story about how the Lions eye bank were harvesting corneas from victims in the Morgue, without their consent. Under Texas law, this appears to be legal (remember Texas has the Veggie liable law). Even if Family says no, this appears to happen, from what the news story said.
They said the only way to prevent this, is to fill out a form, stating not to have this done. So if you don't fill out the form, they can do this. How many people don't know about the form?
This is not only disgusting and appalling, it could be highly infectious. Without proper background checking of the donors, on their physical history, checking on past dementia, and/or family history, some of these unfortunate victims, could be passing a human TSE.
Response Jill Spitler Clevelland Eye Bank:
"No, we are not stealing.........Yes, you do have such a law in the state of Texas, but not all your state Eye Banks utilize the law. The Eye Bank that you're speaking of is only one of 43 certified Eye Bank throughout the USA.
And there are measure taken per the Medical Standards of the Eye Bank Association of America, the certifying body for eye banks and per FDA regulations to address those concerns that you speak of.
I would suggest that those interested/concern with transplant contact their local agencies. The Eye Bank Association of America has a web. site . Further if anyone has problems contacting or finding out about their local organization(s), call me or e-mail me I would be glad to help. My e-mail address is jill@clevelandeyebank.org"
Terry Singeltary responds:
"Explain this to the family in Houston who went to their loved ones funeral, only to find out that the loved one that was in the casket, had their corneas removed without their permission, without the consent of the victim or it's family. They would not have known it, only for the funny look the victim had. So, they questioned, only to find out, the corneas, had in fact, been removed without consent.
I call that stealing, regardless what the law states. This type of legal grave robbing is not a logical thing to do without knowing any type of background of the victims medical past, which really will not prove anything due to the incubation period. Eye tissue being potentially a highly infective source, there are risks here.
Should they not at least know of the potential ramifications of TSE's (the person receiving the corneas)?
Should there not be some sort of screening?
Should there be some sort of moral issue here?
If this is the case, and in fact, they can come take your corneas, without your consent, then what will they start taking next, without your consent?
Lets look at a hypothetical situation:
What would happen if my Mom (DOD 12-14-97 hvCJD) would have gotten into a car wreck and died, before the symptoms of CJD appeared. Not much money, so there was no autopsy. What would have happened to that recipient of those infecting corneas?"
Comment (webmaster): Actual transmission of CJD by means of corneal transplant may or may not be rare. The incidence of infectivity in older people could be fairly high; this is not to be confused with the lower incidence of symptomatic (clinical) CJD. It is very unlikely that familial CJD would have been diagnosed in earlier generations; however, without interviewing the family even known kindreds would not be excluded.
In blood donation, a much stricter policy is followed, even though corneal transplant may be far more dangerous (being a direct link to the brain and not going through purification steps).
Since highly sensitive tests for pre-clinical CJD are now available, it would make sense to screen corneas for CJD, just as they are screened for AIDS, hepatitus, and a host of other conditions.
New DoH guidance on decontaminating lenses
December 4th, 2009
New guidance on decontamination of trial contact lenses and other contact devices has been revealed.
The latest recommendations from the Department of Health’s Advisory Committee on Dangerous Pathogens (ACDP) replace previous guidance issued amid fears that Creutzfeldt-Jakob Disease (CJD) and variant CJD (vCJD), the human form of bovine spongiform encephalopathy (BSE, ‘mad cow disease’), could theoretically be transmitted from person to person by contact lenses and other devices such as tonometer heads and diagnostic lenses.
Details were discussed at the British Contact Lens Association’s Pioneers’ Conference in London late in November.
Professor Roger Buckley (pictured), a member of the ophthalmology subgroup of the ACDP’s Transmissible Spongiform Encephalopathy Working Group established to review this advice, told BCLA members at the Royal Society of Medicine that there had been no known cases of transmission of CJD/vCJD resulting from contact lens wear or diagnostic examination, and there was now thought to be a low level of risk of infectivity of the cornea and ocular surface.
Under the new guidance, six steps are required to minimise the risk of transmission via re-used contact devices. The lens or device should be: decontaminated immediately after contact with the eye surface; rinsed in Water for Irrigation BP (not tap water) for not less than 30 seconds; cleaned on all surfaces with a liquid soap or detergent, then rinsed in Water for Irrigation BP for a further 30 seconds; immersed in a freshly-prepared solution of sodium hypochlorite providing 10,000ppm of available chlorine for ten minutes; rinsed in three changes of Water for Irrigation BP for a total of not less than ten minutes; shaken to remove excess water, dried with a disposable tissue, and stored dry in a suitable container.
Any further measure (such as autoclaving) can then be carried out, if this is necessary and if the device is designed to withstand such a process. Otherwise, it is ready for immediate re-use.
