Emerging disease risksin dogs

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Speakers

William (Bill) Ellis BVMS PhD FRCVS

Bill was educated at University of Glasgow, School of

Veterinary Medicine, where he also obtained his PhD.

He worked at the Veterinary Sciences Division,

Stormont, Belfast from 1973 to 2008, where he held

various positions including Acting Director of the

institute and Head of Department of Veterinary

Science, Queens University Belfast, from 2000- 2006.

He was also, Director of the OIE Leptospira reference

laboratory, at Stormomt from 1989 to 2008.

Since then he has worked as part time consultant to

the OIE Leptospira Reference Laboratory and as a

private consultant specialising in leptospirosis.

His academic interests have been mainly in the area

of leptospirosis, and among his credits, are the first

isolations of serovar Hardjo from aborted foetuses,

milk, male and female genital tracts of cattle and

sheep. The first isolations of Bratislava from pig

foetuses, and pig male and female genital tracts

and Bratislava from horses and dogs. He has also

been interested in vaccinal immunity and along

with his student, Ke-Ting Yan, was the first to

recognise the importance of CMI in veterinary

leptospirosis vaccines.

He has written extensively on leptospirosis and has

lectured on the subject in many parts of the world.

David Sutton BVetMed MRCVS

David Sutton initially qualified as a veterinary

surgeon from the Royal Veterinary College, London

in 1982. After spending some time in general

practice in the UK, he joined the veterinary

pharmaceutical industry as Veterinary Advisor for

a UK animal health company.

In 1988, he joined Intervet, eventually becoming

UK Director of Veterinary Services with overall

responsibility for managing all UK technical product

support and product registration.

Within Intervet, he specialised in the areas of small

animal vaccination, and pharmacovigilance and he

has lectured widely on these topics at many national

and international conferences and symposia.

Currently, David Sutton works as Technical Director

for MSD Animal Health with worldwide technical

responsibility for the company’s small animal

vaccine products.

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Richard Newton BVSc MSc PhD DLSHTM

DipECVPH FRCVS

After graduating in Veterinary Science from

Liverpool University in 1991 and working in mixed

practice, Richard Newton joined the Epidemiology

Unit of the Animal Health Trust in 1994. Since

completing a Masters in Communicable Disease

Epidemiology at the London School of Hygiene and

Tropical Medicine in November 1998 he has worked

on the epidemiology of a variety of diseases of

companion animals, including grass sickness, EIPH

and strangles in horses and influenza, including

cross-species transmission from horses to dogs. He

completed his PhD on the epidemiology of equine

infectious respiratory disease in 2002 and in 2003

was awarded both the Diploma of Fellowship from

the Royal College Veterinary Surgeons and became a

de facto Diplomate of the European College of

Veterinary Public Health. He is currently Head of

Epidemiology and Disease Surveillance at the Animal

Health Trust. The group at the AHT currently has

programmes on infectious disease surveillance in the

UK for which it prepares quarterly disease reports

for Defra. He also oversees dedicated programmes

on grass sickness surveillance and vaccination and

investigation of ‘seasonal canine illness’, an

emerging disease syndrome in dogs walked in

woodland environments in the autumn months.

Richard also has a young family which keeps him

very busy!

Olivia Walter BSc MSc

Olivia graduated from the University of Edinburgh

with a degree in Zoology (later gaining an MSc in

Conservation Ecology from the Durrell Institute of

Conservation and Ecology) and became a keeper of

small mammals at ZSL London Zoo. While at the

zoo, and thereafter, Olivia managed European

breeding programmes for Amur leopards, Amur

tigers, Sumatran tigers, Asiatic lions, Douroucoulis,

South American sealions and Short Snouted

seahorses (a British species). She then became

Conservation/Zoo Programme Coordinator for the

British and Irish Association for Zoos and Aquariums

(BIAZA). Her nine years covered monumental

change from a dwindling membership organisation

to one with a rising membership referred to by

government and non-zoo conservation

organisations on all matters of legislation, animal

welfare and conservation.

In 2009 Olivia took on administration for for the

charity Wildlife Vets International (WVI) on behalf

of International Zoo Veterinary Group, as well as

providing clients guidance on animal welfare,

management and conservation. In addition to the

above, Olivia has worked and carried out research

abroad including; Kipling Camp (India), Tongabezi

(Zambia), Wetlands International (Borneo,

Indonesia), WCS Cambodia and Breeding Centre for

Endangered Arabian Animals, UAE.

In her spare time, Olivia has two young children,

loves sailing, swimming and walking for hours and

growing fruit and vegetables. She supports her

husband growing coral on a Yorkshire hillside!

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Eric Morgan MA VetMB PhD MRCVS DipEPVC

Eric graduated in veterinary medicine and zoology

from the University of Cambridge in 1997 and

entered a short period of general practice in

Wales before embarking on research on the

ecology of parasite transmission in the saiga

antelope in Kazakhstan. After interruptions to

serve with the RAVC in the Balkans and in the

foot and mouth disease epidemic in the UK, this

eventually led to a PhD from the University of

Warwick in 2003. Since then, he has been at the

University of Bristol, where he teaches

parasitology to veterinary students, and conducts

research into the ecology, epidemiology and

control of parasites in wild and domestic animals.

