Aspects of Equine Infectious Disease Control From the ... · against equine inﬂuenza virus among Thor-oughbred racehorses attending race meetings. The introduction and evolution

Aspects of Equine Infectious Disease ControlFrom the United Kingdom Perspective

J. Richard Newton, BVSc, MSc, PhD, DLSHTM, Diplomate ECVPH, FRCVS

Differences in approaches to the control of infectious diseases of horses exist between the UnitedKingdom and North America. Valuable lessons can be mutually learned to better understandrespective approaches. Adoption of novel methods of prevention and control that have proved usefulelsewhere in the world may have significant impacts on horse welfare. The examples of mandatoryinfluenza virus vaccination, use of voluntary Codes of Practice for infectious venereal diseases,increasing acceptance of the significance of the carrier state for strangles and parallel development ofdifferential diagnostics with the introduction of a new modified live strangles vaccine are used toillustrate a variety of different mechanisms by which improvements in equine disease control havedeveloped in the United Kingdom. Author’s address: Centre for Preventive Medicine, AnimalHealth Trust, Lanwades Park, Kentford, Newmarket, Suffolk CB8 7UU, United Kingdom; e-mail:[email protected]. © 2007 AAEP.

1. Introduction

The United Kingdom has periodically encounteredsignificant equine-disease outbreaks, which have inthemselves led to paradigm shifts in methods ofcontrol. A few notable examples are provided anddiscussed below.

● The introduction of mandatory vaccinationagainst equine influenza virus among Thor-oughbred racehorses attending race meetings.

● The introduction and evolution of the volun-tary codes of practice for equine infectious ve-nereal diseases.

● The increasing acceptance of the significanceof the carrier state in the endemic persistenceof equine strangles.

● The introduction of the first modified liveequine vaccine to Europe for the control ofequine strangles. This was followed by the

occurrence of clinical signs of strangles in asmall number of horses in the period aftervaccination, which presented a novel diagnos-tic challenge.

The examples provided here illustrate apparent geo-graphical and possibly cultural differences in ap-proaches to equine infectious disease problemsbetween the United Kingdom and the United States.However, with ever broadening cross linkages be-tween the equine and veterinary industries on theboth sides of the Atlantic, it is hoped that the ap-proaches outlined here will be of interest to and beadopted by a North American audience.

2. Mandatory Equine Influenza Vaccination

Among naı̈ve horses, equine influenza is a highlycontagious respiratory disease that is characterizedby pyrexia, associated depression and anorexia,

AAEP PROCEEDINGS � Vol. 53 � 2007 13

IN-DEPTH: MANAGING INFECTIOUS DISEASE OUTBREAKS AT EVENTS AND FARMS

NOTES

harsh dry cough, nasal discharge, and secondarybacterial respiratory infection. A novel H3N8equine influenza A virus subtype, which firstemerged in Miami, FL in 1963, initiated a worldwidepandemic of equine respiratory disease1 and was thestimulus for the development of multivalent, adju-vanted influenza vaccines for horses.2 This earlywork, based on experience from human vaccines, ledto the development of the now broadly standardizedschedules for equine influenza vaccination. Theseschedules recommend that a primary course of twodoses of vaccines be given �4–6 wk apart followedby a booster vaccination 6 mo after the end of theprimary course; annual boosters are recommendedthereafter. The same schedules are still used todayfor the product datasheet recommendations for thelatest inactivated virus vaccines and are the basisfor the regulatory rules for most internationalequine competitions.

It was recognized during several influenza out-breaks in the United Kingdom during the 1970s,especially in the 1979 outbreak,3 that vaccinatedhorses generally suffered less severe disease thanthose that were unvaccinated. Influenza vaccina-tion of Thoroughbred racehorses in Great Britainbecame mandatory under the Jockey Club Rules ofRacing at the start of the flat racing season in March1981, and it was implemented soon after in Irelandand France.

3. Jockey Club Rules on Influenza Vaccination

The first vaccination of the primary course is givenon day 0. The second vaccination of the primarycourse is given between 21 and 92 days (i.e., 3 wk–3mo) after the first vaccination. The third vaccina-tion of primary course (“6-mo booster”) is given be-tween 150 and 215 days after the second injection(i.e., 5–7 mo). Subsequent booster vaccinations aregiven at intervals of no more than 12 mo (“annualbooster”). No horse is permitted to race unless vac-cinated 7 or more days previously, and the primarycourse must be completed.

