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Bovine spongiform
encephalopathy, Germany
|
|
|
Information received
on 25/02/2014 from Dr. Karin Schwabenbauer, Ministerial Dirigentin and Chief
Veterinary Officer , Directorate of Animal Health, Animal Welfare,
Bundesministerium für Ernährung, Landwirtschaft und Verbraucherschutz (BMELV) ,
Bonn, Germany |
|
Summary
Report
type |
Immediate notification (Final
report) |
Date of start of
the event |
30/01/2014 |
Date of
pre-confirmation of the event |
04/02/2014 |
Report
date |
25/02/2014 |
Date submitted to
OIE |
25/02/2014 |
Date event
resolved |
13/02/2014 |
Reason for
notification |
Reoccurrence of a listed
disease |
Date of previous
occurrence |
16/01/2014 |
Manifestation of
disease |
Sub-clinical
infection |
Causal
agent |
Prion (atypical BSE
H-type) |
Nature of
diagnosis |
Laboratory
(advanced) |
This event
pertains to |
the whole
country |
|
|
Outbreak
1 |
Prädikow, Prötzel,
Märkisch-Oderland, BRANDENBURG |
Date of start of the
outbreak |
30/01/2014 |
Outbreak
status |
Resolved (13/02/2014) |
Epidemiological
unit |
Farm |
Affected
animals |
Species |
Susceptible |
Cases |
Deaths |
Destroyed |
Slaughtered |
Cattle |
714 |
1 |
0 |
1 |
0 |
|
|
Summary
of outbreaks |
Total outbreaks:
1 |
Total animals
affected |
Species |
Susceptible |
Cases |
Deaths |
Destroyed |
Slaughtered |
Cattle |
714 |
1 |
0 |
1 |
0 |
|
Outbreak
statistics |
Species |
Apparent
morbidity rate |
Apparent
mortality rate |
Apparent case
fatality rate |
Proportion
susceptible animals lost* |
Cattle |
0.14% |
0.00% |
0.00% |
0.14% |
|
*Removed
from the susceptible population through death, destruction and/or
slaughter |
|
Epidemiology
Source of the
outbreak(s) or origin of infection |
|
Epidemiological
comments |
As part of the German targeted bovine
spongiform encephalopathy (BSE) surveillance system, a BSE-case classified as
atypical (H-type) was identified in a cow at slaughter. An epidemiological
investigation of the event was conducted. The summary of the event is as
follows: - The cow was slaughtered on 30.01.2014 at the age of eleven years and
four months without clinical signs. - Results from the immuno blot tests at the
NRL (Friedrich Loeffler-Institute) confirmed the animal positive for atypical
BSE of the H-type, a very rare form of the disease not associated with feeding.
- The animal´s carcass has been destroyed. The identified animal did not enter
the food channels; at no time it presented any risk to human health. - The
epidemiological investigation identified eight offspring cattle, three of which
were already slaughtered, one of which has been fallen and four of which have
been traded to another Member State. The tracing of the bovines born on the farm
from one year before until one year after the birth of the identified cow
revealed 371 bovines (177 have been already slaughtered, 63 were fallen stock, 3
have been traded within the territory of Germany, 127 have been traded to other
States, one has been culled and destroyed). The OIE does not recognize an
atypical form of BSE as a distinct entity for the purpose of its international
standards; it is not mentioned in the OIE Terrestrial Animal Health Code, which
does not distinguish between different forms of
BSE. |
|
|
Control
measures
Measures
applied |
- Movement control inside the country
- Screening
- Disinfection of infected
premises/establishment(s)
- Modified stamping out
- No vaccination
- No treatment of affected animals
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Measures to be
applied |
|
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Diagnostic test
results
Laboratory name and
type |
Species |
Test |
Test
date |
Result |
Friedrich Loeffler-Institute
(National laboratory) |
Cattle |
western blot |
04/02/2014 |
Positive |
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Future
Reporting
The event is resolved. No more
reports will be submitted. |
|
Map of outbreak
locations
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Saturday, January 18, 2014
GERMANY DETECTS A CASE OF ATYPICAL BSE Jan 17, 2014
Saturday, January 18, 2014
Bovine spongiform encephalopathy ,Germany Information received on
17/01/2014
Thursday, February 14, 2013
Unique Properties of the Classical Bovine Spongiform Encephalopathy Strain
and Its Emergence From H-Type Bovine Spongiform Encephalopathy Substantiated by
VM Transmission Studies
Saturday, December 15, 2012
*** Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Saturday, August 14, 2010
***BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama)
and VPSPr PRIONPATHY
*** (see mad cow feed in COMMERCE IN ALABAMA...TSS)
However, a BSE expert said that consumption of infected material is the
only known way that cattle get the disease under natural conditons.
