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From: TSS (216-119-136-29.ipset16.wt.net)
Subject: Re: THE SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE OPEN MEETING 11th February 2003
Date: February 11, 2003 at 12:28 pm PST
In Reply to: Re: THE SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE OPEN MEETING 11th February 2003 posted by TSS on February 11, 2003 at 11:05 am:
© SEAC 2003
1
SEAC No: 77/4 OFFSPRING CULL: PAPER FOR SEAC MEETING ON 11th FEBRUARY 2003 Issue 1. The EU TSE Regulation requires all Member States “to cull the last
progeny of a female animal in which [BSE is] confirmed ……. born
within two years prior to, or after, clinical onset of the disease in its
dam”.
The same provisions regarding the culling of offspring that are in the
TSE Regulations also apply in the OIE Codea. In addition, the UK
operates a comprehensive offspring cull. This requires the
compulsory slaughter of all offspring born in the UK after 1 August
1996; the date from which the UK reinforced feed ban is considered
fully effective. This wider cull was seen as necessary to secure the
agreement of other EU Member States to the resumption of UK beef
exports, eventually agreed in September 1998, even though no risk
was apparent in offspring born more than two years before the onset
of clinical symptoms in their dams.
Previous SEAC advice
2. In 1997, SEAC considered a seven-year cohort study (1) on
maternal transmission. The study showed that offspring of clinical
BSE cases have an enhanced risk of developing BSE. The risk
difference for offspring from BSE dams was estimated at 9.6%
compared to non-BSE cases. An additional analysis of this study
concluded that maternal exposure was estimated to be most
important in animals born within 150 days of disease onset in their
dams (2).
3. A separate analysis of the dam-calf pairs from the BSE database
reported that the BSE risk was highest in offspring born after the
onset of clinical symptoms in the dam (3). For offspring born before
the onset of clinical symptoms, the risk was highest in the six
a The OIE International Animal Health Code contains standards, guidelines and
recommendations to prevent the import of infectious agents and diseases pathogenic to
animals and humans during trade in animals, animal genetic material and animal products.
This is done through detailed recommendations on sanitary measures to be used by OIE
member countries in establishing the health regulations applying to the import of animals,
animal genetic material and animal products.
© SEAC 2003
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months before onset but diminished as the interval between birth
and onset increased. No transmission was detected in offspring
born more than two years before the onset of clinical symptoms.
4. SEAC concluded that the research provided some evidence for low
level, direct maternal transmission, however they acknowledged that
the contribution of variation in genetic susceptibility to a feed-borne
infection could not be ruled out as an additional factor.
5. SEAC confirmed that the evidence on maternal transmission did not
call into question existing measures and it was satisfied that the
controls in place (SRM, and OTM supported by the then reinforced
feed ban) to protect the consumer were adequate.
6. SEAC considered the issue of an offspring cull and concluded that a
cull of offspring from BSE affected dams would have only a small
effect both on the incidence of BSE and the duration of the
epidemic. Nevertheless SEAC suggested that Government consider
the possibility of an offspring cull and it effects on the epidemic.
SEAC issued a statement on maternal transmission on 16th April
1997. This is attached at Annex A
7. Although SEAC had advised that existing consumer health
protection measures were appropriate, the Government decided to
introduce an offspring cull in support of DBES. A cull of all offspring
began on a voluntary basis in August 1998 and the BSE Offspring
Slaughter Regulations 1998, which made it compulsory, came into
effect on 4th January 1999.
Advice sought from the Committee
8. The UK continues with a comprehensive offspring cull in which all
offspring (born after August 1996) from BSE cases are culled. To
meet the EU TSE regulations, as applied in other Member States,
the UK would only have to implement an offspring cull with regard to
offspring born 2 years prior to the onset of BSE, or offspring born at
any time after the development of BSE in the dam. Offspring born
outside the two-year period would go into the food chain.
