Sunday, June 17, 2018

Reviews Prion-like Propagation of α-synuclein, Parkinson, and tse prion

Reviews Prion-like Propagation of α-synuclein, Parkinson, and tse prion

Review Prion-like Propagation of α-synuclein in the gut-brain axis 

Author links open overlay panel Ying Chen a Qianhang Shaoa Yu-He Yuana Nai-Hong Chen ab 

a State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica& Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China bCollege of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, China Received 19 April 2018, Revised 4 June 2018, Accepted 5 June 2018, Available online 9 June 2018.

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•There is evidence that Parkinson’s disease may develop from the enteric nervous system and spread to the brain.

•There is evidence that the gut-brain axis may depend on the prion-like propagation of α-synuclein.

•The review shows the α-synuclein as a potential target in therapy of PD. 

Abstract

Parkinson’s disease (PD) is a progressive degenerative disease of the nervous system, which is characterized by movement disorders, such as static tremor, rigidity, and bradykinesia in advanced patients. Gastrointestinal (GI) dysfunction, such as gastric dysmotility, constipation, and anorectic dysfunction, is common non-motor symptom in the early stage of PD. The progression of PD includes the degenerative loss of dopaminergic (DA) neurons and aggregation of α-synuclein in the substantia nigra (SN). Interestingly, both of them are also present in the enteric nervous system (ENS) of PD patients. In this review, we describe the relationship between non-motor symptoms particularly GI dysfunction and the pathogenesis of PD, aiming to show the powerful evidences about the prion-like propagation of α-synuclein and support the hypothesis of gut-brain axis in PD. We then summarize the mechanism of the gut-brain axis and confirm α-synuclein as a potential target for drug design or new clinical treatment.

Abbreviation

CNScentral nervous systemDAdopamineDMVdorsal motor nucleus of the vagusENSenteric nervous systemGIgastrointestinalIL-1interleukin-1LBsLewy bodiesLPSlipopolysaccharideLAG3lymphocyte-activation gene 3MPTP1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineP301Lmutant TauPDParkinson's diseasePNSperipheral nervous systemROSreactive oxygen speciesSCFAshort chain fatty acidsSNsubstantia nigraTHTyrosine hydroxylaseTLR 2Toll-like receptor 2TNTstunneling nanotubes

Keywords

α-synuclein Prion-like Enteric nervous system Gut-brain axis Non-motor symptom Parkinson’s disease


Chapter 17 - Prion-like propagation of pathology in Parkinson disease 

Author links open overlay panelLauraVolpicelli-Daley1PatrikBrundin2

1Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, United States

2Van Andel Research Institute, Center for Neurodegenerative Science, Grand Rapids, MI, United States Available online 7 June 2018.

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Abstract

Over 100 years ago, Lewy bodies and Lewy neurites were defined as a pathologic hallmark of Parkinson disease. Eighty years later, α-synuclein was found to be the primary component of these inclusions. Emerging evidence suggests that α-synuclein pathology propagates across interconnected networks throughout the nervous system in a prion-like manner. Pathologic α-synuclein seeds aggregation of native α-synuclein, resulting in the formation of insoluble inclusions. These seeds can propagate within the neuron and to interconnected neurons, resulting in the spread of pathology throughout the brain. Here, we discuss how the findings that α-synuclein pathology spreads throughout the nervous system has revolutionized our understanding about Parkinson disease pathogenesis and resulted in the development of novel therapeutic strategies to halt disease progression.

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Keywords

alpha-synuclein synucleinopathy Lewy body prion-like protein aggregation novel therapies Lewy body dementias


Sporadic Creutzfeldt-Jakob Disease in a Woman Married Into a Gerstmann-Sträussler-Scheinker Family: An Investigation of Prions Transmission via Microchimerism

Aušrinė Areškevičiūtė, MSc Linea Cecilie Melchior, PhD Helle Broholm, MDLars-Henrik Krarup, MD, PhD Suzanne Granhøj Lindquist, MD, PhD Peter Johansen, PhDNeil McKenzie, PhD Alison Green, PhD Jørgen Erik Nielsen, MD, PhDHenning Laursen, Dr.Med ... Show more Journal of Neuropathology & Experimental Neurology, nly043,https://doi.org/10.1093/jnen/nly043 Published: 07 June 2018 Cite Permissions Share search filtersearch input 

