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From: TSS ()
Subject: Re: MELBOURNE grandmother who died this week from suspected CJD was a blood donor for 25 years
Date: October 24, 2006 at 6:58 pm PST

In Reply to: MELBOURNE grandmother who died this week from suspected CJD was a blood donor for 25 years posted by TSS on October 21, 2006 at 10:15 am:


----- Original Message -----
From: Helane Shields
To: MAD COW - TERRY SINGLETARY
Sent: Tuesday, October 24, 2006 4:11 PM
Subject: Australian CJD "expert" not telling truth about sCJD blood infectivity ? See below - CJD victims in Australia & Canada - blood transfusions


http://www.news.com.au/sundayheraldsun/story/0,21985,20622280-661,00.html

A MELBOURNE grandmother who died this week from suspected Creutzfeldt-Jakob disease was a blood donor for 25 years.

Valerie Powell, 68, died on Tuesday. Her husband Ron, 70, said his wife was a regular blood donor until a year ago.

But he said doctors had told him the type of CJD his wife had could not be transmitted by blood or blood products.

The Australian Red Cross said there had never been a reported case of classical CJD being passed from a blood donor anywhere in the world.

CJD expert Prof Colin Masters, head of the Department of Pathology at Melbourne University, said Victorians who may have received blood from Mrs Powell should not be alarmed because there was no evidence classical CJD was passed through the blood.

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

Email to Dr. Laura Manuelidis, CJD expert - Yale Medical School . . . . .

Helane Shields wrote:


Dear Dr. Manuelidis . . . . . attached is a recent article from Australia regarding a CJD victim who frequently gave blood. As you can see, the victim's doctors claim there is no risk of TSE blood transmission from sporadic CJD patients - saying the only blood risk is from nvCJD victims.

The article mentions the 3 cases of nvCJD transmission in UK from blood.

Regarding your research article below -- were you only referring to nvCJD prions in blood -- or did you find there also a risk from sporadic CJD prions in blood ?

Thank you for your advice . . . . Helane Shields, Alton, NH
----- Original Message -----
From: laura manuelidis
To: Helane Shields
Sent: Tuesday, October 24, 2006 12:10 PM
Subject: Re: to Dr. Laura Manuelidis - CJD prions in blood? Question about your research -" nv" only or also "sporadic" ?


Dear Helane,

I read the comment of Colin Masters. Contrary to his statement, we have published a substantial report of blood infectivity in sCJD infected guinea pigs (transmitted from a classical human sCJD case). This 1978 Science paper demonstrated the sCJD agent in the buffy coat (white blood cells) of blood [Viremia in experimental Creutzfeldt-Jakob disease. Manuelidis EE, Gorgacs EJ, Manuelidis L. Science. 1978 Jun 2;200(4345):1069-71. PMID: 349691], and warned of potential transfusion risks.

In this study, moreover, the amount of the sCJD infectious agent increased at late stages of disease. This increased infectivity can also be appreciated by graphing the incubation periods of the recipient animals who were inoculated with blood from CJD animals at sequential stages post infection. The incubation time gets shorter (meaning more agent) with blood samples taken at the end of the disease (I can send you a slide of this if you like). Your quotes below from our paper (Radebold et al) on our past work was therefore referring to sCJD experiments; the Radebold paper used another CJD agent that is present in Japan, but not yet found in the USA or Europe, and this also indicated transit of this other (non vCJD agent) by the bloodstream.

Additionally, although different agents may have relatively more or less infectivity in blood, spleen and lymphatics, the spleen of Guinea Pigs infected with sCJD is also infectious, and thus is similar to almost all other TSEs. The spleen a place where blood is "filtered" for infectious agents. These data were also published in 1979, and I believe Colin Masters read these papers.

