Thursday, October 25, 2012

Current limitations about the cleaning of luminal endoscopes and TSE prion risk factors there from

Article in Press

Current limitations about the cleaning of luminal endoscopes

R. Hervé, C.W. Keevil

Environmental Healthcare Unit, Centre of Biological Sciences, University of Southampton, Southampton, UK

Received 1 September 2011; accepted 22 August 2012. published online 24 October 2012.



The presence and potential build-up of patient material such as proteins in endoscope lumens can have significant implications, including toxic reactions, device damage, inadequate disinfection/sterilization, increased risk of biofilm development and potential transmission of pathogens.


To evaluate potential protein deposition and removal in the channels of flexible luminal endoscopes during a simple contamination/cleaning cycle.


The level of contamination present on disposable endoscopy forceps which come into contact with the lumen of biopsy channels was evaluated. Following observations in endoscopy units, factors influencing protein adsorption inside luminal endoscope channels and the action of current initial cleaning techniques were evaluated using a proteinaceous test soil and very sensitive fluorescence epimicroscopy.


Disposable endoscope accessories appear to be likely to contribute to the contamination of lumens, and were useful indicators of the amount of proteinaceous soil transiting through the channels of luminal endoscopes. Enzymatic cleaning according to the manufacturer's recommendations and brushing of the channels were ineffective at removing all proteinaceous residues from new endoscope channels after a single contamination. Rinsing immediately after contamination only led to a slight improvement in decontamination outcome.


Limited action of current decontamination procedures and the lack of applicable quality control methods to assess the cleanliness of channels between patients contribute to increasing the risk of cross-infection of potentially harmful micro-organisms and molecules during endoscopy procedures.

Keywords: Luminal endoscope, Decontamination, Prion, CJD


Subject: CJD * Olympus Endoscope

Date: Sun, 10 Oct 1999 16:41:49 –0500

From: "Terry S. Singeltary Sr."

To: GOLDSS@...

Dear Dr. Goldstine,

Hello Sir, I understand that Olympus has issued a letter to the medical institutions and the CDC, about the dangers of _not_ being able to decontaminate the instruments (endoscope's) via modern autoclaving techniques (boil 3 minutes in 3% SDS or another ionic detergent and autoclave for 1 hour at 134 degrees C). I understand that; "Olympus" has issued a warning, _not_ to attempt to decontaminate the instrument, that they are instructed to destroy them.

(very very wise move);

Please Sir, it is imminent that I receive a copy of this letter, it is very important. This could lead to other company's following through, and lead to awareness of the potential health threats from human T.S.E.'s and the risks through surgery, and not just from endoscopes. It would be most appreciated, if you could send a copy of this document to;

Fax: xxxxx

I look forward, to hearing back from you....

Many Thanks,

Terry S. Singeltary Sr./ Mom DOD 12-14-97 hvCJD

Subject: Re: CJD * Olympus Endoscope

Date: Tue, 12 Oct 1999 15:57:03 –0500

From: "Terry S. Singeltary Sr."

To: GOLDSS@...

References: 1

Dear Mr. Goldstine, Hello again, I hope the CDC has not changed your mind, since our phone call, about sending me the information, in which we spoke of. I am still waiting for the information, re-fax. Someone had told me, you would not send me the information, but I told them you would, due to the importance of it pertaining to public safety, and the fact, you are a Doctor. I hope you don't disappoint me, and the rest of the public, and hide the facts, as the CDC and NIH have for years. Olympus can be part of the Truth, or you can be part of the cover-up. We are going to find out, sooner or later.

I already know, as do many more.

Still waiting,

Kind Regards,

Terry S. Singeltary Sr.

"Terry S. Singeltary Sr." wrote:

Dear Dr. Goldstine,

Hello Sir, I understand that Olympus has issued a letter to the medical institutions and the CDC, about the dangers of _not_ being able to decontaminate the instruments (endoscope's) via modern autoclaving techniques (boil 3 minutes in 3% SDS or another ionic detergent and autoclave for 1 hour at 134 degrees C). I understand that; "Olympus" has issued a warning, _not_ to attempt to decontaminate the instrument, that they are instructed to destroy them.

(very very wise move);

Please Sir, it is imminent that I receive a copy of this letter, it is very important. This could lead to other company's following through, and lead to awareness of the potential health threats from human T.S.E.'s and the risks through surgery, and not just from endoscopes. It would be most appreciated, if you could send a copy of this document to;

Fax: xxxxxxx

I look forward, to hearing back from you....

Many Thanks,

Terry S. Singeltary Sr./ Mom DOD 12-14-97 hvCJD



Volume 354, Number 9192 20 November 1999

Contaminated surgical instruments and variant Creutzfeldt-Jakob disease

Sir--John Collinge (July 24, p 317 )1 mentions the possibility of iatrogenic transmission of Creutzfeldt-Jakob disease (CJD). Discussion with surgical colleagues (including colleagues from other institutions) suggests that sterilised instruments do sometimes have tissue visible on them.

To investigate further, we used a dissecting microscope to examine 30 surgical instruments after cleaning. In our Central Sterile Services Department, cleaning consists of visual inspection and removal of gross soiling, ultrasonic cleaning, hot wash, and rinse before air drying. Instruments are then steam sterilised. 16 of 25 artery forceps had blood or tissue visible in the jaws or joints. One of two clamps had blood or tissue at the joint. These instruments proceed to the sterilisation process without further cleaning. A similar situation probably exists in other sterilisation and disinfection units.

These findings support the suggestion that a range of surgical procedures may serve as unrecognised contamination events and account for a proportion of cases of sporadic CJD,2 when procedures involve contact with lymphoreticular tissues such as tonsillectomy, appendicectomy, and lymph-node and gastrointestinal biopsy. This study showed a correlation between increasing surgical exposures and risk of sporadic CJD. Tissue from unrecognised early cases of new variant CJD could contaminate instruments with infectious prions.