In view of this,
Does the Committee agree that this change to the existing UK
offspring cull would not result in significant additional risk to
consumers?
© SEAC 2003
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Background
Background information is provided in Annexes A-E
Annex A SEAC and Epidemiological sub-group statements
from 1997.
Annex B The progress of the BSE epidemic.
Annex C Research on maternal transmission since the
previous SEAC consideration in 1997.
Annex D The impact of the offspring cull on disease
eradication
Annex E Update on cases of BSE born after the real ban
(BARBs)
© SEAC 2003
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ANNEX A
Statement, 16th April 1997
On 29 July 1996, the Spongiform Encephalopathy Advisory
Committee (SEAC) issued a statement on maternal transmission of
BSE following its consideration of an interim report on a study
conducted by the Epidemiology Department, Central Veterinary
Laboratory, Weybridge to investigate the occurrence and incidence
of dam to calf transmission of BSE (the cohort study).
SEAC established an Epidemiology Subcommittee to consider the
final results from the cohort study. The Subcommittee was chaired
by Professor Peter Smith (London School of Hygiene and Tropical
Medicine), a member of SEAC. It included two further members of
SEAC, Dr Richard H Kimberlin (SARDAS) and Professor Will
Hueston (University of Maryland). The Subcommittee also included
Professor Roy Anderson (Oxford University), Professor Robert
Curnow (Reading University), Dr Peter Goodfellow (SmithKline
Beecham Pharmaceuticals), Professor Dr. Ir. Aalt Dijkhuizen
(Wageningen Agricultural University, the Netherlands) Professor
Nicholas Day (Medical Research Council Biostatistics Unit), Dr John
Williams (Roslin Institute), Dr Rosalind Ridley (Cambridge
University) and Mr John Wilesmith (Central Veterinary Laboratory).
The Subcommittee was assisted by Dr Sheila Gore (Medical
Research Council Biostatistics Unit), Dr Neil Ferguson (Oxford
University), Dr Christl Donnelly (Oxford University), Dr John
Woolliams (Roslin Institute), and Ms Judith Ryan (Central Veterinary
Laboratory). The Subcommittee met on four occasions, and
submitted its final report on maternal transmission of BSE to SEAC
on 11 April 1997.
At its meeting on 15 April 1997, SEAC considered and accepted in
full the report from the Epidemiology Subcommittee.
SEAC noted that the results of the cohort study were not
inconsistent with those of the case control study published in 1995
by Hoinville and others of the Epidemiology Department, CVL. That
study, which involved cases of BSE born after the ruminant feed
ban, did not identify significant evidence of maternal transmission,
but the statistical confidence interval included a risk of up to 13 per
cent (Veterinary Record (1995) 136, 312-318).
The cohort study provides no information on the mechanism of
direct maternal transmission of BSE. We recommend that further
research should be undertaken to shed light on the mechanism.
© SEAC 2003
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Some research has already been carried out into potential routes of
transmission from dam to calf, by testing the infectivity of tissues
from BSE-affected animals, including placenta, embryos, blood and
milk: no evidence of infectivity has been found. However, given that
the rate of transmission is probably low, some of these negative
results may be due to the practical difficulties of detecting low levels,
or a low prevalence, of infectivity. SEAC recognises that a low level
of transmission would make research on mechanisms difficult, and
that it would be complemented by a better understanding of the
mechanisms of scrapie transmission in sheep.
Any cull based upon the slaughter of calves born to cows in which
BSE has been confirmed will have only a small effect on the
incidence of BSE and the duration of the epidemic. Nevertheless,
Government should consider the possibilities for such a cull, and its
effects.
SEAC noted that, in its statement of 29 July 1996, it had concluded
that the evidence on maternal transmission did not call into question
existing measures to protect public health. In the light of the
Subcommittee's report, SEAC reconsidered the existing measures.
