Viral Diseases of Swine Flashcards

1
Q

Swine virology is constantly evolving and rapidly changing with new emerging disease

A
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2
Q

Evolving Fields

A

Pseudorabies virus

1983: 18.8% of U.S. breeding herds seropositive
2004: PRV eradicated from U.S. commercial swine
2022: PRV still present in U.S. feral swine

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3
Q

Evolving Field:

Swine Influenza Virus

A

1918: Human Pandemic Strain
1998: New Strains with genes from human and avian viruses appeared in U.S. swine
2009: Pandemic H1N1 derived from pig virus

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4
Q

Evolving Field:

Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)

A

1987: first recognition of disease
2022: considered most costly swine disease in U.S.

Porcine Epidemic diarrhea virus

2013: Emerged in U.S. 7 million pigs died in 1st year

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5
Q

Evolving Field:

African Swine Fever Virus

A

2007: Introduced into eastern europe, caucus and russia

2018-2020: Introduced into China, Belgium, +12 asian countries

2020: Introduced into Germany

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6
Q

Gilt

A

female that has not produced a litter of piglets

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7
Q

Sow

A

female taht has produced a litter of piglets

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8
Q

Boar

A

intact male

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9
Q

Barrow

A

castrated male

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10
Q

farrow

A

to give birth to a litter of piglets

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11
Q

Swine Production:

  1. Breeding and Gestation
A

3 months, 3 weeks, 3 days (114d)

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12
Q

Swine Production:

  1. Farrowing
A

Birth to weaning

3 week weaning common

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13
Q

Swine production:

  1. nursery
A

weaking to 40-50 lbs

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14
Q

Swine Production:

4 Grower - Finisher

A

until market 250-300lbs

~6 months

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15
Q

Swine Production:

Changes in pig production over time

A

Change over time = changes in disease susceptibility

Large Farms – nearly continuous farrowing

Continuous supply of naive pigs, source of viral shedding

Specialized swine finishing facilities

Shipping pigs after weaning

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16
Q

Betaarterivirus

A

Porcine reproductive and respiratory syndrome virus

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17
Q

Arteriviridae

A
  • Arteri:
    • artery
  • Single-stranded, positive-sense, RNA virus, enveloped
  • Ability to establish prolonged or persistent infections
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18
Q

PRRSV:

Commercial Assay

A

measure anti-N antibodies

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19
Q

PRRSV:

A
  • FIrst emerged in late 1980s-early 1990s
  • Two genotypes
    • Genotype 1:
      • European
    • Genotype 2:
      • North American
  • Both Genotypes now present worldwide
    • High genetic diversity within genotype
    • Highest mutation rate for any RNA viruse
    • Quasispecies within farm and individual
20
Q

PRRS is a population disease

A
  • Most costly disease of swine in US
    • seroprevalence estimated at 71.1% of sites in U.S
    • Costs $664 million / year
      • production of herd decreased by 15%
      • Increased pre-weaning mortality 10-40%
      • Animal health costs increased 4x
21
Q

PRRSV:

Kansas Outbreak

A

2006 Kansas Outbreak

5,500 sow farm

>400 abortions in the first week

Mortality in nursing pigs >50%

Estimate after 1st month: cost >$4millio

22
Q

PRRSV:

Transmission

A
  • Routes of Transmission (EFFICIENT transmisstion)
    • Direct: horizontal and vertical transmission
      • primary vector; Infected pig
      • PRRSV can cross the placenta in 3rd trimester
    • Indirect: contact with contaminated Fomites +/- aerosol
      • needles, boots, coveralls, transport vehicles
      • Importance of aerosol transmission controversial
23
Q

Key Concepts for PRRSV

A
  • Disease occurs in:
    • Pregnant gilts and sows :
      • Reproductive Failure
    • Nursery and Grow-finish pigs:
      • Respiratory
  • Primary site of virus replication:
    • MACROPHAGES
24
Q

PRRSV Infection:

Phase 1

A

Initial virus replication occurs in the macrophages and dendritic cells of the lungs and upper respiratory tract

25
Q

PRRSV Infection:

Phase 2

A

Viremia results within 6-12 hours of infection

Viremia may last for several weeks

Replication in macrophages throughout the body

26
Q

PRRSV Infection:

Phase 3: Persistent Infection

A

Virus replication localized to lymphoid tisses, including Tonsils and Lymph Nodes

Virus is 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”)

27
Q

PRRSV: Pathogenesis

A
28
Q

PRRSV:

Pathogenesis:

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

29
Q

PRRSV:

Pathogenesis:

Adaptive Immunity

A

Early Production of non-neutralizing antibodies

Delayed production of neutralizing antibodies

Delayed IFN-y producing cells

30
Q
A

Pathogenesis, with susceptibility

31
Q

PRRSV:

Pathogenesis:

Effect on other pathogens

A

PRRSV infections increases severity of disease caused by other pathogens

Porcine circovirus Type 2

Mycoplasma hyopneumoniae

Bordetella bronchiseptica

PRRSV is the most common virus isolated in clinical cases of porcine respiratory disease complex

32
Q

PRRSV:

Pathogenesis:

Seasonal

A

incidence rate high during fall and winter

Incidence rate low during spring and summer

33
Q

PRRS:

Disease Syndromes:

1, Reproductive Failure

A

All Parties: pregnant sows and gilts

  • Clinical Sings:
    • increased stillborm piglets, mummified fetuses, premature farrowings, weak-born pigs, embryonic death, Late-term abortions
      • Stillbirths and mummies may increase 25-35%
      • Abortions may be >10%
    • Lethargy, reduced appetite and fever
    • May see cyanosis of ears and skin
    • Agalactia in lactating sows
    • Increase in preweaning mortality
  • Outbreaks typically last 1-4 months
34
Q

PRRS:

Gross Lesions

A
35
Q

PRRS:

Disease:

  1. Respiratory Disease
A
  • Newborn, nursery >>>> Grow-finish pigs
  • Clinical sings:
    • 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 mortalitiy
    • Increased bacterial infections
36
Q

PRRS:

Respiratory disease:

Gross lesions

A

Interstitial pneumonia

Lungs wet, heavy

Can be difficult to differentiate form normal

enlarged lymph nodes

37
Q

PRRS:

Microscopic lesions

A
  • Interstitial pneumonia
    • characterisc lesion
    • severe and necrotizing
    • Macrophages and necrotic cells in alveoli
  • Lymphoid hyperplasia
    • polyclonal B-cell activation
    • Typically no lesion in fetuses
38
Q

PRRS:

Clinical Manifestations:

Epidemic

A

Naive herd or new virus strain

All ages affected

Reproductive failure

Acute respiratory disease

Increased bacterial infections

39
Q

PRRS:

Clinical manifestations:

Endemic - breeding herd immune

A

Only affects nursery / grower pigs

Respiratory disease

Increased bacterial infections

40
Q

PRRSV: Diagnosis

Serology

A
  • ELISA: IgG antibody
    • detectable within 7-10 days post-infection
  • Serum neutralization antibody
    • delayed - may not appear until 28 dpi
41
Q

PRRSV: Diagnosis

Virus Detection

A
  • PCR
  • Virus Isolation
  • IHC
  • Sequencing to determine isolate
42
Q

PRRSV: Diagnosis

Oral Fluids

A
  • Antibody and or virus detection
    • population level sample
43
Q

PRRSV:

Control

A
  • No effective treatment for PRRS
    • NSAIDs:
      • reduce pyrexia / inflammation
    • Antibiotics:
      • reduce secondary bacterial infectins
  • PREVENTING INFECTION:
    • 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
44
Q

PRRS:

Vaccination

A
  • killed vaccines considered ineffective when used alone
  • Modified live virus vaccines
    • commercially available
    • used over the last 20+ years
    • Effective in controlling outbreaks, reducing virus replication and clinical disease, decreasing economic losses
    • Limitations:
      • does not provide sterilizing immunity
      • viral sheding and transmission still occurs
      • reduces weight gain in pigs if NOT exposed to wildtype PRRSV
      • Potential for reversion ot virulence and persistent infection
      • Unable to differentiate infected form vaccinated
      • Should not vaccinate bors with MLV
  • Challenges in PRRS vaccine development:
    • antigenic heterogeneity makes broad protection difficult
    • Sophisticated immune evasion strategies of the virus
45
Q

PRRSV:

Elimination

A
  • Strategies to eliminate PRRSV from herd
    • segregated early weaning
      • preventing exposure during nursing
    • Nursery depopulation
      • successful when no virus transmisstion in sow herd but nursery and grow/dinish pigs still actively infected
      • Nursery pigs removed
      • Nurseries disinfected and left empty for 7-14 days
    • Endemic infections:
      • whole herd depopulation - repopulaiton, test and removal, herd closure
46
Q

PRRSV:

Farm Biosecurity

A
  • Strict quarantine and testing programs
  • Obtaining PRRv-naive 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
    • Stable when chilled/frozen