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Toxoplasmosis
FromWikipedia,thefreeencyclopedia

Toxoplasmosisisaparasitic diseasecausedbytheprotozoan Toxoplasmagondii.[1]The parasiteinfectsmostgeneraof warmbloodedanimals, includinghumans,butthe primaryhostisthefelid(cat) family.Animalsareinfectedby eatinginfectedmeat,by ingestionoffecesofacatthat hasitselfrecentlybeeninfected, andbytransmissionfrom mothertofetus.Catsarethe primarysourceofinfectionto humanhosts,althoughcontact withrawmeat,especiallypork, isamoresignificantsourceof humaninfectionsinsome countries.Fecalcontamination ofhandsisasignificantrisk factor.[2]

Toxoplasmosis
Classificationandexternalresources

T.gondiitachyzoites ICD10 ICD9 B58 (http://apps.who.int/classifications/icd10/browse/2010/en#/B58) 130(http://www.icd9data.com/getICD9Code.ashx?icd9=130)

DiseasesDB 13208(http://www.diseasesdatabase.com/ddb13208.htm) MedlinePlus 000637 (http://www.nlm.nih.gov/medlineplus/ency/article/000637.htm)

NicolleandManceauxfirst describedtheorganismin1908, eMedicine med/2294(http://www.emedicine.com/med/topic2294.htm) aftertheyobservedtheparasites D014123(http://www.nlm.nih.gov/cgi/mesh/2013/MB_cgi? MeSH intheblood,spleen,andliverof field=uid&term=D014123) aNorthAfricanrodent, Ctenodactylusgondii.The parasitewasnamedToxoplasma(arclikeform)gondii(aftertherodent)in1909.In1923,Jankureported parasiticcystsintheretinaofaninfantwhohadhydrocephalus,seizures,andunilateralmicrophthalmia. Wolf,Cowan,andPaige(19371939)determinedthesefindingsrepresentedthesyndromeofsevere congenitalT.gondiiinfection.[2]

Uptoathirdoftheworld'shumanpopulationisestimatedtocarryaToxoplasmainfection.[3][4]The CentersforDiseaseControlandPreventionnotestheoverallseroprevalenceintheUnitedStatesas determinedwithspecimenscollectedbytheNationalHealthandNutritionalExaminationSurvey (NHANES)between1999and2004wasfoundtobe10.8%,withseroprevalenceamongwomenof childbearingage(15to44years)11%.[5]AnotherstudyplacedseroprevalenceintheUSat22.5%.[4]The samestudyclaimedaseroprevalenceof75%inElSalvador.[4]OfficialassessmentinGreatBritainplaces thenumberofinfectionsatabout350,000ayear.[6] Duringthefirstfewweeksafterexposure,theinfectiontypicallycausesamild,flulikeillnessornoillness. Thereafter,theparasiterarelycausesanyphysicalsymptomsinotherwisehealthyadults.[citationneeded] However,thosewithweakenedimmunesystems,suchasthosewithAIDSandpregnantwomen,may becomeseriouslyill,anditcanoccasionallybefatal.[citationneeded]Theparasitecancauseencephalitis

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(inflammationofthebrain)andneurologicdiseases,andcanaffecttheheart,liver,innerears,andeyes (chorioretinitis).[citationneeded]Recentresearchhasalsolinkedtoxoplasmosiswithattentiondeficit hyperactivitydisorder,obsessivecompulsivedisorder,andschizophrenia.[7]Numerousstudiesfounda positivecorrelationbetweenlatenttoxoplasmosisandsuicidalbehaviorinhumans.[8][9][10]

Contents
1Signsandsymptoms 1.1Acutetoxoplasmosis 1.2Latenttoxoplasmosis 1.3Cutaneoustoxoplasmosis 1.4Psychiatricdisorders 1.5Contraryevidence 2Diagnosis 3Transmission 3.1Pregnancyprecautions 3.2Rodentbehavior 4Treatment 4.1Acute 4.2Latent 5Epidemiology 6History 7Societyandculture 7.1Notablecases 8Otheranimals 8.1Livestock 8.2Domesticcats 8.3Marinemammals 9Seealso 10References 11Bibliography 12Externallinks

