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POD > 3.5, 3.6, 3.7 RNA Viruses > Flashcards

3.5, 3.6, 3.7 RNA Viruses Flashcards

1
Q

picornaviridae:
- type of genome
- enveloped/nonenveloped
- are they big or small

A
  • (+) ssRNA
  • non-enveloped
  • small
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2
Q

what is the most important veterinary picornavirus

A

food and mouth disease virus

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3
Q

FMD affects what animals

A

cloven-hooved (cows, buffalo, pigs, sheep/goats)

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4
Q

T/F FMD is highly contagious

A

T

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5
Q

what are some lesions seen in FMD

A

ulcers, oral vesicles and erosions, teat lesions, foot lesions

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6
Q

what lesions are more common in pigs and what lesions are less common in pigs infected with FMD

A

hoof and snout lesions; oral

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7
Q

T/F Canada is free of FMD

A

T

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8
Q

what is a unique problem with FMD vaccination

A

7 serotypes of the virus exist so vaccination is not cross-protective

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9
Q

calciviridae:
- type of genome
- enveloped/non-enveloped

A
  • (+) ssRNA
  • non-enveloped
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10
Q

what is an important calicivirus

A

feline calcivirus

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11
Q

what disease caused by calicvirus is similar to FMD in swine

A

vesicular exanthema of swine

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12
Q

vesicular exanthema of swine is caused by what virus

A

calicivirus

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13
Q

feline calicivirus is similar to what other viral disease in cats

A

feline herpesvirus (feline rhinotracheitis virus)

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14
Q

what are clinical signs associated with feline calicivirus

A

conjunctivitis, rhinitis, salivation, tracheitis, pneumonia

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15
Q

does feline calicivirus have high or low mortality

A

low

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16
Q

up to ___% of cats are subclinical carriers of calicivirus

A

25

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17
Q

what is an important consideration for vaccinating cats against calicivirus

A

it will not induce lifelong immunity and will not protect against all strains

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18
Q

flaviviridae:
- genome
- enveloped/nonenveloped

A
  • (+) ssRNA
  • enveloped
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19
Q

what is an important flaviviridae virus

A

bovine viral diarrhea virus

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20
Q

BVD is a complex disease caused by a __________ group of related BVDV that differ in (3):

A

heterogeneous; antigenicity, cytopathogenicity, and virulence

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21
Q

what is the distribution of BVDV

A

worldwide

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22
Q

what are the routes of BVDV transmission

A

vertical and horizontal

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23
Q

what important bovine virus causes vertical and horizontal transmittion

A

BVDV

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24
Q

what are the two types of BVDV and which causes persistent infection

A

cytopathic and non-cytopathic; the latter causes persistent infection

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25
Q

what is the predominant biotype of BVDV in nature

A

non-cytopathic

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26
Q

what 2 factors influence the disease pattern of BVD within and between herds

A

1) herd immunity
2) presence or lack of persistently infected animals

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27
Q

what 2 host factors cause varying clinical and pathological manifestation of BVDV

A

age and pregnancy status of the animal

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28
Q

what are some signs of cytopathic BVDV

A
  • erosive/ulcerative lesions of GI tract
  • thrombocytopenia
  • diarrhea
  • nasal/ocular discharge
  • ulcers in lips, mouth oral cavity
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29
Q

what are the 3 outcomes of fetal infection with BVDV:
1) early pregnancy
2) mid pregnancy
3) later pregnancy

A

1) embryonic death and resorption
2) persistent infection WITH tolerance
3) immune response and elimination of virus

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30
Q

how does mucosal disease from BVDV develop

A

when a persistently infected animal (aka non-cytopathic) becomes infected with a cytopathic strain

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31
Q

what is a critical aspect of BVDV control

A

identifying and culling persistently infected animals within the herd

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32
Q

what 3 diseases in cattle cause oral lesions

A

1) FMD
2) BVDV
3) malignant catarrhal fever

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33
Q

togaviridae:
- type of genome
- enveloped/nonenveloped

A
  • (+) ssRNA
  • enveloped
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34
Q

how are togaviruses spread

A

arthropod vectors (they are arboviruses)

