Epi1 wk3 T12 to T18.pdf

12. Pneumoenteri s of ruminants caused by adenoviruses. NOTFOUNF IN CA Effect every vertebrate Adenoviruses – for topics 12-14 firstisolationsfromhumanadenoidgland  dsDNA g...

12. Pneumoenteri s of ruminants caused by adenoviruses. NOTFOUNF IN CA Effect every vertebrate Adenoviruses – for topics 12-14 firstisolationsfromhumanadenoidgland  dsDNA genome, non-enveloped (high resistance) icosahedral o Double strain so there is enough space for own polymerase enzymes  Biological proper es – wide distribu on, diverse pathogenicity (carriers are frequently asymptoma c), oncogenic effect (some) 3structuralcapsidproteinso Mainly only mild respiratory and intes nal signs, some mes cause severe disease (Rubarth´s disease) AKAknobatthe endofthefibreprotein If c  An genic proper es – strong an gens, surface projec ons (fibres – neutralising an gen), cross- arising at ons within genera (serogroups) reac o Cross-neutralisa on, can be used in vaccines – very stable virus, able to agglu nate (HAI importance for test can be done) cytopath.gePPEejne  Diagnos cs – virus isola on (strong CPE), IF, HA, ELISA, PCR cadv. i o Indirect: VN, ELISA, AGID, CF, HAI Phylogene cs  Genera: o Mastadeno-, Aviadeno-, Atadeno-, Siadeno-, Ichtadenovirus, Testadenovirus genus  Species – named by le ers others Fish Frogs turtle snake  Serotypes – numbered (from 1, based on VN)  Serogroups – based on cross-reac ons between serotypes (AGID, CF)  Mastadenovirus genus: o Bovine mastadenovirus A (BAdV-1) o Bovine mastadenovirus B (BAdV-3) o Bovine mastadenovirus C (BAdV-10) o Canine mastadenovirus (CAdV-1, 2) o Ovine mastadenovirus A (BAdV-2, OAdV-2-5) o Ovine mastadenovirus B (OAdV-1) o Ovine mastadenovirus C (OAdV-6)  Atadenovirus genus: o Duck atadenovirus A (EDSV) o Bovine atadenovirus D (BAdV-4, -5, -8, Rus) o Bovine atadenovirus E (BAdV-6) o Bovine atadenovirus F (BAdV-7)  Aviadenovirus genus: o Fowl aviadenovirus A (FAdV-1 (CELO)) o Fowl aviadenovirus B (FAdV-5) o Fowl aviadenovirus C (FAdV-4, -10) o Fowl aviadenovirus D (FAdV-2, -9, -11) o Fowl aviadenovirus E (FAdV-6, -7, -8a, 8b)  Siadenovirus genus: o Turkey siadenovirus A (TAdV-3)  Ichtadenovirus genus and Testadenovirus genus  Adenovirus pneumoenteri s in calves Mild disease of 1-4 months old calves with nasal discharge, coughing and diarrhoea Causa ve agents: 113 10 A B C respectively o Mastadenovirus genus – “subgroup I”: replica on in bovine kidney cells o Atadenovirus genus – “subgroup II”: replica on in bovine tes cle cells Bathadenovivore Pathogenesis 4 to 7 D E F  PO, air-borne infec on (oronasal route)  mul plica on in the tonsils, lymphoid ssue  main epithelia  viraemia (lymphoid cells): upper respiratory + enteric mucosal iii iii in Introduc on with carrier calves – usually in large farms (crowding), poor colostrum uptake  In adult ca le subclinical  Role of co-infec ons (BVD, IBR, PI-3, Pasteurella, etc.)  Incuba on me: 1-7 days AKAlatentperiod Clinical signs importanceofcolostrum intake  From 6-8 weeks of age on (without colostrum from 3-4 weeks on)  Mild fever, loss of appe te, conjunc vi s, serous nasal discharge, coughing, saliva on, mild diarrhoea  Co-infec ons (1-2 weeks a er the first signs) – pneumonia Pathology, histopathology  Intralobular inters al pneumonia, bronchioli s, atelectasia, virus enteri s, osmo c diarrhoea, aepht kidney tubular epithelial necrosis, release, proteinuria Histopar A typeinclusion ftp  BAdV-10 – New Zealand, Northern Ireland: non-febrile enterocoli s, haemorrhagic gastroenteri s, haemorrhages in renal cortex, bladder and trachea – newly introduced disease to ca le from sheep, more severe clinical signs Diagnosis Virus isola on: PCR, IF, ELISA – Serology: VN (paired sera inves ga ons), with all serotypes Treatment – symptoma c and suppor ve therapy (with an bio cs) Preven on Improve keeping condi ons, improve / check colostrum uptake Farm-specific inac vated vaccines, polyvalent – viral and bacterial an gen components – repeated vaccina on of calves vaccina on of pregnant ca le twice before parturi on I Adenovirus pneumoenteri s in lambs  Respiratory and enteric disease usually in intensively raised lambs  D Causa ve agents: Atoc o Mastadenovirus genus and Atadenovirus genus  Epizoo ology: 4mainlyBadV 2 o Similar to calf pneumoenteri s – mainly in lambs of young ewes (first pregnancy), crowded raising / fa ening farms, frequent asymptoma c carriage Pathogenesis, clinical signs same as calver   Similar to calf pneumoenteri s – in lambs from the age of 3-4 weeks on  Mainly respiratory signs, but haemorrhagic-necro c enteri s may also occur (OAdV-4)  Co-infec ons may complicate affectstheintestinalmucosa  Urolithiasis is a frequent complica on in rams Treatment, control, preven on – symptoma c and suppor ve treatment, closed farming, improved hygiene, inac vated vaccine (currently not available)  13. Canine infec ous hepa s and infec ous laryngotrachei s (caused by adenoviruses). NO ADENOVIRUSES FOUND IN CATS Canine infec ous hepa s (Rubarth disease)– most important adenovirus amongst mammals  Rubarth-disease – acute disease of dogs with vomi ng, diarrhea, bleedings and icterus  Fox encephali s – haemorrhagic encephali s of foxes  Pathogen: CAdV-1 worldwidedistribution but disease is rare due tovaccination  World-wide occurrence, Canidae and Ursidae are suscep ble  Asymptoma c   lethal, frequent seroposi vity due to immunisa ons vaccines especially in young age Pathogenesis d nasal sometimes macrophage associated  Viral intake: PO, conjunc va  tonsils, Peyer’s patches  lymph nodes  viraemia (with lymphoid cells): o liver – hepa s o brain – encephali s mainly o kidneys – glomerulonephri s shedsvia urine o eyes – uvei s, iridocycli s, glaucoma  IMInchronic form Blueeyedisease lookslike Glaucoma  CPE, endothelial damage, DIC, immunocomplex deposi on (type III. hypersensi vity) o Similar to Aleu an mink disease virus!   virus shedding with secre ons (faeces, but urine: up to six months) – long-term carriage (in kidneys) – infec on: direct  Cross-protec on: CAdV-2  Sensi vity: 3-6 months– mortali es over 1 year – mild or subclinical  Maternal immunity – protects up to 3 months  Incuba on me: 1-5 days Clinical signs  Course: o Peracute – death within 1-2 days, non-specific clinical signs o Acute – fever over 40°C for 3-5 days, may look like poisoning o Extended – 1-2 weeks, oedema, convulsions, uvei s (grey / blue eyes) o Fox – acute encephali s, convulsions, haemorrhages in chronicform B e  (usually in dogs under the age of 1 year) o Sudden death may occur o Fever, depression, lymphadenomegaly, oedema, icterus, anorexia, vomi ng, bloody diarrhoea, abdominal pain o Mucosal haemorrhages, tachycardia, leukopenia, coagula on problems (gum bleeding, haematoma) o Apathy, seizures, disorienta on, coma  death o Conjunc vi s, corneal oedema, anterior uvei s, photophobia o Chronic – “blue eye”, cataract, glaucoma, ulcera on in a chroniccare canleadtoblindness Pathology  Oedema, haemorrhages, enlarged yellow liver, centrolobular hepatocyte necrosis, hepa s, icterus   Serosa haemorrhages, nephri s, gall bladder oedema  Nuclear inclusion bodies (Cowdry A), smudge cell  denial Liver parenchymal cell degenera on, invasion of inflammatory cells Diagnosis – anamnesis, clinical signs  Laboratory tests – leukopenia, lymphopenia, neutropenia o Later neutrophilia, lymphocytosis, elevated serum ALT, AST, ALP levels, bilirubinuria, proteinuria, prolonged clo ng me, DIC  Direct virus detec on – immunofluorescence, immunoperoxidase staining, virus isola on (in canine or swine cells), PCR Imost I  Serology – VN, iIF, ELISA, HAI, CF, AGID aimtin Differen al diagnosis II p b ftp.t Ipfii Laboratory values – CPV-2 (Canine parvovirus), CPV-1, CDV (Canine diptheric virus), CHV (Canine herpes) Vomi ng, diarrhoea – CPV-2, – CDV Ocular lesions – CHV, CDV Treatment  Clinical management (IV hydra on, glucose, liver protec ve drugs), hyper-immune serum?  Preven on – immunisa on: More important In HungarycalledBody glob o (A enuated) and inac vated CAdV-1 o A enuated CAdV-2 – cross-protec on between CAdV-1 and 2 o Usually component of polyvalent vaccines – basic immunisa on from 2-3 months of age – yearly (or every 2nd or 3rd year) repe ons Badvacationthe Eyesight up EEEaI IEg us Canine infec ous laryngotrachei s  Mild febrile disease of dogs with upper respiratory tract inflamma on influenza  Causa ve agent: CAdV-2 partof Kennelcough includespasteurella Bordetellapara  Distribu on: world-wide  Clinical manifesta ons usually in young dogs – alone rarely induces clinical signs  Crowded keeping condi ons, coinfec ons – Parainfluenza virus 2, Canine respiratory coronavirus, sometimes canine herpesvirus, Bordetella bronchisep ca, Pasteurella multocida → Kennel causes it cough syndrome diseases that Pathogenesis The 8 9 91 824 therefore Air-borne infec on  virus mul plica on in upper respiratory tract mucosa  rhini s, laryngi s, tracheobronchi s, bronchioli s Clinical signs Mild fever, nasal discharge, dry coughing – with co-infec onsipneumonia notcausedbyadenovirus Diagnosis – case history, clinical signs, quick spread in the popula on Virus isola on: in canine cells – Serology: VN, ELISA 1 mainly PCR Treatment – symptoma c (respira on support) + an bio cs for co-infec ons Preven on – improved keeping condi ons, immunisa on from 2-3 months, usually polyvalent vaccines  rabies likesymptoms anddistemper Fox encephali s pathogen Cad  CNS signs are more important emanhagicencephalitis offoxes  Clinical symptoms – inappetence, apathy, change in behaviour, later incoordina on, convulsions, death)  Pathology – hepa s, lympho-his ocy c encephali s (lymphoid cell cuffing around the blood vessels, neuron degenera on, glial nodules)  Intranuclear inclusion bodies are pathognomic (neurons, hepatocytes, urinary bladder epithelial cells)  Diagnosis – PCR  Differen al diagnosis – rabies, distemper  14. Adenoviral diseases in poultry. Avian adenoviruses NOTspecies specific World-wide distribu on, frequent infec ons – 3 serogroups, 3 genera Germinative Serogroup I. (Aviadenovirus genus) – 12 serotypes: 1-11, but 8a and 8b (differences in andhorizontal pathogenicity and virulence) o FAdV-1, -7, and -8 – Inclusion body hepa s (in broiler chickens) o FAdV-3 – Inclusion body hepa s (in parrots) o FAdV-4 – Hydropericardium syndrome, craw dilata on (chicken, pigeon) veryacuterespiratorydisease in quail o FAdV-1 (CELO) – Quail bronchi s o FAdV-1-8 – Gizzard erosion (Japan) o FAdV-11 – Spiking mortality syndrome (broiler chicken, turkey) horizontalonly  Serogroup II. (Siadenovirus genus) – Galliformes, the same virus causes: o Turkey haemorrhagic enteri s I o Marble spleen disease of pheasants in.ua o Chicken splenomegaly  Serogroup III. (Atadenovirus genus) – in several bird species (waterfowl, chicken, stork, quail, etc.) AKAnowBautha denovirus o Egg drop syndrome virus (DAdV-1) Aviadenoviruses (Serogroup I.)  