Signsandsymptoms
Infectionhastwostages:

Acutetoxoplasmosis
Duringacutetoxoplasmosis,symptomsareofteninfluenzalike:swollenlymphnodes,ormuscleachesand painsthatlastforamonthormore.Rarelywillahumanwithafullyfunctioningimmunesystemdevelop severesymptomsfollowinginfection.Youngchildrenandimmunocompromisedpeople,suchasthose withHIV/AIDS,thosetakingcertaintypesofchemotherapy,orthosewhohaverecentlyreceivedan organtransplant,maydevelopseveretoxoplasmosis.Thiscancausedamagetothebrain(encephalitis)or

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theeyes(necrotizingretinochoroiditis).Infantsinfectedviaplacentaltransmissionmaybebornwitheither oftheseproblems,orwithnasalmalformations,althoughthesecomplicationsarerareinnewborns.The toxoplasmictrophozoitescausingacutetoxoplasmosisarereferredtoasTachyzoites,andaretypically foundinbodilyfluids. Swollenlymphnodesarecommonlyfoundintheneckorunderthechin,followedbytheaxillae(armpits) andthegroin.Swellingmayoccuratdifferenttimesaftertheinitialinfection,persist,and/orrecurfor varioustimesindependentlyofantiparasitictreatment.[11]Itisusuallyfoundatsinglesitesinadults,butin children,multiplesitesmaybemorecommon.Enlargedlymphnodeswillresolvewithinonetotwo monthsin60%ofcases.However,aquarterofthoseaffectedtaketwotofourmonthstoreturntonormal, and8%takefourtosixmonths.Asubstantialnumber(6%)donotreturntonormaluntilmuchlater.[12]

Latenttoxoplasmosis
ItiseasyforahosttobecomeinfectedwithToxoplasmagondiianddeveloptoxoplasmosiswithout knowingit.Inmostimmunocompetentpeople,theinfectionentersalatentphase,duringwhichonly bradyzoitesarepresent,formingcystsinnervousandmuscletissue.Mostinfantswhoareinfectedwhilein thewombhavenosymptomsatbirth,butmaydevelopsymptomslaterinlife.[13]

Cutaneoustoxoplasmosis
Whilerare,skinlesionsmayoccurintheacquiredformofthedisease,includingroseolaanderythema multiformelikeeruptions,prurigolikenodules,urticaria,andmaculopapularlesions.Newbornsmayhave punctatemacules,ecchymoses,orblueberrymuffinlesions.Diagnosisofcutaneoustoxoplasmosisis basedonthetachyzoiteformofT.gondiibeingfoundintheepidermis.Itisfoundinalllevelsofthe epidermis,isabout6mby2mandbowshaped,withthenucleusbeingonethirdofitssize.Itcanbe identifiedbyelectronmicroscopyorbyGiemsastainingtissuewherethecytoplasmshowsblue,the nucleusred.[14]