Since 1981, British racing has not been cancelledbecause of equine influenza, but there have beencontinued seasonal peaks of infection among unvac-cinated non-Thoroughbred horses that are associ-ated with increased mixing at shows in the summermonths. Because of the absence of systematic, con-sistent, and long-term surveillance data, it is notpossible to provide absolutely conclusive evidence ofthe true impact of mandatory influenza vaccinationon reducing the incidence of influenza virus infec-tion and associated disease. However, it is thewidely held belief of many that this is indeed thecase. There were markedly different financial andwelfare consequences of significant influenza out-breaks in Thoroughbreds in 2003 in Great Britainand South Africa in which mandatory vaccinationwas and was not, respectively, adopted. This high-lights the benefits of vaccination in horses at risk ofexposure to this highly contagious disease agent.

Details of these outbreaks of influenza that occurredin 20034 will be described later in this paper.

With changes in equine H3N8 influenza A virusescaused by antigenic drift, influenza outbreaks havecaused periodic disruption to the training schedulesof vaccinated Thoroughbreds in individual yards ortraining centers in the United Kingdom, whichbrings mandatory vaccination under periodic scru-tiny. However, investigations of these largely clin-ically mild and geographically limited outbreakshave permitted closer assessment of factors associ-ated with disease occurrence in vaccinated popula-tions.

Outbreaks of influenza virus infection amongracehorses vaccinated according to Jockey ClubRules were investigated in Newmarket in 19955 and19986 to establish reasons for vaccine failure. In-vestigations showed that, in 1995, horses were pro-tected from infection if they had antibody levelsabove a threshold equivalent to that observed inexperimental-challenge infections using nebulisedaerosol.5 Investigations in 1998 showed no suchprotective threshold.6 Subsequent characteriza-tion showed that the 1998 H3N8 virus was antigeni-cally distinct from the 1995 virus and thosecontained in available vaccines. These outbreakshighlighted the need for potent vaccines to maintainprotective antibody and inclusion of epidemiologi-cally relevant viral strains in vaccines.

Subsequent field vaccine studies were conductedto determine what factors might lead to inadequateantibody levels in Thoroughbreds.5 Investigationsshowed that yearlings receiving their third vaccinedose were protected for only a few months. Toavoid infection during the high-risk period of theautumn sales, they would require further strategicboosters. Subsequent studies confirmed that “timesince last vaccination,” “number of previous doses,”“age first vaccinated,” and “previous vaccine types”were all important antibody-level determinants inyoung racehorses entering training.7 Also, delay-ing the interval between two doses of a new primaryvaccine course in previously primed animals pro-vided more sustainable levels of protective anti-body.8 These findings have important implicationsfor optimal control of influenza by vaccination andare being used to inform strategic vaccination poli-cies.

However, a more recent outbreak in racehorses inthe United Kingdom did serve to confound some ofthe widely held beliefs regarding vaccine breakdownin young horses, and it again highlighted the bene-fits of detailed epidemiological and microbiologicalinvestigation.4

Between March and May 2003, equine influenzavirus infection was confirmed as the cause of clinicalrespiratory disease among both vaccinated and non-vaccinated horses in at least 12 locations in theUnited Kingdom. In the largest outbreak, at least21 Thoroughbred training yards in Newmarket, in-cluding �1300 racehorses, were variously affected;

14 2007 � Vol. 53 � AAEP PROCEEDINGS


horses showed signs of coughing and nasal dis-charge during a 9-wk period (Fig. 1).

An American sublineage H3N8 equine influenzavirus, previously not identified in the United King-dom, was responsible for the outbreak. Many in-fected horses had been vaccinated within theprevious 3 mo with a vaccine that contained repre-sentatives from both the American and Europeanlineages. On the basis of accepted criteria, theredid not seem to be significant antigenic differencesbetween the infecting virus and Newmarket/1/93,the American lineage virus representative in themost widely used vaccine,. Two-year-old horseswere apparently less susceptible to infection than3-yr-olds and older animals, despite broadly equiv-alent single radial hemolysis (SRH) antibody levels.This was consistent with qualitative rather thanquantitative difference in the immunity conveyed byvaccination.

