|
The purpose of the Seminar
was to raise awareness of African Horse Sickness and West Nile Virus
by providing an assessment of the current situation and details of how the
UK can best manage the risk and prepare for the future. With the increase
in global travel, the unpredictable effects of climate change, and the
arrival and rapid spread of Bluetongue in 2007 these diseases are no
longer considered distant threats. “These diseases, and in particular
African Horse Sickness, have the potential to devastate the UK’s $4
billion equine industry and bring all equestrian activity to a halt for
some considerable time”.
The emphasis was very much on
cooperation and communication between the equine industry, veterinary and
other experts, pharmaceutical companies, government, insurance companies
and other interested parties, with conference participants being urged to
spread the word and to play their part in ensuring that an “effective
strategy to manage an outbreak” is put in place. The current EU
legislation Council Directive 92/35 was viewed as outdated and in urgent
need of renewal. The overarching plan is to deliver an alternative disease
control strategy based on preventive vaccination not slaughter, using
state of the art diagnostics and vaccines, and incorporating the wisdom of
those with first hand experience of dealing with these diseases in the
field. There was a clear warning by Professor Guthrie of the dangers of a
slaughter on suspicion approach to disease control. The emphasis was on
being prepared before the disease arrived, so that we did not have a panic
knee-jerk response, with all the unpleasant, far reaching and unforeseen
consequences of that type of approach. It was not a question of if the
diseases arrive, but when.
The morning session was chaired
by Joe Grimwade, Chairman of the TBA Veterinary Committee, and
included presentations by Dr Richard Newton (Animal Health Trust,
Newmarket), Professor Philip Mellor (IAH), Professor Alan Guthrie
(University of Pretoria,
S. Africa), and Dr Josie Traub-Dargatz
(Colorado State University).
The afternoon session was chaired
by Brigadier Paul Jepson (Chief Executive of The Horse Trust), and
included presentations by Professor Alan Guthrie, Dr Chris Oura (IAH), Dr
Jules Minke (Merial, France), and Matthew Hartley (Defra). The seminar was
brought to a close by Kirsten Rausing, Chairman of the Thoroughbred
Breeders’ Association.
Dr Richard Newton gave an overview of the
threat to the UK of emerging equine diseases, Professor Mellor gave
details on AHS and Bluetongue with reference to epidemiology, vectors and
climate change, Professor Guthrie gave presentations on AHS and West Nile
Virus in South Africa, and Dr Josie Traub-Dargatz gave a presentation on
the WNV outbreaks in the USA. Dr Oura gave details of the role of IAH as
an AHS OIE reference laboratory, with details of diagnostics, Dr Minke
gave details on the new vaccine technologies for AHS and WNV and the
imminent trials of recombinant AHS vaccines in S Africa, and Matthew
Hartley spoke about prevention, detection and control of AHS and WNV in
the UK, and “Defra working with industry in partnership”. Brigadier Jepson
spoke about the Working Group set up by The Horse Trust to ensure
preparedness for disease, and both he and Kirsten Rausing stressed the
need for action at European level to update Council Directive
92/35.
Brigadier Jepson gave details of the African Horse Sickness
Working Group.
“The AHSWG, established in 2007 and chaired by The
Horse Trust, has brought together representatives of DEFRA, the IAH,
British Horse Racing Authority, British Horse Society, Animal Health
Trust, The Donkey Sanctuary, the insurance industry, British Equine
Veterinary Association, Cambridge University Veterinary School, veterinary
pathologists and other key interest groups from the British equestrian
industries”.
It is concerned with ensuring that the UK is as
best prepared as possible to prevent and control AHS. During the first
year it concentrated on collecting evidence from scientists and
entomologists, and now the consultation process has been widened to
included insurance industries and other. It has 3 aims:
i) to develop
an acceptable control strategy
ii) to push for the production of
effective vaccines
iii) to raise awareness of AHS, not only amongst the
horse public, but also amongst politicians and at EU level.
The Group
is thus working with two scenarios:
i) how best to cope with AHS under
the existing control strategy
ii) and acceptable future control
strategy
The message is “Invest now in order to prevent problems
later”.
Brigadier Jepson stressed the need to lobby politicians
both in the UK and Europe. He also emphasised the need to campaign for
better border controls in view of the very large number of animal
movements (some probably illegal) into the UK and through
Europe.
NB He drew attention to a forthcoming Conference in
February 2009 at Adlington Equestrian Centre (Macclesfield) on climate
change and disease, when all parts of the equine industry will be
represented.
Dr Richard Newton, Head of Equine Epidemiology and Disease
Surveillance at the Animal Health Trust,
Newmarket.
EMERGING EQUINE DISEASES: OVERVIEW OF THE
THREAT TO THE UK.
Dr Newton’s main message was that prevention
is the key. We must learn lessons from the information available now, as
there is a real threat to the UK posed by such diseases as AHS, WNV,
Equine Infectious Anaemia . We must act to prevent the diseases arriving
and becoming endemic. He cited the arrival of WNV in the USA in 1999, BTV
in Northern Europe in 2006, and EIA in Ireland in 2006. He discussed the
spread of vectors and climate change, but also highlighted the role of
global movements/trade (“allowing” the vector or host to be imported - jet
setting mosquitoes - which could result in the parachuting in of disease),
and of biological factors e.g. the EIA outbreak in
Ireland.
Regarding WNV, he spoke of the 1999 outbreak in the
USA which resulted in the disease spreading rapidly and becoming endemic.
He referred to the success of the vaccination campaign which was started
in 2001. WNV vaccine is now a core vaccine for horses in the USA. Dr Josie
Traub-Dargatz of Colorado State University elaborated on the vaccination
campaign in Nebraska and Colorado in her presentation.
Regarding
the UK, the risk of WNV is currently low for horses resident in the UK.
There is apparently no clinical WNV in UK birds (although Ernie Gould,
Oxford, disputes this). Birds act as the reservoir host with mosquitoes as
the vectors. Although horses (and humans) can get bitten and contract the
disease, they are regarded as dead end hosts i.e. they are not a reservoir
of infection (this is in contrast to AHS). The disease is not infectious
from horse to horse. However, Dr Newton emphasised that the following
points should be borne in mind:
i) role of migrating birds in
introducing/spreading disease
ii) the effect of climate change on
mosquito vector distribution.
iii) presence of susceptible native birds
in the UK
iv) “jet setting” mosquitoes – both malaria and WNV have been
spread in this way.
v) there are no equine vaccines for AHS and WNV
registered for use at present in the EU.
vi) there is currently no
equine surveillance in the UK.
