19th International Congress on Modelling and Simulation, Perth, Austra - PDF document

19th International Congress on Modelling and Simulation, Perth, Australia, 12–16 December 2011 peakprevalenceofapproximately20–50%withtheexceptionofonesmalleroutbreak.TheoutbreaksofRCDsuppresstherabbitpopulationsinitiallybutthepopulationsthenrecovertoapproximately50%ofthecarryingcapacitybeforethenextoutbreakoccurs.Forthecasewheresimultaneousco-infectioncanoccurtheoutbreaksaremorefrequent(approximately1peryear).4CONCLUSIONSWehaveinvestigated,usingamathematicalmodelintheformofasystemofdifferentialequations,theeffectofbothmyxomatosisandRCDonrabbitpopulations.Oursimulationsover20dayshaveshownthatthepresenceofaconcurrentoutbreakofmyxomatosiscansuppressthemaximumnumberofrabbitsinfectedwithRCD.Thiseffectoccursbothwhensimultaneousco-infectionisnotpossibleaswellaswhenitispossible,buttheeffectismorepronouncedwhensimultaneousco-infectionisnotpossible.Wehavealsorunthesimulationoveralongertimescaleof10yearsincludingseasonalbirthratesandlogisticdensitydependentdeathrates.ThepresenceofmyxomatosishereallowsRCDoutbreakstooccur,whereaswithoutmyxomatosisthenRCDdiesout.However,thisconclusionneedsfurtherinvestigationtodeterminehowrobustisthisconclusionwithrespecttochangesinparametervaluesandinitialnumbers.Itwouldalsobevaluabletoinvestigatetheeffectthedifferentinfectionshaveontransmissioncontactrates,usingproximitysensors,suchasinMarshetal.[2010].Furtherworkisplannedtoinvestigatemulti-patchmodelswhererabbitscanmigratebetweendifferenthabitatpatches.TheseimprovedmodelswillallowthestudyofaninvasionofRCDinfectedrabbitsintoaregionpopulatedonlybyrabbitsinfectedwithmyxomatosis,andvisaversa.Othereffectsthatcouldbevaluabletoincludearetheeffectsofwaningimmunityinmyxomatosisforlookingatlongertimescales.ThismightbevaluableindecidingwhereandwhenitcouldbemostoptimaltointroduceRCDtoaregionasanmoreeffectivemeansofcontrollingrabbitpopulations.EFERENCESAnderson,R.andR.May(1982).Coevolutionofhostsandparasites.Parasitology85,411–426.Aparcio,J.P.,H.G.Solari,andN.Bonino(2004).Competitionandcoexistenceinhost-parasitesystems:themyxomatosiscase.PopulationEcology46,71–85.Barlow,N.D.,M.Barron,andJ.Parkes(2002).RabbithaemorrhagicdiseaseinNewZealand:eldtestofadisease-hostmodel.WildlifeResearch29,649–651.Barlow,N.D.andJ.M.Kean(1998).Simplemodelsfortheimpactofrabbitcalicivirusdisease(RCD)onAustralasianrabbits.EcolologicalModelling109,225–241.Cooke,B.(2011).Personalcommunication.Dwyer,G.,S.A.Levin,andL.Buttel(1990).AsimulationmodelofthepopulationdynamicsandevolutionofMyxomatosis.EcologicalMonographs60,423–447.Henning,J.,J.Meers,P.Davies,andR.Morris(2005).Survivalofrabbithaemorrhagicdiseasevirus(RHDV)intheenvironment.EpidemiologyandInfection133,719–730.Marchandeau,S.,S.Bertagnoli,B.Peralta,C.Boucraut-Baralon,J.Letty,andF.Reitz(2004).PossibleinteractionbetweenmyxomatosisandcalicivirosisrelatedtorabbithaemorrhagicdiseaseaffectingtheEuropeanrabbit.VeterinaryRecord155,589–592.Marsh,M.,M.Hutchings,S.McLeod,andP.White(2010).Spatialandtemporalheterogeneitiesinthecontactbehaviourofrabbits.BehavioralEcologyandSociobiology65,183–195.Mutze,G.,P.Bird,J.Kovaliski,D.Peacock,S.Jennings,andB.Cooke(2002).Emergingepidemiologicalpatternsinrabbithaemorrhagicdisease,itsinteractionwithmyxomatosis,andtheireffectsonrabbitpopulationsinSouthAustralia.