However, multivariable analyses comparing in-fected and non-infected animals showed that theapparently counterintuitive inverse age effect wasexplained by elements in the vaccine history of theseanimals. Among factors in the vaccine history as-sociated with influenza infection, there was signifi-cantly increased risk of infection associated withmale gender, a primary course interval �92 days,and a period �3 mo since the last vaccination.

There was a significantly decreased risk of infectionassociated with increasing pre-infection antibodylevel and first vaccinating after 6 mo of age. Therewas also significant variation in risk according toboth the first and last type of vaccine administered.Findings highlight the benefits of relating vaccinehistory with risk of infection among vaccinatedhorses suffering influenza infection.

4. Introduction of the Horserace Betting Levy BoardCodes of Practice for Equine Infectious VenerealDiseases and Its Practical Application in DiseaseControl

The first Horserace Betting Levy Board (HBLB)Code of Practice was published for the 1978 breedingseason after an outbreak of contagious equine me-tritis (CEM) that had first been seen in the UnitedKingdom the previous year. In the 1977 outbreak,large numbers of Thoroughbred mares showed pro-fuse purulent vaginal discharge after mating, andmany studs were eventually forced to stop breeding.However, the disease had already spread, and therewas serious disruption and economic losses in theThoroughbred breeding industry.

The first code was heralded a great success; de-spite the severity of the requirements, which in-cluded swabbing mares three times at weeklyintervals before covering, high compliance was

Fig. 1. Training yards in Newmarket with confirmed equine influenza infection in spring of 2003 (red squares numbered in order inwhich the infection was detected). Blue lines represent horse walks linking different training grounds.



achieved. Only 7 cases were seen in 1978, and nonewere seen in the following season. This initial codeemphasized several important factors that are stillrecognized today for successful infection control andmaintenance. They emphasized the importance ofcareful hygiene measures when teasing, mating,and examining mares. The role of the veterinarianand stud handler in disease transmission wasbrought into sharp focus by this outbreak. Thepractice in Newmarket of “walking in” mares fromboarding studs to stallion studs, which was believedto have effectively propagated CEM, highlighted theimportance of honest and timely communicationsbetween all parties, particularly stud managers andveterinarians. The fastidious nature of the caus-ative organism and the care required to successfullyculture it led to the formation of a register of dedi-cated competent laboratories that subsequentlycame under the umbrella of the annual accreditationprocess. The phenomenon of the healthy carrierstate in mares, stallions, and teasers became recog-nized, and the elimination of these animals from thepopulation was achieved through application of theCodes of Practice.

The favorable impact of the first code for CEM,which also included disease caused by Klebsiellapneumoniae and Pseudomonas aeruginosa, subse-quently resulted in inclusion of disease control onequine herpesevirus (EHV) and equine viral arteri-tis (EVA) and guidelines on strangles (Streptococcusequi). Since this time, CEM and EVA have becomeregulated diseases in the United Kingdom, and ondiagnosis or suspicion, these cases are compulsorilyreferred to the national veterinary authorities, whotake on the responsibility of implementing control.An expert subcommittee was also formed, whichnow meets each year to review and update the rec-ommendations as needed in light of new scientificknowledge or practical experience like outbreaks.Each year, the codes are widely distributed to Thor-oughbred and non-Thoroughbred breeders and vet-erinarians. They can also be downloaded in PDFformat from the HBLB’s website (http://hblb.org.uk/sndFile.php?fileID�%203) and are freely availablefrom the Board, the Thoroughbred Breeders’ Asso-ciation, and the British Horse Society.

5. Codes of Practice and EVA in Europe

The annually updated Codes of Practice continue tobe the practical means by which prevention of EVAis implemented in the United Kingdom, and it isdone particularly but not exclusively by the Thor-oughbred breeding industry. This is based on an-nual pre-breeding serological screening of bothstallions and mares and uses a killed vaccinea installions. This approach has to date been proven tocontrol disease on at least two occasions when pre-viously infected mares have been detected after sub-clinical outbreaks among Thoroughbreds in Francein 2000 and Ireland in 2003. It highlights the im-portance of serosurveillance to detect infected ani-

mals in the absence of clinical signs. This hassubsequently led to heightened control measuresamong imported animals on some U.K. Thorough-bred stud farms.