Eye procedure raises CJD concerns
BySTEVE MITCHELL, Medical Correspondent
WASHINGTON, Nov. 18 (UPI) -- A New York man who died from a rare brain disorder similar to mad cow disease in May underwent an eye procedure prior to his death that raises concerns about the possibility of transmitting the fatal disease to others, United Press International has learned.
The development comes on the heels of the announcement Thursday by U.S. Department of Agriculture officials of a possible second case of mad cow disease in U.S. herds.
Richard Da Silva, 58, of Orange County, N.Y., died from Creutzfeldt Jakob disease, an incurable brain-wasting illness that strikes about one person per million.
Richard's wife Ann Marie Da Silva told UPI he underwent a check for the eye disease glaucoma in 2003, approximately a year before his death. The procedure involves the use of a tonometer, which contacts the cornea -- an eye tissue that can contain prions, the infectious agent thought to cause CJD.
Ann Marie's concern is that others who had the tonometer used on them could have gotten infected.
A 2003 study by British researchers suggests her concerns may be justified. A team led by J.W. Ironside from the National Creutzfeldt-Jakob Disease Surveillance Unit at the University of Edinburgh examined tonometer heads and found they can retain cornea tissue that could infect other people -- even after cleaning and decontaminating the instrument.
"Retained corneal epithelial cells, following the standard decontamination routine of tonometer prisms, may represent potential prion infectivity," the researchers wrote in the British Journal of Ophthalmology last year. "Once the infectious agent is on the cornea, it could theoretically infect the brain."
Prions, misfolded proteins thought to be the cause of mad cow, CJD and similar diseases, are notoriously difficult to destroy and are capable of withstanding most sterilization procedures.
Laura Manuelidis, an expert on these diseases and section chief of surgery in the neuropathology department at Yale University, agreed with the British researchers that tonometers represent a potential risk of passing CJD to other people.
Manuelidis told UPI she has been voicing her concern about the risks of corneas since 1977 when her own study, published in the New England Journal of Medicine, showed the eye tissue, if infected, could transmit CJD.
At the time the procedure was done on Richard Da Silva, about a year before he died, she said it was "absolutely" possible he was infectious.
The CJD Incidents Panel, a body of experts set up by the U.K. Department of Health, noted in a 2001 report that procedures involving the cornea are considered medium risk for transmitting CJD. The first two patients who have a contaminated eye instrument used on them have the highest risk of contracting the disease, the panel said.
In 1999, the U.K. Department of Health banned opticians from reusing equipment that came in contact with patients' eyes out of concern it could result in the transmission of variant CJD, the form of the disease humans can contract from consuming infected beef products.
Richard Da Silva was associated with a cluster of five other cases of CJD in southern New York that raised concerns about vCJD.
None of the cases have been determined to stem from mad cow disease, but concerns about the cattle illness in the United States could increase in light of the USDA announcement Thursday that a cow tested positive on initial tests for the disease. If confirmed, this would be the second U.S. case of the illness; the first was detected in a Washington cow last December. The USDA said the suspect animal disclosed Thursday did not enter the food chain. The USDA did not release further details about the cow, but said results from further lab tests to confirm the initial tests were expected within seven days.
Ann Marie Da Silva said she informed the New York Health Department and later the eye doctor who performed the procedure about her husband's illness and her concerns about the risk of transmitting CJD via the tonometer.
The optometrist -- whom she declined to name because she did not want to jeopardize his career -- "didn't even know what this disease was," she said.
"He said the health department never called him and I called them (the health department) back and they didn't seem concerned about it," she added. "I just kept getting angrier and angrier when I felt I was being dismissed."
She said the state health department "seems to have an attitude of don't ask, don't tell" about CJD.
"There's a stigma attached to it," she said. "Is it because they're so afraid the public will panic? I don't know, but I don't think that the answer is to push things under the rug."
New York State Department of Health spokeswoman Claire Pospisil told UPI she would look into whether the agency was concerned about the possibility of transmitting CJD via tonometers, but she had not called back prior to story publication.
Disposable tonometers are readily available and could avoid the risk of transmitting the disease, Ironside and colleagues noted in their study. Ann Marie Da Silva said she asked the optometrist whether he used disposable tonometers and "he said 'No, it's a reusable one.'"
Ironside's team also noted other ophthalmic instruments come into contact with the cornea and could represent a source of infection as they are either difficult to decontaminate or cannot withstand the harsh procedures necessary to inactivate prions. These include corneal burrs, diagnostic and therapeutic contact lenses and other coated lenses.
Terry Singletary, whose mother died from a type of CJD called Heidenhain Variant, told UPI health officials were not doing enough to prevent people from being infected by contaminated medical equipment.
