Influensautbrottet i Sverige 2007

Intervet AB 

Box 123 

182 12 Danderyd 

Tel 08 - 775 76 50 

www.intervet.se 

INTERVET SYMPOSIUM - Med fokus på hästinfluensan 2007 

INTERVET SYMPOSIUM 

Med fokus på hästinfluensan 2007 

Stockholm Göteborg Malmö 

Solvalla 16/10 Åby 17/10 Jägersro 18/10 

Influensautbrottet i Sverige 2007 

Gittan Gröndahl och Maria Eriksson, SVA 

EquiFluNet och internationella rekommendationer 

Louise Treiberg Berndtsson, SVA 

Influensautbrottet 1993 

– Historik och vad lärde vi oss av detta? 

Peter Forssberg, STC 

Paneldebatt/frågestund 

Föredragshållarna samt 

Stig Hägglund, STC 

Solvalla 16 okt - Åby 17 okt - Jägersro 18 okt


Solvalla 16 okt - Åby 17 okt - Jägersro 18 okt


Program 

INTERVET SYMPOSIUM – 


18.45-19.30 Influensautbrottet i Sverige 2007 

(Gittan Gröndahl och Maria Eriksson, SVA) 

19.30-19.50 EquiFluNet och internationella rekommendationer 

(Louise Treiberg-Berndtsson) 

19.50-20.00 Bensträckare 

20.00-20.20 Influensautbrottet -93 

– Historik och vad lärde vi oss av detta? 

(Peter Forssberg, STC) 

20.20-21.00 Paneldebatt/frågestund 

(föredragshållarna samt Stig Hägglund, STC) 

Equilis ® Prequenza 

Antigen 

→ Subenhetsvaccin 

Adjuvans 

→ ISCOM-Matrix 

Vaccinets skyddande effekt visat 

→ Challenge mot både Nm/05/03 

och SA/04/03 

Förpackningar 

→ Sprutor eller ampuller, båda med 

peel off-etikett 

Solvalla 16/10 - Åby 17/10 - Jägersro 18/10



• Varför fick detta utbrott så stor spridning? 

• Var startade det, och hur/var skedde spridningen? 

• Typ av hästar som drabbades, vaccinationsstatus på 

drabbade? 

• Vad kan vi göra för att förhindra ett liknande utbrott i framtiden? 

• Vad lärde vi oss vi förra stora utbrottet -93? 

• Orsaken till att vaccinationsobligatoriet inom travet upphävdes? 

• Kommer regler/rutiner att ändras, vad händer/gäller utomlands? 

• Hur fungerar det globala nätverket för övervakning av 

hästinfluensa? 

• Hur väljs vaccinstammar ut, hur görs uppföljningar? 

Hästinfluensa… 

Varför ska vi vaccinera..? 


Resultat från studien som ges i denna 

presentation är preliminära. 

För slutgiltiga siffror och resultat hänvisas till 

kommande publikation i 

Svensk Veterinärtidning. 

Oktober 2007 

Gittan Gröndahl 

Epidemin av 

hästinfluensa stinfluensa 

i Sverige 2007 

Gittan Gr Gröndahl dahl, tf statsveterinär, VMD 

Maria Eriksson, vet stud 

SVA, 2007 

Sedan 1980talet: 

Europeisk 

variant 

Amerikansk 

variant 


Hästinfluensa 

orsakas av 

influensavirus av 

olika subtyper 

även 

Sydamerikansk 

variant 

Sydafrikansk 

variant 

© Tf statsvet Gittan Gröndahl, SVA 


Hästinfluensans utbredning 

• A1: inte sedan 1979 

• A2: nya varianter 

• Hästinfluensa förekommer i Sverige årligen 

• Mer epidemiskt vissa år 

• De flesta länder har h ästinfluensa 

• Nya Zeeland och Island fria 

• Australien var fritt tills augusti 2007 

Australiens utbrott 2007 

• Första fallet augusti 2007 

• Tidigare fritt land, 

inga vaccinerade hästar 

• Kraftig spridning på en månad: 

2653 Infected Properties, 

323 Dangerous Contact Properties and 

356 Suspect Properties. (070928) 

• Mål: utrota EI inom 6 månader 

45 

40 

35 

30 

25 

20 

15 

10 

5 

0 

1997 199819992000200120022003200420052006 


Svenska rapporterade utbrott till 

Jordbruksverket 1997-2006 


1 ”utbrott”= 

första fallet, 

men kan vara 

många hästar 

drabbade 



Symptom på hästinfluensa 

Symptom på hästinfluensa A2 

• OBS: Vaccinerade hästar får lindrigare 

symtom – om de över huvudtaget får 

symtom. Sprider mindre mängd virus, och 

återhämtar sig snabbare än ovaccinerade 

Isoleringsrekommendationer 

vid influensa 

• Stallet isoleras 10 dagar efter 

senaste insjuknade hästs 

första febertopp 

OBS - Spridningen av smitta kan begränsas 

om man har m öjlighet att separera/isolera 

den först insjuknade hästen i stallet 




Stor svensk epidemi av 

hästinfluensa 2007 

• Spreds från södra Sverige i januari 2007 

• Nådde hela Sverige, jan jan-juni juni 2007 

• Mest travstallar drabbade, 

inkl de flesta banor 

• 2 unga h ästar akut döda i sviterna 

• Bristande vaccination, åsidos sidosättande ttande av 

smittskyddsregler, mörkande? 

Travronden rapporterade om A2 

• [070924]: Kriterieauktionen direktsänds 

• [070613]: V64-trippel för Kari 

• [070613]: Den nye Gidde... 

• [070613]: V64: Formkusk ligger lågt 

• [070605]: Fler A2-sjuka på Solvalla 

• [070604]: A2 på Solvalla 

• [070509]: Smittoläget 

• [070507]: Misstänkt A2 hos Svensson 

• [070426]: A2-nytt 

• [070420]: Russel, Chaplin och USA-importer 

• [070418]: Ännu mera A2 

• [070417]: Peter Forssberg om A2-influensan 

• [070417]: Nurmos-stall isolerat 

• [070417]: Misstänkt A2 i Boden 

• [070403]: A2 på Vermo 

• [070326]: A2 även på Romme 

• [070325]: "I påsk vill jag vara med igen" 

• [070321]: Konstaterad A2 i Gävle 


• [070320]: Gävle-stall A2-isolerade 

• [070314]: Hallå där Charlotta B... 

• [070305]: Inbrott hos Turja igen 

• [070301]: Nya fall av A2-virus 

• [070220]: "Det måste gå fort i början" 

• [070216]: Laursens överl ägsna 101-oddsare 

• [070210]: Heiskanen tränare i Italien 

• [070206]: Återbud från Adielsson 

• [070123]: A2-läget stabiliserat 

• [070119]: A2-läget: inga nya fall idag 

• [070118]: A2-läget just nu 

• [070117]: Dags för vaccinationstvång? 

• [070117]: Två hästar döda på Axevalla 

• [070116]: Per ställer in Axevallapremiären? 

• [070115]: A2 på Axevalla 

• [070104]: A2 i Skaratrakten 

• [061209]: Champagne i Århus 



Det påstås att……. 

• ”Vaccinerade hästar blir också sjuka och det 

pågår mycket, mycket l ängre än hos 

ovaccinerade” (Travronden blogginlägg av Pelle, april 2007) 

• ”Att vaccinera är att spruta in sjukdom i kroppen 

(…) och vilken idrottsman gör det frivilligt?” (Pelle 

igen) 

• ”Det är bättre att hästarna blir ordentligt sjuka så 

man inte råkar missa det och startar en 

vaccinerad häst som bara är lite sjuk i influensa, 

för då kan den få allvarliga komplikationer” (en av 

våra svarare) 

Studie av epidemin av 

hästinfluensa i Sverige 2007 

• Oberoende studie vid 

Statens veterinärmedicinska anstalt (SVA) 

• Stöd från SVAs Forskningsfond 

Syfte med studien 

• Vilken typ av hästar drabbades? 