Although he works widely across different systems

and questions, this research is assembled around

the impacts of climate and other environmental

change, and how to devise appropriate and

sustainable responses. Recently, angiostrongylosis

in dogs and gastrointestinal nematodes in sheep

have proved to be good examples. Outside work,

his family protects him from over-indulging an

unhealthy interest in the intimate life of slugs, and

an insatiable enthusiasm for rugby (wisely

restricted to watching, not playing).

Richard Wall BSc MBA PhD FRES

After a BSc in Zoology (University of Durham) and a

PhD in insect population ecology (University of

Liverpool), Richard moved to the Tsetse Research

Laboratory in Bristol to work on the behaviour of

tsetse flies, the vectors of African trypanosomiasis,

with field studies largely based in Zimbabwe.

After four years, he transferred to the University of

Bristol’s School of Veterinary Sciences, to work

primarily on sheep blowfly myiasis, but then also

became involved in projects on screwworm fly in

Papua New Guinea and cattle dung ecology. After

the award of a Royal Society Research Fellowship,

Richard moved to the School of Biological Sciences in

Bristol. There, for almost 20 years now, he has

worked on a diverse range of arthropod

ectoparasites and disease vectors of veterinary

importance in many parts of the world. This research

has ranged widely from fundamental studies of

taxonomy and physiology, through to field

population ecology and farm-level investigations of

the application of sustainable control technologies.

In addition to his research, Richard teaches

parasitology to veterinary undergraduates and

entomology and ecology to biologists. The rest of his

life is occupied by his family and his increasingly

unconvincing attempts play the occasional game of

rugby and the piano: unfortunately he plays rugby

like Angela Hewitt and the piano like Richie McCaw

(His words…not ours! (Ed.))

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Agenda

A day exploring some emerging disease trends in canine health and their

potential impact in the United Kingdom.

10.00 am

10.30 am

11.30 pm

12.00 pm

12.30 - 2.00pm

2.00pm

3.00pm

3.30pm

3.45pm

4.45pm

5.15pm

Registration & Coffee

Leptospirosis - time for a change? Dr William Ellis

Towards a new approach to canine leptospirosis David Sutton, MSD

Morning Q&A Session

Lunch & Zoo Visit

Investigating emerging threats - Richard Newton, AHT

understanding the risks posed by canine influenza

and seasonal canine illness

Afternoon Tea

Emergent Disease and the work of Olivia Walter, WVI

Wildlife Vets International

Our changing environment - what does the future Professor Richard Wall

hold for vector-borne disease? (Edinburgh/Bristol)

Eric Morgan

(London/Doncaster)

Afternoon Q&A session

Close

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Bivalent vaccines against Leptospira serovars Canicola andIcterohaemorrhagiae have been available in Europe for around50 years. During that time canine leptospirosis has changedboth in terms of prevalence, the causative serovars, aspects ofthe clinical picture and control measures.

Awareness of these changes was initiated by the reporting ofother serovars being associated with canine leptospirosis inNorth America, namely serovars Bratislava, Pomona,Grippotyphosa and Autumnalis and subsequently a significantrise in the number of cases in the 1990’s. Four componentvaccines containing the additional serovars Pomona andGrippotyphosa became available there in 2002. At the sametime there was an increased awareness of adverse reactionsassociated with canine vaccines in the USA and the need forannual vaccination with Leptospira vaccines came in forcriticism. The situation has been further complicated by the WSAVA guidelines which have listed leptospirosis as a non-core disease.

Adverse reactions were not seen as a problem in Europe, butthe continued use of Canicola vaccination was being questionedon the grounds that clinical Canicola infection had almostdisappeared in some countries. In addition, there was anawareness of continued exposure of dogs toIcterohaemorrhagiae infection and the emergence of otherserovars as causes of canine leptospirosis in Europe – Bratislava,Grippotyphosa and Sejroe/Hardjo. A review of the Europeanliterature indicated the need for the inclusion of serovarsBratislava and Grippotyphosa in European dog vaccines, thecontinued inclusion of serovars Canicola andIcterohaemorrhagiae, but found no case at present for theinclusion of serovar Pomona.

The biologics industry has responded by developing newmultivalent vaccines which not only address efficacy but alsoconcerns about adverse reactions and has also attempted, withpartial success, to rationalise vaccination requirements andprotocols across Europe and north America.

One of the major dilemmas in deciding the appropriateness ofserovars for inclusion has been the difficulty in the laboratorydiagnosis of past and current infections. In addition, up-to-date

surveillance information is not available in many countries. Inthe UK the data is distorted by practitioner bias in requestingonly testing for serovars Canicola and Icterohaemorrhagiae.

This presentation will discuss the rationale for developing a newEuropean vaccine and discuss the challenges in obtainingmeaningful laboratory based diagnostic and surveillance data.