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35
Q

all 3 togaviruses are _________ and __________

A

arboviruses; zoonotic

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36
Q

what is the ultimate outcome of togavirus infection

A

-viral infection invades into brain cortex -> paralysis and death

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37
Q

what are the 3 togaviruses

A

eastern equine encephalitis virus, western equine encephalitis virus, venezuelan equine encephalitis virus

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38
Q

what 4 arboviruses have we discussed

A

1) african swine fever virus
2) eastern equine encephalitis virus
3) western equine encephalitis virus
4) venezuelan equine encephalitis virus

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39
Q

arteriviridae:
- type of genome
- enveloped/nonenveloped

A
  • (+) ssRNA
  • enveloped
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40
Q

in what cells does arteriviridae replicate

A

macrophages and endothelial cells

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41
Q

what is the most important arterivirus discussed

A

PRRS

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42
Q

T/F PRRS is on the OIE list

A

T

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43
Q

what is the most economically important swine disease

A

PRRS

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44
Q

is PRRS frequently subclinical or clinical

A

subclinical

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45
Q

what is unique about PRRS survival and what does this mean for infection

A

survives well in low temperatures so see infections in the winter months

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46
Q

how is PRRS transmitted

A

horizontal via aerosol, semen, direct contact

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47
Q

what are the 2 main RESPIRATORY syndromes observed in an animal with PRRS and why

A

interstitial pneumonia (due to pulmonary macrophage infection and secondary pneumonia) and ear cyanosis

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48
Q

what is the main REPRODUCTIVE syndrome of PRRS

A

SMEDI; abortion; if born alive piglets weak and often die of pneumonia

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49
Q

what are the 2 main coronaviruses

A

enteric coronaviruses (pigs) and feline coronavirus

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50
Q

coronavirus:
- type of genome
- enveloped/nonenveloped

A
  • (+) ssRNA
  • enveloped
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51
Q

does coronaviruses have high or low genetic variability and why

A

high; RNA virus

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52
Q

what are the main families of coronaviruses

A

alpha, beta, gamma, delta

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53
Q

which of the families of coronaviruses are one the OIE list

A

alpha and gamma

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54
Q

what are the 3 main presenting syndromes of coronaviruses

A

1) diarrhea/enteritis
2) respiratory infections
3) immune-mediated disease

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55
Q

what 3 coronaviruses are responsible for enteric disease in pigs

A

1) porcine epidemic diarrhea virus - PEDV
2) transmissible gastroenteritis virus - TGEV
3) Porcine deltacoronavirus - PDCoV

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56
Q

T/F all 3 coronaviruses responsible for enteric disease in pigs are antigenically similar so cross-protection can occur

A

F; they are antigenically distinct so cross-protection cannot occur

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57
Q

enteric coronavirus causes up to ______% mortality in piglets up to ____ weeks of age

A

100%; 2

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58
Q

what are the 3 signs of enteric coronavirus in pigs

A

1) dehydration
2) diarrhea
3) vomiting

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59
Q

how is enteric coronavirus disease spread in pigs

A

oral-fecal; aerosol; direct contact; fomites

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60
Q

where does enteric coronaviruses replicate

A

in villus epithelium (jejunum and ileum)

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61
Q

what are signs on postmortem of enteric coronavirus (PEDV, TGEV, PDCoV)

A
  • villus atrophy
  • distended intestines
  • thin-walled intestines
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62
Q

how is PRRS managed (4)

A

fluid/electrolytes, warm/clean/dry environment, antibiotics, vaccination

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63
Q

what is the distribution of FIP

A

worldwide

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64
Q

what cats tend to get FIP

A

young, immunocompromised

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65
Q

feline coronavirus (FeCV) infects _______ cells whereas FIP infects ________

A

intestinal epithelial cells; macrophages

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66
Q

T/F only a small percentage of cats that are exposed to FeCV get FIP

A

T

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67
Q

what are signs of FeCV infection

A

mild diarrhea

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68
Q

what is necessary for development of FIP

A

immunocompromised or stressed -> cleavage activation and mutation of fusion domains of the spike protein -> macrophage infection

