Fake news.
Gary
Gary
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The same amount that had it before they started testing for it...Originally posted by CrookedArrow View PostComment
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Well thank you Terry, but at my age I'm just not too worried about CWD killing me. I don't hunt any known CWD areas and if it eventually spreads everywhere, just exactly what would you suggest I do about it ? Stop eating venison ? Ain't happening in my lifetime !Originally posted by flounder9 View Postjust hope your luck holds up drycreek, once this species jump makes it, and the cwd mutates to different strains, which it has, only time will tell. bbbut, it's the friendly fire that i am worried about. iatrogenic. medical, surgical, tissue, instruments, all proven, friendly fire, for the genetically unfortunate ones, the ones more susceptible, do you feel lucky, how about your children, and their children, do you want to roll the dice, you might be lucky, like lucky thought, but who has heard from lucky lately ;-)
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]
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract ***> This is very likely to have parallels with control efforts for CWD in cervids.
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2
Abstract
The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity.
Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids.
Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent.
Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA).
A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay.
Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3.
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.
Funding This study was funded by DEFRA within project SE1865.
Competing interests None declared.
Saturday, January 5, 2019
Rapid recontamination of a farm building occurs after attempted prion removal
THURSDAY, FEBRUARY 07, 2019
CWD TSE Prion, and Processing your own meat
kind regards, terryComment
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Pretty sure he isn’t allowed to post on THF anymore.Originally posted by CrookedArrow View PostComment
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Since you’re giving up can I have all your hunting equipment?Originally posted by Passafist View Post
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Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'Originally posted by Drycreek3189 View Post
DIVISION OF NEUROPATHOLOGY University of Texas Medical Branch 114 McCullough Bldg. Galveston, Texas 77555-0785
FAX COVER SHEET
DATE: 4-23-98
TO: Mr. Terry Singeltary @ -------
FROM: Gerald Campbell
FAX: (409) 772-5315 PHONE: (409) 772-2881
Number of Pages (including cover sheet):
Message:
*CONFIDENTIALITY NOTICE*
This document accompanying this transmission contains confidential information belonging to the sender that is legally privileged. This information is intended only for the use of the individual or entry names above. If you are not the intended recipient, you are hereby notified that any disclosure, copying distribution, or the taking of any action in reliances on the contents of this telefaxed information is strictly prohibited. If you received this telefax in error, please notify us by telephone immediately to arrange for return of the original documents. -------------------------- Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Admitting Race: C
Attending Dr.: Date / Time Admitted : 12/14/97 1228 Copies to:
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
Autopsy NO.: AU-97-00435
AUTOPSY INFORMATION: Occupation: Unknown Birthplace: Unknown Residence: Crystal Beach Date/Time of Death: 12/14/97 13:30 Date/Time of Autopsy: 12/15/97 15:00 Pathologist/Resident: Pencil/Fernandez Service: Private Restriction: Brain only
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
***TYPE: Anatomic(A) or Clinical(C) Diagnosis. IMPORTANCE: 1-immediate cause of death (COD); 2.ureterlying COD; 3-contributory COD: 4.concomitant, significant; 5-incidental ***
Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date; Time: 01/30/98 - 0832
Page: 1 Continued .... --------------
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683
Pathology Report
Autopsy NO,: AU-97-00435
MICROSCOPIC DESCRIPTION: The spongiform change is evident in all areas of neocortex, varying from mild to moderate in severity with only very mild neuronal loss and gliosis. In the bilateral occipital lobes, there is severe loss cortical neurons and gliosis, with a corresponding pallor of the underlying white matter. There is only minimal, focal spongiform change in corpus striatum, lentiform nuclei, thalamus, hippocampus, brainstem and cerebellum. There is no significant loss of neurons from the lateral geniculate nucleus, and the optic chiasm and tracts are well-myelinated.
SECTIONS TAKEN: N-l) Pituitary, N-2) Right frontal, N-3) Right inferior frontal, N-4) Right caudate putamen. N-5) Right lentiform nuclei, N-6) Right hippocampus, N-7) optic chiasm. N-8) Left inferior temporal lobe, N-9) Right inferior occipital, N-10} Cerabellum. N-l1) Midbrain, N-12) Pons, N-13) Medulla.
FINAL DIAGNOSES: BRAIN: 1. Clinical history of rapidly progressive dementia, clinically consistent with Creutzfeldt-Jakob Disease.
a. spongiform encephalopathy, most Severe in occipital lobes, consistent with Heidenhain variant of Creutzfeldt-Jakob disease.
b. Ventriculer enlargement, moderate, consistent with atrophy. 1. Communicating spherical enlargement of occipital horn of left lateral ventricle (possible incidental congenital anomaly).