• Blev hästarna sjuka trots att de var 

vaccinerade? (ny virusstam/dåliga vaccin) 

• Eller var det ovaccinerade h ästar som 

framför allt blev sjuka? 

• Skyddade vaccin mot sjukdom/gravare 

sjukdom? 

• Kan rutiner förbättras? 


Underlag: 

Studie av epidemin av 

hästinfluensa i Sverige 2007 

• 68 rapporter vid SVA om positiva influensaprover 

från ca 100 hästar januari-juni 2007 

• Känt att hästinfluensan drabbade 

Sveriges 32 travbanor/regioner enligt följande: 

3/3 storbanor, 8/11 mellanbanor och 13/18 

sm åbanor, totalt 24 st. 

• Mörkertal antal drabbade banor? 

• Varje banregion innefattar många tränare 

Januari: 

Axvall, Aneby, 

Hishult 

Tävling Axevalla 16/1 

under isoleringen och 

3 hästar dör – Åby, 

Mantorp och Jä gersro 

isolerar dagarna efter. 

Virus sprider sig över 

landet….. 

Februari: 

Hammarö, Visby, 

Vårgårda, 

Borensberg, 

Uppsala 

Färjestad o Visby 

isolerar, tävling på 

Färjestad 19/2 

Mars: 

Sala, Järvsö, 

Borlänge, St Skedvi, 

Skattkärr, Saxdalen, 

Glanshammar, Gävle, 

Helsingborg 

Tävling Gävle 20 och 27/2 

under isoleringen. 

Hagmyren ställer in. 

Romme isolerar också. 


Bollnäs, Rättvik, 

Romme, Dannero, 

Solänget, Åmål, 

Skellefteå, Boden, 

Oviken, Halmstad, 

Örebro, Solvalla 

isolerar. 

Finland också A2. 

April: 

Orsa, Rättvik, Tumba, 

Örebro, Boden, Halmstad, 

Edsvalla, Eskilstuna, 

Nossebro, Haparanda, 

Älandsbro, Lindesberg, 

Edsbyn, Åmål, Borlänge, 

Näsviken, Ljungbyhed, 

Bollnäs, Eskilstuna, St 

Skedvi, Kimstad, Norberg 

Insamlingsresultat 

Örebro, Åby, Åmål, 

Skellefteå, Solvalla 

isolerar. 

Finland också A2. 

Maj: 

Tävelsås, Västerljung, 

Söderköping, Linkö ping, 

Skinnskatteberg, 

Enköping, Säffle, St 

Anna, Strömsholm, 

Örebro, Nordingrå 

• 45 av SVA-positiva hästhållare kunde kontaktas 

varav enkätsvar erhållits från 19 st. 

• 13 drabbade travbanor kontaktades. 

Svar från 8: Axevalla, Färjestad, Visby, Romme, 

Örebro, Lindesberg, Solvalla samt Halmstad. 

Inget svar från: Mantorp, Åmål, Rättvik, Gävle, 

Hagmyren och Boden. 

• 63 stallar med 773 hästar analyserade 


Enkätfrågor 

• Sjuka och friska hästars namn, ålder, 

kön, ras, träningsstatus 

• Datum för senaste 2 vaccinationer 

mot hästinfluensa 

• Tidigare sjuk i influensa 

• Temperaturkurvor under utbrottet 

• Antal dagar med hosta +/- näsfl öde 

• Antibiotikabehandlingar 

Subjektiva uppfattningar 

”Var smittades dina hästar tror du?” 

• Många svarar: 

”- På travtävlingar för 2-3 dagar sedan” 

• Jägersro, Mantorp 2/1, Axevalla, 

Gävle 12/3, Romme 16/3 + 16/4, 

Rättvik 26/3, Dannero 15/4 

omnämns t ex 


Kriterier i studien 

• Adekvat vaccinerad = Grundvacc 2 ggr 

eller revacc inom 1 år tillbaka 

• Ej adekvat vaccinerad = Vaccinerad 

men ej som ovan 

• Ovaccinerad = Ingen vacc eller endast 

1 vacc för mindre än 2 veckor sedan 


87% 

Kriterier i studien 

• Feber = Temperatur =38,3°C 

• Hosta, näsflöde = Enl hästhållaren 

• Sjukdomsgrad: 

lindrig = feber i 1 -2 dagar 

måttlig = feber i 3-4 dagar 

kraftig = feber i 5 dagar eller mer 

• Tävlingskondition = Har nyligen startat 

el ska starta i travlopp 

Svar från 63 stallar med 

totalt 773 friska och sjuka hästar 

Tävlingskondition: 233/293 hästar (80%) 

Rasfördelning 

Andel 

20% 

15% 

10% 

5% 

0% 

6% 

3% 

3% 

1% 

Varmblod 

Kallblod 

Ponny 

Halvblod 

Okänt 

23% 

0 – 29 år 

Medelålder = 4,9 år (±3,2) 

0 år 

1 år 

2 år 

3 år 

4 år 

5 år 


Ålder 

35% 

Könsfördelning 

1% 

41% 

Åldersfördelning i hela materialet 

6 år 

7 år 

8 år 

9 år 

10+ år 

okänd 

Ston 

Valacker 

Hingstar 

Okänt 


40,5 

40 

39,5 

39 

38,5 

38 

37,5 

37 

36,5 

2007-01- 

08 


13 

Vaccinationsstatus – 

känt för 530 hästar (friska och sjuka) 

• Ovaccinerade: 213 st (40%) 

• Adekvat vaccinerade: 169 st (32%) 

• Ej adekvat vaccinerade: 148 st (28%) 

• För 1/3 av hästarna visste inte tränarna om 

de var vaccinerade eller inte (243 st) 

• 7% (21/318 svar) hade haft influensa förut 

30% 

25% 

20% 

15% 

10% 

5% 

0% 

Åldersfördelning (friska+sjuka) 

per vaccinationskategori 

Tränare A inne på Axevalla. 

Adekvat vaccinerade hästar (25%) 


18 


23 

2007-01- 2007-02- 

28 02 

0 år 

1 år 

2 år 

3 år 

4 år 

5 år 

Normal temp är upp till 38°C. 

BB 7 år 

CML 6 år 

TL 5 år 

Ovaccinerade hästar f år högre 

feber och i fler dagar (upp till 2 v). 

Ålder 

1 vaccination är bättre än ingen. 

Men för att hinna ge skydd bör det 

ha gått några veckor. 


40,5 

40 

39,5 

39 

38,5 

38 

37,5 

37 

36,5 


08 

40,5 

40 

39,5 

39 

38,5 

38 

37,5 

37 

36,5 

Ovaccinerade 

Adekvat vaccinerade 

Ej adekvat vaccinerade 

6 år 

7 år 

8 år 

9 år 

10+ år 

okänt 


Ej adekvat vaccinerade hästar (42%) 


13 


18 


23 

Andel 

20% 

15% 

10% 

5% 

0% 

0 år 

1 år 

2 år 

3 år 

4 år 

5 år 


28 02 


Ovaccinerade hästar (33%) (3 är vacc, men väldigt 

nära/vid utbrottet) 


08 


13 


18 


23 


28 02 

Ålder 

6 år 

7 år 

8 år 

9 år 

10+ år 

okänd 

CH 2 år 

EK 4 år 

MR 2 år 

RR 2 år 

HC 2 år 

RA 2 år 

RH 2 år 

HJ 2 år 

BFR 3 år 



40,5 

40 

39,5 

39 

38,5 

38 

37,5 

37 

36,5 


03 

32% 

32% 

7 

6 

5 

4 

3 

2 

1 

0 

Tränare B utanför Axevalla. 

