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
2
Q
what is the most important veterinary picornavirus
A
food and mouth disease virus
3
Q
FMD affects what animals
A
cloven-hooved (cows, buffalo, pigs, sheep/goats)
4
Q
T/F FMD is highly contagious
A
T
5
Q
what are some lesions seen in FMD
A
ulcers, oral vesicles and erosions, teat lesions, foot lesions
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
7
Q
T/F Canada is free of FMD
A
T
8
Q
what is a unique problem with FMD vaccination
A
7 serotypes of the virus exist so vaccination is not cross-protective
9
Q
calciviridae:
- type of genome
- enveloped/non-enveloped
A
- (+) ssRNA
- non-enveloped
10
Q
what is an important calicivirus
A
feline calcivirus
11
Q
what disease caused by calicvirus is similar to FMD in swine
A
vesicular exanthema of swine
12
Q
vesicular exanthema of swine is caused by what virus
A
calicivirus
13
Q
feline calicivirus is similar to what other viral disease in cats
A
feline herpesvirus (feline rhinotracheitis virus)
14
Q
what are clinical signs associated with feline calicivirus
A
conjunctivitis, rhinitis, salivation, tracheitis, pneumonia
15
Q
does feline calicivirus have high or low mortality
A
low
16
Q
up to ___% of cats are subclinical carriers of calicivirus
A
25
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
18
Q
flaviviridae:
- genome
- enveloped/nonenveloped
A
- (+) ssRNA
- enveloped
19
Q
what is an important flaviviridae virus
A
bovine viral diarrhea virus
20
Q
BVD is a complex disease caused by a __________ group of related BVDV that differ in (3):
A
heterogeneous; antigenicity, cytopathogenicity, and virulence
21
Q
what is the distribution of BVDV
A
worldwide
22
Q
what are the routes of BVDV transmission
A
vertical and horizontal
23
Q
what important bovine virus causes vertical and horizontal transmittion
A
BVDV
24
Q
what are the two types of BVDV and which causes persistent infection
A
cytopathic and non-cytopathic; the latter causes persistent infection
25
what is the predominant biotype of BVDV in nature
non-cytopathic
26
what 2 factors influence the disease pattern of BVD within and between herds
1) herd immunity
2) presence or lack of persistently infected animals
27
what 2 host factors cause varying clinical and pathological manifestation of BVDV
age and pregnancy status of the animal
28
what are some signs of cytopathic BVDV
- erosive/ulcerative lesions of GI tract
- thrombocytopenia
- diarrhea
- nasal/ocular discharge
- ulcers in lips, mouth oral cavity
29
what are the 3 outcomes of fetal infection with BVDV:
1) early pregnancy
2) mid pregnancy
3) later pregnancy
1) embryonic death and resorption
2) persistent infection WITH tolerance
3) immune response and elimination of virus
30
how does mucosal disease from BVDV develop
when a persistently infected animal (aka non-cytopathic) becomes infected with a cytopathic strain
31
what is a critical aspect of BVDV control
identifying and culling persistently infected animals within the herd
32
what 3 diseases in cattle cause oral lesions
1) FMD
2) BVDV
3) malignant catarrhal fever
33
togaviridae:
- type of genome
- enveloped/nonenveloped
- (+) ssRNA
- enveloped
34
how are togaviruses spread
arthropod vectors (they are arboviruses)
35
all 3 togaviruses are _________ and __________
arboviruses; zoonotic
36
what is the ultimate outcome of togavirus infection
-viral infection invades into brain cortex -> paralysis and death
37
what are the 3 togaviruses
eastern equine encephalitis virus, western equine encephalitis virus, venezuelan equine encephalitis virus
38
what 4 arboviruses have we discussed
1) african swine fever virus
2) eastern equine encephalitis virus
3) western equine encephalitis virus
4) venezuelan equine encephalitis virus
39
arteriviridae:
- type of genome
- enveloped/nonenveloped
- (+) ssRNA
- enveloped
40
in what cells does arteriviridae replicate
macrophages and endothelial cells
41
what is the most important arterivirus discussed
PRRS
42
T/F PRRS is on the OIE list
T
43
what is the most economically important swine disease
PRRS
44
is PRRS frequently subclinical or clinical
subclinical
45
what is unique about PRRS survival and what does this mean for infection