DURA; Left subdural hemorrhage, recent, minimal.
PITUITARY: Severe capillary congestion.
COMMENTS; See also western blot report from Dr. Gambetti's lab Amyloid stains are not completed for this case as of this date. The results, which are not essential for the diagnosis, will be reported separately in an addendum.
(this was hand written notes) no amyloid evident in the special stains. no evidence of plaques.GAE
Gerald A. Campbell, M.D., Pathologist Division of Neuropathology
(Electronic Signature}. (Gross: 01/16/98 Final: 02/08/98
Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date: Time: 02/09/98 - 1120
Page 2 END OF REPORT -------
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 fax (409) 772-5683 Pathology Report
Date/Time of Death: 12/14/97 Autopsy No.: AU-97-00435
NEUROPATHOLOGY CONSULTATION
CLINICAL HISTORY This patient was a 63-year-old white female with recent onset of progressive dementia. She was well until September of this year, when she noted a decrease in her visual activity and was found to have visual field defects as well. MRI revealed no lesions in the orbits or optic pathways. She was admitted to the hospital with the working diagnosis of bilateral optic neuropathy for a course of intravenous methylprednisolone, but her vision continued to deteriorate. She developed increasing memory and speech impairment, weakness and myoclonus. She died on 12/14/97, approximately three and one-half months after her symptoms started.
Date/Time of Death: 12/14/97 13:30 Date/Time Autopsy: 12/15/97 15:00 Pathologist Resident: PENCIL/FERNANDEZ
GROSS DESCRIPTION: Submitted are the brain, convexity dura and pituitary gland.
The pituitary gland is very dark and almost hemorrhagic in appearance, but has no obvious hematoma. It is submitted totally for histology.
The right convexity dura has diffuse but minimal subdura hemorrhage, and the dura is otherwise unremarkable.
The brain is normally developed with normal size for an adult and is symmetric externally. It does not have apparent sulcal widening. There is mild congestion of the leptomeninges, which are transparent. There is no evidence of inflammatory exudete. There is no evidence of internal softenings or other lesions externally. The cerebral arteries have focal atherosclerosis, but are without significant compromise of the vessels lumens. There is no evidence of aneurysms or malformations.
The hemispheres are sliced coronally revealing, a ventricular system which is mildly enlarged. The cortical ribbon is normal in thickness throughout most of the brain, except for the inferior and medial occipital lobes bilaterally, where the cortex is firm, thin and has a brownish discoloration, more severely so on the left than the right. In addition there is a spherical enlargement of the left occipital horn of the lateral ventricle which communicates with the remainder of the lateral ventricle. The tissue of the white matter around this enlargement is somewhat softer then in other areas. Other areas of the brain are grossly unremarkable. The brainstem and cerebellum are sliced transversely, revealing normal development and no evidence of gross changes or lesions.
DICTATED BY: GERALD A. CAMPBELL, M.D., PATHOLOGIST 01/16/98
Page 1 Continued .... ---------------
Patient Account: 90000014-518 Med. Rec. No,: (0160)118511Q
Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex:F Race:C Admitting Dr.: Attending Dr: Date/Time Admitted: 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY REPORT Autopsy Office (409)772-2858 Autopsy No.: AU-97-00435
CLINICAL SUMMARY:
This is a 63-year-old white female with a recent onset of progressive dementia. Her past medical history is significant for hypothyroidism. She was well until September of this year, when she noted visual difficulty. By mid-October, she could not read the newspaper. She was found to have a decrease in visual acuity and visual field defects. One week after her initial evaluation, a panel of blood tests showed no significant abnormalities and a MRI revealed some periventricular white matter "plaque-like" areas but no lesions in the orbits or optic pathways.
The patient had continued deterioration and distortion of her vision. The visual field defects increased, and she was found to have paracentral scotomas which were thought to be consistent with bilateral optic neuropathy. Early in November, she was admitted to the hospital for a course of intravenous methyl prednisolone.
During her hospital stay, she was noted to have short term memory and speech impairment; her vision did not improve. She was discharged with the diagnosis of Creutzfeldt-Jakob disease.
Later, the patient developed progressive dementia with marked impairment of speech and memory. She had complete visual loss, increased weakness and myoclonus. She died on December 14, 1997.