In the event that EVA is confirmed, the Code ofPractice recommends that the local Divisional Vet-erinary Manager of the Department for the Environ-ment, Food, and Rural Affairs (DEFRA) beimmediately notified in accordance with the EVAOrder 1995. In addition, all movements and breed-ing is stopped, all cases and contacts are traced,sampled, and isolated, and all other horses on theaffected premises are screened and grouped accord-ing to infectious status. It is also important thatgood communication exists between interested par-ties including those that have received animals (andsemen if relevant) from the infected stud, those thatare planning to send animals, and those in thebreeder’s association. Testing and screeningshould continue on all possible affected premisesuntil the end of the outbreak; seropositive animalsand pregnant mares should be isolated for 4 wk afterfirst sampling, and stallions must have their shed-ding status investigated. Serosurveillance is usedon stallions vaccinated using Artervac, the onlykilled virus vaccine for equine arteritis virus (EAV)available in Europe. This testing shows thatachievement and maintenance of the immunity re-quired to protect against developing semen sheddingrequires stallions to have several boosters in addi-tion to the 2–3 dose primary course (Fig. 2). Thisindicates that many first-season sires are probablyinadequately protected against EVA infection by useof killed vaccine. This could be overcome by vacci-nation and subsequent boosting of potential stal-lions while they are still racing.

This was particularly highlighted in the 2003breeding season when there were problems withavailability of Artervac in Europe. The conse-quence of this was that first-season sires were leftcompletely susceptible to EAV infection, whereaspreviously well-vaccinated stallions had good levelsof residual immunity that was evidenced by highvirus-neutralization (VN) antibody levels. The out-break in Ireland resulted in infection of a first-sea-son sire, which did not subsequently shed virus in itssemen.

The most important aspect of control programsafter an outbreak of EVA has been traced to a studis to stop covering immediately. If a stallion is notinfected, then attempts must be made to preventinfection of all stallions. If a stallion has alreadybeen infected, then the most efficient means of main-taining the spread of the infection around the studmust be used. The rates of infection on the indexstud in the 1993 outbreak in the United Kingdom9

closely followed the rate of covering in the precedingweek (Fig. 3).

All horse and semen movement should be stoppedon and off the stud, and recently departed animalsshould be traced, placed in isolation, and tested.



The control of outbreaks of EVA can be based on thefact that virus is most unlikely to be present in thehorses (other than stallions) for �3 wk after expo-sure. It is sometimes impossible to determine theprecise day of infection during an outbreak. Thus,horses should be kept in isolation for at least 3 wkafter their first positive blood test. By then, theyare likely to be free from infection. Because EVAusually spreads poorly between animals through therespiratory route, it should be possible to stop thespread of infection around a stud after covering hasceased.

6. Codes of Practice and EHV in Europe

Although spontaneous abortion cannot be com-pletely prevented because of EHV-1, there is muchthat can be done through sensible management, hy-giene, and vaccination to reduce its incidence and tolimit the spread of EHV-1. This will prevent so-called abortion storms and the dreaded paralyticform of the disease that, in the past, accompaniedsome severe abortion outbreaks; more recently, ithas been affecting groups of non-pregnant sportshorses. The HBLB’s Code of Practice outlines

these recommendations for the prevention and con-trol of EHV-1 disease on studs.

● Mares should be foaled away from the stallionstud wherever possible.

● If this is not possible, then pregnant maresshould be kept in small groups and isolatedfrom possible high-risk contact groups such asweanlings, yearlings, and horses out of train-ing.

● Pregnant mares, especially in the later stagesof pregnancy, should not be stressed or trans-ported with other horses.

● Foster (nurse) mares should be isolated, espe-cially from pregnant mares, until it is estab-lished that her own foal did not die fromEHV-1 related disease.

● Sensible and regular hygiene practices shouldbe adopted, preferably with pregnant mareshaving a dedicated staff.

● The adoption of a vaccination program againstEHV-1 is strongly recommended, but it mustbe emphasized that this will not necessarilyprotect all vaccinated mares from abortion andis not a substitute for good management andhygiene.

● Vaccination at 5, 7, and 9 mo of gestation isrecommended in accordance with the manu-facturer’s recommendations to reduce (but noteliminate) the risk of abortion storms.

If disease occurs in the stud and EHV-1 is a pos-sible cause (abortion, neonatal foal death, paralysis,etc.), then control measures need to be implementedimmediately even before the diagnosis is confirmed.

