Viral Diseases of Swine Flashcards
(38 cards)
1
Q
How long has pseudorabies virus been in the US?
A
- 1983 - 18.8% of US breeding herds seropositive
- 2004 - PRV eradicated from S commercial swine
- 2022 - PRV still present in US feral swine
2
Q
How long has Swine Influenza Virus been present in the US?
A
- 1918 - Human pandemic strain
- 1998 - New strains with genes from human and avian viruses appeared in US swine
- 2009 Pandemic H1N1 derived from pig virus
3
Q
How long has Porcine Reporductive and Respiratory syndrome virus (PRRSV) been in the S?
A
- 1987 - first recognition of disease
- 2022 - considered most costly swine disease in US
4
Q
How long has Porcine epidemic diarrhea virus been present in the US?
A
- 2013 - emerged in U.S, 7 million pigs died in 1st year
5
Q
How long has African swine fever virus (ASFV) existed?
A
- 2007 - Introduced into E. Europe, Caucus and Russia
- 2018-2020: introduced into China, Belgium, +12 Asian countries
- estimated loss of >25% of the world’s pig population
- 2020 - introduced into Germany
6
Q
What is a Gilt?
A
female pig that has not produced a litter of piglets
7
Q
What is a sow?
A
female pig that has produced a litter of piglets
8
Q
What is a Boar?
A
intact male pig
9
Q
What is a Barrow?
A
castrated male pig
10
Q
What is Farrowing?
A
Giving birth to a litter of piglets
11
Q
What is the timeline of swine prodction?
A
- Breeding and Gestation
- 3mos, 3wks, 3 days (114days)
- Farrowing
- Birth to weaning
- 3 weak weaning common
- Nursery
- weaning to 40-50 lbs (7-9wks)
- Grower-Finisher
- Until market 250-300 lbs (6 mos)
12
Q
How have changes in swine production lead to changes in swine ssceptibility?
A
- Large farms ⇢ nearly continuous farrowing
- Continuous supply of naive pigs, which are a sources of viral shedding
- Specialized swine finishing facilities
- Shipping pigs after weaning (stress, mixing, etc)
13
Q
What are viruses that belong to the family Arteriviridae like?
A
- Single-stranded
- positive sense
- RNA
- enveloped
- Ability to establish prolonged or persistent infections
- Ex:
- Equine arteritis Virus
- Porcine Reproductive and Respiratory Syndrome virus
- Simian hemorrhagic fever virus
14
Q
What are the Genotypes of Porcine Reproductive and Respiratory Syndrome virus (PRRSV)?
A
- 2 Genotypes:
- Genotype 1 - European
- Genotype 2 - North American
- Both are now present worldwide
- high genetic diversity within genotype
- Highest mutation rate for any RNA virus
- Quasispecies within farm and individual
15
Q
When did Porcine Reproductive and Respiratory Syndrome virus (PRRSV) first emerge?
A
late 1980s / early 1990s
16
Q
How is Porcine Reproductive and Respiratory Syndrome virus (PRRSV) Transmitted?
A
- Routes of Efficient transmission
- Direct: Horizontal and vertical transmission
- Primary vector: infected pigs - all body secretions and fluids contain virus
- PRRSV can cross the placenta in 3rd trimester
-
Indirect: Contact with contaminated fomites +/- aerosol
- Needles, boots, coveralls, transport vehicles
- Importance of aerosol transmission controversial
- Direct: Horizontal and vertical transmission
17
Q
What types of pigs are affected by Porcine Reproductive and Respiratory Syndrome virus (PRRSV)?
A
- Pregnant gilts and sows - reproductive failure
- Nursery and grow-finish pigs - respiratory
18
Q
What is the primary site of virus replication for Porcine Reproductive and Respiratory Syndrome virus (PRRSV)?
A
Macrophages
19
Q
What are the different phases of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) infection?
A
- Phase 1:
- initial virus replication occurs in the macrophages and dendritic cells of the lungs and upper respiratory tract
- Phase 2:
- Viremia results within 6-12 hours of infection
- May last for several weeks
- Replication in macrophages throughout the body
- Phase 3:
- Virus replication localized to lymphoid tissue, including tonsils, and lymph nodes.
- Virus 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”)
20
Q
How does Porcine Reproductive and Respiratory Syndrome virus (PRRSV) modulate 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
20
Q
How does Porcine Reproductive and Respiratory Syndrome virus (PRRSV) modulate adaptive immunity?
A
- Early production of non-neutralizing antibodies
- Delayed production of neutralizing antibodies
- Delayed IFN-y producing cells
21
Q
What is the Pathogenesis of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) ?