***“In view of what we know about BSE after almost 20 years experience,
contaminated feed has been the source of the epidemic,” said Paul Brown, a
scientist retired from the National Institute of Neurological Diseases and
Stroke.
BSE is not caused by a microbe. It is caused by the misfolding of the
so-called “prion protein” that is a normal constituent of brain and other
tissues. If a diseased version of the protein enters the brain somehow, it can
slowly cause all the normal versions to become misfolded. It is possible the
disease could arise spontaneously, though such an event has never been recorded,
Brown said.
*** 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.”
Wednesday, February 12, 2014
*** USDA/APHIS NOTICE: Final Rule Regarding Imports and BSE Effective March
4, 2014
Thursday, February 20, 2014
Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr.
Linda Detwiler 2014
I ask Professor Kong ; Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform
Encephalopathies (BSE): Public Health Risk Assessment ''IS the h-BSE more
virulent than typical BSE as well, or the same as cBSE, or less virulent than
cBSE? just curious.....'' Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or
another, but we have found that H-BSE can infect humans. I hope we could publish
these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong, PhD Associate Professor Department of
Pathology Case Western Reserve University Cleveland, OH 44106 USA END...TSS
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
BSE-H is also transmissible in our humanized Tg mice. The possibility of
more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
please see below from PRION2013 ;
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
AD.56: The emergence of novel BSE prions by serial passages of H-type BSE
in bovinized mice
Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki
Okada, Shirou Mohri and Takashi Yokoyama National Institute of Animal Health;
Tsukuba, Japan
H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE,
and has been detected in several European countries, and North America.
Transmission studies of H-type BSE led to the emergence of the classical BSE
(C-BSE) phenotypes during passages in inbred wild type and bovinized
PrP-overexpressing transgenic mice. In this study, we conducted serial passages
of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice
(TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods
of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage
were constant (~= 220 d), no clear differences were observed in their biological
and biochemical properties. However, at the forth passage, 2 different BSE
phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the
other is longer survival times. TgBoPrP mice with longer incubation period
showed the H-type phenotype of PrPsc profile and pathology. However, those of
shorter incubation period were different phenotypes from previously existed BSE
prions (C-BSE, L-type BSE, and H-type BSE).
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
www.landesbioscience.com
please see ;
Thursday, August 15, 2013
The emergence of novel BSE prions by serial passages of H-type BSE in
bovinized mice
Sunday, September 1, 2013
*** Evaluation of the Zoonotic Potential of Transmissible Mink
Encephalopathy
We previously described the biochemical similarities between PrPres derived
from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations
suggest a link between these two uncommon prion phenotypes in a primate model
(it is to note that such a link has not been observed in other models less
relevant from the human situation as hamsters or transgenic mice overexpressing
ovine PrP [28]). We speculate that a group of related animal prion strains
(L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion
diseases in humans with a type 2 PrPres molecular signature (and more
specifically type 2B for vCJD)
snip...
Together with previous experiments performed in ovinized and bovinized
transgenic mice and hamsters [8,9] indicating similarities between TME and
L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME
outbreaks in North America and Europe during the mid-1900s.
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
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.
snip...
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 ;
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
TSS
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