Control of Canine Leptospirosis in Europe: time for a change

W. A. Ellis BVMS PhD FRCVS

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Canine leptospirosis vaccination for the 21st Century

Leptospirosis is a geographically widespread disease whichaffects many animal species – including man. It is currentlyconsidered to be the most widespread zoonotic infection in theworld1 and in recent years is becoming even more prevalent.

There are many pathogenic strains of leptospires which aretraditionally classified into specific serovars based on surfaceantigens. Antigenically related serovars are then grouped intoserogroups. This classification into serogroups and serovars isbased on serological testing and is therefore most relevant forvaccination purposes.

Infected animals shed bacteria in their urine and transmissioncan occur either directly through contact with the infectedurine, or indirectly, for instance following contact withcontaminated water. The bacteria typically invade a host viamucous membranes in the eyes, nose, or mouth or through skincuts or abrasions. Once leptospires are in the body they enterthe blood system and multiply rapidly. The bacteria theninfiltrate organs such as kidney, liver, spleen, eyes, and centralnervous system where they replicate further. From the kidneysthey are shed in the urine, thus perpetuating the infection cycle.

Chronically infected reservoir host species (often wildlife such asrodents) maintain disease in the environment. These reservoirhosts are usually well-adapted to the particular serovar theyharbor and will not show clinical signs—but can shed leptospiresfor months, even years.

Incidental hosts, such as dogs, can suffer serious clinical diseaseafter infection. Although they normally shed leptospires for a shorter period, they are still important sources of infection. As leptospirosis is a potentially serious zoonotic condition,limiting shedding from infected dogs is a critical component of disease control.

In dogs, the early signs of disease can be vague and non-specificmaking recognition based on clinical signs difficult. However, ifnot successfully treated at this stage the signs may progress toserious, possibly fatal, illness – often culminating in hepaticand/or renal failure.

Confirming a presumptive diagnosis can be complex and time-consuming and as a consequence many cases will almostcertainly go undiagnosed, making it likely that the truefrequency of disease in the canine population is significantlyunderestimated.

Vaccines against canine leptospirosis are readily available and,since many dogs are at risk of disease, vaccination is widespreadin many countries. Traditionally, leptospirosis in dogs has beenassociated with serovars from serogroups Canicola andIcterohaemorrhagiae, and bivalent vaccines containing strainsfrom these serogroups have been successfully used for the last50 years. However over recent years a change has occurred inthe epidemiology of canine leptospirosis and nowadays cases of disease caused by serovars from different serogroups areseen increasingly frequently; in the USA from serogroupsGrippotyphosa and Pomona and in Europe predominantly fromserogroups Grippotyphosa and Australis. In the USA, there arealready a number of tetravalent canine leptospirosis vaccinesavailable containing, in addition to traditionalIcterohaemorrhagiae and Canicola antigens, strains fromserogroups Grippotyphosa and Pomona. In Europe there havebeen only bivalent vaccines used until very recently althoughindependent experts are now recommending the use oftetravalent vaccines.2

David Sutton BVetMed MRCVSTechnical Director, MSD Animal Health

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Nobivac® L4

A new European tetravalent canine leptospirosis vaccine hasrecently been authorised via an EU centralised procedure(Nobivac® L4 – MSD Animal Health). This product is a non-adjuvanted liquid injectable vaccine containing inactivatedwhole cell strains from serogroups Canicola,Icterohaemorrhagiae, Grippotyphosa and Australis.

A number of studies have been undertaken in order toinvestigate the safety and efficacy of this new vaccine.3

Safety

Field safety studyThis was carried out as a randomised, positive controlled,double blinded study. In total 194 dogs (including puppies andpregnant bitches) from a range of breeds were included. Thedogs were randomly assigned to one of two groups andvaccinated with either Nobivac L4 or Nobivac Lepto (a bivalentvaccine). Pups were vaccinated twice and pregnant bitches andother adult dogs were given a single vaccination. Allleptospirosis vaccinations were given mixed with NobivacDHPPi, with exception of the first vaccination of the pups,which was mixed with Nobivac Puppy DP.

All adverse signs following vaccination were recorded and noclinically relevant differences in local and systemic reactions,rectal temperature and outcome of pregnancy were observedbetween the two vaccine groups. This confirms that the safetyprofile of Nobivac L4 for pups, pregnant bitches and other dogsis similar to that for the current bivalent vaccine.

Risk of allergic reactionsBovine serum, containing protein, especially bovine serumalbumin (BSA), is widely used in the manufacture of manyvaccines. This BSA component has been implicated as a cause ofallergic reactions post-vaccination.4.5 During the production ofNobivac L4 a unique VacciPure™ filtration process is used. Thisensures that excess BSA is actively removed from the finalproduct, resulting in much lower levels of BSA in the finalformulation as compared to other leptospirosis vaccines (Table 1).

Table 1. BSA content of canine leptospirosis vaccines

Vaccine Manufacturer batch BSA content (mg/ml)

Nobivac L4 MSD AH A002A 0.4

A003A 0.4

Nobivac Lepto MSD AH A103B 0.3

A101A 0.5

A105B 0.3

Vaccine V Competitor A Batch 1 4

Batch 2 2.4

Vaccine E Competitor B Batch 1 3.6

Batch 2 3.8

Vaccine D Competitor C Batch 1 6.3

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Efficacy

In the following studies, the main efficacy criteria investigatedwere those related to the ability of the vaccine to successfullycontrol leptospira infection and the shedding of infection via urine. Since clinical disease always follows a period ofleptospiraemia which allows the bacteria to reach the targetorgans such as liver or kidneys, it follows that if the vaccine can prevent leptospiraemia it will effectively prevent not only clinical disease, but also the risk of renal infection andurinary excretion.

Immunity against infection and shedding

A series of four challenge studies were undertaken to assess the efficacy of Nobivac L4 in preventing infection and renalexcretion. For these studies the puppies in the vaccine groupswere all vaccinated twice as follows:

1. Nobivac DHPPi/Nobivac L4 and Nobivac KC at 6 weeks of age2. Nobivac DHPPi/Nobivac L4 at 10 weeks of age

The puppies in the control groups were vaccinated withNobivac DHPPi and Nobivac KC at the same ages. All vaccinatesand controls were then challenged three weeks later.

The results demonstrate that Nobivac L4 was able to preventinfection and renal excretion in the majority of animals (Table 2).

It is important to note in the following studies that the criterionfor a “dog positive for infection” is a dog with at least twosamples of blood or serum or urine/kidney on different days or a dog with challenge-induced nephritis or clinical orhaematological evidence for leptospirosis. The criterion for a “dog positive for renal infection” is a dog with at least onepositive sample of urine/kidney from day post-challenge 14 onward or challenge-induced nephritis (demonstrated byhistopathological examination).

Table 2. Efficacy following challenge 3 weeks post-vaccination

* Both dogs had mild, transient clinical signs; no positive cultures

or PCR results, no thrombocytopenia, no interstitial nephritis

Challenge GroupInfection Renal infection

CanicolaVaccine

Control

2/8*

8/8

0/8

8/8

IcteroVaccine

Control

0/7

7/7

0/7

7/7

GrippoVaccine

Control

0/8

7/8

0/8

6/8

AustralisVaccine

Control

0/8

6/8

0/8

1/8

No. dogs positive for:

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Efficacy at 12 months

In order to confirm the ability of Nobivac L4 to provide a full 12 months immunity, a further series of challenge studies wereset up. For these studies the puppies in the vaccine groups wereall vaccinated twice as follows:

1. Nobivac DHPPi/Nobivac L4 and Nobivac KC at 6 weeks of age2. Nobivac DHPPi/Nobivac L4 at 10 weeks of age

The puppies in the control groups were vaccinated withNobivac DHPPi and Nobivac KC at the same ages. All the dogswere housed securely for 12 months following vaccination to avoid any possibility of being exposed to natural (field)infection. All vaccinates and controls were challenged 12 months post-vaccination.

The results demonstrate that Nobivac L4 was able to preventinfection and renal excretion for at least 12 months followingvaccination in the majority of animals (Table 3).

References

1. Adler, B. and De La Pena Moctezuma, A. (2010) Leptospira and

leptospirosis. Veterinary Microbiology, 140: 287–296.

2. Ellis, W.A. (2010) Control of canine leptospirosis in Europe: time for

a change? Veterinary Record, 167: 602-605.

3. Klaasen, H.L.B.M., van der Veen, M., Molkenboer, M.J.C.H. and

Sutton, D. (2012) A novel tetravalent Leptospira bacterin protects

against infection and shedding following challenge in dogs.

Veterinary Record published online November 23, 2012;

doi:10.1136/vr.101100.

4. Ohmori, K., Masuda. K., Maeda, S., Kaburagi, Y., Kurata, K., Ohno,

K., DeBoer, D.J., Tsujimoto, H. and Sakaguchi, M. (2005) IgE

reactivity to vaccine components in dogs that developed immediate-

type allergic reactions after vaccination. Vet Immunol Immunopathol,

104: 249-256.

5. Ohmori, K., Masuda, K., DeBoer, D.J., Sakaguchi, M. and Tsujimoto,

H. (2007) Immunoblot analysis for IgE-reactive components of fetal

calf serum in dogs that developed allergic reactions after non-rabies

vaccination. Vet Immunol Immunopathol, 115: 166-171.

Table 3. Efficacy following challenge at 12 months post-vaccination

* Dog had three positive urine samples; no clinical signs,

no thrombocytopenia, no positive kidney, no interstitial nephritis

** Dog had interstitial nephritis; no positive culture/PCR results,

no clinical signs, no thrombocytopenia

Challenge GroupInfection Renal infection

CanicolaVaccine

Control

1/9

9/9

1/9*

9/9

IcteroVaccine

Control

0/9

6/9

0/9

6/9

GrippoVaccine

Control

1/8**

7/9

1/8**

0/9

AustralisVaccine

Control

2/8

8/9

0/8

4/9

No. dogs positive for:

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Canine Influenza

In March 2004 a press release from the University of Floridareported the first known natural transmission of equineinfluenza to another species. The virus had been isolated from a greyhound affected during an outbreak of respiratory diseasein January 2004. Molecular studies suggested that there was a single transmission event from horses to dogs and that sincethen the virus has transmitted directly from dog to dog.

