Swine 6 Flashcards

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1
Q

PRRS genus, and related virus

A

Genus Arteriveridae - related to:
§ Equine arteritis virus (EAV)

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2
Q

Clinical properties of genus arteriveridae; type of infections and disease, where they replicate, genome feature

A

§ Can cause asymptomatic persistent infections
§ Can cause severe fatal disease
§ Replicate in macrophages
§ Exhibit considerable genome plasticity

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3
Q

carrier state of PRRS, and shedding? what related characteristic makes control very difficult?

A

n Persistent - prolonged carrier state
n >100 d, some evidence >200 d
n Some field observations suggest most infected pigs cease shedding the virus in 60 days
n Shedding carriers are probably the most significant source of virus (think quarantine barn!)
n Can be a persistent carrier and have antibodies
> unique characteristic that makes control very difficult.

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4
Q

PRRSV - infectivity? contagiousness? cross-protection between strains?

A

n Highly infectious
> low minimum infectious dose (10 virions)
n Not considered highly contagious
> slow area spread, anecdotal opinions that it spreads in air
n Heterologous strains are not fully cross-
protective

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5
Q

is PRRSV endemic, or epidemic…….or?

A

Endemic – with epidemics of new strains occurring
n Subclinical - western Canada
n Clinical - virulent strain in Ontario

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6
Q

PRRSV virulence? strains?

A

n Considerable variation in virulence among strains
n Distinct clusters which are antigenically & genetically distinct:
n European strains (Lelysted virus)
n N.A. strains (VR2322)
n Highly pathogenic PRRS – high fever disease (China)

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7
Q

PRSSV; genome changes and significance

A

Antigenic drift within a herd
n Positive herds can become infected
with a 2nd strain

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7
Q

PRRSV incidence

A

Pig-producing countries
(not Australia)
n Approximately 80% of herds in Ontario are +ve
n Not all positive herds have clinical signs

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7
Q

PRRSV environmental survivability and susceptibility

A
  • Environmental survival -temperature dependent
    § Frozen (-20oC): months to years
    § Room temp (20oC): 6 days
  • Susceptible to drying, detergents & disinfectants (Lysol)
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8
Q

PRRSV - Transmission methods

A

vertical
horizontal
fomites
aerosol?

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9
Q

vertical transmission of PRRSV

A

n Shed in semen of infected boars
n Transplacental (mid & late pregnancy)
> Sows infected earlier in pregnancy may deliver viremic piglets

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10
Q

horizontal transmission of PRRSV

A

(pig to pig; dam to piglet)
- Within herd: to naïve nursery piglets as passive antibody wanes
> Pig-to-pig contact: especially if pigs fight
> Needles can transfer virus from one litter to another
- Between herds: by infected replacement gilts & boars***

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11
Q

fomite transmission of PRRSV

A

n Mechanical vectors (trucks, incoming supplies, etc)
n Insects: mosquitoes & flies
> carry live virus in GIT for short periods over short distances ~2.3 km

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12
Q

Aerosol transmission of PRRSV

A

n Highly prevalent in most hog dense regions
n Airborne transmission: at least over short distances

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13
Q

PRRSV: Clinical Signs in pregnant females

A

Infection of pregnant females:
- Anorexia, fever (1-5 days post-infection)
- Sow mortality – if virulent strain

1st & 2nd trimester – minimal impact on pregnancy viability

3rd trimester – transplacental infection (~72 days):
- Reproductive failure (i.e. abortion, premature farrowing) & infertility lasting up to 4 months post-infection

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14
Q

PRRSV effects of late gestation infection ( ~72 days)

A

late gestation ~72 days
n Abortions
n Premature farrowings
- <110 d gestation
- Premature farrowing (<110 d) are indicative of PRRS.
n Stillbirths, mummified, autolysed near- term fetuses
n Weak born piglets congenitally infected

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15
Q

abortions in late gestation (~72 days), differentials:

A

differential diagnosis would include PRRSv, Leptospirosis, pseudorabies & brucellosis.

16
Q

PRRSV Clinical Signs - Respiratory

A

Respiratory (systemic) disease:
n Congenitally infected suckling pigs (vertical transmission)
n Nursery & grower pigs (horizontal transmission)
n Dyspnea “thumping” most typical
n Cyanosis of extremities (“blue-ear disease”)
n Minimal coughing in pure PRRS pneumonia
> coughing more common following secondary bacterial invasion
n Immunosuppressive **virus results in mixed infections

17
Q

what is the cause of “Blue ear disease”? where was it seen?