Psychiatricdisorders
Studieshaveshownthetoxoplasmosisparasitemayaffectbehaviorandmaypresentasorbeacausativeor contributoryfactorinvariouspsychiatricdisorders,suchasdepression,anxiety,and schizophrenia.[15][16][17]In11of19scientificstudies,T.gondiiantibodylevelswerefoundtobe significantlyhigherinindividualsaffectedbyfirstincidenceschizophreniathaninunaffectedpersons. Individualswithschizophreniaarealsomorelikelytoreportaclinicalhistoryoftoxoplasmosisthanthose inthegeneralpopulation.[18]RecentworkattheUniversityofLeedshasfoundtheparasiteproducesan enzymewithtyrosinehydroxylaseandphenylalaninehydroxylaseactivity.Thisenzymemaycontributeto thebehavioralchangesobservedintoxoplasmosisbyalteringtheproductionofdopamine,a neurotransmitterinvolvedinmood,sociability,attention,motivation,andsleeppatterns.Schizophreniahas longbeenlinkedtodopaminedysregulation.[19]Minocycline,anantibioticcapableofpassingtheblood brainbarrierusedfortreatingtoxoplasmosis,hasbeenfoundtoalleviatethesymptomsof schizophrenia.[20] ChronicinfectionwithT.gondiihastraditionallybeenconsideredasymptomaticinimmunocompetent humanhosts.However,accumulatingevidencesuggestslatentinfectionmaysubtlyinfluencearangeof humanbehaviorsandtendencies,andinfectionmayalterthesusceptibilitytoorintensityofanumberof affective,psychiatric,orneurologicaldisorders.[21]

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LatentT.gondiiinfectioninhumanshasbeenassociatedwithimpairedpsychomotorperformance, enhancedrisktakingpersonalityprofiles,andhigherincidenceofautomobileaccidents.[21]Moreover, correlationshavebeenfoundbetweenpositiveantibodytiterstoT.gondiiandOCD,Parkinsonsdisease, Alzheimersdisease,suicideinpeoplewithmooddisorders,andbipolardisorder.[21]Positiveantibody titerstoT.gondiihavebeenshowntobenotcorrelativewithmajordepressionordysthymia.[22] ThemostsubstantialbodyofevidencelinkingT.gondiitoaneurologicaldisorderinvolvesthepotential associationbetweenschizophreniaandinfectionwiththeparasite.[23][24]Asof2013,atleast38studies havefoundapositivecorrelationbetweenT.gondiiantibodytitersandschizophrenia.[21][25]Whilethe vastmajorityofthesestudiestestedpeoplealreadydiagnosedwithschizophreniaforT.gondiiantibodies, significantassociationsbetweenT.gondiiandschizophreniahavebeenfoundpriortotheonsetof schizophreniadiseasesymptoms.[23] InmostofthecurrentstudieswherepositiveassociationshavebeenfoundbetweenT.gondiiantibody titersandcertainbehavioraltraitsorneurologicaldisorders,T.gondiiseropositivitytestsareconducted aftertheonsetoftheexamineddiseaseorbehavioraltraitthatis,itisoftenunclearwhetherinfectionwith theparasiteincreasesthechancesofhavingacertaintraitordisorder,orifhavingacertaintraitordisorder increasesthechancesofbecominginfectedwiththeparasite.[26] Groupsofindividualswithcertainbehavioraltraitsorneurological disordersmaysharecertainbehavioraltendenciesthatincreasethe likelihoodofexposuretoandinfectionwithT.gondiiasaresult, itisdifficulttoconfirmcausalrelationshipsbetweenT.gondii infectionsandassociatedneurologicaldisordersorbehavioral traits.[26]

Contraryevidence
ToxoplasmagondiiisbeneficialtomicewithAlzheimer'sdisease. [27]MurineanaloguestotheComt,DRD4andDAT1human genesalsoexist,andthesegenesarerelatedtoAlzheimer's disease.[28]DAT1,forexample,encodestheneuralmembranes throughwhichdopaminereturnstothecell.DAT1genemutations areresponsiblefortoorapiddopamineuptake,whichresultsin deficiencyinextracellulardopamine.SinceT.gondiiproduces dopamine,ithasapotentialtoovercomethesegenerelated disordersalsoinhumans,mainlybecausethemechanisms encodedbyComt,DRD4,andDAT1arebothmurineandhuman. ToofastDAT1dopamineuptakeisrelatedtootherneurological disorders[29][30]whichcanpotentiallybenefitfromT.gondii dopaminesynthesis.Itisaninterestingopenquestionwhether mammalswithDAT1polymorphismsaregeneticallybetter adaptedtoT.gondiiinfection.

