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Virology > Swine Coronavirus > Flashcards

Swine Coronavirus Flashcards

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
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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
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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)
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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
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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
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6
Q

How is PEDV transmitted?

A
  • Primarily Fecal/Oral transmission
  • Additionally:
    • Contaminated fomites, trucks/trailers, people
    • Contaminated feed
    • Environmental exposure
    • +/- aerosol
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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
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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
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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
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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%
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11
Q

What are the clinical signs of PEDV?

A
  • Vomiting
  • Watery diarrhea
  • decreased appetite
  • weight loss
  • lethargy/depression
  • dehydration
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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
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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
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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
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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
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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
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17
Q

How is PEDV treated?

A
  • Supportive care:
    • maintain hydration
    • Provide clean, dry, draft-free environment
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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
  • 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
Q

What is Porcine Rotavirus?

A
  • 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
Q

How is porcine rotavirus transmitted?

A
  • Primarily fecal/oral
    • exposure to carriers or virus in the environment
27
Q

What is the pathogenesis of Porcine Rotavirus?

A
  • 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
Q

What is the clinical disease of Porcine Rotavirus like?

A
  • 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
Q

What are the lesions associated with Porcine Rotavirus?

A
  • Thin, flaccid and transparent intestinal walls
  • Villus atrophy and fusion, epithelial hyperplasia in crypts
30
Q

How is Rotavirus diagnosed?

A
  • Virus detection
    • PCR, FA, IHC, VI, ELISA, sequencing
    • sample feces/intestines from acutely affected pigs
    • shedding can occur in non-affected pigs
31
Q

How is Porcine Rotavirus Controlled?

A
  • 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
Q

How can Immunity to Porcine Rotavirus be initiated?

A
  • 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
Q

What are characteristics of viruses belonging to the family Parvoviridae?

A
  • Parvo = small
  • Single-stranded
  • DNA virus
  • Nonenveloped
  • Highly resistant to disinfection/temp/pH
    • infectious for months to years
34
Q

What is Porcine Parvovirus (PPV)?

A
  • 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
Q

What are the key concepts of PPV?

A
  • Cause of reproductive failure in naïve dams
  • Much more likely to occur in gilts than in sows
  • disease of first-parity pigs
36
Q

How is PPV transmited?

A
  • 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
Q

What is the susceptibility of pigs to PPV?

A
  • 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
Q

What is the pathogenesis of PPV?

A
  • 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
Q

What are the clinical signs of PPV?

A
  • 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
Q

What lesions are associated with PPV?

A
  • 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
Q

When should PPV be suspected in a herd?

A
  • 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
Q

How is PPV diagnosed?

A
  • 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
Q

How can PPV be controlled?

A
  • 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

Virology (37 decks)

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