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VETM 422 > Porcine Viral Diseases > Flashcards

Porcine Viral Diseases Flashcards

1
Q

Acute Scour of large number of pig litters with acute D+ and high mortality suggest what viruses ? On most mortem no gross lesions just dehydrated carcass w watery intestinal contents.

A

transmissible gastroenteritis (TGE), porcine epidemic diarrhea (PED) and swine delta corona virus associated diarrhea (SDCV)

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2
Q

What does PEDV stand for?

A

porcine epidemic diarrhea Virus

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3
Q

What does TGE stand for?

A

transmissible gastroenteritis

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4
Q

What does SDCV stand for?

A

swine delta corona virus (SDCV)

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5
Q

What is the taxonomic family classification of of PEDV, SDCV and TGE?

A

Family- Coronavirus

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6
Q

What structure of virus are PED, SDCV and TGE?

A

Enveloped, positive sense RNA viruses

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7
Q

What are the routes of infection for PEDV, SDCV and TGE?

A

Mainly fecal oral, with airborne transmission via fecal-nasal route being possible

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8
Q

For PEDV, SDCV and TGE infected pigs shed enormous amounts of virus on what days?

A

7-9 days

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9
Q

Clinical manifestation of PEDV, SDCV and TGE ?

A

D+ and V+ leading to dehydration and possible metabolic acidosis

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10
Q

What is morbidity of PEDV?

A

up to 100%

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11
Q

What is the mortality of PEDV in suckling piglets, piglets over 10 days, and in adult and fattening pigs, respectively?

A

-Suckling piglets: up to 100%
-Piglets older than 10 days: less than 10%
-Adult and fattening pigs: less than 5%

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12
Q

What is the incubation period of PEDV?

A

3-4 days (short)

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13
Q

Histology of PEDV, SDCV and TGE?

A

Corna viruses replicate in the tip of the villi, therefore impact the mature enterocytes. Will have a villus to crypt ration to 3:1 (normal is 7:1).

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14
Q

Gross lesions of PEDV, SDCV and TGE ?

A

liquid intestinal contents with thin walled intestines

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15
Q

Are PEDV, SDCV and TGE reportable in Alberta?

A

Yes

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16
Q

PEDV has been reported where in Canada?

A

Ontario

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17
Q

TGE has occurrence where?

A

Global occurrence

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18
Q

SDCV has been reported where in Canada?

A

Eastern Canada

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19
Q

Mortality rates in piglets are higher with PEDV or SDCV?

A

PEDV
SDCV mortality varies greatly

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20
Q

Acute outbreaks of SDCV occurs in piglets when?

A

3-5 weeks of age

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21
Q

Clinical manifestation of TGE

A

Similar to PEDV and SDCV. V+, dehydration, weight loss,

yellow D+

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22
Q

Piglets with TGE have what mortality

A

Death within a few days

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23
Q

Morbidity of TGE in older pigs?

A

Disease for up to 3 weeks, or no clinical signs

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24
Q

Clinical signs of TGE in sows

A

Anorexia, fever, v+, d+ and agalactia

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25
Q

If see vomitin gin pigs what should another differential besides PEDV, SDCV and TGE be?

A

Porcine hemagglutinating encephalomyelitis virus

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26
Q

What samples can be used for laboratory testing of PEDV, SDCV and TGE?

A

fresh feces, oral fluids, small intestine, serum for antibodies

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27
Q

What laboratory tests can be used to identify the viral agents?of porcine corona viruses

A

-RT-PCR (b/c RNA virus)
-Elisa
-Immunochemistry
-virus isolation

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28
Q

Which is better RT-PCR or immunohistochemistry?

A

PCR tells you the virus is there but you don’t know if it’s active or not. Bit is very sensitive.

Immunohistochemistry stains viral antibodies so you know the virus is active and replicating . But not as sensitive as PCR

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29
Q

What serological tests can be used to check for PEDV, SDCV and TGE?

A

-ELISA
-Immunofluorescence
-Serum neutralization

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30
Q

What are the three prevention methods for PEDV, SDCV and TGE?

A

-Natural immunity
-Biosecurity and ‘all in all out” practices
-Vaccination

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31
Q

Describe how natural immunity helps prevent PEDV?

A

Maternal antibodies in the colostrum from PEDV immune sows help protect neonates against oral infection from 4 to 13 days (the highest mortality rate time)

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32
Q

Are vaccines for PED available in Canada?

A

No, only in South Korea, Japan and china

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33
Q

Another Virus PEDV, SDCV and TGE can be confused with based on histology manifestations?

A

Swine rotavirus, it also causes villus atrophy (virus replicates in mature enterocytes)

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34
Q

When does Rotavirus infect pigs?