● Veterinary advice should be sought.● The mare (and foal) should be isolated.● The fetus and placenta should be sent to the

laboratory.● Movements on and off the stud should be

stopped immediately.● Owners of mares planning to visit the pre-

mises should be notified.

Fig. 2. EAV virus-neutralization (VN) serological status of 108 stallions measured between 320 and 400 days after last vaccinationusing a killed virus vaccine. (A) log10 titer versus number of previous boosters. (B) Proportion with protective titers (�1.9 log10)versus number of previous boosters.

Fig. 3. Numbers of new EVA cases and coverings on the indexstud in the 1993 U.K. EVA outbreak.



Laboratory results are needed to confirm a diag-nosis of EHV-1.

If results confirm EHV-1, isolation and movementrestrictions should be maintained for at least 1 moafter the last case of disease or until extensive lab-oratory testing shows absence of on-going active in-fection.

Mares in contact with the affected animals shouldbe isolated in small groups until after they havefoaled to limit the transmission of EHV-1 shouldfurther disease occur.

The breeder’s association and the owners of horsesthat have left, that are still resident, or that areplanning to visit the premises should be notified.

7. Successfully Managing Equine Strangles

Infectious diseases pose a considerable threat to thesmooth running of any equine premises, and theserisks are, in general, proportionally greater for largepremises than for smaller operations. Of all equineinfectious diseases, strangles can be particularlyproblematic, because it may lead to considerablelong-term problems for infected premises. Addi-tionally, the stigma associated with the disease maypersist long after the infection has been eliminated.Strangles has the ability to become endemic, partic-ularly on studs,10 and its regular recurrence over anumber of years frequently coincides with the newcrop of susceptible weaned offspring. It is impor-tant that horse owners and their veterinarians rec-ognize strangles as early as possible and thatappropriate means of control are implemented.

Strangles in horses is caused by infection with thebacterium Streptococcus equi, and typical signs arepyrexia, anorexia, soft cough, purulent nasal dis-charge, and swollen lymph nodes of the head thatfrequently abscessate and discharge pus. In someoutbreaks, the largely pathognomonic sign of lymph-node abscessation may occur only in later cases ormay not be evident at all. To maximize the chanceof effective containment and control, it is importantthat a diagnosis of strangles is made as early aspossible, even in horses that may not be showingclassic signs. This is best achieved by culture andidentification of the S. equi bacterium on appropri-ate samples by a specialist bacteriology laboratorythat has experience in the typing of specific strepto-coccal species. The optimal chance of confirmingthe diagnosis may be achieved if samples of aspi-rated pus, swabs from discharging abscesses, andswabs of the nasopharynx are each submitted fromas many suspect cases as possible. A negative re-sult for one nasal swab from a single horse, forexample, should not be taken as assurance that S.equi is not involved, and it is always wise to followthe general rule of thumb that “if it looks like stran-gles, then treat it as strangles.”

The cornerstone of control of any infectious dis-ease is prevention of transmission of the causativeorganism from infectious to susceptible animals,and this can only be effectively achieved when con-

trol measures are based on a thorough understand-ing of the epidemiology of the disease. In stranglesoutbreaks, purulent discharges from clinical and re-covering cases are an extremely important and eas-ily visible source of infection. It is important thatall measures are taken to prevent both direct andindirect transfer of these discharges between af-fected and susceptible horses. Direct transmissionhere refers to horse to horse contact, whereas indi-rect transmission can be achieved by sharing of wa-ter sources, feeding utensils, tack, equipment, andother less obvious transmitters such as handlers,farriers, and veterinarians as well as their hands,clothing, and equipment.

