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Solvent extraction as an adjunct to rendering: The effect on BSE and scrapie

agents of hot solvents followed by dry heat and steam

Article  in  The Veterinary record · August 1998

DOI: 10.1136/vr.143.1.6 · Source: PubMed

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6 The Veterinary Record, July 4, 1998
Papers and Articles
Solvent extraction as an adjunct to rendering: the effect on
BSE and scrapie agents of hot solvents followed
by dry heat and steam
D. M. Taylor, K. Femie, I. McConnell, C. E. Ferguson, P. J. Steele
Veterinary Record (1998) 143, 6-9
The study was designed to determine the effect on bovine
spongiform encephalopathy (BSE) and scrapie agents of the
solvent extraction processes used in the past by British ren-
derers. The raw material was mouse spleen infected with
either the 22A strain of scrapie agent or the 301V strain of BSE
agent. Samples were exposed to hexane, heptane, petroleum
spirit or perchlorethylene at the relevant temperatures for the
appropriate times. Control samples were exposed to the same
range of temperatures for the same range of times in saline.
Other samples were exposed to the hot solvents, followed by
treatment with dry heat at 100°C for 30 minutes and steam at
100°C for 30 minutes. Further samples were exposed only to
the dry heat and steam cycles. No single complete process was
significantly more effective than any of the others, and they all
produced only slight inactivation, less than one log on average
for both strains of agent. The average degree of inactivation
produced by exposure to hot saline was generally comparable
to that produced by exposure to the hot solvents. This was also
true for the samples exposed only to dry heat and steam com-
pared with those exposed to hot solvent before treatment with
dry heat and steam, and suggests that the slight inactivation
was caused by the heat rather than by the solvents. It is con-
cluded that the solvent extraction processes used by renderers
in Britain had little capacity to inactivate BSE and scrapie
agents.
WHEN bovine spongiform encephalopathy (BsE) was first
observed in 1986, it was recognised that it belonged to a group of
unusual transmissible degenerative encephalopathies (TDE) which
includes the sheep disease, scrapie (Wells and others 1987).
Scrapie occurs in a number of countries, and is known to have
been endemic in Britain for at least 250 years. No confirmed
scrapie-like disease of cattle had ever been recorded previously;
nor did neurohistopathological investigation of archival bovine
brains reveal any evidence for the existence of such a disease
(Taylor 1995). Epidemiological studies established that there was
a link between feeding cattle with meat and bone meal and their
subsequent tendency to develop BSE (Wilesmith and others 1988).
Meat and bone meal is manufactured by the rendering industry
from animal tissues discarded by abattoirs, butchers, etcetera,
which must have been contaminated from time to time with the
D. M. Taylor, FiBMS, FIScT, CBiol, HIBiol, PhD, K. Fernie, BSc,
L. McConnell, MIAT, HNC, P. J. Steele, BSc, Neuropathogenesis Unit,
Institute for Animal Health, West Mains Road, Edinburgh EH9 3JF
C. E. Ferguson, HNC, Compton Laboratory, Institute for Animal Health,
Compton, Newbury RG20 7NN
transmissible agent that causes scrapie. It therefore seems likely
that BSE was caused initially by the transmission of the scrapie
agent to cattle via feedstuff. However, it is uncertain why this
occurred in the 1980s, given that meat and bone meal had been
fed to cattle for at least 60 years before the emergence of BSE.
Several hypotheses relating to the incidence of scrapie, the
increasing sheep population, and the changes in rendering prac-
tices in the United Kingdom have been proposed (Wilesmith and
others 1988, Taylor 1993). Perhaps the most persuasive argument
was based upon the observation that in Britain during the late
1970s and early 1980s there had been a large scale abandonment
of the solvent extraction process used as an adjunct to rendering.
Given that the average incubation period of BSE is around five
years, and that the disease was first observed in the mid 1980s, it
was considered that the emergence of the disease might have been
associated with the discontinuation of the use of solvent extraction
by the rendering industry. In 1975, approximately 65 per cent of
the meat and bone meal manufactured in Britain had been subject-
ed to solvent extraction, but by 1982 the proportion had dropped
to 10 per cent (Wilesmith and others 1991).
Rendering procedures are essentially cooking processes that
melt the fat in animal tissues and allow it to be drawn off as tallow
for commercial distribution. The remaining solids (greaves) are
then usually pulverised to produce meat and bone meal for incor-
poration into animal feed as a protein supplement. Until the late
1970s it was a common practice in Britain to subject greaves to
solvent extraction processes before producing meat and bone
meal. This increased the yield of tallow, and resulted in low-fat
meat and bone meal which at one time attracted premium prices.
It was considered that the application of solvent extraction to
already rendered tissues might have provided sufficient additional
inactivation of BSE or scrapie infectivity to prevent these agents
being present in meat and bone meal at levels that would consti-
tute an effective oral dose for cattle (Wilesmith and others 1988).
It is known that TDE agents are much more resistant to inactivation
than conventional microorganisms (Kimberlin and others 1983,
Brown and others 1986, Taylor and others 1994), and that organic
solvents do not generally have any significant inactivating activity
on scrapie-like agents in crude tissue preparations (Taylor 1992).
However, nothing was known about the inactivating potential of
the solvent extraction processes used by the rendering industry on
TDE agents (Taylor 1989), processes which had involved the expo-
sure of greaves to hot solvents such as benzene, hexane, heptane,
perchlorethylene, petroleum spirit, or trichlorethylene, usually fol-
lowed by exposure to dry heat and/or steam heat at 100°C to drive
off residual solvent from the remaining greaves. It was therefore
decided to carry out a laboratory study of the effect on BSE and
scrapie agents of exposure to hot solvents, followed by exposure
to dry heat and steam. When these experiments were planned,
studies on the effect of solvent extraction in rendering plants were
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The Veterinary Record, July 4, 1998 7