A

As suckling pigs and weaners

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35
Q

How do you tell the difference between PEDV, SDCV, TGE and swine rota virus since clinical manifestations are the same?

A

RT-PCR and histology

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36
Q

What does PPV stand for?

A

Porcine Parvovirus

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37
Q

What family does PPV belong to?

A

Parvoviridae

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38
Q

What type of virus is PPV?

A

Naked, + ssDNA virus

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39
Q

PPV needs what type of cells?

A

Replicating cells (ie. fetal cells)

GI tract also fast replication but does not have the correct receptors in sows

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40
Q

What was the causative agent for of SMEDI syndrome (stillbirths, mummification, embryonic death, and infertility) in the 1960s?

A

PPV

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41
Q

How is transmission of PPV achieved?

A

Affected sows dont show clinical signs. During acute infection they secrete virus in their faces and other fluids.

But sow to fetus transmission ONLY in seronegative animals

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42
Q

how does the Sow become infected with PPV?

A

Fecal oral route

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43
Q

What days in gestation are fetuses susceptible to PPV?

A

6 -70

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44
Q

If sow is infected between day 6 and 35 what are the possible outcomes for fetus?

A

Embryonic death and reabsorption

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45
Q

If sow is infected between day 35 and 70 what are the possible outcomes for fetus?

A

Fetal death and mummification (ossification)

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46
Q

If sow is infected after 70 what are the possible outcomes for fetus?

A

Immunologic competency- survival and born with seropositivity

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47
Q

After initial infection of the sow vertical transmission to the fetus takes how long?

A

12-18 days

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48
Q

Sows have what kind of placenta? What are the implications of this?

A

Epithelia-chorial
Means the placenta is tightly closed for anything, and the virus cannot replicate in placental cells

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49
Q

So how is vertical transmission achieved for PPV?

A

Not known

Possibly transported by immune cells (macrophages?), lymph or blood (not likely), continuous replication (not likely)

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50
Q

Clinical manifestations of PPV are? And how do these clinical manifestations differ from other species?

A

In swine causes only repro manifestations (stillbirth, abortions, mummification, infertility) some of these can happen in cows and cats also

But other species have GI signs and pigs DO NOT

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51
Q

Does position of fetus impact lesions on still borns with PPV?

A

Yes fetuses closer to the cervical end are effected earlier compared to other’s in the litter

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52
Q

When should PPV infection be strongly considered?

A

When females return to oestrus with no other apparent reasons, when increase numbers of mummified fetuses (especially when first or second litter)

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53
Q

What material should be submitted to the lab for PPV testing?

A

mummified fetuses/fetal remains

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54
Q

How is PPV tested for in fetal tissue?

A

detection of viral antigen in fetal tissue via immunoflorence

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55
Q

What are prenvtion measures for PPV?

A

Killed vaccines

56
Q

When should piglets be vaccinated for PPV? and why?

A

22 weeks with a booster at 28 weeks.

Before this piglet will still have passive immunity (maternal antibodies) even if seronegative. so vx would not be effective

57
Q

What family is pseudorabies part of?

A

Herpesviridae

58
Q

Has psedorabies been reported in Canada?

A

No, and eradicated in USA since 2004

59
Q

Pseudorabies can also infect what other species?

A

cattle, sheep, goats, dogs, cats, mink, foxes, raccoons and rats

60
Q

What type of virus is psuedorabies? Enveloped, naked?

DNA, RNA?

A

enveloped dsDNA virus

61
Q

How is pseudorabies transmitted?

A

Direct contact, sexual contact, inanimate objects, inhalation of droplets, inhalation of aerosols

62
Q

What is the natural host of pseudo rabies?

A

Swine

63
Q

What is the pathogenesis of pseudorabies?

A
  1. Primary replication in respiratory tract
  2. entry into PNS neuron’s and establishment of latency in trigeminal ganglion, retrograde transfer to brainstem
  3. Replication in LNs and viremia. found in blood (monocytes ) and lymph (macrophages)
  4. monocytes and macrophages go to placenta and cause Secondary replication
64
Q

Clinical signs of psedurabies in pigs depend on what?

A

Age

65
Q

Clinical manifestation of pseudo rabies in neonates and suckling pigs?

A

nuero signs: posterior paralisis, ms twitching uncordination.

And fever, V+, decreased appetite

66
Q

What is the mortality of pseudo rabies in neonate and suckling pigs?

A

100%

67
Q

Clinical manifestation of pseudo rabies in weaner pigs?

A

Respiratory signs (coughing, laboured breathing, etc)

68
Q

What is the mortality of pseudo rabies in weaner pigs?

A

5-10%

69
Q

Clinical manifestation of pseudo rabies in grower and finisher pigs?

