Avian Virology Flashcards
Pacheco’s DIsease is caused by what etiologic agent?
What is the family and subfamily of this virus?
What are the clinical signs associated with Pacheco’s disease?
Mucosal papillomas occur in what locations with this disease? What issues do those cause?
What species are particularly prone to papillomas?
What neoplasia is associated with mucosal papillomatosis?
- Psittacid herpesvirus 1 (PsHV-1)
- Alphaherpesviridae; genus Iltovirus – all avian herpes viruses are alphaherpesviruses.
- Others in this group – mareks, columbrid alphaherpes 1.
- Pacheco’s disease
- Acute, rapidly fatal disease of parrots, some passerines
- Mucosal papillomas and associated neoplasms of parrots
- First recognized Brazil, late 1920s
- Species affected and geographic distribution
- Either sex, any age, all species susceptible
- Mucosal papillomas greatest prevalence in Amazon parrots, macaws, Hawk-headed parrots, conures.
- Documented in NA, Eu, Middle East, Japan, NZ, Aus.
- Clinical signs
- Unexpected death or multiple deaths over short period
- Some birds may have biliverdin-stained urates (yellow or green) immediately prior to death
- Mucosal papillomatosis
- Cloaca, oral cavity
- Some birds may exhibit upper resp signs, strain to defecate, have blood in droppings.
- Generalized form of disease in the esophagus, crop, proventriculus, ventriculus – chronic wasting, regurgitation uncommon but may occur.
- Papillomas cauliflower-like or cobblestone and diffuse.
- Oral papillomatous lesions most common along margins of choanae and base of tongue.
- Usually starts as loss of pigment prior to papilloma formation.
- Lesions wax/wane, may disappear or progress.
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Amazons, macaws, hawkheaded parrots, conures.
- Evert cloaca during PE.
- Bile duct and pancreatic duct carcinomas common sequelae to mucosal papillomatosis.
- CS assoc with chronic liver disease – weight loss, overgrown beak, poor feather quality.
- Alphaherpesviridae; genus Iltovirus – all avian herpes viruses are alphaherpesviruses.
How is Pacheco’s disease typically diagnosed?
What changes may be seen on bloodwork?
What lesions would be seen on gross and histology?
What are the inclusion bodies? What organ are they readily seen in?
What treatments are available? How efffective are they?
What is the incubation period for Pacheco’s disease?
Bile duct carcinomas are typically what genotype?
- Diagnosis
- Usually made at necropsy
- Leukopenia, marked elevations in AST
- Gross lesions variable.
- Subtle liver changes that resemble diffuse lipidosis to prominent swelling, necrosis, pancreatitis, enteritis.
- Most birds in good BCS.
- Periportal hepatocytes typically spared
- Pan-nuclear eosinophilic inclusions in liver and especially in spleen.
- Pancreatic necrosis, necrosis of GIT with intralesional inclusion bodies.
- Single report of cockatiel with chronic active pancreatitis secondary to PsHV1.
- May have palpable crop thickening if diffuse papillomatosis.
- Biopsy not necessary for diagnosis; PCR will return all these birds as positive, testing not necessary.
- Rads may show rounded liver margins.
- Bile duct carcinomas visualized on ultrasound.
- Increased GGT with bile duct carcinomas, not specific.
- Diagnosis confirmed by liver biopsy.
- Treatment.
- Acyclovir has been used in aviaries and individuals.
- May be highly effective in preventing mortality during outbreaks.
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Not cured, will become carriers.
- Subclinical birds and survivors high risk for developing mucosal papillomas.
- May lead to hepatic neoplasias/biliary carcinomas.
- Cloacal carcinomas are rare.
- Cases with mucosal papillomas are not impacted by treatment with acyclovir.
- Mucosal papillomas should be left alone.
- Can debulk with sharp dissection, laser surgery, radiosurgery, topical silver nitrate.
