Pseudorabies Flashcards
1
Q
What are the characteristics of Pseudorabies Virus (PRV)?
A
- 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
2
Q
What is the history of Pseudorabies?
A
- 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
3
Q
What animals are susceptible to pseudorabies virus?
A
- Natural host - swine (only reservoir host)
- Dead end hosts - diverse group of vertebrates
4
Q
How does PRV affect dead end hosts?
A
- 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
5
Q
How is PRV transmitted?
A
- Shedding:
- Oronasal and vaginal secretions
- semen, urine, feces
- milk/colostrum
- Transmission:
- Direct contact
- aerosol
- AI
- fomites
- transplacental
- ingestion of infected tissue/milk
6
Q
What is the pathogenesis of PRV?
A
- 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
7
Q
How does the clinical disease of PRV present in nursing piglets?
A
- 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
8
Q
How does the clinical disease of PRV present in weaned piglets?
A
- 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
9
Q
How does the clinical disease of PRV present in adult pigs?
A
- 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
10
Q
What are the Gross lesions associated with PRV
A
- 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
11
Q
What are the histopathologic lesions associated with PRV?
A
- Nonsuppurative meningoencephalitis (characteristic)
- Trigeminal ganglioneuritis, neuronal necrosis
- Necrotic tonsilitis, bronchitis, bronchiolitis, alveolitis
12
Q
What are the NON-porcine Clinical sings of PRV?
A
- Sadden death
- Intense local pruritus
- self mutilation
- CNS signs
- circling
- paralysis
- fever respiratory distress
13
Q
How is PRV diagnosed?
A
- Viral detection
- VI, FA, PCR, IHC
- Brain, spleen, lung, tonsil
- Nasal swabs (acute infections)
-
Serology
- ELISA, SN, latex agglutination
- ONLY SWINE
- detect latent infections
14
Q
How is PRV controlled?
A
- 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
15
Q
What are the Vesicular Disease Viruses?
A
- 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)
16
Q
What is Foot and Mouth Disease Virus?
A
- 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
- A, O, C, Asia 1, SAT 1, 2, 3
17
Q
How is FMDV transmitted?
A
- Direct or indirect contact with infectious secretions, excretions, and tissues
- Mechanical vectors
- Aerosolized virus
18
Q
What are the disease characteristics of FMDV
A
- Fever and vesicles in the oral cavity and around the mouth and feet
- Morbidity ~100% rare fatalities
19
Q
What are the Clinical signs of FMDV
A
- 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
20
Q
What is the pathogenesis of FMDV?
A
- 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
21
Q
How is FMDV diagnosed?
A
- Tissue choice for sampling: vesicular epithelium or fluid
- oropharyngeal fluid or swab if vesicles not present
- Serology:
- ELISA
22
Q
What are the possible differential diagnosis for suspected FMDV?
A
- 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
23
Q
How is FMDV contolled?
A
- Reduce risks of viral introduction
- slaughter infected and susceptible animals during outbreaks
- movement restrictions
- vaccines used in endemic countries
24
Q
What is Senecavirus A (SVA)?
A
- 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
25
Q
What is Vesicular Stomatitis Virus (VSV)?
A
- 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
26
Q
What is Swine vesicular disease virus (SVDV)?
A
- 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