Micrographofalymphnodeshowing thecharacteristicchangesof toxoplasmosis(scatteredepithelioid histiocytes(palecells),monocytoid cells(topcenterofimage),large germinalcenters(leftofimage)) H&Estain

ExamplesofgeneticfactorsinParkinson'sdiseaseareLRRK2mutationsGly2019Ser,I2020T,andothers. SomeevidenceindicatesexposuretopesticidescausesParkinson'sdisease[31]Thediseasepresentswhen 80%oftheneuronsthatproducedopamineinthesubstantianigradie.Thisshortageofdopaminecouldbe compensatedbyT.gondii,whichisknowntoproducedopamine.

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Diagnosis
Toxoplasmosiscanbedifficulttodistinguishfromprimarycentralnervoussystemlymphoma,andasa result,thediagnosisismadebyatrialoftherapy(pyrimethamine,sulfadiazine,andfolinicacid(USAN: leucovorin)),followedbyabrainbiopsyifthedrugsproducenoeffectclinicallyandnoimprovementon repeatimaging. DetectionofT.gondiiinhumanbloodsamplesmayalsobeachievedbyusingthepolymerasechain reaction.[32]Inactivecystsmayexistinahostwhichwouldevadedetection. Toxoplasmosiscannotbedetectedwithimmunostaining.LymphnodesaffectedbyToxoplasmahave characteristicchanges,includingpoorlydemarcatedreactivegerminalcenters,clustersofmonocytoidB cells,andscatteredepithelioidhistiocytes.

Transmission
Transmissionmayoccurthrough: Ingestionofraworpartlycookedmeat,especiallypork,lamb, orvenisoncontainingToxoplasmacysts:Infectionprevalence incountrieswhereundercookedmeatistraditionallyeaten hasbeenrelatedtothistransmissionmethod.Tissuecysts mayalsobeingestedduringhandtomouthcontactafter handlingundercookedmeat,orfromusingknives,utensils,or cuttingboardscontaminatedbyrawmeat.[33] Ingestionofcontaminatedcatfeces:Thiscanoccurthrough handtomouthcontactfollowinggardening,cleaningacat's litterbox,contactwithchildren'ssandpits,ortouchinga leechtheparasitecansurviveintheenvironmentforovera year.[34]
Lifecycleof Toxoplasmagondii Catsexcretethepathogenintheirfecesforanumberofweeksafter contractingthedisease,generallybyeatinganinfectedrodent.Even then,catfecesarenotgenerallycontagiousforthefirstdayortwoafterexcretion,afterwhichthecyst 'ripens'andbecomespotentiallypathogenic.[35]

Pregnancyprecautions
Congenitaltoxoplasmosisisaspecialforminwhichanunbornfetusisinfectedviatheplacenta.Apositive antibodytiterindicatespreviousexposureandimmunity,andlargelyensurestheunbornfetus'safety.A simpleblooddrawatthefirstprenataldoctorvisitcandeterminewhetherornotawomanhashadprevious exposureandthereforewhetherornotsheisatrisk.IfawomanreceivesherfirstexposuretoT.gondii whilepregnant,thefetusisatparticularrisk.Awomanwithnopreviousexposureshouldavoidhandling rawmeat,exposuretocatfeces,andgardening(catfecesarecommoningardensoil).Mostcatsarenot activelysheddingoocysts,soarenotadanger,buttheriskmaybereducedfurtherbyhavingthelitterbox emptieddaily(oocystsrequirelongerthanasingledaytobecomeinfective),andbyhavingsomeoneelse emptythelitterbox.However,whileriskscanbeminimized,theycannotbeeliminated.Forpregnant