With respect to consumption of bovine products the measures
currently in place to protect the consumer are considered
appropriate. In particular, the Committee considered the possibility
of milk being a vehicle of transmission. SEAC concludes that no
evidence has been found to suggest that milk from any species
affected by transmissible spongiform encephalopathies is infectious.
This concurs with the opinion of the Scientific Veterinary Committee,
which advises the European Commission.
With respect to occupational exposure, responsibility for assessing
whether any amendments are needed to the existing Health and
Safety Executive guidance rests with the Advisory Committee on
Dangerous Pathogens.
Epidemiology subcommittee statement to SEAC on maternal
transmission of 11 April 1997
In July 1996 SEAC issued a statement on maternal transmission of
BSE following an interim analysis of data from an ongoing study
(called the "cohort study") being conducted by the Epidemiology
Department, Central Veterinary Laboratory (CVL). The study was
intended to determine whether maternal transmission occurred, and
if so, to inform policy makers with respect to animal health
implications.
© SEAC 2003
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The study involved over 300 "matched-pairs" of calves. One calf in
each pair was the offspring of a confirmed case of BSE and the
other an animal born in the same herd in the same calving season
whose dam had reached the age of 6 years without developing
clinical signs of BSE. The two groups of animals were born between
August 1987 and November 1989, and were taken from their natal
herds between July 1989 and February 1990, aged between 2 and
24 months. They were kept on one of three experimental farms until
they reached the age of 7 years or were culled at an earlier age with
BSE or another disease. All animals surviving to the age of 7 years
were then slaughtered and their brains were examined
pathologically for evidence of BSE.
The preliminary results of the study, when most but not all of the
animals had been followed to the age of 7 years, suggested that the
offspring of BSE cases had an incidence of BSE that was about
10% greater than that of control animals, with statistical confidence
limits (95%) ranging from 5-15%, the range reflecting the limited
numbers of animals that developed BSE in the study.
By November 1996 the last of the animals in the study had reached
the age of 7 years, and by January 1997 the last of their brains had
been examined. As had been anticipated, the final results were not
markedly different from those on which the interim analysis had
been based in 1996. Of the 301 offspring of BSE cases, 42 (14.0%)
developed BSE. Among the 301 offspring of the "control" dams
without BSE, 13 (4.3%) developed BSE. The difference between the
two risks was thus 9.6%, and was highly statistically significant with
a confidence interval ranging from 5.1% to 14.2%. A paper giving
the results of the study will be published shortly in the Veterinary
Record by the Epidemiology Department of CVL.
The cohort study was set up to investigate the occurrence of
maternal transmission, but interpretation of the results was
confounded by the likely exposure of some of the experimental
animals to contaminated feed. The results could be explained by
two hypotheses, acting alone or in combination, namely direct
maternal transmission of infection or inherited genetic variation in
susceptibility to BSE via contaminated feed. Although most of the
animals involved in the study had been born after the ruminant feed
ban in July 1988, feed-borne transmission is thought to have
continued beyond that date. This is consistent with the observation
that the BSE risk in both of the groups was greater among animals
born before the introduction of the feed ban than among animals
born later. However, the difference in risk between the two groups
© SEAC 2003
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was also greater in those born earlier, and this would not be
expected if direct maternal transmission was the sole route of
infection of the calves in the study. Such an effect might be apparent
if cattle vary in their susceptibility to contracting BSE from infected
feed. It is possible that the offspring of BSE cases may inherit, from
their dams, genes associated with increased susceptibility to
disease and that at least some of the difference in BSE risk between
the offspring of BSE affected and non-affected dams in the study
may be due to inherited factors, rather than because of direct
transmission of BSE from dam to calf.
The subcommittee has reviewed the evidence for variation in
genetic susceptibility to BSE in cattle. There is variation in the risk of
TSEs according to genotype in some species. For example,
polymorphisms of the PrP gene are associated with substantial
variation in susceptibility to infection with the scrapie (and in
incubation period ) in sheep and mice and with differences in risk of
CJD in humans. The subcommittee notes, however, that the limited
research so far completed has failed to identify genetic factors as a
major component in the epidemiology of BSE.