MF /AV 12/16/97
Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date / Time: 01//30/98 - 0832 Page: 2 Continued .... --------------
Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Race: C Admitting Dr.: Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston. Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
AU-97-00435
GROSS DESCRIPTION:
EXTERNAL EXAMINATION: The body is that of a 63-year-old well-nourished, well-developed white female. There is no rigor mortis present, and there is unfixed dependent lividity on the posterior surface. The head is normocephalic with a moderate amount of gray, medium length scalp hair. The irides are blue with equal pupils measuring 0.4 mm in diameter. The nares are patent with no exudate. Dentition is fair. Buccal membranes are normal. There is normal female hair distribution. The chest does not have increased anterior-posterior diameter. The abdomen is slightly protuberant. Lymph node enlargement is not present. The extremities are unremarkable. The genitalia are those of a normal female. Two well-healed remote scars are identified in the abdomen: one in the right upper quadrant and another in the superpubic area.
BRAIN: The brain weighs 1450 gm. The gyri and sulci display a normal pattern without edema or atrophy. The meninges show no abnormalities. The circle of Willis, basilar and vertebral arteries show no significant atherosclerosis. The brain is fixed in formalin for later examination by a neuropathologist (see neuropathology report). No indentation of the cingulate gyri, unci or molding of the cerebellar tonsils are noted.
SPINAL CORD: The spinal cord is not removed.
PITUITARY GLAND: The pituitary gland is removed and is fixed in formalin for subsequent examination by a neuropathologist.
MF /AV 12/16/97
Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date / Time: 01/30/98 - 0832
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Patient Account : 90000014-518 Med. Rec. No.: (0160)118511Q patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Race: C Admitting Dr.: Attending Dr,: Date/Time Admitted: 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683
Pathology Report AU-97-00435
MICROSCOPIC DESCRIPTION:
BRAIN: Histologic examination of multiple sampled areas of the brain showed the characteristic features of Creutzfetdt-Jakob disease. These were present in most sections, but were particularly prominent in the occipital cortex. The spongiform degeneration was seen in the neuropil of the gray matter as multiple vacuoles amoung numerous reactive astrocytes and occasional neuronal cell bodies. These changes were most notable in the basal layer of the cortex. PAS and amyloid stains will be performed on selected sections to asses the presence of plaques.
MF /MF 01/28/98
Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date / Time: 01/30/98 - 0832
Page: 4 Continued .... --------------
Patient Account: 90000014-518 Med. Rec. No.: (0160}118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Race: C Admitting Dr.: Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 775550-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
Autopsy office (409)772-2858 Autopsy No.: AU-97-00435
FINAL AUTOPSY REPORT
CLINICOPATHOLOGIC CORRELATION:
The clinical findings in this case strongly suggest the diagnosis of Creutzfeldt-Jakob disease: progressive dementia, typical EEG changes, visual disturbances and myoclonus. These characteristics indicate this is a "probable case of CJD", according the criteria set by the EC Surveillance Group of Creutzfeldt-Jakob Disease in Europe (1).
The definitive diagnosis of Creutzfeldt-Jakob disease, however, is established by neuropathologic findings. There are three changes that are classically described and considered diagnostic: spongiform change, neuronal loss and astrocytic gliosis. The presence of these can vary significantly in proportion and distribution and often correlate with clinical symptoms. This permits classification of the disease into several variants.
Three variants of Creutzfeldt-Jakob disease have been proposed by Roos and Gajdusek (2): frontopyramidal, with pyramidal or lower motor neuron involvement; occipitoparietal {Heidenhain), characterized by disorders in higher cortical function and vision; and diffuse, with cerebral, cortical, basal ganglia, thalamic, cerebellar, midbrain and spinal cord involvement.
Histological examination from multiple samples of the brain in this case revealed astrocytic gliosis, spongiform degeneration and neuronal loss. Although these changes were seen in most sections, they were most prominent in the occipital cortex. This correlates very well with the clinical history of visual disturbances. Based on this finding, the present case corresponds to the Heidenhain variant. It is not uncommon for Creutzfeldt-Jakob disease to present with visual symptoms as the initial manifestation of the disease. Vargas et al (3) has reported three cases with these characteristics.
There have been numerous and significant advances in our understanding of Creutzfeldt-Jakob disease and prion diseases in general. These have been reviewed in several papers written recently, including one by Horowich and Weissman (4).
In summary, this 63 year old female with a history of visual disturbances and dementia of rapid progression was found to have the neuropathologic changes characteristic of Creutzfeldt-Jakob disease, predominantly in the occipital cortex. The occipital tropism and consequent visual symptoms indicate this case corresponds to the Heidenhain variant.
