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Papovavirus
- DNA virus
- Papilloma and Polyoma
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Papilloma virus
- Causes benign skin tumors in some birds - warts or papillomas
- Host-specific (not zoo or communicative)
- African grey parrots - papiliferous plaques on eyelids, commisure of beak and face. Gets more extensive over time, looks like pox.
- Not related to cloacal papillomatosis (herpes)
- No real tx, freeze or burn off warts
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Polyoma virus - virus, types, animals it affects
- world-wide spread, non-enveloped papovavirus
- some genetic variation but all have same host range
- seen in wild cockatoos, raptors in Europe, house sparrow in US
- budgie and non-budgie forms
- Goose hemorrhagic polyomavirus (genetically distinct virus)
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avian polyoma virus major forms and major variation
- Two major forms: Budgerigar and non-budgerigar
- morphologically and antigenically similar
- varies with age of infection
- polyoma virus in mammals are persistent infections that cause tumors in unnatural hosts
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avian polyoma virus - Budgie form
- Virus replicates in wide range of tissues - skin, feathers, liver, spleen, kidney, brain
- "Budgie fledgling disease"
- infected at or aroudn birth. Sudden death around 15 days
- 10% show ataxia, tremors. Often die within 11 days.
- close to 100% morality
- Older budgies: infected as nestlings, abdominal distension, SQ hemorrhages. If survive, reduced down and contour ("feather dusters"), repro.
- English budgies resistant
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Avian polyoma virus - non-budgie form
- Fulminant disease: nestlings. Depression, regurg, diarrhea, SQ hemorrhages, abdominal distension. 12-48h duration (then death).
- Chronic form: rare. Weight loss, polyuria, poor feathers. Often die from renal failure.
- age and severity varies with species. Most affected are hand-fed. >2y often asymptomatic, develop transient viremia, shed, 90d to clear. Persistent infections possible.
- Conures, macaws, eclectus, lovebirds, cockatoos, gouldian finches, green aracari
- Edema and ascites syndrome: survive initial infection, develop signs above, ascites is modified or transudate, viral inclusions rare, looks like nestlings with EEE, PCR of blood and tissue is positive for APV
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Polyoma Virus - French Molt
- Virus damages capillaries of new feathers, causing poor feather formation (esp flight feathers)
- slow, debilitating disease. Young birds, born late in season
- possibly non-lethal form of polyoma
- Looks similar to disease caused by psitticine beak and feather disease
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Transmission of polyoma virus, incubation
- Not experimentally confirmed.
- Feces, feather dust (in environment)
- Respiratory secretions, crop secretions (how veterinarians spread it)
- Incubates 2-14 days in non-budgies
- 11-15 days in budgies.
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Path, histopath and dx of polyoma virus
- Path: hydropericardium, cardiomegaly, hepatomegaly, splenomegaly, renomegaly, ascites, ecchymotic hemorrhages
- Histopath: necrosis of affected organs, intra-nuclear inclusions
- dx: necropsy, DNA probe (Conjunctiva, Choana, Cloaca = active shedding), blood test (infection)
- Tx: none
- Prevention: vax at 5 and 8 weeks (repeat before boarding, over-use may cause glomerulonephritis). Stop breeding until done, move birds and disinfect, test birds before putting them back in.
- don't mix budgies, lovebirds and cockatiels
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Psittacine Beak and Feather Disease virus type, which birds, which cells, history
- only circovirus in psittacines
- pigeon circovirus causes immunosuppression and secondary infections
- Loves rapidly dividing cells - replicates in thymus, bursa, crop, esophagus, intestines, skin and feathers
- reported in the wild since 1887. Seen in wild African Grey parrots and in doves. Rarely disease in captivity. Second serotype for lories and lorikeets. Also in Cockatoos >8mo, chronic progressive form, lesions before 3 years.
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Psitticine Beak and Feather Disease lesions, signs
- First lesion in developing feathers - can be whole body in young, slowly progressive in older. Downy first affected in adults. Shiny black beak. Distribution depends on stage of molt.