A
- Infection of Macrophages + Modulation of Immunity
- Immunosuppression
- Increased susceptibility to primary and secondary pathogens - Polymicrobial Disease
- PRRSV infections increase severity of disease caused by other pathogens
- Porcine circovirus type 2
- Mycoplasma hyopneumoniae
- Bordetella bonchiseptica
- PRRSV infections increase severity of disease caused by other pathogens
22
Q
What is the seasonality of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) ?
A
- Incidence rate high during fall and winter
- Incidence rate low during spring and summer
23
Q
What is the Reproductive syndrome of Porcine Reproductive and Respiratory Syndrome virus (PRRSV) ?
A
- All parities: pregnant sows and gilts
- Clinical signs:
- Increased stillborn piglets, mummified fetuses, premature farrowing, weak-born pigs, embryonic death, late-term abortions
- Stillbirths and mummies may increase 25-35%
- Abortions may be >10%
- Lethargy, reduced appetite and fever of sows/gilts
- May see cyanosis of ears and skin
- Agalactia in lactating sows
- Increase in preweaning mortality (30-50%)
- Increased stillborn piglets, mummified fetuses, premature farrowing, weak-born pigs, embryonic death, late-term abortions
- Clinical signs:
- Outbreaks typically last 1-4 months
24
What is the Respiratory Disease portion of Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)?
* Newborn, nursery \>\> grow-finish pigs
* Clinical Signs:
* **_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 mortality (10-25%)**
* Increased bacterial infections (systemic, pulmonary)
25
What gross lesions does PRRSV cause?
* Interstitial pneumonia
* lungs wet and heavy (do NOT fully collapse)Can be difficult to differentiate from normal
* Enlarged lymph nodes
26
What Microscopic Lesions does PRRSV cause?
* Interstitial pneumonia - **Characteristic lesion**
* Severe and necrotizing
* Macrophages and necrotic cells in alveoli
* Lymphoid Hyperplasia
* Polyclonal B-cell activation
* Typically no lesions in fetuses
27
What are the clinical manifestations of PRRSV in naive herds?
* Epidemic
* All ages effected
* Reproductive Failure
* Acute Respiratory Disease
* Increased bacterial infections
28
What are the clinical manifestations of PRRSV in a herd where the breeding stock is immune?
* Only affects nursery/grower pigs
* Respiratory disease
* Increased bacterial infections
29
How is PRRSV diagnosed?
* Serology:
* **ELISA: IgG Ab (non-neutralizing)**
* Detectable within 7-10 days post infection (dpi)
* Serum neutralizing Ab
* Delayed - may not appear until 28 dpi
* Virus Detection: **PCR**, virus isolation, IHC
* sequencing to determine isolate
* **Oral Fluids:** Ab and/or virus detection
* population level sample
30
What is the treatment for PRRSV?
* No effective treatment
* NSAIDS - reduce pyrexia/inflammation
* Antibiotics - reduce secondary bacterial infections
31
How is PRRSV prevented?
* 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
32
What is the PPRSV Vaccine?
* Killed vaccine ineffective when used alone
* **Modified live virus (MLV) vaccine**
* Commercially available
* sed over the last 20+ years (first approved in 199)
* Effective in controlling outbreaks, reducing virus replication and clinical disease, decreasing economic losses (increasing weight gain and decreasing mortality)
33
What are the limitations of the PRRSV vaccine?
* Does not provide sterilizing immunity (does not prevent infection)
* Viral shedding and transmission still occurs
* Reduces weight gain in pigs if NOT exposed to wildtype PRRSV
* Potential for reversion to virulence and persistent infection
* Unable to differentiate infected from vaccinated (DIVA)
* Should not vaccinate bores with MLV
34
What were some of the challenges in the PRRSV vaccine development?
* Antigenic heterogeneity makes broad protection difficult
* Sophisticated immune evasion strategies of the virus
35
What are some strategies for eliminating PRRSV from herds?
* Segregated early weaning
* Preventing exposure during nursing
* Nursery depopulation
* Successful when no virus transmission in sow herd (12-28 months after initial outbreak) but nursery and grow/finish pigs still actively infected
* Nursery pigs removed (sent to other farms for finishing)
* Nurseries disinfected and left empty for 7-14 days
* Endemic infections: whole herd depopulation-repopulation, test and removal, herd closure
36
What Biosecurity measures have been implemented to control PRRSV?
* Strict quarantine and testing programs
* Obtaining PRRSV-naïve 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 (6.0-7.5)
* Stable when chilled/frozen
37
Is there a possible cure of PRRSV?
* Working on removing Codon 163
* A PRRSV receptor - that allows viral entry into cells
