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Veterinary Virology DMP851 > Viral Diseases of Swine – Porcine Coronaviruses, Porcine Rotavirus and Parvovirus > Flashcards

Viral Diseases of Swine – Porcine Coronaviruses, Porcine Rotavirus and Parvovirus Flashcards

1
Q

Coronaviridae

A

Corona - crown or halo

Single-stranded, postive-sense, RNA virus, enveloped

Fourt Genera:

-Alphacoronavirus

  • Betacoronavirus
  • Deltacoronavirus
  • Gammacoronavirus
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2
Q

Porcine Coronoviruses:

Genus Alphacoronavirus

A
  • Porcine epidemic diarrhea virus (PEDV)
  • Transmissible gastroenteritis viurs (TGEV)
    • Recognized in u.s since 1946, soon after worldwide
    • Widespread in U.S. herds, cases now rare
    • Pathogenesis and clinical disease identical to PEDV
      • no cross protection between TGEV and PEDV
  • Porcine Respiratory Coronavirus
    • derived from TGEV, cross-protective
    • Tropism for lungs, infections usually subclinical
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3
Q

Porcine Coronaviruses:

Genus Deltacoronavirus

A

Porcine detlacoronavirus (PDCoV)

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4
Q

PEDV:

Epidemiology

A
  • Was introduced into U.S. in April 2013
    • identified in Europe and Asia previously
    • Within 1 year: 7 million pigs died (10% of the population)
    • Spread rapidly, now reported in 39 states

PEDV is seasonal,

  • higher incidence during the winter,
  • Pigs are the only known hosts
  • Clinical presentation depends on viral isolate, age of pigs, concurrent infections, rate of group exposure
  • Infectious dose of PEDV is extremely small
    • exposure to a small number of virions is capable of infecting pigs
    • Level of PEDV in piglet feces, 10,000 times higher than a sow feces
    • Young Day old piglets
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5
Q

PEDV:

Monitoring

A

Enacted June 5, 2014: SECD (swine enteric coronavirus diseases) federal order – included PEDV and PDCoV

SECD were reportable: required to report all cases of SECD to federal animals health officials, Federal order ended March 6, 2018

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6
Q

PEDV:

Key Concepts

A

Is characterized by severe enteritis, vomiting, watery diarrhea and weight loss

Severity of PEDV infection is age-dependent

Was recently introduced inot U.S. swine spread rapidly, now widely distributed

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7
Q

PEDV:

Transmission

A
  • Primary fecal/oral transmission
  • some fomite transmission is possible
  • contaminated feed
  • environmental exposure
  • +/- aerosol
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8
Q

PEDV:

Infection

A

oral exposure leads to virus replication in mature intestinal enterocytes

Neonatal pigs have long villi with more mature enterocytes permissive to replication

Neonatal pigs also have slower turnover of enterocytes

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9
Q

Villi:

A

Projections into the intestinal lumen

Involved in digestive absorption functions

Mature enterocytes

Cells survive only a few days

nonproliferative

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10
Q

Crypts

A

invagination of the intestinal epithelium around the villi

Primarily involved in secretory functions

Stem cell progenitors of hte villus enterocytes

Continually dividing

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11
Q

TGEV and PEDV :

Target

A

Villus epithelium for replication

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12
Q

PEDV:

Pathogenesis

A
  • Virus replication in SI enterocytes causes cell lysis
    • enterocytes and virus are sloughed and expelled in feces
  • Viral shedding typically occurs for 3-4 weeks
    • subclinical virus carriage in small intestine possible
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13
Q

Clinical disease inversely related to age

A
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14
Q

PEDV:

Clinical Disease

A
  • All ages susceptible to infection
  • Incubation short: 2-4 days
  • High Morbidity
  • Mortality vaires based on age
    • suckling pigs:
      • typically 50-80%
    • Growing/Adult pigs:
      • typically 1-3%
  • Clinical signs:
    • vomiting, watery diarrhea, decreased appetite, weight loss, lethargy/depression, dehydration
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15
Q

Chronic or Endemic TGEV

A
  • Sows immune and antibodies in colostrum/mils protects pigs while nursing
  • Pigs become susceptible after weaning when lactogenic immunity wanes
  • Signs usually mild:
    • diarrhea, dehydration, unthriftiness
  • Low mortality
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16
Q

PEDV / THEV:

Gross lesions

A

Thin, transparent intestinal walls with accumulation of large amounts of yellow fluid in the interstinal lumen

Congestion of mesenteric vessels

Edematous mesenteric lymph nodes

17
Q

PEDV / TGEV:

Microscopic Lesions

A

Acute, diffuse, severe atrophic eneteritis

Atrophy and fusion of villi in jejunum and ileum

18
Q

When to suspect PEDV in a herd

A

Clinical history of diarrhea in more than 50% of pigs on a site over a short period of time