Cleaning of instruments is extremely difficult if blood, tissue, and other proteinaceous material have dried. Prions exhibit an unusual resistance to conventional chemical and thermal decontamination methods. Heat and some instrument disinfectants (eg, glutaraldehyde and alcohol) are fixatives. Therefore, surgical instruments should be promptly and effectively cleaned before thermal or chemical disinfection or sterilisation takes place. If delay is likely before processing, instruments should be cleaned in a dedicated sink or washer disinfector in the theatre before return to the sterile services department. Otherwise tissue and body fluids containing prions may dry onto the surface.

To overcome these difficulties a validated automated cleaning system should be used before disinfection or sterilisation.3,4 This system includes an initial low temperature clean (normally <35 a="a" and="and" by="by" coagulate="coagulate" detergent="detergent" disinfection.4="disinfection.4" div="div" followed="followed" hot="hot" not="not" preferably="preferably" prion="prion" protein="protein" remove="remove" thermal="thermal" ultrasonics="ultrasonics" using="using" wash="wash" which="which" will="will">

Cleaning failures may occur for the following reasons: delay before processing; initial wash temperature is too high; inappropriate detergent is used; cleaning jets are blocked or poorly adjusted; ultrasonic transducers have failed; washer disinfector is poorly loaded and soiled surfaces are not accessible to cleaning solutions. Use of a properly validated and maintained washer disinfector,5 and careful inspection of each item after cleaning and disinfection, will lower the risk of prion transmission and increase the likelihood of attaining sterility. These solutions have resource implications, as does the alternative of using instruments once only.

To act now (at considerable financial cost) to lessen the risk of iatrogenic prion transmission or do nothing (at unknown cost) is perhaps a political and public health decision. In the meantime, hospital infection control teams can promote good practice as far as current resource allows.

*I F Laurenson, A S Whyte, C Fox, J R Babb

*Department of Microbiology, Fife Area Laboratory, Kirkcaldy KY2 5AH, UK; and Hospital Infection Research Laboratory, City Hospital NHS Trust, Birmingham

1 Collinge J. Variant Creutzfeldt-Jakob disease. Lancet 1999; 354: 317-23.

2 Collins S, Law MG, Fletcher A, et al. Surgical treatment and risk of sporadic Creutzfeldt-Jakob disease: a case-control study. Lancet 1999; 353: 693-97.

3 Advisory Committee on Dangerous Pathogens and Spongiform Encephalopathy. Transmissible spongiform encephalopathy agents: safe working and the prevention of infection. London: HM Stationery Office, 1998.

4 British Standards Institution. BS 2745 parts 1 and 3. Washer disinfectors for medical purposes. London: BSI, 1993.

5 NHS Estates. Washer disinfectors: health technical memorandum 2030. London: HM Stationery Office, 1995.

Sir--John Collinge1 concludes that the early cases of variant Creutzfeldt-Jacob disease (vCJD) may have occurred during the preclinical phase of the bovine spongiform encephalopathy (BSE) epidemic. He also discusses incubation periods for vCJD lasting decades rather than a few years. His argument is based on Kuru as an example of a transmission of a spongiform encephalopathy within human beings and the affect of a species barrier involved in the transmission of BSE to human beings. I agree with his argument but I am convinced that he missed a very important conclusion.

Young age of vCJD may indicate infection in infancy. Oral transmission requires a high load of infectivity such as found in spinal cord or brain rather than in any other tissue. However, the source of food that may have contained such material is unknown.

vCJD affects young adults under 35 years, compared with sporadic CJD, which affects elderly adults. The onset of disease in the 43 cases of vCJD in the UK occurred in 1994-98. Apart from eight patients with an age of onset over 38 years, 35 patients developed vCJD at 35 years or younger (mean age 25 years [SD 6]).

vCJD is the only example of a spongiform encephalopathy with good epidemiological and experimental evidence of transmission across a species barrier. In passing to a new species, the incubation period of the disease is increased. For example, primary and secondary transmissions of BSE to VM mice results in incubation periods of 433 and 116 days, respectively.2 Transmission of BSE and vCJD to mice that have the gene for human BSE-specific amyloid result in incubation perods of 602 and 228 days, respectively.3

Kuru is an example of transmission between human beings of a spongiform encephalopathy via ritual cannibalism. Adult women and very young children of both sexes had the highest exposure to infected brain material. In Kuru, transmission was by the peripheral route and may also have been oral. I have calculated a mean incubation period of 12 years for patients who were exposed to the Kuru agent in early infancy.4 I included only children and adolescents with a ratio of female to male patients of about 1·5. This ratio is similar to that found in patients with vCJD (1·0-1·1). Among older patients the ratio is higher because men did not attend the ceremonies.

If for vCJD we assume exposure in early infancy, the mean incubation period is 25 years. Such an increase in incubation period for an agent crossing a species barrier must be expected in accordance with data for BSE2,3 and vCJD.3

Exposure to BSE during early infancy could be an explanation for the appearance of vCJD in younger adults. Such a possibility would necessitate exposure to the BSE agent in the 1960s and 1970s, well before the BSE epidemic.5 This possibility leaves the hope that the critical phase of exposure may have ended several years before the peak of the BSE epidemic.

Heino Diringer

Ladestrasse 48, D-26180 Rastede, Germany

1 Collinge J. Variant Creutzfeldt-Jakob disease. Lancet 1999; 354: 317-23.

2 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' is caused by the BSE agent. Nature 1997; 389: 498-50 [PubMed].

3 Hill AF, Desbruslais M, Joiner S, Sidle KCL, Gowland I, Collinge J. The same prion strain causes nvCJD snd BSE. Nature 1997; 389: 448-50 [PubMed].

4 Gajdusek DC. Infectious amyloids: subacute spongiform encephalopathies as transmissible amyloidoses. In: Fields BN, Knipe DM, Howley PM, eds. Virology, 3rd edn, vol 2. Philadelphia: Lippincott-Raven, 1996: 2851-900.