survives well in low temperatures so see infections in the winter months
46
how is PRRS transmitted
horizontal via aerosol, semen, direct contact
47
what are the 2 main RESPIRATORY syndromes observed in an animal with PRRS and why
interstitial pneumonia (due to pulmonary macrophage infection and secondary pneumonia) and ear cyanosis
48
what is the main REPRODUCTIVE syndrome of PRRS
SMEDI; abortion; if born alive piglets weak and often die of pneumonia
49
what are the 2 main coronaviruses
enteric coronaviruses (pigs) and feline coronavirus
50
coronavirus:
- type of genome
- enveloped/nonenveloped
- (+) ssRNA
- enveloped
51
does coronaviruses have high or low genetic variability and why
high; RNA virus
52
what are the main families of coronaviruses
alpha, beta, gamma, delta
53
which of the families of coronaviruses are one the OIE list
alpha and gamma
54
what are the 3 main presenting syndromes of coronaviruses
1) diarrhea/enteritis
2) respiratory infections
3) immune-mediated disease
55
what 3 coronaviruses are responsible for enteric disease in pigs
1) porcine epidemic diarrhea virus - PEDV
2) transmissible gastroenteritis virus - TGEV
3) Porcine deltacoronavirus - PDCoV
56
T/F all 3 coronaviruses responsible for enteric disease in pigs are antigenically similar so cross-protection can occur
F; they are antigenically distinct so cross-protection cannot occur
57
enteric coronavirus causes up to ______% mortality in piglets up to ____ weeks of age
100%; 2
58
what are the 3 signs of enteric coronavirus in pigs
1) dehydration
2) diarrhea
3) vomiting
59
how is enteric coronavirus disease spread in pigs
oral-fecal; aerosol; direct contact; fomites
60
where does enteric coronaviruses replicate
in villus epithelium (jejunum and ileum)
61
what are signs on postmortem of enteric coronavirus (PEDV, TGEV, PDCoV)
- villus atrophy
- distended intestines
- thin-walled intestines
62
how is PRRS managed (4)
fluid/electrolytes, warm/clean/dry environment, antibiotics, vaccination
63
what is the distribution of FIP
worldwide
64
what cats tend to get FIP
young, immunocompromised
65
feline coronavirus (FeCV) infects _______ cells whereas FIP infects ________
intestinal epithelial cells; macrophages
66
T/F only a small percentage of cats that are exposed to FeCV get FIP
T
67
what are signs of FeCV infection
mild diarrhea
68
what is necessary for development of FIP
immunocompromised or stressed -> cleavage activation and mutation of fusion domains of the spike protein -> macrophage infection
69
what is the main physiological mechanism by which FIP causes clinical signs
vascular injury and leakage
70
what is the main pathology of FIP
vasculitis and necrosis of the blood vessel wall
71
what are the two forms of FIP
wet and dry
72
what is the telltale sign of wet FIP
peritoneal exudate with plaques and grey-white nodules
73
what effusions are formed as a consequence of FIP
abdominal distension, pericardial effusion, pleural effusion
74
by what tests is FIP presumptively diagnosed and how is a definitive diagnosis reached
PCR; immunohistochemistry showing coronavirus in macrophages
75
T/F FIP is easy to control because there are effective vaccines
F; no vaccines
76
T/F there is a new antiviral drug for FIP
T
77
reoviridae:
- type of genome
- enveloped/nonenveloped
- dsRNA
- nonenveloped
78
what is unique about the reovirus genome
segmented therefore high rates of mutation (genetic drift) and reassortment (genetic shift)
79
rotaviruses cause ___________ in essentially all animal species
gastroenteritis (diarrhea)
80
how are rotaviruses spread
ingestion of contaminated feed and water
81
how many groups of rotaviruses exist
8
82
do rotaviruses have a long or short incubation period
short (16-24h)
83
are young or old animals most likely to get rotavirus
young
84
what is a sign of early infection of rotaviruses
yellow/green diarrhea
85
what is the pathology of rotaviruses
destruction of enterocytes lining tips of the intestinal villi
86
how are rotaviruses diagnosed (3)
- ELISA
- PCR
- histopathology
87
how are rotaviruses treated
antibiotics and electrolytes
88
T/F vaccines are available for rotaviruses
T
89
bluetongue virus affects what animals (4) - what is the main one
sheep, cattle, goats, deer; sheep mainly
90