"They've got to start taking this disease seriously and they simply aren't doing it," said Singletary, who is a member of CJD Watch and CJD Voice -- advocacy groups for CJD patients and their families.
U.S. Centers for Disease Control and Prevention spokeswoman Christine Pearson did not return a phone call from UPI seeking comment. The agency's Web site states the eye is one of three tissues, along with the brain and spinal cord, that are considered to have "high infectivity."
The Web site said more than 250 people worldwide have contracted CJD through contaminated surgical instruments and tissue transplants. This includes as many as four who were infected by corneal grafts. The agency noted no such cases have been reported since 1976, when sterilization procedures were instituted in healthcare facilities.
Ironside and colleagues noted in their study, however, many disinfection procedures used on optical instruments, such as tonometers, fail. They wrote their finding of cornea tissue on tonometers indicates that "no current cleaning and disinfection strategy is fully effective."
Singletary said CDC's assertion that no CJD cases from infected equipment or tissues have been detected since 1976 is misleading.
"They have absolutely no idea" whether any cases have occurred in this manner, he said, because CJD cases often aren't investigated and the agency has not required physicians nationwide report all cases of CJD.
"There's no national surveillance unit for CJD in the United States; people are dying who aren't autopsied, the CDC has no way of knowing" whether people have been infected via infected equipment or tissues, he said.
Ann Marie Da Silva said she has contacted several members of her state's congressional delegation about her concerns, including Rep. Sue Kelly, R-N.Y., and Sen. Charles Schumer, D-N.Y.
"Basically, what I want is to be a positive force in this, but I also want more of a dialogue going on with the public and the health department," she said.
Singletary said CDC's assertion that no CJD cases from infected equipment or tissues have been detected since 1976 is misleading.
"They have absolutely no idea" whether any cases have occurred in this manner, he said, because CJD cases often aren't investigated and the agency has not required physicians nationwide report all cases of CJD.
"There's no national surveillance unit for CJD in the United States; people are dying who aren't autopsied, the CDC has no way of knowing" whether people have been infected via infected equipment or tissues, he said.
Friday, December 04, 2009
New guidance on decontamination of trial contact lenses and other contact devices has been revealed for CJD AND vCJD
SUNDAY, JANUARY 17, 2016
Of Grave Concern Heidenhain Variant Creutzfeldt Jakob Disease
TUESDAY, NOVEMBER 20, 2018
CDC Eyes of CJD patients show evidence of prions concerns for iatrogenic transmission
Disinfection of Multi-Use Ocular Equipment for Ophthalmological Procedures: A Review of Clinical Effectiveness, Cost-Effectiveness, and Guidelines
CADTH Rapid Response Report: Summary with Critical Appraisal
Shirley S. T. Yeung and Mary-Doug Wright.
Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2019 Feb 19. Copyright and Permissions
Context and Policy Issues In ophthalmology, there are certain equipment that are used and reused across different patients within a medical practice that resulting in indirect contact between multiple patients.1 This could pose a risk of cross infection between patients, especially with viruses and bacteria.1 One example of such equipment would be the tonometer, a device to measure the intraocular pressure in patients to determine risk of glaucoma.1 The tonometer tip is in direct contact with the patient’s eye and studies have demonstrated the transmission of hepatitis B virus, hepatitis C virus, human immunodeficiency virus (HIV), and Creutzfeldt-Jakob disease can occur between patients.1 Therefore, equipment cleanliness is critical.
The Canadian Optometrists Association has a general infection control guideline; however, in general, among available guidelines, there is little consistency and guidance in what the best approach would be to reduce transmission of diseases between patients.2 In vitro studies compared various sterilization techniques to determine whether or not viral particles are removed from the ophthalmic equipment but it is important to evaluate the impact of these cleanliness techniques on clinically relevant outcomes, such as infection transmission.1 Various guidelines and recommendations exist but it is unclear if there is any association between these techniques and disease transmission between patients.
The objective of this review is to evaluate the comparative clinical and cost-effectiveness of various disinfection techniques and/or procedures for multi-use ocular equipment in ophthalmology patients, as well as the guidelines for its use.
Go to: Research Questions
snip...
Summary of Findings Comparative clinical effectiveness No relevant evidence regarding the clinical effectiveness of various disinfection techniques and procedures for multi-use ocular equipment in ophthalmology patients was identified; therefore, no summary can be provided.
Cost-effectiveness One cost-effectiveness analysis was identified comparing Canadian patients from the hospital perspective which compared the cost-effectiveness between the use of alcohol swabs and peroxide bleach for cleaning of tonometry trips.6 Alcohol swabs are more cost-effective compared to peroxide bleach as the incremental cost-effectiveness ratio was $12,152 for each EKC case averted.6
Evidence-based guidelines Recommendations from the guidelines are summarized below and details are presented in Appendix 4.
