Scientists identify locations of early prion protein deposition in retina, what if?
NEWS RELEASE 29-JAN-2021
Scientists identify locations of early prion protein deposition in retina
Findings indicate cones precede rods as targets for infection
NIH/NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
Research News
IMAGE IMAGE: (LEFT PANEL) EARLY IN PRION INFECTION, A PRION PROTEIN AGGREGATE (MAGENTA) BLOCKS THE ENTRANCE TO A CILIUM (GREEN) IN A RETINAL PHOTORECEPTOR. (LOWER RIGHT) IN PRION-INFECTED RETINA, PRION PROTEIN (MAGENTA)... view more
CREDIT: NIAID
WHAT:
The earliest eye damage from prion disease takes place in the cone photoreceptor cells, specifically in the cilia and the ribbon synapses, according to a new study of prion protein accumulation in the eye by National Institutes of Health scientists. Prion diseases originate when normally harmless prion protein molecules become abnormal and gather in clusters and filaments in the human body and brain.
Understanding how prion diseases develop, particularly in the eye because of its diagnostic accessibility to clinicians, can help scientists identify ways to slow the spread of prion diseases. The scientists say their findings, published in the journal Acta Neuropathologica Communications, may help inform research on human retinitis pigmentosa, an inherited disease with similar photoreceptor degeneration leading to blindness.
Prion diseases are slow, degenerative and usually fatal diseases of the central nervous system that occur in people and some other mammals. Prion diseases primarily involve the brain, but also can affect the eyes and other organs. Within the eye, the main cells infected by prions are the light-detecting photoreceptors known as cones and rods, both located in the retina.
In their study, the scientists, from NIH's National Institute of Allergy and Infectious Diseases at Rocky Mountain Laboratories in Hamilton, Montana, used laboratory mice infected with scrapie, a prion disease common to sheep and goats. Scrapie is closely related to human prion diseases, such as variant, familial and sporadic Creutzfeldt-Jakob disease (CJD). The most common form, sporadic CJD, affects an estimated one in one million people annually worldwide. Other prion diseases include chronic wasting disease in deer, elk and moose, and bovine spongiform encephalopathy in cattle.
Using confocal microscopy that can identify prion protein and various retinal proteins at the same time, the scientists found the earliest deposits of aggregated prion protein in cone photoreceptors next to the cilia, tube-like structures required for transporting molecules between cellular compartments. Their work suggests that by interfering with transport through cilia, these aggregates may provide an important early mechanism by which prion infection selectively destroys photoreceptors. At a later study timepoint, they observed similar findings in rods.
Prion protein also was deposited in cones and rods adjacent to ribbon synapses just before the destruction of these structures and death of photoreceptors. Ribbon synapses are specialized neuron connections found in ocular and auditory neural pathways, and their health is critical to the function of retinal photoreceptors in the eye, as well as hair cells in the ear.
The researchers say such detailed identification of disease-associated prion protein, and the correlation with retinal damage, has not been seen previously and is likely to occur in all prion-susceptible species, including people.
Next the researchers are hoping to study whether similar findings occur in retinas of people with other degenerative diseases characterized by misfolded host proteins, such as Alzheimer's and Parkinson's diseases.
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ARTICLE:
J Striebel et al. Prion-induced photoreceptor degeneration begins with misfolded prion protein accumulation in cones at two distinct sites: cilia and ribbon synapses. Acta Neuropathologica Communications DOI: 10.1186/s40478-021-01120-x (2021).
RELATED:
J Striebel et al. Microglia are not required for prion-induced retinal photoreceptor degeneration. Acta Neuropathologica Communications DOI: 10.1186/s40478-019-0702-x (2019).
J Carroll et al. Microglia are critical in host defense against prion disease. Journal of Virology DOI: 10.1128/JVI.00549-18 (2018).
WHO:
Bruce Chesebro, M.D., chief of NIAID's Laboratory of Persistent Viral Diseases, is available to comment on this study.
