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 (Christine.Fast@fli.bund.de) Markus Keller (Markus.Keller@fli.bund.de) Anne
Balkema-Buschmann (Anne.Buschmann@fli.bund.de) Bob Hills (Bob.Hills@hc-sc.gc.ca)
Martin H Groschup (martin.groschup@fli.bund.de) 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: Christine.Fast@fli.bund.de Markus Keller1 Email:
Markus.Keller@fli.bund.de Anne Balkema-Buschmann1 Email:
Anne.Buschmann@fli.bund.de Bob Hills2 Email: Bob.Hills@hc-sc.gc.ca Martin H
Groschup1* * Corresponding author Email: martin.groschup@fli.bund.de
1 Friedrich-Loeffler-Institut, Institute of Novel and Emerging Infectious
Diseases, Südufer 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
Abstract
Recently we have described the distribution of bovine spongiform
encephalopathy (BSE) infectivity and/or PrPSc in Peyer’s patches (PP) of the
small intestine of orally BSE infected cattle. In this follow-up study
additional jejunal and ileal PP’s 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 PP’s 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.
Discussion
In this follow-up study we have mapped the exact temporal and spatial
emergence and distribution of infectivity in the PP’s 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
PP’s 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
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE
Wednesday, May 2, 2012
ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND
ANIMAL HEALTH
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.blogspot.com/2013/12/a-parliamentary-inquiry-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
Letters
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.
layperson
MOM DOD 12/14/97 confirm ‘hvCJD’ just made a promise to mom, NEVER FORGET!
and never let them forget. ...
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