The recommendations from the AORN guidelines are general and apply to all multi-use ophthalmic equipment in a surgical setting.7 The guideline indicates there is strong evidence to support the immediate cleaning of ophthalmic equipment according to the manufacturer’s instruction for use.7 There is moderate evidence to ensure the cleaning process is done in an adequate manner, including allowing enough time and personnel to ensure thorough cleaning and sterilization.7
Limitations Since no systematic reviews or primary studies were identified for this report, it is difficult to conclude the comparative clinical effectiveness for various cleaning and sterilization techniques for multi-use ocular equipment in ophthalmic patients. Of note, there were studies that were identified that included in vitro outcomes for various cleaning techniques, these are included in Appendix 5. There remains a research gap in identify the most clinically effective cleaning and sterilizing method for reducing transmission of potential diseases between patients in this setting.
One study examining the cost-effectiveness of various cleaning techniques was included and although it was a based on a Canadian population, the effectiveness outcomes were extrapolated from in vitro outcomes.6 This ultimately reduces the validity of these results as it may over or underestimate the magnitude of effect of the cleaning techniques. Additionally, little detail was provided on the exact cleaning procedures within this study, making it difficult for decision makers to determine what the cost-effective disinfection method may be.6
One guideline from the United States was identified and the recommendations are non-specific and do not provide much insight for policy makers as it was intended for a broad setting.6 Although there are a number of guidelines available in this particular area, many of them do not document rigorous methods or guideline development; therefore, are not included in this report but are listed in Appendix 5.
There remains a paucity of studies with patient relevant outcomes, ultimately making it difficult to inform clinical decisions.
Go to: Conclusions and Implications for Decision or Policy Making One cost-effectiveness study and one guideline were identified regarding cleaning techniques for the disinfection of multi-use ocular equipment.6,7
The identified cost-effective study indicated that the use of alcohol swabs was a more cost-effective technique compared to peroxide bleach as a cleaning method of tonometers for reducing epidemic keratoconjunctivitis in a Canadian population.6 However, no details on the cleaning procedures were provided.
One guideline recommends the importance of following the manufacturer’s instructions for use when cleaning and sterilizing ophthalmic equipment.7 It also stresses the importance of thorough and adequate cleaning and sterilization by ensuring the required conditions.7
No systematic reviews or primary studies were identified to answer the comparative clinical effectiveness between various cleaning techniques. Further research addressing various cleaning and sterilization techniques for multi-use ocular equipment, specifically for clinical outcomes in patients undergoing ophthalmology screening or treatment, would help to reduce uncertainty.
References
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Thank you kindly for this, i have been concerned and warning about this for 21 years.
yep, i said that 20 years ago about this very thing. but did anyone listen...no!
prepare for the storm...terry
year 1999 to 2000
Subject: RE-The Eyes Have It (cjd) and they could be stealing them from your loved one... "pay back time"
Date: Sat, 16 Sep 2000 10:04:26 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
Greetings List Members,
I hate to keep kicking a madcow, but this still is very disturbing to me. Not only for the recipient of the cornea's, but as well, for the people whom would be operated on, using the same tools that were used to put those stolen cornea's in the recipient with. No history of this donor or his family (re-ffi), or anything would be known, using stolen organs and or tissue's. I just think this is not only wrong, but very dangerous to a great many other people, as this is one of the most infectious tissues of TSE's. It seems that this practice of stealing organ/tissue happens more than we think. Anyway, the family of the victim which had their cornea's stolen, are now suing. In the example I used with my Mother, if 3 months before, she would have been in a catastrophic accident (car wreck, whatever), no autopsy (for whatever reason), no family (for whatever reason), she lay in the morgue, and after 4 hours, they come steal the cornea's, lot of people could have been infected, just because of lack of medical history of donor/family. It may be hypothetical, but very real. We need to stop the spread of this disease.
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
===========================================
MONDAY, DECEMBER 03, 2018
Prion Seeds Distribute throughout the Eyes of Sporadic Creutzfeldt-Jakob Disease Patients
Friday, December 04, 2009
*** New guidance on decontamination of trial contact lenses and other contact devices has been revealed for CJD AND vCJD
Thursday, January 29, 2009
***Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan, 1999–2008 (WARNING TO Neurosurgeons and Ophthalmologists)
Wednesday, August 20, 2008
***Tonometer disinfection practice in the United Kingdom: A national survey
2023 .Volume 47
Electronic publication date: 26/06/2023
http://health.gov.au/cdi
Creutzfeldt-Jakob disease surveillance in Australia: update to 31 December 2022
Christiane Stehmann, Matteo Senesi, Shannon Sarros, Amelia McGlade, Victoria Lewis, Laura Ellett, Daniel Barber, Marion Simpson, Genevieve Klug, Catriona McLean, Colin L Masters, Steven Collins
Alzheimer’s disease acquired from historic medical treatment
30 January 2024
Five cases of Alzheimer’s disease are believed to have arisen as a result of medical treatments decades earlier, reports a team of UCL and UCLH researchers.