Because it is harder to identify sources of infec-tion, transmission that originates from outwardlyhealthy horses is of greater importance. Categoriesof outwardly healthy horses that are potentially in-fectious for S. equi include those horses that areincubating the disease and go on to develop signs.It is still not clear for how long horses can be infec-tious while incubating the disease before they de-velop obvious outward signs, and it is assumed thatnormal nasal secretions are the source of infection inthese animals. The other important category ofasymptomatic horses that are potentially infectiousto other animals are those recovered cases that con-tinue to harbor the organism after clinical signs ofdisease have cleared up. There is evidence that amoderate proportion of horses continue to harbor S.equi for several weeks after clinical signs have dis-appeared, but in the majority of horses, the organ-ism is no longer detectable 4–6 wk after totalrecovery.11 It is, therefore, sensible to considerthat all recovered horses may be a potential sourceof infection for at least 6 wk after their purulentdischarges have dried up. However, there is grow-ing evidence that in a small but important propor-tion of recovered cases of strangles, carriage andperiodic shedding of S. equi continues for manymonths and in some cases, even years after appar-ent full and uncomplicated recovery.11-14 Thesehorses are referred to as long-term, asymptomaticstrangles carriers, and there is strong anecdotal ev-idence that they can be a significant source of newoutbreaks, even in well-managed groups of horses.If control measures are to be fully effective, theremust be recognition of the importance of this cate-gory of animal, and appropriate detection and man-agement of them should be adopted in a disease-control strategy.14,15 Although there have beenperiodic references in the scientific literature to thecarrier state for strangles, it has really only been inthe past 15 yr that this has been more widely ac-cepted as the most fundamental factor in the en-demic persistence of S. equi in equine populations.Only targeted identification and resolution of theinfection in these animals can effectively act to bringpreviously recurrent disease under control.

Veterinary investigation of a strangles outbreakon affected premises should begin with a detailed



history through interview with the owners. Thisallows the full extent of the problem, which mayactually extend back several years, to be evaluated.Review of the background to the outbreak shouldidentify affected groups of horses and allow the ge-ography of the premises and the management prac-tices adopted to be examined. The next stage is toagree on and implement a practical disease-controlstrategy. The general aims and measures for sucha strategy are outlined in Table 1.14 This outlinestrategy must be adapted to the individual circum-stances of each specific premise and outbreak.

In summary, all movements of horses on and offthe affected premises should be stopped, and paral-lel segregation and hygiene measures should be im-plemented immediately. Cases of strangles andtheir contacts should be maintained in well-demar-cated “dirty” quarantine areas. The aim of the con-trol strategy is to move horses from the “dirty” to“clean” areas where non-affected and non-infectioushorses are maintained after bacteriological screen-ing. Every care should be taken to maintain highhygiene standards throughout the premises and forthe duration of the investigation. Screening of allconvalescing cases and their healthy contacts shouldbe conducted using nasopharyngeal swabbing or la-

vage. Swabs are taken at weekly intervals overseveral weeks and are tested for S. equi by conven-tional culture and identification techniques. Sensi-tivity for detection of S. equi is improved if swabs orlavage samples are also tested by polymerase chainreaction (PCR) test.14 Because PCR has the abilityto detect dead as well as living bacteria, positivePCR results should only be considered as provisionalpositives subject to further investigation. It hasbeen found that the vast majority of asymptomatic,long-term strangles carriers harbor S. equi in theguttural pouches in association with grossly visiblepathology. Therefore, endoscopy of the upper re-spiratory tract and guttural pouches should be per-formed in all outwardly healthy horses in which S.equi is detected, either by culture or PCR. Lavagesamples from guttural pouches should be tested forS. equi by culture and PCR. S. equi infection andpathology, which range from slight empyemathrough to multiple chondroids and severe empyemain one or both guttural pouches, may be successfullyeliminated without the need for referral or hospital-ization,15 but the intensity and cost of treatment isdependent on the extent of pathology involved.Experience suggests that repeated use of an endo-scopic helical retrieval basket in conjunction with

Table 1. Summary of Aims and Measures to Control Transmission of S. equi on the Stud

Aim Control Measure

1 Prevent spread of infection tohorses on other premises andto new arrivals on theaffected stud farm.

All movement of horses on and off the stud should be stopped immediately until furthernotice.

2 Establish whether horses areinfectious in the absence ofclinical signs of strangles(asymptomatic carriers).

All recovered cases and contacts have at least three nasopharyngeal swabs taken atapproximately weekly intervals and tested for S. equi by culture and PCR.

3 Determine if horses arelikely to be free frominfection with S. equi (non-infectious).

Three consecutive swabs are negative for S. equi by culture and at least the third swab ofthe series is also negative by PCR.

4 Determine if horses arelikely to be harbouring S.equi (infectious).

S. equi is cultured or detected by PCR on any of the screening swabs.

5 Isolation of infectious horsesfrom those screened negativefor S. equi.

Infectious horses are maintained in so-called “dirty” isolation areas which are physicallycordoned from the other “clean” areas of the stud where non-infectious horses are kept.Clustering of cases in groups may allow parts of the stud to be easily allocated as“dirty” and “clean” areas.