CONTACT:
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Published: 29 January 2021
Prion-induced photoreceptor degeneration begins with misfolded prion protein accumulation in cones at two distinct sites: cilia and ribbon synapses
James F. Striebel, Brent Race, Jacqueline M. Leung, Cindi Schwartz & Bruce Chesebro Acta Neuropathologica Communications volume 9, Article number: 17 (2021) Cite this article
Abstract
Accumulation of misfolded host proteins is central to neuropathogenesis of numerous human brain diseases including prion and prion-like diseases. Neurons of retina are also affected by these diseases. Previously, our group and others found that prion-induced retinal damage to photoreceptor cells in mice and humans resembled pathology of human retinitis pigmentosa caused by mutations in retinal proteins. Here, using confocal, epifluorescent and electron microscopy we followed deposition of disease-associated prion protein (PrPSc) and its association with damage to critical retinal structures following intracerebral prion inoculation. The earliest time and place of retinal PrPSc deposition was 67 days post-inoculation (dpi) on the inner segment (IS) of cone photoreceptors. At 104 and 118 dpi, PrPSc was associated with the base of cilia and swollen cone inner segments, suggesting ciliopathy as a pathogenic mechanism. By 118 dpi, PrPSc was deposited in both rods and cones which showed rootlet damage in the IS, and photoreceptor cell death was indicated by thinning of the outer nuclear layer. In the outer plexiform layer (OPL) in uninfected mice, normal host PrP (PrPC) was mainly associated with cone bipolar cell processes, but in infected mice, at 118 dpi, PrPSc was detected on cone and rod bipolar cell dendrites extending into ribbon synapses. Loss of ribbon synapses in cone pedicles and rod spherules in the OPL was observed to precede destruction of most rods and cones over the next 2–3 weeks. However, bipolar cells and horizontal cells were less damaged, indicating high selectivity among neurons for injury by prions. PrPSc deposition in cone and rod inner segments and on the bipolar cell processes participating in ribbon synapses appear to be critical early events leading to damage and death of photoreceptors after prion infection. These mechanisms may also occur in human retinitis pigmentosa and prion-like diseases, such as AD.
snip...
Conclusions The present experiments report two new areas of deposition of abnormal disease-associated PrPSc in prion-infected retina. These regions both involve photoreceptor cone and rod cells which then go on to die as a part of the disease process. The location of the PrPSc deposition suggests that the damage mechanisms may involve interruption of the ciliary transport pathways of molecules between the inner and outer segments of PR cells as well as damage to ribbon synapses found in the synaptic end-feet of rods and cones near the OPL. Possible synergy and specificity between these two mechanisms remains to be worked out. These mechanisms might be active in other human retinal degenerative diseases where protein misfolding occurs, such as retinitis pigmentosa and prion-like diseases, such as AD and PD.
***> Scientists identify locations of early prion protein deposition in retina
***> We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent.
***>The abnormal form of the prion protein is present in the retina in the most common sCJD subtype (MM1), albeit at levels lower than those found previously in vCJD and in sCJD of the VV2 subtype.
what if?
all iatrogenic cjd is, is sporadic cjd, before the iatrogenic event is discovered, traced back, provern, documented, put into the academic domain, and then finally the public domain, this very seldom happens, thus problem solved, it's all sporadic cjd, PLUS, SPORADIC CJD HAS NOW BEEN LINKED TO ATYPICAL AND TYPICAL BSE, SCRAPIE, AND NOW CWD. ...terry
FRIDAY, SEPTEMBER 06, 2019
Disinfection of Multi-Use Ocular Equipment for Ophthalmological Procedures: A Review of Clinical Effectiveness, Cost-Effectiveness, and Guidelines
Wednesday, September 11, 2019
Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion
Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure
Variant Creutzfeldt–Jakob disease was identified in a technician who had cut her thumb while handling brain sections of mice infected with adapted BSE 7.5 years earlier. The long incubation period was similar to that of the transfusion-transmitted form of the disease.
FRIDAY, DECEMBER 04, 2009
New guidance on decontamination of trial contact lenses and other contact devices has been revealed for CJD AND vCJD
Friday, July 17, 2009
Revision to pre-surgical assessment of risk for vCJD in neurosurgery and eye surgery units Volume 3 No 28; 17 July 2009
Wednesday, August 20, 2008
Tonometer disinfection practice in the United Kingdom: A national survey
CJD Human Cornea Tissue, Recall END OF ENFORCEMENT REPORT FOR AUGUST 5, 2009 Posted Aug 07 2009 6:32pm
From: TSS
Subject: Tonometer prism sterilisation: A local and UK national survey (TSE)
Date: August 24, 2007 at 1:24 pm PST
1: Cont Lens Anterior Eye. 2007 Aug 17; [Epub ahead of print]
Tonometer prism sterilisation: A local and UK national survey.