His conclusion was that there is a
great need for better knowledge in the UK on emerging diseases:
i) we
must be better able to recognise and diagnose the disease i.e. “raise our
game regarding diagnosis”.
ii) we must be better prepared and use
expertise of other countries e.g. S Africa and USA.
iii) we need to
improve our basic knowledge about where the threats are, about
transmission, biological agents, endemicity, methods of control and
eradication.
iv) we have to identify what key factor is missing
in the scenario (e.g. if climate and host present, but no vector), analyse
the risk, and take any steps possible to prevent it coming into the
country in the first place or gaining a foothold (presumably preventive
vaccination, spraying aircraft for mosquitoes, strict monitoring of animal
imports and stopovers and quarantine, surveillance and
testing?)
NB. The A. H. Trust is not offering surveillance at
the present time for WNV.
The VLA has capability for diagnosis of
WNV.
WHEN OR IF AHS STRIKES: AHS OIE
REFERENCE LABORATORY ACTIVITIES AND RESPONSIBILITIES
Dr Chris Oura,
Head of Non-Vesicular Reference laboratories, Institute of Animal Health
(IAH).
OIE Reference Laboratories for AHS are located in the UK
at IAH, Pirbright, in Spain, and in South Africa. Dr Oura gave details as
follows:
Principal role of OIE laboratories (now known as World
Organisation for Animal Health):
i) to function as a centre of
expertise and standardisation of diagnostic techniques.
ii) to store
and distribute biological reference products and any other reagents used
in the diagnosis and control of AHS.
iii) to develop new procedures for
diagnosis and control of AHS
iv) to develop new procedures for
diagnosis and control of AHS
v) to gather, process, analyse and
disseminate epizootiological (stet) data relevant to AHS
vi) to place
expert consultants at the disposal of the OIE.
The labs are also
concerned with:
i) provision of scientific and technical training for
Member Countries of OIE
ii) provision of diagnostic testing facilities
to Member Countries
iii) organisation of scientific meetings on behalf
of the Office
iv) coordination of scientific and technical studies in
collaboration with other labs or organisations.
v) publication and
dissemination of information
The IAH tests all UK cases of exotic
disease, it screens imported animals for antibodies (ELISA), it tests
samples from round the world, it monitors movement of disease strains
around the world, and it works on the development of new diagnostic tests
– very rapid development in this field.
Types of tests re
AHS:
1. Group specific tests used to confirm which
disease:
Competitive ELISA
Gel based PCR (the sample is stained
using a polyacrylamide gel. The RNA of the virus is amplified by x
100,000)
Real time RT-PCR
These confirm whether AHS. Based on blood
from live animal.
2. Type specific tests used to confirm which
serotype:
Virus isolation
Serotype specific PCR
Serum
neutralisation SNT
Virus neutralisation VNT Use spleen and lymph
samples if animal dead.
New generation diagnostic tests:
Dr Oura
then described the work taking place at IAH by Peter Mertens on developing
a serotype specific PCR which amplifies the particular RNA of the
serotype, giving a serotype result within 24 hours. The test also does a
fingerprint/sequence analysis which indicates where the virus/serotype
originated. Thus these new generation tests will use real time RT-PCR
tests (instead of gel staining PCR), to identify serogroup and serotype
all in a single assay Rt(TaqManR)PCR i.e. high throughput multiplex rt
RT-PCR for AHS. Results shown on screen. (See Contingency planning table
regarding diagnostic testing).
Dr Philip Mellor, Head, Dept of
Arbovirology,IAH, Pirbright.
AFRICAN HORSE SICKNESS AND BLUETONGUE: EPIDEMIOLOGY, VECTORS
AND CLIMATE CHANGE.
Dr Mellor gave a detailed and
authoritative presentation on the background to bluetongue and African
Horse Sickness and their similarities: both viruses are arboviruses, they
both have vertebrate hosts, and the disease is transmitted between the
hosts by species of Culicoides midge. The virus obviously can only survive
if the insect vector and host are present, but temperature, for example,
is also critical: temperatures need to be sufficiently high for the virus
to multiply inside the vector. Increasing temperatures also increase the
efficiency of transmission by the insect vectors in
Europe.
Climate change
The distribution of the insect
vectors which can transmit both of these diseases has been changing with
the rise in temperatures. He attributed the sudden and massive incursion
of blue tongue northwards to climate change, explaining that the period
1976 to 2000 was a major warming period, and the 1990s were the warmest
decade on record. Also winter temperatures showed a significant rise,
meaning that some areas no longer had a vector free period. He referred to
the movement north of the “Culicoides Imicola line” by 700 km since 1998,
from Africa to the Mediterranean Basin (consequently C Imicola now
overlaps with
C Obsoletus and C pulicaris enabling the virus to
be transferred to novel vectors) and to the series of BTV incursions into
Europe which have had such disastrous consequences, particularly for the
sheep industry with over 1.5 million deaths. He referred to the BTV8 virus
“jumping” to northern Europe from Africa in 2006. Apparently the July
temperatures in Maastricht in 2006 were 6 degrees higher than had ever
been experienced before, and these higher temperatures meant more
efficient spread of disease once it had
arrived.
Research
Dr Mellor also pointed to areas
where research was urgently needed e.g. overwintering, and also the
breeding sites of Culicoides, as these are poorly defined . The midges
need moisture to breed, but the breeding sites are varied e.g. leaf litter
and dung for C. Obsoletus in the UK, wet meadows for C. Pulicaris, cattle
dung for C. Dewulfi, organic enriched but not waterlogged ground for C.
Imicola. He referred to investigations into cases where the cause of a
bluetongue outbreak was not immediately obvious e.g. the source of one
case in Cyprus was eventually traced to C. Imicola found to be breeding in
a leaking irrigation pipe in a sheep pen.
African Horse
Sickness
In 1966 there was an outbreak of AHS Type 1 in Spain. The
disease was eliminated and did not reappear for 20 years. However, in 1987
AHS Type 4 appeared. The source was traced to zebras which had been
brought into Spain from Namibia for a safari park. Zebras provide a
reservoir for AHS but do not display clinical signs. The zebras were put
out to graze in meadows where C. Imicola were breeding, and AHS broke out
and spread. In 1988 the disease reappeared in Malaga and spread into
Portugal, with the outbreak lasting until 1991. Controlled and eradicated
by vaccination. (C. Imicola apparently occurs in most of Spain and
Portugal now).
Disease spread
NB:
i) high
mobility of vector – 10 hour flight over water, and 100km travelled.
Overland spread thought to be 2 km per day. Thus disease can spread very
quickly, and over a wide area, and thus be very difficult to
control.
ii) role of wind (Saharan dust).
iii) big protection zone
needed because of facility to travel.
iv) Culicoides can transmit a
range of viruses – appearance of novel vectors.
