Wednesday, February 26, 2014


Bovine spongiform encephalopathy,
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
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
New outbreaks (1)
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
Source of the outbreak(s) or origin of infection
  • Unknown or inconclusive
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
Measures to be applied
  • No other measures
Diagnostic test results
Laboratory name and type Species Test Test date Result
Friedrich Loeffler-Institute (National laboratory) Cattle western blot 04/02/2014 Positive
Future Reporting
The event is resolved. No more reports will be submitted.
Map of outbreak locations





Saturday, January 18, 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 ;




''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.


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)




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




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 ;



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








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