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From: TSS ()
Subject: Review on the epidemiology and dynamics of BSE epidemics
Date: June 6, 2008 at 7:39 am PST

Thursday, June 05, 2008
Review on the epidemiology and dynamics of BSE epidemics

Vet. Res. (2008) 39:15 www.vetres.org DOI: 10.1051/vetres:2007053 c INRA,
EDP Sciences, 2008 Review article

Review on the epidemiology and dynamics of BSE epidemics

Christian Ducrot1*, Mark Arnold2, Aline de Koeijer3, DagmarHeim4, Didier
Calavas5 1 INRA Unité d’Épidémiologie Animale, 63122
Saint-Genès-Champanelle, France 2 VLA Sutton Bonington, The Elms, College
Road, Sutton Bonington, Loughborough, LE12 5RB, England 3 Division of
Infectious Diseases, Animal Sciences Group, Wageningen, University and
Research Center, PO Box 65, 8200 AB Lelystad, The Netherlands 4 Office
vétérinaire fédéral, Schwarzenburgstrasse 155, Case Postale 3003, Bern,
Suisse 5 AFSSA Lyon, Unité Épidémiologie, 31 avenue Tony Garnier, 69364 Lyon
Cedex 07, France (Received 24 April 2007; accepted 23 October 2007)
Abstract – The paper describes how the comprehensive surveillance of bovine
spongiform encephalopathy (BSE) and studies carried out on these data has
enhanced our knowledge of the epidemiology of BSE. Around 7 000 BSE cases
were detected through the screening of about 50 million cattle with rapid
tests in Europe. It confirmed that the clinical surveillance had a poor
capacity to detect cases, and also showed the discrepancy of this passive
surveillance efficiency between regions and production types (dairy/beef).
Other risk factors for BSE were being in a dairy herd (three times more than
beef), having a young age at first calving (for dairy cattle), being
autumn-born (dairy and beef), and being in a herd with a very high milk
yield. These findings focus the risk on the feeding regimen of
calves/heifers. Several epidemiological studies across countries suggest
that the feedborne source related to meat and bone meal (MBM) is the only
substantiated route of infection — even after the feed ban —, while it is
not possible to exclude maternal transmission or milk replacers as a source
of some infections. In most European countries, the average age of the cases
is increasing over time and the prevalence decreasing, which reflects the
effectiveness of control measures. Consistent results on the trend of the
epidemic were obtained using back-calculation modelling, the R0 approach and
Age-Period-Cohort models. Furthermore, active surveillance also resulted in
the finding of atypical cases. These are distinct from previously found BSE
and classified in two different forms based on biochemical characteristics;
their prevalence is very low (36 cases up to 1st September 2007), affected
animals were old and some of them displayed clinical signs. The origin and
possibility of natural transmission is unknown.

BSE / epidemiology / modelling / review / control

Table of contents

1. Introduction
............................................................................
........................................2 2. Passive and active surveillance
for
BSE.........................................................................
........2 2.1. Passive surveillance
............................................................................
.......................2 2.2. Active surveillance
............................................................................
........................3 3. Risk factors and routes of
infection...................................................................
....................5 3.1. Risk factors
............................................................................
.................................5 3.2. Routes of infection
............................................................................
........................6 4. Control measures and evolution of the BSE
epidemics..............................................................8
4.1. Evolvement of control
measures....................................................................
...............8 4.2. Evolution of the BSE epidemic analysed from modelling
and age of cases.............................9 4.3. Evolution of the BSE
prevalence over years
.................................................................. 10 5.
Atypical BSEs and their epidemiological
meaning................................................................. 13
6.
Conclusion..................................................................
.................................................. 14 * Corresponding
author: ducrot@clermont.inra.fr Article available at http://www.vetres.org
or http://dx.doi.org/10.1051/vetres:2007053

snip...

Cases of atypical BSE have only been found in countries having implemented
large active surveillance programs. As of 1st September 2007, 36 cases (16
H, 20 L) have been described all over the world in cattle: Belgium (1 L)
[23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1
L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland
(1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23.
Another H-type case has been found in a 19 year old miniature zebu in a
zoological park in Switzerland [56]. It is noteworthy that atypical cases
have been found in countries that did not experience classical BSE so far,
like Sweden, or in which only few cases of classical BSE have been found,
like Canada or the USA.

And last but not least, similarities of PrPres between Htype BSE and human
prion diseases like CJD or GSS have been put forward [10], as well as
between L-type BSE and CJD [17]. These findings raise questions about the
origin and inter species transmission of these prion diseases that were
discovered through the BSE active surveillance.

full text 18 pages ;

http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf


EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR)
of the United States of America (USA)

Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group
on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE)
Risk (GBR) were asked by the European Commission (EC) to provide an
up-to-date scientific report on the GBR in the United States of America,
i.e. the likelihood of the presence of one or more cattle being infected
with BSE, pre-clinically as well as clinically, in USA. This scientific
report addresses the GBR of USA as assessed in 2004 based on data covering
the period 1980-2003.