5 Wilesmith JW, Wells GAD, Cranwell MP, Ryan JBM. Bovine spongiform encephalopathy. Epidemiological studies. Vet Rec 1988; 123: 638-44 [PubMed].


now with that said, we must keep in mind, nothing has been proven one way or the other about endoscopy equipment and CJD, other than they do not autoclave them, just clean with soloution, that we know would not kill the Prion Protein or the TSE agent. There are many different types of endoscopy equipment, and they are poked in many different places. (believe me i know, just had my kidneys and prostate scoped, and will have to have it done again in about 2 weeks, and my eyes water just thinking about it, 'OUCH', may not let them do it again, i was very reluctant in the first place).

this question was put to Voice about a year ago, and there was a very positive result of CJD victims, that had an endescopy procedure of some kind done. Doesn't prove anything, but as i have said time and time again, the 85%+ sporadic CJD had to come from somewhere, and i believe the medical/pharmaceutical Industries will be a source of infection from TSE's, for many of the sporadic CJD victims....tss


>I became curious that these two cats which were very

>well cared for, died within 5 days of each other

>after being together for a week in December. I question;

>was there an incubation period for their illness and sudden death?

>Why and how did Don become affected? The cat in Texas has been

>cryogenically preserved, (for no reason related to my

>inquisitiveness), and I would like to have the cat's brain tissue

>evaluated if it at all possible.

>So, Terry, that is the scenario. Do you think that there could

>be a possible connection here? The fact that these two perfectly

>healthy cats died within 5 days of each other with a similar course

>of illness; each cat a half a world away from each

>other...coincidence or what? The incubation period could

>have been the same if they ate BSE infected cat food. If you or

>anyone reading this chronicle have any info or articles pertaining

>to the above, I would greatly appreciate it. Besides Dr

>Gambetti, who else also has a license to look at animal tissue?

>Sara in Massachusetts

cats and man have already been tied together in some cases of sporadic CJD. i don't know who would check these tissues, but it would be good to know what they died from, it is coincidental. maybe call Gambetti and explain to him the scenario;

Research letters

Volume 352, Number 9134 3 October 1998

Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy

Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, GianMaria Fabrizi, Sergio Ferrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, Salvatore Monaco

Transmissible spongiform encephalopathies (TSE) encompass inherited, acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four types of PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prion strain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 in the UK.5 We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.

A 60-year-old man, with no unusual dietary habits, was admitted in November, 1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, and myoclonus. An electroencephalogram (EEG) showed diffuse theta-delta activity. A brain magnetic resonance imaging scan was unremarkable. 10 days later, he was speechless and able to follow only simple commands. Repeat EEGs showed periodic triphasic complexes. 2 weeks after admission, he was mute, akinetic, and unable to swallow. He died in early January, 1994.

His 7-year-old, neutered, female shorthaired cat presented in November, 1993, with episodes of frenzy, twitching of its body, and hyperaesthesia. The cat was usually fed on canned food and slept on its owner's bed. No bites from the cat were recalled. In the next few days, the cat became ataxic, with hindquarter locomotor dysfunction; the ataxia got worse and there was diffuse myoclonus. The cat was killed in mid-January, 1994.

No pathogenic mutations in the patient's PrP gene were found. The patient and the cat were methionine homozygous at codon 129. Histology of the patient's brain showed neocortical and cerebellar neuronal loss, astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a punctate pattern and paralleled spongiform changes (figure B). The cat's brain showed mild and focal spongiosis in deeper cortical layers of all four lobes (figure C), vacuolated cortical neurons (figure D), and mild astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed. Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and caudate nucleus (figure E). Western blot analysis of control and affected human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After digestion with proteinase K and deglycosylation, only samples from the affected patient and cat showed type-1 PrPres, with PrP glycoform ratios comparable to those observed in sporadic CJD1 (details available from author).

Microscopic sections of patient and cat brains

A: Occipital cortex of the patient showing moderate spongiform degeneration and neuronal loss (haematoxylin and eosin) and B: punctate perineuronal pattern of PrP immunoreactivity; peroxidase immunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortex showing mild spongiform degeneration (haematoxylin and eosin).D: vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase immunohistochemistry with antibody 3F4 shows punctate perineuronal deposition of PrP in temporal cortex.

This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5 Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2 Taken together, our data suggest that the same agent strain of sporadic CJD was involved in the patient and in his cat.

It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source, or the chance occurrence of two sporadic forms.

1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypic variablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39: 767-78 [PubMed].

2 Collinge J, Sidle KCL, Meads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996; 383: 685-90 [PubMed].

3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501 [PubMed].

4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJD and BSE. Nature 1997; 389: 448-50 [PubMed].

5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiform encephalopathy: a review. Vet Annual 1993; 33: 1-10.

Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e della Visione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy (S Monaco; e mail rizzuto@...); and Istituto Zooprofilattico Sperimentale della Lombardia e dell' Emilia, Brescia


kind regards,

Terry S. Singeltary Sr.


Re: [CJDVoice] sporadic CJDs and Endoscopy Equipment ???

Posted By: mariek43@...

Send Email Thu Jun 28, 2001 7:22 pm

For everyone's information !!

I recently returned from my infection control conference and they presented new guidelines which recommend that endoscopy equipment does not need special treatment for CJD patients. This is consistent with the WHO guidelines. Remember it is good to search for information but detrimental to cause unneccessary trauma for patients and their families. I know because I fight every day to quell the fear.


Re: [CJDVoice] sporadic CJDs and Endoscopy Equipment ???

Posted By: flounder@... Send Email Thu Jun 28, 2001 10:39 pm

hello Marie,

could you please pass reference to where w.h.o. states no need for special treatment for endoscopy equipment for patients of risk of CJD/TSEs. please pass document or url 'reference' please...

i understand about the fear factor, but some of these same folks are the ones that used to say BSE could not transmit to humans.

it would seem since there is documented iatrogentic case of sporadic CJDs, then this route could pose risk as potential route...

thank you, Terry

Re: [CJDVoice] sporadic CJDs and Endoscopy Equipment ???

