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IVP > Microbiology > Flashcards

Microbiology Flashcards

1
Q

what is a virion?

A

an infectious virus particle

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2
Q

what is a protomer?

A

identical protein subunit making up the capsid

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3
Q

what shapes can a capsid be?

A

icosahedral, helical or complex

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4
Q

name 4 viruses of icosahedral symmetry

A

adenovirus, papillomavirus, parvovirus, herpesvirus

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5
Q

name 2 viruses of helical symmetry

A

rhabdovirus, parainfluenza virus

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6
Q

name a virus of complex symmetry

A

poxvirus

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7
Q

name a non-enveloped DNA virus

A

canine parvovirus

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8
Q

name an enveloped DNA virus

A

feline herpesvirus

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9
Q

name a non enveloped RNA virus

A

foot & mouth disease virus

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10
Q

name an enveloped RNA virus

A

influenza virus

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11
Q

t/f

viral genome can be both DNA or RNA

A

false. can only be one or the other

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12
Q

where do DNA viruses replicate?

A

most in nucleus

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13
Q

where do RNA viruses replicate

A

most in cytoplasm

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14
Q

are DNA or RNA viruses more prone to mutation?

A

RNA viruses

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15
Q

are DNA or RNA viruses stable?

A

DNA viruses

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16
Q

t/f

envelopes derived from viral cell?

A

false. derived from host cell

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17
Q

are enveloped or non-enveloped viruses stable?

A

non-enveloped

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18
Q

t/f

enveloped viruses usually easily inactivated by disinfectants

A

true

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19
Q

what is mutation?

A

structural alteration in nucleic acid

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20
Q

mutation has important effects on…

A
  • virulence of virus

- host range of virus

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21
Q

point mutation

A

single nucleotide substitutions

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22
Q

viral recombination

A

exchange or transfer of genetic material between diff but closely related viruses infecting same cell

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23
Q

antigenic DRIFT

A

gradual accumulation of point mutations (common)

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24
Q

antigenic SHIFT

A

acquisition of new gene from another virus due to recombination or reassortment (rare)

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25
Q

In influenza virus, what allows it to attach and to where?

A

Hemagglutinin, attaches to respiratory epithelium

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26
Q

when did the spanish influenza arise?

A

1918

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27
Q

spanish influenza aka…

A

H1N1 virus

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28
Q

how was H1N1 passed to humans

A

bird-to-human transmission

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29
Q

what are the types of virus-cell interactions?

A
  • Lytic infection

- Persistent infection

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30
Q

What are types of persistent infection?

A
  • productive
  • latent
  • non-productive transforming
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31
Q

example of lytic infections

A
  • canine parvovirus

- foot and mouth disease virus

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32
Q

examples of persistent productive infections

A
  • rabies

- foot and mouth disease

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33
Q

examples of persistent latent infections

A
  • herpes virus

- retrovirus

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34
Q

example of non-productive transforming infections

A

equine sarcoids

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35
Q

types of viral effect on cell morphology

A
  • cytopathic
  • inclusion bodies
  • alterations in cell membrane
  • formation of syncytia
  • haemadosorption
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36
Q

describe cytopathic effect

A
  • seen in vitro
  • seen in cell monocultures infected with virus
  • nature of CPE can be diagnostic
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37
Q

describe inclusion bodies

A

morphological changes seen in cells infected with certain viruses

38
Q

all viral infections produce inclusion bodies. t/f?

A

false.

39
Q

give some examples of inclusion bodies

A
  • masses of viral nucleocapsids (e.g. rabies)
  • masses of viral proteins and nucleic acid (e.g. pox)
  • crystalline aggregates of virions
  • degenerate nuclear DNA (e.g. herpes)
40
Q

give examples of alterations to cell membranes

A
  • increase in permeability
  • altered ion exchange/membrane potential
  • proliferation/rearrangement of membrane
  • insertion of viral glycoproteins
41
Q

what is syncytia?

A

viral proteins inserted into plasma membrane of cell may lead to fusion of between neighbouring cells (e.g. herpes, coronavirus)

42
Q

what is haemadosorption?

A

adherence of RBCs to other cells or particles

43
Q

name ways viruses damage cells

A
  • cell lysis
  • inhibit acid synthesis
  • inhibit protein synthesis
  • cytopathic effects
  • cytolysis
44
Q

how can viral interference occur?

A
  • superinfection exclusion

- interferon mediated interference

45
Q

what are cytokines that are produced rapidly (but transiently) in response to viral infection?

A

interferons

46
Q

what is the paracrine effect?

A

interferons released by infected cell and binding to receptors on neighbouring cells

47
Q

what are some routes of viral entry?

A
  • respiratory system
  • alimentary system
  • skin
  • urogenital tract
  • conjunctiva
48
Q

what is the most common route of viral entry

A

respiratory system

49
Q

how do particles enter respiratory system?

A

impaction - large - nasopharynx
sedimentation - medium - small airways
diffusion - small - alveoli

50
Q

where are sites of defence in respiratory system?