BTV is a wake up
call. “As AHSV is transmitted by the same species of biting midge as is
BTV and under similar environmental conditions, the recent devastating
experiences with TV suggest that Europe could also be vulnerable to future
incursions form AHSV.”
Professor Alan Guthrie, Director of Equine
Research Centre, Faculty of Veterinary Science, University of Pretoria,
South Africa, and served on OIE working groups for AHS, EI and WNV. Also
AHSWG adviser.
LIVING WITH AHS: CLINICAL SIGNS, TREATMENT AND
CONTROL IN SOUTH AFRICA.
Summary
Professor Guthrie
gave an extremely stimulating and informative presentation which was
supplemented by information from papers/articles by him which were
distributed at the Conference. He supported his talk with graphic pictures
of the effects of the disease. The main thrust of his message was:
i)
it is not if but when AHS arrives.
ii) the disease has extremely
serious consequences for the equine industry with high mortality and the
potential for devastating the industry.
iii) with changes in climate
and the potential for all Culicoides to be vectors of AHS the threat is
very real.
iv) although the UK is not the number one risk area, with
blue tongue being currently of much more significance, that does not
diminish the need to act now.
v) there is always a risk the disease
could be parachuted in e.g. Spain, due to international trade/movements of
horses, and being spread by novel vectors. Competent vectors exist in most
parts of the world so one has to take care not to introduce the virus in
the first place.
vi) we should vaccinate even though there are
perceived drawbacks to current vaccines. Vaccination with live attenuated
vaccines has been successful in South Africa.
vii) there is a
very urgent need to develop the new recombinant vaccines acceptable to the
EU. Trials of canarypox platform vaccines (Merial) are going ahead within
the next 2 months in South Africa – based on cooperation/collaboration
between Jules Minke (Merial), Professor Guthrie, and Prof. James
McClachlan of UCDavis
viii) slaughter on suspicion is
counterproductive as it discourages reporting of suspected disease and
encourages illegal movement, both of which have very serious consequences
in terms of disease spread.
ix) strict movement controls, vaccination,
stabling of horses dawn to dusk, vector control, surveillance all
implemented as soon as disease suspected.
Below I have made a
summary of some of the main issues covered in the presentation. Further
detail can be found in the above-mentioned
papers.
Occurrence
AHS is endemic in eastern, central
Africa and much of southern Africa. Progress north blocked by Sahara. It
is not regarded as endemic in most of South Africa, except for the north
eastern area. Here it appears each year, usually in January. It spreads
south, optimum conditions being early heavy rains followed by warm dry
weather. Height of infection usually March and April. Dies off with first
frosts at end of April/May. NB Regionalisation of South Africa for
purposes of trade in 1997 – Cape Town province allowed to export horses to
EU.
Vector and host
i) Culicoides bolitinos and imicola
principally in S Africa, but potential for transmission of AHS by all
Culicoides.
ii) The primary cycle is between Culicoides and the
zebra/African donkey. The secondary cycle is between Culicoides and
horses. “In view of the high mortality in horses, this species is regarded
as an accidental or indicator host”.
iii) In South Africa, zebras (and
probably African donkeys as well), if in large enough numbers, can act as
a reservoir of disease e.g. Kruger National Park where there is a
continuous transmission cycle between midge and zebra.
iv) Zebras and
African donkeys largely asymptomatic or very mild fever. Horses have
severe symptoms with high fatalities, usually 70-95% depending on form of
disease (see below). Mules less susceptible with fatalities of
50-70%
v) Horses are not carriers of the disease –viraemia for only 28
days in horses.
vi) Biting flies, as opposed to midges, may play
a small role in transmission – this is not thought to be significant for a
variety of factors.
vii) Dogs can contract the highly fatal form of AHS
if they have fed on carcase of animal that died of AHS. However,
Culicoides do not readily feed on dogs, so dogs are not associated with
spread or maintenance of AHSV.
Serotypes
There are
9 serotypes in tropical Africa, with 3, 4 and 9 occurring outside
Africa.
All can be found in South
Africa.
Diagnosis
NB Differential diagnosis as clinical
signs of cardiac form of AHS similar to equine encephalosis.
OIE listed
disease so suspected cases must have laboratory confirmation.
Use
blood samples during febrile stage, or specimens of lungs, spleen and
lymph nodes at necropsy.
Forms of disease
Dunkop or
pulmonary form: peracute form with 95% mortality, incubation period of 3
to 4 days, followed by high fever and very rapid progressive respiratory
failure due to severe oedema of the lungs and hydrothorax. Death occurs
usually within 30 minutes to a few hours of first signs of respiratory
problems.
Dikkop or cardiac form: 50%+ mortality, incubation of 5
to 7 days, followed by fever for 3 to 4 days. Death within 4 to 8 days of
onset of fever. Oedamatous swellings of the head (swelling in supraorbital
fossae characteristic) and neck, and tongue sometimes swollen and
cyanotic. Severe lesions in the heart. “Severe hydropericardium is almost
invariably present”. Lesions in digestive tract are more severe than in
Dunkop form.
Mixed form: most common form of AHS but rarely
diagnosed clinically – found on pm.
Two forms: i) mild pulmonary
distress followed by oedematous swellings, then cardiac
failure.
ii) initial “subclinical cardiac form suddenly followed
by marked respiratory distress and other signs typical of the pulmonary
form. Death usually occurs 3 to 6 days after the onset of the febrile
reaction”.
Horsesickness fever: usually just a mild fever. Other
clinical signs rare. Usually in donkeys and zebra or partially immune
horses that succumb to infection.
Treatment
No specific
treatment, just supportive treatment, nursing and rest. Slightest exertion
may cause death. Light work can only be resumed at least 4 weeks after
recovery.
Control
Prophylactic vaccination in South
Africa.
Three courses advocated:
i) as weanlings at 6 to
12 months and then
ii) as yearlings at 12 to 18 months and
then
iii) annual revaccination.
Usually vaccinate in
late winter or early summer (September to November) well before the peak
season for the disease (March/April).
Live polyvalent attenuated
vaccine supplied by Onderstepoort Biological Products.
Two
components given three weeks apart: Bottle 1 - serotypes
1,3,4
Bottle 2 – serotypes 2,6, 7, 8
Cross protection is
afforded by 6 against 9, and by 8 against 5.