A

One of the prominent signs of PRRS in the UK was peripheral cyanosis, particularly affecting the ears, which results from the PRRS induced vasculitis. Any age of pig may be affected, not commonly seen in NA.

18
Q

origins and result of congenital PRRSV?

A

If infected during late gestation, piglets may deliver at term, but will be congenitally infected or viremic at birth. These are typically weak at birth and succumb to neonatal diarrhea, respiratory disease and/or high case fatality.

19
Q

what tissue does PRRSV first infect? where does it replicate? what cells does it have a predilection for?

A

n Infection of tonsil & URT followed by viremia
- Replication within lymphoid tissues
- Predilection for:
> pulmonary alveolar macrophages (PAMs) and
> pulmonary intravascular macrophages (PIMs)

20
Q

pathogenesis of PRRSV

A

Infection of tonsil & URT followed by viremia
- Replication within lymphoid tissues
- Predilection for:
> pulmonary alveolar macrophages (PAMs) and
> pulmonary intravascular macrophages (PIMs)
()()
> Leads to interstitial pneumonia
-> increased susceptibility to other lung pathogens
> Lymphopenia by 4 days post exposure
- decrease lymphocytes, monocytes, neutrophils
- 2o infections +/- increased diarrhea in nursing pigs
()()
n Prolonged viremia > persistent infection
n Not latent infection like herpesvirus
n Crosses placenta in late gestation (>day72) - Fetal death due to vasculitis of umbilical vessels
n Abortion
- either due to death of fetuses or effects of acute disease and fever in sows
- Vasculitis in neonates (if survive)
> Periorbital edema
> Mild rhinitis, conjunctivitis
> Lymphocytic encephalitis
> Lymphocytic myocarditis

21
Q

fetal death due to PRRSV caused by what pathogenesis?

A

Crosses placenta in late gestation (>day72)
n Fetal death due to vasculitis of umbilical vessels

Abortion
n either due to death of fetuses or effects of acute disease and
fever in sows

22
Q

PRRSV - Pathology (PM lesions); what we observe, when most remarkable?

A

n Most remarkable in young piglets
n Gross lesions only observed in a few organ systems:
n Non-suppurative interstitial pneumonia n Systemic vasculitis
n Lymphadenopathy
n No lesions pathognomonic

23
Q

PRRSV – Principles of Diagnosis

A

1) Pathology – suggestive but not definitive
n Interstitial pneumonia, vasculitis, lymphadenopathy

2) Virus detection (antigen & nucleic acid)
n IHC – lesional tissues
n PCR – secretions, tissues, blood
n VI – rarely performed, time consuming

3) Genomic analysis
n RFLP or sequencing – to determine similarity of strains

4) Antibody detection for:
n IgG, IgM and SN (serum neutralizing)

24
Q

PRRSV - Serology;
**Commonly used serologic tests in industry:

A

n **ELISA (IDEXX, DAKO) – most common, detects IgG
> positive/negative test, semi-quantitative
n **PCR (polymerized chain reaction, Tetracore) – in sera and
tissues

25
Q

PRRSV - Serology;
less commonly used serologic tests

A

IFA (indirect fluorescent antibody) – can detect either IgG or IgM
> Quantitative antibody titration test
> IFA often used to confirm suspicious ELISA results, but it is somewhat subjective

SN (serum neutralization) – detects neutralizing antibody
> Rarely performed on a commercial basis
> SN increases corresponding to viral clearance, but SN not required for protection

26
Q

What samples do we use for PRRSV PCR? when are they good for?

A

blood:
> appears 1-2 dpi
> disappears in 2-4 weeks

tissues: lung, lymphatics:
> appears 1-2 dpi
>disappears 10-14d PI (lung) or 100-150d PI (tonsil)

semen: 3-5 dpi
>Shed sporadically for weeks

27
Q

serology tests used for PRRSV? when are they good for?

A
  • IFA (IgM):
    > appears 5 dpi
    > disappears 14 days PI
  • ELISA (IgG):
    > appears 10-14 dpi
    > disappears 4–6 months PI
  • IFA (IgG):
    > appears 7-10 dpi
    > disappears 6+ months PI
  • SN antibody:
    > appears 28-42+ dpi
    > disappears > > >6+ months PI
28
Q

Antibody-Nucleic acid demonstration curve for PRRSV

A

D0 - infection exposure
>after ~5d IgM levels increase, peak
> IgM decreases to 0 around D14

D14 - increasing antibody (seroconverting) (IgG)
>build until max around D20, stays stable for some time, until D28-42, then declining
>antibodies decline as neutralizing (SN) antibody and cellular response increases

29
Q

PRRSV - Immunity; how, and timeline? primary source of infection?

