Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle

Veterinary Research 2013, 44:123 doi:10.1186/1297-9716-44-123 Christine Fast ( Markus Keller ( Anne Balkema-Buschmann ( Bob Hills ( Martin H Groschup ( ISSN 1297-9716

Article type Short report Submission date 6 September 2013 Acceptance date 5 December 2013 Publication date 21 December 2013

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Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle

Christine Fast1 Email: Markus Keller1 Email: Anne Balkema-Buschmann1 Email: Bob Hills2 Email: Martin H Groschup1* * Corresponding author Email:

1 Friedrich-Loeffler-Institut, Institute of Novel and Emerging Infectious Diseases, Sdufer 10, 17493 Greifswald-Insel Riems, Germany

2 Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Suite 14, AL 3000A, 11 Holland Cross, Ottawa, Ontario K1A 0 K9, Canada


Recently we have described the distribution of bovine spongiform encephalopathy (BSE) infectivity and/or PrPSc in Peyers patches (PP) of the small intestine of orally BSE infected cattle. In this follow-up study additional jejunal and ileal PPs and ileocaecal-junction tissue samples from 1, 4, and 24 months post infection (mpi) were examined by mouse (Tgbov XV) bioassay. Infectivity was demonstrated in ileal PPs 4 mpi and the distribution/extent of infectivity at 24 mpi was comparable to those seen at earlier time points, revealing no indication for a decline/clearance. These data are relevant for the definition of Specified Risk Materials in the context of the TSE legislation worldwide.


In this follow-up study we have mapped the exact temporal and spatial emergence and distribution of infectivity in the PPs of the small intestine in orally BSE infected cattle. According to IHC results described previously [10,11], infectivity was first seen four months after the oral challenge. However in IHC only traces of PrPSc were seen in single follicles of the ileal PPs at four mpi [10]. This is not reflected by the results presented here, showing already moderate to high amounts of infectivity comparable to levels at later stages of disease [10]. As the detection of infectivity mostly precedes the detection of PrPSc, these results support the theory that the latent period post exposure during which no detectable infection is present might be around two or three months.

Secondly we were interested in the amount and distribution of PrPSc at 24 mpi, since the extent of this accumulation varied at earlier time points with peaks at 8 and in particular 12 mpi and lows at 16 mpi respectively [10]. However, these earlier studies did also suggest a higher amount in animals at 24 mpi suggesting an undulant pattern of about 12 months. This finding is now supported by the bioassay results, as three out of the four cattle from the 24 mpi group showed levels and distribution of infectivity comparable to the peaks seen at 12 mpi. However it has to be bear in mind that only four animals per time point were investigated here and in earlier studies and that the variations between individuals are very high [10,14]. This is reflected in the present study by variable detection rates in different animals of the 24 mpi group and might explain the differences seen in infectivity levels reported for ileal samples by several authors before [6,9-11,15]. In summary, data presented here clearly showed that infectivity is not detectable in the small intestine of animals up to four months post experimental oral exposure with an extremely high dose. Moreover, the low amounts of infectivity detectable after the peak at 12 mpi as demonstrated previously, does not imply an irreversible clearance of the infectious agent from the gut over time, but is rather a time-dependent individual fluctuation, as a higher infectivity load is seen again at 24 mpi. Hence, the data presented here are important for a risk- based SRM definition.

Competing interests

The authors declare that they have no competing interests.

Sunday, December 15, 2013


Wednesday, May 2, 2012



Saturday, June 12, 2010

PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse

Wednesday, July 28, 2010

re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010

Monday, December 02, 2013 *** A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD the human form of mad cow disease may be being spread by medical procedures http://creutzfeldt-jakob-disease.blo...-has-been.html

Wednesday, December 11, 2013

*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease


Tuesday, September 24, 2013

*** NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)

Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15


Wednesday, December 4, 2013

*** Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products; Final Rule Federal Register / Vol. 78 , No. 233 / Wednesday, December 4, 2013

TO ALL IMPORTING COUNTRIES THAT IMPORTS FROM THE USA, BE WARNED, NEW MAD COW BSE REGULATIONS USDA, AND OIE, not worth the paper the regulations were wrote on, kind of like the mad cow feed ban of August 1997, nothing but ink on paper $$$

full text ;

Friday, November 22, 2013

*** Wasting disease is threat to the entire UK deer population CWD TSE PRION DISEASE Singeltary submission


Friday, August 16, 2013

*** Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and Contaminated blood products induce a highly atypical prion disease devoid of PrPres in primates


Sunday, August 11, 2013

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010


Sunday, October 13, 2013

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012


Thursday, October 10, 2013

*** CJD REPORT 1994 increased risk for consumption of veal and venison and lamb


Thursday, October 10, 2013

CJD REPORT 1994 increased risk for consumption of veal and venison and lamb


Published March 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States

Terry S. Singeltary, retired (medically)

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

Published March 26, 2003


JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Terry S. Singeltary, Sr Bacliff, Tex

Since this article does not have an abstract, we have provided the first 150 words of the full text.

KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.


MOM DOD 12/14/97 confirm hvCJD just made a promise to mom, NEVER FORGET! and never let them forget. ...

Saturday, December 21, 2013

Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle