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Virology > Ch 9 - Resp Infections > Flashcards

Ch 9 - Resp Infections Flashcards

1
Q

3 main clinical outcomes of alphaherpesviruses infection of horses, cattle and cats

A

Resp, Repro, CNS

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2
Q

How are alphaherpesviruses transmitted?

A

primarily short distance aerosol and between moist epithelial surfaces

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3
Q

EHV-1 vs EVH-4 cell tropism

A

EHV-1: resp epithelium, sensory neurons, lymphocytes and endothelium.
EHV-4: resp epithelium and sensory neurons

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4
Q

Both EHV-1 and EHV-4 establish latency in?

A

neurons of the sensory ganglia

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5
Q

How are herpesviruses maintained in a population?

A

Infected for life. Replication occurs with or without clinical disease.

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6
Q

Is there a vaccince for EHV?

A

yes

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7
Q

EHV is/is not a reportable disease

A

is a reportable Dz

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8
Q

main difference between alphaherpesviruses in equine vs cattle

A

BHV-1 is very similar to EHV-1 BUT it does not infect endothelium

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9
Q

EHV-1 extra-respiratory spead is associated with?

A

lymphocyte tropism

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10
Q

EHV-1 extra-respiratory Pathogenesis is due to ?

A

endothelial cell infection

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11
Q

Abortion due to equine alphaherpesvirus is usually caused by EHV-1/EHV-4

A

EHV-1. Rarely EHV-4

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12
Q

uterine ? is necessary and sufficient for abortion with equine alphaherpesviruses

A

uterine vasculitis

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13
Q

EHV abortion frequently occurs with/without resp or CNS disease

A

without

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14
Q

key lesions of EHV-1 neuro Dz

A

vasculitis and ischemia (neurons not infected!)

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15
Q

limitations of the EHV Vaccine

A

does not protect against neurologic disease and protection is short lived. revaccination is required.

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16
Q

two important resp viruses in cats

A

FHV-1, Feline Calicivirus

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17
Q

control of FHV-1

A

Vaccine! FVRCP

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18
Q

FVCRP Vx does/does not prevent infection of FHV-1

A

does not

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19
Q

Dx of FHV-1

A

PCR Nasal swab (animal needs to be actively shedding for detection)

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20
Q

When does active shedding occur with FHV-1?

A

usually lags behind the stressful event. can transmit virus for 3 weeks after.

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21
Q

main betaherpesvirus of veterinary importance

A

elephantine herpevirus 1

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22
Q

cell tropism of elephantine herpevirus 1

A

endothelium

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23
Q

when is antiviral therapy beneficial for elephantine herpevirus 1

A

must be rapid intervention

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24
Q

cell tropism of gammaherpesviruses?

A

lymphocytes (site of latency)

