Wednesday, December 28, 2011

FDA Targets Risks From Reused Devices

FDA Targets Risks From Reused Devices


Some medical devices are reused many times in common surgical and diagnostic procedures, and have been for years. They include instruments used in surgery (like clamps and forceps), and endoscopes (like bronchoscopes and colonoscopes) used to visualize areas inside the body.


And the Food and Drug Administration (FDA) wants to ensure that they are safely reused.


The agency is working with healthcare providers, manufacturers, organizations that set standards, and other government agencies to reduce the risk of infection from the inadequate “reprocessing” of these durable devices designed for repeated use. Reprocessing means cleaning and high-level disinfection or sterilization.


FDA has received reports of patients being exposed to microscopic amounts of blood, body fluids and tissue from other patients that may have occurred because the reusable devices were inadequately reprocessed and these contaminants were not removed. Transmission of infection was extremely rare, but the potential for becoming infected by an inadequately processed device was there.


So if you’re scheduled to have a medical procedure, how worried should you be about this?


Not worried enough to cancel or delay your plans, says FDA.


The risk of acquiring an infection from a reprocessed medical device is low, says William Maisel, MD, deputy director for science at the FDA's Center for Devices and Radiological Health. The benefits of these procedures in diagnosing and treating medical conditions far outweigh any risk, he says.


That said, there are questions you can ask your healthcare providers.


Frank Nemec, MD, a Las Vegas gastroenterologist and patient advocate who spoke at an FDA-sponsored workshop in June, advises his patients to ask this question: What precautions are in place to ensure that the procedure will be done safely?


One person who did ask that question is Pamela D. Scott, a biomedical engineer who has been working on this issue at FDA.


Earlier this year, Scott’s mother, Ophelia, was about to have a colonoscopy. Scott called the gastro-intestinal clinic and asked to speak to the person in charge of reprocessing medical devices. In this case, it was the head nurse.


Scott asked if the clinic staff was aware of news reports about problems with the reprocessing of endoscopes. And, if they were aware, how did these reports affect how they clean and disinfect these tools?


The nurse replied that clinic had recently assessed its reprocessing procedures and called in the manufacturer to make sure staff members are properly cleaning and disinfecting or sterilizing the devices.


“Just to know that they took steps, that they had procedures, that helped me,” Scott says.


So ask questions, just as Nemec recommends and Scott did on her mother’s behalf. Before having any medical procedure, it’s a good idea to learn more about the procedure and steps the healthcare facility takes to keep patients safe.


Health care providers are one source of this information. Many professional organizations, including the American Academy of Family Physicians, offer advice on how to ask such questions of your healthcare provider.


FDA is working with manufacturers and healthcare providers to:


Make sure that the makers of these devices are providing reprocessing instructions that are clear and scientifically validated.


Make sure that staff at hospitals and other healthcare facilities understand and are following the manufacturers’ instructions.


Identify device designs that facilitate optimal cleaning, disinfecting and sterilization.


And FDA has created a new website (www.fda.gov/reprocessingreusabledevices) with information about these medical tools.


To report a problem, the site also provides a link to MedWatch, the FDA Safety Information and Adverse Event Reporting Program.


This article appears on FDA's Consumer Updates page, which features the latest on all FDA-regulated products.


Posted December 28, 2011








2002


Date submitted: 3 Jun 2002


>> eLetter ID: gutjnl_el;21


>> >> Gut eLetter for Bramble and Ironside 50 (6): 888


>> >>Name: Terry S. Singeltary Sr.