Investigating emerging threats - understandingcanine influenza and seasonal canine illness

J Richard Newton BVSc MSc PhD DLSHTM DipECVPH FRCVSHead of Epidemiology and Disease Surveillance, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU

In 2005 in response to the situation in the USA, the AHTconducted an assessment of the situation in the UK, whichwas co-funded by Battersea Dogs’ and Cats’ Home, DogsTrust and The Kennel Club. This study retrospectivelyanalysed samples stored since 1999 from outbreaks ofrespiratory disease among dogs where no aetiological agentwas identified. It also attempted to establish whetherexposure to canine influenza virus was present in thosesections of the UK dog population considered most at riskfrom a cross-species transmission event through feeding ofequine offal. Though it can only now be speculated as to theexact route of infection of dogs by equine influenza virus, themost likely explanation is the feeding to dogs of uncooked,infected horsemeat, particularly the lungs, as these are likelyto have the highest levels of virus. Any dog population fed inthis manner such as quarry hounds or greyhounds should beconsidered vulnerable to cross-species infection by equineinfluenza virus.

The AHT study concluded that an outbreak of canineinfluenza had occurred in the UK in a pack of approximately80 English foxhounds in 2002. During a respiratory diseaseoutbreak within the pack, characterised clinically by suddenonset coughing, some hounds became lethargic and weak. Ina number of these hounds signs progressed to loss ofconsciousness and one animal died. A further 6 hounds wereeuthanased when it became apparent that the prognosis forrecovery was poor. Equine influenza virus was detected byimmunostaining in formalin preserved lung tissue and thepresence of equine influenza specific serum antibodies to thevirus were found in hounds that had survived the outbreakand which were still resident in the pack.

In February 2007 the AHT assisted in the investigation of anoutbreak of respiratory disease in a pack of foxhounds insouthwest England. Although it was concluded that thisparticular outbreak was not caused by EIV infection (due tothe absences of each of i) EIV antigen in post mortemmaterial, ii) seroconversion between acute and convalescentsera and iii) pathology consistent with viral pneumonia infatal cases), investigations did reveal the presence ofantibodies specific to H3N8 EIV in the blood of a proportionof hounds, consistent with likely previous exposure.

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Serological testing demonstrated that 27 of 72 hounds testedpositive for antibodies to EIV, revealing an overall influenzaseropositivity prevalence of 37.5% among the hounds in thepack in 2007. However, ordering of these data by date of birthdemonstrated a 0% (0/42) seropositivity prevalence amonganimals born after 1st April 2003 compared with 90%prevalence (27/30) in hounds born before 1st November 2002.This difference in proportions of seropositive animals was highlystatistically significant (Fisher’s exact P<0.0001). Wehypothesised that this distribution may have arisen from an EIVinfection occurring in the pack in early spring 2003, at a timewhen a variant American lineage H3N8 EIV was known to becirculating in horses in Britain. Further evidence to support thishypothesis was provided by haemagglutination inhibition (HI)assays conducted on the hound sera using a panel of EIVstrains, which showed the highest titres to Newmarket/5/03variant American lineage antigen and lower titres to earlierAmerican and European lineage viruses. Interestingly, thesedata were consistent with patterns of HI data for the sameviruses applied to strain-specific post-infection ferret sera thatare used routinely in our laboratory to antigenically characterisenew EIV isolates. The possibility of direct respiratory spreadbetween EIV infected horses and susceptible hounds as aconsequence of the two species being in close proximity in ashared airspace during road transportation to hunt meets hasbeen proposed by the hunt themselves as a potential route ofcross-species transmission in this case.

The interspecies transmission of EIV to dogs was subsequentlyshown not to be unique to the USA or the UK. Transmission ofequine influenza virus to dogs during the 2007 outbreak inAustralia has been reported and interspecies transmission of EIVto dogs upon close contact with experimentally infected horseswas demonstrated in Japan. To date, there is no documentedevidence on the transmission of influenza virus from dogs tohorses. Other influenza viruses have been isolated in dogs,including avian H3N2 in South Korea and H1N1 (pandemicswine flu) in China and the USA, although the latter is restrictedto far fewer cases than the former.

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Seasonal Canine Illness (SCI)

In September 2010 the Sandringham Estate, Norfolk, alertedthe Animal Health Trust (AHT) to an emerging syndrome thathad been reported over the previous couple of years in dogsbeing walked in woods on the estate. The AHT also becameaware around this time of reports of a similar syndromeoccurring in dogs walked in other woodland areas, particularlyin several sites in Nottinghamshire. Due to its apparentautumnal occurrence but unknown aetiology the conditionbecame known as ‘Seasonal Canine Illness’ or SCI. SCI isassociated with dogs being walked in woodland areas andpresents as a sudden onset syndrome of vomiting, diarrhoeaand lethargy, which if not treated appropriately may proceedto recumbency and death, although most cases do recover over 7-10 days, especially when receiving re-hydration therapy.The current working case definition is based on i) signs shown,ii) time of year and iii) recent exposure to a woodlandenvironment.

Analysis of geographical dog walk data from Sandringham in2010, which spatially evaluated the ratio of dog walkingintensity between SCI cases and non-affected controls, helpedidentify potentially ‘higher risk’ areas for SCI on theSandringham Estate. SCI was not reported from any of the fourstudy sites of Sandringham Estate and Thetford Forest inNorfolk and Clumber Park and Sherwood Forest inNottinghamshire, between November 2010 and August 2011.However, the syndrome recurred markedly in September 2011and review of cases from Sandringham recorded

In 2010 and 2011, highlighted the seasonal nature of SCI andthe ‘higher risk’ sites identified in 2010 were indeed where mostcases were reported in September 2011.

With the recurrence of SCI cases in 2011, expert assistance waspromptly sought to survey habitats where SCI cases hadrecently walked, based on the premise that the seasonal re-occurrence would likely relate to the recent re-emergence ofthe causal factor within that habitat. For several toxic causaltheories proposed in 2010, there should have been clearevidence for them within the dog walk habitat. On 16thSeptember 2011 a field visit was conducted in areas of ‘higher

risk’ for SCI at Sandringham with a botanist from the NaturalHistory Museum, London. Based on that expert botanicalopinion, previously proposed toxic causes of SCI, includingtoxins from blue-green algae (as no significant bodies of waterpresent to hold them), toxic non-native plants (no evidence ofthem being present), bracken spores (the abundant brackenwas not spore forming) and fungi (were not abundant andwhat was there was not recent, consistent with recent dryweather) were considered to be most unlikely.

Based on accumulating and independent observations made oncases from several different sites, during autumn 2011 the AHTdeveloped a working hypothesis for SCI. This is related toexposure of dogs to harvest mites (Neotrombicula autumnalis)which are active at the same time as SCI and quite a number ofaffected dogs have shown signs of being exposed to the bitinglarval stages (‘chiggers’) of this insect. It is hypothesised,therefore, that SCI is associated with an as yet unidentifiedpathogen transmitted via bites from the larval stages of harvestmites to dogs as dogs pass through these habitats in latesummer/autumn.

On the basis of evidence from the last three years, SCI will be a recurring seasonal problem, which has the potential tohave significant welfare impact for dogs being walked inwoodland areas in the autumn. SCI illustrates the need todevelop improved surveillance methods for emergingsyndromes of unknown aetiology in companion animals. These are necessary in order to better characterise the natureand frequency of the syndromes, to identify high risk areas and animal populations and to indicate where to best targetinvestigations and interventions.

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The emergence of disease issues is increasingly recognized as amajor factor affecting the survival of endangered species,forcing “at risk” wildlife populations into ever closer anddamaging proximity to human habitation and the disease poolwithin domestic pets and livestock. Such proximity carriespotentially devastating risks of natural disease outbreaks inever smaller and fewer endangered colonies. It is noexaggeration to say that infectious diseases such as distemperand rabies in small or fragmented populations, such as theAmur leopard or island populations in Mauritius, could inthemselves spell the final step to extinction. Catastrophic die-offs in carnivore populations, for instance, are more frequentlyrelated to disease than any other cause.

Wildlife Vets International (WVI) is at the forefront of wildlife

Emerging diseases and the work ofWildlife Vets International

Olivia Walter BSc MScWildlife Vets International, info@wildlifevetsinternational.org

and conservation medicine – capable of exerting a profoundlypositive influence on attempts to ensure species survivalglobally. We fund specialist wildlife veterinary surgeons todeliver on-site skills, training and field management toconservation organisations battling to save endangeredwildlife worldwide.

Our multi-species expertise addresses an underdevelopedaspect of conservation at a time of increasing and urgent needas wildlife populations become increasingly vulnerable to theeffects of infectious disease. As a small but effectiveorganisation, our work is typified by programmes helpingresolve conflict between local people and the man-eatingtigers of Bangladesh, preserving Africa’s disappearing painteddogs and rare primate rehabilitation in Nigeria.

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The WVI preventative medical programme for the Bangladeshtiger population, now down to around 350 animals is a keycomponent of a long term project. Perhaps the most ambitiousof all is WVI’s pivotal role in the proposed re-introduction to thewild of the rarest big cat on earth – the Amur leopard.

As we have been working successfully in projects in theBangladesh Sundarbans, Vietnam, Sumatra, Russia, Nigeria,Mauritius, Zimbabwe and the Seychelles, WVI has becomerecognised as a leader in its field. Therefore we are increasinglybeing asked to tackle new projects and new challenges.Demand for veterinary backup and services, including in situtraining of conservation staff, is set to increase as threats of thistype become increasingly obvious and conservationorganizations become aware of the availability and impact of

WVI to tackle the risk of extinction from disease.