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womenwithnegativeantibodytiters,indicatingnopreviousexposuretoT.gondii,serologytestingas frequentasmonthlyisadvisableastreatmentduringpregnancyforthosewomenexposedtoT.gondiifor thefirsttimedecreasesdramaticallytheriskofpassingtheparasitetothefetus. Despitetheserisks,pregnantwomenarenotroutinelyscreenedfortoxoplasmosisinmostcountries (Portugal,[36]France,[37]Austria,[37]Uruguay,[38]andItaly[39]beingtheexceptions)forreasonsofcost effectivenessandthehighnumberoffalsepositivesgenerated.Asinvasiveprenataltestingincurssome risktothefetus(18.5pregnancylossespertoxoplasmosiscaseprevented),[37]postnatalorneonatal screeningispreferred.Theexceptionsarecaseswherefetalabnormalitiesarenoted,andthusscreening canbetargeted.[37] SomeregionalscreeningprogrammesoperateinGermany,SwitzerlandandBelgium.[39] Treatmentisveryimportantforrecentlyinfectedpregnantwomen,topreventinfectionofthefetus.Sincea baby'simmunesystemdoesnotdevelopfullyforthefirstyearoflife,andtheresilientcyststhatform throughoutthebodyareverydifficulttoeradicatewithantiprotozoans,aninfectioncanbeveryseriousin theyoung. In2006,aCzechresearchteamdiscoveredwomenwithhighlevelsoftoxoplasmosisantibodieswere significantlymorelikelytohavebabyboysthanbabygirls.Inmostpopulations,thebirthrateisaround 51%boys,butwomeninfectedwithT.gondiihaduptoa72%chanceofaboy.[40]

Rodentbehavior
InfectionwithT.gondiihasbeenshowntoalterthebehaviorofmiceandratsinwaysthoughttoincrease therodentschancesofbeingpreyeduponbycats.[23][41][42]Infectedrodentsshowareductionintheir innateaversiontocatodorswhileuninfectedmiceandratswillgenerallyavoidareasmarkedwithcat urineorwithcatbodyodor,thisavoidanceisreducedoreliminatedininfectedanimals.[23][42][43] Moreover,someevidencesuggeststhislossofaversionmaybespecifictofelineodors:whengivena choicebetweentwopredatorodors(catormink),infectedrodentsshowasignificantlystrongerpreference tocatodorsthandouninfectedcontrols.[44][45] T.gondiiinfectedrodentsshowanumberofbehavioralchangesbeyondalteredresponsestocatodors. Ratsinfectedwiththeparasiteshowincreasedlevelsofactivityanddecreasedneophobicbehavior.[41][46] Similarly,infectedmiceshowalterationsinpatternsoflocomotionandexploratorybehaviorduring experimentaltests.Thesepatternsincludetravelinggreaterdistances,movingathigherspeeds,accelerating forlongerperiodsoftime,andshowingadecreasedpausetimewhenplacedinnewarenas.[47]Infected rodentshavealsobeenshowntohavedifferencesintraditionalmeasuresofanxiety,suchaselevatedplus mazes,openfieldarenas,andsocialinteractiontests.[47][48]

Treatment
Treatmentisoftenonlyrecommendedforpeoplewithserioushealthproblems,suchaspeoplewithHIV whoseCD4countsareunder200,becausethediseaseismostseriouswhenone'simmunesystemisweak. Trimethoprim/sulfamethoxazoleisthedrugofchoicetopreventtoxoplasmosis,butnotfortreatingactive disease.

Acute
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Themedicationsprescribedforacutetoxoplasmosisare: Pyrimethamineanantimalarialmedication Sulfadiazineanantibioticusedincombinationwithpyrimethaminetotreattoxoplasmosis Combinationtherapyisusuallygivenwithfolicacidsupplementstoreduceincidenceof thrombocytopaenia. CombinationtherapyismostusefulinthesettingofHIV. Clindamycin Spiramycinanantibioticusedmostoftenforpregnantwomentopreventtheinfectionoftheir children (otherantibiotics,suchasminocycline,haveseensomeuseasasalvagetherapy).