WildlifeResearch29,577–590.Story,G.,D.Berman,R.Palmer,andJ.Scanlan(2004).Theimpactofrabbithaemorrhagicdiseaseonwildrabbit(Oryctolaguscuniculus)populationinQueensland.WildlifeResearch31,183–193. Figure2.Simulationofmodelwithoutinclusionofnaturalbirthanddeathsoveratimescaleofasingleoutbreak.ThesolidlinesareforbothdiseasespresentwithbothRCDandmyxomatosispresent(blacklinesfornoco-infectionandthinredlinesforco-infection)andthedashedlinesareforRCDalonewithnoinitialmyxomatosis.HerereferstothetotalprevalenceofRCD,=(=Nwithasimilartermforthetotalmyxomatosisprevalence. Figure3.Simulationsincorporatingbothdiseaseswithadensity-dependentdeathrateandaseasonalbirthrate.Thethickblacklineisfornosimultaneousco-infectionandthethinredlineallowsco-infectiontooccur. Table1.Diseaseparametervalues,fromBarlowandKean[1998]forRCDandandAparcioetal.[2004]formyxomatosis. Parameter(units)SymbolValue density-independentper-capitabirthrate(daysdensity-independentper-capitadeathrate(dayscarryingcapacity(rabbitsha transmissioncoefcient(rabbitshadaysper-capitamortalityrateduetodisease(daysper-capitarecoveryrate(days transmissioncoefcient(rabbitshadaysper-capitamortalityrateduetodisease(daysper-capitarecoveryrate(days ),andtherestofthepopulationevenlydividedinto.Aninitialprevalenceof10%forRCDwasusedinallcases,sotheinitialnumbersforallcompartmentsareS;I;I;R;R;J;J;I;R)=(0InFigure2thetotalpopulations,scaledwithrespecttothecarryingcapacity,wereplottedalongwiththeprevalenceforRCDandformyxomatosis.Acomparisonismadeofwheretheinitialmyxomatosisprevalenceof20%andwithnomyxomatosiswaspresentinitiallyinthepopulation,andnallywith20%initialmyxomatosisprevalencewheresimultaneousco-infectionispossible.Forthescenariowherenomyxomatosisispresentinitially,(0)=0,theinitialnumberofrabbitssusceptibletobothdiseasesisthenchangedfromThecasewherenoco-infectioncanoccurisdiscussedrst.IncomparisontoasingleRCDoutbreak,withnomyxomatosispresentinitially,theRCDoutbreakwithmyxomatosispresentissuppressed;itreachesapeakRCDprevalenceofonlyslightlyover15%comparedwithover30%.Ifsimultaneousco-infectionisallowedthenthepeakRCDprevalenceisstillsuppressed,butnowreachesavalueofapproximately0.24.Anexplanationforthesuppressioneffect,forthecaseofnoco-infection,isthatrabbitscurrentlyinfectedwithmyxomatosisremovepossiblesusceptiblerabbitsfrombeinginfectedbyRCD;akindof`vaccination'effectofmyxomatosisonRCD.Thetotalpopulationat20daysisreducedto0.46oftheinitialpopulationcomparedtolessthan0.3oftheinitialpopulationforwhenthereisnocurrentoutbreakofmyxomatosis.Whenthepossibilityofco-infectionexiststheresultsareintermediatebetweentheno-myxomatosisandwithmyxomatosisbutnoco-infectioncases.Apossibleexplanationisthepresenceofrabbitssimultaneouslyinfectedwithbothdiseasesreducestheprevalenceofmyxomatosis.InFigure3populationdynamicswithaseasonalbirthratewasassumed,withlogistic,density-dependentdeaths.Theseasonalbirthrate,thesameasusedbyBarlowandKean[1998],hasthefunctionalform)=1+t ;d=0toreplacetheconstantrate.Thus,theper-capitabirthrateoscillatesfromeveryyear.Usingthisvalueresultsinmonthlyexponentialnetgrowthratesrangingfrom,whichisofthesameorderofmagnitudeasthevaluesreportedinMutzeetal.