- Feathers clubbed, pinched, hemorrhagic. Fall out easily, slowly or not replaced
- Beak lesions: start shiny due to loss of down, then elongated and brittle, broken or necrotic
- Peracute form in neonates, esp in cockatoos: Depression and regurgitation, pneumonia, enteritis, crop stasis, weight loss, severe feather lesions. Death in 2-3 days.
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Psittacine Beak and Feather Disease - French Molt
- acute form in young birds during first adult plumage molt
- Depression followed by sudden changes in feathers - necrosis, fractures, hemorrhages
- Birds usually die within 2 weeks
- Concurrent infection with APV in some.
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Psittacine Beak and Feather Disease in African Grey Parrots (acute and chronic), lovebirds, budgies, lories
- Acute: develop pancytopenia, virus in bone marrow. No feather lesions. Die suddenly from opportunistic infections
- Chronic: dystrophic feathers. New contour feathers are red.
- Lovebirds: very prevalent, transient infection in asymptomatic, dz in feathers in young adults
- Budgies: less common, no wing feathers
- Lories: feather changes in fledglings, some recover and have normal feathers. Others have chronic form
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Psittacine Beak and Feather Disease - age, incubation, Transmission, Diagnosis, tx, control.
- Age-related resistance = >3y resistant to disease, may develop transient viremia and shedding
- Incubation period: 21-25d in chicks and fledglings. Months to years in older.
- Transmission: ingestion/inhalation. Feces, feather dust, oral secretions, fomites. Stable in environment. Vertical transmission possible
- Dx: DNA probes (Conjunctiva, Choana, Cloaca for shedding, blood for infection). Feather dust in environment, tissues of dead birds.
- Hemagglutination activity - shows exposure (past or present).
- Basophilic intranuclear or intracytoplasmic inclusions on necropsy or feather follicle biopsy.
- Tx: No tx. Chronic dz may live for years. Supportive care - soft food, prevent secondary, warm environment.
- Control: new birds tested in quarantine. Test + birds again in 90 days.
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Avian Polyoma Virus vs Psittacine Beak and Feather Disease
2 types of each
virus
dx
histo
tx
prevention
- APV: budgie (death at fledging/15d vs feather dusters) vs non-budgie (nothing if >2y, abd distension and hemorrhage).
- PBFD: Young (Chronic progressive loss of feathers then brittle beak (<3). Old (>3) asymptomatic.
- APV virus: papova
- PBFD virus: circo
- dx for APV and PBFD: swab (CCC) or blood (PCR)
- APV Histo: intranuclear inclusions
- PBFD histo: intranuclear or intracytoplasmic inclusions
- Tx for APV and PBFD: none
- prevention for APV: vax at 5 and 8 wks, keep babies away from adults
- prevention for PBFD: keep babies away
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French molt
what is it?
Which virus?
- infection in birds that gets first adult feathers, affects WHOLE feather. Come in patchy and strange.
- Virus: circo and papova (Avian Polyoma virus and Psitticine Beak and Feather Disease)
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Herpesviridae
- DNA viruses, wide variety of avian hosts
- usu host specific, but some can affect several species
- Latent lifelong infections
- periodic viral shedding (+/- clinical signs)
- Tansmission by direct contact
- alpha-herpes virus in parrots
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Pacheco's disease - type of virus, species affected, most common
- Herpes viral hepatitis in South American species (Amazons, macaws, conures, disease are but reported in African Grey parrot, cockatiel and cockatoo)
- most common in aviaries, quarantines and pet stores (esp mixed collections, Patagonian conures may be carriers)
- Signs: acute death, depression, lethargy, loss of appetite, yellow urates and diarrhea, CNS signs, regurg often terminal, elevated liver enzymes and leukopenia in survivros, hepatomegaly, renomegaly, splenomegaly on rads
- Outbreaks follow stressful events, incubation 5-14d, persists in oral and cloacal mucosa
- Transmission through oral secretion, droppings, vomit. Outcome and infection depend on genotype and species.
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Pacheco's Disease diagnosis
- Hard to dx in a live bird. Hx, signs, lab findings suggestive. Strongly positive on PCR but die before test results come back. Response to treatment
- Necropsy - well muscled, enlarged liver, spleen and kidney. Serosal and epicardial hemorrhage, necrotic hepatitis, splenitis and nephritis. Eosinophilic intra-nuclear inclusions
- DNA probes (PCR) - tissue, blood, feces
- Viral isolation
- Antibody levels, used to detect carriers.