how many serotypes of bluetongue virus exist
24
91
how is bluetongue virus transmitted
insect vectors (arbovirus)
92
where do we see bluetongue virus
tropical and temperate regions - CANADA IS FREE OF THE DISEASE
93
are most bluetongue virus infections subclinical or clinical
subclinical
94
in what cells does bluetongue virus replicate
macrophages and endothelial cells
95
what is the main pathology of bluetongue virus (3)
vascular injury:
- thrombosis/infarction
- cyanosis of lips, tongue, coronary band
- ulceration
96
what are the main signs of bluetongue virus (5)
- fever
- reluctant to move
- edema of face
- ulcers in nose and mouth
- abortion
97
how is bluetongue disease diagnosed
ELISA
98
T/F a vaccine for bluetongue disease exists
T
99
orthomyxoviridae:
- type of genome
- enveloped/nonenveloped
- where does replication take place
- segmented (-) ssRNA
- enveloped
- nucleus
100
orthomyxoviridae viral replication takes place in the _________ and protein synthesis occurs in the __________
nucleus; cytoplasm
101
orthomyxoviridae is classified based on what surface antigens (2)
hemagglutinin and neuraminidase
102
what is hemagglutinin essential for
viral attachment and fusion
103
what is neuraminidase essential for
release of virus from infected cells
104
there are __ subtypes of hemagglutinin (__ -___ in bats) and __ subtypes of neuraminidase (__ - ___in bats)
18; H17-H18; 11; N10-N11
105
what are hemagglutinin and neuraminidase
surface antigens of orthomyxoviridae
106
how many genera of orthomyxoviridae are there
4 (A, B, C, D)
107
what is an important disease caused by influenza A virus (orthomyxoviridae)
avian influenza
108
what are the 4 diseases caused by influenza A viruses
avian influenza, equine influenza, swine influenza, canine influenza
109
what H:N combinations exist in:
- avian influenza
- equine influenza
- swine influenza
- canine influenza
avian: many
equine: H3N8 and H7N7
swine: H1N1 and H3N2
canine: H3N2 and H3N8
110
what influenza can cause antigenic shift and what can cause antigenic drift
influenza A can cause both antigenic shift and antigenic drift; influenza B can cause antigenic drift as well
111
what causes re-assortment of H and N
exchange of the RNA segments of coding for H and N proteins during co-infection of one animal with different subtypes
112
what is a common source of transmission of avian influenza
wild bird populations
113
what are the notifiable avian influenza viruses
anything H5 and H7
114
what is a highly pathogenic avian influenza virus present worldwide right now and does it cause disease in humans
H5N1; rarely causes disease in humans
115
how might humans contract H5N1 avian influenza
close contact with infected birds or heavily infected environments
116
what species has H5N1 been jumping from birds into
cows
117
what must happen to hemagglutinin for the virus to fuse with the cell membrane
must be cleaved post-translationally
118
what is similar between LPAI and HPAI and what is the main difference that contributes to the different virulence between the two viruses
both are produced in a non-infectious form; LPAI is cleaved extracellularly whereas HPAI is cleaved intracellularly by many proteases
119
how is LPAI cleaved and how does this relate to its site of infection
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
how is HPAI cleaved and how does this relate to its site of infection
there are several amino acids at the cleavage site, and it can be done by ubiquitously expressed enzymes throughout many different tissues
121
what is the name of the enzymes that are responsible for cleaving HPAI
endopeptidase furins
122
how is HPAI transmitted
fecal-oral
123
T/F avian influenza causes specific clinical signs
F; signs are non-specific and resemble other diseases such as newcastle disease (a paramyxoviridae)
124
what is the process of diagnosing avian influenza
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
what is key to HPAI detection and protection
surveillance, detection and depopulation of affected flocks
126
what are 4 steps for control and prevention of avian influenza (specifically HPAI)
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
paramyxoviridae:
- genome
- enveloped/nonenveloped