19
Q

PEDV:

Diagnosis

A
  • Viral antigen and nucleic acids
    • feces or intestine
      • best to collect form acutely-affected live pigs
    • PCR, IHC, VI, Sequencing
  • Serology
    • IFA, SN, ELISA
20
Q

PEDV:

Treatment and Prevention

A
  • Treatment is supportive:
    • maintain hydration and provide clean, dry, draft-free environment
  • Commercial Vaccines in U.S.
    • 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
21
Q

Immunity:

A
  • Passive Lactogenic immunity very important
    • 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
22
Q

PEDV:

Introduction Risk Factors

A

Exact mechanisms for introduction and rapid dissemination throught U.S. pig farms unknown

Potential contributions:

Contaminated feed ingredients

Contaminated fomites such as boots, cloting, equipment, trucks, people, and movement of infected pigs

23
Q

PEDV:

Biosecurity

A

PEDV is sensitive to heat and disinfectants, stable inc old

cleaning/disinfection farrowing unit, trailers, trucks, equipment

Limit traffic onto farm and feedmill

Isolation of new animals – ensure introduction of negative animals

Showers/coveralls/boots for entry into faclity

24
Q

PDCoV

A
  • Intoruduced into U.S. in January 2014
  • Disease presentation very similar to PEDV and TGEV
    • atrophic enteritis, diarrhea, vomiting
    • Diagnosis by PCR on feces/instestine
    • Overall lower prevalence than PEDV
25
Q

PRCV

A

Porcine Respiratory Coronavirus

TGEV with mutation in spike protein gene

Replicates in respiratory tract

Aerosol spread

Widespread in U.S

Usually subclinical

Immunity gives gross protection for TGEV

Significant decrease in clinical TGEV

26
Q

Rotaviruses

A

Porcine rotavirus

27
Q

Reoviridae

A
  • Reo = Respiratory enteric orphan viruses
  • Double-stranded, segmented, RNA virus, nonenveloped
  • Rotaviruses are classified by group, subgroup, serotype
    • 9 primary groups:
      • A, B, C, D, E, F, G, H, I
    • Group A historically most common
    • Immunity is not cross-protective
28
Q

Rotavirus

A
  • Typically species specific
  • Uniquitous among swine worldwide
    • common disease:
      • likely all swine herds infected
      • All ages susceptible but significant disease usually only seen in young pigs
      • Sows have varying levels of Anitbody in clostrum and milk which provide varying degrees of passive protection to nursing piglets
29
Q

Rotovirus:

Transmission

A

Primary fecal/oral transmission

Exposure to carriers or virus in the environment

30
Q

Rotovirus

Infection

A

virus infects and destroys mature enterocytes near the tips of the villi throughout the small intesting

Results in villus atrophy, malabsorption, and osmotic diarrhea

31
Q

Porcine Rotavirus:

Clinical Disease

A
  • Infections can be clinical or subclinical
    • C/S:
      • diarrhea usually seen during nursing or immediately after weaning between 3-6 weeks of age
        • White gray to yellow pasty diarrhea, or watery diarrhea lasting 2-5 days
        • Moderate dehydration, rough hair coat, poor growth, decreased appetite, +/- vomiting
        • Variable morbitity
        • Annual mortality rates of 7-20% of nursing piglets and 3-15% weaned
  • Co-pathogens and poor husbandry increase severity
32
Q

Porcine Rotavirus:

Lesions

A

Thin, flaccid and transparent interstinal walls

Villus atrophy and fusion, epithelial hyperplasia in crypts

33
Q

Rotavirus:

Diagnosis

A

Virus detection

PCR, FA, IHC, VI, ELISA, sequencing

sample feces/intestines form acutely affected pigs

Shedding can occur in non-affected pigs

34
Q

Rotavirus:

Control

Lactogenic Immunity

A
  • Important for protecting
    • endemic infections common:
      • varying levels of maternal Antibody provided in milk/colostrum
35
Q

Rotavirus:

Control:

Good Husbandry and Supportive therapy

A

Cand reduce severity of outbreaks

36
Q

Rotavirus:

Control:

Virus is very stable and persists in Environment for Months

A
  • Fairly resistant to temperatur, pH, disinfectants
    • Bleach effective
  • Hish Standards fo sanitation
    • cleaning / disinfection between farrowings
37
Q

Rotavirus:

Control

Commercial Vaccines

A

Both modified live and killed vaccines

Limitaitons due to lack of cross-protection

38
Q

Rotavirus:

Immunity

A

Require antibodies in the intestine

IgA important

IgA in colostrum and milk protective

Mother susceptible = piglets susceptible at birth

Mother immune = piglets susceptible 1-3 days after weaning

Difficult to stimulate acitve immunity while piglets are nursing immune dams

Veterinary Virology DMP851 (12 decks)

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