- Repeated surgical intervention may result in cloacal scarring.
- Epizootiology and preventive measures
- Incubation 5-7 days.
- Lifelong infections, future outbreaks.
- When nonadapted parrots are exposed, Pacheco disease occurs.
- Densely housed indoor collections are more prone to outbreaks of Pacheco disease.
- All birds that developed bile duct and pancreatic duct carcinomas were tested as genotype 3.
- PCR assays to detect all 4 genotypes of PsHV-1 have been developed.
- Vaccines may prove useful in high-risk flocks.
- Unkonwn if vaccination with one serotype will protect against others.
What species are commonly affected by Psittacine Herpesvirus 2?
What are teh clinical signs?
How is this disease diagnosed?
What treatments are available?
- Psittacine herpesvirus 2 (PsHV-2)
- Aphaherpesviriniae; genus Iltovirus.
- Most closely related to PsHV-1 but not associated with Pacheco-like dz.
- Species affected and geographic distribution
- Only Congo African Grey Parrots in US and Germany
- Only other bird known to be infected was a blue and gold macaw.
- Clinical signs
- Subclinical or mucosal and mucocutaneous papillomas of oral cavity and eye.
- Benign but extensive.
- Ddx include cutaneous papillomas by parrot papillomavirus 1 (PePV1), other oral neoplasias.
- Rare, causes extensive face lesions, only reported in wild-caught birds.
- Subclinical or mucosal and mucocutaneous papillomas of oral cavity and eye.
- Diagnosis
- Gross lesions characteristic, can confirm by biopsy
- Virus inclusions not reported
- PCR to detect in tissue or oral/cloacal swabs
- Treatment
- No attempts have been made
- Acyclovir is not effective – lesions not associated with replicated virus.
- Aphaherpesviriniae; genus Iltovirus.
What are the clinical signs associated with Psittacine Herpesvirus 3?
How is this disease typically diagnosed?
What lesions are present on necropsy?
What histologic findings are typically seen?
What treatment and control measures are typically used?
- Psittacine herpesvirus 3 (PsHV-3).
- History and description of the virus
- Alphaherpesvirinae; genus Iltovirus.
- Occurs sporadically in a range of parrots in NA, Eu.
- Targets trachea.
- Species affected and geographic distribution
- Only confirmed by sequencing an outbreak in Bourke’s parrots in US and two eclectus parrots in Aus.
- Similar disease has been described in others.
- Clinical signs
- Coughing, difficulty breathing, ocular and nasal discharge.
- Died within 3-7 days of signs.
- Nonspecific clinical signs.
- Diagnosis
- Diagnosis in the live bird
- No work has been done on diagnosis in live birds for PsHV3.
- Cytology of conjunctiva and trachea has potential to detect syncytial cells and eosinophilic intranuclear inclusion bodies.
- Can detect with panherpesvirus primers on PCR.
- No work has been done on diagnosis in live birds for PsHV3.
- Postmortem diagnosis
- Conjunctivitis, tracheitis, changes in lungs suggestive of diffuse or locally extensive pneumonia and air sacculitis.
- Pale foci pancreatic necrosis.
- Syncytial cells containing pan-nuclear eosinophilic inclusion bodies in bronchi, parabronchi, trachea, conjunctiva, air sac, respiratory epithelium of turbinates.
- Numerous other tissues – spleen, pancreas, inner ear, meninges, kidney, thymus, bursa, gonads.
- Lymphoplasmacytic inflammation, hyperplasia respiratory epithelium.
- Unlike PsHV-1, liver is NOT primary target.
- Treatment
- Acyclovir may be helpful, unknown.
- Epizootiology and preventive measures
- Persistent infected birds likely to keep shedding.
- Possible to detect subclinical carriers with PCR oral swabs, cloacal swabs, blood samples.
- Diagnosis in the live bird
- History and description of the virus
What are the clinical signs of Columbid herpesivirus 1?
