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Virology > Viral Diseases of Swine > Flashcards

Viral Diseases of Swine Flashcards

1
Q

How long has pseudorabies virus been in the US?

A
  • 1983 - 18.8% of US breeding herds seropositive
  • 2004 - PRV eradicated from S commercial swine
  • 2022 - PRV still present in US feral swine
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2
Q

How long has Swine Influenza Virus been present in the US?

A
  • 1918 - Human pandemic strain
  • 1998 - New strains with genes from human and avian viruses appeared in US swine
  • 2009 Pandemic H1N1 derived from pig virus
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3
Q

How long has Porcine Reporductive and Respiratory syndrome virus (PRRSV) been in the S?

A
  • 1987 - first recognition of disease
  • 2022 - considered most costly swine disease in US
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4
Q

How long has Porcine epidemic diarrhea virus been present in the US?

A
  • 2013 - emerged in U.S, 7 million pigs died in 1st year
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5
Q

How long has African swine fever virus (ASFV) existed?

A
  • 2007 - Introduced into E. Europe, Caucus and Russia
  • 2018-2020: introduced into China, Belgium, +12 Asian countries
    • estimated loss of >25% of the world’s pig population
  • 2020 - introduced into Germany
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6
Q

What is a Gilt?

A

female pig that has not produced a litter of piglets

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7
Q

What is a sow?

A

female pig that has produced a litter of piglets

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8
Q

What is a Boar?

A

intact male pig

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9
Q

What is a Barrow?

A

castrated male pig

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10
Q

What is Farrowing?

A

Giving birth to a litter of piglets

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11
Q

What is the timeline of swine prodction?

A
  • Breeding and Gestation
    • 3mos, 3wks, 3 days (114days)
  • Farrowing
    • Birth to weaning
    • 3 weak weaning common
  • Nursery
    • weaning to 40-50 lbs (7-9wks)
  • Grower-Finisher
    • Until market 250-300 lbs (6 mos)
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12
Q

How have changes in swine production lead to changes in swine ssceptibility?

A
  • Large farms ⇢ nearly continuous farrowing
    • Continuous supply of naive pigs, which are a sources of viral shedding
  • Specialized swine finishing facilities
    • Shipping pigs after weaning (stress, mixing, etc)
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13
Q

What are viruses that belong to the family Arteriviridae like?

A
  • Single-stranded
  • positive sense
  • RNA
  • enveloped
  • Ability to establish prolonged or persistent infections
  • Ex:
    • Equine arteritis Virus
    • Porcine Reproductive and Respiratory Syndrome virus
    • Simian hemorrhagic fever virus
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14
Q

What are the Genotypes of Porcine Reproductive and Respiratory Syndrome virus (PRRSV)?

A
  • 2 Genotypes:
    • Genotype 1 - European
    • Genotype 2 - North American
  • Both are now present worldwide
    • high genetic diversity within genotype
    • Highest mutation rate for any RNA virus
    • Quasispecies within farm and individual
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15
Q

When did Porcine Reproductive and Respiratory Syndrome virus (PRRSV) first emerge?

A

late 1980s / early 1990s

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16
Q

How is Porcine Reproductive and Respiratory Syndrome virus (PRRSV) Transmitted?

A
  • Routes of Efficient transmission
    • Direct: Horizontal and vertical transmission
      • Primary vector: infected pigs - all body secretions and fluids contain virus
      • PRRSV can cross the placenta in 3rd trimester
    • Indirect: Contact with contaminated fomites +/- aerosol
      • Needles, boots, coveralls, transport vehicles
      • Importance of aerosol transmission controversial
17
Q

What types of pigs are affected by Porcine Reproductive and Respiratory Syndrome virus (PRRSV)?

A
  • Pregnant gilts and sows - reproductive failure
  • Nursery and grow-finish pigs - respiratory
18
Q

What is the primary site of virus replication for Porcine Reproductive and Respiratory Syndrome virus (PRRSV)?

A

Macrophages

19
Q

What are the different phases of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) infection?

A
  • Phase 1:
    • initial virus replication occurs in the macrophages and dendritic cells of the lungs and upper respiratory tract
  • Phase 2:
    • Viremia results within 6-12 hours of infection
    • May last for several weeks
    • Replication in macrophages throughout the body
  • Phase 3:
    • Virus replication localized to lymphoid tissue, including tonsils, and lymph nodes.
    • Virus no longer detectable in blood and lungs
    • No clinical signs of disease
    • Most pigs clear virus by 3-4 months; but replication can be maintained for 250 days (“life-long”)
20
Q

How does Porcine Reproductive and Respiratory Syndrome virus (PRRSV) modulate innate immunity?

A
  • Inhibits IFN-a
  • Modulates TNF-a and IL-1B production
  • Induces regulatory cytokines, such as IL-10
  • Inhibits Toll-like receptors
  • Inhibits NK cells
  • Modulates antigen presentation and T cell activation
20
Q

How does Porcine Reproductive and Respiratory Syndrome virus (PRRSV) modulate adaptive immunity?

A
  • Early production of non-neutralizing antibodies
  • Delayed production of neutralizing antibodies
  • Delayed IFN-y producing cells
21
Q

What is the Pathogenesis of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) ?