Latent
Inpeoplewithlatenttoxoplasmosis,thecystsareimmunetothesetreatments,astheantibioticsdonot reachthebradyzoitesinsufficientconcentration. Themedicationsprescribedforlatenttoxoplasmosisare: AtovaquoneanantibioticthathasbeenusedtokillToxoplasmacystsinsideAIDSpatients[49] Clindamycinanantibioticwhich,incombinationwithatovaquone,seemedtooptimallykillcysts inmice[50]

Epidemiology
T.gondiiinfectionsoccurthroughouttheworld,althoughinfectionratesdiffersignificantlybycountry.[51] Forwomenofchildbearingage,asurveyof99studieswithin44countriesfoundtheareasofhighest prevalencearewithinLatinAmerica(about5080%),partsofEasternandCentralEurope(about20 60%),theMiddleEast(about3050%),partsofSoutheastAsia(about2060%),andpartsofAfrica(about 2055%).[51] IntheUnitedStates,datafromtheNationalHealthandNutritionExaminationSurvey(NHANES)from 1999to2004found9.0%ofUSbornpersons1249yearsofagewereseropositiveforIgGantibodies againstT.gondii,downfrom14.1%asmeasuredintheNHANES19881994.[52]Inthe19992004 survey,7.7%ofUSbornand28.1%offoreignbornwomen1544yearsofagewereT.gondii seropositive.[52]Atrendofdecreasingseroprevalencehasbeenobservedbynumerousstudiesinthe UnitedStatesandmanyEuropeancountries.[51] Becausetheparasiteposesaparticularthreattofetuseswhenitiscontractedduringpregnancy,[53]much oftheglobalepidemiologicaldataregardingT.gondiicomesfromseropositivitytestsinwomenof childbearingage.SeropositivitytestslookforthepresenceofantibodiesagainstT.gondiiinblood,so whileseropositivityguaranteesonehasbeenexposedtotheparasite,itdoesnotnecessarilyguaranteeone ischronicallyinfected.[54]

History

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TheT.gondiiprotozoanwasfirstdiscoveredbyNicolleandManceaux,whoin1908isolateditfromthe AfricanrodentCtenodactylusgundi,thenin1909differentiatedtheorganismfromLeishmaniaandnamed itToxoplasmagondii.[37]Thefirstrecordedcongenitalcasewasnotuntil1923,andthefirstadultcasenot until1940.[37]In1948,aserologicaldyetestwascreatedbySabinandFeldman,whichisnowthe standardbasisfordiagnostictests.[55]

Societyandculture
Notablecases
ArthurAshe(tennisplayer)developedneurologicalproblemsfromtoxoplasmosis(andwaslater foundtobeHIVpositive).[56] MerrittButrick(actor)wasHIVpositiveanddiedfromtoxoplasmosisasaresultofhisalready weakenedimmunesystem.[57] PrinceFranois,CountofClermont(pretendertothethroneofFrance)hisdisabilitycausedhimto beoverlookedinthelineofsuccession. LeslieAsh(actress)contractedtoxoplasmosisinthesecondmonthofpregnancy.[58] SebastianCoe(Britishmiddledistancerunner)[59] MartinaNavratilovasufferedfromtoxoplasmosisduringthe1982USOpen.[60] LouisWain(artist)wasfamousforpaintingcatshelaterdevelopedschizophrenia,whichsome believewasduetotoxoplasmosisresultingfromhisprolongedexposuretocats.[61] JaroslavFlegr(biologist)isaproponentofthetheorythattoxoplasmosisaffectshumanbehavior.[62]

Otheranimals
AlthoughT.gondiihasthecapabilityofinfectingvirtuallyallwarmbloodedanimals,susceptibilityand ratesofinfectionvarywidelybetweendifferentgeneraandspecies.[63]Ratesofinfectioninpopulationsof thesamespeciescanalsovarywidelyduetodifferencesinlocation,diet,andotherfactors.