Hästar som är adekvat vaccinerade (18%) 


08 


13 


18 

Adekvat vaccinerade 

(n=91) 


23 

QS 4 år 

SJ 3 år 

40,5 

39,5 

38,5 

37,5 

Ju fler ovaccinerade hästar, 

desto högre smittryck 

(högre virusmängd i stallet) 

Tränare B utanför Axevalla. 

Ovaccinerade hästar/okänt vaccinationsstatus (72%) 

36,5 

2007-01-03 2007-01-08 2007-01-13 2007-01-18 2007-01-23 

och desto fler sjuka (sjukare) hästar. 

68% 

68% 


(n=80) 

55% 

55% 

45% 

45% 

79% 

79% 

CL 4 år 

LJS 2 år 

LJ 2 år 

CLA 4 år 

HG 2 år 

HP 7 år 

LM 6 år 

LP 10 år 

LL 2 år 


Ovaccinerade: majoriteten fick feber 

• Av samtliga hästar fick 311/562 st feber (=38,3°C) minst en dag, 

uppdelat på vaccinationsstatus ser det ut så här: 

Feber 

Ej feber 

Ovaccinerade 

(n=168) 

21% 21% 

Ovaccinerade: högre febertoppar och 

fler dagar sjuka 

Antal feberdagar hos de hästar 

som hade feber (medel ± SD) 

*** 

** 

Vaccinerade 

(n=91) 


41 

40,5 

40 

39,5 

39 

38,5 

38 

37,5 

37 

36,5 


(n=80) 

Högsta febertopp hos hästar med 

feber (medel ± SD) 

*** 

* 

Ovaccinerade 

(n=168) 


100% 

1 häst 

Hosta 

90% 

80% 

70% 

60% 

50% 

40% 

30% 

20% 

10% 

0% 

Vaccinerade 

(n=91) 

Feberperiod 

Ej adekvat 

vaccinerade 

(n=80) 

Ovaccinerade 

(n=168) 

Hur länge tar det för ett stall att 

bli feberfritt? 

Ingen feber 

Kortare feberperiod 

(1-2 d) 

Måttlig feberperiod 

(3-4 d) 

Längre feberperiod 

(5 d el mer) 

• 2 – 22 dagar 

• Medelvärde 7 dgr (±3,4) 

• När började mätningarna? 

– Sannolikt längre perioder i verkligheten 

• 202 st (45 %) hostade 

• 1-23 dagar 

• Medel 6,1 dgr (±3,7) 

• n=453 svar 


Hosta & Näsflöde 

Näsflöde 

Hälften av alla 

ovaccinerade 

hästar fick feber 

3 d eller längre 

(25% >5d) 

• 208 st (45 %) hade 

näsflöde 

• 1-15 dagar 

• Medel 6,1 dgr (±3,0) 

• n=460 svar 


80% 

70% 

60% 

50% 

40% 

30% 

20% 

10% 

0% 

Hosta 

Näsflöde 

Ovaccinerade Adekvat 

vaccinerade 

Ovaccinerade: fler hostar och snorar 

och under längre tid 

Hur många hästar har 

hosta eller näsflöde? 

Ej adekvat 

vaccinerade 

Antal dagar 

4,5 

4 

3,5 

3 

2,5 

2 

1,5 

1 

0,5 

0 

Hur många dagar har 

dessa hosta eller näsflöde i 

snitt? 

Medel hostdagar 

Medel näsflödesdagar 

Ovaccinerade Adekvat 

vaccinerade 

Antibiotikabehandlingar 

• 9 % behandlades sekundärt (30/319) 

– vanligast penicillin (18) och trimsulfa (7) 

– behandling 5,9 dgr (±1,03) 

– genomsnittlig ålder 3,7 år (±1,91)*** 

jmfr 4,9 år för hela materialet. 

• Inga av dessa 30 hästar var adekvat 

vaccinerade… 

Vaccinerade h ästar jämfört med ovaccinerade: 

• Färre hästar med feber 

• Färre feberdagar/häst 

• Lägre feber 

• Färre hästar får hosta och näsflöde 

• Färre dagar/häst med hosta resp. näsflöde 

• Färre (inga!) hästar behövde behandlas 


Take home message 

32% 

Adekvat vaccinerade (n=91) 

68% 

Ovaccinerade (n=168) 

79% 

Ej adekvat 

vaccinerade 

21% 


Konklusion 

Hästar som vaccineras mot influensa 

på ett adekvat s ätt 

blir inte sjuka eller 

får en mildare sjukdom under kortare tid 

jämfört med ovaccinerade individer. 

Förebygg influensa! 

• Vaccinera fölen 

efter 6 månaders ålder (2 ggr) 

• Vaccinera alla hästar i stallet 

• Vaccination helst var 6 mån. 

(unga hästar) t.o.m. 4 års ålder 

• Årlig vaccination fr.o.m. 5 år 

• FEI, internationell ridsport: 

Vaccination var 6 mån. 

• Vaccinera när utbrott närmar sig! 

• Inför obligatorisk vaccination av 

svenska travhästar igen? 


Att diskutera… 

• Hur länge är prestationen nedsatt? 

• 1 veckas vila för varje feberdag 

rekommenderas 

• Varje dag i ett travträningsstall kan kosta 

ca 300 kr. 10 dagars isolering/sjukdom = 

3000 kr/häst i träningsavgift till spillo för 

travhästägaren 

• Vaccination kostar mindre än 1 kr/dag 

• Bättre isoleringsåtgärder vid utbrott? 


Rätt tt sk skötsel tsel 

och 

hästh sthållnings llnings- 

rutiner 

med 

smittskydd i 

fokus 


Bättre ttre djurskydd 

Kortare avbrott i 

verksamheten 

Ekonomiskt 

mycket att vinna 


Equi Flu Net och internationella 

rekommendationer 

Louise T Berndtsson 

Avd för virologi 

Influensa hos häst 

• Först isolerad i 

Tjeckoslovakien 1956 

A1, H7N7 

(A/eq1/Prague/56) 

• Isolerad i Miami 1963 

A2, H3N8 

(A/eq2/Miami/63) 

Influensavirus 



HA – för införsel 

av virus in i cellen 

Hemagglutinin och 

Neuraminidas 

Faktorer som vidmakthåller 

epizootier av hästinfluensa 

Na – för att ta sig 

ut ur cellen efter 

virus 

replikationen 

• Antigen drift 

När existerande antikroppar inte längre 

känner igen HA-gp och därmed ej virus. 

• Kort duration av immunitet 

• (Sprids över speciesgränserna?) 

Amerikansk och Europeisk 

variant 



A1 

Prag/56 

† ? 

A2 

Miami/63 


fylogenetiskt träd 

A2 

Europeisk 

Amerikansk 

Newmarket/1/93 

Kentucky/94 

Kentucky/98 

South Africa/4/03 

Newmarket/5/03 

Internationell övervakning av 

hästinfluensa 

• Expert Surveillance Panel 

– SVA ett av 6 laboratorier globalt 

– Möts varje år för genomgång av 

utbrott och karakterisering av 

stammar 

– På grundval av utvecklingen 

rekommenderas bibehållande 

eller utbyte av vaccinstammar 

– Rekommendationer för 

harmonisering och standardisering 

av metoder för antigenbestämmning 

i vacciner 

• South Africa/4/03 täcker väl 

stammar av amerikanska 

varianten 

• Newmarket/2/93 täcker väl de 

flesta stammar av europeiska 

varianten, men några isolat 

från 2002 ”outgroups” 

• Antigenic Cartography en 

metod för framtida 

karakterisering? 