already in progress in Britain. However, it was recognised that
these would be limited because there were only two sites (now
none) using solvent extraction at that time. Because the British
rendering industry had largely abandoned the use of solvent
extraction by the mid to late 1970s, it was difficult to plan the pre-
sent study because discussions with renderers showed that there
was no clear recollection of the precise technical details of some
of the processes that had been used. As a result, although the
details of the processes involving petroleum spirit and per-
chlorethylene may not be precise, those involving heptane and
hexane are based upon reliable data provided by the last two
British renderers to have used solvent extraction until the 1990s.
The laboratory scale solvent extraction procedures described in
this paper are not claimed to be precise reproductions of the
industrial processes, but are intended to provide a yardstick by
which it can be judged whether there is any substance to the
hypothesis that the abandonment of solvent extraction processes
by British renderers facilitated, or contributed to, the emergence
of BSE.
The original intention had been to use mouse brain infected
with mouse-passaged BSE and scrapie agents as the test material.
However, it was recognised that the fat content of mouse brain
would be significantly higher than that of the greaves customarily
subjected to solvent extraction. It is known that the efficiency of
heat inactivation of conventional microorganisms is impaired by
the presence of fat. The only other organ of any appreciable size
that becomes infected to a significant degree in mice infected with
TDE agents is the spleen, and this was selected as the tissue for
these studies because of its relatively low fat content. The fat con-
tent of the spleen tissue used in these studies was not measured,
and a literature search for such information relating to mouse
spleen was fruitless. However, from an analysis of a variety of
data provided by Dr R. Oberthur it was possible to arrive at the
following figures for the typical composition of mammalian
spleen: 75 per cent moisture, 7 per cent fat, 17 per cent protein
and 1 per cent ash. In contrast, greaves prepared from ovine and
porcine tissues had the following analysis before solvent extrac-
tion: 4 per cent moisture, 19-5 per cent fat, 49 per cent protein and
31.8 per cent ash (Taylor and others 1997). The large difference
between the fat contents of these two types of samples (even
allowing for some variation between mammalian species) con-
firms the appropriateness of having selected mouse spleen as the
tissue to be used in these solvent extraction studies; it could even
be argued that the infectivity in the mouse spleen samples might
be more readily inactivated than the infectivity in greaves because
of their lower fat content. In another context, the use of spleen tis-
sue was considered to represent a worst-case scenario as far as
inactivation is concerned because (unlike the spleens of cattle
with BSE) the spleens of sheep with scrapie and experimentally
induced BSE (Foster and others 1996) become infected and the
spleen is a relatively solid tissue. In contrast, the other principal
'high-risk' tissues (brain and spinal cord) are much softer, and
would tend to become smeared over the surface of other more
solid particles during rendering and solvent extraction.
For the experiments, it was decided to use the spleens of mice
infected with the 22A strain of scrapie agent which has been
shown to be more thermostable than other strains of scrapie agent
(Dickinson and Taylor 1978, Kimberlin and others 1983), and the
301V strain of BSE agent, for which no inactivation data were
available.
Materials and methods
Preparing samples of infected spleen tissue
To create the required pools of 301V- or 22A-infected spleens,
vM mice were injected intracerebrally with these agents. The mice
were culled when they developed clinical signs of terminal neuro-
logical disease, according to well defined criteria (Dickinson and
others 1968). The spleens were removed and weighed aseptically;
and average weights were 26 mg for the 301V-infected mice, and
43 mg for the 22A-infected mice. To minimise any variation in
the titre of the spleen samples used in the test procedures, the fol-
lowing strategy was adopted. The 301V-infected spleens were
halved aseptically, and each half was allocated to a different pool.
The 22A-infected spleens were divided into three approximately
equal pieces that were placed in three different pools. For the
experiments, samples of 22A- or 301V-infected spleen tissue each
containing six pieces of spleen, were prepared by randomly com-
bining portions of spleen taken from the different main pools.
These samples of pooled pieces of spleen weighed from 78 to 80
mg and were stored at -30°C until required. The standard devia-
tion in the infectivity in these samples attributable to random mix-
ing is estimated to be around 0-3 of a log.
Test procedures
The tissue samples were exposed to the following five proce-
dures.
(1) Exposure to physiological saline at 22°C for six hours (as a
titre control for the experiments overall).
(2) Exposure to a) hexane at 60°C for six hours, or b) heptane at
80°C for 10 minutes, or c) petroleum spirit at 70°C for four hours,
or d) perchlorethylene at 80°C for four hours.
(3) Exposure to physiological saline for the same ranges of times
and temperatures applied in (2).
(4) Exposure (without solvent treatment) to dry heat at 100°C for
30 minutes, followed by exposure to steam at 100°C for 30 min-
utes. The samples were then allowed to dry.
(5) Exposure to the heat processes described in (4) after treatment
with the solvents as in (2), after which the samples were allowed
to dry.
To carry out these procedures, the 78 to 80 mg subsamples of
spleen tissue from the different pools were placed in sterile,
unsealed 50 ml boiling tubes.
For procedure (1), 10 ml of sterile physiological saline was
added to the samples which were then kept at room temperature
for six hours. The saline was then drawn off and discarded, and
the samples were prepared for bioassay as described below.
For procedures (2) and (3), 10 ml of either sterile saline or the
appropriate solvent (from newly-opened containers) was added, and