Germina ve and horizontal infec ons   Transmission – eggs, day-old chicken, fomites make diseasemoresevere infectiousbors.tt Co-infec ons, roletheof yolk immunity FIB Ii anaemia Cav fewweeks forofathe only  Mainly in 4-12 weeks-old herdsprotects (because yolk immunity) notb eingefficient  Pathogenesis: germina ve / PO  viraemia  gut, liver, kidneys and trachea  Clinical signs – frequent subclinical infec ons o Embryo damages, decreased egg produc on, tenosynovi s (+ reovirus!), respiratory dependingon strain signs, hepa s a a L t.iq gffg Isestn it H Ab defe  Diagnosis – direct: IF, IP, ELISA, AGID, PCR, hybridisa on – indirect: VN, ELISA, IF, AGID, (HAI) as Chicken inclusion body hepa s jiffy.EE i.i ii iii iii arena www in  Chicken, turkey, pigeon, goose suscep ble – FAdV-1, -7, -8 (rarely other serotypes)  i eiima.name Age dependency – from 28-30 days on (rarely from 6 days to 20 weeks of age), concluded within  3 weeks soso.azÉ f Mortality - 2-10 % within 3-5 days  Clinical signs – anaemia, diarrhoea weakness similartoHepatitishydro pericardium syndrome he  Pathology – anaemia, enlarged, pale liver, petechial haemorrhages (in skeletal and heart muscles)yellow necroticfociintheliver drooping  Histopathology – nuclear inclusion bodies mainly nots ignificant erosions cellsinfiltrationofi nflammatorycells deathofepithelial  Hepa s-hydropericardium syndrome in goose chickenmany goosepigeon southAmerica  FAdV-4   10-24 days,man Age ofannoying mortalityhaha 4-6 % i.fi ittjiijio EEEmie severedisease than IBI aeeettoee ienee fÉ star Clinical signs – si ng (for 5-6 hours), weakening ÉÉ  Pathology, histopathology lesions – hepa s,ahydropericardium, focalinfinitely enticewooooendresses hepa c necrosis with en nuclear idq.ge yqeIt inclusion bodies, myocardial necrosis (without inflamma on) e aad mode 1ns oedema  Diagnosis – PCR, virus isola on  Differen al diagnosis – from Derzsy’s disease Si adenoviruses Groups the.gg hngnta.EtinttgEn3ErIenIhe'T.hr Turkey haemorrhagic enteri s HEV possible at a nucleic acid level  22 0at Siadenovirus – over 4 weeks of age, usually in 6-11 weeks old poults (mortality: 6-8 %) p.tt ddek9  World-wide distribu on immunosuppe neeation  Pathogenesis: frabzfeld deepe o PO, cloaca  mul plica on in enterocytes  viraemia  immune suppressive, blood bloodvessel damages  haemorrhages (spleen, liver, kidneys, lungs) severe immunosuppression  Clinical signs – varies (subclinical, mild,not sudden death): weakness depression,weight bloody faeces, anaemia thirst, loss  Pathology lesions – anaemia, enteri s, enlarged mo led spleen, haemorrhages, fluid in thoracic–  abdominal cavity ved edematous I wall HE gen / an body detec onp(i.e.t.EE Diagnosis – virus isola on, PCR, anintestinal hgEffyfgIeenEatittg ftp.hitisinienfusionbod ELISA)  Differen al diagnosis – Avian influenza, non-velogenic NDV, enteri s: Turkey coronavirus nospiffed p oultry theseafirst.in (bluecomb) (no splenomegaly); enlarged,always mo exclude led spleen: re culoendotheliosis, leucosis, paratyphus, yersiniosis E coli Salmonella Pasteurellamulticida  Treatment –Forconvalescent spleen s econd serum a (?), an bio c treatment for co-infec ons (immune suppressive virus!)  Preven on: a enuated vaccine duetowidespread intensified ÉÑ notthatcommonnowadays Marble Spleen Disease and Splenomegaly 2 similardiseases P YES  Marble spleen disease (in pheasant, between 3-8 months of age) o Acute Atypicalrespiratory clinical signs, no bloody diarrhoea j signs éde Intestinallesion o Pathology lesions – enlarged, mo led spleen n  man hisIaas Splenomegaly (USA / in broiler chicken usually) o Enlarged liver and spleen, hyperplasia store qq.in nqggnggfEEy Barthadenovin Egg Drop Syndrome YET Iyheand me horizontalinfection  Enteric disease of layer hens with decreased egg produc on  History – The Netherlands 1976, quick dispersal in Europe and world-wide occurrence o Presumably spread with Marek’s disease vaccine infectedwith LIEBFEE fehztf.hnKEIPfebgot  Suscep bility – chicken, duck, goose, stork, quail, etc. nonadotter  Causa ve agent: Duck atadenovirus 1 (DAdV-1, EDSV)  Atadenovirus chiffen hkdbseyethegdenov.ws Respsigns In quails same as Pathogenesis 44 5 7 5 Thevirus becomesactivelaterin theoviduct i chickenshatchedfromaninfectedegg mature latentuntilthebirdsbecomesexually only in thelaying