Pseudorabies

Question 1

What are the characteristics of Pseudorabies Virus (PRV)?

Answer 1

• Herpesviridae
• Herpein = to creep
• dsDNA enveloped virus
  
  • 140kb
• Known for ability to establish lifelong infections, immune evasion and latency
• Sensitive to disinfectants, relatively unstable outside hose

Question 2

What is the history of Pseudorabies?

Answer 2

• 1813 - earlies reports in US - cattle “Mad-itch”
• 1902 - PRV isolated as etiologic agent
• 1960s - PRV oubreaks increased significantly in US
• 1983 - 18.8% of US herd seropositive
• 2004 - US PRV-free
  
  • eradicated in commercial swine, endemic in feral swine
• 2011 - PRV variant emerged in China
  
  • more virulent

Question 3

What animals are susceptible to pseudorabies virus?

Answer 3

• Natural host - swine (only reservoir host)
• Dead end hosts - diverse group of vertebrates

Question 4

How does PRV affect dead end hosts?

Answer 4

• High mortality due to fatal encephalitis, neurologic signs
  
  • death typically within 2-3 days
• Carnivores - infected after consuming infected carcass
• Humans and high order primates - rare and sporadic cases

Question 5

How is PRV transmitted?

Answer 5

• Shedding:
  
  • Oronasal and vaginal secretions
  • semen, urine, feces
  • milk/colostrum
• Transmission:
  
  • Direct contact
  • aerosol
  • AI
  • fomites
  • transplacental
  • ingestion of infected tissue/milk

Question 6

What is the pathogenesis of PRV?

Answer 6

• Primary site of viral replication is nasal, pharyngeal, or tonsillar epithelium
• Virus spreads via lymphatics to regional lymph nodes then becomes systemic
• Virus spreads via nervous tissue to the brain, where replication continues
• incubation period: 2-6 days
• Viral shedding for >2weeks
• Latency after acute infection
  
  • virus harbored in the trigeminal ganglia
• Reactivation and shedding resumes
  
  • Stress, illness, transport, poor husbandry, farrowing, crowding
• Disease severity depends on age immune status, route of infection and virulence of isolate

Question 7

How does the clinical disease of PRV present in nursing piglets?

Answer 7

• Primary neurologic disease
• Mortality as high as 100% in < 2week old pigs
• Clinical Signs:
  
  • Fever, tremors hypersalivation, incoordination, seizures, hind limb paralysis, ataxia, recumbency, nystagmus, paddling, death

Question 8

How does the clinical disease of PRV present in weaned piglets?

Answer 8

• Primary respiratory disease, occasionally CNS signs
• Mortality 5-10%
• Clinical Signs:
  
  • fever, listlessness, decreased appetite, sneezing, nasal discharge, harsh cough, conjunctivitis, dyspnea, loss of condition

Question 9

How does the clinical disease of PRV present in adult pigs?

Answer 9

• Grower/Adult
  
  • Primary respiratory disease
  • usually mild or subclinical
  • mortality 1-2%
• Gilts/Sows (all parities)
  
  • Reproductive failure - 20% on infected farms
  • Resorption, abortion, stillbirths, mummified fetuses, weak piglets

Question 10

What are the Gross lesions associated with PRV

Answer 10

• Serous or fibrinonecrotic rhinitis
• Keratoconjunctivitis
• Pulmonary edema, congestion, consolidation, hemorrhage
• Congested and hemorrhagic lymph nodes
• Necrotic foci in liver, tonsils, spleen, lymph nodes, adrenals
  
  • aborted fetuses

Question 11

What are the histopathologic lesions associated with PRV?

Answer 11

• Nonsuppurative meningoencephalitis (characteristic)
• Trigeminal ganglioneuritis, neuronal necrosis
• Necrotic tonsilitis, bronchitis, bronchiolitis, alveolitis

Question 12

What are the NON-porcine Clinical sings of PRV?

Answer 12

• Sadden death
• Intense local pruritus
• self mutilation
• CNS signs
• circling
• paralysis
• fever respiratory distress

Question 13

How is PRV diagnosed?

Answer 13

• Viral detection
  
  • VI, FA, PCR, IHC
  • Brain, spleen, lung, tonsil
  • Nasal swabs (acute infections)
• Serology
  
  • ELISA, SN, latex agglutination
  • ONLY SWINE
  • detect latent infections

Question 14

How is PRV controlled?