Livestock
Amonglivestock,pigs,sheep,andgoatshavethehighestratesofchronicT.gondiiinfection.[64]The prevalenceofT.gondiiinmeatproducinganimalsvarieswidelybothwithinandbetweencountries,[64] andratesofinfectionhavebeenshowntobedramaticallyinfluencedbyvaryingfarmingandmanagement practices.[65]Forinstance,animalskeptoutdoorsorinfreerangingenvironmentsaremoreatriskof infectionthananimalsraisedindoorsorincommercialconfinementoperations.[65][66] IntheUnitedStates,thepercentageofpigsharboringviableparasiteshasbeenmeasured(viabioassayin miceorcats)tobeashighas92.7%andaslowas0%,dependingonthefarmorherd.[66]Surveysof seroprevalence(T.gondiiantibodiesinblood)aremorecommon,andsuchmeasurementsareindicativeof thehighrelativeseroprevlanceinpigsacrosstheworld.[67]Alongwithpigs,sheepandgoatsareamong themostcommonlyinfectedlivestockofepidemiologicalsignificanceforhumaninfection.[64]Prevalence ofviableT.gondiiinsheeptissuehasbeenmeasured(viabioassay)tobeashighas78%intheUnited States,[68]anda2011surveyofgoatsintendedforconsumptionintheUnitedStatesfounda seroprevalenceof53.4%.[69]

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Duetoalackofexposuretotheoutdoors,chickensraisedinlargescaleindoorconfinementoperationsare notcommonlyinfectedwithT.gondii.[65]Freerangingorbackyardraisedchickensaremuchmore commonlyinfected.[65]AsurveyoffreerangingchickensintheUnitedStatesfounditsprevalencetobe 17%100%,dependingonthefarm.[70]Becausechickenmeatisgenerallycookedthoroughlybefore consumption,poultryisnotgenerallyconsideredtobeasignificantriskfactorforhumanT.gondii infection.[71] AlthoughcattleandbuffalocanbeinfectedwithT.gondii,theparasiteisgenerallyeliminatedorreduced toundetectablelevelswithinafewweeksfollowingexposure.[65]Tissuecystsarerarelypresentinbuffalo meatorbeef,andmeatfromtheseanimalsisconsideredtobelowriskforharboringviable parasites.[64][66] HorsesareconsideredresistanttochronicT.gondiiinfection.[65]However,viablecellshavebeenisolated fromUShorsesslaughteredforexport,andseverehumantoxoplasmosisinFrancehasbeen epidemiologicallylinkedtotheconsumptionofhorsemeat.[66]

Domesticcats
TheseroprevalenceofT.gondiiindomesticcats,worldwide,hasbeenestimatedtobearound3040%.[72] IntheUnitedStates,noofficialnationalestimatehasbeenmade,butlocalsurveyshaveshownlevels variedbetween16%and80%.[72]A2012surveyof445purebredpetcatsand45sheltercatsinFinland foundanoverallseroprevalenceof48.4%.[73]A2010surveyofferalcatsfromGiza,Egypt,foundan overallseroprevalenceof97.4%.[74] T.gondiiinfectionratesindomesticcatsvarywidelydependingonthecats'dietsandlifestyles.[75]Feral catsthathuntfortheirfoodaremorelikelytobeinfectedthandomesticcats.TheprevalenceofT.gondii incatpopulationsdependsontheavailabilityofinfectedbirdsandsmallmammals,[76]butoftenthisprey isabundant. Mostinfectedcatswillshedoocystsonlyonceintheirlifetimes,foraperiodofaboutonetotwo weeks.[72]Althoughthisperiodofsheddingisquitetransient,millionsofoocystscanbeshed,witheach oocystcapableofspreadingandsurvivingformonths.[72]Anestimated1%ofcatsatanygiventimeare activelysheddingoocysts.[65]