Amyloid.jpeg
Alzheimer’s disease is caused by the amyloid-beta protein, and is usually a sporadic condition of late adult life, or more rarely an inherited condition that occurs due to a faulty gene. The new Nature Medicine paper provides the first evidence of Alzheimer’s disease in living people that appears to have been medically acquired and due to transmission of the amyloid-beta protein.
The people described in the paper had all been treated as children with a type of human growth hormone extracted from pituitary glands from deceased individuals (cadaver-derived human growth hormone or c-hGH). This was used to treat at least 1,848 people in the UK between 1959 and 1985, and used for various causes of short stature. It was withdrawn in 1985 after it was recognised that some c-hGH batches were contaminated with prions (infectious proteins) which had caused Creutzfeldt-Jakob disease (CJD) in some people. c-hGH was then replaced with synthetic growth hormone that did not carry the risk of transmitting CJD.
These researchers previously reported that some patients with CJD due to c-hGH treatment (called iatrogenic CJD) also had prematurely developed deposits of the amyloid-beta protein in their brains.* The scientists went on to show in a 2018 paper that archived samples of c-hGH were contaminated with amyloid-beta protein and, despite having been stored for decades, transmitted amyloid-beta pathology to laboratory mice when it was injected.** They suggested that individuals exposed to contaminated c-hGH, who did not succumb to CJD and lived longer, might eventually develop Alzheimer’s disease.
This latest paper reports on eight people referred to UCLH’s National Prion Clinic at the National Hospital for Neurology and Neurosurgery in London, who had all been treated with c-hGH in childhood, often over several years.
Five of these people had symptoms of dementia, and either had already been diagnosed with Alzheimer’s disease or would otherwise meet the diagnostic criteria for this condition; another person met criteria for mild cognitive impairment. These people were between 38 and 55 years old when they started having neurological symptoms. Biomarker analyses supported the diagnoses of Alzheimer’s disease in two patients with the diagnosis, and was suggestive of Alzheimer’s in one other person; an autopsy analysis showed Alzheimer’s pathology in another patient.
The unusually young age at which these patients developed symptoms suggests they did not have the usual sporadic Alzheimer’s which is associated with old age. In the five patients in whom samples were available for genetic testing, the team ruled out inherited Alzheimer’s disease.
As c-hGH treatment is no longer used, there is no risk of any new transmission via this route. There have been no reported cases of Alzheimer’s acquired from any other medical or surgical procedures. There is no suggestion that amyloid-beta can be passed on in day-to-day life or during routine medical or social care.
However, the researchers caution that their findings highlight the importance of reviewing measures to ensure there is no risk of accidental transmission of amyloid-beta via other medical or surgical procedures which have been implicated in accidental transmission of CJD.
The lead author of the research, Professor John Collinge, Director of the UCL Institute of Prion Diseases and a consultant neurologist at UCLH, said: “There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care. The patients we have described were given a specific and long-discontinued medical treatment which involved injecting patients with material now known to have been contaminated with disease-related proteins.
“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future.
“Importantly, our findings also suggest that Alzheimer's and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future.”
Co-author Professor Jonathan Schott (UCL Queen Square Institute of Neurology, honorary consultant neurologist at UCLH, and Chief Medical Officer at Alzheimer’s Research UK) said: “It is important to stress that the circumstances through which we believe these individuals tragically developed Alzheimer’s are highly unusual, and to reinforce that there is no risk that the disease can be spread between individuals or in routine medical care. These findings do, however, provide potentially valuable insights into disease mechanisms, and pave the way for further research which we hope will further our understanding of the causes of more typical, late onset Alzheimer’s disease.”
First author Dr Gargi Banerjee (UCL Institute of Prion Diseases) said: “We have found that it is possible for amyloid-beta pathology to be transmitted and contribute to the development of Alzheimer’s disease. This transmission occurred following treatment with a now obsolete form of growth hormone, and involved repeated treatments with contaminated material, often over several years. There is no indication that Alzheimer’s disease can be acquired from close contact, or during the provision of routine care.”
The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR UCLH Biomedical Research Centre, Alzheimer’s Research UK, and the Stroke Association.
If you were treated with the growth hormone (c-hGH) in the UK between 1959 and 1985 and would like further information about this research, please contact the National Prion Clinic via email (uclh.prion.help@nhs.net) or by telephone (020 7679 5142 or 020 7679 5036).