Control of
outbreaks
Define Infected Area and apply strict controls swiftly:
no movement in or out of horses, stabling of horses dusk to dawn, vector
control, rectal temperatures of horses taken twice daily, animals with
fever may be killed (welfare) or “housed in insect-free stables to prevent
spread of the disease”, vaccination of all susceptible animals (S Africa
vaccinates with modified live vaccine even in the face of an outbreak –
probably not acceptable to Europe). Movement restrictions plus vaccination
in the Protection and Surveillance zones, and vector insect control. No
euthanasia of suspected AHS (unless welfare grounds). This policy
encourages reporting and reduces the urge to move animals illegally. S
Africa now has 20 to 40% overreporting of the disease as a result of this
approach. The crucial benefits of this approach are that it stops the
movement of animals and encourages cooperation in effecting the disease
control policy.
For more detail see “African Horse sickness” by J
A W Coetzer and AJ Guthrie, Page 1231 onwards, Volume 2 Infectious
Diseases of Livestock edited J Coetzer and R C Tustin,
OUP.
Outbreaks outside Africa e.g.
1950s-60s Middle East
and South West Asia – had huge effect on disadvantaged
communities.
1987-91 European outbreaks. Costs in excess of £30
million. Virus overwintered. On
June 1, 1987 shipment of zebras
left Namibia, arrived in Europe on 16 June, and in Spain on 18 June.
Destination a safari park. On 14 July first deaths occurred of horses
adjacent to the safari park. Disease not diagnosed until 14 September –
thus awareness paramount. Vaccination used in Europe including
Onderstepoort Biological Products Combination
Bottle 1 (modified
live vaccine), and Equipest (Merial) inactivated monovalent vaccine for
strain 4 (no longer commercially available).
Types of
vaccine:
Live Vaccines
Advs:
Very effective
Simple
production
Stable for years. Major impact in endemic
areas.
Disadvantages:
Variable attenuation – some
reaction and even death.
Variable immune response
Vector
transmission – fears that in these polyvalent vaccines insect vector can
pick up other strains in the vaccines and transmit them.
Reassortment
possible.
Possible maternal antibody interference by vaccine in foals
born to immune dams, so vaccination not recommended until foals 6 months
old. However, levels of antibodies in foals depend on immunity of dam, and
with foals which only acquire low levels of antibody they could be
vulnerable when not vaccinated or only vaccinated once (it is recommended
that horses should be vaccinated twice – as weanlings (6 to 12 months),
and then as yearlings (12 to 18 months) and then
yearly.
Inactivated
vaccines
Advs:
Efficient
Safe
No
transmission
Disadvantages:
Complex to produce and
store
Monovalent – one serotype
Slowish response
Have to balance
inactivated/immunogenicity
Costly
No stocks
Low shelf
life
Less useful in endemic areas because of the above
factors.
Recombinant vaccines (See Jules Minke, Merial notes
also)
There is an urgent need to develop recombinant vaccines for AHSV.
At present none available commercially for AHSV but the success of these
vaccines with West Nile Virus and BTV (which is closely related to AHSV)
gives real grounds for optimism. Hence trials in South Africa over the
next two months with experimental Merial AHSV recombinant canarypox
vaccine.
There are many advantages of the recombinant
canarypox vectored vaccines listed in Merial literature
including:
i) safe and effective
ii) swift onset of
immunity
iii) non replicating thus eliminating the risk of viral
shedding and reversion to virulence
iv) provides broad protection
– generates both a humoral and cell-mediated immune response
v)
provides highly targeted immune response
vi) can be used as part
of DIVA strategy
Questions
Tim Morris of the British
Horseracing Authority asked Prof. Guthrie about quarantine and vector
protected conditions. The precautions were rigorous e.g. sealed buildings,
double door entry, forced ventilation systems with evaporative coolers
with filters. Horses were allowed to exercise from 2 hours post sunrise to
2 hours pre sunset. Insecticides applied.
Dr Jules Minke, Merial,
Lyons.
Adviser to The Horse Trust Working Party on AHS and
WNV.
NEW VACCINE TECHNOLOGIES FOR AHS
AND WNV: CURRENT STATUS AND FUTURE POSSIBILITIES
Dr Minke gave
an extremely stimulating presentation about the new vaccine technologies,
providing much optimism. Both he and Professor Guthrie, together with Dr
Josie Traub-Dargatz of Colorado State University, provided the vital
expertise and pragmatism needed in any discussion on West Nile Virus and
African Horse Sickness Virus disease control policies.
I quote from
the summary provided by Dr Minke on the new vaccine technologies. Below
that I list some of the main points from his presentation. As has been
said earlier, due to a combined effort by Dr Minke, Professor Guthrie and
Professor James McClachlan of
UC Davis, trials of a new
recombinant vaccine for AHS, using the canarypox technology, are scheduled
to take place in the next two months in South Africa. If successful this
would have enormous implications for the control and eradication of the
disease, not only in South Africa but in the EU, where up till now the
modified live vaccines currently in use for AHSV are viewed with some
concern.
Abstract from Newmarket Conference brochure
"One
of the most significant changes in the field of veterinary medicine has
been the introduction of several recombinant vaccines based on the
canarypox (ALVAC) vector platform. Its high safety profile and ability to
induce both humoral and cellular immune responses against the transgene
without the need for adjuvants have been the driving forces for the
generation of a number of commercial vaccines.
The Alvac
technology platform facilitated the rapid generation of new constructs and
as soon as the sequences of the protective genes of a micro organism are
know, synthetic genes can be made and inserted into the ALVAC genome. This
has proven to be an advantage in the case of emerging diseases such as WNV
and Nipah virus and could be a major asset for the development of safe and
efficacious vaccines for AHS. Notwithstanding the evident success of the
polyvalent modified live vaccines against AHS in endemic areas, there are
concerns about their use in epidemic situations because of their inherent
biological safety risks. Therefore, their deployment in case of an
outbreak in Europe would be viewed with concern by some veterinary
authorities. The recent successful demonstration of efficacy of a
canarypox vaccine expressing the VP2 and VP5 proteins of the related BTV
confirms the viability of an ALVAC vaccination strategy for AHS. An
additional advantage of the use of the ALVAC platform is that tests based
upon the non- structural proteins will enable differentiation between
naturally infected and vaccinated animals."
Supplementary notes from presentation
West
Nile Virus vaccine
New vaccines are now in use in the USA e.g.
Merial Recombitek (canarypox recombinant), and Intervet Chimerivax. Very
safe. Used routinely as one of the core vaccines. Can be made commercially
available under temporary licence in Europe.
African Horse
Sickness Virus vaccine
Currently use modified live attenuated
polyvalent vaccines in S Africa supplied by OBProducts. There is some
nervousness in Europe about these vaccines – the perceived possible risks
include reversion to virulence, possibility of establishing the vaccine
virus in the midges (as polyvalent, many strains besides the current
threat) and thus spreading other strains), risk in pregnant
animals.