Abstract 

This is the first report of presumed sporadic Creutzfeldt-Jakob disease (sCJD) and Gerstmann-Sträussler-Scheinker disease (GSS) with the prion protein gene c.305C>T mutation (p.P102L) occurring in one family. The father and son were affected with GSS and the mother had a rapidly progressive form of CJD. Diagnosis of genetic, variant, and iatrogenic CJD was ruled out based on the mother’s clinical history, genetic tests, and biochemical investigations, all of which supported the diagnosis of sCJD. However, given the low incidence of sCJD and GSS, their co-occurrence in one family is extraordinary and challenging. Thus, a hypothesis for the transmission of infectious prion proteins (PrPSc) via microchimerism was proposed and investigated. DNA from 15 different brain regions and plasma samples of the CJD patient was subjected to PCR and shallow sequencing for detection of a male sex-determining chromosome Y (chr. Y). However, no trace of chr. Y was found. A long CJD incubation period or presumed small concentrations of chr. Y may explain the obtained results. Further studies of CJD and GSS animal models with controlled genetic and proteomic features are needed to determine whether maternal CJD triggered via microchimerism by a GSS fetus might present a new PrPSctransmission route. Keywords: Chromosome Y, Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker disease, Microchimerism, PRNP, Prions, Transmission Issue Section: Original Article



WEDNESDAY, JUNE 13, 2018 

Sporadic Creutzfeldt-Jakob Disease in a Woman Married Into a Gerstmann-Sträussler-Scheinker Family: An Investigation of Prions Transmission via Microchimerism


wonder how many inectious tse prions are shed from skin in a home in ones lifetime???

could that expose and cause sCJD or vpspr or familial type tse prion disease, or some other tse prion from those exposed over time???

did that question make you uncomfortable? 

why?

these questions must be answered.

85%+ of all human tse prion disease i.e. sporadic creutzfeldt jakob disease scjd comes from somewhere, and all iatrogenic cjd is, is sporadic cjd, until route and source of the iatrogenic event is discovered, traced back, confirmed, put into the academic domain, and finally put into the public domain, which very seldom happens. we must continue asking the hard questions, or our loved ones died for nothing...

what if, ***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent. *** ???

THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984

THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE

R. G. WILL

1984

snip... 

F. Familial Associations

The overall familial incidence of 6% in the retrospective section of this study contrasts with the estimated familial incidence of 15% in a review of the world wide epidemiology of C.J.D. (Masters et al., 1979a). In individual series higher figures are quoted with, for example, a familial incidence of 47% in Chile (Galvez et al., 1980) and 35% in Libyan born Israelis (Neugut et al., 1979). In a comprehensive retrospective survey of C.J.D. in France (Brown et al., 1979b), however, a 9% familial incidence was discovered, a figure comparable with this series. The low familial incidence may reflect either the difficulties of retrospectively obtaining an accurate family history or an artificially high familial incidence in relatively selected series due to extensive investigation of individual families.

The paradox of an apparently dominantly inherited condition (Masters et al., 1981a) which is yet transmissible is unresolved. Detailed investigation of individual families suggests that, if case to case transmission occurs, the incubation period must extend to decades (Masters et al., 1981a). Although this is compatible with the suspected incubation period of kuru (Gajdusek, 1979), the tendency for siblings to die at the same age rather than the same time (Masters et al., 1981a) supports the presence of a genetic influence. ***The discovery of a discordant identical twin pair in the present study suggests that even if there is an inherited susceptibility an environmental factor is necessary for the development of the condition. It further suggests that genetic integration of the agent is unlikely, in accordance with experimental evidence in which nuclear fractions are non-infectious (Millson et al., 1971) and vertical trans- mission has not been found in the laboratory (Amyx et al., 1981).

An unexpected but interesting finding in the context of familial associations is the group of nine patients with a first degree relative dying of a different 'degenerative' neurological condition. The extraordinary family with apparently dominantly inherited Alzheimer's disease and carcinoma of the colon is under investigation at another centre.

In other systematic studies of the epidemiology of C.J.D. an association with other neurological conditions has not been described but Masters (1981a) has reported four cases of C.J.D. occurring within four pedigrees of familial Alzheimer's disease. Adam et ale (1982) have described a family with a dominantly inherited neurological disorder sharing features of cerebral amyloidosis, spongiform encephalopathy and Alzheimer's disease. ***The relationship of C.J.D. to other degenerative neurological disorders may be a fruitful avenue of further epidemiological research.

CASE CONTROL STUDY

The objective of the case control study was to obtain quantitative data on putative risk factors and to identify potential common exposure to an environmental source of infection. The difficulties of such a study have been described by Bobowick et al. (1973) and Kondo and Kuroiwa (1982) in the only previous case control studies of C.J.D. In a rare condition such as C.J.D. it is difficult to obtain sufficient patient numbers to achieve statistically valid results. In this study 22 patients were included in the first 18 months, a number sufficient to exclude any ubiquitous risk factor but inadequate to distinguish relative risk. The case control study has, however, continued beyond the time limits of this analysis and to date over a hundred patients have been included.