What types of pigeons are more commony affected?
How is this disease diagnosed?
What lesions are seen on necropsy?
How can it be treated?
COLUMBID HERPESVIRUS
Agent
· Columbid herpesvirus-1 (Smadel’s disease)
Demographics
· Pigeons – common in racing and fancier pigeon lofts more commonly than free-ranging pigeons
· If coinfected w/ circovirus: immunosuppression 🡪 clinical disease
Clinical manifestation
· Often subclinical
· More often clinical in squabs – lethargy, anorexia, weight loss, distended coelom
· Small, solid, grayish foci (sialiths) near choana
Diagnosis
· Antemortem
· Virus isolation
· Serology
· Postmortem
· Gross – hepatomegaly, splenomegaly
· Histo – necrotic foci in liver/spleen without inflammatory response; eosinophilic inclusion bodies
Treatment
· Acyclovir may be attempted
What are the three herpesviruses affecting raptorial birds?
How are these related to columbid herpesvirus 1?
What species is particularly susceptible?
What clinical signs are typically observed?
How is this diagnosed?
What lesions occur on necropsy? What are the inclusion bodies?
How can this be treaed and prevented?
RAPTOR HERPESVIRUSES
Agents
· Falconid herpesvirus-1 (FaHV-1)
· Strigid herpesvirus-1 (SHV-1)
· Accipitrid herpesvirus-1 (AHV-1)
Demographics
· Gyrfalcons appear particularly susceptible
Clinical manifestation
· Hepatosplenitis – multifocal necrosis of liver and spleen
· Signs – anorexia, lethargy, regurgitation, lime green urates, white plaques in the throat, unilateral keratitis/conjunctivitis, sudden death
Diagnosis
· Antemortem
· Virus isolation, serology
· Postmortem
· Gross – hepatomegaly, splenomegaly
· Histo – necrotic foci in liver/spleen without inflammatory response; eosinophilic inclusion bodies
Treatment
· Acyclovir may be attempted
Prevention
· Avoid feeding infected pigeons to raptors (main cause of infection)
FaHV-1 and SHV-1 are identical to columbid herpesvirus-1 (owls/falcons are aberrant hosts 🡪 severe disease)
Herpesviruses affect a wide range of avian species.
What are the clinical signs in the following groups?
Pigeons
Psittacines
Galliformes
Eagles
Falcons & Owls
Ducks
Cranes & Storks
Cormorants
Penguins
Toucans
Finch
Frigatebirds
Herpesvirus (MISC)
- Etiology: Herpesvirus
- Synonyms:
- IBDF (falcons); owl herpes, pigeon herpes encephalo-myelitis, psittacine herpes
- Geography: No. America, Middle East, Asia, Russia, Africa, Australia
- Morbidity & Mortality: Varied
- Seasonality: Unknown
- Clinical Signs: Varied, see gross path
- Pathology:
- Chickens: Marek’s disease, infectious larnygotracheitis.
- Pigeons and doves: encephalomyelitis.
- Cranes and storks: hepatitis.
- Quail and pheasant: hepatitis.
- Songbirds: conjuctivitis.
- Marine birds (cormorants (unknown)
- Diagnosis: Viral isolation. Intranuclear inclusion bodies (Cowdry type A); serology to test for antibodies (likely a carrier)
- Control: Isolation, depopulation
- Human Issues: None
What is the etiologic agent of Duck Plague?
What species are susceptible?
Where is this disease found naturally?
What is the morbidity and mortality?
Is there a seasonality to this disease in the wild?
What are the clinical signs?
What are the findings on pathology?
How is this diagnosed?
How is it controlled?
Duck Plague
- Etiology: Herpesvirus
- Synonyms: Duck viral enteritis, DVE
- Susceptible Species: Ducks, geese, swans. Blue winged teal redhead duck, wood duck highly susceptible. Least susceptible pintail duck.