[2002]forseveraldifferenteldstudiesinSouthAustralia.Forthesesimulationsmaximumstep-sizewassetto0.1days,topreventoutbreaksbeingmissed,andanoptiontopreventpopulationsbecomingnegativewasimposed.Thisgaveconsistentresultswithamaximumstepsizeof0.05.Forthecasewherethereisnomyxomatosispresentinitially(notshown)thenRCDdiesoutquickly.Forthecasewherebothdiseaseswerepresentinitially,withnosimultaneousconfectionallowed,thenmajoroutbreaksaresustained,occurringapproximately2yearsapart,butirregularlyspaced,andwith Includingalsothepopulationdynamics,thedifferentialequationscorrespondingtothecompartmentdiagraminFigure1are S; dt=�(b+cN)Ic+cS�(\rc+c)Ic;dIm dt=�(b+cN)Im+mS�(\rm+m)Im;dRc dt=�(b+cN)Rm+\rcIc�(m+b)Rc;dRm dt=�(b+cN)Rm+\rmIm�(c+b)Rc;dJm dt=�(b+cN)Jm+m+b)Rc�(\rm+m)Jm;dJc +( +(+( +(+(+(isthesumoftheninesubpopulations.Herewehaveassumedconstantper-capitabirthrateandalogisticdensity-dependentdeathrate.Here=(isthecarryingcapacity.and,withm;carethedisease-induceddeathrates.ThissystemofdifferentialequationsissolvedinMATLABusingtheroutine,whichisarobustadaptivetime-steppingprocedurebasedona4thorderRunge-Kuttaapproachwith5thordererrorestimation.Theoptions(setat0.1days)andwereusedforthesimulationsinvolvingoutbreaksover10yeartopreventthepopulationsfrombecomingnegativeandtopreventtoosmallstepsbeingtakensothatoutbreaksweremissed.Wefoundthatsettingthemaximumstepssizeto0.05daysgaveoutbreaksatthesametime.Thepopulationdynamicsrates(sourcedfromBarlowandKean[1998])wereobtainedfromrabbitpop-ulationsestimateddirectlyfromdata.Thecarryingcapacity=15wasprovidedfromBarlowandKean[1998],basedonSouthAustraliandata.ThesearesummarisedinTable1.RCDparameterswereobtainedfromBarlowandKean[1998].ForthemodelsdevelopedinBarlowandKean[1998],itismen-tionedthattheadditionofanincubationclass(i.e.theexposed,,inthenetworkmodel)didnotaffectthenaloutcomeofthemodel,solongasthetotaldurationofthedisease(frominfection)remainedconstantandthecontactrateincreasesproportionaltothedecreaseininfectiousperiod.Fortherabbitssimultaneouslyinfectedwithbothdiseasesweassumethetransmissioncoefcientandthedisease-inducedmortalityratecoefcienttobethesameasforRCDbutweassumethereisnorecoveryinthiscase(=0).Myxomatosisinrabbitshavebeenwell-studiedandcanbecategorisedintodifferentstrainsbythedurationofinfectionaswellasthemortalityratecausedbythestrain.Forthepurposeoftheinvestigationtobecarriedouthere,thenaturallydominant,andmostabundantstrainofthemyxomavirusinAustralia(GradeIIIB)wastheonlyoneconsidered(AndersonandMay[1982]).TheparametervaluesweresourcedfromAparcioetal.[2004](for)andAndersonandMay[1982](forAnalternatevaluefor=0isgiveninDwyeretal.[1990].3RESULTSOFSIMULATIONSSimulationsofthemodelwereproducedwherethebirthanddeathratesweresettozerotocapturethesoleeffectofthediseasesinteracting,independentofpopulationdensityeffects.Thisisrepresentativeofasinglepairofoutbreaksofbothdiseasespassingthroughthepopulationinashorttimescale,withthepopulationhavingexperiencedpreviousoutbreakssothatthearesomerabbitsinthepopulationwhohavepreviousrecoveredfromwithorbothdiseases.Forthesimulationsgeneratedinthissection,itisassumedthattheinitialpopulationdensity=15)compriseswhohaverecoveredfrombothdiseasesinfectiouswithRCDandmyxomatosiseach,havingnotcaughtanyotherdiseasesbefore( 