To assist the CVL Epidemiology Department in the interpretation of
the results of the cohort study, independent analyses of the data
were conducted by three additional groups with expertise in
statistical analysis (based in the Wellcome Trust Centre for the
Epidemiology of Infectious Disease, University of Oxford; the MRC
Biostatistics Unit, Cambridge; and the Department of Applied
Statistics, University of Reading). In so far as was possible, they
tried to evaluate the contributions to the risk difference between the
animals in the two groups from inherited differences in susceptibility
to disease caused by infected feed and from direct transmission of
BSE from dam to calf. In the absence of detailed information on the
genetic make up of the animals in the study, the possible genetic
contribution could only be assessed by statistical modelling.
The analyses by the three groups have been submitted for
publication later this year. These analyses reached broadly the
same conclusions. That there was a highly significant difference in
risk between the two groups of animals was clear. The findings did
not definitively establish direct maternal transmission as the sole
explanation for the difference in risk. The statistical model which
fitted the data best involved contributions from both direct maternal
transmission and inherited susceptibility. The main evidence for
direct maternal transmission is that the risk of BSE in the calf of an
affected dam was greatest for calves born close to the onset of BSE
in the dam. However, the power of the study to detect differences
© SEAC 2003
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related to the time between BSE onset and the date of birth of a calf
was limited by the design of the study which resulted in 83.4% of the
calves being born within the six months prior to onset of clinical
disease in the dam.
Further investigation was necessary of the possible variation in the
risk of BSE associated with the time between the birth of an animal
and the onset of BSE in the dam. This was undertaken mainly by
the group from the Wellcome Centre for the Epidemiology of
Infectious Diseases, University of Oxford through analyses of data
on all cases of BSE born after the ruminant feed ban, which are
recorded on the BSE database held by the Epidemiology
Department at the CVL. The findings will be submitted for
publication shortly. Evidence was found that the subsequent BSErisk
was greatest in calves born after the date of BSE onset in the
dam. For calves born before onset, the risk was lower, and
diminished as the interval between birth and onset increased, and
no risk was apparent more than two years before onset (see next
paragraph). Thus, although possibly subject to some biases, these
analyses also suggested that enhanced BSE-risk in the offspring of
BSE dams involves a low level of direct maternal transmission in the
late stages of the incubation period.
In view of the findings of the analyses that are summarised above,
the subcommittee concludes that there is some evidence for direct
maternal transmission of BSE at a low level, but some variation in
genetic susceptibility to BSE following feed-borne exposure may
occur. The risk of transmission of BSE from dam to calf is likely to
be less than 10%, and appears to be confined to animals born after
the onset of BSE in the dam or up to two years beforehand. This
level of transmission is not sufficient, by itself, to perpetuate BSE in
the cattle population and is likely to have only a minor effect on the
rate at which the incidence of BSE declines. It is inevitable that
cases infected via animal feed will continue to appear in diminishing
numbers for several years. Therefore, although the number of cases
infected maternally will be small, they may represent an increasing
proportion of the remaining cases detected.
Given the evidence that variation in genetic susceptibility may have
contributed to the results of the cohort study, and of the importance
of genetic factors in TSEs in other species, the subcommittee
considers that further research is necessary to clarify whether or not
variations in the PrP gene or other genes may be influencing the
transmission of, or susceptibility to, BSE in cattle. Research should
seek to identify polymorphisms of the PrP gene which may be
associated with BSE susceptibility, including stored samples from
© SEAC 2003
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the cohort study. There should also be a search [AVMC1] for other
genetic markers, outside the PrP gene, which may be associated
with an increased BSE risk in.
