Atypical H-TYPE BSE Case Confirmed in Norway
Atypical BSE Case Confirmed in Norway
29 January 2015 NORWAY – A bovine spongiform encephalopathy (BSE) case has
been diagnosed as atypical by Europe’s reference laboratory after officials were
alarmed earlier this week.The Veterinary Laboratories Agency in the UK found
that the fifteen year old animal had H-variant atypical BSE after routine
inspections in Norway found unusual prion proteins in the brain on 12 January. A
spokesperson at the Norwegian Veterinary Institute said the animal, from North
Trondelag, was the first positive case out of over 273,000 screened cattle.
Norway has monitored cattle over two years old for BSE since 2001, passing
around 20,000 cattle as BSE free each year. The animal has been destroyed. - See
more at:
Wednesday, January 21, 2015
Norway detects "probable" case of mad cow disease
American Association of Zoo Veterinarians Infectious Disease Committee
Manual 2013
BOVINE SPONGIFORM ENCEPHALOPATHY (BSE)
Little is known about atypical BSE. The origin and natural routes of
transmission, if any, have yet to be determined. Almost all cases have been in
older cattle (usually > 8 years of age) that have shown little resemblance to
the clinic-pathological picture seen in classical disease. It has been suggested
that the disease may be sporadic or be caused by a genetic mutation, but no
convincing evidence has been found to support either of these ideas. The correct
answer will probably only come by study of the future annual incidence curves of
both types of disease. Regardless of the origin of atypical BSE, the possibility
of recycling the disease in cattle and other ruminants, as well as the potential
for transmission to humans, mandate a continuation of feed and specified-risk
materials (SRM) bans, together with diagnostic testing programs for some time to
come.
snip...
Naturally occurring cases of BSE in species other than cattle have been
very limited and have been linked to exposure to contaminated feed or infected
carcasses. The majority of cases originated in the UK and like BSE in cattle,
have declined with the implementation of feed controls. None of the exotic
animals were infected in the wild.
Experts who may be consulted: Linda A. Detwiler, DVM Clinical Professor
Department of Pathobiology and Population Medicine
College of Veterinary Medicine Mississippi State University 732-580-9391
Fax: 732-741-7751 ldetwiler@belle-terre.com
Atypical BSE: Transmissibility
BASE (L) transmitted to: cattle (IC) - inc < 20 mos and oral?)
Cynomolgus macaques (IC)
Mouse lemurs (IC and oral)
wild-type mice (IC)
bovinized transgenic mice (IC and IP)
humanized transgenic mice (IC)
H cases transmitted to:
cattle – IC incubations < 20 months
bovinized transgenic mice (IC)
ovinized transgenic mice (IC)
C57BL mice (IC)
One study did not transmit to humanized PrP Met 129 mice
Evaluation of Possibility of Atypical
BSE Transmitting to Humans
Possble interpretation:
L type seems to transmit to nonhuman primates with greater ease than
classical BSE
L type also transmitted to humanized transgenic mice with higher attack
rate and shorter incubation period than classical?
H type did not transmit to Tg Hu transgenic mice
Linda Detwiller, 5/10/2011
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
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.
P.4.23 Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw
Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1
1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale,
Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research
Institute, Poland; 5Kansas State University (Previously at USDA National Animal
Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the
classical BSE strain (BSE-C) has led to over 200 cases of clinical human
infection (variant CJD). Atypical BSE cases have been discovered in three
continents since 2004; they include the L-type (also named BASE), the H-type,
and the first reported case of naturally occurring BSE with mutated bovine PRNP
(termed BSE-M). The public health risks posed by atypical BSE were argely
undefined.
Objectives: To investigate these atypical BSE types in terms of their
transmissibility and phenotypes in humanized mice.