Chandra A, Barsam A, Hammond CJ. West Kent Eye Centre, Princess Royal University Hospital, Orpington, Kent BR6 8ND, UK.
PURPOSE: First to audit local adherence to a protocol of use of an alcohol wipe for each tonometry, and secondly to assess current practice nationally in the UK.
METHOD: The audit was carried out at two units: The West Kent Eye Centre at the Princess Royal University Hospital (Orpington, UK) and Queen Mary's Hospital (Sidcup, UK). The standard set for this audit was 100% sterilisation. During a 1-week period in November 2005, the number of alcohol wipes was counted in each consultation room after outpatient clinics, with the doctors being assessed blind to the survey. The number of Goldman applanation tonometry intra-ocular pressures recorded by each clinician was counted by inspection of the medical records of patients seen. Secondly, departments listed in the UK Directory of Training Posts were contacted by telephone and the senior nurse was interviewed. They were asked directly about their department's tonometer prism sterilisation and management.
RESULTS: The local audit showed only 54% of tonometry measurements were associated with sterilisation using an alcohol-impregnated wipe. The national survey included 140 of the 152 UK training departments. Thirty-three (23.6%) departments used disposable tonometer prisms routinely. The remaining 107 (76.4%) used non-disposable prisms. Eighty-five (60.7%) departments provided sodium hypochlorite for prism sterilisation, with 69 (81.2%) of these departments providing more than one prism/clinician to allow full exposure to the disinfectant. Twenty-two (15.7%) departments used alcohol wipes. Only 8 (7.5%) of the 107 departments using non-disposable prisms tracked these prisms, despite Royal College of Ophthalmologists guidelines that they should be. These same 8 (7.5%) departments replaced the non-disposable prisms as per manufacturer guidelines. 19.3% of charge nurses were aware of a policy for tonometry in patients with, or at risk of, prion disease.
CONCLUSIONS: This study highlights that sterilisation of tonometer prisms was inconsistent in a local audit. Nationally, practices were varied. The majority of ophthalmology departments continued to use non-disposable tonometer prisms, but few seemed aware of the Royal College of Ophthalmologists' recommendation that disposable prisms are used in patients at risk of prion disease, and few track tonometer heads or replace them according to manufacturers guidelines. Use of disposable tonometer prisms would seem to reduce concerns about sterilisation, as well as prevent spread of common pathogens.
PMID: 17703987 [PubMed - as supplied by publisher]
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PA-34
SPORADIC CREUTZFELDT-JAKOB DISEASE: PRPRES IS CONSTANTLY PRESENT IN THE RETINA, AND RARELY IN THE OPTIC NERVE
M. Mangieri1, G. Giaccone1, L. Limido1, G. Di Fede1, S. Suardi1, R. Capobianco1, P. Fociani2, O. Bugiani1, F. Tagliavini1 1 Istituto Nazionale Neurologico Carlo Besta, Division of Neuropathology and Neurology 5, Milano, Italy and 2 Ospedale Luigi Sacco, Division of Pathology, Università di Milano, Milano, Italy
e-mail: mmangieri@istituto-besta.it
Creutzfeldt-Jakob disease (CJD) is marked by the presence of the protease-resistant prion protein (PrPres) in the brain. Studies of the retina and optic nerve in patients with CJD are scanty and on very small series of patients. We analysed ocular tissues of sporadic CJD patients (retina of 58 and optic nerve of 51), representing all combinations of PRNP codon 129 polymorphisms and PrPres types by Parchi, except VV1. Ocular tissue from 24 patients with other neurological diseases were used as controls. The ocular tissue was collected at autopsy and the samples were fixed in Carnoy solution or frozen. Before immunohistochemistry with 3F4 antibody, the sections were pretreated with proteinase K and guanidine thiocyanate. In all cases of sCJD the retina showed immunoreactivity for PrPres localized in the inner and outer plexiform layers, with a synaptic type of labelling. No difference in the pattern of labeling was detected between CJD patients with different PRNP codon 129 polymorphisms and PrPres types in the brain. In all cases with frozen retinal tissue available (n = 18), the immunoblot was positive for PrPres . Two out of the 51 sCJD showed the deposition of PrPres also in the optic nerve, corresponding to an immunostaining delineating stellate cells and associated with the presence of numerous CD68- and CD45-positive cells. Our results demonstrate the presence of the pathological form of prion protein not only in the retina of all sCJD cases analysed, but also in optic nerve in a small subset of sCJD patients, a finding previously described only in variant CJD and in experimental animal models. Moreover, our data suggest a correlation between the deposition of PrPres and inflammatory changes in the optic nerve in sCJD.