period Thevirusremains Germinative vertical infection  In S EEEEE.IE EEIEIagfE EEE.EEEEEE  E.EE PO, germina ve infec on  viraemia  oviduct, intes nal mucosa  edema in genital tract, fjffffff tevenimiexaaate 1  É i a T increased mo lity of the oviduct Ver cal transmission – in eggs, on the shell (if yolk immunity)  Before the egg produc on season only a few seroposi ve chickens are found even in infected manysickbirdsinfectedlayers flocks  Horizontal transmission – with faeces  quick spread in the herd  The epizoo c lasts for 5-6 weeks – egg produc on drops by 30 – 50% severeeconomic loss Clinical signs in chickens laying Soft thin noset to Usually in the 3rd-7th week of egg produc on (peak) –of diarrhoea, so -shelled eggs, fragile shell, deformed eggs an Diagnosis – clinical signs, virus isola on, PCR, HAI Differen al diagnosis I Reduced egg produc on – Newcastle disease, Avian influenza, Avian encephalomyeli s + egg shell deformi es – Infec ous bronchi s, Turkey rhinotrachei s, Avipox shellbrokenshell ME Eng clinical Preven on, control – no hatching during 82,4signs2 and 2 weeks a thinerwards, disinfec on of egg shells, (waterfowl) EI manure treatment, eradica on from primary breeder toprovideyolkimmunity flocks, preven on of contact with infected birds Iguana parentflows exclusionofinfectedbreedinganimals at 14 16weeks of Immunisa on – inac vated vaccines before the egg laying season: milder signs, less frequentzedo.name germina ve infec on due to yolk immunity Egg Drop Syndrome in goose gosling  In 1-2 weeks of age – mortality 4-5 % – frequent seroposi vity, clinical manifesta on is rare  Clinical signs – respiratory signs, nasal discharge, lacrima on, laboured breath  Pathology, histopathology lesions – rhini s, tracheobronchi s, nuclear inclusion bodies in trachea ons pneumonia thetrachea and bronchus epithelial cells, with co-infecteeeukdiedtein hyperplasia  Diagnosis – clinical signs, pathology, histopathology: virus isola on, PCR  Differen al diagnosis – from Derzsys disease – only respiratory signs NOTE! Biotechnology  Adenoviruses are used as vectors to express inserted foreign genes in: o Rabies oral vaccine for foxes o SARS-CoV-2 vaccine for humans Sputnik and Astrazeneca  Better off As vectors to express inserted foreign genes  15. Infec ous bovine rhinotrachei s (IBR, IPV). Herpesvirales – for topics 15-25  Herpesvirales order – 3 family, 3 subfamily, 23 genera, more than 200 species  Herpesviridae family: Ortho her perviridaefamily o Alphaherpesvirinae subfamily o Betaherpesvirinae subfamily o Gammaherpesvirinae subfamily  Alloherpesviridae family fish notimportant  Malacoherpesviridae family Herpesviridae family  Alphaherpesvirinae subfamily o Simplexvirus genera (11 species):  HHV-1, HHV-2, BoHV-2 (herpesmamilli s) o Varicellovirus genera (17 species):  HHV-3, BoHV-1 (IBR, IPV), -5 – EHV-1,-3, -4,-8, -9 – SuHV-1 (Aujeszky’s) – CaHV-1 – FeHV-1 – CpHV-1 o Mardivirus genera (4 species):  GaHV-2, -3 (Marek 1, 2) – MeHV-1 (turkey herpes 1) – CoHV-1 (pigeon herpes) o Iltovirus genera (2 species):  GaHV-1 (ILTV) – PsHV-1 (Pacheco’s disease) o Unassigned species:  AnHV-1 (duck plague)  Betaherpesvirinae subfamily o Unassigned (3 species):  SuHV-2 (inclusion body rhini s)  Gammaherpesvirinae subfamily o Lymphocryptovirus genera (8 species):  HHV-4, (Epstein-Barr virus) o Macavirus genera (9 species):  OvHV-2 (malignant catharral) – AlHV-1, -2 – CpHV-2 – BHV-6 – SuHV-3, -4, -5 o Percavirus genera (3 species):  EHV-2, -5 o Unassigned (3 species):  EHV-7 Herpesvirus general  dsDNA, enveloped icosahedral  More than 20 structural proteins, 10-12 of them in the envelope: can be deleted (marker)  Resistance: weak o 60℃, disinfectants destroy within minutes, sensi ve to detergents o Survive in excre ons in the environment for few days and few weeks   Stenoxen: most of them – some of them euryxen: Aujeszky’s disease, malignant catarrhal fever, turkey herpes  Monkey herpes B: zoono c storathogeniceffect  Strong CPE, difference between subfamilies: o Alphaherpesvirinae – mp.int changing (narrow-wide) host range, replica on cycle (< 24 h) lessthan1day s lower o Betaherpesvirinae – narrow host range, replica on cycle > 24 than much h Alpha o Gammaherpesvirinae – narrow host range, B and T cell tumour, immunosuppression intothnootsena.fi iii aenepefEtiminiympn allieding incorporated  Latency, persis ng infec ons: o Viral latency – virus is dormant within the host cell, no virus mul plica on, no virus produc on, the host is seronega ve for the virus o Persistent infec on – virus is persis ng in the host cells (mostly in lymphoid cells), virus mul plica on and virus produc on take place, an -viral an bodies can be detected in the host o Prolonged/life-longinfection  α: neuron – β: gland, lymphoid ssue – γ: lymphoid cells  Reac va on can occur  An genicity: o Weak an gens (envelop glycoproteins) o Vaccine protec on – only for a few months o Cross-reac ons within genera (rarely cross-protec on) strong  Marker vaccines (Differen a ng Infected from Vaccinated Animals: DIVA) o Dele on mutants puncoproteine (IgE nega ve Aujeszky virus) o Point-muta ons (missense) o Risk of recombina on (marker rescue) Potentilyreintroducingt hefullviralg enomeand www.isvedior betweenvaccinatedandnatundlyineectedmim.fi makingitharder deferen  Detec on of the infec on: o PCR, isola on, an gen detec on methods o Latent infec on: co-cul va on, PCR, NA hybridiza on o Serology: (discrimina ve) ELISA, VNT  Treatment – in human medicine: nucleoside analogues (acycloguanozin), not registered for veterinary use, expensive  Preven on – hygiene, vaccina on, eradica on asusual Infec ous Bovine Rhinotrachei s (IBR) Febrile illness of the ca le with general signs, nasal discharge, conjunc vi s, respiratory inflamma ons, encephali s, abor on and inflamma on of the genital mucosae  Causa ve agent – Bovine herpesvirus 1 and 5 (BoHV-1, -5)  Differences in ssue-tropism:response o BoHV-1 – IBR, IPV, IBP (cause disease in mucosal membranes) abortion respiratorydisease gen o BoHV-5 – nervous ssue (encephali s)  Differences in virulence – inapparent to severe in ca le (main host)  Inapparent infec on in other ruminants – sheep, goat, wild ruminants verycommon Occurrence – world-wide, mainly in large farms, eradica on programs in several countries of EU Epizoo ology   Introduc on into the farm with infected animals or semen  Bulls may shed the virus in semen for months  Rela ve slow spread in the popula on – contact, airborne  Convalescent animals are long-term/life-long carriers  The parallel presence of respiratory and genital forms is not common in a farm  Abor on and encephali s are o en accompanied or followed by respiratory form Pathogenesis  Infec on route: aerogene, PO, venereal  viraemia  mul plica on in respiratory epithelial cells  inflamma on  Calf: a er viraemia, or ascending from nose along nerves  brain  encephali s  Suscep ble ca le: viraemia  resorp on of foetus, abor on  Genital form: viraemia  vesicles on the mucosal membranes, inflamma on, crusts, nodules  Latency in nervous ssue (reac va on) mucosallesions  Long-term/life-long shedding (intermi ent)  Symptoms are modified – age, amount of the inoculum, pathogenicity, route of infec on, host- immune status virus  Respiratory form – incuba on: 2-5 days o 1-6 months old calves – fever, respiratory symptoms, occasionally diarrhoea tite islowat 1433  Colostrum-protected calves – clinical symptoms from 6-8 weeks of age  Non-protected calves – clinical symptoms from 1-2 weeks of age (liver damage) o From 6 months of age (older animals) – fever, respiratory symptoms, “red nose disease”, mucosald amage nasal discharge (necro c material), conjunc vi s (some mes the main symptom), decreased milk produc on exudative o Bacterial seconder infec on  pneumonia o 20-50% morbidity, < 5% mortality relativelyhigh Clinical signs Manlyincalveunder smonths CNSform  Encephali s – under 5 months of age, uncommon o Conjunc vi s, nasal discharge, fever, later lameness, tremor, opisthotonus, death a er 5- 7 days Ataxia  Abor on: theeldersarealreadyprotected o Sporadic, mainly in heifers in It at.i Eia o During the acute infec on or p I few weeks later EE.EE o All phases of the pregnancy (embryo resorp on-abor on) – aborted foetus autoly c, mul ple necro c foci in the organs NOTcharacteristic  Infec ous pustular vulvovagini s (IPV): o Ini ally oedema of the vulva and vagina – later pustules, which tend to coalesce o Mucosal membrane covered by yellowish white membrane o Painful: frequent urina on, and tail flapping o Healing selfl imiting within 10-14 days o NO ABORTION!!!  Infec ous pustular balanoposthi s (IBP): o Oedema of the prepuce o Painful: loss of libido erosionso nthem ucousmembranes  IPV and IBP are both part of the genital form of the disease Diagnosis  Live animal: o Clinical symptoms o Secre ons – PCR, isola on, an gen detec on tests (IF, an gen-ELISA) o Serology – blood, milk (ELISA, VN) orplacenta o Differen al diagnosis – diseases of the respiratory, diges ve and nervous systems reproductivesystem  Dead animal: characteristic fetch o Pathological examina on – nasal cavity, pharynx, larynx, trachea: inflamma on, haemorrhages, erosions, pseudo membranes o Histological examina on – acidophilic nuclear inclusion bodies teriainfection  Trachei s-bronchi s, inters al pneumonia ithenabrinou.it Hyh  Abor on – mul focal, acute necrosis in foetal organs  Lymphohis ocy c encephali s o Virus detec on – PCR, isola on, an gen detec on tests (IF, IHC, an gen-ELISA) Preven on  Therapy – an bio cs against seconder bacterial infec ons  Epidemiological rules – closed herds, separa on of different age groups  Vaccines – prevent clinical diseases o Live and inac vated vaccines – control of epidemics: live vaccines o Breeding animals inac vated vaccines – safe for the foetus o Cows – immunisa on 6 and 3 weeks before breeding, and 6 months a er breeding (from the following pregnancy: immunisa on before breeding and 6 months a er breeding) o Their calves – immunisa on at 4-6 months of age 2× in 2-3 weeks, repeat in every 6 months o Beef ca le – 2× in 2-3 weeks, repeat in every 6 moths Eradica on  