REFERENCES:
Patient Name: POULTER, BARBARA Patient location: AUTOPSY Room/Bed: Printed Date / Time: 01/30/98 * 0832
Page: 5 Continued .... --------------
Patient Account: 90000014-518 Med. Rec. No.: (0160)118511Q Patient Name: POULTER, BARBARA Age: 63 YRS DOB: 10/17/34 Sex: F Race: C Admitting Dr.: Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409} 772-5683 Pathology Report
Autopsy No.: AU-97-00435
FINAL AUTOPSY REPORT
CLINICOPATHOLOGIC CORRELATION:
1. Budka H, et al: Tissue handling in suspected Creutzfeldt-Jakob disease (CJD) and other human spongiform encephalopathies (prion diseases), Brain Pathology. 5:319-322,1995.
2. Roos R, Gajdusek DC, Gibbs CJ Jr: The clinical characteristics of transmissible Creutzfeldt-Jakob disease. Brain 96: 1-20, 1973.
3. Vargas ME, et al: Homonymous field defect as the first Manifestation of Creutzfeldt-Jakob disease. American Journal of Ophthalmology. 119:497-504, 1995.
4. Horowich AL, Weissman JS: Deadly conformations - protein misfolding in prion disease. Cell Vol.89, 499-510, 1997.
MF /MF 01/28/98
SCOT D. PENCIL, M.D., PATHOLOGIST MARTIN FERNANDEZ, M.D. 01/29/98 (Electronic Signature)
Patient Name: POULTER, BARBARA Patient Location: AUTOPSY Room/Bed: Printed Date / Time: 01/30/98 - 0832
Page: 6 END OF REPORT --------------
The University of Texas Medical Branch at Galveston
Gerald A, Campbell, Ph.D., M.D, Associate Professor and Director Division of Neuropathology Department of Pathology
February 26, 1998
Pierluigi Gambetti, M.D. Professor Institute of Pathology Case Western Reserve University 2085 Adelbert Road Cleveland Ohio 44106
Dear Dr, Gambetti:
Enclosed please find the microscopic slides and autopsy report from our patient, Barbara Poulter (Hosp.# 11851lQ, Autopsy # AU97-435). These slides are being sent for consultation at the request of Mr. Singletary, Ms. Poulter's son and next of kin. We will also send frozen tissue from the brain on dry ice next week, and someone will call you on the day the tissue is shipped. Please return the slides when you have finished with your examination. If you need any further information, please do not hesitate to call me. Thanks for your assistance with this case.
Sincerely, Gerald A. Campbell ------------------ CASE WESTERN RESERVE UNIVERSITY
February 26, 1988
Gerald Campbell, M.D,, PhD. Division of Neuropathology, G85 University TX Medical Branch Galveston, TX 77555-0785
Dear Dr. Campbell,
As per our telephone conversation concerning a recent case of CJD, I Will be willing to examine slides and the frozen tissue on western blotting, I will issue a report to you about our conclusions. Below is my address, Our Fed Ex number is ***************.
Thank your for your assistance in this matter,
Best personal regards,
Pierluigi Gambetti, M.D.
PG:In
Division of Neuropathology Pierluigi Gambetti, M.D. Director Institute Of Neuropathology 2085 Adelbert Road Cleveland, Ohio 44106
Phone 216-368-0587 Fax 216-368-2546 ------------------ CASE WESTERN RESERVE UNIVERSITY
February 27, 1998
Dr. Gerald A. Campbell The University of Texas Medical Branch at Galveston Division of Neuropathology, G85 Galveston. TX 77555-0785
Dear Dr. Campbell,
We are in receipt of the slides you sent on Mrs. Barbara Poulter (your #: AU97-435;our#098-28).
Best personal regards, Pierluigi Gambetti, M.D.
PG:sb
Division of Neuropathology Pierluigi Gambetti, M.D., Director ----------------------------------- CASE WESTERN RESERVE UNIVERSITY
March 30, 1998
Dr. Gerald A, Campbell The University of Texas Medical Branch at Galveston Division of Neuropathology Department of Pathology Galveston, Texas
Dear Dr Campbell,
We performed Western immunoblot analysis on the frozen tissue from your case #AU97-435 (our #098-28). The Immunoblot reveals the presence of protease-resistant prion protein (PrPres) confirming the diagnosis of prion disease. The immunoblot pattern of PrPres is consistent with the diagnosis of Creutzfeldt-Jakob disease.
Thank you for referring to us this interesting case.
Sincerely,
Piero Parchi, M.D.
Pierluigi Gambetti, M.D.