neuroprion 2006 abstract book
----- Original Message -----
From: "Terry S. Singeltary Sr." <[log in to unmask]>
To: <[log in to unmask]>
Sent: Thursday, December 28, 2006 10:23 AM
Subject: Ophthalmic Surgery in Prion Diseases
Volume 13, Number 1–January 2007
Dispatch
Ophthalmic Surgery in Prion Diseases
Tsuyoshi Hamaguchi,*1 Moeko Noguchi-Shinohara,* Yosikazu Nakamura,†2 Takeshi Sato,‡2 Tetsuyuki Kitamoto,§2 Hidehiro Mizusawa,¶2 and Masahito Yamada*2 *Kanazawa University Graduate School of Medical Science, Kanazawa, Japan; †Jichi Medical University, Shimotsuke, Japan ‡National Center for Neurology and Psychiatry, Ichikawa, Japan; §Tohoku University Graduate School of Medicine, Sendai, Japan; and ¶Tokyo Medical and Dental University, Tokyo, Japan
Suggested citation for this article
Abstract
Eleven (1.8%) of 597 patients underwent ophthalmic surgery within 1 month before the onset of prion disease or after the onset. All ophthalmologists reused surgical instruments that had been incompletely sterilized to eliminate infectious prion protein. Ophthalmologists should be aware of prion diseases as a possible cause of visual symptoms and use disposable instruments whenever possible.
Visual impairment occurs in 10% to 20% of patients with sporadic Creutzfeldt-Jakob disease (sCJD) during an early stage of the disease (Heidenhain variant) (1,2). Some patients with prion diseases may visit ophthalmologists with visual impairment due to prion diseases or with coexisting age-related eye diseases (3,4).
Infectious prion protein (PrPSc) was identified in the retina and optic nerve in patients with variant CJD (vCJD) and sCJD (5,6), and CJD has been transmitted by corneal transplantation (7,8). In the World Health Organization (WHO) guidelines, eyes were classified as highly infectious tissues (9).
Secondary transmission of PrPSc through ophthalmic surgery could possibly be prevented around the onset of prion diseases, although surgery that is performed long before the onset of prion diseases would not have that potential. It is important to understand the current status of ophthalmic surgery for patients with prion diseases and to clarify the clinical features of the patients with prion diseases who undergo ophthalmic surgery. Here, we describe the relevant data from CJD surveillance in Japan.
The Study.....snip full text ;
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what if ???
Greetings Friends, Neighbors, and Colleagues,
Eye procedure raises CJD concerns
November 19, 2004 United Press International by STEVE MITCHELL
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 casesof 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.
Cadaver corneal transplants -- without family permission
Houston, Texas channel 11 news 28 Nov 99
Reported by Terry S. Singeltary Sr.son of CJD victim
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
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Previous story--
Cadaver corneal transplants -- without family permission...
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Sept. 15, 2000, 11:39PM
Slain woman's family sues over missing eyes
By BILL MURPHY
Copyright 2000 Houston Chronicle
The family of a woman who was stabbed to death last year has filed a lawsuit accusing the Lions Eye Bank of Houston of removing the woman's eyes without permission and inserting plastic discs in their place.
Daisy Diaz's relatives were horrified when they saw her body and noticed her eyes were missing, said their lawyer, Duncan Neblett III.
"They're a Catholic family," Neblett said. "They have strong beliefs about the body and burial. They were really upset by this."
Dorey Zidrow, the eye bank's spokeswoman, said she could not specifically discuss the Diaz case because it was in litigation. But Zidrow said a state law allows doctors to remove corneas -- the dime-sized lens near the eye's surface -- from a corpse without the family's permission.
The eye bank's usual procedure calls for removing the corneas, Zidrow said, but not the entire eyes.
"There are an awful lot of people who benefit from this program in the state of Texas," she said.
Diaz, 25, was stabbed to death in her apartment in the 400 block of Thornton in October. Her brother-in-law, 30-year-old Raudel Quiroz, is charged in the killing but has not been caught.