ESP 2007 - antigen 

karakterisering 



H3N8 stammar som används i 

nuvarande amerikanska och 

europeiska vaccin 

• Europeisk variant: 

– Suffolk/89 

– Borlänge/91 

– Newmarket/2/93 

• Amerikansk variant: 

– Newmarket/1/93 

– Kentucky/92 





2006 OIE recommendations 

Update vaccines to contain : 

• an A/equine/South Africa/4/03 (H3N8)-like virus (American 

lineage) and 

• an A/equine/Newmarket/2/93 (H3N8)-like virus (European 

lineage) remains 

Olika möjligheter för 

influensavacciner 

• uppgradera nuvarande vacciner - 

kan ta flera år 


• Testa existerande vaccin - 

challenge studie mot Syd Afrikanska 

varianten 







Conclusions and recommendations from the Expert Surveillance Panel on Equine 

Influenza Vaccines - January 2006 

These recommendations relating to the composition of vaccines for 2006 were made 

following review of the data arising from equine influenza surveillance by the panel of 

international collaborators for the period January 2005 – January 2006. The 

recommendations for vaccine strains remain as for 2005. 

Influenza activity 2005 

Outbreaks of equine influenza in Denmark, France, Sweden, Tunisia, United Kingdom, and 

the USA were reported during 2005. Some outbreaks occurred in vaccinated animals but 

disease was generally mild. 

All influenza activity was associated with H3N8 viruses. There were no reports of serological 

or virological evidence of H7N7 (equine-1) subtype viruses circulating in the equine 

population. Nevertheless, diagnostic laboratories should continue serological and virological 

monitoring and when using polymerase chain reaction (PCR) for rapid diagnosis, should 

ensure that primers specific for H7N7 virus as well as H3N8 virus are used. 

Characteristics of recent isolates 

All viruses characterised antigenically and/or genetically from Europe and North America 

during 2005 belonged to the ‘American' lineage with the exception of one isolate in the UK. 

In haemagglutination inhibition (HI) tests using post infection ferret antisera American 

Lineage viruses isolated in Europe and North America were closely related to the prototype 

vaccine strain A/South Africa/4/2003 and the A/eq/Newmarket/5/2003 reference strain. The 

HA1 sequences of American lineage viruses isolated since 2003 in America, Europe and 

South Africa all fall within a single phylogenetic sub-group, previously referred to as the 

‘Florida' lineage (Lai et al., 2001; 2004). The sequences of viruses isolated in America since 

2003 and represented by A/eq/South Africa/4/2003 (and A/eq/Ohio/2003) are characterised 

by two further amino acid changes in antigenic sites compared with the HA1 sequences of 

viruses isolated in Europe; these additional changes appear to contribute to greater antigenic 

drift from A/eq/Newmarket/1/93-like viruses currently included in vaccines. The European 

lineage virus isolated in 2005 reacted well in HI tests with ferret antisera against the 

European lineage reference strain A/eq/Newmarket/2/93. 

Recommendations for the composition of equine influenza vaccines 

During the period January 2005 to January 2006, H3N8 viruses of the ‘American’ lineage 

continued to circulate in Europe and North America with some vaccinated horses affected. 

These viruses, together with those responsible for the 2003/4 outbreaks in South Africa and 

circulating in North America were antigenically closely related to the currently recommended 

vaccine strains, A/eq/South Africa/4/2003-like. Only one virus belonging to the ‘European’ 

lineage was characterised during 2005 and no serious clinical episodes have been attributed 

to these viruses. Nonetheless, the recommendation remains that a European lineage virus be 

included in vaccines and surveillance for European lineage viruses be continued. 


It is recommended, therefore, that vaccines contain the following: 

• an A/eq/South Africa/4/2003 (H3N8)-like virus (American lineage) 1 

1 

A/eq/Ohio/2003 is as equally acceptable as A/eq/South Africa/4/2003. 

• an A/eq/Newmarket/2/93 (H3N8)-like virus (European lineage) 2 

2 

A/eq/Suffolk/89 and A/eq/Borlänge/91, currently used vaccine strains, continue to be 

acceptable. 

Reference reagents 

Reference reagents specific for the recommended European lineage vaccine strains are 

available for standardisation of vaccine content by single radial diffusion (SRD) assay and 

can be obtained from the National Institute for Biological Standards and Control (NIBSC). 

Preparation of reagents for the 2005 recommendation is under review. 

Three equine influenza horse antisera (anti-A/eq/Newmarket/77 [H7N7], anti- 

A/eq/Newmarket/1/93 [H3N8] and anti-A/eq/Newmarket/2/93 [H3N8]) are available as 

European Pharmacopoeia Biological Reference Preparations (EP BRPs) for serological 

testing of equine influenza vaccines by the single radial haemolysis assay. These antisera are 

also available from the Office International des Epizooties International Reference 

Laboratory in Newmarket (UK) for use as primary standards in diagnostic serological testing. 

Pooled equine serum obtained post infection with A/eq/South Africa/4/2003 (H3N8) virus is 

currently the subject of an international collaborative study to establish this serum as an EP 

BRP / OIE primary standard to supersede the anti-A/eq/Newmarket/1/93 (H3N8) serum. 

SRD reference reagents EP BRPs for serological 

testing of equine influenza 

vaccines 

NIBSC, Blanche Lane, 

South Mimms, Potters Bar, 

Herts, EN6 3QG, UK 

Fax: +44 (0)1707 646730 

e-mail: 

enquiries@nibsc.ac.uk 


European Directorate for 

the Quality of Medicines, 

BP 907, F-67029 

Strasbourg Cedex, France 

Website: 

http://www.pheur.org 

OIE primary standards 

for diagnostic serological 

testing 

Animal Health Trust, 

Lanwades Park, Kentford, 

Newmarket, Suffolk, 

CB8 7UU, UK 

Fax: +44 (0)8700 50 24 61 

e-mail: info@aht.org.uk 

References: 

Lai A.C.K., Chambers T., Holland R.E., Morley P.S., Haines D.M., Townsend H.G.G. & 

Barrandeguy M. (2001). Diverged evolution of recent equine-2 influenza (H3N8) viruses in 

the Western Hemisphere. Arch. Virol., 146 , 1063–1074; 

Lai A.C.K., Rogers K.M., Glaser A., Tudor L. & Chambers T. (2004). Alternate circulation 

of recent equine-2 influenza viruses (H3N8) from two distinct lineages in the United States. 

Virus Res., 100 , 159–164. 


Influensautbrottet 1993 

- Historik och vad lärde vi oss av detta? 

Peter Forssberg, STC 

amerikansk 

stam 

A2-influensa 

Historik 

Större utbrott 


europeisk 

stam 

1979, 1985, 1992, 2006 


Vaccinationsobligatorium 

Ej i Finland, ej i Sverige 

Framställan om obligatorium 

Nordisk djurskyddskommitté 

Banveterinärkonferens 

Utbrott A2 


november 1992 – maj 1993 

< 1 år efter föregående utbrott 


Pia Törnqvist et.al 1991 

effekt 81% 

intervaller? 

• Förväntningar 

•Biverkningar 

• Ekonomi 

• Avvecklat obligatorium 

Borttaget obligatorium 

• Lokala smittskyddsgrupper 

• Ändrade intervaller 

• ”öppnare” isolering 



1993 

färre sjuka 19% 8% 

vaccinationsgrad dålig: 

Solvalla 90-100% 

Mantorp 27% 

Gävle 34% 

Östersund 15% 

25% 

Fördelning kallblod 

25% 

25% 

25% 

Påstådda biverkningar 

12% 

55% 


18% 

15% 



Vet. Res. 35 (2004) 411–423 

© INRA, EDP Sciences, 2004 

DOI: 10.1051/vetres:2004023 

411 

Review article 

Current perspectives on control of equine influenza 

Janet M. DALY*, J. Richard NEWTON, Jennifer A. MUMFORD 

Centre for Preventive Medicine, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, 

CB8 7UU, United Kingdom 

(Received 7 July 2003; accepted 31 October 2003) 

Abstract – Influenza A viruses of the H3N8 subtype are a major cause of respiratory disease in horses. 