6 Prevent cross infection fromhorses in the “dirty” area tothose in the “clean” area ofthe premises.

Potentially infectious horses in the “dirty” area are preferably looked after by dedicatedstaff or are dealt with after non-infectious horses in the “clean” area. Strict hygienemeasures are introduced including provision of dedicated clothing and equipment foreach area, disinfection facilities for personnel and thorough stable cleaning anddisinfection methods.

7 Monitoring of horses in the“dirty” areas for persistenceof S. equi infection andestablishment of sites ofcarriage.

Nasopharyngeal swabbing is continued with endoscopic examination of the upperrespiratory tract including guttural pouches in those horses in which S. equi wasisolated after clinical signs had disappeared. Horses that satisfy the non-infectiouscriteria of measure 3 above are returned to the “clean” area.

8 Elimination of gutturalpouch inflammation and S.equi infection

Removal of pathology through a combination of flushing and aspiration of saline andremoval of chondroids using endoscopically guided instruments. Topical and systemicadministration of penicillin antimicrobial treatment to eliminate S. equi infection.



topical and systemic administration of penicillin an-timicrobial therapy is appropriate for even the mostrefractory cases.

8. Investigating Strangles Post-Vaccination

The first strangles vaccine to be licensed in theUnited Kingdom was a modified-live stranglesvaccine16b that became available in 2004. Al-though clinical signs in horses apparent within sev-eral days of vaccination might seem like an adversereaction to the vaccination, the possibility of concur-rent natural infection with wild-type S. equi alsoneeds to be considered.

In response to several suspected adverse reac-tions, several differential diagnostic methods havebeen developed and successfully applied.17 Theseinclude (1) PCR to differentiate vaccine from field S.equi strains (Fig. 4), (2) DNA sequencing to rule outpossible reversion to virulence of the vaccine strain,and (3) DNA sequencing of M-protein regions tosubtype and differentiate S. equi strains.

One horse developed pyrexia and painful subman-dibular lymph-node swelling 7 days post-vaccina-tion, and vaccine-strain S. equi was isolated fromthe nose at that time. Field-strain S. equi was sub-sequently isolated from the discharging lymph node.DNA sequencing confirmed that the field strain didnot occur through recombination with S. zooepi-demicus, and the M protein was different from thatof the vaccine strain. In another incident, a foaldeveloped parotid lymph-node abscessation aftervaccination, and S. equi was isolated. Shortly af-terwards, a nearby non-vaccinated horse also devel-oped clinical signs of strangles, and S. equi wasisolated from mucopurulent nasal discharge. PCRand DNA sequencing applied to these isolatesshowed that they were both field strains that did notcome from recombination with S. zooepidemicus;again, these cases were not caused by infection withvaccine S. equi strains. Further investigationssubsequently identified an infected carrier fromwhich field-strain S. equi was isolated. M-protein

sequencing showed that this “carrier” isolate wasidentical to that isolated from the non-vaccinatedcase with the nasal discharge. Other investiga-tions have subsequently identified a few cases ofstrangles in which the vaccine strain has been iso-lated in pure culture from abscessed lymph nodes,and it was associated with administration of thevaccine in accordance with the manufacturer’s rec-ommendations. Therefore, there is limited poten-tial for the vaccine strain to cause disease.

This work highlights the discriminatory potentialprovided by modern molecular techniques. In as-sessing strangles-like clinical presentations post-vaccination, consideration should be given to twopossibilities: modified live vaccines being responsi-ble for clinical disease or carriers contributing to S.equi persistence.

9. Concluding Remarks

The limited examples provided above are intendedto illustrate the variety of different mechanisms bywhich improvements in disease control may be in-troduced and subsequently, evolve. This rangesfrom the introduction of a mandatory vaccinationprogram, which within the defined sector of Thor-oughbred racing has been able to be effectively po-liced through the use of equine passports, to thevoluntary codes of practice, which through wide-spread compliance continue to achieve their in-tended aims. However, delayed recognition of theimportance of other significant epidemiological fea-tures, such as strangles carriers, has consequentlytaken longer to bring improvements in disease-con-trol measures, although there has been progress onthis front. Finally, the application of sensitive mo-lecular techniques in diagnostic applications is im-proving our understanding of disease investigationand control.