>>Email: flounder@wt.net


>>Title/position: disabled {neck injury}


>>Place of work: CJD WATCH


>>IP address: 216.119.162.85


>>Hostname: 216-119-162-85.ipset44.wt.net


>>Browser: Mozilla/5.0 (Windows; U; Win98; en-US; rv:0.9.4)


>>Gecko/20011019 Netscape6/6.2


>> >>Parent ID: 50/6/888


>>Citation:


>> Creutzfeldt-Jakob disease: implications for gastroenterology


>> M G Bramble and J W Ironside


>> Gut 2002; 50: 888-890 (Occasional viewpoint)






>>-----------------------------------------------------------------


>>"CJDs (all human TSEs) and Endoscopy Equipment"


>>----------------------------------------------------------------- >> >> >>


>>regarding your article;


>>


>> Creutzfeldt-Jakob disease: implications for gastroenterology >>


>>I belong to several support groups for victims and relatives


>>of CJDs. Several years ago, I did a survey regarding


>>endoscopy equipment and how many victims of CJDs have


>>had any type of this procedure done. To my surprise, many


>>victims had some kind of endoscopy work done on them.


>>As this may not be a smoking gun, I think it should


>>warrant a 'red flag' of sorts, especially since data now


>>suggests a substantial TSE infectivity in the gut wall


>>of species infected with TSEs. If such transmissions


>>occur, the ramifications of spreading TSEs from


>>endoscopy equipment to the general public would be


>>horrible, and could potential amplify the transmission


>>of TSEs through other surgical procedures in that


>>persons life, due to long incubation and sub-clinical


>>infection. Science to date, has well established


>>transmission of sporadic CJDs with medical/surgical


>>procedures.


Terry S. Singeltary Sr. >>CJD WATCH


Again, many thanks, Kindest regards,


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder@wt.net CJD WATCH


[scroll down past article for my comments]


snip...




========================================================


Greetings List Members,


This is _very_ disturbing to me:


snip...


The distribution of PrPSc in the body is different in sporadic and variant CJD, reflecting the different pathogenesis of the two forms. In the case ot sporadic CJD, prion infectivity is largely limited to the CNS (including the retina) and only operations involving the brain and eye have resulted in iatrogenic transmission of the disease. Gastro-intestinal endoscopy is unlikely to be a vector for the transmission of sporadic CJD as infected tissue is not encountered during the procedure. No special precautions are necessary during or after the procedure and the endoscope should be cleaned and disinfected in the normal thorough way.4


snip...


i personally believe it is irresponsible for anyone to state in this day and time, that sporadic CJDs (now at 6 variants) will not transmit the disease by this route. considering infective dose cannot be quantified, only speculated, such a statement is thus, irresponsible. to hypothosize that sporadic CJD just happens spontaneously (with no scientific proof), that the PrPSc distribution in tissues of all sporadic CJDs is entirely different than that of vCJD, without being able to quantify the titre of infection, or even confirm all the different variants yet, again is _not_ based on all scientific data, then it's only a hypothosis. who is to say that some of these variants of sporadic CJD were not obtained _orally_?


also stated:


snip...


Although thorough cleaning of flexible endoscopes ensures patient safety for ''normal'' pathogens, the same process may not be adequate for the PrPSc.


snip...


The sporadic form of CJD affects approximately one person per mil-lion per annum in the population on a worldwide basis.


who is to say how much infectivity are in some of these variants of sporadic CJDs, without confirming this? if we look at the 6 different variants of sporadic CJDs, has the infective dose for all 6 _documented_ variants been quantified, and documented as being 'measurable'?


will there be more variants of sporadic CJDs, and what of the ramifications from them?


what of other strains/variants of TSE in cattle, BSE in sheep, CWD in cattle, or any of the 20+ strains of Scrapies in deer/elk? i get dizzy thinking of the different scenerio's. what would the human TSEs from these species look like and how can anyone quantify any tissue infectivity from these potential TSE transmissions to humans, and the risk scenerio described here from this potential route? could not some of these sporadic CJDs have derived directly or indirectly from one of these species, and if so, pose a risk by the route described here?


something else to consider, in the recent finding of the incubation period of 38 years from a _small_ dose of human growth hormone;


snip...


