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Avian Borna Virus: PDD or really AAG? – Dr OroszA disease that needs some changes of thinkingPDD = Avian Ganglio Neuritis New insights into PDDOriginally reported in macaw species (macaw wasting disease)Reported in more than 50 species of psittacine birds including African greys, macaws, conures, lovebirds, amazons, cockatoos, cockatiels, parakeetsdisease of captive birdsappears to be widespread30-50% of population affecteddepends on locale and testingClinical disease is variable – how it presents is variable, old world vs new worlddistribution of lesions in CNS, PNS, ANSseverity of lesions‘Classic’ Disease – gastro tract, most often observed in New World species.Classic presentation:depression, anorexia, loss of body condition, regurgitation, loss of pectoral mass, undigested stuff in fecesPathology view, end stageno suppurativelymphocytic, plasmatcyticganglioneuritisPCR: presence avian bornavirus (ABV)sometimes, but not all the time Historically viruses proposed: adenovirus, coronavirus, Eastern equine encephalitis, togavirus paramyxovirus, deno-like viruses, Enteroviruses Reoviruses documented in PDD 2007 suspected paramyxovirus like dx, blood PDD positive birds2 independent reports BVD in summer of 2008, with a 3rd group shortly afterCorrelation of Borna Virus Disease (BVD) with avian cases of PDDNewcastle is a paramyxovirus Virus Chipinterrogated confirmed PDD and control case seriessamples independently collected on 2 continentsMicroarray tissues screened for most known viral pathogensNovel Borna virus signature detectedTexas A&M researchersABV was cultured from confirmed PDD caseInfected 3 healthy cockatiels with ABV2/3 birds developed clinical PDDABV was detected in 3/3 cloacal swas3/3 birds histopathy lesionsBDV – very conserved, 2 genotypes identifiedABV – more diversecurrently 6 genotyes knownrelationship between genotype, specific host disease unknown at this timeBDV and ABV share similar structure BVD is mammalian formABV presents in healthy birdscauses a viremia without clinical diseaseBlood ABV testing:Europe 46% healthy birds are ABV positive30% infection rate in US33% BVD infection rate in healthy humansIncubation period unknownSexually transmitted in the vitolene membrane of the eggPsittacine nursery outbreak, 20 daysCockatiels – loss of body weight and condition by 20-30 days post infectionDetermined, release P40 (glyco) protein with bornavirus infection, ganglia or nuclei. P40 protein released Research Rossie Groupinjected protein into normal cockatielsbirds developed symptoms of PDD but did not have ABVPDD is actually an autoinflammatory response/diseaseBirds can have PDD without ABVThe virus gets into the body, it depends on the immune system of the bird – if the virus attacks the glyco proteins and where, the symptoms develop. Like Guillain barre disease – THIS IS IMPORTANT LOOK IT UPInfectious agent:ABV or other neurotropic virusesCauses release, proteinHistopathologic lesions compatible with autoimmune dxInvasion, T lymphocytes, plasma cells {Paramyxovirus and ABV gene blast are so close it’s scary – federal government might be concerned}inflammation in glial cellsleakage of proteinsCAN, ANS, associated, GI dysfunction and neurological signs, cerebrum and cerebellumPNS: spinal cord ANS:ParasympatheticLong preganglionic fiberShort postganglionic, organ wallMixing and digestionSympatheticBoth are longGanglia outside of the organVagus NerveNuclei that innervate:Nucleus ambiguousDorsal nucleus, GI tract -> colonTaste fibersSpinal nucleus: sensory, face, motor jawABV: Autonomic NSDorsal vegal nucleusLesionssmooth muscle atrophy/neurogenic atrophyAtony, dilatation, impaction – crop, proventriculus, ventriculus, intestines Adrenal glandLymphocytes, medullaClusters near cortexOften used for histopathologyCerebrumLymphocytic perivascular cuffingGlial cells affectedSite determines the neurologic signsCerebellumGlia + granular cell layerDisruption/loss Purkinje cell layerGlia + molecular cell layerProprioceptionConscious proprioception – know where the body isFascilus gracilus and cuneatus – tracts to go conscious centers If lymphocites are