A
  • nasal passages
  • nasopharynx
  • larynx
  • lower respiratory tract
51
Q

where are cough receptors located?

A

larynx

52
Q

where is the mucociliary escalator?

A

lower respiratory tract

53
Q

where are turbinate bones?

A

nasal passages

54
Q

where are lymphoid nodules in submucosa?

A

nasopharynx

55
Q

what is the 2nd most common route of viral entry?

A

alimentary system

56
Q

what are some defences of the alimentary system?

A

perstalsis, mucous, bile, proteases, gastric acid, secretory IgA, tight junctions, lymphoid tissue (peyers patches), constant cell turnover

57
Q

what are some barrier disruptions to skin defences?

A
  • cuts, abrasions, trauma
  • biting arthropods
  • animal bites
  • latrogenic
58
Q

where would defence mechanisms of tear production and mechanical ‘wiping’ occur?

A

conjunctiva

59
Q

what are some defence mechanisms of the urogenital tract?

A
  • urinary flushing
  • anatomical barriers
  • low pH
  • secretory IgA
60
Q

how can viruses spread from site on entry?

A
  • apical release

- basolateral release

61
Q

what type of directional spreading moves to contagious surfaces?

A

apical release

62
Q

what is basolateral release?

A

directional shedding favouring internal dissemination

63
Q

once in sub-epithelial tissues, virus disseminates via…

A
  • lymphatics
  • bloodstream
  • nerves
64
Q

in haematogenous spread, how can virions be transported through the blood?

A
  • free virions in plasma

- absorbed to, or within blood cells

65
Q

what is neural spread?

A

viral spread through peripheral nerves

66
Q

retrograde (centripetal) transport

A

allows access to CNS

67
Q

anterograde (centrifugal) transport

A

allows access to peripheral tissue

68
Q

what is viraemia?

A

presence of infectious virus in the blood

69
Q

what are the 3 requirements for successful infection?

A
  • sufficient viral particles present at site of infection
  • cells at site of infection susceptible and permissible
  • host defences inactive or absent
70
Q

how do dogs get distemper?

A
  • transmission from recently infected animal or fresh formites
  • virus enters host via aerosol droplets that contact upper respiratory tract epithelium
  • viral replication within 24hrs in local tissue macrophages then spreads via these cells to local lymphoid tissue
  • widespread viraemia and viral proliferation within lymphoid, acute fever and leukopaenia
  • viral invasion of epithelial tissue and CNS depending on dogs humoral & cell mediated immunity and viral virulence
71
Q

what is viral tropism?

A

ability of virus to selectively infect particular cell types

72
Q

what is enterotropic?

A

virus replicates in cells of GIT

73
Q

what is it called when virus replicates in cells of nervous system?

A

neurotropic

74
Q

what are determinants of tissue tropism?

A
  • accessibility
  • susceptibility
  • permissiveness
  • immune response
75
Q

viruses passed in faeces generally more resistant to environmental inactivation. true/false?

A

true

76
Q

what are some possible outcomes of foetal infection?

A
  • abortion/stillbirth
  • foetal malformation
  • foetal tolerance
  • recovery with no adverse effects
77
Q

with BVDV, what happens if infection occurs 80-125 days?

A
  • defects in brain and eye tissues
  • surviving calves remain infected for life
  • become immune tolerant of virus
  • later die of mucosal disease from viral mutation
78
Q

with BVDV, when would foetal death and resorption occur?

A

<80days gestation

79
Q

with BVDV, what is the 125 day gestation threshold significance?

A

immune system fully developed in foetus by 125 days

80
Q

what are patterns of infection a result of?

A

interplay between characteristics of viral lifecycle and host immune response

81
Q

acute infection is…

A

brief, self-limiting infection

82
Q

chronic infection is…

A

long-lasting, from months to life

83
Q

latent infection is…

A

resting/hiding, viral recrudescence

84
Q

slow infection is…

A

maybe long preclinical phase, can infect others in this time

85
Q

what viruses cause epithelial damage leading to secondary bacterial infections?

A
  • canine parvovirus - septicemia

- foot & mouth - bacterial infection

86
Q

what viruses cause immune damage leading to secondary infection?

A
  • FIV - infecting lymphocytes and monocytes - reduced cell mediated immunity
  • measles cause immunosuppression
87
Q

what is immunopathology

A

damage caused by host immune response

88
Q

what is a result of immunopathology?

A

hypersensitivity reactions

89
Q

what is an example of a virus that causes immunopatholgy?

A

feline infectious peritonitis (FIP)

90
Q

what happens when immune system recognises host proteins as foreign?

A

autoimmune disease

91
Q

what can cause autoimmune disease?

A
  • molecular mimicry
  • revealing previously hidden antigens
  • incorporation of host proteins in virions
  • persistent infection
92
Q

what is viral oncogenesis?

A

viral infection leading to tumour production

IVP (1 decks)

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