Posted By: flounder@... Send Email Thu Jun 28, 2001 11:49 pm


what infection control safety conference were you at ???

For everyone's information, here is a bit of data from the FDA and other sources.

the 85%+ of the many different strains of sporadic CJD have to be coming from somewhere. not saying this is definately the cause, but does not hurt to ask.

if CDC/NIH/DH had questionnaire sent to every family, maybe they could put something together.

but they don't even want it reportable $$$

kind regards, Terry

In addition:

Provide all labeling including advertisements, appropriate directions for reprocessing/disinfection/sterilization, maintenance, etc. Include all cautions, warnings, precautions, contraindications or limitations.

If a reusable scope, provide a warning/contraindication within the labeling that this should not be used in patients suspected of having Creutzfield-Jakob Disease (CJD).

Meeting held at the Department of Health on the 4th October

... the above precautions would minimise risk of transmission. However, the destruction of all endoscopes used on CJD patients would reinforce the level of safety. ...

Decontamination of a patient-care device after use on patients with CJD: Although there is no evidence of CJD transmission via body substances (e.g., blood, urine, bronchial fluid, GI secretions), some experts recommend that when a patient-care device is contaminated with body substances it should be sterilized as follows (1-3):

A. Steam autoclave for 1 hour at 132°C.

B. Immerse in 1 N sodium hydroxide for 1 hour at room temperature.

C. Immerse in 0.5% sodium hypochlorite for 2 hours at room temperature.

The Decontamination of Surgical Instruments and OTHER Medical Devices

Report of a Scottish Executive Health Department Working Group

Feb 2001

A conservative endoscopic approach, therefore, is:

ß Seek alternative diagnostic studies or therapeutic approaches in patients with known or suspected spongiform encephalopathies.

ß Where such procedures are totally unavoidable, refer such patients to a large centre where specific endoscopes are reserved for patients with CJD.

ß Discard all endoscopic accessories used in patients with known or suspected CJD.

ß No change can be recommended to the indications for endoscopy or current cleaning and disinfection protocols in patients who have no increased risk of CJD.

kind regards, Terry


Posted By: flounder@... Send Email Fri Jun 29, 2001 6:30 pm

Greetings CJD Voice,

i suppose one could interpret this in many ways. seems the way i interpret it, is they do seem very concerned about all instruments and diagnostic equipment, but the one's they cannot destroy, use with 'extreme' caution.

some might want to read this and pass on to there next conference.....


''unnecessary trauma for patients and families''

i don't suppose being concerned about the many different potential routes of TSEs would fit into that category, i would hope not, especially on a list of Families of TSE victims, looking for answers.

the following was scanned and there may be character errors, did not have time to correct...


WHO/CDS/CSR/APH/2000.3 WHO Infection Control Guidelines for TSEs. Report of a WHO Consultion

Geneva, Switzerland 23-26 March 1999


3.3 Diagnostic

During the earlier stages of disease, patients with TSE who develop intercurrent illnesses may need to under go the same kinds of diagnostic procedures as any other hospitalized patient. These could include ophthalmoscopic examinations, various types of endoscopy, vascular or urinary catheterization, and cardiac or pulmonary function tests. In general, these procedures may be conducted without any special precautions, as most tissues with which the instuments come in contact contain no detectable infectivity (see sub-Section 2.4.2). A concervative approach would nevertheless try to schedule such patients at the end of the day to allow more strict environmental decontamination (see Section 6.3) and instrument cleaning (see Section 6.2). When there is known exposure to high or low infectivity tissues, the instruments should be subjected to the strictest form of decontamination procedure which can be tolerated by the instrument. Instrument decontamination is discussed in more detail in Section 6.2 and decontamination methods are specifically described in Annex III.


3.4 Surgical procedures Before admission to a hospital or healthcare facility, the infection control team should be informed of the intention to perform a surgical procedure on any person with confirmed or suspected TSE. Every effort should be made to plan carefully not only the procedure, but also the practicalities surrounding the procedure, e.g. instrument handling, storage, cleaning and decontamination or disposal. Written protocols are essential. All staff directly involved in these procedures or in the subsequent re-processing or disposal of potentially contaminated items, should be aware of the recommended precautions, and be adequately trained. The staff should be made aware of any such procedures in sufficient time to allow them to plan and to obtain suitable instruments and equipment (such as single use items), and it may be useful to schedule the patient at the end of the day's operating list. Staff must adhere to protocols that identify specifics regarding pre­operative, peri-operative and post-operative management of the patient, disposable materials, including bandages and sponges, and re-usable materials. Ancillary staff, such as laboratory and central instrument cleaning personnel, must be informed and appropriate training provided. Basic protective measures are described in Table 4. Recommendations listed in Section 6 and Annex III for decontamination of equipment and environment, and in Section 7 for disposal of infectious waste should be followed. Supervisors should be responsible for ensuring that the appropriate procedures are followed and that effective management systems are in place.

Table 4 Precautions for surgical procedures

Wherever appropriate and possible, the intervention should: 1. be performed in an operating theatre;

2. involve the minimum required number of healthcare personnel;

3. use single, use equipment as follows: i) liquid repellent operating theatre gown, over a plastic apron ii) gloves iii) mask iv) visor or goggles v) linens and covers;

4. mask all non - disposable equipment;

5. maintain one. way flow of instruments;

6. treat all protective clothing, covers, liquid and solid waste by a method listed in Section 6; and Annex III; incineration is preferred

7. mark samples with a 'Biohazard" label;

8. clean all surfaces according to recommendations specified in Section 6 and Annex III.

Procedures which are normally carried out at the bedside (e.g. lumbar puncture, bone marrow biopsy) may be performed at the bedside, but care should be taken to ensure ease of environmental decontamination should a spillage occur.