There are no inactivated vaccines produced now. “Equipest”
produced by Merial for Spain in 1990s against AHSV 4 is no longer
commercially available. There is a need for second generation inactivated
vaccines because there are many disadvantages including:
i) at present
inactivated vaccine production requires Level 3 (high level
containment)
ii) there is limited production capacity
iii) no DIVA
capability
iv) relatively slow onset of immunity
v) short shelf
life
(For more details see Prof. Guthrie’s presentation).
New
vaccines
1. Baculovirus platform recombinant vaccine (see work by
Roy and Sutton). Effective for bluetongue so have potential be effective
against AHS.
2. Live vectored vaccines:
a) Replicative
type have been used to combat rabies in foxes by air dropping food packs
with vaccine inside. Also fowlpox.
b) Non replicative vector: canarypox
virus (ALVAC). This canarypox platform used for Equine Influenza
(Proteqflu, used in Australia 2008), West Nile Virus (Merial Recombitek,
used in 2002 onwards USA), feline influenza. ALVAC platform vaccine has
also been used to protect endangered species e.g. Santa Catalina Island
Fox
This ALVAC canarypox platform has many advantages:
i) Rapid
onset of immunity
ii) Efficacious
iii) Can be used as part of DIVA
strategy – tests can differentiate between vaccinated and non vaccinated
animals.
iv) Long lasting protection
v) No replication,
shedding, and reversion to virulence
vi) Convenience – stable longer
shelf life than inactivated vaccines
vii) Biosecurity level lower – no
need to work with highly virulent organisms (just selected
genes).
These new vaccines thus provide a platform of choice
regarding emerging diseases enabling the rapid generation of new
constructs (4 months) i.e. relatively quick production of vaccine possible
from platform.
See Veterinary Record 2005 Edlund
Toulemande.
Summary
1. New technology platforms are very
promising e.g. canarypox, baculo, and chimera (Intervet Chimerivax for WNV
and yellow fever)
2. Canarypox very promising/significant because of
rapid immunity onset and DIVA technology e.g. sheep gain good immunity
against BTV8.
3. Feasibility to be demonstrated for AHS in S Africa
trials (Guthrie, Minke, McClachlan).
Professor Josie
Traub-Dargatz, Pofessor of Equine Medicine at Colorado State University
(CSU), College of Veterinary Medicine and Biomedical Sciences, Fort
Collins, Colorado.
LIVING WITH WNV IN THE USA:
EPIDEMIOLOGY, CLINICAL ASPECTS AND CONTROL.
Prof. Dargatz has
worked at the CSU veterinary hospital since 1983, and her principal
interests are in respiratory and gastrointestinal tract infectious
diseases. However she is also closely interested in government networks
for monitoring diseases and how information is communicated. She gave an
extremely informative presentation on WNV, and the arrival and spread of
the disease in the USA. Particularly valuable was the insight gained from
the study, spearheaded by Professor Dargatz, into the outbreaks of West
Nile Equine Encephalomyelitis (WNEE), caused by WNV, in Nebraska and
Colorado. Her main conclusions are listed below. Prof. Dargatz also
provided additional supporting written material:
“Living with
West Nile Virus in the USA: epidemiology, clinical aspects and prevention
199 through 2007” by J Traub-Dargatz and T Cordes.
I have also included
supplementary notes which were taken by me at the
presentation.
Conclusions
1. Vaccination is the
single most effective means of preventing WNV disease.
2. WNV
vaccine is now considered a core vaccine for horse owners in the
USA.
3. Vets and owners play a critical role in disease detection i.e.
in detection of the unusual.
4. There must be a plan in place for
efficient communication of information to equine owners and vets e.g.
website. (During the outbreaks the veterinary hospital received a huge
number of phone calls, but was at the same time expected to be nursing
cases of WNEE at the hospital).
5. There must be an effective
laboratory infrastructure for rapid diagnosis with options for fast track
development and approval of prevention and treatment options when emerging
diseases occur.
6. It is absolutely critical to have pharmaceutical
companies poised ready to take action.
Supplementary notes
taken at the Conference.
WNV is an arbovirus now endemic in the
USA. It is the causative agent of West Nile Equine Encephalomyelitis
(WNEE). It is seasonal, occurring mainly in late summer and
autumn.
Insect vector and host
Many varieties of birds
act as the amplifying host for the virus. Mosquitoes are the insect
vector, primarily Culex. The main cycle is thus between bird and insects.
However, horses and humans can contract WNV if bitten by a mosquito, but
they are regarded as “dead end” hosts because they do not have enough
virus in their blood to act as source for mosquitoes.
NB
i) Person
to person transmission possible? – blood transfusion, pregnant mother to
foetus, breast milk of mother.
ii) Other animals besides horses may
become infected: squirrels, alligators
iii) May be bird to bird
infection without mosquito vector. This has only been demonstrated under
laboratory conditions, so it has been suggested there may be a remote
possibility in the wild e.g. perhaps birds eating birds, faecal
material
iv) Cats and dogs are susceptible – may eat dead birds –
rarely show signs of disease
Symptoms
Ataxia (unsteady), twitching
muscles, altered mentation (ranging from hyperexcitability to extreme
lethargy), weakness and unusual gait. May become recumbent (at greater
risk of death). Can be confused clinically with other neurological
diseases. Relatively high mortality rates without vaccination – 30%, but
40% in some areas. Those that recover may have residual problems, which
may be long lasting.
Diagnostic tests
1. Blood: MAC ELISA
(antibodies) on serum (no confusion with vaccination). Illustrates recent
exposure. This test available in many veterinary diagnostic
laboratories.
2. Blood: PRNT or Microtiter for antibodies. Different
from MAC ELISA. Diasadvantage: can confuse with vaccination, and also “one
gets a positive result to wild virus”.
3. Tissue tests to identify
virus in tissue. NB precaution.
History
1999 Unusually
large number of bird deaths in USA. John Andresen (New York state vet) was
the first to spot higher than usual cluster of horses with neurological
problems. WNEE can be difficult on clinical signs alone to differentiate
from other neurological diseases, so if disease is not endemic i.e. not
expected (this was the case before 1999) this can cause problems re
diagnosis. The message is preparedness, with dissemination of up to date
knowledge, plus vigilance, regarding emerging diseases.
Equine
cases
1999 25
2000 60
2001 738
2002 15, 259 (actual
figure probably 3 times this)
2003 5000
2004 1000
2007
468
Further details available at
www.aphis.usda.gov/vs/nahss/qeuin/wnv
With use of vaccination in 2002
and 3 there was a dramatic drop in horse and human cases.