Answer 14

• Reported to state/federal authorities
• PRV inactivated by sunlight, drying, high temps, several disinfectants
• Biosecurity:
  
  • protect domestic pigs from contact with feral or wild suids
• MLV Vaccine
  
  • generally prohibited in PRV-free countries
  • Decreases clinical signs, reduces viral shedding, improves survival
  • Does NOT provide sterile immunity or prevent latent infections
  • DIVA (Differentiating Infected from Vaccinated Animals)
    
    • Gene deletions in vaccine allow Ab differentiation

Question 15

What are the Vesicular Disease Viruses?

Answer 15

• Foot and mouth disease virus (FMDV)
• Seneca Virus A (SVA)
• Vesicular stomatitis virus (VSV)
• Swine vesicular disease virus (SVDV)
• Vesicular exanthema of swine virus (VESV)

Question 16

What is Foot and Mouth Disease Virus?

Answer 16

• Picornaviridae, genus Aphthovirus
• ssRNA+, nonenveloped (environmentally resistant)
• Highly contagious disease of cloven-hooved livestock and wildlife
• Outbreaks can severely disrupt livestock production and require significant resources to control
• 7 major serotypes:
  
  • A, O, C, Asia 1, SAT 1, 2, 3
    
    • O most common
  • Immunity not cross-protective

Question 17

How is FMDV transmitted?

Answer 17

• Direct or indirect contact with infectious secretions, excretions, and tissues
• Mechanical vectors
• Aerosolized virus

Question 18

What are the disease characteristics of FMDV

Answer 18

• Fever and vesicles in the oral cavity and around the mouth and feet
• Morbidity ~100% rare fatalities

Question 19

What are the Clinical signs of FMDV

Answer 19

• lameness and blanching around the coronary band
• high fever
• lethargy
• huddling
• reduced appetite
• vesicles develop on the coronary band, heel of foot including accessory digits, snout, mandible, and tongue

Question 20

What is the pathogenesis of FMDV?

Answer 20

• Primary site of infection is the nasopharyngeal epithelium
• Virus is then distributed throughout the body and replicates in the epithelium of the mouth, muzzle, teats, feet, and areas of damaged skin
• Vesicles develop and rupture within48 hours

Question 21

How is FMDV diagnosed?

Answer 21

• Tissue choice for sampling: vesicular epithelium or fluid
  
  • oropharyngeal fluid or swab if vesicles not present
• Serology:
  
  • ELISA

Question 22

What are the possible differential diagnosis for suspected FMDV?

Answer 22

• SVA, VSV, SVDV, VESV
• Clinical disease is identical
• Laboratory confirmation is essential (FAD investigation required)
• Contact authorities and DO NOT REMOVE any samples from the premise

Question 23

How is FMDV contolled?

Answer 23

• Reduce risks of viral introduction
  
  • slaughter infected and susceptible animals during outbreaks
  • movement restrictions
  • vaccines used in endemic countries

Question 24

What is Senecavirus A (SVA)?

Answer 24

• AKA: Seneca Valley Virus (SVV)
• Picornaviridae, genus Senecavirus (only member)
  
  • ssRNA+ non-enveloped
• discovered in 2002
• Swine thought to be natural host
• SVA infrequently associated with outbreaks of idiopathic vesicular disease in pigs
• July 2015: significant emergence of SVA
• 2016: confirmation that SVA isolates cause vesicular disease in pigs
• Significant concern due to the inability to distinguish lesions for FMDV!
• A widespread emerging Swine Production Disease

Question 25

What is Vesicular Stomatitis Virus (VSV)?

Answer 25

* Rhabdoviridae, genus *Vesiculovirus* * ssRNA- enveloped * Clinical disease in cattle, horses, and pigs * can cause self-limiting influenza-like disease in humans * Morbidity in herd 10-20% * 2 distinct serotypes: New Jersey and Indiana * Disease seen sporadically in US (primarily horses and cattle) * Transmission through direct contact with infected animals or by blood-feeding insects

Question 26

What is Swine vesicular disease virus (SVDV)?

Answer 26

* Picornaviridae, genus *enterovirus* * +ssRNA non-enveloped * Pigs only natural host * Reported in Europe and Asia * economically important due to cost of eradication and embargoes on export of pigs/pork * Transmission by direct or indirect contact or by feeding infected pork products