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69
Q

what is the main physiological mechanism by which FIP causes clinical signs

A

vascular injury and leakage

70
Q

what is the main pathology of FIP

A

vasculitis and necrosis of the blood vessel wall

71
Q

what are the two forms of FIP

A

wet and dry

72
Q

what is the telltale sign of wet FIP

A

peritoneal exudate with plaques and grey-white nodules

73
Q

what effusions are formed as a consequence of FIP

A

abdominal distension, pericardial effusion, pleural effusion

74
Q

by what tests is FIP presumptively diagnosed and how is a definitive diagnosis reached

A

PCR; immunohistochemistry showing coronavirus in macrophages

75
Q

T/F FIP is easy to control because there are effective vaccines

A

F; no vaccines

76
Q

T/F there is a new antiviral drug for FIP

A

T

77
Q

reoviridae:
- type of genome
- enveloped/nonenveloped

A
  • dsRNA
  • nonenveloped
78
Q

what is unique about the reovirus genome

A

segmented therefore high rates of mutation (genetic drift) and reassortment (genetic shift)

79
Q

rotaviruses cause ___________ in essentially all animal species

A

gastroenteritis (diarrhea)

80
Q

how are rotaviruses spread

A

ingestion of contaminated feed and water

81
Q

how many groups of rotaviruses exist

A

8

82
Q

do rotaviruses have a long or short incubation period

A

short (16-24h)

83
Q

are young or old animals most likely to get rotavirus

A

young

84
Q

what is a sign of early infection of rotaviruses

A

yellow/green diarrhea

85
Q

what is the pathology of rotaviruses

A

destruction of enterocytes lining tips of the intestinal villi

86
Q

how are rotaviruses diagnosed (3)

A
  • ELISA
  • PCR
  • histopathology
87
Q

how are rotaviruses treated

A

antibiotics and electrolytes

88
Q

T/F vaccines are available for rotaviruses

A

T

89
Q

bluetongue virus affects what animals (4) - what is the main one

A

sheep, cattle, goats, deer; sheep mainly

90
Q

how many serotypes of bluetongue virus exist

A

24

91
Q

how is bluetongue virus transmitted

A

insect vectors (arbovirus)

92
Q

where do we see bluetongue virus

A

tropical and temperate regions - CANADA IS FREE OF THE DISEASE

93
Q

are most bluetongue virus infections subclinical or clinical

A

subclinical

94
Q

in what cells does bluetongue virus replicate

A

macrophages and endothelial cells

95
Q

what is the main pathology of bluetongue virus (3)

A

vascular injury:
- thrombosis/infarction
- cyanosis of lips, tongue, coronary band
- ulceration

96
Q

what are the main signs of bluetongue virus (5)

A
  • fever
  • reluctant to move
  • edema of face
  • ulcers in nose and mouth
  • abortion
97
Q

how is bluetongue disease diagnosed

A

ELISA

98
Q

T/F a vaccine for bluetongue disease exists

A

T

99
Q

orthomyxoviridae:
- type of genome
- enveloped/nonenveloped
- where does replication take place

A
  • segmented (-) ssRNA
  • enveloped
  • nucleus
100
Q

orthomyxoviridae viral replication takes place in the _________ and protein synthesis occurs in the __________

A

nucleus; cytoplasm

101
Q

orthomyxoviridae is classified based on what surface antigens (2)

A

hemagglutinin and neuraminidase

102
Q

what is hemagglutinin essential for

A

viral attachment and fusion

103
Q

what is neuraminidase essential for

A

release of virus from infected cells

104
Q

there are __ subtypes of hemagglutinin (__ -___ in bats) and __ subtypes of neuraminidase (__ - ___in bats)

A

18; H17-H18; 11; N10-N11

105
Q

what are hemagglutinin and neuraminidase

A

surface antigens of orthomyxoviridae

106
Q

how many genera of orthomyxoviridae are there

A

4 (A, B, C, D)

107
Q

what is an important disease caused by influenza A virus (orthomyxoviridae)

A

avian influenza

108
Q

what are the 4 diseases caused by influenza A viruses

A

avian influenza, equine influenza, swine influenza, canine influenza

109
Q

what H:N combinations exist in:
- avian influenza
- equine influenza
- swine influenza
- canine influenza