2006
equine population in USA c 6 million, and 4.1 million doses of vaccine
manufactured NB. Equine industry and pharmaceutical companies responded
quickly, meaning that there was a rapid and widespread response to
challenges posed by the disease.
Vaccines
Only 3 are
licensed and commercially available for use in horses in US:
1.
Killed/inactivated vaccine with adjuvant 2001 granted a conditional
licence. In February 2002 a full licence was granted. Licensed for
prevention of viraemia (i.e virus development in blood) but not
disease.
2. 2003 January Merial Canarypox recombinant vaccine with
adjuvant in which WNV protective proteins are expressed by canarypox
vector. 2 doses are given, 3 weeks apart, then yearly after that. Licensed
for prevention of viraemia.
3. The chimera vaccine consisting of
“protective proteins of WNV spliced into an attenuated human yellow fever
virus (WN-YF)” Intervet vaccine “Chimerivax”. Single dose and annual
booster.
NB In 2005 DNA vaccine was licensed but it is not
yet commercially available.
Efficacy
Very efficacious. Vaccines
never 100%.
No safety issues to date. Some initial concern re pregnant
mare e.g. loss of pregnancy, but this was not substantiated.
Most cases
of WNV are in unvaccinated horses.
See www.aaep.org
Nebraska
and Colorado Study of WNV Outbreaks
This was spearheaded by
Professor Dargatz as it was obvious the government was not in a position
to do this as it was overwhelmed. Also cost was a factor. Veterinary
students at CSU were employed as this was less expensive, but also
beneficial to their studies. They conducted telephone surveys, and
contacted 536 individuals. There was a 92% participation rate. NB A clear
plan for collecting data is essential, so for countries not yet affected,
but at risk, it is vital that a system is already in place before disease
strikes.
Information gained/lessons learned (see also
Conclusions on first page)
Relatively high fatality 30%
Of those
with clinical signs majority were not vaccinated or only partially
vaccinated.
Fatalities more common in older horses.
If disease
at stage where animal recumbent, then more likely to be fatal.
Other
animals infected e.g. mules.
Residual problems of disease – some
animals who survive never return to normal.
Vaccination the most
effective means of preventing WNV
Better to prevent than to wait
until disease arrives.
Regional occurrence
First season
just a few cases
Second season – amplification explosion.
Then
reduction to maintenance levels.
Decline in disease due
to:
Widespread, regular use of vaccination.
Preventive
management and control – mosquito control – insecticides, repellents,
vector-resistant housing.
Natural immunity because of
exposure.
Stagnant water removal, dung and tall
weeds.
Costs
In Nebraska and Colorado the cost of
treatment, prevention and lost use was in the order of 4 million dollars.
See avma and usda links below for further details.
Further
information
This can be obtained through the
link
http://www.avma.org/onlnews/javma/jun03/030615l.asp
“In 2002,
378 and 1,100 equine cases of West Nile infections were confirmed in
Colorado and Nebraska, respectively….. Of the cases studied, 8 percent
were mild, 58 percent were moderate, and 34 percent were severe…..
Approximately 47 percent of equids with WNV in Colorado and Nebraska
received at least one WNV vaccination in 2002, according to the owner
survey”.
Regarding costs:
“… researchers estimate that
prevention costs of WNV vaccination likely exceeded a combined $2.75
million in Colorado and Nebraska in 2002…”
“Veterinarians then
estimated the cost of treatment for each category and determined that it
costs approximately $200 to treat animals with mild disease, $400 for
those with moderate disease, and $250 for equids with severe disease.
Severe cases cost less, on average, because many severely infected equids
were likely euthanatized before incurring high treatment
expenses….”
The entire report on costs to the equine industry in
Colorado and Nebraska can be viewed and/or downloaded at
www.aphis.usda.gov/vs/ceah/cahm/Equine/wnv-info-sheet.pdf
(PDF).
Professor Alan Guthrie, Director of Equine Research
Centre, Faculty of Veterinary Science, University of Pretoria, South
Africa, and served on OIE working groups for AHS, EI, WNV. Also AHSWG
adviser.
WEST NILE VIRUS IN SOUTH
AFRICA: COMPARISONS AND CONTRASTS WITH THE USA
Disease of
humans and animals with an insect vector – the Culex mosquito e.g. Culex
univittatus. Birds are reservoir hosts. Humans and horses get bitten and
can become infected but they are regarded as dead end
hosts.
1937 Ugandan woman discovered with West Nile Fever in
West Nile province.
1974, 1986-7 virus isolated in humans in South
Africa.
Extensive epidemics recently in Mediterranean and E Europe,
North Africa, Asia and more recently North America. With climate change
possible spread further north from the Mediterranean.
Neurological
disease with 40 % fatality. However in S Africa an avirulent or mildly
pathogenic virus strain (lineage 2 virus) in horses; in humans it can
cause fever plus muscle/joint pain in humans – death very
rare.
South Africa
1. WNV is endemic in S Africa with
very widespread transmission of the virus.
2. Distribution is
linked to vector distribution.
3. Rarely causes neurological
disease in horses. S Africa has avirulent or mildly pathogenic virus
strains (Lineage 2 viruses). This is in contrast to the USA (Lineage 1
viruses), which result in major neurological disease. Lineage 1 also in
Europe and Asia epidemics.
A serological survey of all thoroughbreds by
SNT (Serum Neutralisation Test) showed that 75% adult mares were
seropositive but had no clinical signs. (Also maternal antibody detected
in colostrum).
4. Experimental infection with Lineage 2 virus led
to nothing significant regarding disease – no observed clinical signs or
viraemia.
5. Horses and humans are dead end hosts and therefore the
disease should not be a barrier to International Trade.
Summary
(Quote from Prof. Guthrie’s Conference paper):
“Asymptomatic or
subclinical WNV infection of horses (and humans) is common throughout much
of South Africa, and the experimental infection of horses with a S.
African Lineage 2 isolate of WNV resulted in neither clinical disease nor
viraemia. The difference between the clinical signs observed following
infection with WNV in horses in South Africa and those infected with WNV
the USA is due to difference in pathogenicity between the virus strains
that circulate in the two regions.”
(See Guthrie AJ, Howell PG,
Gardner I, Swanepoel R, Nurton JP, Harper CK, Pardini AD, Groenewald D,
Visagé CW, Hedges J, Balasuriya UBR, Cornel AJ, MacLachlan NJ: 2003. West
Nile virus infection of Thoroughbred horses in South Africa (2000 -
20001). Equine Veterinary Journal 35 (6), pp 601-605).
