Korbel Rinder Emerg viral infections in pet birds 141126 · Clinic for Birds, Reptiles, Amphibians & Ornamental Fish Center for Clinical Veterinary Medicine University Ludwig Maximilian

27.11.14

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Rüdiger Korbel & Monika Rinder Clinic for Birds, Reptiles, Amphibians & Ornamental FishCenter for Clinical Veterinary MedicineUniversity Ludwig Maximilian of Munich/Germany

EMERGING VIRAL DISORDERS IN PET BIRDS- A review on the past 30 years -

Rinder et al. 2014: ORT bei Masthähnchen. Fortbildung Hähnchenaufzucht – Brüterei Süd – Bogen, Gankhofen, Pfahlheim

Viral Disorders?

•  Pathology & Epizootiology (1890s)

•  Poultry Medicine (1920s)

•  Pet Bird Medicine (1970s (USA) resp. 1980s (Europe)

•  Reptile Medicine (1990s (USA, later Europe)

•  (Ornamental) Fish Medicine (2010s)

History of Exotic Animal Medicine

Viral Disorders – History

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Fact sheet – Psittacid Herpesviruses (Pacheco‘s Disease (PD), Internal Parrot Papillomatosis (IPP), Amazon Tracheitis)

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Fact sheet – Psittacid Herpesviruses (Pacheco‘s Disease (PD), Internal Parrot Papillomatosis (IPP), Amazon Tracheitis)

1.  Virus description:•  Alphaherpesvirus, Iltovirus (enveloped DNA virus)•  PsHV-1: genetically diverse (4 genotypes and probably 3 serotypes):

cause of PD and IPP, broad host range•  PsHV-2: cause of IPP, in African Grey parrots and Blue and Yellow

macaws•  PsHV-3: respiratory disease, detected in Bourke’s parrots and

Eclectus parrots so far•  Herpesvirus serologically more closely related to ILT virus than to

PsHV-1, not genetically characterized so: far Amazon Tracheitis, in amazons and other psittacid species: respiratory disease)

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Fact sheet – Psittacid Herpesviruses (Pacheco‘s Disease (PD), Internal Papillomatosis of Parrots (IPP), Amazon Tracheitis)

2.  History:•  1930: severe disease of parrots in Brazil by Pacheco and Bier •  1933: disease was named Pacheco’s Disease by Findlay•  1975: identification of herpesviruses as the causal pathogens

during an outbreak in Florida by Simpson and colleagues•  1979: first description of Amazon Tracheitis in Germany by

Winteroll and Gylstorff•  1996: classification as an alphaherpesvirus based on first DNA

sequence information by Van Devanter and colleagues•  2005: first description of PsHV-2 by Styles and colleagues•  2012: genetic charachterization of a PsHV-3 as cause of

respiratory disease by Shivaprasad and Phalen

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3.  Epidemiology:•  Distribution:

•  PSHV-1 worldwide, •  PsHV-2 and PsHV-3: only a few cases so far

•  persistent infections, latency common (USA: PsHV-1 prevalence estimations 7 % of the parrot population)

•  Transmission: •  oral and probably aerogen ingestion of contaminated

materials from oral secretions or faeces•  introduction of (nonclinically) infected animals into a flock•  contact to infected birds•  vertical transmission probably not relevant

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4.  Clinical signs•  incubation periods 2-3 weeks, sometimes longer•  external factors (stress...) can lead to outbreaks•  peracute – acute: Pacheco’s Disease

•  sudden death•  diarrhoe with yellow droppings•  sometimes unspecific signs (lethary, fluffing feathers)

respiratory symptoms•  chronic: Internal Papillomatosis: papillomes of intestinal mucosas

(mostly oral and cloacal), liver and pancreatic tumors•  respiratory disease: bronchopneumonia, tracheitis, syringitis

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5.  Diagnosis•  clinical symptoms unspecific•  until 1990ies:

•  virus cultivation (Chicken embryofiboblasts): not all virus strains•  electron microscopy•  histology: intra-nuclear inclusion bodies in affected internal

organs (not always present)•  today:

•  PCR: from combi-swabs oral+cloacal mucosa or blood, in dead birds from internal organs (liver, brain, proximal intestines)

•  serology: limited cross reactivity of serotypes in virus neutralisation tests, ELISA/Western blot

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6.  Control (treatment and prevention)•  treatment:

•  acyclovir: reducing clinical symptoms of Pacheco Disease (not eliminating virus)

•  surgical resection of papillomas (palliative, recidives common)•  prevention:

•  no vaccine available•  isolation of infected birds•  prevention of pathogen introduction into aviary (quarantine and

testing)

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Fact sheet – Avian Polyomavirus(Budgerigar Fledgling Disease)

1.  Virus description:•  Budgerigar Fledgling Disease Virus, Avian Polyomavirus

(Polyomavirus, Polyomaviridae)•  small non-developed DNA virus•  nearly identical viruses in psittacids, falconiformes,

accipitriformes and chicken•  closely related viruses: canary polyomavirus, finch polyomavirus,

butcherbird polyomaviarus, crow polyomavirus, goose polyomavirus

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2.  History:•  1981: first description and virus characterisation in an acute fatal

disease in young budgerigars with high mortality in Florida, disease named budgerigar fledgling disease (Bernier et al 1981, Bozemann et al 1981)

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3.  Epidemiology:•  worldwide distribution•  common in budgerigars but also in other psittacid species

(lovebirds, macaws, eclectus parrots, conures, caiques, ring-necked parakeets)

•  persistent infection assumed•  virus shedding high in young birds, low in older birds (immunity)•  transmission

•  horizontal: faeces, crop secretions, feather dust, aerosols•  vertical: confirmed in budgerigars, but not in other psittacid

species•  virus highly stable in environment

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4.  Clinical signs•  virus with affinity for epithelial, lymphoreticular, and endothelial

cells•  disease of young birds•  Feather dystrophy, abnormal feather growth à deformed or lost

flight feathers (“runners” or “creepers”)•  other symptoms: subcutaneous bleeding, crop stasis,

regurgitation, stunting, abdominal distension, head tremor, death•  not unequivocally distinguishable from beak and feather disease

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5.  Diagnosis•  clinical symptoms•  virus detection

•  PCR: from blood, cloacal swabs, feathers#•  serology: virus neutralisation test, ELISA•  in carriers lifelong antibody persistence

•  post mortem:•  pathology: hepatosplenomegaly, ascites, subcutaneous and

subserosal hemorrhages. •  Histopathology: large, intranuclear inclusion bodies in affected

tissues membranous glomerulopathy of the kidneys.

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6.  Control (treatment and prevention)•  no treatment available•  Vaccine:

•  USA: vaccine Psittimune ® APV (Biomune) (inactivated vaccines)

•  in affected aviaries: breeding with older pairs (virus shedding low, possibly no transmission to offspring)

•  prevention: •  hygiene •  prevention of pathogen introduction into aviary (quarantine and

testing)•  separation of young birds (shedding high amount of virus) from

susceptible birds

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Fact sheet – Circovirus infection in psittacids:Psittacid beak and feather disease (PBFD)

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1.  Virus description:•  Beak and feather disease virus, psittacid circovirus, Family

Circoviridae•  Small non-enveloped virus with a small circular single-stranded

DNA genome (about 2 kb)•  broad host range: more than 60 species of Psittaciformes •  High genetic heterogeneity:

•  Host specificity of genetic clusters assumed•  Extensive recombination events assumed

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2.  History:•  1982: first animal virus with circular, single-stranded DNA

detected as a contaminant in pig kidney cell culture: •  Named porcine circovirus

•  1989: PBFD•  first characterization of a virus from feather follicles of a

diseased cockatoo by Ritchie and colleagues

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Fact sheet – Circovirus infection in psittacids: Psittacid beak and feather disease (PBFD)

3.  Epidemiology:•  worldwide distribution•  Transmission:

•  Virus shedding: excretions, secretions and feather dust•  direct contact with infected animals: •  Virus ingestion by inhalation or ingestion•  Speculation about certain host specificity of genetic variants

•  Some birds can eliminate virus, other may be lifelong and persistently infected