TABLE 1: Numbers of affected/unaffected mice injected with dilutions of 22A- or 301 V-infected spleen samples treated with hexane
22A 301V
Dilution Titre Dilution Titre
Treatment 10-2 10-3 10-4 10-5 (IDso/g) 10-3 10-4 10-5 10-6 (IDso/g)
Saline at 220C for six hours 11/11 11/12 5/10 0/9 105.6 12/12 12/12 8/12 1/11 107.0
Saline at 600C for six hours 10/10 4/9 1/8 0/6 104.8 12/12 8/11 1/12 0/10 106.0
Hexane at 600C for six hours 10/10 6/11 0/10 0/9 104-7 12/12 9/9 5/8 0/10 1o6 8
Dry heat at 1000C for 30 minutes plus
steam at 1000C for 30 minutes 8/8 5/9 0/9 0/10 104.8 12/12 11/12 0/5 1/8 106.2
Hexane at 600C for six hours plus
dry heat at 1 000C for 30 minutes
plussteamat100Cfor30minutes 11/11 2/11 0/10 0/10 104.4 11/11 10/11 2/10 2/8 106.5
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8 The Veterinary Record, July 4, 1998

TABLE 2: Numbers of affected/unaffected mice injected with dilutions of 22A- or 301 V-infected spleen samples treated with heptane
22A 301V
Dilution Titre Dilution Titre
Treatment 10-2 10-3 10-4 105 (ID5o/g) 10-3 10-4 10-5 10-6 (ID50/g)
Saline at 22°C for six hours 11/11 11/12 5/10 0/9 105.6 12/12 12/12 8/12 1/11 107.0
Salineat80°Cfor10minutes 11/11 11/11 0/11 0/9 105.2 12/12 10/12 1/10 0/12 106.1
Heptane at 80°C for 10 minutes 11/11 10/11 2/10 0/12 105-4 12/12 12/12 8/10 0/11 107-°
Dry heat at 1 000C for 30 minutes plus
steam at 1000 Cfor 30 minutes 8/8 5/9 0/9 0/10 104.8 12/12 11/12 0/5 1/8 106.2
Heptane at 800C for 10 minutes plus
dry heat at 1 000C for 30 minutes
plussteam at 1OO0Cfor30 minutes 12/12 8/12 0/11 0/12 1049 12/12 7/11 1/11 0/10 105

the tubes were immersed in a water-bath at the appropriate tempera-
ture. The exposure period was timed from the point at which the
required temperature was achieved in the saline or solvent, as mea-
sured by thermometers immersed in the fluids. Because there was
some evaporation of the solvents, small volumes were added during
the exposure period to maintain the volume at 10 ml. The bubbling
action of the solvents kept the spleen samples constantly agitated.
At the end of the exposure period, the fluids were drawn off and
discarded, and the samples were prepared for bioassay as described
below.
For procedure (4), samples were placed in a thermostatic hot-air
oven (R. E. Pickstone) which had a forced convection fan and had
been set to run at 100°C. After the samples were placed in the
oven, the temperature dropped. The 30 minute exposure period
was timed from when the temperature returned to 100°C, as indi-
cated by the oven thermometer. The samples were then placed in
an autoclave (British Steriliser Co) set to run at 100°C under grav-
ity-displacement conditions, according to the thermocouple posi-
tioned in the drain-line. After a 10 minute heating up period, the
sample were exposed to steam at 100°C for 30 minutes. The sam-
