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Virology > Swine Influenza > Flashcards

Swine Influenza Flashcards

1
Q

What are the characteristics of viruses of the family Orthomyxoviridae?

A
  • Orthomyxo - stright mucus
  • Single-stranded
  • negative-sense
  • RNA virus
  • Enveloped
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2
Q

What are the Genera of Orthomyxoviridae?

A
  • 4 primary genera:
    • Influenza A virus (human, birds, mammals)
    • Influenza B virus (almost exclusively humans)
    • Influenza C virus (humans, pigs, dogs
    • Influenza D virus (cattle, pigs
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3
Q

What is the genome of a influenza virus like?

A
  • Segmented genome
    • 8 segments
    • ssRNA: 14 kb
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4
Q

How are influenza viruses classified?

A
  • Based on hemagglutinin and neuraminidase:
    • spike-like proteins that project from the surface, important in pathogenesis
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5
Q

How are Influenza viruses named?

A
  • Standardized:
    • Type/ animal of origin/ geographic origin/ strain number/ year of isolation/ subtype in parentheses
    • No animal species given in Human viruses
    • Ex:
      • A/swine/Kansas/B4553/2010 (H1N1)
  • Clade system:
    • Clade - group of viruses with common ancestor
    • Based on genomic sequences
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6
Q

What is hemagglutinin (HA or H)?

A
  • Binds to sialic acid receptors on host cells
  • Virus entry into cells
  • 18 subtypes (H1 - H18)
  • High rates of mutation
  • Target of vaccination
  • Dominant Antigen recognized by immune system
    • Antibodies to hemagglutinin will neutralize the virus
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6
Q

What is Neuraminidase (NA or N)?

A
  • Cleaves sialic acid on host cells
  • Virus release from host cells and penetration of mucus
    • virus is released from parent cell and surrounding mucous layer
    • Repenetrates mucous layer and attaches to new respiratory epithelial cell
  • 11 subtypes (N1 - N11)
  • Oseltamivir (Tamiflu): neuraminidase inhibitor (limits viral spread)
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7
Q

What happens when 2 different strains infect a cell simultaneously?

A
  • Genetic reassortment can occur
    • can generate viruses containing a new HA, new NA, or both
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8
Q

How is Genetic reassortment different from antigenic drift?

A
  • Genetic Reassortment (antigenic shift)
    • Allows rapid major changes in the genetic make-up of influenza viruses
    • Exchange of gene segments ⇢ Subtype change
      • Can cause pandemics
  • Antigenic drift:
    • Subtle point mutations & small changes that occur gradually over time
    • Driven by host immune system
    • Affects antigenic sites in HA and NA
    • Ab no longer fully protective
      • Reason for seasonal flu changes
    • Does NOT result in pandemics
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9
Q

What is Swine influenza virus (SIV)?

A
  • Caused by influenza type A virus
  • Classified by 2 proteins::
    • Hemagglutinin (HA)
    • Neuraminidase (NA)
  • Different combinations of H and N proteins create subtypes
  • Little or no cross-protection between subtypes
  • Worldwide distribution
  • One of the most important causes of Acute respiratory disease in pigs
    • 2009 Pandemic strain of H1N1
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10
Q

Is SIV zoonotic?

A
  • Yes, but relatively rare
  • human to human transmission inefficient
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11
Q

What is the Avian-human species barrier?

A
  • For Influenza A viruses
  • Avian influenza virus prefers a2-3 sialic acid receptors
    • in the respiratory and GI cells of birds
  • Human influenza virus prefers a2-6 sialic acid receptors
    • in the respiratory cells of humans
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12
Q

How do pigs affect the Avian-human species barrier?

A
  • Considered intermediate “mixing-vessel” host
    • Can be infected with both avian and human influenza viruses
    • Potential for genetic shift and Evolution of pandemic viruses
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13
Q

What are the key Concepts for SIV?

A
  • Acute, highly contagious, respiratory disease of swine
  • Common and widespread in US swine
    • nearly all herd in Midwest seropositive
  • Effective vaccination becoming difficult due to increased viral diversity
  • Primary subtypes circulating in swine:
    • H1N1, H1N2, H3N2
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14
Q

What is the epidemiologic information for SIV?

A
  • Outbreaks historically common in fall and winter but can occur year-round
  • Sudden onset, Rapid spread
    • Clinical signs 1-3 dpi
    • Shedding 1-2dpi can continues for 5-8dpi
    • Asymptomatic long-term carrier pigs are rare
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15
Q

How do Ab+ swine herds fair in new SIV outbreaks?