Replacing of the herd – quick, safe, but expensive  Raising free genera on – me-consuming o Immunisa on of the whole herd o Separa on of the suckling calves a er 3 days of age (a er consuming colostrum), isolated raising o Monitoring every 6 moths (ELISA ) – free status if the herd is nega ve in two consecu ve tests  Selec on – the most popular method o < 10 % seroposi vity – removal of posi ve animals o > 10 % seroposi vity – selec on by using marker vaccines  Immunisa on of the whole herd with marker vaccine – repea ng every 6 months: reduce the amount and frequency of virus shedding  Repeated discrimina ve ELISA – IgE posi ve animals are removed  A er 3-4 years the rate of infec on below 10% - all posi ve animals removed theslaughtered animalscanbeconsumed  Maintaining the free status: o Epizoo ology rules – monitoring: 10% of the herd have to be tested every 6 months I ELISA) (discrimina ve (IgE) Followthenational veterinary policyforeradication  16. Bovine herpesmamilli s, inclusion body rhini s of swine. Bovine herpesmamilli s Oedema, pustules and erosions on the skin of the teats and the udder. i nitiallythen and onthe Englandpustule u dder History, occurrence – world-wide: mainly Africa, Australia, USA (warm rainy weather); rare in Europe pseudolumpy skindisease Causa ve agent – Bovine herpesvirus 2 (BoHV-2), Alfaherpesvirinae subfamily Affected: ca le (rarely buffalo, other ruminants) Epizoo ology  Introduc on with infected animals  Spread by milking in herd (hand/machine), arthropods (mechanical vectors) – more common in late summer and early fall  The virus can invade only through skin lesions; immunosuppression contributes to the disease  In endemic herds heifers and their calves are mainly affected Pathogenesis contact Skin lesion: local mul plica on  viremia  pustules (udder mainly)  inflamma on, oedema  erosions  crusts Canbe on part ofthe udder Clinical signs my bodybutmainlyfound inthe  Incuba on me: 3-7 days  Europe – localized form o Painful, refuse milking – healing within 1-2 weeks o Heifers – oedema, red discolora on, pustules, erosions, crusts o Bacterial seconder infec on  mas s o Suckling calves – pustules on mouth, oral cavity, face, ears o Damage – decrease in milk produc on, blood in milk (confiscates), teats scab: difficulty in milking 1 ith Evenlyeconomicall osses o Subclinical infec on is common likeotherHerpevivurer  Africa, rarely other con nents – generalized form o Very similar to the Lumpy skin disease (laboratory examina on is inevitable) onlythiscand istinguishbetweenthem Diagnosis – clinical symptoms man Skin lesion – PCR, isola on (histological examina on: intranuclear inclusion bodies, syncy al cells) (Serology: VNT) notveryhelpfulduetolargenumberofsubclinical infections Differen al diagnosis – disease with pustules: FMD, vesicular stoma s, Pox viruses (cowpox, pseudocowpox, papillomatosis, Lumpy skin disease): prolifera ve altera ons (lump) Therapy – symptoma c local (disinfec on), isola on (milking) of affected animals, no vaccine Inclusion body rhini s of swine Beta SubHV2  Causa ve agent – Suid herpesvirus 2 (SuHV-2): unassigned cytomegalovirus  o World-wide, rarely occurring disease, 100% of animals infected within a herd o ITiWAinfeions Disease only in swine, in vitro propaga on is difficult  Epizoo ology, pathogenesis: o Horizontal spread:  Contact, aerogene (saliva, nasal discharge)  mul plica on in nose, lacrimal gland  cell-associated viraemia  seconder mul plica on mainly in lymphocytes, lung macrophages o Ver cal spread:  Pregnant sows – foetuses get infected  abor on, s llbirth, weak new-borns Clinical signs  Incuba on me: 10-20 days  Disease un l 3 weeks of age – infec on in the uterus or during delivery  Sudden death  Fever, inappetence, sneezing, mucous, rarely bloody nasal discharge  Even 10-50 % mortality Diagnosis  Live animal: o Nasal swab, unclo ed blood: PCR - (Serology: indirekt IF, ELISA)  Dead animal: o Gross pathological, histological examina on:  Disseminate haemorrhages, subcutaneous oedema, hydropericardium, hydrothorax  Giant cells containing basophil intranuclear inclusion bodies in the nasal mucosal membrane o Detec on of the agent – nasal mucosal membrane: PCR, IF, (isola on)  Differen al diagnosis – SMEDI, PRRS, Aujeszky’s disease, PCV-2, classical swine fever Preven on – good husbandry, colostrum of convalescent sows protects the piglets un l 3-4 weeks of age  17. Malignant catarrhal fever. Acute, usually lethal, febrile illness with general sings, kerato- conjunc vi s, encephali s, haemorrhagic pneumonia, and enteri s mainly in ca le Occurrence: world-wide Causa ve agents newnameovidgammaherpesvirus2COUGH2 AIGHV1  Ovine herpesvirus 2 (OHV-2), Alcelaphine herpesvirus 1 (AlHV-1): Gammaherpesvirinae subfamily (rarely other herpesviruses as well)  AlHV-1 can be propagated in cell culture, OHV-2 not  AlHV-1 – wildebeest inapparent infec on, only ca le is affected  OHV-2 – sheep inapparent infec on, affected: ca le, rarely buffalo, bison, deer, goat, swine  CpHV-2 – goat inapparent infec on, affected: buffalo, deer, swine  Mainly