ples were then allowed to dry before preparing them for bioassay
as described below.
In procedure (5) the samples were processed in solvents, as in
procedure (2), and then exposed to procedure (4). The samples
were then prepared for bioassay as described below.
Solvents
The solvents used were hexane SBP 65/70 (Shell Chemicals UK)
heptane (Chemitrade), Analar petroleum spirit 60-800C (BDH),
and HPLC grade perchlorethylene (Sigma-Aldrich)
Bioassay
After treatment, each of the spleen samples was homogenised
in 0-72 ml of sterile physiological saline to provide a 10-1 (w/v)
dilution. Further serial (v/v) 10-fold dilutions were prepared in
saline from these homogenates. All the dilutions were injected
intracerebrally (0-02 ml) into weanling vM mice to determine the
titres of infectivity in the samples, using the method of Karber
(1931). If carried out carefully, the reproducibility of the results
from such bioassays are extremely reliable (I. McConnell, C. E.
Ferguson and D. M. Taylor, unpublished observations). The mice
were scored for clinical neurological disease by using a standard
protocol (Dickinson and others 1968). Mice were culled either
when they developed terminal neurological disease, or 500 days
after having been injected. The brains were immersion-fixed in 10
per cent formol saline. Sections were prepared from nine areas of
the brain, stained with haematoxylin and eosin, and examined for
the presence of spongiform vacuolation by a standard procedure
(Fraser and Dickinson 1968).
Results
The titres of infectivity in the various spleen samples are shown
in Tables 1 to 4. No single process was significantly more effec-
tive than any of the others, and they all produced only slight inac-
tivation. After exposure to hot solvents, dry heat, and steam, the
average loss of titre for both 22A and 301V was only 0.8 of a log.
The average loss of titre after treatment with hot solvent (but
without exposure to dry heat and steam) was generally compara-
ble with that after exposure to hot saline. This was also true for
the samples exposed only to dry heat and steam, compared with
those exposed to hot solvent before treatment with dry heat and
steam, indicating that it was the heat, rather than the solvents, that
caused the reductions in the levels of infectivity.
Discussion
From the time of the earliest probable dietary exposure of cattle
to the agent that causes BSE the only two surviving solvent extrac-
tion facilities that existed within the UK were in Scotland, but these
ceased to operate in the early 1990s. These plants are known to
have manufactured a large proportion of the meat and bone meal
used, at least in 1988, in Scotland (Wilesmith and others 1991).
Given the low incidence of BSE in Scotland, and the fact that the
reported incidence has been increased through the known acquisi-
tion of subclinically BSE-affected cattle from England, it has been