The necessity of obtaining information at second hand introduces a potential source of error in the study of C.J.D. In this study the level of co-operation and detail of information was clearly enhanced by interviewing relatives prospectively and for this reason cases ascertained after death were not included in the prospective study. The checking of information given by relatives of control cases with the patients themselves suggested that the quality of information given at second hand was remarkably accurate.

The selection of controls is critical to the potential significance of a case control study. In this study age- and sex-matched controls were obtained from concurrent inpatients. Although in some cases the discovery of a suitable control proved both difficult and time-consuming, and in a few cases impossible, it was felt essential to persevere with the stated protocol in order to avoid the introduction of bias. Both previous case control studies were carried out retro- spectively and used 'healthy' and potentially over-matched controls.

Despite the differences between previous studies and the present case control study, the results were, almost without exception, both concordant and negative. No difference between patients and controls was discovered in past surgical or medical history, occupational history, educational history, eating habits or exposure to animals. Kondo and Kuroiwa (1982) discovered a correlation between physical injuries and the development of C.J.D. but could not exclude a methodological bias. No such correlation was discovered in this study and the subject was not examined in the study by Bobowick et ale (1973).

In the latter study the consumption of hog brains by patients was stressed but did not differ from the control group and in both this study and the study in Japan (Kondo and Kuroiwa, 1982) no dietary factory was related to increased risk of developing C.J.D.

***The successful oral transmission of C.J.D. and scrapie to primates (Gibbs et al., 1980) and the close resemblance between the properties of the transmissible agent in the two conditions (Gibbs and Gajdusek, 1976) has raised the possibility that the human disease is contracted from sheep. No direct evidence is available and the concept is based on inference and interesting but unconvincing anecdotes

(Alter et al., 1971; Lo Russo et al., 1980; Kamin and Patten, 1984). The patient discovered in this study who had never been known to eat meat suggests that eating scrapie infected meat cannot be the only source of C.J.D. in man. C.J.D. occurs in countries in which natural scrapie has not been observed (Galvez et al., 1980; Kondo and Kuroiwa, 1982) and no relationship was discovered in France (Chatelain et al., 1981) between the geographic distribution of scrapie and the incidence of C.J.D. A similar investigation could not be carried out in England and Wales as notification of scrapie to the Ministry of Agriculture is inconsistent and sheep farmers often destroy affected animals without seeking veterinary advice for fear of financial loss.

A detailed residential history was obtained in cases and controls. Although over-representation of cases was discovered in certain areas, similar but distinct areas of previous residence common to an apparent excess of controls was discovered. If C.J.D. does have a prolonged incubation period extending to decades the detailed study of residential history may, however, establish potential contact between individual cases which would be otherwise undetectable. The detailed study of individual cases in the prospective study has revealed the possibility of tenuous but extraordinarily coincidental contact between patients.

This may only be a reflection of intensive investigation, but if C.J.D. is transmitted by relatively minor surgical or dental procedures many years prior to death it is only by the systematic study of individual cases that potential cross-contamination may be discovered.

EVIDENCE FOR CASE-TO-CASE TRANSMISSION OF C.J.D.

The possible iatrogenic transmission of C.J.D. by neurosurgery, corneal transplantation and stereotactic electrodes has been suggested in the past (Duffy et al., 1974: Bernouilli et al., 1977; Masters et al., 1979a). In this series the close temporal relationship of neurosurgical procedures on two affected patients and three patients, unaffected at the time but who subsequently developed the disease is described. This provides strong circumstantial evidence of iatrogenic transmission by neurosurgery. Although sterilisation procedures have improved since the cases described, the unusual resistance of the agent and the recent description of probable neurosurgical transmission in France (Foncin et al., 1980) suggests that there is a continued risk of accidental transmission. However, brain biopsy to confirm the diagnosis of C.J.D. is now an unusual event and computed tomography has obviated the need for ventriculography.

The depth electrodes putatively responsible for one case of iatrogenic transmission in this series were inadequately sterilised in formalin and were subsequently used in over 200 patients. The neurosurgical instruments used in the cases of presumed neurosurgical transmission were sterilised using autoclaving procedures which were inadequate according to current advice (Gajdusek et al., 1978). However, despite detailed investigation, no cases other than those described above are known to have developed C.J.D. Thus, despite the possible implantation of the agent directly into the central nervous system, a large number of patients failed to develop the disease. This provides circumstantial evidence of an inherited susceptibility to the agent and suggests that cases of iatrogenic transmission may have occurred due to the unfortunate temporal proximity of susceptible individuals exposed to the agent.

