Canine, Equine, Avian Influenza Flashcards

1
Q

What is the structure of influenza viruses?

A
  • (-)ssRNA
  • enveloped
  • 8 segments - ~14kb
  • Classified based on hemagglutinin (16+2) and neuraminidase (9+2): spike-like proteins that project from the surface; important for cell entry and targets for neutralizing Abs
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2
Q

What are the 4 genera of Influenza viruses?

A
  • A - humans birds mammals
  • B - humans seals
  • C - humans, pigs, dogs
  • D - cattle pigs
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3
Q

What is Hemagglutinin?

A
  • Binds to sialic acid receptors on hos cells
  • Allows virus entry into cells
  • 18 subtypes (H1-H18)
  • high rate of mutation
  • Target of neutralizing Abs (vaccines
  • dominant Ag recognized by the immune system
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4
Q

What is Neuraminidase?

A
  • Cleaves sialic acid on host cells
  • Allows virus release from host cells and penetration of mucus
  • 11 subtypes
  • Oseltamivir (Taiflu): neuraminidase inhibitor
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5
Q

How are influenza viruses named?

A

Type/creature/origin/StrainID/year isolated (H#N#)

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6
Q

How does the Influenza virus evolve?

A
  • Antigenic drift:
    • subtle point mutations & small changes that occur gradually over time
    • driven by RNA polymerase and hose immune system
    • Affects antigenic sits in HA and NA
    • Ab no longer fully protective
    • Reason for seasonal flue changes
    • does NOT usually result in pandemics
  • Genetic Reassortment:
    • Allows rapid major changes in the genetic make-up of influenza viruses (antigenic shift)
    • Exchange of gene segments
    • Results in subtype change
    • Can cause pandemics
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7
Q

What is Avian Influenza (AI)?

A
  • Caused by influenza type A viruses (IAVs)
    • Natural reservoir is aquatic birds
  • Classified by 2 proteins;
    • Hemagglutinin
    • Neuraminidase
    • differnt combos creat different subtypes
  • Classified by pathogenicity based on the ability of a particular strain to produce disease in domestic poultry
    • Low pathogenic avian influenza viruse (LPAIV)
    • Highly pathogenic avian influenza virus (HPAIV; “fowl plague”)
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8
Q

What is the Avian-human species barrier?

A
  • Avian influenza viruses prefer a2-3 sialic acid receptors
    • respiratory and GI tract of birds
  • Human influenza viruses prefers a26 sialic acid receptors
    • upper respiratory
    • a2-3 in lower respiratory
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9
Q

What are Low Pathogenic Avian Influenza viruses

A
  • Worldwide distribution
  • Subclinical, respiratory signs, reduced egg production
  • frequently recovered from clinically normal shorebirds and migrating waterfowl
  • found in backyard flocks, live-poulty markets
  • Most commercial poulty are free
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10
Q

What are highly pathogenic avian influenza viruses?

A
  • Arise from mutations in the cleavage sit fo the H5 and H7 hemagglutinins of LPAI viruses
  • Sever systemic disease, epidemics, high mortality, sudden death
    *
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11
Q

How are AIs transmitted?

A
  • Direct or indirect contact with feces or respiratory secretions
    • Inhalation or ingestion
  • between farms;
    • breaches in biosecurity practices
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12
Q

What is the incubation period for AIs?

A
  • variable
  • Few days to 2 weeks
  • Usually 1-7 days
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13
Q

What are the results of a LPAI infection?

A
  • Subclinical
  • respiratory signs: sneezing, coughing, ocular and nasal discharge, swollen infraorbital sinuses
  • Lesions: sinusitis, congestion and inflammation of the trachea and lungs
  • Layers/breeders: 5-30% decrease in egg production, reduced fertility, ova rupture or involution, mucosal edema and exudate in oviduct lumen
  • Low morbidity and low mortality
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14
Q

What are the results of a HPAI infection?