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Pacheco's Disease Treatment
- Acyclovir: TID during outbreak
- Vaccination: NOT during outbreak. Inactivated virus. Can cause granulomas and paralysis, use ONLY in high risk groups.
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Marek's Disease
- Fowl paralysis, neurolymphatomatosis.
- Highly contagious
- economically important in poultry industry
- Neurotropic virus - peripheral nerve - mononuclear infiltrate - lymphoid neoplasia
- rare in turkey, quail
- Transmission: replicates and sheds in feather dander throughout life of bird. Stable in environment. No egg transmission.
- Chicks in first weeks of life highly susceptible.
- Several types of clinical dz. Peracute in unvaccinated 3-5wk old chicks.
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Marek's disease clinical signs and lesions, dx and control
- Acute: tumors, sudden death, blindness (grey eye)
- Classic paralysis (neurolymphomatosis): wings, legs, neck, CNS = asymmetric paralysis.
- vagus nerve - GI stasis, dilation, dyspnea
- Lesions: peripheral nerve swelling/discoloration, Lymphoid accumulation in skin, liver, spleen, kidneys, heart, lung, gonads. Loss of bursa, thymus, bone marrow degeneration. Immunized birds may develop skin tumors
- Dx: clinical signs, post-mortem findings, virus isolation (WBC, feather pulp, tissue), AB detection (VN, ELISA, IFA, AGID)
- Control: Vax in ovo or at 1 day old. Vax prevents tumor formation NOT INFECTION. Acyclovir could reduce severity.
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Amazon Tracheitis virus
- possibly related to ILT
- More common in Europe than US. Acute dyspnea and death or chronic URD. Necrotic tracheitis, pharyngitis, and esophagitis
- intranuclear inclusions are harder to find
- diagnosis by viral isolation
- no vax
- Acyclovir as tx is unknown
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Infectious Laryngotracheitis
- Chickens and pheasants
- Transmission: resp, intraocular, fomites. Carrier birds? 6-12d incubation
- High morbidity, 10-20% mortality
- Severe: coughing, gasping, wheezing, open-mouth breathing, blood in trachea
- mild: nasal d/c, conjunctivitis, drop in egg production (recovery in 2-4wks)
- lesions: inflammation and hemorrhage in trachea. Pseudomembranes in trachea.
- dx: signs, history, virus isolation, PCR, serology.
- Control: vax, biosecurity
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Herpes virus warts of cockatoos
- wart-like lesions on the feet of cockatoos and macaws (like papilloma on the face)
- low level of infectivity. Lesions may be horny or plaque-like. Lesions persist for years without a problem. No tx necessary.
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Duck Plague
- Duck viral enteritis
- acute, highly contagious disease
- Ducks, geese and swans
- Europe, Asia, N. America, Africa
- High mortality (esp in OLDER ANIMALS), high economic loss. Decimates wild populations
- viral-induced vascular damage (results in hemorrhages)
- Direct and indirect (water) transmission
- 3-7d incubation time
- Possible LATENT FORM in survivors. Wild birds may contaminate domestic pools
- Signs: acute death, large numbers, adult>young, weakness, lethargy, pale, dyspnea, diarrhea. Hemorrhages on body surfaces (petechia, ecchymoses, heart, GI, spleen, free blood in body cavities).
- Dx: PCR, viral isolation
- Prevention: no tx (cull and separate), vax for zoos and private breeders. Control exposure to wild birds.
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Falcon and Owl Herpesvirus
- Inclusion body disease
- Caused hepatitis/splenitis with necrosis and intranuclear inclusion bodies in cells
- same virus as pigeon herpesvirus type (2008). In Asia, North America, Europe. Free living and captive raptors
- Acts like Pacheco's disease
- Acute death is the first sign of disease
- Depression, lethargy, anorexia. 24-72h prior to death.