- (-) ssRNA
- enveloped
128
T/F paramyxoviridae can cause respiratory or systemic illness
T (think of newcastle disease, rinderpest and canine distemper)
129
of the paramyxoviruses studied, which are on the OIE list
rinderpest and newcastle disease virus
130
what virus causes newcastle disease virus
avian paramyxovirus 1
131
how many serotypes of avian paramyxovirus are there
9
132
what bird species are susceptible to newcastle disease
all to some level
133
in avian hosts, paramyxovirus causes what characteristic disease (4)
respiratory, circulatory, gastrointestinal, nervous system
134
T/F newcastle disease is zoonotic
T (causes conjunctivitis in humans)
135
what are the 4 pathotypes of newcastle disease virus
1) asymptomatic
2) lentogenic
3) mesogenic
4) velogenic
136
describe the severity of newcastle disease caused by the following:
1) asymptomatic:
2) lentogenic:
3) mesogenic:
4) velogenic:
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
what are the 2 subtypes of velogenic newcastle disease
1) velogenic neurotropic
2) velogenic viscerotropic
138
describe the following:
1) velogenic neurotropic
2) velogenic viscerotropic
1) respiratory and neurological
2) hemorrhagic intestinal
139
what is a major contributor to strain differences in newcastle disease virus virulence? what disease is this similar to
cleavability of the fusion protein; similar to avian influenza
140
T/F the difference in virulence between newcastle disease virus and avian influenza is due to idential mechanisms
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
T/F clinical signs of newcastle disease are non-specific
T
142
outbreaks of what virus have historically cause destruction of entire cattle populations and resulted in famines, only eradicated by vaccines
rinderpest
143
rinderpest gains entry via receptors on what two types of cells
leukocytes and epithelial cells
144
what are 2 important signs of rinderpest
erosions and necrosis of oral mucosa; nasal/ocular discharge
145
what is the main host of canine distemper
dogs 2-6 months old
146
T/F canine distemper only affects dogs
F
147
how is canine distemper shed
urine, feces, nasal/ocular secretions
148
canine distemper infects and kills what cells
leukocytes
149
most canine distemper infections are subclinical/clinical
subclinical
150
what are some common signs of distemper
- enteritis
- purulent conjunctivitis and rhinitis
- pus in bronchi
- neurologic signs (ex. chewing motion)
- pneumonia
151
what are the 4 forms of canine distemper
1) peracute
2) acute
3) subacute neurologic
4) late form
152
describe the 4 forms of canine distemper:
1) peracute
2) acute
3) subacute neurological
4) late form
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
rhabdoviridae:
- genome
- enveloped/nonenveloped
- segmented (-) ssRNA
- enveloped
154
what two rhabdoviruses are on the OIE list
- rabies
- vesicular stomatitis
155
vesicular stomatitis affects what species mainly
horses
156
vesicular stomatitis resembles what disease
FMD
157
how is vesicular stomatitis spread
sandflies and blackflies as vectors
158
T/F vesicular stomatitis was last reported in the US in 1949 but cases exist in Canada
F; other way around
159
all vesicular diseases produce
fever with vesicles that will progress to erosions in:
- mouth
- feet
- nares
- muzzle
- teats
160
T/F all mammals can theoretically get rabies
T
161
what is the incubation period of rabies
2 weeks to 6 months
162
what happens in the early and advanced stages of rabies virus infection in dogs
early: behaviour change
advanced: paralysis; fury
163
what are some clinical signs of rabies
- aggression
- salivation (difficulty swallowing)
- convulsions
- paralysis
164
how is rabies spread
saliva
165
T/F rabies can rarely but theoretically be spread by inhalation of aerosol particles containing the virus
T
166
what is the name for rabies contained in wildlife reservoirs
sylvatic rabies
167
what is the pathogenesis of rabies
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
how is rabies diagnosed
post-mortem only:
- flourescencce
- RT PCR
- negri bodies
169
what are inclusions of rabies present in neurons on histology
negri bodies
170
how do negri bodies look
- eosinophilic
- sharply outlined