TABLE 3: Numbers of affected/unaffected mice injected with dilutions of 22A- or 301V-infected spleen samples treated with petroleum spirit
22A 301 V
Dilution Titre Dilution Titre
Treatment 10-2 10-3 10-4 10-5 (IDso/g) 10-3 10-4 10-5 1 0-6 (IDso/g)
Salineat220Cforsixhours 11/11 11/12 5/10 0/9 105.6 12/12 12/12 8/12 1/11 107.0
Saline at 700C for four hours 7/7 7/7 0/9 0/11 105.2 10/12 3/11 1/11 0/9 <105-4
Petroleum at 700C for four hours 12/12 10/10 2/11 1/12 105.5 12/12 10/10 1/10 0/12 106.3
Dry heat at 1 000C for 30 minutes plus
steam at 1OOtCfor 30 minutes 8/8 5/9 0/9 0/10 104.8 12/12 11/12 0/5 1/8 106.2
Petroleum at 700C for 10 minutes plus
dry heat at 1 000C minutes plus
steamat100°Cfor30minutes 8/8 6/6 0/11 0/12 105.2 11/11 7/11 0/10 0/10 105.8
 Downloaded from veterinaryrecord.bmj.com on March 8, 2013 - Published by group.bmj.com

The Veterinary Record, July 4,1998 9

TABLE 4: Numbers of affectedlunaffected mice injected with dilutions of 22A- or 301V-infected spleen samples treated with perchlorethylene
22A 301 V
Dilution Titre Dilution Titre
Treatment 10-2 10- 104 10-5 (ID50/g) 10-3 10-4 10-5 10-6 (ID50/g)
Salineat220Cforsixhours 11/11 11/12 5/10 0/9 105.6 12/12 12/12 8/12 1/11 1070
Saline at 800C for four hours 11/11 7/7 0/11 0/9 105.2 12/12 7/12 1/11 0/12 105.9
Perchlorethylene at 800C for four hours 12/12 10/10 0/9 1/10 105.2 12/12 11/12 0/11 0/12 106.1
Dry heat at 1 000C for 30 minutes plus
steam at 100°C for 30 minutes 8/8 5/9 0/9 0/10 1048 12/12 11/12 0/5 1/8 1062
Perchlorethylene at 800C for four hours
plus dry heat at 1 000C for 30 minutes
plussteamat10OCfor30minutes 12/12 8/10 0/12 0/12 105.0 12/12 5/11 1/11 0/12 105-7

suggested that the solvent process may have had the capacity to
inactivate, or significantly reduce the titres of infectivity of BSE or
scrapie agents (Wilesmith and others 1988). However, the small
overall losses of titre observed after solvent processing in this
study suggest that the capacity of these procedures to reduce BSE or
the British rendering industry throughout the late 1970s may have
played a part, despite the relatively modest associated reduction in
the titres of infectivity.
Acknowledgements. The funding of this project by MAFF iS
-