We describe the second patient with hGH related CJD in the Netherlands. The patient developed the disease 38 years after hGH injections. To our knowledge, this is the longest incubation period described for any form of iatrogentic CJD. Furthermore, our patient was _not_ treated with hGH, but only received a _low_ dose as part of a diagnostic procedure. (see full text below).


snip...


so my quesion is, how low is 'low' in quantifing the infectious dose in vCJD, comparing to _all_ sporadic CJDs, from the different potential routes, sources, and infectivity dose?


will the titre of infectivity in every tissue and organ of all sporadic CJDs stay exact or constant, no matter what the infective dose, route and species may be? this is considering you don't buy the fact that sporadic CJDs 85%+ of _all_ CJDs, are a happen stance of bad luck, happen spontaneously without cause, and are one-in-a-million world wide, with no substantial surveillance to confirm this.


Diagnosis and Reporting of Creutzfeldt-Jakob Disease T. S. Singeltary, Sr; D. E. Kraemer; R. V. Gibbons, R. C. Holman, E. D. Belay, L. B. Schonberger




and what of Dr. Prusiner et al recent work about tissue infectivity;


Prions in skeletal muscle


snip...


Our data demonstrate that factors in addition to the amount of PrP expressed determine the tropism of prions for certain tissues. That some muscles are intrinsically capable of accumulating substantial titers of prions is of particular concern. Because significant dietary exposure to prions might occur through the consumption of meat, even if it is largely free of neural and lymphatic tissue, a comprehensive effort to map the distribution of prions in the muscle of infected livestock is needed. Furthermore, muscle may provide a readily biopsied tissue from which to diagnose prion disease in asymptomatic animals and even humans.


snip...






can the science/diagnostic measures used to date, measure this, and at the same time guarantee that no titre of infectivity exists from sporadic CJDs (all of the variants), from this potential mode and route of transmission?


i don't think so, this is just my opinion. this is why i get paid nothing, and these scientists get the big bucks. i just hope i am wrong and the big bucks are correct in their _hypothisis_ of this potential mode/route of transmission with endoscopy equipment, from _all_ human TSEs.


i understand we have to weigh the risks of what we know to what we don't know, to the disease we _may_ catch to what we are having the procedure for, but to categorically state at this present time of scientific knowledge;


snip...


"Gastro-intestinal endoscopy is unlikely to be a vector for the transmission of sporadic CJD as infected tissue is not encountered during the procedure. No special precautions are necessary during or after the procedure and the endoscope should be cleaned and disinfected in the normal thorough way.4"


snip...


but, to categorically state this, in my opinion, is not only wrong, but potentially very dangerous to the future of human health...TSS


SHORT REPORT


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


E A Croes, G Roks, G H Jansen, P C G Nijssen, C M van Duijn ...............................................................


J Neurol Neurosurg Psychiatry 2002;72:792-793


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.


Prion diseases are potentially transmissible. Human to human transmission was first reported in 1974, when a 55 year old woman was described who developed symptoms of Creutzfeldt-Jakob disease (CJD) 18 months after a corneal transplant.1 Since then, transmission has been reported after stereotactic electroencephalographic (EEG) depth recording, human growth hormone (hGH) and gonadotrophin treatment, and dura mater transplantation.2-5 More than 267 patients with iatrogenic CJD are known today and their number is growing.6 The most important iatrogenic cause of CJD is still contaminated cadaveric hGH. Exposure to contaminated hGH occurred before 1985, when recombinant growth hormone became available. In a recent study, incubation periods in 139 patients with hGH associated CJD were found to range from 5-30 years, with a median of 12 years.6 One of the factors influencing incubation time is genotype on polymorphic codon 129 of the prion protein gene.7 The incubation time is significantly shorter in people who are homozygous for either methionine or valine on this polymorphism.7


We describe the second patient with hGH related CJD in the Netherlands. The patient developed the disease 38 years after hGH injections. To our knowledge, this is the longest incubation period described for any form of iatrogenic CJD. Further-more, our patient was not treated with hGH but only received a low dose as part of a diagnostic procedure.