A

Respiratory disease

70
Q

What is the mortality of pseudo rabies in grower and finisher pigs?

A

1-2%

71
Q

Clinical manifestation of pseudo rabies in adult pigs?

A

mild or unapperant signs

Gilts or sows may have reproductive signs

72
Q

Gross lesions of pseudo rabies

A

-lung edema and hemorrhages
- stomach- hemorrhages
- hyperemia/necrosis of tonsils
- leptomeningeal hyperemia

73
Q

What is the pathogenesis of pseudorabies in other species?

A

1) primary replication in respiratory system
2)Entry into PNS and productive replication on trigeminal ganglion

NOT GOING TO BLOOD OR LYMPH

74
Q

What sign do non natural hosts get with pseudo rabies?

A

Neuropathic itch
AKA Mad itch

75
Q

What causes mad itch?

A

Pseudorabies replication in PNS neurons cause transmission of neuroinflammatory itch signals to the brain and the central inhibition of itch pathways are nonfunctional

76
Q

Dogs can also get pseudorabies how?

A

Eating wild boar meat

77
Q

Gross lesions of pseudorabies in nonnatural hosts?

A

hyperaemia in meninges and miningeal vessels

78
Q

Diagnosis of psedo rabies?

A

gross lesions along with herd hx, clinical signs and diagnostic serology

isolation of virus via nasal swabs 8-25days post infection

Surviving swine have detectable antibodies for life

Immunohistochemistry (shows when active)

79
Q

In a herpes virus if high antibody load are detected what’s does that mean? What about low?

A

High antibodies means currently not infectious (in latent phase)

If low then shedding so in active phase

80
Q

How is pseudo rabies prevented?

A

BIOSECURITY, strict import regulations

81
Q

Is pseudo rabies a reportable disease?

A

yes

82
Q

How has pseudo rabies been eradicated?

A

Serological survaleince, culling of those who react, BIOSECURITY and deletion mutant/DIVA Vx

83
Q

What is a deletion mutant /DIVA Vx and how has it made serological surveillance possible?

A

Allows for discrimination between antibody produced in response to vx and in response to natural exposure (gE protein is delated in vaccine antibody). ELISA allows for determination of which antibody the pig has

84
Q

What family does swine influenza belong to?

A

Orthomyxoviridae

85
Q

What type of virus is swine influenza?

A

enveloped -ssRNA virus
SEGMENTED genome

86
Q

There are many Types of swine influenza, what type are we most concerned with? How is it subtyped?

A

Type A (has potential for cross transmission)

Subtyped based on HA(18) and NA(11) proteins

87
Q

HA binds to what on host cells?

A

Sialic acid

88
Q

What allows for swine to be the perfect mixing pot for avian and human influenza strains?

A

Avian strains have receptors with high affinity for silica acid residues in the gut, while human strains have receptors with high affinity for resp tract. Both of these receptor types are present in pigs leads to antigenic shift and reassortment (b/c segmented genome!)

Also true for quails

89
Q

Reassortment requires what?

A
  1. Viral genome must be segmented
  2. the viruses must be in the same cell
90
Q

How did the 2009 H1N1 virus happen?

A

Triple reassortment

Swine+human+ avian flu virus= North American swine flu virus+ Euro-Asia Swine flu virus = H1N1

91
Q

Clinical signs of Swine influenza?

A

Coughing, nasal discharge, fever, decreased appetite

Abbortion fever in pregnant sow

92
Q

What is the morbidity and mortality of swine influenza?

A

Morbidity: 100%
Mortality: low

93
Q

How is SIV transmitted?

A

Nasal discharge and aerosols

94
Q

Gross lessions of SIV?

A

Lung lesions that last upto 14 days

95
Q

What subtype usually induces a longer impact, H1N1, H1N2 or H3N2?

A

H1N1

96
Q

How is SIV detected?

A

Nasal/tonsil swabs then RT-PCR followed by sequncing

Immunohistochemistry

97
Q

What serology test can be used to detect SIV?

A

Heamagglutination inhibition test, ELISA

98
Q

How can SIV be prevented?

A

Combination vx of all 3 subtypes along with a bacterium

99
Q

What does PCV2 stand for?

A

Porcine circovirus

Type 2 (other types not clinically important)

100
Q

What family is PCV2?

A

Circoviridae (encodes only 2 proteins)

101
Q

What type of virus is PCV2?

A

naked ssDNA virus

102
Q

PCV2 can cause 4 syndromes, what are they?

A

-Subclinical infection
-PCV-2 systemic disease/Post weaning multisystemic wasting syndrome (PWMS)
-PCV2 Reproductive disease
-porcine dermatitis and nephrpathy syndrome (PDNS)

103
Q

What factors determine what syndrome and how severe of PCV2 pigs get?