Subclinical infection with virus shedding can occur in vaccinated horses, particularly where there is 

a mismatch between the vaccine strains and the virus strains circulating in the field. Such infections 

contribute to the spread of the disease. Rapid diagnostic techniques are available for detection of 

virus antigen and can be used as an aid in control programmes. Improvements have been made to 

methods of standardising inactivated virus vaccines, and a direct relationship between vaccine 

potency measured by single radial diffusion and vaccine-induced antibody measured by single radial 

haemolysis has been demonstrated. Improved adjuvants and antigenic presentation systems extend 

the duration of immunity induced by inactivated virus vaccines, but high levels of antibody are 

required for protection against field infection. In addition to circulating antibody, infection with 

influenza virus stimulates mucosal and cellular immunity; unlike immunity to inactivated virus 

vaccines, infection-induced immunity is not dependent on the presence of circulating antibody to 

HA. Live attenuated or vectored equine influenza vaccines, which may better mimic the immunity 

generated by influenza infection than inactivated virus vaccines, are now available. Mathematical 

modelling based upon experimental and field data has been applied to examine issues relating to 

vaccine efficacy at the population level. A vaccine strain selection system has been implemented 

and a more global approach to the surveillance of equine influenza is being developed. 

equine influenza / epidemiology / vaccine strain selection / surveillance 

Table of contents 

1. Introduction...................................................................................................................................... 412 

2. Epidemiology................................................................................................................................... 412 

3. Vaccine potency............................................................................................................................... 413 

4. Natural immunity and live vaccines ................................................................................................ 414 

5. Optimising vaccination schedules .................................................................................................. 416 

6. Vaccine strain selection ................................................................................................................... 417 

7. Diagnosis ......................................................................................................................................... 419 

8. International control......................................................................................................................... 420 

9. Conclusion ....................................................................................................................................... 420 

* Corresponding author: janet.daly@aht.org.uk 


412 J.M. Daly et al. 

1. INTRODUCTION 

Management procedures aimed at limiting 

the severity of disease and the spread of 

infection, whether on a local or international 

basis, require sensitive diagnostic 

techniques for rapid detection of clinical 

and subclinical infection. Equine influenza 

vaccines were first developed in the 1960s 

[4], and are used widely for control of 

equine influenza however, in spite of intensive 

vaccination programmes in some groups, 

equine influenza infections remain a serious 

problem. The H3N8 component of 

inactivated vaccines has been the subject of 

intense investigation with a view to identifying 

the reasons for vaccine breakdown 

against this subtype. Research has focussed 

on vaccine potency, adjuvants, vaccination 

schedules and antigenic drift. During the 

last decade, progress has been made in all 

these areas of investigation, providing new 

approaches to the control of equine influenza. 

2. EPIDEMIOLOGY 


Equine influenza was first recognised in 

1956, when influenza was recovered during 

a widespread epidemic of respiratory disease 

among horses in Eastern Europe [58]. 

The virus (A/eq/Prague/56), which has an 

H7 haemagglutinin (HA) and an N7 neuraminidase 

(NA), was designated as the 

prototype equine influenza virus, historically 

referred to as equine subtype 1. The 

last confirmed outbreak caused by an H7N7 

subtype virus was in 1979; however H7specific 

antibody has been reported in 

horses believed to be unvaccinated, suggesting 

that the virus may still circulate in 

a subclinical form. 

In 1963, an equine influenza virus of a 

different antigenic subtype (H3N8), originally 

designated as equine subtype 2, 

caused a major epidemic in the USA [64]. 

The prototype virus, A/eq/Miami/63, was 

introduced into the equine population of 

Florida with the importation of horses from 

Argentina [57]. Field evidence suggested 

that regular vaccination provided protection 

against H7N7 infections, but that the 

H3N8 component of the vaccine was less 

effective [53]. For example, in January 

1976 a localised outbreak of H3N8 occurred 

in Thoroughbred horses in Newmarket 

(UK) at a time when many animals had 

recently been vaccinated [59]. Clinical 

influenza affected unvaccinated and some 

vaccinated horses, with the severity of disease 

corresponding with the period since 

vaccination. Stables in which over 75% of 

horses were vaccinated were not affected 

seriously [59]. Between 1978 and 1981, 

widespread epidemics of H3N8 viruses 

were reported in Europe and North America 

with infections occurring in vaccinated as 

well as unvaccinated horses [7, 28, 30, 52, 

62]. In Britain in 1979, influenza was confined 

to unvaccinated horses during the first 

six months of the year, but spread to vaccinated 

Thoroughbreds in June 1979, providing 

clear evidence that the vaccines did not 

provide immunity against field infection 

for the full year between “booster doses” 

[6]. Racing was affected, and this led to the 

subsequent introduction of mandatory vaccination 

in the UK and Ireland in 1981. 

In 1989, there was again a major epidemic 

of influenza H3N8 in Europe affecting 

not only unvaccinated but also large 

numbers of vaccinated horses [33]. This 

represented the first major outbreak in Britain 

since 1979. Outbreaks of equine influenza 

have occurred sporadically in Europe 

and on the American continent since the 

1989 epidemic. 

In the last 15 years, there have also been 

a number of serious outbreaks of H3N8 

influenza in populations with no previous 

history of the disease. In 1986 and 1987, the 

infection was introduced into South Africa 

and India, respectively. The source of these 

outbreaks could be traced to the transportation 

of infected horses by air from areas 

where influenza was endemic. Inadequate 

quarantine at the port of entry allowed the 

introduction of infected horses into the local 



susceptible populations with subsequent 

explosive spread of disease and some mortality. 

Analysis of the HA genes of the South 

African and Indian viruses have confirmed 

their close relationship to viruses circulating 

in the USA and Europe at the time. In 

1989, an influenza epidemic was reported 

in horses in China with morbidity rates as 

high as 80% and mortality rates reaching 

20% in some herds. Fatal cases were always 

associated with bacterial infection [21]. 

The origin of this outbreak was not traced 

to the importation of equidae and indeed the 

antigenic characteristics of this virus appear 

markedly different from other equine H3N8 

isolates [22]. On the basis of sequence 

information, it was proposed that this virus 

was derived from an avian source and as 

such represented a new interspecies transmission 

event [65]. Although this avianderived 

virus successfully transmitted to 

horses and lost its ability to infect ducks, it 

did not spread beyond China and did not 

persist in the local horse population beyond 

1990 [23]. Further outbreaks in Hong Kong 

in 1992 [54], Dubai in 1995 [66], and the 

Philippines in 1997 highlighted the ease 

with which equine influenza outbreaks can 

be introduced into susceptible populations 

as a result of international movement of 

horses. 

3. VACCINE POTENCY 

Currently, the principal markers for 

resistance to and recovery from influenza 

virus infection are circulating antibodies 

specific for the HA and NA glycoproteins 

[1]. These glycoproteins are the principle 

determinants for cell entry in infection 

(HA) and for exit from the cell after virus 

replication (NA). Progress in assessing the 

protective efficacy of early vaccines was 

hampered by a lack of reliable methods to 

measure the HA content of vaccines and the 

host’s antibody response to the HA. Additionally, 

there was no reproducible challenge 

method in horses for assessing the 

protection provided by vaccination. The 

Control of equine influenza 413 

HA content of vaccines was measured in 

chick cell agglutination (CCA) units and 

antibody responses to the HA were measured 

by the haemagglutination inhibition 

(HI) test. In some instances these methods 

are both still used. Early attempts to analyse 

the relationship between vaccine-induced 

antibody and protection against infection 

were confused by technical problems, and 

HI titres ranging from 8 to 128 were quoted 

as being protective [5, 31, 55, 59]. Improved 

methods of measuring vaccine potency, 

antibody responses and protection against 

infection have since been developed, facilitating 

progress in vaccine standardisation 

and design. A reliable in vitro potency test, 

the single radial immunodiffusion (SRD) 

test, has been introduced for measurement 

of immunologically active HA in equine 

influenza vaccines and has been evaluated 

in an international collaborative study [68]. 