WVI patrons Steve Leonard, Matt Brash and Kate Humble shareour determination to establish veterinary issues as an integraland natural part of all endangered wildlife projects. Ourveterinary specialists such as WVI founder, director and worldrenowned big cat expert, Dr John Lewis, ensure that WVI holdsits own on the world conservation stage.

However, in order to continue to push the boundaries ofconservation medicine, and really make a difference, we need YOUR help and support. Please visit us atwww.wildlifevetsinternational.org and follow us onFacebook/WildlifeVetsInternational to discover more about our work.

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Global changes in the incidence and distribution of vector-bornediseases in animal and human populations have been evident inrecent years. North America has seen the importation of andsubsequent rapid spread of West Nile viral encephalitis, wherebirds are the primary reservoir. Europe has witnessedunexpected outbreaks of bluetongue virus (BTV) and, recently,Schmallenberg virus in northern countries. There has been acontinued spread and establishment of the exotic mosquitoAedes albopictus, a major vector of dengue fever, to most ofthe Mediterranean region. Crimean-Congo haemorrhagic fevervirus and its Hyalomma tick vector have also emerged in parts ofTurkey, and for the first time caused clinical disease in humansin both Turkey and Greece. Usutu virus has emerged in Austria,Hungary and Spain and outbreaks of West Nile virus continueto appear in France, Hungary and Romania and has emerged inItaly and Greece. Tick-borne encephalitis has expanded its rangein central Europe and Scandinavia, and many new tick-transmitted rickettsial pathogens have been identified ofconcern to both human and veterinary health. In recent years,babesiosis has been recorded in northern Germany and The

Our changing environment: the future for vector-borne disease in the UK

Richard Wall BSc MBA PhD FRES & Eric Morgan MA VetMB PhD MRCVS DipEPVCVeterinary Parasitology & Ecology Group, School of Biological Sciences, University of Bristol, Bristol BS8 1UG, UKE-mail: richard.wall@bristol.ac.uk

Netherlands, canine monocytic ehrlichiosis (CME) in southernEurope, Anaplasma platys anaplasmosis in France, and A. phagocytophilum anaplasmosis in cattle, horses, dogs andcats in northern Europe. The UK has seen a dramatic rise in theincidence of tick-borne Lyme borreliosis and has been affectedby the waves of BTV and Schmallenberg virus which have sweptacross northern Europe.

These patterns of disease incidence appear to be a result ofcomplex interactions between factors such as increasingmovements of people and their pets, changes in approaches to management, insecticide and drug resistance, economic andsocietal changes and changes in climate. Each of these factorsmay carry a different weight and play a different role underspecific local circumstances. The result is a highly complex andlabile disease aetiology about which, in many cases, appropriatedetailed information is lacking. As a result there is little tosupport clear advice about risk, transmission or diseasemanagement; a point well illustrated by the recent outbreaksof Schmallenberg virus.

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The potential impact of climate change on vector distributionand vector-borne disease incidence is of particular interest.There is considerable evidence which demonstrates thatchanges in the phenology and distribution of a wide range ofspecies have occurred in response to climate change worldwide.Nevertheless, as yet an unambiguous link between climatechange and disease incidence has proved difficult todemonstrate; this difficulty however does not imply that no linkexists! Increases in temperature are likely to lead to increasednumber of generations and prolonged periods during whichconditions are favourable for survival and transmission. Forsome pathogens that have an obligatory development phasewithin a vector, the rate of pathogen maturation istemperature-dependent. As the summer temperatures increaseabove a certain threshold the pathogen completes itsdevelopment more rapidly within the vector. This increases thepotential for onward transmission, as well as the vectorpotential of each individual vector. Similarly the speed ofdevelopment and moulting of certain tick species is increased athigher temperatures, thus making it more likely that tropicaland sub-tropical species will establish in more temperatehabitats. On the other hand, higher temperatures may alsodecrease the survival of the off-host stages, offsetting the directeffects of temperature on higher prevalence. In addition, sincemany parasites and their vectors are at least as limited byhumidity as by temperature, effects of climate change willdepend critically on the interaction between temperature andrainfall. Hence, the net effect of climate change may becomplex and not easily predicted. Depending on the relativeeffects of temperature on development and mortality atdifferent stages of development, the outcome in terms ofabundance are likely to vary dramatically, especially when

seasonality is taken into account. For most vectors, the greatesteffect of climate change on transmission is likely to be observedat the extremes of the range of temperatures at whichtransmission occurs.