A

-Coinfection
-Immune modulation
-Host susceptibility
-differences in PCV2 isolates

104
Q

PCV2 infects what organ?

A

LNs

105
Q

Diagnostic criteria for subclinical PCV2?

A

1) Lack of clinical signs (possible decreased average gain)
2) no or minimal histopathological lesions
3) low amount of PCV-2 in few Lymph tissued

106
Q

Clinical manifestations of PCV-2 systemic disease/ Post-weaning multi-systemic wasting syndrome?

A

Wasting, weight loss, pale skin, poor doing, possible Resp or GI signs

107
Q

Diagnostic criteria for PCV-2 systemic disease/ Post-weaning multi-systemic wasting syndrome?

A

moderate to severe lymphocyte depletion with granulomatous inflammation

Moderate to high amount of PCV-2 inclusion bodies in lymphoid tissue (evident by immunohistochemistry). scored 1-3

108
Q

Where is PCV-2 found?

A

Globally

109
Q

What type of infection is PCV-2?

A

Chronic

110
Q

If PCV-2 is causing GI signs where would inclusion bodies be?

A

Crypts

111
Q

Clinical manifestations of PCV-2 reproductive disease?

A

Abortions, mummifications or regular return to estrus/ infertility

112
Q

What is the diagnostic criteria for PCV-2 reproductive disease?

A

-Fibrous to necrotizing myocarditis in fetuses, with evidence of PCV-2 in heart (confirmed by immunohistochemistry)
-PCR positivity around time of return to estrus

113
Q

Clinical manifestations of porcine dermatitis and nephropathy syndrome?

A

hemorrhagic and necrotizing skin lesions mainly on hind limbs and perineal area and/or pale kidneys

114
Q

Evidence of porcine dermatitis and nephropathy syndrome is histology?

A

vasculitis and/or glomerulonephritis

115
Q

What are the target cells of PCV-2 in fetal life to postnatal life?

A

Fetal: cardiomyocytes, hepatocytes, macrophages
Postnatal: Macrophages

116
Q

How is PCV-2 diagnosed?

A

-Clinical hx
-post mordem findings
-immunohistochemistry of virus in lymphatic tissues
-PCR swab or serum (just provides info on if infected or not, infection does not necessarily lead to signs)
-qPCR

117
Q

PCV-2 vx are based on PCV-2a isolates but do they protect against other isolates?

A

Yes, through cross-protection. All vaccines demonstrate a cellular and humoral immune response

118
Q

Explain how PCV-2 vx works?

A

They do not prevent infection but decrease the diseases associated with infection. If get vaccinated will be infected.

119
Q

What does PRRSV stand for ?

A

Porcine Respiratory and reproductive syndrome virus

120
Q

What family does PRRSV belong to?

A

Arteriviridae

121
Q

What type of virus is PRRSV?

A

Enveloped + RNA virus, Segmented

Bc RNA and segmented there are numerous strains (European and American strain common)

122
Q

Where is PRRSV found?

A

Globally

123
Q

What is the pathogenesis of PRRSV?

A

Viruses targets avelor and tissue macrophages, in acute disease the virus targets lung and lymphoid tissue and many other sites. Chronic disease virus found in peripheral LN and tonsils

124
Q

What are the clinical signs of PRRSV?

A

Reproductive problems typically in late gestation. Respiratory disease, typically in grower/feeder pigs. blue ears. Fever

125
Q

Does PRRSV cause mortality in adult pigs?

A

Typically no

126
Q

Is persistent infection common in PRRSV?

A

Yes, subclincally

127
Q

Describe the immune response to PRRSV?

A

At acute infection there is a weak immune response; do to decoy antibodies

There is then reactivation of replication which either leads to a persistent infection or a strong immune response that clears the virus

128
Q

In PRRSV when do neutralizing antibodies develop?

A

Peaks at around 2.5 months, has a very DELAYED immune response.

Total antibodies will start to develop quickly but they are decoy antibodies

129
Q

Gross lesions of PRRSV?

A

blood spots on lungs and liver

130
Q

Best way to confirm PRRSV?

A

Isolation of virus and RT- PCR

131
Q

How to determine if have an immune response to PRRSV?

A

ELISA

132
Q

How to control PRRS if we decide to live with it?

A

Vaccinate, and practice good biosecurity)- mantian herd immunity

133
Q

How does PRRSV spread?

A

Aerosols and fomites

134
Q

If we want to be PRRSV free how can that happen?

A

depopulate, surveillance via virological and serological testing, prevention of reintroduction

135
Q

Is PRRSV endemic?

A

Yes

VETM 422 (7 decks)

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