A further international collaborative study 

demonstrated that the single radial haemolysis 

(SRH) assay is more reproducible than 

the HI test for measuring antibody to HA 

[38]. Furthermore, there is a direct relationship 

between vaccine potency, in terms of 

microgrammes of HA, and antibody to HA 

stimulated by inactivated vaccines as measured 

by SRH [41, 67]. 

Vaccine evaluation by experimental challenge 

infection of horses was slow to progress 

because of difficulties encountered in reproducing 

clinical disease [8, 31, 35, 56]. These 

difficulties have been overcome by using 

nebulised aerosols. This delivery system 

mimics a natural infection by producing 

infectious droplets (diameter < 5 mm) capable 

of reaching the upper and lower airways 

(D. Hannant, unpublished data) and avoids 

a concentration of challenge inoculum at 

the site of sampling. Using this challenge 

method, a series of experiments to measure 

the protection afforded by inactivated virus 

vaccines with a variety of adjuvants and 

antigen presentation systems have been performed. 

A number of experiments have 

used the SRD test to standardise inactivated 

vaccines, the SRH test to measure antibody 

responses in the horse and challenge infections 




to assess protection from infection and disease. 

These studies have determined the 

relationships between vaccine potency, circulating 

antibody to HA and protection 

against infection and disease. Levels of antibody 

required for virological protection against 

challenge with an antigenically similar 

virus were between 120 to 154 mm 2 , with 

evidence that a higher threshold was required 

for protection with increasing doses of nebulised 

virus [39]. The influenza epidemic in 

South Africa in 1986 provided a rare opportunity 

to examine vaccine efficacy in the 

field in a population where no natural 

immunity exists. From pre-infection antibody 

levels it was possible to estimate that 

an SRH value of around 160 mm 2 was consistent 

with a 90% protection rate based on 

the proportion of horses that seroconverted 

when exposed to infection [39]. 

The majority of current equine influenza 

vaccines contain inactivated whole virus 

(with adjuvants, which include oil, alhydrogel 

or carbomer) or subunit vaccines (ISCOMs 

or micelles combined with Quil A). It was 

found that antibody responses stimulated 

by vaccines containing aluminium phosphate 

or hydroxide were more durable than 

those induced by aqueous vaccines of 

equivalent antigenic content. Antibody nevertheless 

declined to low levels by 16 to 

20 weeks after the second and third dose of 

vaccine. In contrast, the incorporation of a 

polymer adjuvant was found to stimulate 

antibody that remained at a high level for at 

least six months after the third dose of vaccine 

[43]. Similarly, vaccination with three 

doses of ISCOMs containing 15 mg HA 

resulted in the level of SRH antibody persisting 

at around 70 mm 2 for 15 months following 

the third dose [42]. 

The historical lack of standardisation of 

vaccines from different sources, and the 

undemanding standards of some licensing 

authorities, has resulted in the use of products 

with inadequate potency in terms of 

ability to stimulate antibody to the HA. 

Morley et al. [37] described a large doubleblind 

field trial using a commercial killed 

vaccine that failed to demonstrate a significant 

difference in the rate of disease between 

vaccinated and unvaccinated animals in the 

face of a naturally occurring outbreak of 

disease in a population of horses stabled at 

a racetrack. The situation is improving with 

the establishment of European Pharmacopoeia 

international reference preparations 

to standardise serological tests for potency 

evaluation of vaccines, and the introduction 

of federal regulations on equine influenza 

vaccines in Europe [17] and, more recently, 

in the USA (9CFR parts 112 and 113). 

4. NATURAL IMMUNITY AND LIVE 

VACCINES 

Immunity provided by inactivated influenza 

virus vaccines, is dependent on high 

levels of circulating antibody to HA and, in 

the absence of such antibody, vaccinated 

horses are susceptible to infection. In contrast, 

infection with influenza induces longterm 

immunity independent of circulating 

antibody against HA. For example, ponies 

with low or undetectable anti-HA antibodies 

were clinically and virologically protected 

from challenge infection more than 

one year after natural infection [26]. This 

suggests an important difference in the 

immune response following infection compared 

with vaccination using inactivated 

virus. Additional components of the immune 

response that may be involved are the cellular 

immune and mucosal antibody responses 

local to the site of infection. 

Cellular immune responses to influenza 

are well defined in man. The key cell-mediated 

immune response is the development 

of MHC class I restricted CD8 + cytotoxic 

T lymphocytes (CTL), which are usually 

detectable within 3 to 4 days after infection. 

CD8 + CTL lyse virus-infected host cells 

[70]. The epitopes recognised by CTL on 

the HA, nucleoprotein (NP), matrix (M1) 

and polymerase PB2 proteins are more 

highly conserved than those involved in 

humoral immunity. MHC class II-restricted 

CD4 + T helper cells facilitate both humoral 



and cellular immune responses and can 

exert cytolytic effects, though to a lesser 

extent than CD8 + CTL. Whereas antibodies 

reduce virus load and restrict re-infection, 

cellular immune mechanisms probably play a 

more important role in clearance of virus 

during the convalescent period [12, 36]. 

Less is known about cellular immune 

responses in horses. Experimental infection 

of ponies with influenza induces a genetically 

restricted, antigen-specific CTL response 

that persists for at least six months [25]. 

Generation of CTL in this case probably 

occurs through endogenous antigen processing 

followed by peptide presentation via 

MHC class I molecules. In contrast, inactivated 

virus vaccines fail to stimulate a significant 

CTL response because the antigens 

undergo exogenous processing and presentation 

via MHC class II. 

Equine influenza virus infection has been 

demonstrated to generate virus-specific mucosal 

IgA and serum IgGa and IgGb responses, 

whereas an inactivated virus vaccine induced 

only a serum IgG(T) response [44]. 

The qualitative differences between the 

immune responses that follow infection or 

vaccination with inactivated virus suggest 

that improvements can be made in vaccine 

design. Ideally, vaccines should induce 

broadly reactive, local and systemic, antibody 

and cellular immune responses, establish 

memory and consequently generate a 

rapid anamnestic response upon field exposure 

to equine influenza virus. The incidence 

of free and cell-associated virus is 

thereby reduced and recovery enhanced. 

Live attenuated and live, vectored equine 

influenza vaccines that should more closely 

mimic natural infection are available. The 

Merial vaccine PROTEQ Flu is a live 

recombinant vaccine that uses canarypox as 

the vector to express the HA genes of 

equine influenza viruses. The recombinant 

virus undergoes an abortive infection in 

mammalian cells so that no progeny viruses 

are made but the expressed viral antigens 

are processed endogenously and presented 

as peptides via MHC class I by the host cell 


in the same manner as occurs in natural 

infection but without associated infection 

risks. There is a wealth of evidence for 

canarypox vaccines inducing cellular immune 

responses to human immunodeficiency 

virus in man [18, 20], but this has yet to be 

demonstrated for the PROTEQ Flu vaccine. 

A cold-adapted, temperature-sensitive, 

modified-live virus equine influenza vaccine 

(FluAvert IN Vaccine), which is delivered 

intranasally, is now licensed for sale in 

the USA. The safety and efficacy of the vaccine 

has been demonstrated in experimental 

studies, however the vaccine does not provide 

sterile immunity [10, 34, 60, 71]. No 

correlation was found between the concentration 

of serum antibody induced by vaccination 

and protection against infection, 

though an anamnestic response was demonstrated 

at seven days post infection [61]. 

Although there is evidence to show that 

primed animals will develop a serological 

response [71], it appears that the use of 

serum antibody response as a measure of 

live virus mucosal vaccines in naïve animals 

is inappropriate. Our ability to measure 

alternative correlates of immunity has 

lagged behind the development of these 

alternative vaccination strategies. 