2MODELDESCRIPTIONBoththeeffectsofRCDandofmyxomatosisonrabbitpopulationswerecombinedintoasinglemodeltoinvestigatepossibleinteractionsbetweenthetwodiseasesandthecombinedeffectsofthediseasesontherabbitpopulationdensity.Additionalvariablesareincludedtoincorporatetheinteractionofthediseases.Forthisparticularmodel,referstothepopulationdensitythatissusceptibletobothRCDandmyxomatosis,whereasrefertothepopulationdensitysusceptibletoeitherRCDbutnotmyxomatosis,ormyxomatosisbutnotRCDrespectively.Theinfectiouspopulationisdividedintofourseparatecategories:thoseinfectiouswithRCD,butarenotimmunetomyxomatosis();thoseinfectiouswithmyxomatosisbutarenotimmunetoRCD();thoseinfectiouswithRCDbutareimmunetomyxomatosis();andthoseinfectiouswithmyxomatosisbuthavealreadydevelopedimmunitytoRCDTherecoveredpopulationdensity,,referstotherabbitpopulationthathavesurvivedbothinfections(RCDandmyxomatosis),andhencedevelopedimmunitytoboththediseases.Immunityobtainedbyrabbitsisassumedtobelifelongforthetimescalesofinterestinthisstudy.Forsimplicityitisassumedthatgettinginfectedwithonediseasedoesimpactonthediseasecharacteristicsoftheotherdisease,suchastransmissionrate,mortalityrateandrecoveryrate.ThisassumptionissupportedbythefactthatRCDandmyxomatosisaretwocompletelyseparatediseasessoitisunlikelythatonewillconferanyimmunityfortheother.Acompartmentdiagramforthediseasetransmissionmodelwithbothdiseasesisprovidedbelow.InthisdiagramaretheforceofinfectionforRCDandmyxomatosis,respectively,;;,wherem;c,aretransmissioncoefcientswherewehaveassumeddensity-dependenttrans-missioninbothcases.WehavetakenthecoefcientforrabbitsinfectedwithbothdiseasessimultaneouslytobethesameasforRCD,whichisthemorevirulent,althoughitislikelythevaluewillbesmallerduetotheprobablediminishedcontactratesofalreadysickrabbits.Therecoveryratecoefcientsarerespectively,foreachinfectiousagent.Inthismodelthepossibilityforco-infectionwithbothdiseasesisincluded,withnumbersgivenbythevariable.Itisnotcurrentlyknownifco-infection(simultaneousinfectionwithbothdiseases)actuallyoccursinpractice.Cooke[2011]suggeststhatitisrareornon-existent.RCDinfectsfor4daysorso,myxomatosisfor15days.Whetherthisactuallyhappensornotwillalsodependinpartonseasonaleffects.ItseemsthatinSA,thetwodiseasesareunlikelytobeactiveatthesametimebutitmaybetrueinQueenslandthattheyare.Nevertheless,weincludeco-infectioninthemodelandlatercomparethesituationswhereitispossibleornotpossible.Hereweassumethatifsimultaneousco-infectionoccursthatthemortalityrateisthesameasforRCDalthoughinpracticeitislikelytobehigherduetothecompromisedheathoftherabbitalreadyinfectedwithmyxomatosis. S Ic Im Rc Rm Jm Jc R Ib cS \rcIc (m+b)Rc \rmJc mS \rmIm (c+b)Rm \rcIcm (m+b)Ic (c+b)Im bS Figure1.Compartmentdiagramillustratingtheowsbetweencompartmentsinthemodel,excludingthenaturalbirthsanddeaths 1INTRODUCTIONBecauseoftheirnotoriousbreeding,adaptabilityandinvasivecapabilities,theEuropeanrabbit(laguscuniculus)hasbeenestimatedtocausearound$600milliondamageannually,includingthecostofcontrolmeasures,aswellastheendangermentandextinctionofnativeoraandfauna.TheAus-traliangovernmenthastakenvariouscontrolmethodsinattemptstoreduce,oratleastlimit,therabbitpopulationinAustralia.Shootingwasoneofthemorecommonapproachestriedbuttolittlesuccess.Poisoningandwarrenrippingwerealsostandardconventionalcontrolmethodsbutwerebothlabourin-tensiveandexpensive.Thisleadresearcherstotheconsiderationofspecies-selectivebiologicalcontrolagents,morespecically,theMyxomavirusin1950,andlater,calicivirustocombatthedecliningeffectoftheMyxomavirus.TheMyxomaviruswasextremelylethalwhenrstintroduced,eliminatingintheexcessofofrabbitpopulations,althoughtheeffectsvariedfromsitetosite.Duringsubsequentyears,thevirulenceoftheMyxomavirusexperiencedasteadydecline.ThelessvirulentstrainofMyxomavirusiscompetitivelydominant,whichexplainwhyalthoughmyxomatosiswasintroducedusingthestrainwithhighestviru-lence(gradeI),withinafewyears,gradeIIIandgradeIVwerethemostabundantstrainsintheeld(Dwyeretal.