- 100% mortality
- Ingesting infected pigeons
- Falcon vax available
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Paramyxoviruses
- RNA viruses, enveloped
- Significant impact in pet birds and poultry
- 9 serotypes
- Most important diseases: Newcastle Disease (PMV1), PMV 1 of pigeons, PMV 3 of psittacines
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Newcastle Disease basics - pathotypes
- Major importance to poultry industry (started in 1927). Intermittent in US.
- Paramyxovirus
- Most species of birds susceptible.
- 4 pathotypes: Lentogenic (mild), mesogenic (moderate), velogenic neurotropic (HIGHLY pathogenic), Velogenic viscerotropic (most pathogenic - Exotic Newcastle Disease)
- Clinical signs vary wildly betweens species and strains--geese and ducks resistant to chicken strains, lentogenic needs specific cells, virulent virus replicate in many cells = fatal systemic infection
- HIGHLY contagious
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Newcastle transmission, incubation, clinical signs
- Transmission: inhalation, ingestion or exposure of mucus membranes to feces/respiratory secretions. Virus shed up to 1 year after infection. Insects, rodents, humans act as vectors. No egg transmission. Virus stable in environment. Fomites are serious concern
- incubation: 2-15d
- Signs: acute death vs acute disease. Lethargy, weakness, edema of head or lower eyelid, diarrhea, dyspnea, oculonasal discharge, neuro signs, interrupted egg laying.
- commercially important ($180mil), highly infective. High mortality (95-100% unvax). From imported psittacines.
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Newcastle necropsy, histo, dx, prevention
- Resp GI splenic inflammation
- Diptheritic membranes in mouth, trachea, esophagus, PV, cloaca, infammation in cecal tonsils, hemorrhage, necrosis and perivascular cuffing in the brain, hemorrhage conjunctiva/cloaca only sign in last outbreak.
- Intra-nuclear or intracytoplasmic inclusions are rare (IFA helps)
- dx: viral isolation (feces, pharyngeal swab), antibodies differentiate between serotypes
- Prevent with quarantine and testing, vax for gallinacious species (in other countries).
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PMV 1 in Pigeons
- captive and wild birds (like old dog vestibular, head tilt)
- neuro signs: tremors, ataxia, severe torticollis, weight loss, anorexia, death.
- Mortality highest in nestlings
- older birds spontaneous recovery in 3-4wks
- dx: viral isolation, ab levels.
- vax: inactivated available. USED DURING OUTBREAK to reduce clinical signs and duration. No value after CNS signs develop. Annual boosters
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PMV3 in psittacines
- Like PMV1 in pigeons, serotype seen in poultry and psittacines
- passerines get diarrhea, dyspnea and dysphagia. CNS signs in psittacines. African greys get ocular lesions, nasal hemorrhage and paralysis.
- High morbidity, low mortality.
- Necropsy similar to PMV1 in pigeons. Perivascular cuffing in brain.
- Vax for turkeys, doesn't protect psittacines.
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Pox viruses
- Large complex DNA viruses that replicate in cytoplasm. All birds are susceptible to some type, but each species group has their own. Varied virulence, not transmissible to other avian groups
- Three major forms: dry, wet and septicemic forms
- transmission: requires damaged skin - vectors (biting arthropods and mosquitos) or trauma! latently infected are a problem.
- VAX: canary pox q6-12mo, reduces mortality if given during outbreak. Autogenous vax of limited use.
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Dry form of pox
- discrete nodules on unfeathered skin
- papules, then vesicles, then erosions, then scabs.
- Can be secondarily infected (rare)
- May persist up to a year
- Mortality low (secondary - prevent seeing or eating or breathing)
- tx: prevent secondary infections. Can induce self-vax.