CASE REPORT


This patient presented at the age of 47 years with paraesthesia in both arms for six months, difficulty with walking for four weeks, and involuntary movements of mainly the upper extremities of two weeks' duration. He did not notice any change in cognitive function, although his twin sister had noticed minor memory disturbances. There was no family history of neurological disease. During childhood the patient had experienced a growth delay compared with his twin sister and with the average in the Netherlands. When he was 9 years old, a nitrogen retention test with 6 IU hGH over five days was performed to exclude growth hormone deficiency. Since the result was not decisive, a quantitative amino acid test was performed, which measures 30 amino acids during fasting and one, two, and three hours after growth hormone injection. No abnormal amino acid concentrations were found making the diagnosis of primordial dwarfism most likely. Therefore, no treatment with hGH was given.


On neurological examination we found a slight dysarthria without aphasia. Cranial nerve function was normal. Walking was unstable and wide based. During movements of the upper extremities myoclonic jerks were present. Sensation, muscle tone, and strength were normal. Co-ordination was impaired in all four limbs with a disturbed balance. Tendon reflexes were brisk at the arms and increased at the legs with a clonus in the ankle reflex. Plantar responses were both normal. On the mini mental state examination, the patient scored 30/30. Routine laboratory investigation, thyroid function, vitamin concentrations (B-1, B-6, B-12, and E), and copper metabolism were normal. Admission EEG examination showed generalised arrhythmic slow activity with diffuse spikes and spike waves. EEG examination two months later showed a further slowing of the rhythm with bilateral diphasic sharp waves but was not typical for CJD. Cerebral magnetic resonance imaging was normal. Cerebrospinal fluid examination showed 1 cell/3 µl, normal glucose and protein concentrations, and a strongly positive 14-3-3 protein test. The patient was homozygous for methionine on the PRNP codon 129 polymorphism. On clinical grounds, CJD was diagnosed. Within one month the patient's condition deteriorated rapidly and because of severe disturbances in coordination and progressive myoclonus he became bedridden. An eye movement disorder developed with slow saccadic and dysmetric eye movements. Temperature became unstable with peaks of 39°C without an infectious focus, for which a disorder of autoregulation was presumed. Until a very advanced stage, cognitive function was intact. The patient died five months after admission. The diagnosis of CJD was confirmed at necropsy. The brain weighed 990 g and showed clear cortical and cerebellar atrophy. Spongiosis, neuronal loss, and gliosis were found predominantly in the putamen, caudate nucleus, and basotemporal and cerebellar cortex; the cerebellum was the most severely affected of these. Vacuoles ranged from 2-12 µm. No amyloid or Kuru plaques were found. Immunohistochemical staining (3F4 antibody 1:1000, Senetek, USA) was clearly positive for prion protein accumulation in a "synaptic" distribution. Most deposition was found in the stratum moleculare of the cerebellum.


DISCUSSION


We describe a 47 year old patient who developed pathology proven CJD 38 years after hGH injections. The patient was never treated with hGH but received a small dose as part of a diagnostic procedure. The onset of CJD was signalled by prodromal symptoms of paraesthesia followed by a rapidly progressive ataxia. The disease presentation and course with predominantly cerebellar and eye movement disorders are compatible with iatrogenic CJD caused by hGH treatment.6 8


Growth hormone treatment was first described in 1958 but hGH was not produced on a larger scale from human pituitary glands until the beginning of the 1960s. In the Netherlands growth hormone extraction started in 1963 and was soon centrally coordinated. Until 1979 growth hormone was extracted non-commercially from pituitaries by a pharmaceutical company. In 1971 commercial products also became available. Our patient was one of the first to receive hGH in the Netherlands but the origin of this product was not recorded. A causal relation can therefore not be established with full certainty, but coincidentally receiving growth hormone and developing this very rare disease is unlikely. Since the clinical course in this relatively young patient is in accordance with an iatrogenic cause, we think the probability is high that the hGH injections explain the development of CJD in this patient.


The first Dutch patient with hGH related CJD died in 1990. 9 During several periods from 1963 to 1969 she received intramuscular injections of hGH. During an unknown period the hGH was derived from South America. At age 39, 27 years after starting the treatment, she developed an ataxic gait, slurred speech, sensory disorders, and myoclonus, but her cognitive function remained normal. Postmortem examination of the brain confirmed the diagnosis of CJD.9 Following the identification of this patient, a retrospective study was started to trace all 564 registered hGH recipients who were treated before May 1985. Until January 1995, none of these was suspected of having CJD.10 Since 1993 prospective surveillance for all forms of human prion disease has been carried out in the Netherlands and, apart from the patient described above, a further two patients with iatrogenic CJD have been identified, who developed the disease after dura mater transplantation.11


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.