[1990]).Inordertocombatthedecline,newvectorsofthedisease,inparticulartheEu-ropeanandSpanisheas,wereintroducedaswellasreintroductionoftheMyxomavirusinattemptstokick-startthediseaseagain.Whiletheseactionsincreasedtheimpactofthediseasetemporarily,myxo-matosiswasstillunabletoreachthelevelsofrabbitmortalityseenwhenitwasrstintroduced.ModelsthatstudythedifferentstrainsofmyxomatosisinrabbitpopulationshavebeendevelopedbyAndersonandMay[1982].In1995,thecalicivirus,orrabbithaemorrhagicdiseasevirus(RHDV),wasaccidentallyreleasedinAus-traliawhenitwasbeingunderconsiderationasanewpotentialbiologicalcontrolagent,followingthedevastatingimpactofitsreleaseinEurope.Calicivirusisthecausativeagentofrabbitcalicivirusdisease(RCD)whichhasamortalityrateofinrabbitsthatare3monthsorolder(Henningetal.[2005]).However,theeffectsofRCDvariedamongthesitesthatwereunderobservationforRCDoutbreaks.Inparticular,itappearedthatenvironmentalconditionssuchasincreasedrainfallandhightemperaturesdecreasedtheeffectivenessofRCDasacontrol(Storyetal.[2004]).AlsoreportedinStoryetal.[2004],therewerenooccurrenceofRCDoutbreaksinrabbitpopulationswherethedensityofsusceptibleswerelessthan12rabbitskmandthattheoveralleffectofRCDwasleastinsitesthatweremostsuitableforItwasreported(Mutzeetal.[2002])thatatsitesthathadmyxomatosis,theintroductionofRCDdelayedtheyearlyoutbreaksofmyxomatosis.Mutzeetal.[2002]suggestedthatRCDoutcompetesmyxomatosiswhenRCDismostactive(inspring)duetothelongerincubationperiodofmyxomatosis(daysasopposedtodaysforRCD).Thus,RCDwouldhavekilledmostrabbitsbeforetheybecomeinfectiousformyxomatosis.However,incertainhabitattypes,morespecically,swampyareasthatmayharbourmosquitoes,theshiftintheoutbreaksofmyxomatosiswasnotobserved.ItwassuggestedthatitwasbecausemosquitoeswerethemainvectorformyxomatosisandthusitwasmorefavourableoverRCDinsuchareas.Also,itwaspostulatedthatforareaswithlowrabbitdensity(whereRCDwouldbelesseffective),myxomatosiscouldprovetobeabettercontrolagent(Storyetal.[2004]).Marchandeauetal.[2004]showedstatisticallythatformostoftheirstudyareas,priorinfectionofmyxomatosiswasasignicantfactorinthepredictionofcontractionofRCD,andvice-versa.However,ingeneral,therehasbeenalackoftheoreticalresearchonthecombinationeffectofbothmyxomatosisandRCDonrabbitBarlowandKean[1998]andBarlowetal.[2002]developedmodelsforRCDandsuggestedthatindirecttransmissionofthevirusandjuvenileimmunitymayberequiredinthemodelforthediseasetopersistlocally.Then2-yearlysustainedoutbreakswereobserved.ThispaperattemptstoextendtheBarlowandKean[1998])modeltothatincorporatesbothRCDandmyxomatosisandinvestigatewhethermyxomato-siscansuppresstRCDprevalence.Theeffectofaseasonalbirth-rateisalsoinvestigated,butweneglecttheeffectsofjuvenileimmunityandindirecttransmission,todetermineifthepresenceofmyxomatosiscanalsostimulate2-yearlycycles. InteractionOfMyxomatosisAndRabbitHaemorrhagicDiseaseInWildRabbitG.R.Fulford ,X.J.Lee,D.BermanandG.HamiltonFacultyofScienceandTech.,QueenslandUniversityofTechnology,2GeorgeSt,Brisbane,QLD,4001RobertWicksPestAnimalResearchCentre,203TorStreet,Toowoomba,QLD4350Email:g.fulford@qut.edu.au IncreasingresistanceofrabbitstomyxomatosisinAustraliahasledtotheexplorationofRabbitHaemorrhagicDisease,alsocalledRabbitCalicivirusDisease(RCD)asapossiblecontrolagent.WhiletheinitialspreadofRCDinAustraliaresultedinwidespreadrabbitmortalityinaffectedareas,thepossiblepopulationdynamiceffectsofRCDandmyxomatosisoperatingwithinthesamesystemhavenotbeenproperlyexplored.Herewepresentearlymathematicalmodellingexaminingtheinteractionbetweenthetwodiseases.Inthisstudyweuseadeterministiccompartmentmodel,basedontheclassicalSIRmodelininfectiousdiseasemodelling.Weconsider,here,onlyasinglestrainofmyxomatosisandRCDandneglectlatentperiods.Wealsoincludelogisticpopulationgrowth,withtheinclusionofseasonalbirthrates.Weassumethereisnocross-immunityduetoeitherdisease.Themathematicalmodelallowsforthepossibilityofbothdiseasestobesimultaneouslypresentinanindividual,althoughresultsarealsopresentedforthecasewhereco-infectionisnotpossible,sinceco-infectionisthoughttoberareandquestionsexistastowhetheritcanoccur.Thesimulationresultsofthisinvestigationshowthatitisacrucialissueandshouldbepartoffutureeldstudies.AsinglesimultaneousoutbreakofRCDandmyxomatosiswassimulated,whileignoringnaturalbirthsanddeaths,appropriateforashorttimescaleof20days.SimultaneousoutbreaksmaybemorecommoninQueensland.Forthecasewhereco-infectionisnotpossiblewendthatthesimultaneouspresenceofmyxomatosisinthepopulationsuppressestheprevalenceofRCD,comparedtoanoutbreakofRCDwithnooutbreakofmyxomatosis,andthusleadstoalesseffectivecontrolofthepopulation.ThereasonforthisisthatinfectionwithmyxomatosisremovespotentiallysusceptiblerabbitsfromthepossibilityofinfectionwithRCD(likeavaccinationeffect).WefoundthatthereductioninthemaximumprevalenceofRCDwasapproximately30%foraninitialprevalenceof20%ofmyxomatosis,forthecasewheretherewasnosimultaneousoutbreakofmyxomatosis,butthepeakprevalencewasonly15%whentherewasasimultaneousoutbreakofmyxomatosis.However,thismaximumreductionwilldependonotherparam-etervalueschosen.Whenco-infectionisallowedthenthissuppressioneffectdoesoccurbuttoalesserdegree.Thisisbecausetherabbitsinfectedwithbothdiseasesreducestheprevalenceofmyxomatosis.Wealsosimulatedmultipleoutbreaksoveralongertimescaleof10years,includingnaturalpopulationgrowthrates,withseasonalbirthratesanddensitydependent(logistic)deathrates.Thisshowshowbothdiseasesinteractwitheachotherandwithpopulationgrowth.Hereweobtainsustainedoutbreaksoccurringapproximatelyeverytwoyearsforthecaseofasimultaneousoutbreakofbothdiseasesbutwithoutsimultaneousco-infection,withtheprevalencevaryingfrom0.1to0.5.WithoutmyxomatosispresentthenthesimulationpredictsRCDdiesoutquicklywithoutfurtherintroductionfromelsewhere.Withthepossibilityofsimultaneousco-infectionofrabbits,sustainedoutbreaksarepossiblebutthentheoutbreaksarelesssevereandmorefrequent(approximatelyyearly).Whilefurthermodeldevelopmentisneeded,ourworktodatesuggeststhat:1)thediseasesarelikelytointeractviatheirimpactsonrabbitabundancelevels,and2)introductionofRCDcansuppressmyx-omatosisprevalence.Werecommendthatfurthermodellinginconjunctionwitheldstudiesbecarriedouttofurtherinvestigatehowthesetwodiseasesinteractinthepopulation.Keywords:rabbits,calicivirus,myxomatosis,RCD,RHDV,pestcontrol