MONDAY, SEPTEMBER 11, 2023
Professor John Collinge on tackling prion diseases
“The best-known human prion disease is sporadic Creutzfeldt-Jakob disease (sCJD), a rapidly progressive dementia which accounts for around 1 in 5000 deaths worldwide.”
There is accumulating evidence also for iatrogenic AD. Understanding prion biology, and in particular how propagation of prions leads to neurodegeneration, is therefore of central research importance in medicine.
***> Singeltary Reply
Published: 09 September 2015
Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Singeltary Comment at very bottom of this Nature publishing;
re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.
First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.
Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.
where have we all heard this before? it's been well documented via the BSE Inquiry. have they not learned a lesson from the last time?
we have seen this time and time again in England (and other Country's) with the BSE mad cow TSE Prion debacle.
That 'anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.
The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients ?
who got pooled extracts injected from thousands of cadavers ? were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.
That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find 'alarming' is pathetic.
Sounds like the journalists had it right in the first place: 'Alzheimer's may be a transmissible infection' in The Independent to 'You can catch Alzheimer's' in The Daily Mirror or 'Alzheimer's bombshell' in The Daily Express
if not for the journalist, the layperson would not know about these important findings.
where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?
when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.
to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer's, the price of poker goes up drastically.
so, who makes that final decision, and how many more decades do we have to wait?
the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?
Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.
FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.
in my opinion, it's one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.
greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it's bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.
my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer's of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.
I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer's and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
Singeltary Comment at very bottom of this Nature publishing, takes a while to load...terry
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
CJD1/9 0185 Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1
http://web.archive.org/web/20090506012455/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?
3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1 BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
http://collections.europa...
''on the possible transmissibility of Alzheimer's''
9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly
(1) concerning a farmer with CJD who had BSE animals,
(2) on the possible transmissibility of Alzheimer's and
(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
THURSDAY, FEBRUARY 7, 2019
In Alzheimer's Mice, Decades-Old Human Cadaveric Pituitary Growth Hormone Samples Can Transmit and Seed Amyloid-Beta Pathology
Subject: CWD GSS TSE PRION SPINAL CORD, Confucius Ponders, What if?
REVIEW
***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***
***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<***
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<***
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***
Saturday, February 2, 2019
CWD GSS TSE PRION SPINAL CORD, Confucius Ponders, What if?
Friday, January 29, 2016
Synucleinopathies: Past, Present and Future, iatrogenic, what if?
FRIDAY, JANUARY 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Greetings Friends, Neighbors, and Colleagues,
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Confucius is confused again.
I was just sitting and thinking about why there is no genetic link to some of these TSE prion sGSS, sFFi, and it’s really been working on my brain, and then it hit me today.
what if, vpspr, sgss, sffi, TSE prion disease, was a by-product from iatrogenic gss, ffi, familial type prion disease ???
it could explain the cases of no genetic link to the gss, ffi, familial type prion disease, to the family.
sporadic and familial is a red herring, in my opinion, and underestimation is spot on, due to the crude prehistoric diagnostic procedures and criteria and definition of a prion disease.
I say again, what if, iatrogenic, what if, with all these neurological disorders, with a common denominator that is increasingly showing up in the picture, called the prion.
I urge all scientist to come together here, with this as the utmost of importance about all these neurological disease that are increasingly showing up as a prion mechanism, to put on the front burners, the IATROGENIC aspect and the potential of transmission there from, with diseases/disease??? in question.
by definition, could they be a Transmissible Spongiform Encephalopathy TSE prion type disease, and if so, what are the iatrogenic chances of transmission?
this is very important, and should be at the forefront of research, and if proven, could be a monumental breakthrough in science and battle against the spreading of these disease/diseases.
the US National Library of Medicine National Institutes of Health pub-med site, a quick search of the word SPORADIC will give you a hit of 40,747. of those, there are a plethora of disease listed under sporadic. sporadic simply means (UNKNOWN).
the US National Library of Medicine National Institutes of Health pub-med site, a quick search of the word FAMILIAL will give you a hit of 921,815. of those, there are a plethora of disease listed under familial.
again, sporadic and familial is a red herring, in my opinion.
also, in my opinion, when you start have disease such as sporadic Fatal Familial Insomnia, (and or sporadic GSS, or the VPSPr type prion disease), and there is NO familial genetic linkage to the family of the diseased, I have serious questions there as to a familial type disease, and thus, being defined as such.
snip...see full text;
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
22 years ago;
2001 Singeltary on CJD
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
26 MARCH 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Terry S. Singeltary, retired (medically)
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
Singeltary 2001
Subject: CJD or Alzheimer's or the same ???