Induction of a cellular immune response 

to a conserved protein such as NP may 

potentially provide protection when the 

viral strains incorporated in the vaccine do 

not match circulating strains. Such crossreactive 

immunity may even extend to partial 

protection against infection with a virus 

of a different subtype (heterosubtypic immunity). 

Infection of mice with a human influenza 

A virus of one subtype can induce partial 

protection against infection with virus of a 

different subtype [47], and a similar study 

in pigs suggested that CD8 + T lymphocytes 

have a role in this heterosubtypic immunity 

[27]. Generation of such cross-reactive 

immunity in the horse could be advantageous 

in the event of a new subtype of influenza 

A virus emerging (or re-emerging) in 

the horse population. 




5. OPTIMISING VACCINATION 

SCHEDULES 

The early vaccination schedules for 

inactivated virus vaccines required two primary 

doses 4 to 6 weeks apart followed by 

annual booster doses. The current minimum 

requirements imposed for competition 

animals by the Federation Equines 

International are a primary course of two 

doses 4 to 6 weeks apart and a booster six 

months later followed by annual boosters. 

Mathematical models validated against experimental 

and field data have demonstrated 

that vaccination dramatically reduces both 

the incidence and size of epidemics, with 

larger outbreaks of equine influenza being 

exceptional amongst groups of vaccinated 

animals [19]. Thus the vaccination policy 

ensures a sufficient level of herd immunity 

to prevent large-scale outbreaks that are 

likely to lead to cancellation of race meetings 

and other equestrian events. However 

it is questionable whether the preliminary 

programme of three doses followed by 

annual vaccination provides sufficient immunity 

to protect young horses from the disease 

or individual training yards from small 

outbreaks of influenza. The short-lived 

immunity provided by inactivated vaccines 

has been acknowledged for some years, and 

it is apparent from various studies [13, 61, 

63] that vaccination in accordance with the 

minimum requirements of Jockey Club 

rules and the vaccine manufacturer’s recommendations 

leaves horses with low antibody 

titres for several months between their 

second and third vaccination. Newton et al. 

[46] found that SRH antibody levels in 

yearling Thoroughbreds on studs in Newmarket 

declined below a protective level 

within four months of a booster vaccination. 

Importantly, this also coincided with 

the autumn sales, a recognised risk period 

for transmission of influenza in young 

Thoroughbreds [45]. Later observations in 

yearlings entering training yards in Newmarket 

confirmed that antibody levels at 

this time were influenced by both time 

elapsed since the last vaccination and the 

total number of vaccines that had been previously 

administered [46]. Cullinane et al. 

[13] demonstrated that an additional 6monthly 

booster would benefit horses that 

may be at high risk during this interval. 

Intensive vaccination regimes, involving 

booster doses every 30 to 60 days, have 

been practised in the USA. However, little 

is known about the potential adverse effects 

of administering a potent vaccine too frequently, 

which may attenuate the immune 

response. Using a stochastic model to assess 

the risk of an outbreak occurring in a Thoroughbred 

population in a typical flat racing 

training yard, Park et al. [51] suggested that 

increasing the frequency of vaccination in 

horses aged 2-years and upwards to include 

six monthly boosters would offer a significant 

increase in protection over annual vaccination. 

Timing of the first vaccination may be 

critical to the subsequent development of 

antibody. Although it is recognised that maternal 

antibody generally inhibits the development 

of neonatal antibody synthesis, it has 

often been assumed that these antibodies 

have decayed to an insignificant level by 3 

to 4 months. The temptation is to vaccinate 

elite stock prior to the loss of maternal antibodies 

to avoid any window of susceptibility. 

Foals born to mares vaccinated during 

the gestation period have high levels of 

maternal antibody within two days of birth 

[13, 61, 63]. In contrast to Liu et al. [32], 

who reported that maternal antibody persisted 

for only a short period, several 

authors [13, 61, 63] found that the majority 

of foals they tested had detectable (HI) antibody 

titres at three months of age but these 

had virtually disappeared at six months. 

Cullinane et al. [13] suggested that not only 

does vaccination in the face of maternal 

antibody interfere with the development of 

active immunity but that repeat vaccination 

in the face of maternal antibodies may induce 

tolerance. On the basis of their findings, 

they recommended that mares should be 

vaccinated against equine influenza in the 

last 6 to 4 weeks of pregnancy to ensure the 

transfer of protective levels of antibody in 



the colostrum, and that foals should not be 

vaccinated until their maternal antibodies 

have waned (i.e. not until six months of age 

or they are seronegative). 

6. VACCINE STRAIN SELECTION 

Surveillance of antigenic drift is a cornerstone 

of influenza control programmes 

based on vaccination. As with other RNA 

viruses, influenza virus replication is highly 

error-prone, therefore newly synthesised 

viral genes have a high frequency of mutation. 

Many of these mutations are either 

inconsequential or detrimental to the virus, 

but mutations affecting the antigenic sites 

of the HA (and NA) can lead to the virus not 

being recognisable by pre-existing antibodies 

generated by infection or vaccination 

with an earlier strain, a process known as 

“antigenic drift”. The formulation of human 

influenza vaccines is reviewed on an annual 

basis and in most years is changed to reflect 

the virus strains most representative of 

those in worldwide circulation. 

Historically, antigenic drift in equine 

H3N8 viruses has been examined in HI tests 

employing post infection or post vaccination 

sera prepared in a number of different 

species. Conclusions about the antigenic 

relatedness of equine H3N8 viruses and the 

significance of observed differences with 

respect to the immunity induced have varied. 

For example, Hinshaw et al. [28] concluded 

than the majority of viruses isolated 

between 1979 and 1981 were substantially 

different from the prototype virus, Miami/ 

63 included in the vaccine when compared 

using post infection ferret sera in HI assays, 

and that representatives of the new variant 

should be included in the vaccines. On the 

other hand, Burrows et al. [6, 7] concluded 

that the minor antigenic drift that they 

detected in viruses isolated between 1963 

and 1979 did not justify a change in vaccine 

strains because post vaccination sera from 

horses immunised with Miami/63 virus 

were highly cross-reactive in HI tests with 

viruses from 1979. This conclusion did not 


take into account the findings of Haaheim 

and Schild [24] that strain-specific antibody 

is more effective than cross-reactive 

antibody in conferring protection. 

Horse sera are relatively cross-reactive, 

particularly when taken from repeatedly 

vaccinated animals whereas ferrets develop 

a more strain-specific antibody response [39]. 

During the 1989 outbreak of influenza in 

the UK, only horses with very high levels 

of vaccine-induced antibody were protected 

against infection, raising the possibility 

that there had been significant antigenic 

changes in the 1989 isolate that 

prevented its neutralisation by antibody 

stimulated by vaccines containing Miami/63, 

Fontainebleau/79 or Kentucky/81. Sequencing 

of the HA1 gene and antigenic analysis 

using monoclonal antibodies suggested that 

there were significant differences between 

a representative 1989 strain and the vaccine 

strains in current use at the time [2]. The 

hypothesis was tested by vaccinating groups 

of ponies with monovalent vaccines containing 

either of the vaccine strains or a 

1989 strain and experimentally challenging 

them with a 1989 virus [15]. Although all 

vaccines provided clinical protection, vaccine 

efficacy in terms of ability to eliminate 

virus excretion correlated directly with the 

degree of antigenic relatedness between 

vaccine and challenge strain. Following a 

meeting of OIE and WHO experts on newly 

emerging strains of equine influenza, it was 

recommended that equine influenza vaccines 

be updated to include a 1989 isolate, 

and that efforts be made to increase surveillance 

and virus characterisation [40]. 

Phylogenetic analysis of HA sequences 

revealed that equine H3N8 viruses, which 

had been evolving as a single lineage [29], 

apparently diverged into two distinct lineages 

during the mid-1980s [14] and, to 

date, both lineages continue to co-circulate 

independently (Fig. 1). Viruses in one lineage 

were predominantly isolated from 

horses in Europe, with the exception of one 

virus isolated in Canada in 1990, whereas 




Figure 1. Phylogenetic tree constructed from equine influenza H3 HA1 amino acid sequences using 

parsimony method. 

viruses in the other lineage were predominantly 

from horses on the American continent. 