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25
gammaherpesvirus of veterinary importance
ovine-herpesvirus 2
26
why do we see cases of malignant catarrhal disease sporadically ? what affects the number of animals with disease?
MCF does not cause disease in the natural host. Bison are more susceptible to OvHV-2 than cattle. Susceptible animals are dead-end hosts.
27
MCF **localized/systemic** disease
systemic
28
MCF common clinical signs in bison and cattle
sudden death, upper resp and intestinal tract ulceration and erosion, keratitis, corneal edema. can affect any system with blood vessels.... so all of them.
29
can MCF transmit between susceptible hosts (bison/cattle)?
No, susceptible hosts are dead-end hosts.
30
Is there a Vx for MCF?
No
31
how do you control MCF?
management practices are KEY
32
Why care about knowing macacine herpesvirus-1?
it is zoonotic and fatal (causes encephalitis in people)
33
3 main determinants of host range (influenza virus)
receptor, HA protein, and fusion protein
34
2 main envelope proteins of influenza virus
HA, NA
35
HA protein function
contains fusion protein, critical for **entry** and allowing release of nucleic acid to replicate
36
NA protein function
binds and cleaves the sialic acid. critical for **exit.**
37
antigenic drift
minor antigenic change due to **point mutations** in viral RNA. The usual source of change (like seasonal influenza)
38
antigenic shift
MAJOR antigenic change due to **re-assortment** of viral genes. usual source of pandemics. - New viral "subtypes"
39
how are influenza viruses generally subtyped?
H# and N#
40
Explain how influenza virus is maintained in nature and the role of waterfowl.
Influenza A - fundamentally a virus of waterfowl. Harbor all H and N types (Except new bat types.) They distribute influenza A viruses worldwide by migration.
41
? serve as "mixing vessels" for avian, human and swine flu strains.
swine
42
swine are an important source of reassortment events that leads to antigenic **Drift/shift** & **seasonal change/pandemics**
shift, pandemics
43
host and ciral factors that affect pathogenicity of flu virus
**Host determinants: ** * Availability of receptors on cells * Host proteases that cleave HA fusion protein (trypsin-like or fur in-like proteases) * Internal biochemistry of the cells * Immunity against the specific viral HA and NA epitopes (i.e. subtype of virus) * Immunity of a population **Viral factors:** * Binding to host cells (HA) * Release of virions from cells (NA) * Virus genetics (driven by selective pressure)
44
canine and equine influenza: diagnosis
RT-PCR detects viral RNA. Antigen detection ELISA. Serology.
45
canine and equine influenza: control
vaccination, isolation/quarantine
46
canine influenza: (H3N8/H3N2) severe disease more common
H3N2
47
molecular difference of HPAI vs LPAI
HPAI oncy seen with H5 and H7 subtypes
48
LPAI vs HPAI disease
LPAI: resp disease most common HPAI: causes severe systemic infections (including CNS!)
49
List the two distinguishing clinical features associated with avian influenza virus infection in birds that are not observed in influenza virus infections in mammals.
1. replicates in/sheds from both resp and enteric tracts 2. there is a systemic form of AIV infection (HPAI)
50
emergence of HPAI strains
all mutants derived from LPAI in wild bird populations
51
HPAI mutation occurs in ..?
within infected poultry
52
T/F: HPAI is a reportable disease
T
53
T/F: HPAI is a zoonotic disease
T
54
how is AI controlled/prevented
* biosecurity * surveillance * depopulation * disinfection * Vx use must be approved by USDA
55
T/F: antivirals are approved by the USDA for use with AI
F
56
T/F: equine influenza is not a reportable Dz in WA
F
57
Indicate where the two different currently circulating subtypes of canine influenza originated from and generally what genetic changes occurred to allow them to infect dogs.
H3N8 from cross-species transmission of H3N8 equine influenza cirus. H3N2: avian origin (cross species transmission, adaptation in dogs)
58
basic structure of paramyxoviruses
enveloped, -RNA (non-segmented) genomes.
59
major organ systems targeted by the Morbillivirus genus.
resp, enteric, CNS
60
List several animals susceptible to Canine Distemper Virus (CDV) and indicate which species serves as the principal reservoir for the virus
dogs, dingo, fox, raccoons, bears, ferrets, lions.... dogs are the main reservoir
61
pathogenesis of CDV
1. entry via aerosols into URT 2. replication in phagocytic cells of tonsils and trachea 3. replication in DCs, monocytes, lymphocytes of regional LNs 4. Primary viremia (may be missed clinically) 5. Secondary viremia (slinically significant)
62
Acute CDV disease signs
**bi-phasic fever,** rhinitis/nasal D/C, conjunctivities, bronchitis, catarrhal pneumonia, secondary infections, gastroenteritis, anorexia, depression
63
CDV CNS disease usually follows ? signs by ? weeks
acute, 1-3
64
CDV CNS disease usually in animals with....
overwhelming infections and/or inadequate immune responses
65
CDV acute CNS disease signs
acute encephalitis +/- ataxia, paresis, seizures, tremors, myoclonus
66
presenting signs for chronic persistent distemper
hyperkaratosis or "hard pad", encephalitis (immune mediated), old dog encephalitis
67
sign of CDV young puppy infection
enamel hypoplasia
68
CDV neurologic signs (acute or chronic) prognosis?
progressive/poor
69
CDV infection most often coincides with with ? at what age?
loss of maternal Ab (~3-4 mo of age)
70
What is Newcastle Dz?
distemper in birds (highly infectious)
71
Which organ systems are usually involved with Newcastle Dz?
resp, nervous, and digestive
72
why is Newcastle Dz important in the poultry industry?
it impacts poutry production worldwide

Virology (5 decks)

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