3.5 Handling of surgical instruments 3.5.1 General measures Methods for instrument decontamination are fully discussed in Section 6. Determination of which method to use is based upon the infectivity level of the tissue and the way in which instruments will subsequently be re-used. For example, where surgical instruments eontact high infectivity tissues, single-use surgical instruments are strongly recommended. If single-use instruments are not available, maximum safety is attained by destruction of re-usable instruments. Where destruction is not practical, re-usable instruments must be handled as per Table 5 and must be decontaminated as per Section 6 and Annex III. Although CSF is classified as a low infectivity tissue and is less infectious than high infectivity tissues it was felt that instruments contaminated by CSF should be handled in the same manner as those contacting high infectivity tissues. This exception reflects the higher risk of transmission to any person on whom the instruments would be re-used for the procedure of lumbar puncture.

Table 5 General measures for cleaning instruments and environment

1. Instruments should be kept moist until cleaned and decontaminated.

2. Instruments should be cleaned as soon as possible alter use to minimize drying of tissues, blood and body fluids onto the item.

3. Avoid mixing instruments used on no detectable infectivity tissues with those used on high and Iow infectivity tissues.

4. Recycle durable items for re-use only alter TSE decontamination by methods found in Section 6 and Annex II1.

5. Instruments to be cleaned in automated mechanical processors must be decontaminated by methods described in Section 6 and Annex III before processing through those machines, and the washers (or other equipment) should be run through an empty cycle before any fuRher routine use.

6. Cover work surfaces with disposable material, which can then be removed and incinerated; otherwise clean and decontaminate underlying surfaces thoroughly using recommended decontamination procedures in Section 6 and Annex III.

7. Be familiar with and observe safety guidelines when working with hazardous chemicals such as sodium hydroxide (NaOH, 'soda lye') and sodium hypochlorite (NaOCI, 'bleach') (see Annex III for definitions).

8. Observe manufacturers' recommendations regarding care and maintenance of equipment.

Those instruments used for invasive procedures on TSE patients (i.e. used on high or low infectivity tissues) should be securely contained in a robust, leak-proof container labelled "Biohazard". They should be transferred to the sterilization department as soon as possible after use, and treated by a method listed in Annex III, or transferred to the incinerator as per Section 3.5.2. A designated person who is familiar with this guideline should be responsible for the transfer and subsequent management.

The consultation did not address the issue of post-exposure notification in the event that an instrument used on a high-risk tissue and/or high-risk patient was subsequently re­used without adequate decontamination.

3.5.2 Destruction of surgical instruments

Items for disposal by incineration should be isolated in a rigid clirdcal waste container, labelled 'Hazardous' and transported to the incinerator as soon as practicable,in line with the current disposal of chincai waste gindance described in the Teachers Guide: Management of Wastes from Health-care Facilities12 published by WHO. To avoid unnecessary destruction of instruments, quarantine of instruments while determining the final diagnosis of persons suspected of TSEs may be used.

3.5.3 Quarantine If a facility can safely quarantine instruments until a diagnosis is confirmed, quarantine can be used to avoid needless destruction of instruments when suspect cases are later found not to have a TSE. Items for quarantine should be cleaned by the best non-destructive method as per Section 6 and Annex III, sterilized, packed, date and 'Hazard' labelled, and stored in specially marked rigid sealed containers? Monitoring and ensuring maintenance of quarantine is essential to avoid accidental re-introduction of these instruments into the circulating instrument pool. If TSE is excluded as a diagnosis, the instruments may be returned to circulation after appropriate sterilization.

3.6 Anaesthesia 3.6.1 General anaesthesia TSEs are not transmissible by the respiratory route; however, it is prudent to treat any instruments in direct contact with mouth, pharynx, tonsils and respiratory tract by a method described in Annex III. Destruction by incineration of non re-usable equipment is recommended.

3.6.2 Local anaesthesia

Needles should not be re-used, and in particular, needles contacting the CSF (e.g. for saddle blocks and other segmental anaesthetic procedures) must be discarded and destroyed.

3.7 Pregnancy and childbirth TSE is not known to be transmitted from mother to child during pregnancy or childbirth; familial disease is inherited as a result of genetic mutations. In the event that a person with TSE becomes pregnant, no particular precautions need to be taken during the pregnancy, except during invasive procedures as per Section 3.4. Childbirth should be managed using standard infection control procedures, except that precautions should be taken to reduce the risk of exposure to placenta and any associated material and fluids. These should be disposed of by incineration. Instruments should be handled as for any other clinical procedure (Table 5). In home deliveries, the midwife (or any other persons in charge of delivery) should ensure that any contaminated material is removed and disposed of in accordance with correct procedures for infected clinical waste.


13 Pruess A, Tomend WK. Teacher's Guide: Management of Wastes from Health-care Activities. Geneva, World Health Organization, 1998. WHO/EOS/98.6. Although the intention of quarantine is to avoid destruction of instruments and will permit the re-introduction of instruments only if TSEs are not diagnosed, the use of a decontamination method for TSEs will confer additional safety should an instrument unintentionally come in contact with staff or patients.