Matthew
Hartley
Deputy Head of Exotic Notifiable Diseases, Defra.
Member of
AHS Working Group.
Mr Hartley provided very useful information on
both WNV and AHS: occurrence, symptoms, etc. which was supported by a very
detailed article in the Conference brochure However, what was of
particular significance was his information on current disease control
policies in the UK, and possible future policy. He emphasised that policy
was based on EU legislation, (1992/35 for AHS) which was now considered to
be in urgent need of revision, in the light of advances in vaccine
technology and diagnostic tests, increased global movements of livestock
and people, climate change, potential for novel vectors (as illustrated by
the BTV8 outbreak in northern Europe in 2006). We were urged to lobby the
EU to review policy, as combined pressure from Defra, the equine industry
and other stakeholders would be far more effective than Defra
alone.
What however was not mentioned was the power given to
the Secretary of State in the Animal Health Act 2002, to slaughter any
animal (including dogs, cats, birds etc) he sees fit. This includes not
only animals that are confirmed by laboratory diagnosis to be infected,
but also those suspected of being infected (but not confirmed positive by
testing) and crucially those not infected. This then opens the gates to
firebreak killing of healthy animals to create a barrier around an
infected area. This mass killing of healthy stock took place in FMD 2001,
and as Elliot Morley acknowledged in his evidence to the EFRA Select
Committee on 6 November 2001 when he said “We do not have powers for a
firebreak cull”, the legal powers for this did not in fact exist in FMD
2001. They do now. I mentioned this to the Chairman of the TBA after the
meeting.
It was evident that there were those in the audience who
feared that Defra might attempt to behave in similar fashion to FMD 2001
(and 2007) and slaughter on suspicion. We were not totally reassured after
close questioning of Mr Hartley that this would not happen if an outbreak
of AHS were to occur in the near future. Neither was a remark by Dr Oura
reassuring when I understood him to indicate that if a few more horses had
to be killed to prevent the disease spreading then so be it. The
impression therefore was that, as things stood under current legislation,
there may not necessarily just be slaughter of infected horses. For
further details of the Defra control strategy see later in text under
individual disease headings.
What was particularly encouraging was
the initiative taken by the equine industry to set up an Animal Horse
Sickness Working Group in 2007 to tackle these issues, working in
partnership with government (see Brigadier Jepson’s comments). Defra’s
presence at, and contribution to the Conference was particularly
significant. Of course the setting up of the Newmarket Conference itself
was another example of the tremendous cooperation and determination
between a wide spectrum of interested parties to:
i) raise
awareness/educate, by bringing together world experts with first hand
knowledge of WNV and AHS and its control in order to provide us with
accurate, up to date information at the cutting edge of
science;
ii) to move the debate forward and to examine ideas for
future strategy/policy, with a view to lobbying the EU. See also the
closing speech by Kirsten Rausing, Chair of the TBA.
Mr Hartley
mentioned the development of the AHS Strategy which would be a “model for
the future” and cost sharing with industry. He also mentioned that
government would set up a Core Stakeholder Group on AHS to ensure
consultation and “working in partnership”. There understandably is a
degree of scepticism about how successful this will be as experiences from
some in the FMD Stakeholder Group regarding the degree/type of
consultation have been worrying. Furthermore, Mr Hartley made the point
that Defra’s resources and priorities had “to be factored in” to any
strategy, and that says it all. There is for example no equine
surveillance in horses at present for as this is considered be too costly.
See
http://www.defra.gov.uk/animalh/diseases/vetsurveillance/profiles/west_nile-virus-full.pdf
Furthermore,
I understand that horse owners who submit samples for testing for WNV to
the VLA have to pay for the cost of the tests.
Below is a brief
summary of some of the points covered on the individual diseases. Quotes
from the article by Matthew Hartley in the Conference brochure are
indicated in italics.
West Nile
Virus
Spread of disease
1. The mosquito vectors are primarily
the Culex species which are known to occur in the UK. 2.The nearest
outbreaks to the UK were in Italy (1998) and southern France (2000).
3.
Mr Hartley stated that “migrating birds are the most likely mechanism for
the infection being introduced into the UK”. This should be qualified as
the introduction of WNV into the USA was apparently not likely to have
been due to migratory birds. The US virus was very closely related to a
lineage 1 strain found in Israel in 1998, but the migration routes of
birds do not correlate with this. Some explanations suggest an imported
(illegally) infected bird, or the “import” of an infected mosquito of the
jet setting variety. Thus the UK could be at the same level of risk as the
USA in 1999.
4. Regarding the bird hosts, some species are particularly
susceptible e.g. the crow family, and can be subject to mass
“die-offs”.
5. No active virus has apparently been found in UK birds
(Phipps et al Veterinary Record (2008), 162, 413-415), but evidence of
antibodies has been found.
Action taken by Defra
1. VLA
surveys on deaths in wild birds since 2001. No evidence of mass die-offs.
See 5. above.
2. It is now possible to send samples to the VLA for
testing via the local Animal Health Office. There is a charge for this
service.
3. Research has been commissioned for a large scale study of
mosquitoes in the UK.
4. The health Protection Agency (HPA) tests for
the presence of WNV in mosquitoes.
5. The Health and Safety Executive
(HSE) have carried out a study of the approved pesticides for use in
mosquito control.
Disease prevention
“Prevention and
control, in the event of clinical disease being identified in the UK, is
primarily to reduce the numbers of vectors and prevent contact with
them:
i) Vector control – eliminate breeding sites of mosquitoes
(stagnant water, rainbutts etc) with possible use of insecticides
ii)
Vector avoidance – for animals keep them away from vector sites, apply
insect repellent, house in insect proofed accommodation when mosquitoes
are active”.
Control strategy
1. Statutory notification
of suspected disease plus veterinary investigation.
2. Restrictions on
infected premises
3. Local and national risk assessments.
4. Dept of
Health contingency plan followed and an infection control team (ICT) set
up locally.
5. Overall control at national level undertaken by Defra
and DoH. The ICT will advise on further local actions e.g. vector control,
extra surveillance, publicity.
6. There is no requirement for statutory
slaughter of horses. If horses slaughtered there is no provision for
compensation.
For further information - Click here! and here!
African Horse
Sickness
Risk of introduction/spread
Closely related to
bluetongue, so sudden spread of bluetongue to northern Europe has led to
reevaluation of potential for introduction – BTV8 does not require
presence of C. Imicola in northern Europe. Local species of midge have
become novel vectors. These are obviously adapted to local climatic
conditions so climate change e.g. rising temperatures not necessary to
maintain the vector.