A
  • Ab mitigate severity of disease and spread throughout herd
  • Outbreaks occur when immunity wanes
16
Q

What is the virulence of SIV?

A
  • Field isolates vary
    • Infection ranges from subclinical to acute severe disease
    • May depend on co-factors, co-pathogens (secondary bacterial infections are common)
      • Haemophilus parasuis, Actinobacillus pleuropneumoniae, Mycoplasma hyopneumoniae, PRRSV
17
Q

How is SIV transmitted

A

By aerosolization and pig-to-pig contact (primarily nasal secretions)

18
Q

How does SIV infect an animal?

A
  • Gains access by nasopharyngeal route
  • Replicates in the epithelial cells of the nasal mucosa, tonsils, trachea, and lungs
  • Epithelium of the bronchi, bronchioles and alveoli can be severely compromised
  • Influx of neutrophils and other inflammatory cells leads to epithelial cell necrosis of cells lining the bronchi and bronchioles
  • Inflammatory exudate can block smaller airways, leading to atelectasis, emphysema, and bronchointerstitial pneumonia
  • Epithelium usually heals within 5-7 days
19
Q

What does the Clinical Disease of SIV look like?

A
  • Sudden onset, rapid spread within 1-3 days
  • Clinical signs: pyrexia, deep hacking cough, depression, etc
  • Morbidity high: up to 100%
  • Mortality low 1-4%
  • Duration: 3-7 days
  • Economic loss: reduced growth rates and increased time to market weight
  • Potential for abortions in late pregnancy
20
Q

What are the clinical signs of SIV?

A
  • Depression
  • Pyrexia
  • Decreased appetite
  • Deep hacking cough
  • Sneezing
  • weight loss
  • huddling
  • dyspnea
  • tachypnea
  • weakness
  • conjunctivitis
  • mucoid oculonasal discharge
21
Q

What are the common gross lesions of SIV?

A
  • Usually confined to thorax
  • Lung:
    • Cranioventral bronchointerstitial pneumonia
      • lobular distribution of congestion, firmness, atelectasis, emphysema
      • Lesions typically well-demarcated, consolidated and purple/red
      • Lesions tend to be more extensive in apical and cardiac lobes
  • Airways:
    • Necrotizing bronchitis/bronchiolitis
      • may contain mucopurulent or blood-tinged exudate
  • Lymph Nodes:
    • variably enlarged and congested
22
Q

When should SIV be suspected in a herd?

A
  • History of sudden onset of severe respiratory illness affecting most animals, along with typical signs and lesions
23
Q

How is SIV diagnosed?

A
  • Samples should be collected within 24-72 hours of clinical onset
  • Nucleic acid or Ag detection
    • Acute phase: nasal swabs, lung tissue
    • Virus isolation, PCR, sequencing, FA, IHC, ELISA
  • Antibody
    • ELISA
    • Hemagglutination inhibition (HI)
      • paired acute and convalescent titers
      • H1 and H3 subtype antigen
24
Q

What is the treatment for SIV?

A
  • No effective treatment
  • Supportive care:
    • Antimicrobials for secondary bacterial infections
    • NSAIDs for severely affected pigs
25
Q

Is there a vaccine for SIV?

A
  • Commercial killed viruses in US
    • Combinations of H1N1, H1N2, H3N2
    • Vaccination of sow/gilts, boars, and piglets
    • Reduce clinical signs but do not always prevent infection
  • Autogenous killed vaccines - commercial RNA vaccine, commercial intranasal live attenuated influenza vaccine
26
Q

Are there maternal Abs for SIV?

A
  • Decrease severity of illness in piglets but can also impair the development of immunity
    • Colostral Ab may protect piglets for 5-14 weeks
    • Potential interference with vaccine efficacy
    • Vaccines typically given in 2 doses 3 weeks apart
27
Q

What is VAERD?

A
  • Vaccine-associated enhanced respiratory disease
  • Combinations SIV vaccine and poorly matched challenge viruses may exacerbate disease in pigs
28
Q

How can SIV be controlled?

A
  • Virus unlikely to survive in environment >2weeks (unless cold conditions/protected from sun)
    • Readily inactivated by heat/disinfectants
    • All in/all out with cleaning and disinfecting facilities
  • Strict import controls and biosecurity
    • Maintain closed herd to avoid introducing infected pigs
    • Stabilizing breeding herd by acclimatization or vaccination
    • Isolating clinical animals may reduce transmission among herd
  • management practices and reducing stress
    • Overcrowding, air quality, reducing dust
    • People with influenza-like illness should avoid contact with pigs
  • Determine sequence/subtype of circulating SIV

Virology (37 decks)

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