6.2 Decontamination of instruments Policy makers should be guided by the infectivity level of the tissue contaminating the instrument and by the expectations of how the instrument will be re-used, as per Section 2.4. In this way, the most stringent recommendations are applied to instruments contacting high infectivity tissues of a person with a known TSE, which will also subsequently be re-used in the CNS or spinal column. Policy makers are encouraged to adopt the highest decontamination methods feasible until studies are published which clarify the risk of re-using decontaminated instruments. Annex III lists the decontamination methods recommended by the consultation in order of decreasing effectiveness. It was emphasized that the safest and most unambiguous method for ensuring that there is no risk of residual infectivity on surgical instruments is to discard and destroy them by incineration. While this strategy should be universally applied to those devices and materials that are designed to be disposable, it was also recognized that this may not be feasible for many devices and materials that were not designed for single use. For these situations, the methods recommended in Annex III appear to remove most and possibly all infectivity under the widest range of conditions. Those surgical instruments that are going to be re-used may be mechanically cleaned in advance of subjecting them to decontamination. Mechanical cleaning will reduce the bio-load and protect the instrument from damage caused by adherent tissues. If instruments are cleaned before decontamination, the cleaning materials must be treated as infectious waste, and the cleaning station must be decontaminated by one of the methods listed in Annex III. The instruments are then treated by one of the decontamination methods recommended in Annex III before reintroduction into the general instrument sterilization processes. A minority opinion held that instruments should be decontaminated before mechanical cleaning, and then handled as per general instrument sterilization processes. Annex III recommends that, where possible, two or more different methods of inactivation be combined in any sterilization procedure for these agents. Procedures that employ heat and NaOH (either consecutively or simultaneously) appear to be sterilizing under worst-case conditions ( e.g., infected brain tissue partly dried on to surfaces). Moreover, hot alkaline hydrolysis reduces biological macromolecules to their constituent sub-units, thereby cleaning as well as inactivating. The consultation recognized that complex and expensive instruments such as intracardiac monitoring devices, fiberoptic endoscopes, and microscopes cannot be decontaminated by the harsh procedures specified in Annex III. Instead, to the extent possible, such instruments should be protected from surface contamination by wrapping or bagging with disposable materials. Those parts of the device that come into contact with internal tissues of patients should be subjected to the most effective decontaminating procedure that can be tolerated by the instrument. All adherent material must be removed and, if at all possible, the exposed surfaces cleaned using a decontamination method recommended in Annex III. Some instruments can be partly disassembled (e.g. drills and drill bits). Removable parts that would not be damaged by autoclaving, NaOH, or bleach should be dismounted and treated with these agents. In all instances where unfamiliar decontamination methods are attempted, the manufacturer should be consulted. These cleaning procedures should be applied even if the instrument has been re-used before discovery of its potential contamination.

Contaminated instruments or other contaminated materials should not be cleaned in automated washers without first having been decontaminated using a method recommended in Annex III.

6.3 Decontamination of work surfaces

Because TSE infectivity persists for long periods on work surfaces, it is important to use disposable cover sheets whenever possible to avoid environmental contamination, even though transmission to humans has never been recognized to have occurred from environmental exposure. It is also important to mechanically clean and disinfect equipment and surfaces that are subject to potential contamination, to prevent environmental build-ups. Surfaces contaminated by TSE agents can be disinfected by flooding, for one hour, with NaOH or sodium hypochlorite, followed by water rinses (see Annex III for detailed instructions). Surfaces that cannot be treated in this manner should be thoroughly cleaned; consider use of a partially effective method as listed in Table 8. Cleaning materials treated as potentially contaminated (see Section 6.4).

6.4 Decontamination of wastes and waste-contaminated materials Decontamination of waste liquid and solid residues should be conducted with the same care and precautions recommended for any other exposure to TSE agents. The work area should be selected for easy containment of contamination and for subsequent disinfection of exposed surfaces. All waste liquids and solids must be captured and treated as infectious waste. Liquids used for cleaning should be decontaminated in situ by addition of NaOH or hypochlorite or any of the procedures listed in Annex III, and may then be disposed of as routine hospital waste. Absorbents, such as sawdust, may be used to stabilize liquids that will be transported to an incinerator; however, this should be added after decontamination. Cleaning tools and methods should be selected to minimize dispersal of the contamination by splashing, splatters and aerosols. Great care is required in the use of brushes and scouring tools. Where possible, cleaning tools such as brushes, towelling and scouting pads, as well as tools used for disassembling contaminated apparatus, should either be disposable or selected for their ability to withstand the disinfection procedures listed in Annex III. Upon completion of the cleaning procedure, all solid wastes including disposable cleaning materials should be collected and decontaminated. Incineration is highly recommended. The cleaning station should then itself be decontaminated using one of the methods in Annex III. Automated cleaning equipment must not be used for any instrument or material that has not previously been thoroughly decontaminated following the recommendations in Section 6.2 and Annex III.

6.5 Personal protection during decontamination procedures Persons involved in the disinfection and decontamination of instruments or surfaces exposed to the tissues of persons with TSE should wear single-use protective clothing, gloves, mask and visor or goggles, as noted in Section 5.1, Table 6. The recommendations found in Table 6 can be adapted to different situations. All individuals involved with disinfection and decontamination procedures should be familiar with these basic protective measures and precautions. Handling of contaminated instruments during transfers and cleaning should be kept to a minimum.

Annex III Decontamination methods for Transmissible Spongfform En cep halopa thies

The safest and most unambiguous method for ensuring that there is no risk of residual infectivity on contaminated instruments and other materials is to discard and destroy them by incineration. In some healthcare situations, as described in the guidance, one of the following less effective methods may be preferred. Wherever possible, instruments and other materials subject to re-use should be kept moist between the time of exposure to infectious materials and subsequent decontamination and cleaning. If it can be done safely, removal of adherent particles through mechanical cleaning will enhance the decontamination process.

The following recommendations are based on the best available evidence at this time and are listed in order of more to less severe treatments. These recommendations may require revision if new data become available.

1. Incineration

1. Use for all disposable instruments, materials, and wastes. 2. Preferred method for all instruments exposed to high infectivity tissues.