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wet form of pox
- Erosions on mucous membranes, greyish yellow to brown
- Become diphtheritic or fibrinonecrotic
- Mortality much higher - can be systemic. Inhibit respiration and eating. Can be secondarily infected
- tx: debridement and topical/systemic antibiotics. Difficult to treat lesions in esophagus/trachea
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Septicemic form of pox
- Acute onset ruffle feathers, lethargy, cyanosis
- die within 3 days of clinical signs
- Moratlity rate 70-99%
- Cutaneous lesions rare
- antemortem diagnosis difficult
- Tx: usually die before/despite tx
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Pox virus in psittacines
- amazons, macaws and pionus parrots
- conjunctivitis and ocular discharge. Forms dry scabs, can be secondarily infected. Resolve in 2-6 weeks if not infected
- Lovebirds develop wet and dry forms
- Budgies get mild dyspnea, no skin or feather changes (septicemic form in lungs)
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Canary pox
- Endemic in large flocks
- Separate in passerine pox
- dry, wet or septicemic forms occur
- swollen eyes and dyspnea
- die quickly from lung lesions
- Finches in cage can be affected
- Vax: commercially available, prevents temporary immunity. Give every 6-12mo, esp fledglings. Reduces mortality if given during outbreak. Good results in other species.
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Eastern Equine Encephalitis Virus
- Affects galliforms, cranes, sparrows, emu, pigeons
- Native birds less susceptible. Become viremic but no disease
- Non-native birds die without signs after short course of enteritis, CNS signs.
- Psittacines, pheasants, emus and cranes
- Transmission by mosquitos
- Survivors resistant to further disease (NOT reserviors
- Necropsy: soft cerebrum, hepatosplenomegaly, enteritis. histo = non-supportive encephalitis, perivascular cuffing, hepatic/myocardial necrosis
- Dx: ab levels
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Western Equine Encephalitis
- usu asymptomatic
- emus, pheasants, english sparrows, ducks, chickens, turkeys
- lethargy, fluffed feathers, incoordination, torticollis, paresis
- Necropsy like EEE (soft cerebrum, hepatosplenomegaly, enteritis. Histo = non-supportive encephalitis, perivascular cuffing, hepative/myocardial necrosis) + pericardial fluid in emu
- Transmission by mosquito
- Nestling English sparrows are amplifying host
- Diagnosis by viral isolation or antibody levels
- Vaccine for horses efficacious in emus
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Proventricular dilatation Disease
- Bornavirus in 5/7 cases in one study? So maybe that.
- Bornavirus causes CNS disease in lots of mammals and ostriches
- Macaw wasting disease?
- Avian bornavirus affects myenteric and CNS, causes lymphoplasmacytic ganglioneuritis. Neuritis causes nerve dysfunction.
- Signs: weight loss, appetite changes, delayed crop emptying, passage of undigested food in droppings. CNS - ataxia, akinesia, progressive paresis to paralysis to seizures. No GI signs.
- Rads: enlarged, food-filled proventriculus. Ventriculus and intestines may be affected. Normal with CNS form
- Fluoroscopy: aids in dx but not definitive. Barium (20min). Poor contractility of ventriculus, isthmus and ventriculus. Lack of closure of isthmus typical. Intestines hyper or hypomotile.
- Biopsy: Proventricular, isthemus or ventricular best but crop biopsy better (70% success), take medium to large blood vessel (you want the NERVE)
- Transmission: unknown. Direct contact? Feces, oral secretions, mating.
- Detection: ELISA, PCR, Antigangliocide antibodies in the future
- Tx: Diet, bacterial supplementation, COX-2 inhibitors. cyclosporin with itraconazolevax in future
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West Nile Virus
- ssRNA virus (Flavivirus)
- Mosquito-borne
- mortality in >300 species of birds
- susceptibility varies: corvids, raptors, songbirds, flamingos (HIGH), domestic geese (HIGH), chickens/turkeys (resistant), Parrots (low - acute death, no signs)
- Seasonal occurrence (with mosquitos), all year in Southern US
- Clinical signs: peracute death, acute disease with progressive neuro signs, ataxia, tremors. Chronic disease with survivors, often permanent neuro signs
- Lesions: inflammation grey matter brain and spinal cord. Lymphoplasmacytic inflammation and necrosis.
- Antigen tests: tissues, choana/cloacal swabs, PCR, Immunohistochemistry, virus isolation, serology.
- Tx: symptomatic (fluids, tube feeding, abx, antifungals, B vitamins), NSAIDs (decreases CNS inflammation).
- Vax: horse vax gives some protection, only for highly susceptible species.