- Geography: No. America, Canada Netherlands, England. Atlantic flyways.
- M/M: Mortality variable, 5-100%. Variation with species. May be variation with age and sex. Decreased egg production.
- Seasonality: All year except Aug/Sep; late spring peak season.
- Clinical Signs: Hypersensitive to light, extreme thirst bloody discharge from vent or bill, droopiness, penile prolapse, cold sore under tongue (think HERPES), inability to fly, convulsions
- Pathology: GI hemorrhage; mallards: circum-scribed hemorrhagic band around intestine; goose: circular ulcers; ‘cheesy’ plaques in esophagus proventriculus, SI. Necrotic spots on liver. Heart=hemorrhagic areas
- Diagnosis: Presumptive Dx on lesions. Viral isolation.
- Control: Destroy entire flocks, including eggs b/c of inapparent carriers. Low virulence vaccine available (Pekin Duck). Not approved in other ducks and geese.
- Other: Acute contagious fatal; inapparent infections. During latency, virus cannot be detected. Hardy-survives weeks. 4degC=water, 60d. Inactivated at pH< 3 and >1. Burn litter, chlorination helps. Sick birds dies: 3-7d after exposure. Wild birds-14d after exposure
- Human Issues: None
What is the etiologic agent of inclusion body disease of cranes?
What species are susceptible?
Where is this disease found naturally?
What is the morbidity and mortality?
Is there a seasonality to this disease in the wild?
What are the clinical signs?
What are the findings on pathology?
How is this diagnosed?
How is it controlled?
Inclusion Body Disease of Cranes (IBDC)
- Etiology: Herpesvirus
- Synonym: Crane Herpes
- Susceptible Species: Stanley, Sandhill, Manchurian, Hooded cranes most susceptible. Experimental infection to young Pekin & coots
- Geography: U.S., Austria, France, China, Soviet Union, Japan
- Morbidity & Mortality: UNK
- Seasonality: Unknown
- Clinical Signs: Lethargy, loss of appetite, death in 48 hours, sometimes bloody diarrhea
- Pathology: Swollen livers and spleens. Pin-point to pinhead lesions (yellow-white) in tissue. Hemorrhage in thymus and intestines.
- Diagnosis: Gross lesions. Viral isolation.
- Control: Destroy entire flock. When not possible, isolate.
- Other: Inapparent infections. Antibody response last for several years, unknown if exposed or carrier.
- Human Issues: None
What type of virus is Usutu Virus?
How is it transmitted?
What genus adn family does this virus belong to?
- Usutu virus
- Mosquito-borne Flavivirus, African origin
- Belongs to Japanese virus encephalitis group
- Significant mortality European blackbirds, Vienna 2001
- Emerging zoonotic potential – immunocompromised individuals
- In healthy individuals may lead to skin rash or seroconversion
- Some USUV naïve Strigiformes seem predisposed
- Potential for spread to other than African or Eurasian continents is unknown
- Taxonomy and description
- Family Flaviviridae; genus flavivirus
- ssRNA virus, icosahedral nucleocapsid
- USUV polyprotein contains three structural proteins
- Capsid protein (C)
- Precursor membrane protein/membrane protein (PrM/M)
- Envelope protein (E)
- Seven nonstructural (NS) proteins
- USUV is a member of the JEV serocomplex
- Large scale bird mortality in naïve populations
- Same group as WNV
- Family Flaviviridae; genus flavivirus
- Physical and chemical properties
- Flaviviruses inactivated by drying, organic solvents, low pH, and proteases.
- Mosquito-borne Flavivirus, African origin
What are the most susceptible species to Usutu virus?
What species have seroconverted without clinical signs?
What is the mosquito vector for this virus?
- Biologic properties
- Susceptible species
- European blackbird (Turdus merula)
- Most widely reported affected spp
- Captive great gray owls (Strix nebulosa)
- House sparrows in Switzerland
- European blackbird (Turdus merula)
- Seroconversion without clinical signs
- Rock pigeons
- Mallards
- Magpies
- Preference by the mosquito vector for certain hosp species.
