Swine Coronavirus Flashcards
(43 cards)
1
Q
What is the virus family Coronaviridae?
A
- Corona = halo / crown
- Single-stranded
- Positive sense
- RNA virus
- enveloped
- Four Genera:
- Alphacoronavirus, Betacoronavirus, Deltacoronavirus, Gammacoronavirus
2
Q
What does a corona virus look like?
A
- ssRNA: 28 kb
- Spike proteins:
- projects from envelope
- binds to host cell receptor
- mediates viral entry
- induces neutralizing antibodies
3
Q
What are the Porcine Coronaviruses?
A
- Genus Alphacoronavirus:
- Porcine epidemic diarrhea virus (PEDV)
-
Transmissible gastronteritis virus (TGEV)
- pathogenesis and clinical disease identical to PEDV
- Porcine respiratory coronavirus (PRCV)
- derived from TGEV
- Genus Deltacoronavirus
- Porcine deltacoronavirus (PDCoV)
4
Q
what is the epidemiologic information of PEDV?
A
- Introduced into US in April 2013
- Within 1 year, 7 million pigs died
- Spread rapidly, now reported in >39 states
-
Seasonal:
- higher incidence during winter
- Pig only known hosts
- Clinical presentation depends on viral isolate, pigs age, concurrent infections, rate of group exposure
-
Infectious dose is extremely small
- level in piglet feces 10,000 x higher than sow feces
5
Q
What are the Key concepts of PEDV?
A
- Characterized by severe enteritis, vomiting, watery diarrhea and weight loss
- Severity of infection is age-dependent
- Recently introduced to US swine, spread rapidly and now widely distributed
6
Q
How is PEDV transmitted?
A
- Primarily Fecal/Oral transmission
- Additionally:
- Contaminated fomites, trucks/trailers, people
- Contaminated feed
- Environmental exposure
- +/- aerosol
7
Q
What is the pathogenesis of PEDV?
A
- Oral exposure leads to virus replication in mature intestinal enterocytes
- neonatal pigs have long villi with more mature enterocytes permissive to replication and a slower turnover of enterocytes
- Virus replication in SI enterocytes causes cell lysis
- cell and virus expelled in feces
- Viral shedding typically occurs for 3-4 wpi
8
Q
What are Villi?
A
- Projections into the intestinal lumen
- Involved in digestive & absorptive function (some secretory activities
- Mature enterocytes
- Cells survive only a few days
- Nonproliferative
9
Q
What are intestinal crypts?
A
- Invaginations of the intestinal epithelium around the villi
- Primarily involved in secretory functions
- Stem cell progenitors of the villus enterocytes
- Continually dividing
10
Q
What is the clinical disease of PEDV?
A
- All ages susceptible to infection
- disease inversely related to age - suckling pigs most severe
- Incubation short: 2-4 days
- High morbidity (up to 100%)
- Mortality varies based on age
- suckling pigs: typically 50-80%
- Growing/adult pigs: typically 1-3%
11
Q
What are the clinical signs of PEDV?
A
- Vomiting
- Watery diarrhea
- decreased appetite
- weight loss
- lethargy/depression
- dehydration
12
Q
What is Chronic/Endemic TGEV?
A
- Sows immune and antibodies in colostrum/milk protect pigs while nursing
- Pigs become susceptible after weaning when lactogenic immunity wanes
- Signs usually mild - diarrhea, dehydration, unthriftiness and runting
- Low mortality
13
Q
What are the Gross Lesions associated with PEDV/TGEV?
A
- Thin, transparent intestinal walls with accumulation of large amounts of yellow fluid in the intestinal lumen
- Congestion of mesenteric vessels
- Edematous mesenteric lymph nodes
14
Q
What are the Microscopic Lesions are associated with PEDV/TGEV?
A
- Acute, diffuse, severe atrophic enteritis
- Atrophy and fusion of villi in jejunum and ileum
- Results in malabsorptive diarrhea and dehydration
15
Q
When should PEDV be suspected in a herd?
A
- Clinical history of diarrhea in more than 50% of pigs on a site over a short period of time
16
Q
How is PEDV diagnosed?