ca le is affected, other ruminants can show some symptoms Epizoo ology  In Africa – wildebeest-associated MCF o Most of the wildebeest over one year of age are carriers: shedding the virus with the amnio c fluid and with different secrets o Ca le are infected on the shared pasture  Outside Africa – sheep-associated MCF o Sheep (and other ruminants) are asymptoma c carriers o Virus shedding of sheep is most intensive in 6-9 months of age o Ca le get infected a er prolonged (few months) contact with sheep o Ca le are not able to spread the virus cattlegetinfectedafterprolongedcontactwithsheep o Only sporadic cases in a herd, rarely several animals are affected o Elder animals are more sensi ve (young animals can survive) Pathogenesis  Not known in several aspects – contribu on of other latent virus infec on in ca le?  Aerogene  cell-associated viraemia Tcells  Immunopathological process is responsible for the lesions: CD8 + lymphocytes-associated severe vasculi s and ssue necrosis Path lesions arebasedonthese  Inapparent infec on is common in ca le – only small part of ca le show clinical symptoms Clinical signs  Incuba on me: 2 weeks – several months  Peracute – high fever, inappetence, lethargy, saliva on, enlarged lymph nodes, bloody diarrhoea, Notascommon tremor, convulsion, death within 1-2 days  Acute – more common, lesions are o en only on the head: AKAHeadform o Fever, lethargy, rumen-atonia, reduced milk produc on o Bilateral keratoconjunc vi s (beginning at the periphery) o Nasal discharge (containing necro c ssue), laboured breathing: erosive, necro c, fibrinous rhini s  o Saliva on, bad breath – erosive, necro c, fibrinous stoma s o Loose of hoofs and horns – lamini s o Enlarged lymph nodes o Abdominal pain, bloody diarrhoea – bloody urine – haemorrhages, necrosis in the genital mucosae and in the skin (muzzle!) CNSsymptomsdueto CNS o vasculitis Depression, then excitement  convulsions  paralysis  death o 50% can survive – healing, or chronic disease  Chronic – prolonged disease (weeks) o High fever, enlarged lymph nodes o Erosions in nasal and oral mucosal membranes: saliva on, nasal discharge containing necro c ssue o Bilateral uvei s o Skin – hyperkeratosis, papular derma s lookslike lesions pox o Clinical symptoms can disappear, then few months later return  death o Young animal – mild clinical symptoms, can return a er healing in few moths usuallyasymptomatic eldera nimalsaremuchmoresensitive Diagnosis  Live animals: o Clinical symptoms ofb lood lowviralloadinthe d uetothe r equired duetotheimmuno bloodstream process pathological Engaggent o PCR: non-clo ed blood – (serology: VNT, iIF, ELISA)  Dead animals – gross pathological, histological examina on: seeabove PCRanaffectedagar o Peracute:  Respiratory tract, intes nes – reddened mucosal membranes, acute haemorrhages  Liver, kidney enlarged  Urinary bladder – oedema, reddened mucosal membranes, acute haemorrhages  Enlarged lymph nodes, and lymphoid follicles o Acute:  Keratoconjunc vi s  Respiratory tract, intes nes – reddened mucosal membranes, acute haemorrhages, erosions covered by fibrin  Enlarged lymph nodes, and lymphoid follicles  Small blood vessels – lymphocy c inflamma on, fibrinoid necrosis, ssue necrosis  Lymphocy c encephali s very similar Differen al diagnosis – IBR, BVD-MD, bluetongue virus, FMD, Rinderpest Therapy – not exist, no vaccine Preven on – isola on from inapparent carriers (sheep)  18. Aujeszky´s disease of swine and in other animals. Swine disease with febrile, general signs, abor on, respiratory and central nervous system signs. In other suscep ble species manifests as severe, acute and lethal encephali s. History, occurrence  Known for long me – pseudorabies, mad itch, Juckreiz  Aujeszky 1902 – differen a on from rabies  Rátz 1914 – first descrip on in swine  Bartha 1961 – a enuated vaccine strain (K/61)  World-wide occurrence, eradicated in several European countries Causa ve agent  Suid herpesvirus 1 (SuHV-1), an genically similar to BHV-1, Alphaherpesvirinae subfamily  Well-propaga ng in cell culture (intranuclear inclusion body, syncy um, cell rounding)  Muta ons and dele ons a er passages in cell culture  a enua on no e e (IgE, IgC, IgM, rIgG, TK defect)  Risk of recombina on – use of mul ple-defected strains are safe for vaccines Epizoo ology carriersonly diseasedDiseaseinhuntingdog r arely  Swine and wild boar are natural hosts (reservoir) of SuHV-1 spreader  Disease can detect in other species as well – dog, cat, ca le, sheep, mouse, rat, several wild animal species (limited viraemia and virus shedding  dead-end for the virus) o Acute, lethal disease of the nervous system Fatalin Ca Ru sporadicc avespruritush eadache  Humans not suscep ble, birds only experimentally infected  Large amount of virus is necessary for infec on  Swine infected PO, aerogene, breeding  viraemia  during the acute phase, large amount of virus is secreted in every secrets for 2-3 weeks (crosses the placenta)  Convalescence swine is life-long carrier and (can be) shedder (latent or persistent infec on), intermi ent shedding  Stress, pregnancy-lacta on  reac va on pharynxtrachealungs  High virus amount in pig’s respiratory ssues – slaughterhouse side-products!  