- Adult female Culex pipiens will seek certain avian hosts
- Then virus replication and dissemination through infected saliva
- Has been isolated from many spp of mosquitoes but vector significance is unknown.
- Cx neavei from Senegal strongly suggested as vector for USUV.
*
- Adult female Culex pipiens will seek certain avian hosts
- Susceptible species
What are the clinical signs associated with Usutu virus infection in birds?
What are the most common findings on necropsy?
What histologic findings are typically seen?
- Clinical findings
- Many avian spp show seroconversion without clinical signs
- CS vary from nonspecific (immobility, ruffled plumage, eyes closed, anorexia) to neuro signs (depression, ataxia, jerky movements, torticollis, nystagmus, mortality).
- Often goes unnoticed in humans.
- From benign skin rash to neuroinvasive form.
- Pathology
- Peracute mortality, few obvious gross lesions
- Splenomegaly, hepatomegaly, pulmonary hyperemia
- Multifocal neuronal degeneration and perineuronal clustering of glial cells.
- Cerebellar lesions may include degeneration of Purkinje cells, formation of glial shrubberies, lymphoplasmacytic perivascular cuffs, mild degeneration and necrosis.
- Milliary pattern of liver necrosis, scattered myocardial necrosis.
- IHC, potential for cross reactivity; ISH
How is usutu virus diagnosed?
How do you expect serology to follow exposure?
What is teh gold standard?
How does USUV spread?
Where do most oubreaks occur? Why does urbanization favor outbreaks? Is there a seasonality to these outbreaks?
What is the key to preventing disease outbreaks?
- Diagnostics
- Serologic response follows viremia
- Circulating IgM produced within 6 days followed by IgG.
- Fourfold rise in titer beterrn acute and convalescent sera 10 days apart for acute infection.
- False-positive possible
- Acute mortality may not have enough time to seroconvert.
- Initial screening – hemagglutination inhibition test (HIT).
- Not specific.
- Cross reacts with other flaviviruses.
- More specific plaque reduction neutralization test (PRNT).
- Considered gold standard for Flaviviridae, cross reactivity does occur.
- Most reliable diagnosis is RT-PCR, USUV specific.
- Serologic response follows viremia
- Epizootiology
- USUV spreads in cycles between ornithophilic mosquito vectors and avian reservoir host.
- Humans dead-end hosts.
- May transmit arboviruses through blood transfusions.
- Has been seen with WNV, not yet USUV.
- Most European USUV epornitics have occurred in urban areas.
- May enhance detection of new cases.
- Urbanization favors the propagation of Cx. Pipiens by proliferation of artificial container habits.
- Peak of mosquito reproductive season is between mid-July and mid-September.
- USUV spreads in cycles between ornithophilic mosquito vectors and avian reservoir host.
- Prophylaxis
- Surveillance
- Targeted, with special attention to blackbirds and house sparrows.
- Rock pigeons and mallards.
- Vaccination
- No specific USUV vaccine
- Mosquito prevention
- Prevention of stagnant pools of water
- Cyclopoid crustaceans or fish/terrapins can reduce larvae in pools or tanks.
- Indoor housing of naïve Passeriformes and Strigiformes
- Screens on windows and doors
- Air conditioning
- Humans should wear loose-fitting, long-sleeved clothes, stay indoors at dusk and dawn, use DEET.
- Reduce the heat in urban areas i.e. shade trees, light-colored, highly reflective roof and paving materials.
- Surveillance
What is the etiologic agent of Beak and Feather disease?
What psittacine species are susceptible?
What are the two forms?
What groups of psittacines may be super-distributors of the virus in Australasia?
How is this virus transmitted?