- Prevention: exposure to mosquitos
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Infectious Bronchitis
- Coronavirus in chickens
- very contagious (wind)
- survivors can become carriers
- signs: depression, resp disease, coughing, tracheal rales, nasal d/c, reduced egg production/quality (layers)
- Lesions: serous to caseous exudate in resp, air sacculitis with exudate, swollen pale kidneys, egg yolk peritonitis, small cystic oviducts
- Dx: clinical signs, history. Viral isolation and serology
- Vax: available
- prevent: good biosecurity (air flow between flocks, prevent wild birds)
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Avian influenza
- RNA virus, family orthomyxovirus
- subtypes based on surface glycoproteins, hemagglutinin, neuraminidase, etc.
- Most avian strains are low path, mild dz. But can evolve.
- High path: severe disease and mortality in poultry. Human illness ranges.
- Virus sources: feces, resp secretions, saliva, eggs, water, people. High path viable for longer periods. Virus shedding varies with strain.
- Transmission: direct contact with secretions, contaminated feed/water/equipment/clothing. Waterfowl and seabirds.
- signs: morbidity/mortality depends on species and strain. Sudden death, anorexia, depression, diarrhea, resp signs like cyanosis, discharge. Neuro signs, edema of head and neck.
- Postmortem lesions: edema and hemorrhages of comb, head. Petechia, exudate in sinuses, air sacs, pericardial sacs, trachea. Catarrhal or hemorrhagic tracheitis, enteritis, air sacculitis and pneumonia
- Dx: antigen detection via surveillance testing, swabs or trachea, PCR. Ab detection in poultry only
- Prevention/control: biosecurity, attenuated vax (limited protection), inactive vax (reduce Mo/Mr)
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If you had a chicken with edema of the head and comb, which viruses would you be thinking about? (2)
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Between Newcastle and Avian Influenza, which could also have dyspnea and respiratory disease as another sign?
both
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How do you differentiate Newcastle and Avian Influenza? (given edema of head and comb, dyspnea and resp disease)
- PCR
- Newcastle: pharyngeal swab
- Avian Influenza: tracheal swab
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If you had a chicken with blood in its trachea on post mortem, which viruses should you consider? (3)
- Infectious LaryngoTracheitis
- Avian Influenza
- Newcastle
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Why would blood in the trachea of a chicken not suggest infectious bronchitis?
LOWER respiratory disease, not upper
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What does a chicken doing the splits have? What kind is it? What other diseases does this kind cause in psittacines? (3)
- Marek's Disease
- Herpesvirus
- Pacheco's (liver disease in New World Psittacines)
- Warts on Cockatoo feet
- Tracheitis in Amazons
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What vaccines are available for viral infections in pet birds? (4)
- Polyoma
- West Nile (less - not as susceptible)
- Pacheco's
- Canary Pox
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What vaccines are safe to give in the face of an outbreak?
- PMV-1 in pigeons
- Pox in canaries
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Which vaccine protects against the side effects of the virus but not the virus itself?
Marek's
-
mycobacterium
- worldwide, all species (mostly elim in commercial poultry)
- M. avium intracellulare or avium, M. genavense mostly.
- More in zoos, then psittacine pets.
- zoo: immuno-compromised. May be contaminated environment.
- Survive a long time in environment. No confirmed bird-to-bird. Aerosol from humans. Fecal to birds? Stress, grounded birds.
- Lives in macrophages subclinically. Long incubation, bad serologic tests, hard to ID an infected bird.
- Transmission: dz dep on route of infection. Ingestion (hematogenous spread to BM, lungs, air sacs, spleen, etc). Inhalation (pulmonary). Wounds (wing web tattoo). Egg transmission (rare), contaminated egg SHELL.
- signs: nonspecific and variable. WEIGHT LOSS late in dz process. Poor feathers, diarrhea, polyuria, abdominal distension, dyspnea, GRANULOMAS, lameness, neuro, bumblefoot
- 3 presentations: cutaneous, atypical (organomegaly, no granulomas), nodular
- dx: hard to dz. Antemortem. leukocytosis? signs? FNA and cytology, acid-fast stain on feces. Intradermal tuberculin test on poultry. Look for nodules, organomegaly, foamy macrophages.