ACKNOWLEDGEMENTS


We are grateful to M Jansen PhD MD for his search for the origin of the growth hormone and P P Taminiau MD. CJD surveillance in the Netherlands is carried out as part of the EU Concerted Action on the Epidemiology of CJD and the the EU Concerted Action on Neuropathology of CJD, both funded through the BIOMED II programme, and is supported by the Dutch Ministry of Health. This surveillance would not have been possible without the cooperation of all Dutch neurologists and geriatricians.


........................................




Authors' affiliations


E A Croes, G Roks*, C M van Duijn, Genetic Epidemiology Unit, Department of Epidemiology and Biostatistics, Erasmus University Medical Centre Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands


P C G Nijssen, Department of Neurology, St Elisabeth Hospital, PO Box 90151, 5000 LC Tilburg, Netherlands


G H Jansen, Department of Pathology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands


*Also the Department of Neurology, St Elisabeth Hospital


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 In revised form 1 March 2002 Accepted 12 March 2002


Competing interests: none declared


REFERENCES


1 Duffy P, Wolf J, Collins G, et al. Possible person-to-person transmission of Creutzfeldt-Jakob disease. N Engl J Med 1974;290:692-3.


2 Bernoulli C, Siegfried J, Baumgartner G, et al. Danger of accidental person-to-person transmission of Creutzfeldt-Jakob disease by surgery. Lancet 1977;i:478-9.


3 Koch TK, Berg BO, De Armond SJ, et al. Creutzfeldt-Jakob disease in a young adult with idiopathic hypopituitarism: possible relation to the administration of cadaveric human growth hormone. N Engl J Med 1985;313:731-3.


4 Cochius JI, Burns RJ, Blumbergs PC, et al. Creutzfeldt-Jakob disease in a recipient of human pituitary-derived gonadotrophin. Aust NZ J Med 1990;20:592-3.


5 Thadani V, Penar PL, Partington J, et al. Creutzfeldt-Jakob disease probably acquired from a cadaveric dura mater graft: case report. J Neurosurg 1988;69:766-9.


6 Brown P, Preece M, Brandel JP, et al. Iatrogenic Creutzfeldt-Jakob disease at the millennium. Neurology 2000;55:1075-81.


7 Huillard d'Aignaux J, Costagliola D, Maccario J, et al. Incubation period of Creutzfeldt-Jakob disease in human growth hormone recipients in France. Neurology 1999;53:1197-201.


8 Billette de Villemeur T, Deslys JP, Pradel A, et al. Creutzfeldt-Jakob disease from contaminated growth hormone extracts in France. Neurology 1996;47:690-5.


9 Roos RA, Wintzen AR, Will RG, et al. Een patiënt met de ziekte van Creutzfeldt-Jakob na behandeling met humaan groeihormoon. Ned Tijdschr Geneeskd 1996;140:1190-3.


10 Wientjens DP, Rikken B, Wit JM, et al. A nationwide cohort study on Creutzfeldt-Jakob disease among human growth hormone recipients. Neuroepidemiology 2000;19:201-5.


11 Croes EA, Jansen GH, Lemstra AF, et al. The first two patients with dura mater associated Creutzfeldt-Jakob disease in the Netherlands. J Neurol 2001;248:877-81.


re-CJD after diagnostic use of human growth hormone


from a donor sourcing aspect, seems the record keeping here has a lot to be desired for, let us hope it has improved for recipients sake.


also, they speak of 'low dose fitting long incubation'. what about KURU still existing after some 40 years exposure had ceased. i don't believe in most instances the dose with kuru is low. just something else to ponder?


TSS






1: Ann Neurol 1999 Aug;46(2):224-33


Classification of sporadic Creutzfeldt-Jakob disease based on molecular and phenotypic analysis of 300 subjects.


Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.


snip...


The present data demonstrate the existence of six phenotypic variants of sCJD. The physicochemical properties of PrP(Sc) in conjunction with the PRNP codon 129 genotype largely determine this phenotypic variability, and allow a molecular classification of the disease variants.


snip...






were not all CJDs, even nvCJD, just sporadic, until proven otherwise?


Terry S. Singeltary Sr., P.O. BOX 42, Bacliff, Texas 77518 USA




Professor Michael Farthing wrote:


Louise Send this to Bramble (author) for a comment before we post. Michael


snip...see full text ;




Saturday, January 16, 2010


Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al


Evidence For CJD/TSE Transmission Via Endoscopes


From Terry S. Singletary, Sr flounder@wt.net 1-24-3




snip...please see full text ;


2011


Monday, December 26, 2011


Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites




Friday, December 23, 2011


Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model


Volume 18, Number 1—January 2012 Dispatch






Thursday, December 22, 2011


Risk of Prion Disease Transmission through Bovine-Derived Bone Substitutes: A Systematic Review Clin Implant Dent Relat Res. 2011 Dec 15. doi: 10.1111/j.1708-8208.2011.00407.x. [Epub ahead of print]






Saturday, December 3, 2011


Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies


Volume 17, Number 12—December 2011






Monday, December 12, 2011


Second iatrogenic CJD case confirmed Korea






2011 Monday, September 26, 2011


L-BSE BASE prion and atypical sporadic CJD






Tuesday, November 08, 2011


Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance?


A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011


Original Paper


Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.






FC5.1.1


Transmission Results in Squirrel Monkeys Inoculated with Human sCJD, vCJD, and GSS Blood Specimens: the Baxter Study


Brown, P1; Gibson, S2; Williams, L3; Ironside, J4; Will, R4; Kreil, T5; Abee, C3 1Fondation Alliance BioSecure, France; 2University of South Alabama, USA; 3University of Texas MD Anderson Cancer Center, USA; 4Western General Hospital, UK; 5Baxter BioSience, Austria


Background: Rodent and sheep models of Transmissible Spongiform Encephalopathy (TSE) have documented blood infectivity in both the pre-clinical and clinical phases of disease. Results in a (presumably more appropriate) non-human primate model have not been reported.


Objective: To determine if blood components (red cells, white cells, platelets, and plasma) from various forms of human TSE are infectious.


Methods: Blood components were inoculated intra-cerebrally (0.1 ml) and intravenously (0.5 ml) into squirrel monkeys from 2 patients with sporadic Creutzfeldt- Jakob disease (sCJD) and 3 patients with variant Creutzfeldt-Jakob disease (vCJD). Additional monkeys were inoculated with buffy coat or plasma samples from chimpanzees infected with either sCJD or Gerstmann-Sträussler-Scheinker disease (GSS). Animals were monitored for a period of 5 years, and all dying or sacrificed animals had post-mortem neuropathological examinations and Western blots to determine the presence or absence of the misfolded prion protein (PrPTSE).


Results: No transmissions occurred in any of the animals inoculated with blood components from patients with sporadic or variant CJD. All donor chimpanzees (sCJD and GSS) became symptomatic within 6 weeks of their pre-clinical phase plasmapheresis, several months earlier than the expected onset of illness. One monkey inoculated with purified leukocytes from a pre-clinical GSS chimpanzee developed disease after 36 months.


Conclusion: No infectivity was found in small volumes of blood components from 4 patients with sporadic CJD and 3 patients with variant CJD. ***However, a single transmission from a chimpanzee-passaged strain of GSS shows that infectivity may be present in leukocytes, and the shock of general anaesthesia and plasmspheresis appears to have triggered the onset of illness in pre-clinical donor chimpanzees.


Saturday, September 5, 2009


TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS


snip...




Wednesday, June 29, 2011


TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood and blood products






Wednesday, August 24, 2011


All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD




Wednesday, August 24, 2011


There Is No Safe Dose of Prions






layperson


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

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