It was apparent, however, that American 

lineage viruses had been introduced into 

Europe on at least one occasion. The 

genetic divergence of American and European 

lineage viruses was reflected in their 

antigenic reactivity, raising the question of 

the potential importance of geographical 

variations in antigenic character for vaccine 

efficacy. Further vaccination and experimental 

challenge studies in ponies suggested 

that vaccines containing virus from 

the American lineage may not be as effective 

in protecting against infection as the 

homologous vaccine against challenge with 

virus from the European lineage [69]. Field 

observations have supported the hypothesis 

that antigenic differences between viruses 

of the American and European lineages are 

sufficient to adversely affect vaccine efficacy. 

During an outbreak caused by a European 

lineage virus in vaccinated Thoroughbred 

horses in the UK in 1995, horses with antibody 

levels of more than around 140 mm 2 were 

protected against infection [46]. However, 



during an outbreak caused by an American 

lineage virus in 1998, when the vaccines 

used contained only European lineage viruses, 

a quarter of horses with antibody levels 

higher than 140 mm 2 became infected [45]. 

The co-circulation of antigenic variants 

means that it is important to base the selection 

of new vaccine strains on knowledge of 

the dominant virus circulating in the field. 

Following a further consultation of OIE and 

WHO experts in 1995, a more formal surveillance 

system was established for equine 

influenza [48]. An international panel of 

experts including representatives from OIE 

and WHO influenza reference laboratories 

reviews data collected on outbreaks of 

influenza, vaccine performance in the field, 

and antigenic and genetic characteristics of 

new virus isolates annually. The expert surveillance 

panel make recommendations on 

the need to update vaccine strains, which 

are published in the OIE Bulletin. The criteria 

used for deciding on the need to update 

equine influenza vaccine strains are based 

largely on those used for human influenza 

vaccine strain selection, i.e. detection of 

changes in the HA as characterised by HI 

tests using ferret and horse antisera, genetic 

sequencing of the HA1 gene and vaccine 

breakdown in the field. Improved surveillance 

in the field, standardisation of the 

potency of vaccines and the introduction of 

a vaccine strain selection system has enabled 

the development of a fast-track licensing 

system for vaccines containing updated 

strains [16]. 

7. DIAGNOSIS 


We have demonstrated that vaccinated 

horses are often only partially immune to 

influenza (particularly if vaccine strains are 

a poor match for circulating viruses) and 

may shed virus in the absence of clinical 

signs. Such animals present a significant 

risk for the spread of infection. Thus our 

ability to diagnose both clinical and sub 

clinical infections in partially immune ani- 

mals is critical in attempts to control equine 

influenza. 

For many years the diagnosis of equine 

influenza has relied on culture of virus in 

embryonated hens’ eggs (and more recently 

Madin-Darby canine kidney cells) and 

measurement of antibody responses to the 

HA. Although a useful epidemiological 

tool, serological diagnosis of equine influenza 

tends to be retrospective because a 

convalescent sample taken around two 

weeks after an acute sample is required for 

a definitive diagnosis. This is because 

infection-induced antibody detected in an 

acute sample cannot be distinguished from 

vaccine-induced antibody. 

An ELISA to detect antibody to the nonstructural 

protein NS1 has been developed 

[3, 50]. As this protein is produced during 

an infection but is not incorporated into 

inactivated whole virus vaccines, it theoretically 

enables differentiation of antibody 

responses to infection from responses to 

vaccination with a traditional vaccine. With 

the introduction of live attenuated equine 

influenza vaccines, the potential usefulness 

of this test for confirmation of infection in 

vaccinated animals will probably be considerably 

reduced. However, the current 

trend towards genetically engineered vaccines 

may facilitate the development of 

DIVA (differentiation of infected from vaccinated 

animals) vaccines in which a specific 

gene encoding a highly immunogenic 

protein is modified or removed. 

Detection of the presence of infectious 

virus by culture of virus in nasal secretions 

can take a minimum of 2 or 3 days, and if 

multiple passages are required confirmation 

of diagnosis is delayed further. A 

number of alternative assays based upon the 

use of a monoclonal antibody to detect 

nucleoprotein in nasal swab abstract provide 

a diagnosis within 24 h. An equine 

influenza-specific ELISA has been described 

[11]. When used in parallel with virus isolation 

during the 1989 equine influenza epidemic 

in Britain, the ELISA enhanced the 

virus detection rate by 44% [33]. Kits for 




detection of human influenza are commercially 

available, and, because of the high 

degree of conservation of the nucleoprotein 

among influenza A viruses, one of these, the 

Directigen Flu-A assay, has been shown to 

be applicable to the diagnosis of equine 

influenza [9]. These direct detection methods 

are useful in the application of control 

measures, as they can be used as a basis for 

isolating horses excreting virus in order to 

reduce infection pressure and for a decision 

on curtailing exercise, which may exacerbate 

disease. They are also a useful adjunct 

to virus isolation, which remains essential 

for characterising new viruses and to provide 

future vaccine strains, as they permit 

virus isolation efforts to be focussed on 

samples known to be positive for equine 

influenza. 

8. INTERNATIONAL CONTROL 

The ever-increasing international movement 

of horses for competition and breeding 

purposes presents a challenge with 

regard to the control of equine influenza. 

Several explosive outbreaks of equine influenza 

attributable to the introduction of 

infected animals into susceptible indigenous 

populations have been described during 

the last 20 years [54, 66]. Due to economic 

and competitive issues, it is desirable 

for the disruption to training programmes 

caused by quarantine to be kept to a minimum 

when horses are moved. There is, 

therefore, a reliance on surveillance of 

influenza in the population that animals are 

leaving and on the effectiveness of vaccines 

to prevent viral shedding. When these 

measures fail, and subclinically infected 

horses shedding virus are transported, the 

short quarantine periods that are often used 

fail to prevent introduction of infection. 

Regulations relating to the movement of 

animals based on the use of improved diagnostic 

techniques and vaccination policies 

that recognise the limitations of current products 

are now in place. The Code Commission 

of the OIE recommends that importing 

countries that are free of equine influenza 

should require that all horses travelling 

from endemic areas are fully vaccinated 

and have received their last booster dose 

within 2 to 8 weeks of travel [49]. A simple 

additional measure that can be implemented 

is the screening of antibody using 

the SRH assay, which can identify potentially 

susceptible animals that require revaccination 

to boost their antibody levels 

before travelling. The advent of more rapid 

diagnostic tests for equine influenza means 

that animals can be screened for viral shedding 

while still in quarantine at their destination 

before being released into potentially 

susceptible local populations. 

9. CONCLUSION 

There are still important goals to be met 

in the control of equine influenza. These 

include increased surveillance, virus recovery 

and characterisation from large equine 

populations in the Americas and Far East, 

and international harmonisation of vaccine 

standards and licensing procedures. However, 

many of the activities are now in place 

to provide vaccine manufacturers with the 

necessary information for production of 

effective vaccines containing epidemiologically 

relevant strains, and the development 

of rapid diagnostic assays has increased our 

ability to monitor equine influenza activity 

worldwide and avoid transmission of infection 

via movement of horses from areas 

where the infection is active. 

ACKNOWLEDGEMENTS 

Much of the data presented in this paper have 

been generated through the collaborative efforts 

of research teams at the Animal Health Trust, 

which currently includes A. Park, L. Spencer and 

D. Hannant, and at the Gluck Equine Research 

Centre, University of Kentucky, USA, headed 

by T. Chambers. The authors greatly appreciate 

the continued financial support of the Horserace 

Betting Levy Board, Animal Health Trust, and 

the equine influenza vaccine manufacturers. 


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