•  Budgerigars at least in Germany presently very frequently infected

•  Virus stable in environment for years, very resistant to disinfectants

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Fact sheet – Circovirus infection in psittacids: Psittacid beak and feather disease (PBFD)4.  Clinical signs

•  Immunosuppression •  Clinical picture varying among bird species and depending on the

age at infection•  Peracute and acute disease in neonates and very young birds

•  Depression, crop stasis, enteritis, pneumonia, death•  Acute form in African grey parrots < 6 months:

•  pancytopenia (severe immunosuppression) and death•  Chronic disease in birds up to 3 years of age:

•  Feather loss in roughly symmetrical pattern•  Abnormal feathering

•  short, curled, deformed•  Hemorrhages in feather pulp, circumferential

constriction at feather base•  Death resulting from secondary infections

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5.  Diagnosis•  clinical symptoms•  Standard:

•  Detection of virus DNA using PCR•  Serology:

•  ELISA using recombinant antigen•  Hemagglutination inhibition test

•  Histology•  Feather shaft epidermis: necrosis, hyperplasia, hyperkeratosis•  Inflammation of feather pulp: cellular infiltrates•  Atrophy and necrosis of lymphatic tissues (Bursa fabricii,

thymus)•  Basophilic nuclear and cytoplasmic inclusion bodies in

macrophages

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6.  Control (treatment and prevention)•  no treatment available•  Vaccine not commercially available•  prevention:

•  hygiene •  prevention of pathogen introduction into aviary (quarantine and

testing)•  Separating groups of infected birds

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Fact sheet – pox virus infection in pet birds

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1.  Virus description:•  large enveloped DNA virus (- 400 nm)•  genus Avipox (subfamily Chordopoxvirinae, family Poxviridae)•  10 species (recognized by the International Committee on the

Taxonomy of Viruses) forming 3 genetic clades: •  Fowlpox virus, Pigeonpox virus, Turkeypox virus, Mynahpox

virus, Juncopox virus•  Canarypox virus, Sparrowpox virus, Starlingpox virus •  Psittacinepox virus

•  more species proposed•  species with more or less strict host specificity

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2.  History:•  first animal virus detected using microscopy and cultured in the

laboratory•  in the past: fowl pox included all pox virus infections of birds

now only diseases in commercial poultry•  2000: first full genome sequence of fowlpox virus by Alonso and

colleagues

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3.  Epidemiology:•  worldwide distribution•  detected in more than 200 bird species•  transmission:

•  pox viruses cannot penetrate intact skin or mucosa, require small lesions

•  mechanical vectors (blood feeding insects or mites) of high importance

•  direct contact with infected animals or contaminated objects•  latent infections?•  very resistant in environment: infective after months to years in

dried scabs

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4.  Clinical signs•  incubation time several days to weeks•  cutaneous or “dry” form: skin nodules (proliferative)

•  localisation: featherless areas: eye lids, base of beak, legs & feet•  impaired vision or feed intake

•  diphteritic or “wet” form: moist, yellowish, necrotic materials •  localisation: internal mucosa of upper alimentary tract or of

respiratory tract, conjunctiva•  respiratory symptoms, anorexia, frequent death

•  systemic or septicemic: common in canaries•  internal organs•  acute depression, anorexia, dyspnoe, death

•  tumors•  complication by secondary infections

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5.  Diagnosis•  clinical symptoms•  eosinophilic intracytoplasmatic epidermal inclusions (Bollinger

bodies)•  virus cultivation (embryonated chicken eggs or cell cultures) •  Electron microscopy•  Detection of virus DNA using PCR

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6.  Control (treatment and prevention)•  no antiviral treatment available•  secondary infections: antibiotics, antifungals•  survivors: strain-specific immunity lasting 6 – 12 months•  Vaccines:

•  pigeonpox, fowlpox: available in Germany, Netherlands?•  canarypox: registered in Germany, but not commercially

available•  prevention:

•  hygiene •  vector control (mosquitoes, red fowl mite)•  Separating groups of infected birds

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Fact sheet – paramyxovirus infection in pet birds