PP:sb
Division of Neuropathology Pierluigi Gambetti, M.D., Director Case Western Reserve University
This Autopsy report is for the use of anyone, who is trying to understand this hideous disease CJD. I hope it can be beneficial for some in researching human TSE. Please remember, this was my Mom, and to use this with great respect.
thank you, kind regards,
Terry S. Singeltary Sr., Bacliff, Texas USA
-------------------------------
BARBARA FREDERICK POULTER
DIED 12-14-97
If I had one last thing I could tell you, it would be, I love you. I'm sorry for the stupid argument we had the last few months, BEFORE this hideous disease ROARED through your body. BUT, I PROMISE MOM, YOUR DEATH WILL NOT GO UNANSWERED!
HEIDENHAN VARIANT CREUTZFELDT JAKOB DISEASE
We got a call from my Mother around the end of Oct. saying "the ****'est thing has happened, I can't see, and if I'm talking to you and I don't make sense, bare with me, I'll come back". It was a shock to all of us. It seems that a few days before, she was crossing the ferry and became frightened because she was having problems seeing. She explained it as looking down a tunnel or not being able to see from the sides, and seeing brown spots.
We had NOT been talking, over something, we had NO control of, for a few months. So I did not know she had been having these visual problems, until she was blind. These were her first symptoms. From that point on, I was with her most everyday. I had to cross the Galveston/Bolivar ferry, and its about 30 minutes each way, so as the disease progressed, it gave me a great deal of time to think. When the visual problems started, it was about 2 weeks later, and she was blind. That led to coordination, and balance problems starting. But as this hideous disease progresses, it just GOES. You don't seem to catch up with it. It was like a fire in a hurricane. We would go out and get her things she needed one day, and the next day it would be obsolete, because the disease had gone to another stage. So you started over. Her coordination and balancing led to being in a wheel-chair. She was starting to get these trembles. I also noticed how her hands and feet started to go inward. Her speech was nothing more than jerble at this time, and this was probably about the 6th week, (at this point we had to tie her to the wheel chair, to keep her from falling out). The trembles had turned into SEVERE JERKS, that at times would take 3 of us to hold her down. I will never forget that....About her 8th week she became comatose....She died around the 10th week. I had spent the night, she had problems through the night, so the nurse came. She checked her out and comforted us, (HOSPICE IS A WONDERFUL ORGANIZATION). The nurse said she seemed to be alright and that it would probably be alright to go home for a few hours. I was on the Ferry, going back to Galveston, when I got the call, she was gone. What can you do, Mom was gone, and I was stuck on the **** Ferry, going the wrong direction.
She knew what she had. I remember, before she had lost her speech completely. After a doctors conference, and CJD had come up. She heard us say CJD, and she screamed, SHE knew! At that point, I didn't know what was, much less, CREUTZFELDT JAKOB DISEASE.....I have learned a lot since. I have learned I truly miss my Mom and I am MAD as hell that she is gone!
Terry/MADSON!!!
SYMPTOMS:
VISION - BLIND IN ABOUT 10 TO 14 DAYS
COORDINATION AND MUSCLE CONTROL SWALLOWING DIFFICULTY CONFUSION AND DEMENTIA SPEECH PROBLEMS HALLUCINATIONS TREMBLES TOO SEVERE JERKING LOSS OF WEIGHT HANDS AND FEET GREW INWARD UPPER TRUNK STIFFNESS, SHOULDER, UPPER ARMComment
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and what's your point texans42, what are you scared of?Originally posted by Texans42 View Post
just because you want to stick your head in the sand, does not meant everyone else does, unless your part of the problem.
instead of censorship, as you are suggesting, why don't you bring something to the table?
just saying...
what are you scared of?
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
here is the latest;
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
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..
***> 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. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip...
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry
kind regards, terryComment
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*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
Boni Pettite folks...Comment
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Ok someone including the OP help me out here. Whats the message??? I kinda get the anti hunter, humans play a role in CWD but what gives???Comment
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Wow, lotta information there. Sorry for your loss, but question ? Did she hunt, clean infected Deer, Elk, a Mad Cow, or Eat other contaminated meats that would directly associate her illness with hunting ?
I look at CJD like the Flesh Eating Bacteria, it is a living organism out there in our world that everyone has "theoretically a chance" to be exposed to.Comment
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And still not one case of variant CJD in humans in the endemic area here in Wyoming since it has been recognized.Comment
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Might as well get the foil hats going
Maybe big government is trying to off hunters by introducing cwd.
After all hiv and was to reduce a certain class
And planned parenthood was originally started to keep the # of darker skin folks down.
Now they are after rednecksComment
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