Swine Influenza Flashcards
What are the characteristics of viruses of the family Orthomyxoviridae?
- Orthomyxo - stright mucus
- Single-stranded
- negative-sense
- RNA virus
- Enveloped
What are the Genera of Orthomyxoviridae?
- 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
What is the genome of a influenza virus like?
- Segmented genome
- 8 segments
- ssRNA: 14 kb
How are influenza viruses classified?
- Based on hemagglutinin and neuraminidase:
- spike-like proteins that project from the surface, important in pathogenesis
How are Influenza viruses named?
- 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
What is hemagglutinin (HA or H)?
- 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
What is Neuraminidase (NA or N)?
- 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)
What happens when 2 different strains infect a cell simultaneously?
- Genetic reassortment can occur
- can generate viruses containing a new HA, new NA, or both
How is Genetic reassortment different from antigenic drift?
- 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
What is Swine influenza virus (SIV)?
- 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
Is SIV zoonotic?
- Yes, but relatively rare
- human to human transmission inefficient
What is the Avian-human species barrier?
- 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
How do pigs affect the Avian-human species barrier?
- Considered intermediate “mixing-vessel” host
- Can be infected with both avian and human influenza viruses
- Potential for genetic shift and Evolution of pandemic viruses
What are the key Concepts for SIV?
- 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
What is the epidemiologic information for SIV?
- 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
How do Ab+ swine herds fair in new SIV outbreaks?
- Ab mitigate severity of disease and spread throughout herd
- Outbreaks occur when immunity wanes
What is the virulence of SIV?
- 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
How is SIV transmitted
By aerosolization and pig-to-pig contact (primarily nasal secretions)
How does SIV infect an animal?
- 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
What does the Clinical Disease of SIV look like?
- 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
What are the clinical signs of SIV?
- Depression
- Pyrexia
- Decreased appetite
- Deep hacking cough
- Sneezing
- weight loss
- huddling
- dyspnea
- tachypnea
- weakness
- conjunctivitis
- mucoid oculonasal discharge
What are the common gross lesions of SIV?
- 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
-
Cranioventral bronchointerstitial pneumonia
- Airways:
- Necrotizing bronchitis/bronchiolitis
- may contain mucopurulent or blood-tinged exudate
- Necrotizing bronchitis/bronchiolitis
- Lymph Nodes:
- variably enlarged and congested
When should SIV be suspected in a herd?
- History of sudden onset of severe respiratory illness affecting most animals, along with typical signs and lesions
How is SIV diagnosed?
- 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
What is the treatment for SIV?
- No effective treatment
- Supportive care:
- Antimicrobials for secondary bacterial infections
- NSAIDs for severely affected pigs
Is there a vaccine for SIV?
- 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
Are there maternal Abs for SIV?
- 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
What is VAERD?
- Vaccine-associated enhanced respiratory disease
- Combinations SIV vaccine and poorly matched challenge viruses may exacerbate disease in pigs
How can SIV be controlled?
- 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