1.  Virus description: avian paramyxovirus•  enveloped virus with a nonsegmented single-stranded RNA

genome•  genus Avulavirus, family Paramyxoviridae•  high genetic heterogeneity leading to differing phenotypical

properties •  9 species (recognized by the International Committee on the

Taxonomy of Viruses) •  Avian paramyxovirus 1 including Newcastle Disease Virus•  Avian paramyxovirus 2 – 9

•  additional species/serotypes of avian paramyxovirus (10 - 12) described

•  differing host ranges

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2.  History:•  first outbreaks of Newcastle Disease

•  1926 in Newcastle-upon-Tyne, England and in Java, Indonesia

but probably also earlier•  1896 in chicken in the Western Islands of Scotland •  1924 in Korea

•  Newcastle Disease Virus: name reserved for virulent viruses, others named PMV-1

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3.  Epidemiology:•  worldwide distribution•  transmission PMV-1:

•  virus shedding in feces•  oral and aerogenic infection

•  notifiable disease of high economic impact•  host range of paramyxovirus: table next page

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species usual host clinical signs

PMV-1 numerous enteritis, ZNS disorders, respiratory

PMV-2 turkeys, passerines, chickens, passerines

respiratory

PMV-3 (2 types)

turkeys / psittacines, passerines

conjunctivitis, respiratory signs, enteritis, ZNS signs

PMV-4 ducks, geese, rails apathogenic or mild resp. disease

PMV-5 budgerigars diarrhea, dyspnoe, torticollis,

PMV-6 ducks, geese unknown

PMV-7 pigeons, doves apathogenic

PMV-8 ducks, geese unknown

PMV-9 ducks unknown

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Fact sheet – pigeon paramyxovirus 1

•  history•  first recognized in the middle East in the late 1970ties•  in Europe in 1981•  closely related to Newcastle Disease Virus, but can be

differentiated based on molecular (sequences) and serological (monoclonal antibodies) techniques

•  host range: domesticated pigeons, doves, wood pigeons•  clinical signs:

•  acute: polyuria, anorexia, diarrhea, •  chronic: ZNS symptoms including paralysis, torticollis

•  nestlings, young birds with highest mortality•  Often mild or no disease in adult birds

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Fact sheet – pigeon paramyxovirus 1

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5.  Diagnosis•  clinical symptoms•  RT-Realtime-PCR or RT-PCR for Newcastle Disease, PMV-1•  virus isolation in embryonated chicken eggs•  haemagglutination test and haemagglutination inhibition test

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6.  Control (treatment and prevention)•  Newcastle Disease and pigeon PMV-1

•  vaccination•  treatment for other serotypes/species unknown•  hygiene

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Fact sheet – Proventricular Dilatation Disease and avian bornavirus

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1.  Virus description:•  enveloped virus with a single-stranded RNA genome•  genus Bornavirus, family Bornaviridae, Order Mononegavirales•  genetic heterogeneous , existence of multiple genotypes

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Fact sheet – Proventr. Dilatation Disease & Avian Borna V.

2.  History:•  Proventricular dilatation disease (PDD) known since the 1970s•  2008: avian bornavirus discovered in psittacids with PDD by two

independent working groups in the United States (Kistler et al., Honkavuori et al.)

•  2009: first description of an avian bornavirus in a non-psittacid species (canary) by Weissenböck and colleagues

•  2011: detection of bornavirus in waterfowl (swans, goose) and a balded eagle by Payne and colleagues, Delnatte and colleagues

•  2014: Estrildid finches as natural hosts of avian bornavirus by Rubbenstroth et al.