We also transmitted CJD from the blood (buffy coat cells) of sCJD human patients. One of these reports was published in Lancet [Manuelidis EE, Kim JH, Mericangas JR, Manuelidis L. Transmission to animals of Creutzfeldt-Jakob disease from human blood. Lancet. 1985 Oct 19;2(8460):896-7. PMID: 2864612] We also transmitted the agent from the blood cells of a patient diagnosed with AD, but on subsequent autopsy found to have CJD. I can supply you with some of that published data as well.

We are not the only lab to have transmitted from the blood of human CJD patients prior to the vCJD outbreak. Tateishi transmitted CJD from the a human case in Japan (Lancet publication of 1980s as well)...All of this data was generated BEFORE vCJD was found.

Finally, there are by now many confirming reports of blood infectivity with other TSE strains (not just vCJD) including many scrapie strains experimentally and in natural infections. Saying infectivity of blood is limited to vCJD is therefore misleading. Similarly, some pharmaceutical companies tried to convince the FDA that human ~10 years ago that CJD blood (unlike virtually all other TSEs with confirmed blood infectivity) must be different than animal bloods, a conclusion that cannot be justified. Even a simple logical question should raise doubts about the absolute statement of Masters. How does a TSE agent reach the spleen much sooner than the adjacent nerve and spinal cord when it is inoculated in a leg muscle? The bloodstream is the obvious route, first implicated in the classic paper of Hadlow, the one that led to our original experiments that were able finally to uncover the TSE infectivity in blood.

The science above however, needs some perspective in terms of human transmission. It is important to recognize that the levels of TSE agents in blood are typically quite low, and thus the risks are not as great as with inoculation of brain, or as with repeated inoculation of a single infected blood into one recipient.

I hope this helps.

Best,
laura




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

BioMed Central
BMC Infectious Diseases
BMC Infectious Diseases 2001, 1 :20
Research article
Blood borne transit of CJD from brain to gut at early stages of
infection
Klaus Radebold, Mark Chernyak, Daniel Martin and Laura Manuelidis*
Address: Section of Neuropathology, Yale Medical School, 310 Cedar St, New Haven, CT 06510, USA
E-mail: Klaus Radebold - radebold@usa.net; Mark Chernyak - laura.manuelidis@yale.edu; Daniel Martin - laura.manuelidis@yale.edu;
Laura Manuelidis* - laura.manuelidis@yale.edu


The present studies therefore indicate these agents
spread via blood, with neural routes playing a secondary
role. Original studies in CJD revealed a hematogenous
route for agent spread after ic inoculation, and agent
could also be detected in white blood cells later in disease
[11,12].


For example, white blood cells from guinea pigs
infected with CJD repeatedly caused disease in recipients,
including the initial three weeks after ic inoculation
[11]. This early appearance of blood infectivity coincided
with the loss and/or clearance of most infectivity away
from the brain [9]. At later stages of the disease, when
the CJD agent had replicated substantially in brain, even
higher levels of agent reappeared in the blood. In contrast,
blood is claimed not to contain infectivity in a
scrapie mouse model [13].


However mice do not survive
inoculation with 20% white blood cell homogenates as
was used to detect infectivity in guinea pigs. Furthermore
others have found white blood infectivity in ham-

sters, mice and humans [14] and Houston and coworkers
recently demonstrated that BSE could be transmitted
by transfusion from a sheep that had been orally
infected with BSE [5]. The wide dissemination of agent to
many distant tissues and the perivascular PrP pathology
in the brain after ip infection also support a hematogenous
route of agent spread [6,8]. There is also a danger
of over interpreting high levels of PrP in some neurons
where the histologic picture may not be specific for infection,
as in the myenteric plexus neurons noted here.

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

Other researchers have also linked sporadic CJD to blood:

"Prion transmission in blood and urine: what are the implications

for recombinant and urinary-derived gonadotrophins?