A
- Viral Ag or nucleic acid
- feces or intestine - best to collect from actually-affected live pigs
- PCR, IHC, VI, sequencing
- Serology
- IFA, SN, ELISA
17
Q
How is PEDV treated?
A
- Supportive care:
- maintain hydration
- Provide clean, dry, draft-free environment
18
Q
How can PEDV be preented?
A
- Commercial vaccines in US
- vaccinate sows/gilts pre-farrowing
- killed virus vaccine
- generally considered incomplete protection in naive animals
- vaccinate sows/gilts pre-farrowing
-
Feedback: intentional and controlled oral exposure of sows/gilts to virulent autogenous PEDV
- Establish consistent whole-herd immunity
19
Q
Is there Immunity against PEDV?
A
- Passive lactogenic immunity very important (IgA)
- neutralizes virus in GI tract of piglet, prevents infection
- Even though PEDV is very similar to TGEV, the viruses are genetically and immunologically distinct
- No cross-protection between TGEV and PEDV
20
Q
What are the introduction risk factors of PEDV?
A
- Exact mechanisms for introduction and rapid dissemination throughout US pig farms unknown
- Potential contributors:
- Contaminated feed ingredients
- Contaminated fomites such as boots, clothing, equipment, trucks, people, and movement of infected pigs
21
Q
What are the Biosecurity measure to prevent PEDV outbreaks?
A
- PEDV is sensitive to heat and disinfectants, stable in cold
- Cleaning/disinfecting farrowing unit, trailers, trucks, equipment
- Limit traffic (people/equipment) onto farm and feedmill
- Maintain visitor log, require downtime between farms
- Isolation of new animals - ensure introduction of negative animals
- Showers/coveralls/boots for entry into facility
22
Q
What is PDCoV?
A
- Introduced into US in Jan 2014
- Disease presentation very similar to PED and TGE
- atrophic enteritis, diarrhea, vomiting
- Diagnosis by PCR on feces/intestine
- Overall lower prevalence than PEDV
23
Q
What is PRCV?
A
- Porcine repiratory coronavirus
- TGEV with mutation in spike protein gene
- Replicates in respiratory tract
- Aerosol spread
- Widespread in US
- Usually subclinical
- Immunity gives cross protection for TGEV
- significant decrease in clinical TGE
24
Q
What are the characteristics of viruses in the family Reoviridae?
A
- Reo = Respiratory enteric orphan virus
- Double-stranded
- Segmented
- RNA virus
- Noneveloped
- Classified by group, subgroup, serotype
- 9 primary groups: A, B, C, D, E, F, G ,H, I
- Immunity not cross-protective
25
What is Porcine Rotavirus?
* Typically are species specific
* Ubiquitous among swine worldwide
* Common disease
* All ages susceptible - more severe for younger pigs
* Sows have varying levels of Ab in colostrum and milk
26
How is porcine rotavirus transmitted?
* Primarily fecal/oral
* exposure to carriers or virus in the environment
27
What is the pathogenesis of Porcine Rotavirus?
* Virus infects and destroys mature enterocytes near the tips of the villi in the SI
* Viral protein has toxin-like activity: increases fluid secretion
* Results in villus atrophy, malabsorption and osmotic diarrhea
28
What is the clinical disease of Porcine Rotavirus like?
* Infections can be clinical or subclinical
* Co-pathogens (TGEV, PEDV, E. coli, salmonella) and poor husbandry increase severity
* Clinical signs:
* Diarrhea usually seen during nursing or immediately after weaning between 3-6 weeks of age
* White/gray to yellow pasty diarrhea (nursing) or watery( weaned) lasting 2-5 days
* Moderate dehydration, rough hair coat, poor growth, decreased appetite, +/- vomiting
* Variable morbidity
* Annual mortality of 7-20% (nursing) and 3-15% (weaned)
29
What are the lesions associated with Porcine Rotavirus?
* Thin, flaccid and transparent intestinal walls
* Villus atrophy and fusion, epithelial hyperplasia in crypts
30
How is Rotavirus diagnosed?
* Virus detection
* PCR, FA, IHC, VI, ELISA, sequencing
* sample feces/intestines from acutely affected pigs
* shedding can occur in non-affected pigs
31
How is Porcine Rotavirus Controlled?