•  2010/2014: ? first detection of bornavirus in a reptile species by Stenglein and colleagues

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3.  Epidemiology:•  worldwide distribution of ABV in psittacid species•  detected in more than 80 parrot species so far•  23 % prevalence estimated in Europe (Heffels-Redmann et al 2011)•  virus shedding via feces, vomits, feather dust, saliva, lacrimal

fluids,...•  transmission:

•  exact route unknown so far, fecal-oral route assumed•  Virus seems to be transmitted slowly and by close contact from

bird to bird•  vertical route (transovarial) assumed, but probably not very

efficient•  time to seroconversion and virus shedding unknow

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4.  Clinical signs•  incubation time variable, from about 2 weeks (chicks) to several

years•  gastro-intestinal and neurological symptoms

•  regurgitation, enteritis, shedding of undigested feed, emaciation

•  ataxia, seizures, tremors of head or wings•  ocular manifestations

•  chorioretinitis•  pathogenesis not fully understood, immuno-pathological

processes assumed

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5.  Diagnosis•  clinical symptoms•  radiographs: dilated proventriculus•  in the past: crop biopsies •  Virus detection:

•  virus DNA using RT-PCR and RT-Realtime-PCR (multiple assays because of genetic heterogeneity)

•  antibodies: ELISA, indirect immunofluorescence assay, Western Blot

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6.  Control (treatment and prevention)•  no etiological treatment available•  no vaccine available•  infected birds: easily digestible feed (pellets), anti-inflammatory

treatment (celecoxib)•  separation of infected birds•  quarantine, testing of birds to be introduced into the flock

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Fact sheet – avian influenza

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5.  Diagnosis•  clinical symptoms•  diagnostic cascade:

•  Realtime PCR for Influenza A virus using combined choanal/cloacal swab or tissues of dead animals

•  if positive: realtime PCR for H5 and H7 hemagglutinin type (and for N1)

•  H5 and H7: realtime PCR or PCR + sequencing for genetic markers related to high pathogeneity

•  confirmation of high pathogeneity by biological test using spf-chickens and cultured virus

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3.  Epidemiology:•  Broad host range: many bird species are susceptible

•  But: many strains of AIV with certain degree of host specificity•  Water fowl as reservoirs: in general subclinical infections

•  Transmission.•  Virus shedding via respiratory tract, conjunctiva, feces•  Virus intake aerogen or oral•  Direct or indirect (over long distances)

•  Incubation time•  Depending on virus type, infection dose, host factors (species

and age)•  Few hours to 6-12 days

•  Course peracute (chicken, turkeys) to asymptomatic (waterfowl)

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Pandemic

•  Avian influenza viruses: use other cell receptors than human influenza viruses•  Pig: mixture of differing receptors•  Emergence of new influenza viruses with differing host range or pathogenicity

•  genetic shift (reassortment, mix of genomic segments of different „parent viruses“ in the new virus

•  Antigenic drift: point mutation in genome leading to a change in antigen structure

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4.  Clinical signs caused by highly pathogenic strains•  Sudden death (mortality - 100 %)•  Severe apathy•  Drop in egg production•  Head edema•  cyanoses of head and •  Respiratory signs•  Diarrhea•  Neurological signs

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5.  Diagnosis•  clinical symptoms•  diagnostic cascade:

•  Realtime PCR for Influenza A virus using combined choanal/cloacal swab or tissues of dead animals

•  if positive: realtime PCR for H5 and H7 hemagglutinin type (and for N1)

•  H5 and H7: realtime PCR or PCR + sequencing for genetic markers related to high pathogenicity

•  confirmation of high pathogenicity by biological test using spf-chickens and cultured virus

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6.  Control (treatment and prevention)•  no etiological treatment available•  vaccination prohibited in Europe•  culling of infected birds •  actions to prevent further distribution of pathogen•  general measurements for prevention of infection:

•  biosecurity •  keeping poultry indoors•  no contact with wild birds (especially waterbirds)

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6.  Control (treatment and prevention)•  no etiological treatment available•  vaccination prohibited•  culling of infected birds •  actions to prevent further distribution of pathogen•  general measurements for prevention of infection:

•  biosecurity •  keeping poultry indoors•  no contact with wild birds (especially waterbirds)

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Rinder et al. 2014: ORT bei Masthähnchen. Fortbildung Hähnchenaufzucht – Brüterei Süd – Bogen, Gankhofen, Pfahlheim

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Korbel Rinder Emerg viral infections in pet birds 141126 · Clinic for Birds, Reptiles, Amphibians & Ornamental Fish Center for Clinical Veterinary Medicine University Ludwig Maximilian