A

avian: many
equine: H3N8 and H7N7
swine: H1N1 and H3N2
canine: H3N2 and H3N8

110
Q

what influenza can cause antigenic shift and what can cause antigenic drift

A

influenza A can cause both antigenic shift and antigenic drift; influenza B can cause antigenic drift as well

111
Q

what causes re-assortment of H and N

A

exchange of the RNA segments of coding for H and N proteins during co-infection of one animal with different subtypes

112
Q

what is a common source of transmission of avian influenza

A

wild bird populations

113
Q

what are the notifiable avian influenza viruses

A

anything H5 and H7

114
Q

what is a highly pathogenic avian influenza virus present worldwide right now and does it cause disease in humans

A

H5N1; rarely causes disease in humans

115
Q

how might humans contract H5N1 avian influenza

A

close contact with infected birds or heavily infected environments

116
Q

what species has H5N1 been jumping from birds into

A

cows

117
Q

what must happen to hemagglutinin for the virus to fuse with the cell membrane

A

must be cleaved post-translationally

118
Q

what is similar between LPAI and HPAI and what is the main difference that contributes to the different virulence between the two viruses

A

both are produced in a non-infectious form; LPAI is cleaved extracellularly whereas HPAI is cleaved intracellularly by many proteases

119
Q

how is LPAI cleaved and how does this relate to its site of infection

A

there is only a single arginine at the cleavage site, and the proteases that can cleave it are present only in the GI and respiratory tract

120
Q

how is HPAI cleaved and how does this relate to its site of infection

A

there are several amino acids at the cleavage site, and it can be done by ubiquitously expressed enzymes throughout many different tissues

121
Q

what is the name of the enzymes that are responsible for cleaving HPAI

A

endopeptidase furins

122
Q

how is HPAI transmitted

A

fecal-oral

123
Q

T/F avian influenza causes specific clinical signs

A

F; signs are non-specific and resemble other diseases such as newcastle disease (a paramyxoviridae)

124
Q

what is the process of diagnosing avian influenza

A

1) PCR
2) if PCR is positive, test for specific H5 and H7 genes to rule out HPAI
3) if PCR positive, sequence the cleavage site
4) if several amino acids present at cleavage site, HPAI

125
Q

what is key to HPAI detection and protection

A

surveillance, detection and depopulation of affected flocks

126
Q

what are 4 steps for control and prevention of avian influenza (specifically HPAI)

A

1) monitor flocks with LPAI H5 and H7 strains
2) biosecurity and depopulation if HPAI detected
3) segregate wild and domestic bird populations
4) educate workers

127
Q

paramyxoviridae:
- genome
- enveloped/nonenveloped

A
  • (-) ssRNA
  • enveloped
128
Q

T/F paramyxoviridae can cause respiratory or systemic illness

A

T (think of newcastle disease, rinderpest and canine distemper)

129
Q

of the paramyxoviruses studied, which are on the OIE list

A

rinderpest and newcastle disease virus

130
Q

what virus causes newcastle disease virus

A

avian paramyxovirus 1

131
Q

how many serotypes of avian paramyxovirus are there

A

9

132
Q

what bird species are susceptible to newcastle disease

A

all to some level

133
Q

in avian hosts, paramyxovirus causes what characteristic disease (4)

A

respiratory, circulatory, gastrointestinal, nervous system

134
Q

T/F newcastle disease is zoonotic

A

T (causes conjunctivitis in humans)

135
Q

what are the 4 pathotypes of newcastle disease virus

A

1) asymptomatic
2) lentogenic
3) mesogenic
4) velogenic

136
Q

describe the severity of newcastle disease caused by the following:
1) asymptomatic:
2) lentogenic:
3) mesogenic:
4) velogenic:

A

1) asymptomatic: no disease
2) lentogenic: subclinical to mild respiratory disease in chicks
3) mesogenic: moderately virulent respiratory or neurological disease
4) velogenic: generalized disease in all ages