In the UK particular concern is focussed on the changes indistribution and abundance of ticks. Ticks are an extremelyimportant group of disease vectors and existing data stronglysuggest that the distribution and abundance of important tickspecies, such as Ixodes ricinus, have changed in recent years;further changes might be expected in response to changes inclimate. Longer summer seasons with a warmer and wetterspring or autumn, might be expected to promote higherchallenge and longer exposure. Tick mortality may be lowergiven milder winters but higher in hotter drier summers. Ticksthough will adapt their seasonal activity and some species mayaestivate during very hot conditions and perhaps adopt a morebimodal pattern of activity, pushing the period of feeding toearlier and later in the year. The distribution of I. ricinus in GreatBritain has been estimated to have expanded by 17% and theirabundance to have increased at 73% of locations surveyed.Human cases of Lyme disease have increased 30-fold between1999 and 2008 in Scotland. The distribution of the Europeanmeadow tick, Dermacentor reticulatus, an important vector ofcanine babesiosis in Europe, is also believed to have extendedand populations have become established in southern England.Lyme borreliosis, has also seen an increase in incidence andrecent studies in the UK have suggested that up to 2% of adultticks biting dogs are likely to be infected with Lyme diseasespirochaetes. There are a range of tick borne pathogens thatare present in central Europe that have the potential to spreadto the UK, particularly if we import some of the tick vectors norcurrently established here. The risk of the latter has beengreatly increased by recent changes to the pet passport scheme.

Climatic conditions for other vector-borne diseases such asDirofilaria heartworm are also improving in the UK, and withcompetent mosquito vectors already present, increased dogmovement could lead to importation and establishment infuture. Parasitic diseases that are already endemic and havenon-arthropod vectors, such as canine angiostrongylosis, alsoappear to have increased in incidence and geographic rangewithin the UK in recent decades.

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The Future

Vector-borne diseases of animals remain considerably less wellresearched than diseases of human concern. Our veterinarydisease surveillance services are relatively poorly developed,especially for companion animals, and are currently beingeroded by economic cuts. We have limited data in the UK onthe distribution of most of our important vectors or vector-borne diseases, in part as a result of the difficulties in diagnosis.Hence, changes in distribution, particularly if subtle or at theearly stages of an epidemic curve, are hard to spot.

In the future, particularly pets are more likely to travel withtheir owners, making them more exposed to new pathogensfor which their owners may have little or no knowledge ofappropriate prophylaxis. What we do not know is whetherperceived increased disease incidence will also provoke changesin owner behaviours. Such changes might include alteredmanagement practices, as well as changes in their approach tochemical prophylaxis and reactive treatment. A change in theperception of disease risk may lead to changes in approach tointervention, with perhaps a greater willingness to treatprophylactically or to intervene with treatment earlier.

As a result, for the future, we need to establish more effectivesurveillance systems for most vector-borne diseases, to allowinformed risk analysis and the evaluation of the potentialspread to new areas or the new introduction of exotic speciesor diseases. This is particularly important given the risks linkedto climate change and changes in land use patterns. This willrequire a clear and exhaustive knowledge of the distribution of arthropod-borne diseases in different areas, monitoring ofnew strains or unrecognized disease agents transmitted byarthropods, continuous monitoring of insecticide resistance and the development of management strategies to minimise its onset.

Further reading

1. Beugnet, F. (2009) Emerging arthropod-borne diseases of companion

animals in Europe. Veterinary Parasitology, 163, 298-305

2. Gratz, N.G. (1999) Emerging and resurging vector-borne diseases.

Annual Review of Entomology, 44, 51-75.

3. Helm, J.R., Morgan, E.R., Jackson, M.W., Wotton, P. & Bell, R. (2010)

Canine angiostrongylosis: an emerging disease in Europe. Journal of

Veterinary Emergency and Critical Care, 20, 98-109

4. Jameson LJ & Medlock JM (2011) Tick surveillance in Great Britain.

Vector-borne & Zoonotic Diseases, 11, 403-41

5. Morgan, E.R. & Wall, R . (2009) Climate change and parasitic disease:

farmer mitigation? Trends in Parasitology, 25, 308-313

6. Morgan, E.R., Jefferies, R., Krajewski, M., Ward. P. & Shaw, S.E.

(2009) Canine pulmonary angiostrongylosis: The influence of climate

on parasite distribution. Parasitology International 58, 406-410

7. Parmesan, C. & Yohe, G (2003) A globally coherent fingerprint of

climate change impacts across natural systems. Nature, 421, 37-42

8. Pietzsch, M.E., Medlock, J.M., Jones, L., Avenell, D., Abbott, J.,

Harding, P. & Leach, S. (2005) Distribution of Ixodes ricinus in the

British Isles: investigation of historical records. Medical and Veterinary

Entomology, 19, 306-314

9. Randolph, S.E. & Rogers, D.J. (2010) The arrival, establishment and

spread of exotic diseases: patterns and predictions. Nature Reviews

Microbiology, 8, 361-371

10. Scharlemann, J.P.W., Johnson, P.J., Smith, A.A., Macdonald, D.W. &

Randolph, S.E. (2008). Trends in ixodid tick abundance and

distribution in Great Britain. Medical and Veterinary Entomology, 22,

238-247

11. Smith, F.D., Ballantyne, R., Morgan, E.R. & Wall, R. (2012) Estimating

Lyme disease risk using pet dogs as sentinels. Comparative

Immunology Microbiology and Infectious Diseases 35, 163-167.

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