Date: Sun, 29 Apr 2001 12:45:28 -0700
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Bovine Spongiform Encephalopathy
Greetings List,
thought some might be interested in this. I have always wondered if CJD and or all TSEs and Alzheimer's could be linked. i have been of the opinion that Alzheimer's is a TSE for a long time, just at the low end of the titre of infectivity scale. i also believe in the accumulation theory. by dose, you could be killed by one sitting, or one injection, or one whatever, depending on the titre of infectivity of that whatever. on the other hand, if the dose is not a lethal dose, over a period of time, the accumulation will become lethal (if consumption continued), and i believe the route/source/titre of infectivity, will be a key roll to the incubation period, and symptoms.
just my opinion...
Prusiner has spent the last 18 years trying to distance himself from a joint paper with GG Glenner in which prion diseases were recognized as just another amyloid. The recent keynote speech was especially amusing/annoying in that now he is completely turning the tables, trying to adsorb some strains of Alzheimer etc into "prions." The fact is, cross-recruitment has been a standard topic in amyloidoses since the late 70's.
Who would want plasma from someone with the ApoA2 mutation below, given that it can recruit the normal protein?
-=-=-
The context of the paper below is systemic hereditary amyloidosis, by which they mean an inherited condition with amyloid spread far and wide by the circulatory system. Damage from cross-beta fibril deposition occurs in kidneys, heart, periferal neurons, liver, or cornea. in contrast to CNS amyloid like CJD or AD.
The first was observed in 1950 by Ostertag, though it wasn't until 1978 that a constituent protein was identified (transthyretin, today 77 known mutational forms). Table I of the paper lists cystatin C (1 mutation), gelsolin (2), apolipoprotein A1 (9), lysozyme (2), and fibrinogen Aalpha (4).
None of these proteins are related. There are no sequence similarities or shared motifs. Most have alpha helix; large semi-speculative literature has these destablized by mutation or amphipathic with respect to beta sheet, or kinetically trapped during folding.
About a quarter of the mutations are frameshifts or stop codon read-thrus, ie mutations that generate random, unadapted polypeptide stretches. They are generally autosomal dominant, indicative of toxic gain-of-function, eg fibril formation. This means heterozygous; sometimes the normal product is recruited to amyloid, the mutant product is always there.
In some amyloids, the entire protein is present; in others just a proteolytic fragment. In the case here, the entire normal protein, as well as the extended read-through product, was found in amyloid. The patient studied spent 9 years on hemodialysis during which considerable readsorption of amyloid occurred, ie amyloid formation is balanced against amyloid degradation.
The most interesting observation in this paper is that there are now 4 lipid binding proteins seen in amyloid, serum amyloid A, ApoA1, ApoE, and now ApoA2.
"As a class, these proteins exist in a partly folded state in solution. The helical content is increased and stabilized upon binding to lipid ... any change in lipid metabolism or mutation in the protein that alters lipid binding will favor aggregatin and fibrillogenesis." That suggests that some apoA2 cases will appear sporadic, eg, be attributable to the disruption of lipid metabolism rather than be a mutation in this gene.
A New Human Hereditary Amyloidosis: The Result of a Stop-Codon Mutation in the Apolipoprotein AII Gene Genomics pp. 272-277 (doi:10.1006/geno.2000.6499) published electronically April 02, 2001
Merrill D. Benson1, ... Barbara Kluve-Beckerman Telephone: (317) 278-3428 . E-mail: mdbenson@iupui.edu .
Hereditary systemic amyloidosis may be caused by mutations in a number of plasma proteins including transthyretin, apolipoprotein AI, fibrinogen A-chain, lysozyme, and gelsolin. Each type of amyloidosis is inherited as an autosomal dominant disease and is associated with a structurally altered protein that aggregates to form amyloid fibrils. Here we report that the amyloid protein in a family with previously uncharacterized hereditary renal amyloidosis is apolipoprotein AII (apoAII) with a 21-residue peptide extension on the carboxyl terminus. Sequence analysis of the apoAII gene of affected individuals showed heterozygosity for a single base substitution in the apoAII stop codon. The mutation results in extension of translation to the next in-frame stop codon 60 nucleotides downstream and is predicted to give a 21-residue C-terminal extension of the apoAII protein identical to that found in the amyloid. This mutation produces a novel Bst NI restriction site that can be used to identify individuals with this gene by restriction fragment length polymorphism analysis. This is the first report of apoAII amyloid in humans and the first mutation identified in apoAII protein. Amyloid fibril formation from apoAII suggests that this lipoprotein, which is predicted to have an amphipathic helical structure, must undergo a transition to a beta -pleated sheet by a mechanism shared by other lipoproteins that form amyloid.
=-=-=-=-=
This can't be studied in the human genome because it lies in a wholly unsequenced region.