A
  • Antibodies
    > measurable as soon as 10 – 14 d post
    infection
    > Not detectable at 6 months post infection
  • Passive immunity lasts 30 days
  • But virus may persist for 6 months
    in tonsils
  • Carrier pigs
    > Primary source of infection
30
Q

PRRSV - Treatment of affected animals:

A

n Supportive: anti-inflammatories (acetaminophen)
n Prevent secondary infections (immunosuppressive):
> Strategic parenteral or mass medication as required

31
Q

Steps to control & eliminate PRRSv in populations:

A
  • Herd closure
  • Gilt acclimation
  • Mass exposure
    > Vaccination
    > Serum inoculation
  • Implement McRebel
  • Off-site weaning
  • Prevent re-infection
32
Q

PRRSV Control: Breeding Herd Stabilization
> Long term control after an outbreak:

A

n is best achieved by mass exposure of the breeding herd to live homologous PRRSV
n which ensures the development of sterilizing immunity and the cessation of ongoing vertical transmission from sow to piglet.
n this is referred to as “breeding herd stabilization”.

33
Q

Mass PRRSV exposure by: vaccination
> what vaccines are available and effective? what animals should they be used with and what should we consider about shedding?

A
  • Attenuated live vaccines licensed:
    >Ingelvac PRRS - MLV and PRRS MLV/ATP : BIVM
    > Fostera PRRS MLV: Zoetis
  • Killed vaccines are ineffective in North America
  • In naive animals, the vaccine virus will be shed for a period of time following vaccination
  • Not licensed for use in boars or pregnant sows – may result in congenital infections if used in later gestation
34
Q

Mass PRRSV exposure by: Serum Inoculation
> issues and risks?

A
  • PRRS MLV may not provide 100% cross protection against heterologous challenge
  • Sterilizing immunity can be produced by exposing animals with the homologous strain present on the farm
  • Serum inoculation is a high risk procedure that involves the inoculation of the breeding herd with a live virulent PRRSV

> Many risks: bacterial and viral contamination, excessive viral concentration, sow mortality

35
Q

what pigs is the modified live PRRSV labeled for? what are issues with using this vaccine? is it commonly used for prevention?

A

n Labeled for use in nursery pigs and open sows
n Can multiply in pigs, spread to non-vaccinates, reduce lung
macrophages and increase disease incidence
n Reproductive problems when vaccinate naïve pregnant sows, decreases semen quality
n Not typically done as part of a preventive vaccine program

36
Q

timing for modified live PRRSV vaccination

A

Breeding herd (repro):
*Prior to breeding (gilts)
*During lactation (sows)
Progeny (respiratory disease):
*After passive antibody decay (usually at weaning)

37
Q

PRRSV vaccine pros and cons

A
  • Prevents clinical problems for some wild viruses
  • Reduces clinical problems for most wild types
  • Ineffective against some wild types
  • A good way to ensure uniform immunity in sows (to the vaccine strain)
  • Does not cause clinical problems in non- pregnant sows or in pregnant sows that have been exposed to the virus before
38
Q

options for breeding herd stabilization for PRRSV aside from mass exposure

A
  • Nursery depopulation – empty for 14 days, clean, disinfect and dry twice
  • Herd Depopulation: clean and disinfect and dry all barns, twice. Repopulate with negative stock**
  • Close herd to in-coming breeding stock for 6-12 months.
    > Serological test of sows for uniform immunity (all low positive or all negative) and test newly weaned pigs for viremia
39
Q

What is McREBEL for PRRS? purpose?

A

Management changes to reduce exposure to bacteria to eliminate losses from PRRS

  • Good Management Procedures:
    used to help eliminate pig-to- pig transmission/exposure during lactation and early post- weaning & enhance passive immunity
40
Q

How to maintain a negative PRRSV herd? what must we keep in mind about transmission?

IMPORTANT

A
  • Isolate herd from all other pigs
  • Incoming breeding stock must be negative
    > House gilts in quarantine for 90 days
  • Purchase semen from PRRS-negative stud
    > Ensure packages entering barn are negative
  • Vehicles carry virus on tires in winter (snow)
    > Clean, disinfect, dry trucks after use
  • Bird proof the building (birds/ducks MAY carry PRRS)
  • Mosquitoes and biting flies can transmit the virus