In the close geographic group of three cases possible nodes of transmission can be suggested, either iatrogenic or through dental procedures, but these must remain conjectural. It is known, however, that the similar scrapie agent can be transmitted from the gums of animals (Adams and Edgar, 1978). Such close spatial clustering of cases is extremely unusual, being previously reported in England (Matthews, 1975a), Czechoslovakia (Mayer et al., 1977) and Hungary (Majtenyi, 1978), but not detected in the study of the epidemiology of C.J.D. in urban Paris (Cathala et al., 1978) where the incidence was found to be relatively high.

The occurrence of the disease in a patient who had contact with cases of familial C.J.D., but was not genetically related, has been described in Chile (Galvez et al., 1980) and in France (Brown et al., 1979b). In Chile the patient was related by marriage, but with no consanguinity, and had social contact with subsequently affected family members for 13 years before developing the disease. The contact case in France also married into a family in which C.J.D. was prevalent and had close contact with an affected member. In neither instance did the spouse of the non-familial case have the disease. The case described in this report was similarly related to affected family members and social contact had occurred for 20 years prior to developing C.J.D. If contact transmission had occurred, the minimum transmission period would be 11 years. Contact between sporadic cases has not been described and it is remarkable that possible contact transmissions have all been with familial cases. No method of transmission by casual social contact has been suggested. 

***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent. 

snip...see full text here;

***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent. ***



snip...see full text ;

TUESDAY, JUNE 20, 2017

Prion 2017

Conference Transmissible prions in the skin of Creutzfeldt-Jakob disease patients

Prion 2017 Conference Transmissible prions in the skin of Creutzfeldt-Jakob disease patients

Dr. Wenguan Zou1, Dr. Christina Orru2, Jue Yuan1, Brian Appleby1, Baiya Li1, Dane Winner1, Yian Zhan1,3, Mark Rodgers1, Jason Rarick1, Robert Wyza1, Tripti Joshi1, Gongxian Wang3, Mark Cohen1, Shulin Zhang1, Bradley Groveman2, Robert Petersen1, James Ironside4, Miguel Quinones-Mateu1, Jiri Safar1, Qingzhong Kong1, Byron Caughey2

1Case Western Reserve University, Cleveland, United States, 2Rocky Mountain Laboratories, National Institutes of Health, Hamilton, United States, 3Nanchang University, Nanchang, China, 4Universitv of Edinburgh, Edinburgh, United Kingdom

Aims: Sporadic Creutzfeldt-Jakob disease (sCJD), the most common human prion disease, is transmissible by neuroinvasive iatrogenic routes due to abundant prion infectivity in the central nervous system (CNS). The disease-associated prion protein (PrPSc) and its infectivity have never been detected in skin from sCJD patients; however, some epidemiological studies have associated sCJD risk with skin-involved non-CNS surgeries. The aims of our study were to explore potential prion seeding activity and infectivity of skin and the feasibility of skin-based CJD diagnosis.

Methods: Skin samples were collected at autopsy or biopsy from twenty-one sCJD, two variant CJD, and fifteen non-CJD patients and analysed by Western blotting and real-time quaking-induced conversion (RT- QulC) for PrPSc. Infectivity of skin from two sCJD patients was determined by bioassay using two lines of humanized transgenic (Tg) mice.

Results: Western blotting demonstrated PrPSc in the skin of one of five deceased sCJD patients examined. However, the more sensitive RT-QuIC assay detected prion-seeding activity in skin from all 23 CJD decedents but not in non-CJD controls, indicating preliminary ClD diagnostic sensitivities and specificities of 100% (95% confidence intervals of 85-100%, and 78-100%, respectively). Although sCJD skins contained ~102-105-fold lower RT-QuIC seeding activity than sCJD brains, ten out of twelve mice from two Tg mouse lines inoculated with skin homogenates of two patients with two different subtypes of sCJD succumbed to prion disease within 450 days after inoculation.

Conclusions: sCJD patients' skin may contain both detectable prion seeding activity and transmissible prions. Our findings not only suggest a new basis for diagnostic sCJD testing, but also raise concerns about the potential for iatrogenic sCJD transmission via skin. (Funded by the CJD Foundation, the National Institute of Neurological Disorders and Stroke, the Centers for Disease Control and Prevention, as well as others)

DISORDERS PRION 2017 DECIPHERING NEURODEGENERATIVE


*sCJD patients' skin may contain both detectable prion seeding activity and transmissible prions.

*Our findings not only suggest a new basis for diagnostic sCJD testing, but also raise concerns about the potential for iatrogenic sCJD transmission via skin.