© SEAC 2003
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Annex B
The BSE Epidemic
The number of cases, month and year of birth of BSE cases is shown in
figure 1. The inset shows the numbers of BSE cases born after the
reinforced feed ban became fully effective on 1 August 1996 (BARB
cases). One set of analyses (4) has indicated that the BSE control
measures introduced in 1988, mainly the ruminant derived protein ban,
resulted in a 67% reduction in the risk of contracting the disease for
animals born in the first 12 months after the introduction of the ban in July
1988. The subsequent SBO ban of 1990 reduced the risk of the disease
(in animals born in the first 12 months after introduction) by a further 46%.
There is evidence of a further marked reduction in risk for animals born
after 31 July 1996, but this not yet quantifiable using the same method as
for the earlier control measures.
Figure 1: Progress of the BSE Epidemic
0
2000
4000
6000
8000
10000
Jan-80 Jan-82 Jan-84 Jan-86 Jan-88 Jan-90 Jan-92 Jan-94 Jan-96 Jan-98
Month of Birth
No of BSE cases
Feed ban introduced (July 1988)
Figure 1: Progress of the BSE Epidemic
0
2000
4000
6000
8000
10000
Jan-80 Jan-82 Jan-84 Jan-86 Jan-88 Jan-90 Jan-92 Jan-94 Jan-96 Jan-98
Month of Birth
No of BSE cases
Feed ban introduced (July 1988)
© SEAC 2003
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ANNEX C
Research on maternal transmission since the previous SEAC
consideration and the 1997 cohort study
A paper published by Donnelly et al in 2002 (4) based on the BSE
survey and clinical incidence data estimated maternal transmission
at 0.5% (0 - 2.8%). When the effects of the offspring cull were taken
into account, the estimate increased to 0.7% (0- 4.0%). These
estimates are substantially lower than the 9.6% estimated in the
1997 cohort study.
These analyses are based on data from Defra's BSE database,
which provides information on the relationship between cases, and
from modelling itself. The figures are derived from cumulated data
from the whole epidemic and therefore provide estimates of the
average. More specifically they have relatively large confidence
bounds, which include zero. The estimated rates do not therefore
apply to the more recently born animals, as the evidence suggests
that maternal risk has declined over time.
It has been suggested that the evidence to date support a
maternally associated risk factor rather than direct maternal
transmission per se. That is, offspring of dams that develop clinical
BSE are more susceptible to BSE infection than offspring of dams
that do not develop clinical BSE. Defra has adopted a working
hypothesis that as the feedborne risk declines so does the apparent
risk for offspring. The results of the 1997 cohort study supports this
hypothesis as it showed that the maternal risk declined in
successive cohorts born after the feed ban.
In November 1999, SEAC was asked to advise on a proposal to
investigate possible mechanisms of maternal transmission using
offspring of BSE affected cattle (that would otherwise have been
slaughtered). SEAC agreed that the offspring were valuable
animals. However, SEAC concluded that in view of the revised
predictions of the decline of the epidemic and the long-term nature
of the experiment, such a study would not yield results within a
useful time frame. As such SEAC did not consider such research as
high priority. Members agreed that although maternal transmission
would not sustain the epidemic, it was important that further studies
exploring this route of transmission were undertaken.
No further research has been commissioned on maternal
transmission to date. This is due to a combination of limited
resources and competing priorities within Government. Additionally,
© SEAC 2003
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the offspring cull has destroyed potential research animals.
However, the continued monitoring of the epidemic and associated
analyses has indicated that the rate of maternal transmission
predicted after the original cohort study (9.6%) has not occurred in
the later born cohorts. That is, the incidence in animals born after 31
July 1996 is considerably less than would have been expected if
maternal transmission of BSE was taking place from dams that did
not live long enough to develop clinical signs.
© SEAC 2003
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Annex D
Impact of the offspring cull on disease eradication
As at 13th January 2003 13,809 offspring have been culled since
August 1998. The peak of the potential contribution of the offspring
cull to the decline in the incidence of BSE would have passed by
now.