137
Q

what are the 2 subtypes of velogenic newcastle disease

A

1) velogenic neurotropic
2) velogenic viscerotropic

138
Q

describe the following:
1) velogenic neurotropic
2) velogenic viscerotropic

A

1) respiratory and neurological
2) hemorrhagic intestinal

139
Q

what is a major contributor to strain differences in newcastle disease virus virulence? what disease is this similar to

A

cleavability of the fusion protein; similar to avian influenza

140
Q

T/F the difference in virulence between newcastle disease virus and avian influenza is due to idential mechanisms

A

T

Context: non-virulent has a single amino acid in the cleavage site activated by extracellular proteases in respiratory and GI tract; virulent has multiple basic amino acids activated by a variety of proteases in many types of infected cells

141
Q

T/F clinical signs of newcastle disease are non-specific

A

T

142
Q

outbreaks of what virus have historically cause destruction of entire cattle populations and resulted in famines, only eradicated by vaccines

A

rinderpest

143
Q

rinderpest gains entry via receptors on what two types of cells

A

leukocytes and epithelial cells

144
Q

what are 2 important signs of rinderpest

A

erosions and necrosis of oral mucosa; nasal/ocular discharge

145
Q

what is the main host of canine distemper

A

dogs 2-6 months old

146
Q

T/F canine distemper only affects dogs

A

F

147
Q

how is canine distemper shed

A

urine, feces, nasal/ocular secretions

148
Q

canine distemper infects and kills what cells

A

leukocytes

149
Q

most canine distemper infections are subclinical/clinical

A

subclinical

150
Q

what are some common signs of distemper

A
  • enteritis
  • purulent conjunctivitis and rhinitis
  • pus in bronchi
  • neurologic signs (ex. chewing motion)
  • pneumonia
151
Q

what are the 4 forms of canine distemper

A

1) peracute
2) acute
3) subacute neurologic
4) late form

152
Q

describe the 4 forms of canine distemper:
1) peracute
2) acute
3) subacute neurological
4) late form

A

1) peracute: fever and sudden death
2) acute: variety of signs including respiratory, nervous and GI
3) subacute neurologic: seizures, convulsions, encephalitis
4) late form: hard pads, encephalitis, progressive loss of neurologic function

153
Q

rhabdoviridae:
- genome
- enveloped/nonenveloped

A
  • segmented (-) ssRNA
  • enveloped
154
Q

what two rhabdoviruses are on the OIE list

A
  • rabies
  • vesicular stomatitis
155
Q

vesicular stomatitis affects what species mainly

A

horses

156
Q

vesicular stomatitis resembles what disease

A

FMD

157
Q

how is vesicular stomatitis spread

A

sandflies and blackflies as vectors

158
Q

T/F vesicular stomatitis was last reported in the US in 1949 but cases exist in Canada

A

F; other way around

159
Q

all vesicular diseases produce

A

fever with vesicles that will progress to erosions in:
- mouth
- feet
- nares
- muzzle
- teats

160
Q

T/F all mammals can theoretically get rabies

A

T

161
Q

what is the incubation period of rabies

A

2 weeks to 6 months

162
Q

what happens in the early and advanced stages of rabies virus infection in dogs

A

early: behaviour change
advanced: paralysis; fury

163
Q

what are some clinical signs of rabies

A
  • aggression
  • salivation (difficulty swallowing)
  • convulsions
  • paralysis
164
Q

how is rabies spread

A

saliva

165
Q

T/F rabies can rarely but theoretically be spread by inhalation of aerosol particles containing the virus

A

T

166
Q

what is the name for rabies contained in wildlife reservoirs

A

sylvatic rabies

167
Q

what is the pathogenesis of rabies

A

1) animal gets bit and comes into contact with saliva contaminated with rabies
2) virus enters motor end plates near site of injury and starts moving up the motor nerve
3) virus replicates in the spinal cord neurons
4) virus moves up the spinal cord to eventually reach the hippocampus

168
Q

how is rabies diagnosed

A

post-mortem only:
- flourescencce
- RT PCR
- negri bodies

169
Q

what are inclusions of rabies present in neurons on histology

A

negri bodies

170
Q

how do negri bodies look

A
  • eosinophilic
  • sharply outlined

POD (13 decks)

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