Porcine Reproductive and Respiratory Syndrome Virus Flashcards

1
Q

How long is the gestation of a pig?

A

115 days

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2
Q

What are the two paths for piglets when they are born?

A

Piglets are either selected to be used as meat or for further breeding

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3
Q

How long does growing and finishing take between weaning and slaughter?

A

20-24 weeks

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4
Q

After weaning how long it is until a sow will commence heat?

A

Around 6 months

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5
Q

Describe the characteristic replication of Arteriviruses

A

Arteriviruses replicate in the perinuclear cytoplasm of their host cells.
New virions are released by exocytosis from the surface of the cell.

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6
Q

Which cells are the primary targets for the virus?

A

Alveolar macrophages

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7
Q

How is PRRSV transmitted?

A
Inhalation
Ingestion
Coitus
Skin damage 
Contaminated needles
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8
Q

Where does replication of PRRSV take place?

A

Replication in mucosal, pulmonary, or regional macrophages

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9
Q

Describe how the clinical signs/disease differ in the following:

  • Sow
  • Neonatal pig
  • Nursey or grower pig
  • Finishing pig
  • Boar
A
  • Sow: abortion of premature farrowing, still born pigs, weak live born pigs
  • Neonatal pig: dyspnoea, CNS signs, high mortality
  • Nursery or grower pig: increased mortality, secondary infections, failure to thrive
  • Finishing pig: fever and less fed consumption
  • Boar: Fever, semen changes
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10
Q

Describe the reproductive damage caused by PRRSV

A
  • Premature farrowings
  • Stillborn or mummified piglets
  • Weak PRRSV-positive piglets
    (50% die soon after birth)
  • Delayed return to service
  • Mixture of clinical signs in piglets from the same farrowing
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11
Q

What other non-reproductive signs may sows and gilts with PRRSV show?

A
  • Anorexia
  • Fever
  • Lethargy
  • Pneumonia
  • Agalactica
    Red/blue discolouration of the ears and vulva
  • Subcutaneous and hind limb oedema
  • Delayed return to oestrus after weaning
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12
Q

In which pigs is PRRSV usually subclinical?

A

Growers and finishers

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13
Q

Describe the subclinical PRRSV infection

A
  • Destruction of macrophages
  • Thickening of the alveolar septa
  • Occasional lesions in blood and lymphatic vessels
  • Minor heart lesions
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14
Q

Describe the respiratory clinical signs of clinical PRRSV

A
Fever
Sneezing
Hyperpnea
Dyspnoea
Coughing
Pneumonia
Lethargy
Periocular oedema
Oculonasal discharge.
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15
Q

Describe PRRSV in the first 6-12 hours of infection

A

Following oronasal exposure, PRRSV replicates in macrophages and dendritic cells in tonsils, upper respiratory tract, and lungs resulting in viremia by 6 to 12 h post-infection

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16
Q

How does PRRSV damage cells?

A
  • Induces cell lysis of pulmonary alveolar macrophages and pulmonary intravascular macrophages which are the primary sites of replication of the virus in the lung.
  • PRRSV appears to induce apoptosis in bystander cells, thus damaging more macrophages than just those infected with the virus.
17
Q

How is the lung grossly affected by PRRSV?

A

Interstitial pneumonia pathology

  • purple/grey discoloration
  • firm consistency
18
Q

Describe the histological changes of interstitial pneumonia

A

The alveolar wall was enlarged by hyperaemia and inflammatory cell infiltration (lymphocyte and macrophage are abundant)

  • Loss of airspaces
  • Inflammatory cells
19
Q

Describe the effects of PRRSV being a primary pathogen

A

Areas and defence mechanisms are affected by primary pathogens of the pig, allowing them and opportunistic pathogens to establish infection, leading to co-infections
PRRSV interacts with other pathogens to cause severe respiratory symptoms in finishing pigs

20
Q

Describe the mechanism by which PRRSV interacts with other pathogens?

A

It is still under investigation but it has been demonstrated experimentally that:

  • Mycoplasma enhances the pathological effects of PRRSV
  • PRRSV enhances the pathological effects of Porcine Influenza virus
  • PRRSV predisposes pigs to infection and disease caused by Streptococcus suis
  • PRRSV can cause a loss of the bactericidal function of pulmonary intravascular macrophages
21
Q

What are the 3 methods of laboratory diagnosis of PRRSV?

A
  • Serology
  • ELISA
  • Immune fluorescence
22
Q

What serological testing used for?

A

Serological testing can be used to determine the status of a herd: infected or free. Paired samples are required to confirm the involvement of PRRSV in the clinical problem seen in the herd at a particular point in time

23
Q

What is oral fluid?

A

Oral fluid is a mixture of saliva and “oral mucosal transudate”
Contains both pathogens and antibodies

24
Q

How should oral fluid samples be handled?

A

Freeze samples promptly to optimize quality.Oral fluid samples for same day submission may be chilled and submitted on wet ice. Maintain the cold chain to preserve sample integrity.

25
Q

Prognostic profiling relies on testing oral fluid samples how often?

A

At 2 week intervals

26
Q

Where are PRRSV vaccine targetting?

A

The surface glycoproteins

27
Q

What are the effects of PRRSV vaccines?

A

These vaccines are effective in reducing clinical signs and the duration of viral shedding, but they are not likely to completely prevent infection. Also, the vaccine efficacy tended to drop significantly upon heterologous challenge.