2. Autoclave/chemical methods for heat-resistant instruments

1. Immerse in sodium hydroxide (NaOH)2° and heat in a gravity displacement autoclave at 121°C for 30 min; clean; rinse in water and subject to routine sterilization. 2. Immerse in NaOH or sodium hypochlorite2~ for 1 hr; transfer instruments to water; heat in a gravity displacement autoclave at 121 °C for 1 hr; clean and subject to routine sterilization. 3. Immerse in NaOH or sodium hypochlorite for 1 hr.; remove and rinse in water, then transfer to open pan and heat in a gravity displacement (121 °C) or porous load (134°C) autoclave for 1 hr.; clean and subject to routine sterilization. 4. Immerse in NaOH and boil for 10 min at atmospheric pressure; clean, rinse in water and subject to routine sterilization. 5. Immerse in sodium hypochlorite (preferred) or NaOH (alternative) at ambient temperature for 1 hr; clean; rinse in water and subject to routine sterilization. 6. Autoclave at 134°C for 18 minutes.22

20 Unless otherwise noted, the recommended concentration is IN NaOH. 22 Unless otherwise noted, the recommended concentration is 20 000 ppm available chlorine. 22 in worse-case scenarios (brain tissue bake-dried on to surfaces) infectivity will be largely but not completely removed.

Chemical methods for surfaces and heat sensitive instruments

1. Flood with 2N NaOH or undiluted sodium hypochlorite; let stand for 1 hr.; mop up and rinse with water. 2. Where surfaces cannot tolerate NaOH or hypochlorite, thorough cleaning will remove most infectivity by dilution and some additional benefit may be derived from the use of one or another of the partially effective methods listed in Section 5.1 (Table 8).

Autoclave/chemical methods for dry goods 1. Small dry goods that can withstand either NaOH or sodium hypochlorite should fu'st be immersed in one or the other solution (as described above) and then heated in a porous load autoclave at -> 121 °C for 1 hr. 2. Bulky dry goods or dry goods of any size that cannot withstand exposure to NaOH or sodium hypochlorite should be heated in a porous load autoclave at 134°C for 1 hr.

Notes about autoclaving and chemicals Gravity displacement autoclaves: Air is displaced by steam through a port in the bottom of the chamber. Gravity displacement autoclaves are designed for general decontamination and sterilization of solutions and instruments. Porous load autoclaves: Air is exhausted by vacuum and replaced by steam.

Porous load autoclaves are optimized for sterilization of clean instruments, gowns, drapes, towelling, and other dry materials required for surgery. They are not suitable for liquid sterilization. Sodium Hydroxide .(NaOH, or soda lye): Be familiar with and observe safety guidelines for working with NaOH. 1N NaOH is a solution of 40 g NaOH in 1 litre of water. 1 N NaOH readily reacts with CO2 in air to form carbonates that neutralize NaOH and diminish its disinfective properties. 10 N NaOH solutions do not absorb CO2, therefore, 1N NaOH working solutions should be prepared fresh for each use either from solid NaOH pellets, or by dilution of 10 N NaOH stock solutions. Sodium hypochlorite (NaOCI solution, or bleach..): Be familiar with and observe safety guidelines for working with sodium hypochlorite. Household or industrial strength bleach is sold at different concentrations in different countries, so that a standard dilution cannot be specified. Efficacy depends upon the concentration of available chlorine and should be 20 000 ppm available chlorine. One common commercial formulation is 5.25% bleach, for which a 1:2.5 dilution (1 part bleach plus 1.5 parts water ) yields the desired working solution. Working solutions should be prepared fresh for each use.


but i think you will get the big picture :-(





Something I submitted to GUT previously;

Subject: Re: gutjnl_el;21 Terry S. Singeltary Sr. (3 Jun 2002) "CJDs (all human TSEs) and Endoscopy Equipment"

Date: Thu, 20 Jun 2002 16:19:51 –0700

From: "Terry S. Singeltary Sr."

To: Professor Michael Farthing

Greetings again Professor Farthing and BMJ,

I was curious why my small rebuttal of the article described below was not listed in this month's journal of GUT? I had thought it was going to be published, but I do not have full text access. Will it be published in the future? Regardless, I thought would pass on a more lengthy rebuttal of mine on this topic, vCJD vs sCJDs and endoscopy equipment. I don't expect it to be published, but thought you might find it interesting, i hope you don't mind and hope to hear back from someone on the questions I posed...

Here is my short submission I speak of, lengthy one to follow below that:

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:
>>Title/position: disabled {neck injury}
>>Place of work: CJD WATCH
>>IP address:
>>Browser: Mozilla/5.0 (Windows; U; Win98; en-US; rv:0.9.4)
>>Gecko/20011019 Netscape6/6.2
>> >>Parent ID: 50/6/888
>> 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

Terry S. Singeltary Sr. >>CJD WATCH

Again, many thanks, Kindest regards,

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

[scroll down past article for my comments]
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
see full text ;


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 1-24-3

Friday, August 10, 2012

Incidents of Potential iatrogenic Creutzfeldt-Jakob disease (CJD) biannual update (July 2012)

Tuesday, June 26, 2012

Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012

type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA

Monday, August 6, 2012


BSE Final report in USA August 6, 2012

Monday, July 23, 2012

The National Prion Disease Pathology Surveillance Center July 2012

North America has NO surveillance system for iatrogenic CJD. a few mishaps of late ;

Tuesday, July 31, 2012

11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital

Thursday, August 02, 2012

CJD case in Saint John prompts letter to patients Canada CJD case in Saint John prompts letter to patients

Wednesday, May 16, 2012

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

Proposal ID: 29403


Friday, October 05, 2012

Differential Diagnosis of Jakob-Creutzfeldt Disease

Original Contribution| ONLINE FIRST

Differential Diagnosis of Jakob-Creutzfeldt Disease

Ross W. Paterson, MRCP; Charles C. Torres-Chae, MPA; Amy L. Kuo, MS, RN, GNP; Tim Ando, BA; Elizabeth A. Nguyen, BS; Katherine Wong, BS; Stephen J. DeArmond, MD, PhD; Aissa Haman, MD; Paul Garcia, MD; David Y. Johnson; Bruce L. Miller, MD; Michael D. Geschwind, MD, PhD Arch Neurol. 2012;():1-5. doi:10.1001/archneurol.2013.79. Text Size: AA A Published online September 24, 2012 ABSTRACT


Objectives To identify the misdiagnoses of patients with sporadic Jakob-Creutzfeldt disease (sCJD) during the course of their disease and determine which medical specialties saw patients with sCJD prior to the correct diagnosis being made and at what point in the disease course a correct diagnosis was made.