Legislation
“Council Directive
92/35 provides for compulsory notification, and the setting up of a
protection zone of at least 100 kms radius around an infected premises.
This, together with a surveillance zone of at least a further 40 kms,
would have to remain in force for at least 12 months. AHS is included in
The specified Disease (Notification and Slaughter) Order 1992 to implement
the slaughter requirements of the EU council Directive 92/35/EEC which
lays down control rules and measures to combat AHS. Imported horses from
at-risk countries outside the European Union are routinely tested for
AHS.
The severity of disease and the controls to monitor and restrict
movement of horses could significantly affect the equine industry in the
UK”.
When a suspect case is reported the horse(s) is brought
indoors, isolated, tested. Insect eradication in
neighbourhood.
If sample positive, horse killed. Horse may be
euthanised at any stage on welfare grounds at veterinary discretion. (NB
Animal Health Act gives additional powers of slaughter).
Control zone
set up of 20 km radius around IP.
Protection zone of 100
km
Surveillance zone of 150 km radius around infected premises. Varies
according to epidemiological and geographical factors.
Tracing
investigations are carried out.
Equine surveillance in surrounding
areas plus surveillance of midge vector.
Professor Mellor also warned
that some Culicoides activity during the day, so just bringing in horses
from dusk to dawn may not be good
enough.
Vaccination
Mr Hartley stated that EU
legislation “requires vaccination” in an outbreak but “there are no
licensed vaccines” and there is a perceived risk that the multivalent live
vaccines may introduce other serotypes, but see comments by Prof. Guthrie
regarding the value of these vaccines in the face of an
outbreak.
According to Mr Hartley:
“The last outbreak of
AHS in Europe, in Spain and Portugal in the early 1990s was controlled
after an intensive local vaccination programme was instigated. There are 9
different serotypes of AHS and there are no vaccines available in Europe
against any of them. Using currently available vaccination approaches,
each of the 9 serotypes would require its own vaccine”. (This refers to
inactivated vaccines, none of which are currently available in Europe.
However, the advent of new vaccine technologies e.g. using the canarypox
platform, may well transform the situation in the near future). “The only
vaccines in regular use overseas in AHS endemic areas are polyvalent
modified live vaccines which are not suitable for use in free areas such
as Europe that would try to eradicate the disease – and might also result
in introduction of new serotypes.”
NB AHS is not endemic in all
parts of South Africa e.g. an area around Cape Town can export to the EU
under a regionalisation agreement and specified quarantine arrangements.
http://www.nda.agric.za/vetweb/Animal%20Disease/AHS_Image40.htm
For
further details of AHS and vaccination in S Africa visit the AHS Trust
website:
http://www.africanhorsesickness.co.za/default.asp
Control
strategy
“Defra is participating in an equine industry led working
group to develop a UK AHS Strategy. The strategy takes forward current
legislation and describes how it would be implemented in partnership
should AHS arrive in the UK. This is currently in the drafting phases and
will be available for consultation later this year”. See earlier
references to this by Brigadier Jepson.
We were advised that
the strategy was in two parts:
i) current disease control
strategy based on current legislation
ii) an improved updated control
strategy drawn up after consultation with industry, scientific experts,
government and other stakeholders. This to be presented to the EU to lobby
for change of Directive 92/35.
“The generic contingency plans for
notifiable disease outbreaks in the UK have been revised to include the
outcomes of the consultation on the Specified Type Equine Exotic Diseases
(STEED) plan.”
Questions:
Imports of
horses
Mr Hartley was asked for details of import figures and source
countries and questioned about the import checks. He was unable to give
details, but the questioner himself made it clear that the UK was the
biggest importer in the EU of horses from Asia, the second biggest from
South America, and the third biggest importer of horses from Africa, and
asked about import testing and surveillance as there were obvious risks.
It seems that there is no import testing for emerging diseases and that
the horses undergo clinical inspection only. There is also no equine
surveillance. Mr Hartley advised the meeting that there is apparently no
legal requirement for the location of horses to be registered, so this
would pose problems for surveillance. (However, as one of Defra’s own
reports makes clear the critical factor is cost – see Defra report links
in WNV section above).
The questioner continued to push on the
issue of stopovers, where horses may be exported from a not at risk
country or disease free zone within that country, and yet on stopovers
these animals may be taken off the aeroplane. If this is in an affected
country and precautions are not adequate then there is an obvious risk. It
would appear that the details of stopovers (location, precautions,
inspections) may not always be recorded. Also as there are apparently no
specific checks/blood tests routinely carried out on import for these
emerging diseases then this is cause for further concern. Certainly Mr
Hartley was not able to provide reassurance on this. This would obviously
be a point worth investigating further.
Kirsten Rausing, Chair of
The Thoroughbred Breeders’ Association
Kirsten Rausing brought the
Conference to a close urging conference-goers to spread the word and to
take urgent action. The industry could not afford to sit back. She said
that the EU had to be approached to amend the “obsolete” 93/35 Directive.
She advised us that the Commissioners are far more likely to take notice
if the industry acted on a united front, and suggested that one such
umbrella organisation could be the European Federation of Horse Breeders
Associations, based in Switzerland (Chairman Hans Peter Meier. Vice
Chairman Richard Jones, UK). The EU is far more likely to act if it has
representations from an organization that it recognizes as supranational
i.e. represented all member states. What are needed are written and
physical representations to the Commissioners regarding the amendment of
the Directive. ( Jules Minke comment: possibly a consortium of the equine
industry, EU, and the pharmaceutical industries could provide the
mechanism for change).
Finally she reminded us that it was a case
of when, not if, these diseases arrive, and action was needed now, despite
the fact that the UK may be at apparently lower risk than elsewhere in
Europe at present, and that other diseases such as bluetongue were more
pressing.
My comment: the risk is very real and should not be
ignored. We are at risk of unforeseen “parachuting in” of disease (in
addition to the “expected” northward spread of some diseases) with the
very real possibility of disease being maintained and spread by novel
vectors. The consequences for the equine industry could be disastrous if
we are not adequately prepared. There is the expertise/technology
available and there is obviously tremendous commitment and determination
within the equine industry to put a workable disease control strategy
based on sound, up to date science, in place. What is needed is the
political will within the EU not only to acknowledge the real threats
posed by the emerging diseases, but to take swift action to employ the
very best of its scientific expertise in order to bring its disease
control legislation into the 21st century, with preventive vaccination at
the fore. As the EC document “A new Animal Health Strategy for the EU
(2007-2013)EU” states “Prevention is better than cure”. Enough of the
words, now we need the action.
Anne Lambourn - 19th July
2008 |