in the way, they can’t tell where they are – will fall, stumble, etcABV(AAG) Clinical signs – CNSoften in old world species+/- GI tract signsCNS signs only -> histopathology: GI tract lesions+/- cortical blindness (can see but can’t interpret images properly)ataxia, incoordinationproprioceptive & motor deficitsprogressive paresisless commonly paralysis and seizuresABV(AAG) PNS AnatomyThoracolumbar spinal cord greatly affectedFocal microgliosis Swollen axons, myelin degenerationPeripheral neuritis in birdsMay be contributory to feather and self mutilation disordersPDD diagnosis, ABV testingpresumptive diagnosis – history, clinical signs, radiological evidence of diseaseDefinitive diagnosis – characteristic lymphoplasmocytic ganlioneuritisCropVentricularBiopsy majority of testing just shows if bird has borna, NOT PDD. Use as clueABV RT- PCR-Tested 791 blood and/or cloacal swab samples up through 2008- 34.3% were positive- present in all major speciesABV detected in: highest concentration in retina, brain, and spinal cordSignificant percentage of avian population affectedA continuum of clinical diseases existsA wasting bird represents an extreme caseMajority of birds DO NOT SHOW clinical disease Clinical disease, intermittent or more continuous – can exhibit symptoms only during certain times of the year, especially during hormonal periods. As a sexually transmitted the disease, the virus has to be activated by the gonadal hormones to then pass down the disease to the chick via the egg membrane. OR virus is passed vent to vent or via eating feces of infected bird. More commonly during hormonal periodsCNSHyperexcitableWobblyBlindness (can be reversed if properly treated)Anything that is neurotropic as a virus can potentially cause the problemAAG IS A RETAINED VIRUSVirus can’t live for long outside of its environment – is NOT airborneTreatment: [has to be based on the symptoms that the bird has]ANS signs:Altered GI tract function, bacterial overgrowthOften clostridiumAvian gastric yeastsReduced/altered motilityGI signsOften affects liver function – commonly treated with milk thistle and dandelionBacterial showers?Inflammation, liverDoxycyclineNSAIDSGingerOnsiorTreatment for CNS signsCelebrexOnsiorAmantidineGabapentin (control seizures)Adjunct to decrease inflammationDepo Lupron (shot)Reduction of hormonal behaviorsCortical BlindnessCelebrexB complex vitaminsOmega 3 PUFAs – eggs, walnuts, pumpkin, flax seedTreatment for PNS signsNeuritis = pain: tramadol, NSAIDs, nerve/ring/line blocksOLD concept of ABV parallels early BDV:low incidence of infectionfatal clinical diseasestrong pathogen1890 epidemic, fatal neurological dx, military horses in borna GermanyBVD was thought to be a deadly virus to allNEW concept of BVDHigh incidence – 60% avg infection rate, healthy horses/etcLow disease prevalence, 5-10% clinical diseasePathogenicity inversely related to prevalence of infectionBVD:High prevalence of silent infectionsLow level of clinical diseaseANY AGENT CAUSES RELEASE of P40 PROTEINGullian Barre PathophysiologyAutoimmune dx triggered by bacterial or viral infectionGangliosides are immune targetsDifferent gangliosides predominate, different areasPeripheral nervesGangliaGullian Barre Clinical ManifestationsDepends on subtypeNumbness, painParasthesiasWeakness of the limbsWeakness plateaus about 4 weeks Avian AutoImmune GanglioneuritisBetter description of the pathologic processT lymphocytes, plasma cells invade where P40 proteins releasedLike G Barre, varies by locationSeverity depends, immune health individual Site of infection varies based on ganglioside targetsWhen affects peripheral nerves:Possible feather damagePossible self mutilationcan get neurogenic atrophy from damaged peripheral nervescachexia from poor absorption – feather changes should also occurAutonomic ganglia – dorsal vagal nucleusCan be very localized, just the crop/stomach/heart etcNew approaches are immune directed – immune modulating therapeutic approachBirds can’t HEAL from AAG, but they can get better – symptoms can get treated, but the actual infection can never leave the body ................
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