* Lactogenic immunity important for protection (IgA)
* Endemic infections common:
* varying levels of maternal Ab provided in milk/colostrum neutralizes virus in gut lumen of piglet
* Good husbandry and supportive therapy can reduce severity of outbreaks
* Virus is very stable and persists in environment for months
* Fairly resistant to temperature, pH, disinfectants (bleach effective)
* High standards for sanitation
* clean/disinfection between farrowings
* Commercial vaccines available (Group A)
* both modified live and killed
* limitations due to lack of cross-protection
32
How can Immunity to Porcine Rotavirus be initiated?
* Requires antibodies in the intestine
* IgA important
* IgA in colostrum and milk is protective
* Mother susceptible = piglets susceptible at birth
* Mother immune = piglets susceptibel 1-3 days after weaning
33
What are characteristics of viruses belonging to the family Parvoviridae?
* Parvo = small
* Single-stranded
* DNA virus
* Nonenveloped
* Highly resistant to disinfection/temp/pH
* infectious for months to years
34
What is Porcine Parvovirus (PPV)?
* First described in 1967 as a cause of reproductive failure
* Endemic in most swine herds worldwide
* usually a subclinical and ubiquitous infection
* losses are well-controlled
* Almost all females naturally infected before or during their first pregnancy
* immunity is lifelong after infection
* All isolates are similar antigenically
* Not a cause of diarrhea
35
What are the key concepts of PPV?
* Cause of reproductive failure in naïve dams
* Much more likely to occur in gilts than in sows
* disease of first-parity pigs
36
How is PPV transmited?
* Virus shed in secretions/excretions for 2weeks after infection
* Infected dam sheds virus in feces, placental fluids, and mummified fetuses
* Naturally infected boars may shed PPV in semen for a few weeks
* Routes:
* Oronasal - Direct or Indirect
* Reproductive
* Transplacental
37
What is the susceptibility of pigs to PPV?
* All ages can be susceptible
* Transplacental infection of embryos and fetuses is the result of dams failing to develop active immunity prior to pregnancy
* Passive immunity in some gilts may persist and interfere with development of active immunity prior to breeding
* Gilts then loose passive immunity near breeding age and can be infected during their first pregnancy
* virus may cross placenta and infect some or all of their embryos or fetuses
38
What is the pathogenesis of PPV?
* Pregnant infected dams develop a viremia during the acute phase of PPV infection
* Virus may then cross some or all of the separate placentas of developing embryos or fetuses
* Time of gestation at infection:
* \<30 days
* death and resorption of embryos
* irregular return to estrus or reduced litter size
* 30-70 days
* Fetal death and mummification
* Not all fetuses are infected at the same time, death at different stages of pregnancy
* Farrow after normal gestation period (abortion rare)
* \>70 days
* Fetuses immunologically competent
* Most mount a immune respones, clear the virus, and are born healthy and seropositive
39
What are the clinical signs of PPV?
* Characterized by large numbers of mummified fetuses
* increase in the number of return to estrus
* small litter size
* failure to farrow
* decreased farrowing rate
* prolonged gestation
* rarely abortion
40
What lesions are associated with PPV?
* Dams - lesions inapparent
* Fetuses/embryos
* **mummification**
* PPV infects rapidly dividing cells and tissues of several organs
* many cell types affected, especially mitotically active capillary endothelium and neurons
41
When should PPV be suspected in a herd?
* Litters with dead fetuses of varying sizes, including mummified fetuses, along with stillborn and healthy pigs born to first-parity gilts
* Problem almost exclusively of seronegative gilts infected during first half of pregnancy
42
How is PPV diagnosed?
* Virus detection in lungs of mummified fetuses
* Preferred specimen - lung tissue form several mummified fetuses \< 16cm long
* Serology
* Compare unmated gilts to gilts exhibiting signs of ingertility
* Positive precolostral Ab titers in piglets
43
How can PPV be controlled?
* Contaminated facilities are the most important source of exposure
* **Vaccination**!
* vaccinate **all susceptible breeding stock 2x** (2weeks apart) several weeks before breeding
* Killed vaccines available and effective