Marinemammals
AUniversityofCalifornia,Davisstudyofdeadseaotterscollectedfrom1998to2004found toxoplasmosiswasthecauseofdeathfor13%oftheanimals.[77]Proximitytofreshwateroutflowsintothe oceanwasamajorriskfactor.Ingestionofoocystsfromcatfaecesisconsideredtobethemostlikely ultimatesource.[78]Surfacerunoffcontainingwildcatfaecesandlitterfromdomesticcatsflusheddown toiletsarepossiblesourcesofoocysts.[79]Theparasiteshavebeenfoundindolphinsandwhales.[17] ResearchersBlackandMassiebelieveanchovies,whichtravelfromestuariesintotheopenocean,maybe helpingtospreadthedisease.

Seealso
TORCHinfection

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TheT.GondiiHost/Pathogeninteractome(http://www.polygenicpathways.co.uk/tgondii.htm)

References
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Toxoplasmosis - Wikipedia, the free encyclopedia

themarineenvironment". IntJParasitol 35(1112):115568.doi:10.1016/j.ijpara.2005.07.002 (http://dx.doi.org/10.1016%2Fj.ijpara.2005.07.002).PMID16157341 (//www.ncbi.nlm.nih.gov/pubmed/16157341). 78. ^17:3022:00"TreatingDiseaseintheDevelopingWorld"(http://www.npr.org/templates/story/story.php? storyId=5058325). TalkoftheNationScienceFriday.NationalPublicRadio.December16,2005. 79. ^"Parasiteincatskillingseaotters"(http://www.magazine.noaa.gov/stories/mag72.htm). NOAAmagazine (NationalOceanicandAtmosphericAdministration).21January2003.Retrieved24November2007.

PartsofthisarticlearetakenfromthepublicdomainCDCfactsheet:Toxoplasmosis (http://www.cdc.gov/toxoplasmosis/)

Bibliography
LouisMWeissKamiKim(28April2011).ToxoplasmaGondii:TheModelApicomplexan. PerspectivesandMethods(http://books.google.com/books?id=yTUkJEphM_IC).AcademicPress. ISBN9780080475011.Retrieved12March2013. J.P.Dubey(15April2010).ToxoplasmosisofAnimalsandHumans,SecondEdition (http://books.google.com/books?id=5Nm7t5p9APAC).CRCPress.ISBN9781420092370. Retrieved12March2013.

Externallinks
Toxoplasmosis(http://www.merck.com/mmpe/sec14/ch186/ch186h.html)atMerckManualof DiagnosisandTherapyProfessionalEdition Toxoplasmosis (http://www.hpa.org.uk/webw/HPAweb&HPAwebStandard/HPAweb_C/1195733799638)at HealthProtectionAgency(HPA),UnitedKingdom PicturesofToxoplasmosis(http://rad.usuhs.edu/medpix/medpix.html? mode=image_finder&action=search&srchstr=toxoplasmosis#top)MedicalImageDatabase VideoInterview(http://www.youtube.com/watch?v=m3x3TMdkGdQ)withProfessorRobert SapolskyonToxoplasmosisanditsaffectonhumanbehavior.(24:27min) Retrievedfrom"http://en.wikipedia.org/w/index.php?title=Toxoplasmosis&oldid=566312154" Categories: Catdiseases Apicomplexa Protozoaldiseases Zoonoses Mindalteringparasites Parasiticinfestations,stings,andbitesoftheskin Poultrydiseases Healthissuesinpregnancy Thispagewaslastmodifiedon29July2013at17:45. TextisavailableundertheCreativeCommonsAttributionShareAlikeLicenseadditionaltermsmay apply.Byusingthissite,youagreetotheTermsofUseandPrivacyPolicy. WikipediaisaregisteredtrademarkoftheWikimediaFoundation,Inc.,anonprofitorganization.

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