The BSE agent was probably imported into USA and could have reached domestic
cattle in the middle of the eighties. These cattle imported in the mid
eighties could have been rendered in the late eighties and therefore led to
an internal challenge in the early nineties. It is possible that imported
meat and bone meal (MBM) into the USA reached domestic cattle and leads to
an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle imports
from BSE risk countries were slaughtered or died and were processed (partly)
into feed, together with some imports of MBM. This risk continued to exist,
and grew significantly in the mid 90’s when domestic cattle, infected by
imported MBM, reached processing. Given the low stability of the system, the
risk increased over the years with continued imports of cattle and MBM from
BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is likely
but not confirmed that domestic cattle are (clinically or pre-clinically)
infected with the BSE-agent. As long as there are no significant changes in
rendering or feeding, the stability remains extremely/very unstable. Thus,
the probability of cattle to be (pre-clinically or clinically) infected with
the BSE-agent persistently increases.

http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/573.html

http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/573.Par.0004.File.dat/sr03_biohaz02_usa_report_v2_en1.pdf


This study further confirms that BASE is caused by a distinct prion isolate
and discloses a novel disease phenotype in cattle, closely resembling the
phenotype previous reported in scrapie-inoculated cattle

*** and in some subtypes of inherited and sporadic Creutzfeldt-Jakob
disease.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


The Italian cases (11 and 15 years of age) originally named bovine
amyloidotic spongiform encephalopathy (BASE) were characterized by an
unglycosylated protein band with a lower molecular mass (thus named L cases)
and the predominance of the monoglycosylated band. In addition,
immunohistochemical detection of PrPres in these cases found greater
deposits in the cerebral cortex and thalamus versus the brain stem. The
French cases found a higher molecular mass associated with the
unglycosylated protein band and were called H cases (see figure 1). *** The
different "strains" are now called atypical BSE. ...

full text, skroll down to page 6 ;

http://www.usaha.org/committees/reports/2006/report-fe-2006.pdf


However, unusual or "atypical" cases of BSE have been reported in the past 3
years by investigators from several countries. Most of these animals were
greater than 8 years of age and of various breeds. There have been two
molecular types of "atypical" BSE isolates described in the literature so
far: (i) a type with a lower molecular mass of the unglycosylated isoform
also called the L-type and (ii) a type with a higher molecular mass of the
unglycosylated isoform, also called the H-type. The L-type has been found in
cattle in Italy (10), Japan (11), Germany (12) and Belgium (13). So far, the
H-type has been described in cattle from France (14), Germany (12) and the
United States (15). The U.S. cases were animals born and raised in the U.S.
(Texas, Alabama). Unusual cases of BSE are an unexpected finding since it
was previously believed that BSE disease in cattle is caused by a single
strain of infectious agent, which has been shown to be very consistent and
uniform in appearance, even after transmission to other species. The reports
of unusual phenotypes of BSE in cattle suggest that different PrPSc
phenotypes exist in cattle with BSE. There are several hypotheses which can
explain these findings: (i) there are variants of the BSE agent with
different molecular features in cattle; (ii) cattle may have been infected
by another source of an infectious prion agent (e.g. scrapie or CWD); or
(iii) a rare sporadic or genetic form of TSE disease could exist in cattle
as described for humans.

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=208195


Please remember, the last two mad cows documented in the USA i.e. Alabama
and Texas, both were of the 'atypical' BSE strain, and immediately after
that, the USDA shut down the testing from 470,000 to 40,000 in the U.S. in
2007 out of about 35 million cattle slaughtered. also, science is showing
that some of these atypical cases are more virulent to humans than the
typical UK BSE strain ;

***Atypical forms of BSE have emerged which, although rare, appear to be
more virulent than the classical BSE that causes vCJD.***

Progress Report from the National Prion Disease Pathology Surveillance
Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008

http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45


In this context, a word is in order about the US testing program. After the
discovery of the first (imported) cow in 2003, the magnitude of testing was
much increased, reaching a level of >400,000 tests in 2005 (Figure 4).
Neither of the 2 more recently indigenously infected older animals with
nonspecific clinical features would have been detected without such testing,
and neither would have been identified as atypical without confirmatory
Western blots. Despite these facts, surveillance has now been decimated to
40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and
invites the accusation that the United States will never know the true
status of its involvement with BSE.