- Tx: quarantine, support immune, LOTS of drugs, damages human/animal bond. Often euth.
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mycoplasma
- no cell wall, hard to culture and transport, so hard to dx.
- transmission: resp and repro (close contact). Horizontal and vertical (crop milk, secretions).
- gallispeticum (turkey/chicken), synoviae (t/c), meleagridis (t), iowae (t)
- signs: resp, repro, joints, brain. Damage epithelial. Chronic and often silent. Conjunctivitis, nasal d/c, sacculitis, repro failure. Mortality from secondary.
- Dx: serology in chx, parrots, culture.
- Control/tx: dz-free breeder, abx, vax not available. NO PENICILLINS/CEPH. Fluoroquinolones, tetracyclines, macrolides, aminoglycosides. ALLEVIATE SIGNS BUT STILL INFECTED.
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Chlamydiosis
- 1879. Gram - intracellular. Worldwide, all species subtypes.
- zoo: Worse for preg women. READILY TRANSMISSIBLE TO HUMANS. asymptomatic to severely systemic, intersitial pneumonia and encephalititis
- REPORTABLE.
- transmission: shed in feces or resp secretions, esp in stress. Survives in environment. Inhalation or ingestion. Scavengers, chicks, ectoparasites. Rarely vertical.
- Lesions: enlarged mottled liver, enlarged friable purple spleen, fibrinous cloudy thick air sacs, fibrinous pericarditis, enteritis, conjunctivitis, keratitis
- Seen in newly acquired bird or after intro or stress. Incubates 3d to 1yr.
- BIRDS THAT HAVE THE DISEASE ARE FULLY SUSCEPTIBLE TO RE-INFECTION
- signs: variable, nonspecific. Overt clinical disease and mortality to non-diagnosed effects on growth, health and repro. Breeding asymptomatic parents may infect nestlings.
- 3 forms: peracute, acute, chronic.
- Concurrent GI and resp infections with gram - bacteria or yeast. Could obscure diagnosis
- dx: LEUKOCYTOSIS on CBC, liver enzymes elevated, glc normal or decreased, non-regen anemia. PCR on blood or CCC, sensitive and specific. ELISA - serology NOT DIAGNOSITC. rare. No abs in acute. Final dx is difficult, esp with asymptomatic. No single test method.
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Chlamydia life cycle
- Biphasic
- Alimentary body infective. adhere to host cell membrane, penetrate as vesicle to avoid detection. Avoid/inhibit immune system. TX INEFFECTIVE AGAINST MO IN HOST CELL
- Reticulate body metabolically active (binary fission), extremely fast. Cells can lyse, infect new cell with division or revert to alimentary body and infect nearby cells.
- Incubation from 3d to 1yr
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3 forms of chlamydia presentation
- peracute form: rapid death, can be single case or outbreak. Few premontory signs. Profuse diarrhea.
- Acute form: few days to weeks, profuse diarrhea with yellow/green urates, weight loss, depression, rhinitis, keratoconjunctivitis, resp signs.
- Chronic form: milder and slower but similar to acute. Weight loss, nasal d/c, labored breathing, abdominal distension (liver, spleen, ascites)
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ddx for severe leukocytosis
- Chlamydophila
- Mycobacteriosis
- Aspergillosis
- Gout
- Severe osteomyelitis
- severe salpingitis
- Egg-yolk peritonitis
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Leukcytosis
tx, follow-up, prevention
- Tx: isolate, protective gear, NOTIFY the health dept. TPN for severe, medicated feed if they can handle it. Doxy (inj better). Watch for hepatotoxicity and stress. Azithro, Enroflox. Supportive - low stress, ensure food intake, control/prevent secondary, NO Ca!!
- Follow-up: Clean/disinfect aviary, allow RECOVERY PERIOD before breeding. Repeat rads and immunodx.
- Prevent: quarantine, test suspicious birds, Prophylactic tx of aviary with new bird? Tx whole aviary yearly?
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Clostridium path, diseases
- gram +, anaerobic and spore-forming rods
- part of normal GI flora. Proliferate due to stress, dietary change, increased sugar consumption, immunosuppression, coccidiosis, toxin-producing.