Methods: Transgenic mice expressing human PrP were inoculated with several
classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the
transmission rate, incubation time, characteristics and distribution of PrPSc,
symptoms, and histopathology were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected
with minimal spongiosis and an average incubation time of 20-22 months, whereas
only one of the C-type BSE-inoculated mice developed prion disease after more
than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse
brains was biochemically different from bovine BASE or sCJD. PrPSc was also
detected in the spleen of 22% of BASE-infected humanized mice, but not in those
infected with sCJD. Secondary transmission of BASE in the humanized mice led to
a small reduction in incubation time. The atypical BSE-H strain is also
transmissible with distinct phenotypes in the humanized mice, but no BSE-M
transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than
classical BSE, has a lymphotropic phenotype, and displays a modest transmission
barrier in our humanized mice. 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.
14th International Congress on Infectious Diseases H-type and L-type
Atypical BSE January 2010 (special pre-congress edition)
18.173 page 189
Experimental Challenge of Cattle with H-type and L-type Atypical BSE
A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H.
Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany,
2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch,
Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy
Secretariat, Ottawa, Canada
Background: After the detection of two novel BSE forms designated H-type
and L-type atypical BSE the question of the pathogenesis and the agent
distribution of these two types in cattle was fully open. From initial studies
of the brain pathology, it was already known that the anatomical distribution of
L-type BSE differs from that of the classical type where the obex region in the
brainstem always displays the highest PrPSc concentrations. In contrast in
L-type BSE cases, the thalamus and frontal cortex regions showed the highest
levels of the pathological prion protein, while the obex region was only weakly
involved.
Methods:We performed intracranial inoculations of cattle (five and six per
group) using 10%brainstemhomogenates of the two German H- and L-type atypical
BSE isolates. The animals were inoculated under narcosis and then kept in a
free-ranging stable under appropriate biosafety conditions. At least one animal
per group was killed and sectioned in the preclinical stage and the remaining
animals were kept until they developed clinical symptoms. The animals were
examined for behavioural changes every four weeks throughout the experiment
following a protocol that had been established during earlier BSE pathogenesis
studies with classical BSE.
Results and Discussion: All animals of both groups developed clinical
symptoms and had to be euthanized within 16 months. The clinical picture
differed from that of classical BSE, as the earliest signs of illness were loss
of body weight and depression. However, the animals later developed hind limb
ataxia and hyperesthesia predominantly and the head. Analysis of brain samples
from these animals confirmed the BSE infection and the atypical Western blot
profile was maintained in all animals. Samples from these animals are now being
examined in order to be able to describe the pathoge esis and agent distribution
for these novel BSE types.
Conclusions: A pilot study using a commercially avaialble BSE rapid test
ELISA revealed an essential restriction of PrPSc to the central nervous system
for both atypical BSE forms. A much more detailed analysis for PrPSc and
infectivity is still ongoing.
14th ICID International Scientific Exchange Brochure - Final Abstract
Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America.
Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE
have all been documented in North America, along with the typical scrapie's, and
atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME.
All these TSE in different species have been rendered and fed to food producing
animals for humans and animals in North America (TSE in cats and dogs ?), and
that the trading of these TSEs via animals and products via the USA and Canada
has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only
enhances and helps the spreading of human TSE from the continued belief of the
UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to
continue to validate this old myth, will only spread this TSE agent through a
multitude of potential routes and sources i.e. consumption, medical i.e.,
surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics
etc.
Conclusion: I would like to submit a review of past CJD surveillance in the
USA, and the urgent need to make all human TSE in the USA a reportable disease,
in every state, of every age group, and to make this mandatory immediately
without further delay. The ramifications of not doing so will only allow this
agent to spread further in the medical, dental, surgical arena's. Restricting
the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD
knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante,
Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis,
Marsh, et al and many more, that the world of TSE Transmissible Spongiform
Encephalopathy is far from an exact science, but there is enough proven science
to date that this myth should be put to rest once and for all, and that we move
forward with a new classification for human and animal TSE that would properly
identify the infected species, the source species, and then the route.