In short, a great deal of further work will need to be done before the
phenotypic features and prevalence of atypical BSE are understood. More than
a single strain may have been present from the beginning of the epidemic,
but this possibility has been overlooked by virtue of the absence of
widespread Western blot confirmatory testing of positive screening test
results; or these new phenotypes may be found, at least in part, to result
from infections at an older age by a typical BSE agent, rather than neonatal
infections with new "strains" of BSE. Neither alternative has yet been
investigated.

http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm


CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006

The U.S. Department of Agriculture was quick to assure the public earlier
this week that the third case of mad cow disease did not pose a risk to
them, but what federal officials have not acknowledged is that this latest
case indicates the deadly disease has been circulating in U.S. herds for at
least a decade.

The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is
thought that cows usually contract the disease from contaminated feed they
consume as calves. The concern is that humans can contract a fatal,
incurable, brain-wasting illness from consuming beef products contaminated
with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the
National Institutes of Health's Laboratory for Central Nervous System
Studies and an expert on mad cow-like diseases, told United Press
International. "The question was, 'How many?' and we still can't answer
that."

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before
one year ago" because of the agency's reluctance to retest the Texas cow
that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end

http://www.upi.com/

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul
Brown is Senior Research Scientist in the Laboratory of Central Nervous
System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05,
...

http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm

PAUL BROWN COMMENT TO ME ON THIS ISSUE

Tuesday, September 12, 2006 11:10 AM

"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy
detailed critiques and recommendations to both the USDA and the Canadian
Food Agency."

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=8125


MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or
Italian L-BASE (THE LAST TWO MAD COWS IN THE USA, IN ALABAMA AND TEXAS WERE
ATYPICAL BSE, CONFIRMED!)

http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html


AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to
other species will invariably present pathology typical of a scrapie-like
disease.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf


NOT to forget the 5 cases of the NOR-98 atypical scrapie documented in the
USA in 2007, in five different states. WHICH pathologically looks like some
sub-types of sporadic CJD, of which Stanely Prusiner warns of a public
health risk ;

***The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


Here we report that both Nor98 and discordant cases, including three sheep
homozygous for the resistant PrPARR allele (A136R154R171), efficiently
transmitted the disease to transgenic mice expressing ovine PrP, and that
they shared unique biological and biochemical features upon propagation in
mice. These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.

Edited by Stanley B. Prusiner, University of California, San Francisco, CA,
and approved September 12, 2005 (received for review March 21, 2005)

http://www.pnas.org/cgi/content/abstract/0502296102v1


http://nor-98.blogspot.com/

Tuesday, June 3, 2008SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA

http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html


Journal of American Medical Association

Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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.

Terry S. Singeltary, Sr Bacliff, Tex

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

http://jama.ama-assn.org/


2 January 2000 British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117


15 November 1999 British Medical Journal vCJD in the USA * BSE in U.S.

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406


JOURNAL OF NEUROLOGY

MARCH 26, 2003

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

Terry S. Singeltary:

http://www.neurology.org/cgi/eletters/60/2/176#535


THE PATHOLOGICAL PROTEIN

Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam

CHAPTER 14 LAYING ODDS

Answering critics like Terry Singeltary, who feels that the U.S. under-
counts CJD, Schonberger conceded that the current surveillance system has
errors but stated that most of the errors will be confined to the older
population.

http://www.thepathologicalprotein.com/


***Atypical forms of BSE have emerged which, although rare, appear to be
more virulent than the classical BSE that causes vCJD.***

Progress Report from the National Prion Disease Pathology Surveillance
Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008

http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45


Communicated by: Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to the
steady increase in the "type unknown" category, which, according to their
definition, comprises cases in which vCJD could be excluded. The total of 26
cases for the current year (2007) is disturbing, possibly symptomatic of the
circulation of novel agents. Characterization of these agents should be
given a high priority. - Mod.CP]

http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html


http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963


There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf


2008

The statistical incidence of CJD cases in the United States has been revised
to reflect that there is one case per 9000 in adults age 55 and older.
Eighty-five percent of the cases are sporadic, meaning there is no known
cause at present.

http://www.cjdfoundation.org/fact.html


BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS

http://bseyoungestage.blogspot.com/


http://flounder068.vox.com/library/post/bse-youngest-age-statistics-under-30-months.html


Tuesday, May 27, 2008

FDA BSE/Ruminant Feed Inspections Firms Inventory Report Texas Legend Ranch
OAI 05/10/2008

http://madcowfeed.blogspot.com/2008/05/fda-bseruminant-feed-inspections-firms.html


Tuesday, June 3, 2008

Thursday, April 03, 2008 A prion disease of cervids: Chronic wasting disease
2008

1: Vet Res. 2008 Apr 3;39(4):41

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html


Thursday, June 05, 2008

Review on the epidemiology and dynamics of BSE epidemics

http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518




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