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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
Q

gammaherpesvirus of veterinary importance

A

ovine-herpesvirus 2

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26
Q

why do we see cases of malignant catarrhal disease sporadically ? what affects the number of animals with disease?

A

MCF does not cause disease in the natural host. Bison are more susceptible to OvHV-2 than cattle. Susceptible animals are dead-end hosts.

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27
Q

MCF localized/systemic disease

A

systemic

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28
Q

MCF common clinical signs in bison and cattle

A

sudden death, upper resp and intestinal tract ulceration and erosion, keratitis, corneal edema. can affect any system with blood vessels…. so all of them.

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29
Q

can MCF transmit between susceptible hosts (bison/cattle)?

A

No, susceptible hosts are dead-end hosts.

30
Q

Is there a Vx for MCF?

A

No

31
Q

how do you control MCF?

A

management practices are KEY

32
Q

Why care about knowing macacine herpesvirus-1?

A

it is zoonotic and fatal (causes encephalitis in people)

33
Q

3 main determinants of host range (influenza virus)

A

receptor, HA protein, and fusion protein

34
Q

2 main envelope proteins of influenza virus

A

HA, NA

35
Q

HA protein function

A

contains fusion protein, critical for entry and allowing release of nucleic acid to replicate

36
Q

NA protein function

A

binds and cleaves the sialic acid. critical for exit.

37
Q

antigenic drift

A

minor antigenic change due to point mutations in viral RNA. The usual source of change (like seasonal influenza)

38
Q

antigenic shift

A

MAJOR antigenic change due to re-assortment of viral genes. usual source of pandemics. - New viral “subtypes”

39
Q

how are influenza viruses generally subtyped?

A

H# and N#

40
Q

Explain how influenza virus is maintained in nature and the role of waterfowl.

A

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
Q

? serve as “mixing vessels” for avian, human and swine flu strains.

A

swine

42
Q

swine are an important source of reassortment events that leads to antigenic Drift/shift & seasonal change/pandemics

A

shift, pandemics

43
Q

host and ciral factors that affect pathogenicity of flu virus

A

**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
Q

canine and equine influenza: diagnosis

A

RT-PCR detects viral RNA. Antigen detection ELISA. Serology.

45
Q

canine and equine influenza: control

A

vaccination, isolation/quarantine

46
Q

canine influenza: (H3N8/H3N2) severe disease more common

A

H3N2

47
Q

molecular difference of HPAI vs LPAI

A

HPAI oncy seen with H5 and H7 subtypes

48
Q

LPAI vs HPAI disease

A

LPAI: resp disease most common

HPAI: causes severe systemic infections (including CNS!)

49
Q

List the two distinguishing clinical features associated with avian influenza virus infection in
birds that are not observed in influenza virus infections in mammals.

A
  1. replicates in/sheds from both resp and enteric tracts
  2. there is a systemic form of AIV infection (HPAI)
50
Q

emergence of HPAI strains

A

all mutants derived from LPAI in wild bird populations

51
Q

HPAI mutation occurs in ..?

A

within infected poultry

52
Q

T/F: HPAI is a reportable disease

A

T

53
Q

T/F: HPAI is a zoonotic disease

A

T

54
Q

how is AI controlled/prevented

A
  • biosecurity
  • surveillance
  • depopulation
  • disinfection
  • Vx use must be approved by USDA
55
Q

T/F: antivirals are approved by the USDA for use with AI

A

F

56
Q

T/F: equine influenza is not a reportable Dz in WA

A

F

57
Q

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.

A

H3N8 from cross-species transmission of H3N8 equine influenza cirus.

H3N2: avian origin (cross species transmission, adaptation in dogs)

58
Q

basic structure of paramyxoviruses

A

enveloped, -RNA (non-segmented) genomes.

59
Q

major organ systems targeted by the Morbillivirus genus.

A

resp, enteric, CNS

60
Q

List several animals susceptible to Canine Distemper Virus (CDV) and indicate which species serves as the principal reservoir for the virus

A

dogs, dingo, fox, raccoons, bears, ferrets, lions….

dogs are the main reservoir

61
Q

pathogenesis of CDV

A
  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
Q

Acute CDV disease signs

A

bi-phasic fever, rhinitis/nasal D/C, conjunctivities, bronchitis, catarrhal pneumonia, secondary infections, gastroenteritis, anorexia, depression

63
Q

CDV CNS disease usually follows ? signs by ? weeks

A

acute, 1-3

64
Q

CDV CNS disease usually in animals with….

A

overwhelming infections and/or inadequate immune responses

65
Q

CDV acute CNS disease signs

A

acute encephalitis +/- ataxia, paresis, seizures, tremors, myoclonus

66
Q

presenting signs for chronic persistent distemper

A

hyperkaratosis or “hard pad”, encephalitis (immune mediated), old dog encephalitis

67
Q

sign of CDV young puppy infection

A

enamel hypoplasia

68
Q

CDV neurologic signs (acute or chronic) prognosis?

A

progressive/poor

69
Q

CDV infection most often coincides with with ? at what age?

A

loss of maternal Ab (~3-4 mo of age)

70
Q

What is Newcastle Dz?

A

distemper in birds (highly infectious)

71
Q

Which organ systems are usually involved with Newcastle Dz?

A

resp, nervous, and digestive

72
Q

why is Newcastle Dz important in the poultry industry?

A

it impacts poutry production worldwide

Virology (5 decks)

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