Oral Session14：45～15：00O-12 Wenquan Zou

*** PrPSc in the skin of CJD patients


Unexpectedly, our latest preliminary study identified two types of PK-resistant PrP molecules [with gel mobility similar to the PrPSc types 1 and 2 from the brain of sporadic CJD (sCJD)] in the fibroblast cells extracted from the skin of clinical sCJD patients and asymptomatic subjects carrying PrP mutations linked to familial CJD (fCJD). We also detected PrPSc in the skin of humanized transgenic (Tg) mice inoculated intracerebrally with a human prion. Moreover, prion infectivity has been observed in the skin of infected greater kudu (Cunningham et al., 2004) and a murine prion inoculated to mice via skin scarification can not only propagate in the skin, but also spread to the brain to cause prion disease (Wathne et al., 2012). We hypothesize that the skin of patients with prion disease harbors prion infectivity and the presence of PK-resistant PrP in the skin is a novel diagnostic marker for preclinical CJD patients.


A Kiss of a Prion: New Implications for Oral Transmissibility

The transmissibility of scrapie among sheep (intraspecies) is well recognized. It must be emphasized that horizontal transfer (from one individual to another) of scrapie is the main route of infection, because vertical transmission of disease from mother to offspring via milk or placental tissue occurs infrequently. Thus, in view of the report by Maddison et al, the oral transmissibility of prions among sheep may serve as a major route for horizontal scrapie transfer. This occurrence is plausible because sheep often lick each other. Maddison et al [10] indicate that, because of the similarities in prion tissue distribution, their implications for the oral transmission of ovine scrapie might be true for other prion diseases, such as cervid chronic wasting disease and human vCJD. If this is true for humans, a kiss of a prion may sometimes have lethal consequences.



PERSON TO PERSON TRANSMISSION OF THE TSE PRION DISEASE, never say never. as the disease mutates, it becomes more virulent in some cases, and cwd is efficiently transmitted from cervid to cervid. there are now multiple strains of CWD in cervids, as with the TSE prion disease in bovine, sheep and goats, and we now have the atypical TSE in these species, that have mutated, and some strains _have_ become more virulent. we now have younger humans dying from the TSE prion disease, with shorter incubation period, and that are much younger. human to human casual transmission of the TSE prion disease...again, never say never. ...TSS

see more here;


-----Original Message-----
From: Terry Singeltary <flounder9@verizon.net>
To: Sent: Thu, Nov 23, 2017 10:22 am

Subject: re-NIH scientists and collaborators find infectious prion protein in skin of CJD patients

>>>Although sCJD patient skin contained ~103- to 105-fold lower prion seeding activity than did sCJD patient brain tissue, all 12 mice from two transgenic mouse lines inoculated with sCJD skin homogenates from two sCJD patients succumbed to prion disease within 564 days after inoculation<<<

for something to be 103 to 105 fold lower prion seeding, yet still be 100% fatal in all test subjects, very disturbing...terry

WEDNESDAY, NOVEMBER 22, 2017

NIH scientists and collaborators find infectious prion protein in skin of CJD patients


WEDNESDAY, NOVEMBER 22, 2017

Prion seeding activity and infectivity in skin samples from patients with sporadic Creutzfeldt-Jakob disease


PRION 2018

17:00 Wen-Quan Zou (Case Western Reserve University): Preclinical detection of prions in skin samples of scrapie-infected animals by serial PMCA and RT-QuIC assays.

THURSDAY, MAY 24, 2018

Prion 2018 May, 22-25 2018 Santiago de Compostela


Skin as a Potential Source of Prion Infectivity Mammalian skin is composed of different strata and cell types, which are both innervated and carry blood vessels. There is therefore the potential for skin to harbor prions and facilitate its excretion into the environment. Cunningham and coworkers demonstrated the presence of prion infectivity in the skin of BSE-affected kudu.87 Subsequently, Thomzig et al. used a rodent model to demonstrate that skin-associated prions could be identified from late preclinical stages of disease for both scrapie and BSE,88 estimating that there is likely to be 5,000–10,000 times less prion in the skin of hamsters challenged with scrapie than in the brains of those same animals. This study also demonstrated the presence of prions in the skin of sheep during the late stages of naturally acquired scrapie where PrPSc was generally associated with small nerve fibers within the dermis. More recently, PrPSc was found within the skin of a vCJD patient.89 In addition, cervine CWD prions have been found within antler velvet,90 a vascularized skin layer covering the developing antler of male deer, which is shed after the ossification of antlers.
Skin may therefore represent another route by which prions contaminate the environment. Mechanisms of prion shedding from this organ could include natural sloughing of skin, abrasions of the skin and, in the case of sheep, skin cuts and nicks that are introduced during shearing.



UCSF 

 Office of Environment, Health and Safety (EH&S) 

 Prion Exposure Protocol 

 Organism or Agent: 

Prions 

Exposure Risk: 

Human Prion Disease (Creutzfeldt-Jakob Disease/New variant CDJ, BSE, etc.) 