Only low amount of virus is present in the pig’s meat a er the acute phase – inac vated a er 40 days in frozen meat  Introduc on with infected swine, fomites, liquid manure (survive for weeks)  Rodents play a minor role  Spread within herd – contact, air-borne, drinking water and food, arthropods mechanical vectors, semen, transplacental  Wild boars are carriers, disease only rarely – hun ng dogs!  Other species get infected from swine: o Common stable, or pasture (liquid manure) – access of dogs and cats into the stables (swine urine, placenta) – feeding raw slaughterhouse products (pharynx, trachea, lungs) Pathogenesis  In swine:  o Primer mul plica on in the infec on site: nasal and pharyngeal cavity, tonsils o  viraemia, spreading along the nerves to the brain o  secondary viral mul plica on in large amount in organs  Adults – fever, respiratory symptoms  Suckling – encephali s, mass-mortality o Piglets of convalescent or vaccinated sows are protected by colostrum un l 8-14 weeks of age – they can contract inapparent infec on during this me  Other species:dead endhosts o Direct access to the brain from the oral mucosa along the nerves (limited viraemia, and virus shedding)  encephalomyeli s, death exceptlambs theycanexcretethevirusinlargeamounts Clinical signs  In swine: o Incuba on me: 1-8 days (1-21 days) o New-borns (1-7 days old) – sudden death o Suckling (2-3 weeks old) – fever, tremor, vomi ng, incoordina on, convulsions, ataxia, paralysis, swallowing disorders, saliva on, whimpering  New-borns + suckling – even 100% mortality o 3-6 weeks old pigs – neurological symptoms for 4-6 days  Maximal 50% mortality o Growing:  Fever, inappetence  Mucous nasal discharge, sneezing, heavy breathing  Trembling nasal and facial muscles, incoordina on, munching  Healing a er 5-7 days  Residual symptoms – head shaking, tremor on head  Maximal 5% mortality o Adult:  O en no symptoms 1Asymptomaticusually  Temporary inappetence, mild respiratory symptoms  Pregnant sow: - Repeated breading, abor on, mummifica on, s llbirth, weak new-borns - Necro c placen s, endometri s  Other species: o Ca le, sheep, goat:  Incuba on me: 2-3 days  Fever, inappetence, reduced milk produc on, restlessness  Convulsions, itching, si ng, laying, dyspnoea, pharyngeal paralysis, saliva on, meteorism – death within 1-2 days, recovery very rare o Carnivores:  Depression, then excitement, itching, saliva on, convulsions, paralysis, death Diagnosis  Live swine: o Clinical symptoms – swabs from secrets: PCR, isola on – serology: VNT, (discrimina ve) dviwinrect.im  ELISA Dead swine: EE.EEKiEEEIsa feI5E i in aE.EE ra iiiEE.it g III  o Gross pathological examina on:  Suckling – mul ple necro c foci in tonsils, liver, spleen  Adult – lung oedema  Aborted foetus – mul ple necro c foci in organs, splenomegaly o Histopathological examina on:  Mul focal acute necrosis associated with acidophilic intranuclear inclusion bodies – lymphohis ocy c meningoencephali s – inters al pneumonia  Other species: o Clinical symptoms o Gross pathology – traces of scratching o Histology – lymphohis ocy c meningoencephali s, glial nodules o Detec on of the virus in dead animals – spleen, tonsils, lung, brain: PCR, IHC, IF, isola on  Differen a on – diseases presen ng neurological symptoms: rabies, classical swine fever, Teschen disease Preven on, control  Separa on of swine from other species (secrets, liquid manure)  Not to feed carnivores with raw pork meet and organs  Vaccina on in infected country (swine) – prevent clinical symptoms, decrease viral shedding o IgE nega ve marker vaccine, a enuated / inac vated o Protec on a er 7-10 days un l 3-4 months o Basic immunisa on with a enuated live virus o First vaccina on of maternally protected pigs on the 10th-12th week of age, repeat vaccina on in 2 weeks o Gilts – vaccina ons at the age of 6 months, at fer liza on and at the 70th-90th day of pregnancy o Older sows – vaccina on at fer liza on o Ruminants, carnivores – a enuated live can cause disease, inac vated vaccine only few months protec on RE cankill Can noteffective Eradica on veryimportant  The virus can maintain in vaccinated pig herds  Replacement – (UK, Denmark) – expensive  Raising virus-free genera on – early weaning of pigs from vaccinated sows, isolated keeping, serological tes ng  Selec on with the help of marker vaccines: o Immuniza on of the whole herd with marker vaccine in every 4 months – regular checking with discrimina ve ELISA o Isola on of the different age-groups  reduced virus shedding, slower spread o Posi ve animals will be removed from the herd when the number of seroposi ve animals is low o “Vaccinated virus free” animals  serological monitoring: 10% in every 6 months + tes ng of abor ons, s llbirths – ceasing vaccina on, becoming seronega ve  Maintenance of the virus-free status – epidemiological measures: import from free herds, quaran ne, regular serological monitoring (ELISA)