- Psittacine beak and feather disease
- Chronic, ultimately fatal virus of Psittaciformes
- Acute form – nestling and fledglings
-
All parrots, lorikeets, cockatoos considered susceptible
- Wild Australian parrots
- Captive psittacine spp
- Etiologic agent
- Beak and feather disease virus (BFDV)
- Family circoviridae
-
Hemagglutinating virus, agglutinates erythrocytes from GP, geese, many psittacines.
- Unlike other circoviruses.
- Ongoing massive viral excretion, readily detected with hemagglutination assay HA as an antigen detection diagnostic test.
- Beak and feather disease virus (BFDV)
- Origins
- 1907 South Australia; red-rumped grass parakeets
- Aka French molt
- Feather loss syndromes
- All psittacine birds are susceptible to a diversity of BFDV clades, with no clear association based on host-virus cospeciation.
- No one genotype is more virulent than another.
-
Loriinae subfamily – lorikeets, lories, budgies, may be most robust, super-distributors of the virus in Australasia.
- Do not have advanced feather and beak lesions, but may have some feather lesions.
- Anecdotal evidence of complete recovery from infection.
- 1907 South Australia; red-rumped grass parakeets
- Transmission
- Excreted in feather dander and feces
- High concentrations of virus can be detected in liver tissue, bile, crop secretions, feces, and feathers
- Suspected to be transmitted vertically.
- Can be found in embryos from infected hens.
- Unlikely to be significant mechanism for circovirus maintenance.
- Horizontal transmission, esp in Australia – tree nest hollows.
- BFDV persists in the environment, high titers excreted
What are the clinical signs associated with Psittacine Beak and Feather Disease?
How does the acute form manifest?
What about the chronic form?
In cockatoos, what is the first feather type that’s damaged? How does this appear clinically?
What are some sequelae to the damage caused by PBFD?
What changes on clinical pathology may be seen?
- Clinical signs
- Juvenile or young adult psittacine birds most susceptible to PBFD.
- Acute form in nestlings and fledglings, esp Grey parrots.
- Can die within a week of signs.
- Rapid depression, leukopenia, anemia, green diarrhea, biliverdinuria, and death due to hepatic necrosis.
- Systemic illness, anorexia or regurgitation.
- Pterylodinia with edematous and painful wing tips, inflammation, vasculitis, SQ edema.
- High viral tiers in liver and bile, may die of liver failure.
- Affected feathers may shed all at once, or only primary feathers affected.
- Usually seen in bilaterally symmetric pattern.
- Fractures of developing calamus and intrapulp hemorrhage.
- Chronic form, more common.
- Slow subtle development and progression.
- As molt progresses, dystrophic feathers replace normal.
- Birds gradually lose plumage, often without other clinical signs of illness.
- Usually bilaterally symmetric and slowly progressive.
- Dystrophic feathers usually short, fault lines across vanes, thickened or retained feather sheath, blood within calamus, annular constriction of calamus, or curling.
- Acute form in nestlings and fledglings, esp Grey parrots.
-
In cacatuidae, powder down feathers aka pulviplumes, often first feathers affected.
- Results in glossy/shiny or dark pseudodiscoloration of beak and claws.
- Plumage may become dull.
- PBFD-affected pulviplumes fragile or develop abnormally thickened outer sheath that fails to disintegrate.
- Beak may also develop fracture lines/slough.
- Sunlight-exposed skin may become darkly pigmented.
- Chronic ulcers at elbows and wing tips.
- Predisposed to hypothermia, secondary infections from immunosuppression.
- Most chronic cases lead to difficulty eating, weight loss, death.
- Some spp, feathers falling out may be only clinical sign.
- First clinical sign in birds with green plumage may be development of yellow feathers.
- Beak abnormalities happen LATE in disease.
- Clinical pathology
- Acute – severe leukopenia in juvenile birds
- Chronic – lower serum protein concentrations, low prealbumin and gammaglobulin
- Juvenile or young adult psittacine birds most susceptible to PBFD.