 UCSF Occupation Health: 415-885-7580 (work hours, 8am to 5pm) 

 Exposure Hotline Pager: 415-353-7842 (24 hours) 

 Environment, Health & Safety: 415-476-1300 (work hours) 

 UCSF Police Department; 415-476-1414 or 9-911 (In case of emergency, 24 hours) 

 EH&S Public Health Officer: 415-514-3531 (work hours) 

Campus Bio-Safety Officer 415-514-2824 California Poison Control: 800-222-1222 SFDPH Emergency Number

415-554-2830 

 CDC Emergency Operation

770-488-7100

Occ Hlth Proto Button 

 *****************************************************************************************

In the event of an accidental exposure or injury, the protocol is as follows: 

 1. Modes of Transmission: 

 Skin puncture or injection 

 Ingestion 

 Contact with mucous membranes (eyes, nose, mouth) 

Contact with non-intact skin 

 Exposure to aerosols 

 2. First Aid: There is no evidence of occupational transmission of prion disease to healthcare workers. Perform first aid as self-care according to the type of exposure/ injury. 

 a. First Aid for an unbroken Skin Exposure: Wash with soap and abundant quantities of warm water (avoid scrubbing), rinse, and dry. Apply for 1 minute, 0.1N Sodium Hydroxide (NaOH) or a 1:10 dilution of bleach (sodiumhypochlorite). 

 When decontaminating with 0.1N NaOH or sodium hypochlorite, a face shield and eye goggles or eye goggles with mask should be worn for protection. It is important to decontaminate the wound with the appropriate agent for the appropriate length of time in order to denature the protein as soon as possible. See the special precautions for NaOH below. 

 After decontamination, rinse well with soap and water to neutralize the base. 

 Bring the 0.1N sodium hydroxide SDS to the ED 

b. First Aid for lacerations or needlestick injuries: Gently encourage bleeding; wash (avoid scrubbing) with warm soapy water, rinse, dry and cover with a waterproof dressing. Further treatment (e.g. sutures) should be appropriate to the type of injury. 

 c. First Aid for splashes to the Eye, Nose or Mouth: Immediately flush the area with running water or normal saline. Continue washing for 15 minutes. Do not use sodium hydroxide or sodium hypochlorite in or around your eyes. Do not rub or keep eyes closed. 

 d. Following the administration of first aid, the employee will: 

 Inform your supervisor of the exposure. 

Remove any garments that may have become soiled/contaminated with prions or NaOH, and place them in a double plastic bag. Close the bag securely, label it as contaminated, and wash your hands thoroughly. 

Identify any equipment involved in the exposure and the mechanism of exposure. Make sure that the area has been secured and that notification of contamination has been posted to prevent other individuals from entering the area. 

If you need immediate care for your injury, proceed to the Emergency Department(ED). When you injury is stable, Contact the Needlestick Exposure Hotline (415-353-7842) to report the exposure. The injured employee will need to follow up in the UCSF Occupational Health Clinic. Be sure to go to the clinic for medical evaluation and complete all necessary workers’ compensation paperwork. 

 e. Splash Affecting Garments, remove garments that may have become soiled or contaminated and place them in a double biohazard red plastic bag. Disposable gloves and gowns should dispose of by incineration, according to World Health Organization guidelines. 

 3. Treatment 

 snip...end 


see updated version here;


c. Operating Rooms

Operating room air may contain microorganisms, dust, aerosol, lint, skin squamous epithelial cells, and respiratory droplets. The microbial level in operating room air is directly proportional to the number of people moving in the room.351 One study documented lower infection rates with coagulase-negative staphylococci among patients when operating room traffic during the surgical procedure was limited.352 Therefore, efforts should be made to minimize personnel traffic during operations. Outbreaks of SSIs caused by group A beta-hemolytic streptococci have been traced to airborne transmission from colonized operating-room personnel to patients.150154 Several potential health-care-associated pathogens (e.g., Staphylococcus aureus and Staphylococcus epidermidis) and drug-resistant organisms have also been recovered from areas adjacent to the surgical field,353 but the extent to which the presence of bacteria near the surgical field influences the development of postoperative SSIs is not clear.35

snip...

and transfer of an epidemic strain of Acinetobacter from patients’ skin to health-care workers’ hands has been demonstrated experimentally.591 

snip...

Infectious RSV has been recovered from skin, porous surfaces, and non-porous surfaces after 30 minutes, 1 hour, and 7 hours, respectively.1145 Parainfluenza viruses are known to persist for up to 4 hours on porous surfaces and up to 10 hours on non-porous surfaces.1146 Rhinoviruses can persist on porous surfaces and non-porous surfaces for approximately 1 and 3 hours respectively; study participants in a controlled environment became infected with rhinoviruses after first touching a surface with dried secretions and then touching their nasal or conjunctival mucosa.1147 Although the efficiency of direct transmission of these viruses from surfaces in uncontrolled settings remains to be defined, these data underscore the basis for maintaining regular protocols for cleaning and disinfecting of hightouch surfaces.


what about tse prion and skin?

never say, never...