scrapie infectivity was extremely limited. The data indicate that the
hot solvents per se had little effect on infectivity, and that the slight
inactivation produced was due mainly to the application of heat. In
a study in which scrapie-infected tissues were subjected to solvent
extraction with heptane in an actual rendering plant, there was no
detectable loss of infectivity (Taylor and others 1997). The process
involved the exposure of scrapie-infected greaves to heptane at
80°C for 10 minutes, followed by a 10-minute, and then a 20-
minute exposure to steam at 100°C. In this study, the spiked raw
materials had been rendered before subjecting them to solvent
extraction. It is therefore possible that the failure of the solvent
extraction process to further reduce the titre of scrapie infectivity
was due to the survival of a thermostable subpopulation of scrapie
agent after rendering. The existence of such thermostable subpopu-
lations has been demonstrated by Taylor and Femie (1996). These
results raise the possibility that the reduction in infectivity
achieved in commercial solvent extraction plants may have been
even less than those achieved in the present study.
The procedure for exposing the infected materials to hot sol-
vents was not truly representative of the industrial processes. The
principal difference was that in the industrial processes, fat-con-
taining solvent was continuously removed and replaced by redis-
tilled solvent, whereas in these experimental studies the solvent
was not recycled. Thus, it might be argued that if significant
amounts of infectivity partitioned with the fat fraction during
commercial solvent extraction, the infectivity could have been
'siphoned off in the solvent/tallow fraction, and resulted in an
appreciable reduction of infectivity in the resulting meat and bone
meal. However, no infectivity has been detectable in tallow pro-
duced under 'worst-case' conditions during experimental render-
ing studies involving BSE- and scrapie-spiked raw materials
(Taylor and others 1995, 1997). Furthermore there was no
detectable difference between the titres of scrapie agent in spiked
materials before and after exposure to a real solvent extraction
process with heptane (Taylor and others 1997). Collectively, these
studies indicate that there is no predilection for scrapie-like agents
to associate with tallow. As a result, the fact that in the present
studies the solvents were not recycled is unlikely to have affected
the results significantly. In another respect, the experimental
methods are considered to have provided rather more rigorous
conditions than the normal commercial processes. The average
diameter of the individual spleen fragments was around 4 mm,
whereas the average particle diameter of the greaves processed in
commercial solvent extraction plans was around 15 mm. In the
experimental procedure the solvents therefore had a greater poten-
tial to percolate into the fragments of spleen than would have been
the case for the fragments of greaves in the commercial process.
The data suggest that the abandonment of solvent extraction
processes by renderers in Britain was not the single key factor that
permitted the emergence of BSE. However, if, as seems likely, a
number of factors conspired to allow the disease to emerge, then
the accelerating abandonment of the solvent extraction process by
gratefully acknowledged. The authors are also grateful to Dr
D. Matthews (MAFF, Tolworth) and Mr J. W. Wilesmith (VLA,
Weybridge) for their constructive comments, and to Dr
R. Oberthur (Labor Dr Oberthur GmbH) for providing data relating
to the analysis of mammalian spleen tissue.
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Notices and divisional events
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Record for each meeting that they organise. Notices should contain
the date, time, venue and town of the meeting, details of the subject,
any speakers and sponsors and the address and telephone number of
the person from whom details can be obtained. They should be
addressed to: Kathryn Clark, Veterinary Record, 7 Mansfield Street,
London WIM OAT, fax 0171 637 0620.
 Downloaded from veterinaryrecord.bmj.com on March 8, 2013 - Published by group.bmj.com

Solvent extraction as an adjunct to

rendering: the effect on BSE and scrapie
agents of hot solvents followed by dry heat
and steam
D. M. Taylor, K. Fernie, L. McConnell, et al.

Veterinary Record 1998 143: 6-9

doi: 10.1136/vr.143.1.6

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