snip... see more breaches in the BSE aka mad cow Triple Firewall, that
never was here ;
Friday, January 23, 2015
*** Replacement of soybean meal in compound feed by European protein
sources and relaxing the mad cow ban $
Comment from Terry Singeltary Sr. This is a Comment on the Animal and Plant
Health Inspection Service (APHIS) Notice: Agency Information Collection
Activities; Proposals, Submissions, and Approvals: Bovine Spongiform
Encephalopathy; Importation of Animals and Animal Products
For related information, Open Docket Folder Docket folder icon
--------------------------------------------------------------------------------
Show agency attachment(s) AttachmentsView All (0) Empty
--------------------------------------------------------------------------------
Comment View document:Docket No. APHIS-2014-0107 Bovine Spongiform
Encephalopathy; Importation of Animals and Animal Products Singeltary Submission
;
I believe that there is more risk to the world from Transmissible
Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from
the United States and all of North America, than there is risk coming to the USA
and North America, from other Countries. I am NOT saying I dont think there is
any risk for the BSE type TSE prion coming from other Countries, I am just
saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present
mad cow risk factors in North America like they are not here?
North America has more strains of TSE prion disease, in more species
(excluding zoo animals in the early BSE days, and excluding the Feline TSE and
or Canine TSE, because they dont look, and yes, there has been documented
evidence and scientific studies, and DEFRA Hound study, that shows the canine
spongiform encephalopathy is very possible, if it has not already happened, just
not documented), then any other Country in the world. Mink TME, Deer Elk cervid
CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type
BSE cattle, atyical HG type BSE cow (the only cow documented in the world to
date with this strain), typical sheep goat Scrapie (multiple strains), and the
atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical
Scrapie has spread from coast to coast. sporadic CJD on the rise, with different
strains mounting, victims becoming younger, with the latest nvCJD human mad cow
case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL
CDC.
typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al),
and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical
Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid
populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk
assessments for each country, and then made BSE confirmed countries legal to
trade mad cow disease, which was all brought forth AFTER that fateful day
December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats
the day it all started. once the BSE MRR policy was shoved down every countries
throat by USDA inc and the OIE, then the legal trading of Scrapie was validated
to be a legal trading commodity, also shoved through by the USDA inc and the
OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion
disease typical and atypical strains, and the BSE TSE Prion aka mad cow type
disease was thus made a legal trading commodity, like it or not. its all about
money now folks, trade, to hell with human health with a slow incubating
disease, that is 100% fatal once clinical, and forget the fact of exposure,
sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion
disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its
all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the
infamous VPSPr. ...problem solved $$$
the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing
but ink on paper.
for this very reason I believe the BSE MRR policy is a total failure, and
that this policy should be immediately withdrawn, and set back in place the BSE
GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all
TSE PRION disease in all species of animals, and that the BSE GBR risk
assessments be made stronger than before.
lets start with the recent notice that beef from Ireland will be coming to
America.
Ireland confirmed around 1655 cases of mad cow disease. with the highest
year confirming about 333 cases in 2002, with numbers of BSE confirmed cases
dropping from that point on, to a documentation of 1 confirmed case in 2013, to
date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad
cow feed ban, and the enforcement of that ban, has drastically reduced the
number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the
USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in
2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD
COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in
my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow
disease in the USA, we still have no clue as to the true number of cases of BSE
mad cow disease in the USA or North America as a whole. ...just saying.
Number of reported cases of bovine spongiform encephalopathy (BSE) in
farmed cattle worldwide* (excluding the United Kingdom)
Country/Year
snip...please see attached pdf file, with references of breaches in the USA
triple BSE mad cow firewalls, and recent science on the TSE prion disease.
...TSS No documents available. AttachmentsView All (1) Empty Docket No.
APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and
Animal Products Singeltary Submission View Attachment:
Sunday, January 11, 2015
Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of
Animals and Animal Products Singeltary Submission
Friday, January 23, 2015
*** Replacement of soybean meal in compound feed by European protein
sources and relaxing the mad cow ban $
Saturday, January 24, 2015
*** Bovine Spongiform Encephalopathy: Atypical Pros and Cons
Monday, December 1, 2014
Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review
December 1, 2014
Thursday, January 29, 2015
Identification of H-type BSE in Portugal
TSS
posted by Terry S. Singeltary Sr. at
9:07 AM
0 Comments:
Post a Comment
Subscribe to Post Comments [Atom]
<< Home