A
  • severe systemic disease with high mortality
    • morality can approach 100% within days
  • Peracute form: sudden death with no premonitory signs
  • Acute:
    • Cyanosis and edema of the head, comb, wattle
    • Edema and red discoloration of the lower limbs and feet due to subcutaneous ecchymosis
    • Petechia in visceral organs and muscles
    • Blood-tinged oral and nasal discharge
    • Green colored diarrhea
    • CNS signs: torticollis, opisthotonos, incoordination, paralysis, drooping wings
  • Gross lesions: variable - edema, hemorrhage and necrosis in visceral organs, skin and CNS
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15
Q

How is AI diagnosed?

A
  • Virus detection:
    • oropharyngeal/cloacal swabs
    • pooled organs or feces
    • virus isolation, RT-PCR
  • Antibody:
    • HI, AGID, or ELISA
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16
Q

Is there a vaccine for AIs?

A
  • requires the approval of state veterinarian
  • prevents clinical signs and death
  • reduces viral replication and shedding
17
Q

What is Equine Influenza Virus (EIV)?

A
  • Highly contagious
  • Widespread
  • Caused by H3N8 equine influenza A - and H7N7 (extinct?)
  • Clinical disease varies widely
18
Q

What are the clinical signs of EIV?

A
  • high fever 106F
  • serous nasal discharge
  • submandibular lymphadenopathy
  • nonproductive cough
  • depression
  • decreased appetite
  • weakness
19
Q

What is the pathogenesis fo EIV?

A
  • Virus replicates in respiratory epithelial cells:
    • destruction of tracheal and bronchial epithelium and cilia
    • Inflammation, hyperemia, edema, desquamation
  • 3 weeks for respiratory tract epithelium to regenerate
    • risk for secondary bacterial infections:
      • mucopurulent nasal dischange, pneumonia, pleuropneumonia, chronic bronchitis
20
Q

What lesions are seen with EIV?

A
  • early: Rhinitis and tracheitis with epithelial degeneration and loss of ciliated epithelium
  • Late: epithelial hyperplasia and suppurative bronchopneumonia, proliferation of type II pneumocytes
21
Q

How is EIV diagnosed?

A
  • Nasopharyngeal swabs:
    • collect soon after clinical onset
    • virus isolation, RT-PCR or ELISA
    • commercial rapid antigen detection kit
  • Paired serum samples
22
Q

How is EIV treated?

A
  • Non-specific: rest and supportive care
    • NSAIDS fever >104
    • Antibiotics if fever longer than 3-4 days, purulent nasal discharge or signs of pneumonia
  • Minimize complications:
    • restriction of strenuous activity
      • min 3 weeks
    • avoid stress
    • control dust
    • provide superior ventilation
    • Environmental hygiene
23
Q

Is there a EIV vaccine?

A
  • AAEP: Risk-based vaccinations
  • 2 types:
    • Intranasal modified live virus vaccine
    • Intramuscular inactivated, adjuvanted vaccine
  • duration limited - may need boosters every 6 months if high risk
24
Q

What causes Canine influenza?

A
  • Influenza A H3N8 or H3N2
25
Q

How is CIV transmitted?

A
  • Spread via aerosolized respiratory secretions (coughing, barking, sneezing) or contaminated fomites
    • virus infectious for up to 48hrs on surfaces
26
Q

What are the clinical signs of CIV?

A
  • Mild form:
    • cough (dry/moist, 10-21 days) fever, oculonasal discharge, sneezing, lethargy, decreased appetite
  • Severe form:
    • high fever 104-106, tachypnea, dyspnea
    • Radiographs may show evidence of pneumonia
27
Q

How is CIV diagnosed?

A
  • Virus detection:
    • Nasal or pharyngeal swabs
    • lung and trachea if post-mortem
    • RT_PCR, Virus Isolation
  • Ab detection
    • paired serum samples - 4x increase in titer
    • hemagglutination inhibition
28
Q

What is the treatment for CIV?

A
  • most dogs recover uneventfully within 2-3 weeks
  • If sever disease:
    • NSAIDS, fluids, antibiotics, oxygen
29
Q

What is the prognosis for CIV?

A
  • Morbidity 80%
  • Mortality < 10 %
30
Q

Is there CIV vaccinations?

A
  • AAHA risk-based for dogs:
    • H3N8 - inactivated virus
    • H3N2 - inactivated virus
    • bivalent available
    • none approved for use in cats