Reichl H, Balen A, Jansen CA. : Hum Reprod. 2002 Oct;17(10):2501-8. "

and

http://www.biomedcentral.com/1471-2334/1/20

"Blood borne transit of CJD from brain to gut at early stages of infection
Klaus Radebold , Mark Chernyak , Daniel Martin and Laura Manuelidis

Brain lacks significant lymphatic drainage, and has little infectivity before 40 days, even after ic inoculation. Thus the infectious inoculum must spread to the gut by a vascular route, a direction opposite to that generally assumed. This interpretation is consistent with previous studies demonstrating white blood cell infectivity as well as perivascular PrP accumulations in CJD. "

"

Manuelidis EE, Kim JH, Mericangas JR, Manuelidis L. Transmission to animals of Creutzfeldt-Jakob disease from human blood. Lancet 1985;2:896-7.

Tateishi J. Transmission of Creutzfeldt-Jakob disease from human blood and urine into mice. Lancet 1985;2:1074. "

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

http://www.cdc.gov/ncidod/eid/vol3no2/ricketts.htm

Synopses

Is Creutzfeldt-Jakob Disease Transmitted in Blood?
Maura N. Ricketts,* Neil R. Cashman,† Elizabeth E. Stratton,* Susie ElSaadany*
*Laboratory Centre for Disease Control, Health Canada, Ottawa, Ontario, Canada; and †Montreal Neurological Institute, Montreal, Canada

"Four Australians have been reported with CJD following transfusion (49). The patients had cerebellar signs; however, no other evidence of iatrogenic cause was described (50). The source of blood transfusions was undocumented. Genetic testing results were not provided; it is uncertain if cases were of the familial type, and no other information on alternative iatrogenic sources was provided.

In Canada, an albumin recipient died of neuropathologically confirmed CJD after receiving albumin from a pool containing blood from a person who died of neuropathologically confirmed CJD (D.G. Patry, pers. comm.). Eight months separated the receipt of albumin and development of symptoms, a much shorter period by a factor of three than seen in any other putative iatrogenic case, which makes iatrogenic transmission unlikely. A complete investigation is under way. "

", , , CJD may be uniformly underdiagnosed in older age groups; because of nv-CJD there will likely be increased attention to differential diagnoses among elderly persons dying of rapidly progressing dementing illnesses. We do not suggest that all sporadic cases are due to external exposure such as blood, but rather we draw attention to an important epidemiologic characteristic of CJD that is not consistent with an entirely stochastic or age-related event.

AUSTRALIA - ANOTHER sCJD VICTIM

Sent: Saturday, October 21, 2006 3:00 PM

Subject: australia another CJD victim - blood donor -

http://www.news.com.au/sundayheraldsun/story/0,21985,20622280-661,00.html

A MELBOURNE grandmother who died this week from suspected Creutzfeldt-Jakob disease was a blood donor for 25 years.

Valerie Powell, 68, died on Tuesday. Her husband Ron, 70, said his wife was a regular blood donor until a year ago.

But he said doctors had told him the type of CJD his wife had could not be transmitted by blood or blood products.

The Australian Red Cross said there had never been a reported case of classical CJD being passed from a blood donor anywhere in the world.

CJD expert Prof Colin Masters, head of the Department of Pathology at Melbourne University, said Victorians who may have received blood from Mrs Powell should not be alarmed because there was no evidence classical CJD was passed through the blood.

But he said in the past year there had been three cases, all in Britain, of variant CJD -- more widely known as mad cow's disease -- passed from blood donors.

Mr Powell said his wife went to her GP in July because she was feeling unwell.

"He diagnosed depression and put her on medication," he said. "It didn't help. Valerie's symptoms became worse."

Mrs Powell's family was told a test of her spinal fluid showed she "probably" had sporadic CJD, which makes up 90 per cent of all classical CJD cases.

It was not known how she developed the rare, but fatal, brain disease. Only a biopsy will confirm suspicions that Mrs Powell died from CJD.

Prof Masters said there was no way of screening blood donors. About 20 Australians a year die from classical CJD.

THERE are support groups for families of victims of CJD. Contact Suzanne Solvyns 1800 052 466, Carol Wilson 1800 181 683 or Mandy Newton 1800 884 897.

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

TSS





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