Design Retrospective medical record review.

Setting A specialty referral center of a tertiary academic medical center.

Participants One hundred sixty-three serial patients over a 5.5-year period who ultimately had pathologically proven sCJD. The study used the subset of 97 patients for whom we had adequate medical records.

Main Outcome Measures Other diagnoses considered in the differential diagnosis and types of medical specialties assessing patients with sCJD.

Results Ninety-seven subjects' records were used in the final analysis. The most common disease categories of misdiagnosis were neurodegenerative, autoimmune/paraneoplastic, infectious, and toxic/metabolic disorders. The most common individual misdiagnoses were viral encephalitis, paraneoplastic disorder, depression, vertigo, Alzheimer disease, stroke, unspecified dementia, central nervous system vasculitis, peripheral neuropathy, and Hashimoto encephalopathy. The physicians who most commonly made these misdiagnoses were primary care physicians and neurologists; in the 18% of patients who were diagnosed correctly at their first assessment, the diagnosis was almost always by a neurologist. The mean time from onset to diagnosis was 7.9 months, an average of two-thirds of the way through their disease course.

Conclusions Diagnosis of sCJD is quite delayed. When evaluating patients with rapidly progressive dementia with suspected neurodegenerative, autoimmune, infectious, or toxic/metabolic etiology, sCJD should also be included in the differential diagnosis, and appropriate diagnostic tests, such as diffusion brain magnetic resonance imaging, should be considered. Primary care physicians and neurologists need improved training in sCJD diagnosis.

Wednesday, June 27, 2012

First US BSE Case Since 2006 Underscores Need for Vigilance

Neurology Today 21 June 2012

PO-028: Oral transmission of L-type bovine spongiform encephalopathy (L-BSE) in primate model Microcebus murinus

Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel Verdier1 1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux Civils de Lyon; Lyon, France

An atypical form of bovine spongiform encephalopathy has been identified in cattle in Europe, North America and Japan and was designed as L-type BSE (L-BSE) due to the lower apparent molecular mass of the unglycosylated, protease-

resistant prion protein (PrPres) detected by western blot compared with classical BSE. Experimental evidences from studies in transgenic mice expressing human PrP and in primate models suggest a higher risk of transmission to humans of the L-BSE form than for classical BSE agent. However, a major unresolved issue concerns the potential transmissibility of the L-BSE agent by oral route. To address this question, we infected mouse lemurs (Microcebus murinus), a non-human primate model, with L-BSE by intracerebral or oral route.

Four adult lemurs were intracerebrally (IC) inoculated with 5mg of L-BSE infected brain homogenate of an atypical French BSE case (02-2528). Four young and four adult animals were fed with 5 mg or 50 mg of infected brain. After sacrifice, the brain tissues were biochemically and immunocytochemically investigated for PrPres.

The 4 animals IC inoculated died at 19 and 22 months postinoculation (mpi). They developed blindness, tremor, abnormal posture, incoordinated movements, balance loss. Symptoms get worse according to the disease progression, until severe ataxia. Severe spongiosis was evidenced into the thalamus, the striatum, the mesencephalon, and the brainstem, whereas into the cortex the vacuolisation was weaker. Strong deposits of PrPres were detected into the thalamus, the striatum, and the hippocampus whereas in the cerebral cortex, PrPres was prominently accumulated in plaques.

The orally inoculated animals showed similar clinical symptoms occurring between 27 and 34 mpi. Disease was characterized by progressive prostration, loss of appetite and poor appearance of the fur. Only one adult animal showed disequilibrium. PrPres was strongly accumulated only in the striatum and thalamus and weakly into the cortex. No plaques were evidenced. Two animals that were orally challenged at the age of two years are still alive and healthy 34 months after inoculation. The western blot analysis showed uniform molecular profiles, irrespective of the route or dose of infection, and included notably a PrPres form with low apparent molecular mass (~19 kDa) similar to the PrPres in the original cattle brain. However, the PrPres profile in lemurs was characterized by a higher proportion of di- and mono-glycosylated species (up to 95% of the total signal) than in the bovine L-BSE inoculum (~80%). In addition, small amounts of PrPres were detected by western blotting in the spleen of three animals (one intra-cerebrally inoculated and two fed with 5 mg of cattle brain).

Here, we demonstrate that the L-BSE agent can be transmitted by oral route from cattle to young and adult mouse lemurs. In comparison to IC inoculated animals, orally challenged lemurs were characterized by longer survival periods as expected with this route of infection.

EFSA Journal 2011 The European Response to BSE: A Success Story


EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.


see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

Wednesday, August 01, 2012

Behavioural and Psychiatric Features of the Human Prion Diseases: Experience in 368 Prospectively Studied Patients

Monday, August 06, 2012

Atypical neuropathological sCJD-MM phenotype with abundant white matter Kuru-type plaques sparing the cerebellar cortex

Monday, August 20, 2012


Tuesday, June 26, 2012

Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012

type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA

Monday, August 6, 2012

TAFS BSE in USA August 6, 2012


Saturday, May 26, 2012

Are USDA assurances on mad cow case 'gross oversimplification'?


What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”

The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”

“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.

In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said

The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.



Saturday, August 4, 2012

Final Feed Investigation Summary - California BSE Case - July 2012



Summary Report BSE 2012

Executive Summary

Saturday, August 4, 2012

Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation

Sunday, August 26, 2012

Detection of PrPSc in peripheral tissues of clinically affected cattle after oral challenge with BSE

2011 Monday, September 26, 2011

L-BSE BASE prion and atypical sporadic CJD

see the Duke, Pa, Yale, and Mexican study here, showing the misdiagnosis of CJD TSE prion disease as Alzheimers ;

Wednesday, May 16, 2012

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

Proposal ID: 29403


Monday, August 20, 2012