References and Footnotes1. Anon. The 1963 equine influenza epizootic. Journal of the

American Veterinary Medical Association 1963;143:1108.2. Bryans JT, Doll ER, Wilson JC, et al. Immunisation for

equine influenza. Journal of the American Veterinary Med-ical Association 1966;148:413–417.

3. Burrows R, Goodridge D, Denyer M, et al. Equine influenzainfections in Great Britain, 1979. Veterinary Record 1982;110:494–497.

4. Newton JR, Daly J, Spencer L, et al. Description of the 2003UK equine influenza (H3N8) outbreak, during which recentvaccination failed to prevent signs of respiratory disease inracehorses in Newmarket. Veterinary Record 2006;158:185–192.

5. Newton JR, Townsend HGG, Wood JLN, et al. Immunity toequine influenza: relationship of vaccine-induced antibody inyoung Thoroughbred racehorses to protection against fieldinfection with influenza A/equine-2 viruses (H3N8). EquineVeterinary Journal 2000;32:65–74.

6. Newton JR, Verheyen K, Wood JLN, et al. Equine influenzain the United Kingdom in 1998. Veterinary Record 1999;145:449–452.

7. Newton JR, Lakhani KH, Wood JLN, et al. Risk factors forequine influenza serum antibody titres in youngThoroughbred racehorses given an inactivated vaccine.Preventive Veterinary Medicine 2000;46:129–141.

Fig. 4. S. equi from a discharging abscess that generated anaroA PCR product of 1364 bp (lane 2) compared with an aroA genePCR from the vaccine strain that yielded a 432-bp product (lane3); lane 1 is a DNA ladder.



8. Newton JR, Texier MJ, Shepherd MC. Modifying likelyprotection from equine influenza vaccination by varyingdosage intervals within the Jockey Club Rules of Racing.Equine Veterinary Education 2005;17:314 –318.

9. Wood JLN, Chirnside ED, Mumford JA, et al. First recordedoutbreak of equine viral arteritis in the United Kingdom.Veterinary Record 1995;136:381–385.

10. Holland RE, Harris DG, Monge A. How to control stranglesinfections on the endemic farm. Proceedings of the Ameri-can Association of Equine Practitioners 2006;52:78–80.

11. Newton JR, Wood JLN, De Brauwere MN, et al. Detectionand treatment of asymptomatic carriers of Streptococcus equifollowing strangles outbreaks in the UK. In: Proceedings ofthe 8th International Conference on Equine Infectious Dis-eases, Dubai 1998. Eds., U Wernery, JF Wade, JA Mumfordand O Kaaden. R&W Publications, 1999; pp. 82–87.

12. Newton JR, Wood JLN, Dunn KA, et al. Naturally occurringpersistent and asymptomatic infection of the gutturalpouches of horses with Streptococcus equi. Veterinary Record1997;140:84–90.

13. Newton JR, Wood JLN, Chanter N. Strangles: long termcarriage of Streptococcus equi in horses. Equine VeterinaryEducation 1997;9:98–102.

14. Newton JR, Verheyen K, Talbot NC, et al. Control of stran-gles outbreaks by isolation of guttural pouch carriers identi-fied using PCR and culture of Streptococcus equi. EquineVeterinary Journal 2000;32:515–526.

15. Verheyen K, Newton JR, Talbot NC, et al. Elimination ofguttural pouch infection and inflammation in asymptomaticcarriers of Streptococcus equi. Equine Veterinary Journal2000;32:527–532.

16. Jacobs AA, Goovaerts D, Nuijetn PJ, et al. Investigationstowards an efficacious and safe strangles vaccine: submuco-sal vaccination with a live attenuated Streptococcus equi.Veterinary Record 2000;147:563–567.

17. Kelly C, Bugg M, Robinson C, et al. Sequence variation ofthe SeM gene of S. equi allows discrimation of the source ofstrangles outbreaks. Journal of Clinical Microbiology 2006;44:480–486.

aArtervac, Fort Dodge Animal Health, Fort Dodge, IA 50501.bEquilis StrepE, Intervet International B.V., 5831 AN

Boxmeer, The Netherlands.



Documents

Aspects of Equine Infectious Disease Control From the ... · against equine inﬂuenza virus among Thor-oughbred racehorses attending race meetings. The introduction and evolution