987696512-14444-6374
MKLLAATVLLLTICSLEGALVRRQAKEPCVESLVSQYFQTVTDYGKDLMEKVKSPELQAEAKSYFEKSKEQLTPLIKKAGTELVNFLSYFVELGTQPATQ
1 aggcacagac accaaggaca gagacgctgg ctaggccgcc ctccccactg ttaccaacat
61 gaagctgctc gcagcaactg tgctactcct caccatctgc agccttgaag gagctttggt
121 tcggagacag gcaaaggagc catgtgtgga gagcctggtt tctcagtact tccagaccgt
181 gactgactat ggcaaggacc tgatggagaa ggtcaagagc ccagagcttc aggccgaggc
241 caagtcttac tttgaaaagt caaaggagca gctgacaccc ctgatcaaga aggctggaac
301 ggaactggtt aacttcttga gctatttcgt ggaacttgga acacagcctg ccacccagtg
361 aagtgtccag accattgtct tccaacccca gctggcctct agaacaccca ctggccagtc
421 ctagagctcc tgtccctacc cactctttgc tacaataaat gctgaatgaa tcc
kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA
http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
SATURDAY, JULY 22, 2023
Alzheimer's Disease Update
TSE Prion and Endoscopy Equipment
Subject: Re: CJD * Olympus Endoscope
Date: Tue, 12 Oct 1999 15:57:03 –0500
From: "Terry S. Singeltary Sr."
To: GOLDSS@...
References: 1
Dear Mr. Goldstine, Hello again, I hope the CDC has not changed your mind, since our phone call, about sending me the information, in which we spoke of. I am still waiting for the information, re-fax. Someone had told me, you would not send me the information, but I told them you would, due to the importance of it pertaining to public safety, and the fact, you are a Doctor. I hope you don't disappoint me, and the rest of the public, and hide the facts, as the CDC and NIH have for years. Olympus can be part of the Truth, or you can be part of the cover-up. We are going to find out, sooner or later.
I already know, as do many more.
Still waiting,
Kind Regards,
Terry S. Singeltary Sr.
Wednesday, March 02, 2016
Endoscope Maker Olympus Agrees To $646 Million Settlement Over Kickbacks, while still ignoring the elephant in the room, CJD TSE PRIONS Health Inc.
*** Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al ***
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary
see full text;
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
I have researched human/animal TSEs now for over 5 years due to the death of my Mother from the Heidenhain Variant Creutzfeldt Jakob disease, one of six - known - variants of the infamous 'sporadic' CJD.
I did a little survey several years ago about CJD and ENDOSCOPY in 2001, and then went there again when another article was released recently. However, they seemed to only be concerned with the vCJD strain and risk from endoscopy equipment.
My concerns are if vCJD can be transmitted by blood, and there are now 6 variants of the infamous sporadic CJDs that they are documenting to date, how do they know that none of these 6 variants will not transmit the agent (prion) via blood?...especially since the sporadic CJDs are the only ones documented to date to transmit via the surgical arena and now that the CWD is spreading more and more, who knows about the cattle?
I would always read this study and it would bring me back to reality as to how serious/dangerous this agent is in the surgical/medical arena. You might want to read this short abstract from the late, great Dr. Gibbs twice, and let it really sink in. And please remember while reading some of these transmission studies, that most all, if not ALL these agents transmit freely to primates. Humans, of course, are primates.
Regarding claims that:
'Well, it has never been documented to transmit to humans."
There are two critical factors to think about:
A. CJD/TSEs in the USA are NOT reportable in most states and there is NO CJD/TSE questionnaire for most victims and their families, and the one they are now issuing asks absolutely nothing about route and source of the (prion) agent, only how the disease was diagnosed. Furthermore, the elderly are only very rarely autopsied, ie looking for Alzheimer's or 'FAST Alzheimer's' OR prion disease-related factors and phenomena, such as heart failure caused by disease.
B. It is unethical and against the law to do transmission studies of TSEs to humans, they are 100% FATAL.
I suggest you read these case studies about medical arena CJD transmission very carefully:
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Singeltary, Posted by flounder on 05 Nov 2014 at 21:27 GMT
WEDNESDAY, JANUARY 31,
Creutzfeldt Jakob Disease, CJD Support Group for short statured children of the 1970's and 1980's And 2024 Alzheimer’s iatrogenic Transmission
Thursday, January 25, 2024
TSE Prion Disease, Eyes, Ophthalmology Diagnostic Equipment, Iatrogenic, What If?
MONDAY, JANUARY 29, 2024
Iatrogenic Alzheimer’s disease in recipients of cadaveric pituitary-derived growth hormone
''The clinical syndrome developed by these individuals can, therefore, be termed iatrogenic Alzheimer’s disease, and Alzheimer’s disease should now be recognized as a potentially transmissible disorder.''
Terry S. Singeltary Sr.
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