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. 

These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. 

Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification 


Terry S. Singeltary Sr.




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.


sporadic CJD, along with new TSE prion disease in humans, of which the young are dying, of which long duration of illness from onset of symptoms to death have been documented, only to have a new name added to the pot of prion disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be sporadic with no genetic link to any family member? when the USA is the only documented Country in the world to have documented two different cases of atypical H-type BSE, with one case being called atypical H-G BSE with the G meaning Genetic, with new science now showing that indeed atypical H-type BSE is very possible transmitted to cattle via oral transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old excuse, better surveillance. You can only use that excuse for so many years, for so many decades, until one must conclude that CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a blip or a reason of better surveillance, it is a mathematical rise in numbers. More and more we are seeing more humans exposed in various circumstance in the Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same time in North America, more and more humans are becoming exposed to the TSE prion disease via consumption of the TSE prion via deer and elk, cattle, sheep and goats, and for those that are exposed via or consumption, go on to further expose many others via the iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I pondered this mode of transmission via the victims of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or sGSS ? what if?



Thursday, March 8, 2018 

Familial human prion diseases associated with prion protein mutations Y226X and G131V are transmissible to transgenic mice expressing human prion protein



Furthermore, GSS A117V infected vole brains were able to induce the same disease phenotype in recipient voles within 3–4 months after challenge, proving that a prion agent propagated in the brains of infected animals. These findings imply that brains of GSS patients harbor infectious prions with transmissibility features similar to those found in other human and animal TSEs.



*** 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 


Morbidity and Mortality Weekly Report

274 MMWR / March 9, 2018 / Vol. 67 / No. 9 US Department of Health and Human Services/Centers for Disease Control and Prevention

Update: Dura Mater Graft–Associated Creutzfeldt-Jakob Disease — Japan, 1975–2017

Ryusuke Ae, MD, PhD1; Tsuyoshi Hamaguchi, MD, PhD2; Yosikazu Nakamura, MD1; Masahito Yamada, MD, PhD2; Tadashi Tsukamoto, MD, PhD3; Hidehiro Mizusawa, MD, PhD3; Ermias D. Belay, MD4; Lawrence B. Schonberger, MD4


The cases described in this report indicate that recipients of prion-contaminated grafts could remain at risk for CJD for at least 30 years after receiving grafts. Given the known potential for even longer latency periods for prion diseases, this outbreak is expected to continue. The dCJD cases underscore the importance of establishing measures to eliminate or greatly reduce the possibility of CJD transmissions (e.g., strict donor screening, appropriate record keeping, prevention of crosscontaminations, and ideally, the use of validated sterilization methods) whenever human tissues, particularly of cadaveric origin, might be used to treat other patients. In addition, a system of human disease surveillance to detect the possible emergence of new sources of prion disease transmissions is needed. Furthermore, physicians maintaining a high index of suspicion for unusual prion disease cases, as well as a system of human disease surveillance to detect the emergence of new sources of prion disease transmissions, is needed to enable the prevention of infections Finally, maintaining surveillance for CJD in Japan is important to better assess the impact of the outbreak of dCJD and to identify additional cases.


SUNDAY, MARCH 11, 2018 

Dura Mater Graft–Associated Creutzfeldt-Jakob Disease — Japan, 1975–2017 Update


Thursday, August 13, 2015 

Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years 


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, 


Thursday, January 14, 2016 

*** Preventable Tragedies: Superbugs and How Ineffective Monitoring of Medical Device Safety Fails Patients REPORT ***

how can it be, HOW CAN IT BE $$$ not a word about CJD GSS FFI VPSPR TSE Prions that I saw...absolutely crazy, WE ARE MISSING THE BIGGER PICTURE! 

how many victims that will never be reported ??? 