A
  1. Infection of Macrophages + Modulation of Immunity
  2. Immunosuppression
  3. Increased susceptibility to primary and secondary pathogens - Polymicrobial Disease
    • PRRSV infections increase severity of disease caused by other pathogens
      • Porcine circovirus type 2
      • Mycoplasma hyopneumoniae
      • Bordetella bonchiseptica
22
Q

What is the seasonality of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) ?

A
  • Incidence rate high during fall and winter
  • Incidence rate low during spring and summer
23
Q

What is the Reproductive syndrome of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) ?

A
  • All parities: pregnant sows and gilts
    • Clinical signs:
      • Increased stillborn piglets, mummified fetuses, premature farrowing, weak-born pigs, embryonic death, late-term abortions
        • Stillbirths and mummies may increase 25-35%
        • Abortions may be >10%
      • Lethargy, reduced appetite and fever of sows/gilts
      • May see cyanosis of ears and skin
      • Agalactia in lactating sows
      • Increase in preweaning mortality (30-50%)
  • Outbreaks typically last 1-4 months
24
Q

What is the Respiratory Disease portion of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)?

A
  • Newborn, nursery >> grow-finish pigs
  • Clinical Signs:
    • Dyspnea
    • Tachypnea, open-mouth breathing, lethargy, depression, increased mortality, reduced appetite and poor growth, diarrhea, nasal discharge, coughing, sneezing, fever, aural cyanosis or “blue ear”
      • Reduced daily weight gain of pigs by 85%
      • Increase in postweaning mortality (10-25%)
    • Increased bacterial infections (systemic, pulmonary)
25
Q

What gross lesions does PRRSV cause?

A
  • Interstitial pneumonia
    • lungs wet and heavy (do NOT fully collapse)Can be difficult to differentiate from normal
  • Enlarged lymph nodes
26
Q

What Microscopic Lesions does PRRSV cause?

A
  • Interstitial pneumonia - Characteristic lesion
    • Severe and necrotizing
    • Macrophages and necrotic cells in alveoli
  • Lymphoid Hyperplasia
    • Polyclonal B-cell activation
  • Typically no lesions in fetuses
27
Q

What are the clinical manifestations of PRRSV in naive herds?

A
  • Epidemic
  • All ages effected
  • Reproductive Failure
  • Acute Respiratory Disease
  • Increased bacterial infections
28
Q

What are the clinical manifestations of PRRSV in a herd where the breeding stock is immune?

A
  • Only affects nursery/grower pigs
  • Respiratory disease
  • Increased bacterial infections
29
Q

How is PRRSV diagnosed?

A
  • Serology:
    • ELISA: IgG Ab (non-neutralizing)
      • Detectable within 7-10 days post infection (dpi)
    • Serum neutralizing Ab
      • Delayed - may not appear until 28 dpi
  • Virus Detection: PCR, virus isolation, IHC
    • sequencing to determine isolate
  • Oral Fluids: Ab and/or virus detection
    • population level sample
30
Q

What is the treatment for PRRSV?

A
  • No effective treatment
  • NSAIDS - reduce pyrexia/inflammation
  • Antibiotics - reduce secondary bacterial infections
31
Q

How is PRRSV prevented?

A
  • Primary means of control
  • Testing replacement gilts and boars
  • Isolation/acclimatization of incoming animals
    • Test on arrival to isolation facility and 45-60 days later prior to introduction into the herd
32
Q

What is the PPRSV Vaccine?

A
  • Killed vaccine ineffective when used alone
  • Modified live virus (MLV) vaccine
    • Commercially available
    • sed over the last 20+ years (first approved in 199)
    • Effective in controlling outbreaks, reducing virus replication and clinical disease, decreasing economic losses (increasing weight gain and decreasing mortality)
33
Q

What are the limitations of the PRRSV vaccine?

A
  • Does not provide sterilizing immunity (does not prevent infection)
  • Viral shedding and transmission still occurs
  • Reduces weight gain in pigs if NOT exposed to wildtype PRRSV
  • Potential for reversion to virulence and persistent infection
  • Unable to differentiate infected from vaccinated (DIVA)
  • Should not vaccinate bores with MLV
34
Q

What were some of the challenges in the PRRSV vaccine development?

A
  • Antigenic heterogeneity makes broad protection difficult
  • Sophisticated immune evasion strategies of the virus
35
Q

What are some strategies for eliminating PRRSV from herds?

A
  • Segregated early weaning
    • Preventing exposure during nursing
  • Nursery depopulation
    • Successful when no virus transmission in sow herd (12-28 months after initial outbreak) but nursery and grow/finish pigs still actively infected
    • Nursery pigs removed (sent to other farms for finishing)
    • Nurseries disinfected and left empty for 7-14 days
  • Endemic infections: whole herd depopulation-repopulation, test and removal, herd closure
36
Q

What Biosecurity measures have been implemented to control PRRSV?

A
  • Strict quarantine and testing programs
  • Obtaining PRRSV-naïve breeding stock and semen
  • Sanitation of transport vehicles
  • Strict protocols of fomite and personnel movement between farms
  • Air filtration (+/- aerosol)
  • Disinfection:
    • PRRSV is labile in environment
    • Inactivated by lipid solvents
    • Heat sensitive
    • Narrow pH stability range (6.0-7.5)
    • Stable when chilled/frozen
37
Q

Is there a possible cure of PRRSV?

A
  • Working on removing Codon 163
    • A PRRSV receptor - that allows viral entry into cells

Virology (37 decks)

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