The transmission rate of 9.6% derived from the 1997 cohort study is
an estimate derived from animals born from August 1987 to
November 1989, with the majority born at the peak of exposure,
between July to December 1988. This essentially represents field
data and the results were in agreement with the dam-calf pairs
analyses conducted by Defra and previous analyses by the Imperial
Group (1996/97 and earlier work).
TSE Testing
As at 15 January 2003, 1,402 offspring aged over 30 months have
been tested for BSE. All animals tested negative.
Table: Age distribution of Offspring tested for BSE
September 2001 - 15 January 2003
Age Group Number tested in
GB
Number tested in
NI
Data pending 76 4
Under 30 months 11 335
30-35 months 162 34
3 years 325 20
4 years 252 26
5 years 138 6
6 years 12 1
Total tested 976 426
BARB cases
Data on the first 16 BARBs born in GB was presented to SEAC in
September 2002 by Professor Wilesmith (VLA). This data has
subsequently been published in the Veterinary Record
(SEAC/INF/75/24). An update for the first 27 BARBs born in GB has
© SEAC 2003
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been provided by Professor Wilesmith and is attached at Annex E.
The author suggests that the observations do not provide evidence
that any of these cases are maternally associated.
Other Data
The data and information from SSC opinions and other EU member
states do not provide support for the hypothesis that a maternally
associated factor plays a role in transmission of the disease. This
may be due to the generally low risk of exposure from feed.
© SEAC 2003
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ANNEX E
SUMMARY OF INITIAL EPIDEMIOLOGICAL FINDINGS OF 27
CASES OF BSE BORN AFTER 31 JULY 1996 IN GREAT BRITAIN
AS AT 31 DECEMBER 2002
1. The following provides a summary of the initial epidemiological
findings, from routine investigations, of the first 27 BARB cases born
in Great Britain. Complete information has so far been received for
all but two purchased cases, for which the questionnaires for the
natal (breeder) herds have not been received.
METHOD OF DETECTION
2. The method of detection is summarised in Table 1.
Table 1
METHOD NO. CASES
Clinical suspects 9
Casualty slaughter 12
Fallen stock 2
OTM survey 4
It is notable that only one third of the cases to date were detected as
clinically suspect animals. All of the cases found as a result of the
screening of casualty slaughtered animals had, however, exhibited
clinical signs associated with BSE, as had one of the two positive
cases detected in the fallen stock survey. Of the four cases detected
in the OTM survey, two animals had exhibited clinical signs of BSE,
one was an apparently healthy animal and one was a member of a
herd that was slaughtered as a result of the death of the owner.
© SEAC 2003
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DATES OF BIRTH
The distribution of the 27 cases by their month and year of birth is shown
in Table 2.
Table 2
MONTH AND YEAR OF
BIRTH
NO. CASES
August 1996 3
September 1996 2
October 1996 1
November 1996 1
December 1996 1
January 1997 2
February 1997 4
March 1997 1
April 1997 2
May 1997 1
June 1997 1
July 1997 2
September 1997 1
November 1997 1
February 1998 1
March 1998 1
July 1998 2
AGE AT ONSET OF CLINICAL SIGNS/SLAUGHTER
The age at onset of clinical signs or at slaughter ranged from 46 to 72
months, with a mean of 58 months. This remains greater than for the first
20 confirmed cases in the previous BAB cohorts and preliminary analyses
indicate that this is a statistically significant increase. The three oldest
animals (70m, 71m and 72 months of age) were detected in the OTM
survey.
HERD TYPE
Twenty-three of the 27 cases were in dairy herds and four were in
beef suckler herds. This is not remarkable in that it does not
represent a change in the incidence in the two herd types. All four
© SEAC 2003
17
of the cases occurring in the suckler herds had received commercial
concentrates in their early life.
GEOGRAPHICAL DISTRIBUTION
Seven of the cases were in purchased animals. From the time
spent in the natal herds and ultimate herds, and taking account of
the apparent i.p. distribution, it is most likely that these seven
animals were infected in their natal herds. The distribution of the 27
cases by the county in which they were most likely exposed is given
in Table 3.