Neblett said authorities have told him Quiroz may have returned to his native Guatemala.
Neither Diaz nor her family had given permission to donate any of her organs, Neblett said.
Although state law allows corneas to be removed from corpses without first gaining the family's permission, they cannot be removed over the family's stated objection.
The eye bank is located at, and staffed by, the Baylor College of Medicine, and receives part of its funding from the Lions Club.
The Diaz lawsuit is the second such suit to be filed against the eye bank in recent years.
The family of Levi Perry Jr., a Houston teacher shot to death in MacGregor Park in 1994, also alleged in their suit that Perry's eyes were removed. The family was awarded $345,000 from the eye bank in April 1999.
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THE LEGALITY OF STEALING ORGAN/TISSUE...
TEXAS STATUTES
Sec. 693.012. Removal of Corneal Tissue Permitted Under Certain Circumstances.
On a request from an authorized official of an eye bank for corneal tissue, a justice of the peace or medical examiner may permit the removal of corneal tissue if:
(1) the decedent from whom the tissue is to be removed died under circumstances requiring an inquest by the justice of the peace or medical examiner;
(2) no objection by a person listed in Section 693.013 is known by the justice of the peace or medical examiner; and
(3) the removal of the corneal tissue will not interfere with the subsequent course of an investigation or autopsy or alter the decedent's postmortem facial appearance.
Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.
Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.
Search 1999 Legislation for: 693.012
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TEXAS STATUTES
Sec. 693.003. Consent Required in Certain Circumstances.
(a) A medical examiner or a person acting on the authority of a medical examiner may not remove a visceral organ unless the medical examiner or person obtains the consent of a person listed in Section 693.004.
(b) If a person listed in Section 693.004 is known and available within four hours after death is pronounced, a medical examiner or a person acting on the authority of a medical examiner may not remove a nonvisceral organ or tissue unless the medical examiner or person obtains that person's consent.
(c) If a person listed in Section 693.004 cannot be identified and contacted within four hours after death is pronounced and the medical examiner determines that no reasonable likelihood exists that a person can be identified and contacted during the four-hour period, the medical examiner may permit the removal of a nonvisceral organ or tissue.
Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.
Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.
Search 1999 Legislation for: 693.003
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PLEASE NOTE; the bottom would only pertain to those who know of the law. if you don't know about it, you cannot dispute, so in four hours, they can legally remove body organs, as long as they don't disfigure. and who is to know the difference? makes me wonder of some of my dead relatives, and if they were burried with their eye's and or any of their organs. This is very disturbing, if not for moral reasons, but for the risk of dangerous pathogens (human TSE's, etc.) to be transmitted. only time will tell, but i am very disturbed. these laws are not morally correct. They should be re-written as to they cannot so easily take your organs, with no one knowing. The Family or Victim, must consent. There should be some kind of research on donor/family medical history...TSS
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Sec. 693.013. Persons Who May Object to Removal.
The following persons may object to the removal of corneal tissue:
(1) the decedent's spouse;
(2) the decedent's adult children, if there is no spouse;
(3) the decedent's parents, if there is no spouse or adult child; or
(4) the decedent's brothers or sisters, if there is no spouse, adult child, or parent.
Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.
Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.
Search 1999 Legislation for: 693.013
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to cover one's butt....
Sec. 693.014. Immunity From Damages in Civil Action.
(a) In a civil action brought by a person listed in Section 693.013 who did not object before the removal of corneal tissue, a medical examiner, justice of the peace, or eye bank official is not liable for damages on a theory of civil recovery based on a contention that the person's consent was required before the corneal tissue could be removed.
(b) Chapter 104, Civil Practice and Remedies Code, applies to a justice of the peace, medical examiner, and their personnel who remove, permit removal, or deny removal of corneal tissue under this subchapter as if the justice of the peace, medical examiner, and their personnel were state officers or employees.
Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.
Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.
Search 1999 Legislation for: 693.014
[[[as you can see, they knew it was wrong when they wrote the laws. or they would not have covered the rear-ends so well...TSS]]]
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thanks again, kind regards, Terry S. Singeltary Sr.
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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.
PMID: 8006664 [PubMed - indexed for MEDLINE]
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease
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..
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
iatrogenic tse prion
Terry S. Singeltary Sr.