- diseases: ulcerative enteritis, necrotic enteritis, gangrenous dermatitis, botulism, neuroparalytic disease, heptatitis, enterotoxemia, tyzzer's disease
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necrotic enteritis
- Clostridium perfringens A and C with alpha and beta toxins. In chickens 1wk-6mo = subclinical, decreased growth rate, decreased feed utilization.
- pathophys: in normal gut flora. Exacerbated by diet or ingestion of contaminated feces, soil, litter, feed.
- signs: depression, decreased appetite, reluctance to move, diarrhea, piloerection, short duration before death. Many MO on fecal gram stain. Foul-smelling diarrhea and voluminous stools.
- Lesion: confined to SI (jejunum and ileum, rarely ceca). Friable, gas-distended intestines, green/yellow pseudomembranes on mucosa, small amounts of blood, concurrent infection with coccidia
- tx: responsive to abx, probiotics, hygiene, diet change.
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Ulcerative Enteritis
- Clostridium colinum
- young captive quail. Sometimes young chickens, turkeys, pigeons. Worldwide.
- Transmission: fecal-oral from chronic carrier, contaminated litter, water and feed. Incubation 1-3d, acute death (100% in quail). +/- white watery diarrhea.
- signs: piloerection, listless, weakness
- Peak mortality 5-14d after signs.
- lesions: hemorrhagic enteritis, petechial hemorrhages, intestinal ulcerations, perforation of ulcers.
- immunity: protective in survivors. If tx with abx, remain susceptible
- tx: abx in water and feed if eating, removal of contaminated feed/bedding/etc, tx underlying diseases.
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Gangrenous dermatitis
- C. perfringens, C. septicum, C. novyi. Secondary s. aureus. Bacteria found on environment and on skin
- young chickens. Bubbly tail in Turkeys.
- Infection follows skin wound. Semen collection, caponization. Sequel to disease, environmental factors combined with viral immune suppression. Similar cellulitis in crows with open fracture (trauma, gunshot).
- signs: depression, incoordination, inappetance, leg weakness, ataxia, short illness then death in <24h
- lesions: SQ and muscle edema and gas. Discrete white foci in liver, bursa. Cellulitis and edema around tail in turkeys, abnormal tail feathers.
- abx of limited efficacy due to underlying disease, improve hygiene, minimize trauma.
- organisms in tissues.
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Degredation of nitrogenous waste in birds
- mammals: urea
- birds: BUN unimportant. Reduced quantities except in penguins. Excrete uric acid without losing water. Precipitates on egg shell.
- Plasma levels maintained below saturation levels. Colloid solution - lots of mucus, bound by protein matrix, prevents precipitation and protects epithelia.
- Uric acid secreted from cloaca, reverse peristalsis sends urine and urates into colon to resorb water.
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Gout
- pathophys: plasma uric acid levels, acute severe increase, chronically elevated levels.
- Precipitation of urate crystals on visceral surfaces (frosting), in joints, in renal parenchyma (3 forms)
- any factor that increases production or decreases elimination, often multifactorial
- contributing: dietary, renal dz, dehydration, stress, cold
- conservation: asian vultures, gyps, diclofenac toxicity
- signs: depression and weakness, visceral usu ante-mortem dz. Sudden death, swollen and painful joints (shifting weight, unable to fly, decreased activity)
- BW: elevated WBC (heterophils), elevation of uric acid, increased CK and AST.
- Uric acid: decreased with PUPD or liver dz, increased with renal disease (70% destruction), dehydration and post-prandial. Should be <10, 10-20 = re-test after rehydrated or fasted
- dx: UA, arthrocentesis, rads, laparoscopy, frosting on serosa, tophi in joints and SQ.
- URIC ACID WILL DISSOLVE IN FORMALIN, so FIX IN ALCOHOL
- Tx: determine and eliminate primary cause and concurrent diseases. Fluids, correct electrolytes. Analgesics PRN, NSAIDs, corticosteroids? Colchine for acute attacks, allopurinol to reduce serum uric acid. Diet, avoid nephrotoxic, monitor response.
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