Table 3
Region County No. Cases
Cumbria 1
Lancashire 1
S. Yorkshire 1
Greater Manchester 1
Northern England
Cheshire 3
Staffordshire 1
Shropshire 1
Mid and West
England
Leicestershire 1
East England Cambridgeshire 1
Oxfordshire 1
Buckinghamshire 2
South-East England
Hampshire 2
Somerset 1
Dorset 2
Devon 2
South-West England
Gloucestershire 1
Gwynedd 1
Pembrokeshire 1
Carmarthenshire 1
Wales
Powys 1
Scotland Dumfrieshire 1
This geographical distribution remains different from the major part
of the epidemic, comprised of cases born before the initial feed ban
in 1988, during which the incidence was greatest in the southern
part of England. It is also notably different from the geographical
distribution of BAB cases, which was concentrated in the eastern
region of England. The distribution of BARB cases is consistent
© SEAC 2003
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with the major risk factor being simply the number of cattle dairy
herds per county. The only apparent “cluster” of cases are the three
animals in the Buckinghamshire/Oxfordshire area.
PREVIOUS INCIDENCE OF BSE IN BARB AFFECTED HERDS
The owners of seven of the 20 natal herds, in which homebred
cases occurred, have not reported any suspect cases in their herds
previously and no confirmed cases are associated with these herds.
The other BARB-affected herds do not represent the high withinherd
incidence BSE-affected herds nor those herds with,
numerically, the greatest number of cases.
BSE STATUS OF THE DAMS
None of the dams of the cases, or the other offspring of these dams,
has developed clinical signs of BSE. The survival of the dams is
summarised in Table 4.
Table 4
Age (yr.) of Dams Alive
At Time Of Investigation
Of BARB
Survival Time (mths), Post Birth of BARB, of
Dams That Were Dead or Untraceable
6 8 11 NK <3 3-5 6-11 12-23 24-35 >36 N
No.Cases 1 2 2 1 2 2 2 7 2 2 5
* BSE 1 questionnaires for the breeders not yet received for two
purchased cases.
OTHER POSSIBLE SOURCES OF INFECTION
For one case, there was a possibility of it being accidentally fed dog
food.
© SEAC 2003
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SUMMARY
This updated analysis has not indicated any change in the basic
epidemiological picture compared to the examination of the first
sixteen BARB cases that were born in Great Britain. There is some
additional evidence of a prolonged incubation period for the BARB
cases and the geographical distribution of the cases is indicative of
a wide-scale distribution of a low risk of exposure.
J.W.W.
December 2002
© SEAC 2003
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References
(1) WILESMITH JW, WELLS GAH, RYAN JBM, GAVIER-WIDEN D,
SIMMONS MM (1997) A cohort study to examine maternally
associated risk factors for bovine spongiform encephalopathy.
Veterinary Record 141, 239-243.
(2) DONNELLY CA, GHANI AC, FERGUSON NM, WILESMITH JW,
ANDERSON RM. (1997) Analysis of the Bovine Spongiform
Encephalopathy Maternal Cohort Study: Evidence for Direct
Maternal Transmission. Applied Statistics 46, (3) 321-344.
(3) DONNELLY CA, FERGUSON NM, GHANI AC, WILESMITH JW,
and ANDERSON RM. (1997) Analysis of dam-calf pairs of BSE
cases: confirmation of a maternal risk enhancement.
Proceedings of the Royal Society of London, Series B. 264, 1647-
1656.
(4) STEVENSON MA, WILESMITH JW, RYAN, JBM, MORRIS, RS,
LOCKHART, JW, LIN, D and JACKSON, R. (2000) Temporal
aspects of the bovine spongiform encephalopathy epidemic in
Great Britain: individual animal-associated risk factors for the
disease. Veterinary Record 147, 349-354 http://www.defra.gov.uk/ TSS
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