Sunday, January 17, 2016 

*** Of Grave Concern Heidenhain Variant Creutzfeldt Jakob Disease *** 


J Neurol Neurosurg Psychiatry 2002;72:792-793 doi:10.1136/jnnp.72.6.792 Short report

Creutzfeldt-Jakob disease 38 years after diagnostic use of human growth hormone

E A Croes1, G Roks1,*, G H Jansen3, P C G Nijssen2, C M van Duijn1

+ Author Affiliations 1Genetic Epidemiology Unit, Department of Epidemiology and Biostatistics, Erasmus University Medical Centre Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands 2Department of Neurology, St Elisabeth Hospital, PO Box 90151, 5000 LC Tilburg, Netherlands 3Department of Pathology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands

Correspondence to: Professor C M van Duijn, Genetic Epidemiology Unit, Department of Epidemiology and Biostatistics, Erasmus University Medical Centre Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands; vanduijn@epib.fgg.eur.nl Received 27 December 2001 Accepted 12 March 2002 Revised 1 March 2002

Abstract

A 47 year old man is described who developed pathology proven Creutzfeldt-Jakob disease (CJD) 38 years after receiving a low dose of human derived growth hormone (hGH) as part of a diagnostic procedure. The patient presented with a cerebellar syndrome, which is compatible with iatrogenic CJD. This is the longest incubation period described so far for iatrogenic CJD. Furthermore, this is the first report of CJD after diagnostic use of hGH. Since the patient was one of the first in the world to receive hGH, other cases of iatrogenic CJD can be expected in the coming years.

snip...

An incubation period as long as 38 years had never been reported for iatrogenic CJD. Huillard d'Aignaux et al7 studied the incubation period in 55 patients with hGH related CJD in a cohort of 1361 French hGH recipients. The median incubation period was between 9 and 10 years. Under the most pessimistic model, the upper limit of the 95% confidence interval varied between 17 and 20 years. Although the infecting dose cannot be quantified, it can be speculated that the long incubation period in our patient is partly explained by the administration of a limited amount of hGH. This hypothesis is supported by experimental models, in which higher infecting doses usually produce shorter incubation periods.6 Since our patient was one of the first in the world to receive hGH, this case indicates that still more patients with iatrogenic CJD can be expected in the coming years. Another implication of our study is that CJD can develop even after a low dose of hGH. This case once more testifies that worldwide close monitoring of any form of iatrogenic CJD is mandatory.


SHORT REPORT

Creutzfeldt-Jakob disease 38 years after diagnostic use of human growth hormone


THURSDAY, FEBRUARY 15, 2018 

Iatrogenic Creutzfeldt-Jakob disease with Amyloid-β pathology: an international study

http://creutzfeldt-jakob-disease.blogspot.com/2018/02/iatrogenic-creutzfeldt-jakob-disease.html

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





Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease 

*** Singeltary comment PLoS *** 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? 

Posted by flounder on 05 Nov 2014 at 21:27 GMT 


IN CONFIDENCE

5 NOVEMBER 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

[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.]




snip...see full Singeltary Nature comment here; 

re-Evidence for human transmission of amyloid-? 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)


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. ...




2012

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 ?

source references ...end...tss 

Hello Nicole,

by all means, please do use my poster. but I thought this was already taken care of, and I could not attend for my poster presentation, therefore, it was not going to be presented. I have some health issues and could not make the trip.

please see old correspondence below...

From: Nicole Sanders Sent: Tuesday, April 10, 2012 5:37 PM To: Terry S. Singeltary Sr. Subject: RE: re-submission

Dear Terry,

The decline of proposal number 30756 is registered in the system. Thank you for your consideration.

Best Regards,

Nicole

Nicole Sanders

Senior Specialist, Membership & Conference Programming

______________________________________


From: xxxx 

To: Terry Singeltary 

Sent: Saturday, December 05, 2009 9:09 AM 

Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'

Your preliminary abstract number: 670

Dear Mr. Singeltary,

On behalf of the Scientific Committee, I am pleased to inform you that your abstract

'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'

WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.

Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.

Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Author: T. Singeltary; Bacliff, TX/US

Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange

This abstract has been ACCEPTED.

#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Authors: T. Singeltary; Bacliff, TX/US

Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

Body: Background

An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

Methods

12 years independent research of available data

Results

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion

I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.

I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion

page 114 ;

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf

http://www.isid.org/14th_icid/

http://www.isid.org/publications/ICID_Archive.shtml

http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf

TUESDAY, DECEMBER 12, 2017 

Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017

http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html

Tuesday, December 12, 2017 

Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology

http://tauopathies.blogspot.com/2017/12/neuropathology-of-iatrogenic.html

MONDAY, OCTOBER 02, 2017 

Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species

http://creutzfeldt-jakob-disease.blogspot.com/2017/10/creutzfeldt-jakob-disease-united-states.html

THURSDAY, AUGUST 17, 2017 

*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017

Singeltary et al

http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html

SUNDAY, APRIL 8, 2018 

Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018


Wednesday, May 30, 2018 

Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago


SUNDAY, JUNE 17, 2018 

Houston Chronicle Texas deer population would welcome good soaking, deer herd, the largest in the nation, will remain stunningly healthy, what about CWD TSE Prion?

Oh what a tangled web we weave when first we practice to deceive?




Terry S. Singeltary Sr.

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