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block 4 > Rhabdovirus, reovirus, birnavirus > Flashcards

Rhabdovirus, reovirus, birnavirus Flashcards

1
Q

rhabdoviruses of interest

A
  • rabies

- vesicular stomatitis virus

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2
Q

reoviruses of interest

A
  • blue tongue virus
  • African horse sickness virus
  • rotavirus
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3
Q

birnaviruses of intrest

A
  • infectious bursal dx virus
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4
Q

rhabdoviridae general characteristics

A
  • neg sense RNA
  • enveloped
  • distance bullet shape
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5
Q

rhabdoviridae life cycle

A
  • entry = membrane fusion, take up by endocytosis and that acid of endoscope -> triggers fusions
  • raps rna in nuceloprotein; can’t produce any protein until transcribe genome -> mrna which can turn into varied of different proteins
  • exit= via budding
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6
Q

rabies distribution

A
  • worldwide distribution
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7
Q

rabies transmission

A
  • biting, primarily by bat bite
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8
Q

rabies presenations

A
  • urban: dogs

- syllabic rabies: wildlife (primarily what we see in us)

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9
Q

sylvatic rabies effects who

A
  • bats
  • racoons
  • foxes
  • skunks
  • woodchucks
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10
Q

raccoon out during the day

A
  • rv and distemper
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11
Q

rabies pathogenesis

A

inoculation from bite of rabid animal -> local replicaiton -> attachment and infection or peripheral nerves at motor end plate -> retrograde spread w/ in axoplasm of peripheral nerves -> spread to spinal cord and brain -> replicate in brain -> centrifugal spread from brain to salivary glands and other tissues -> secretion into saliva and transmission via biting

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12
Q

how does rabies gain access to cns

A

neurons endocytosis through cell body then gain access to cns then spreads neuron to neuron;

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13
Q

what happens if rabies infects through sensory nerve endings

A

gets stuck in dorsal root ganglion

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14
Q

rabies gross id

A

normal appearance brain and spinal cord

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15
Q

rabies histopathology

A
  • mild changes

- cytoplasmic eosinophilic inclusion bodies in neurons of hippocampus and cerebellum- negri

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16
Q

rabies pathology

A
  • mild perivascular cuffing and mononuclear cell infiltrates
  • no neuronal loss, see disorganization axon and dendritic connections
  • no gross changes
  • no histopath
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17
Q

incubation period of rabies

A
  • 14-90 days
  • up to 2 years
    length incubation period depends on where bitten
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18
Q

phases of rabies

A
  • prodromal phase

- one of two forms (furious rabies or dumb/ paralytic rabies)

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19
Q

prodromal phase

A

change in temperament (normally friendly animal -> dnt recognize owner, aggressive, normally fearful animal seems friendly)

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20
Q

two forms of second phase or rabies

A
  • furious rabies

- dumb or paralytic rabies

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21
Q

furious rabies signs

A
  • restlessness, nervousness, aggression
  • loss fear humans
  • hypersalviarion
  • hypersensitivity to sound/ light
  • hyperesthesia
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22
Q

dumb or paralytic rabies

A
  • depression
  • paralysis
  • seizures
  • coma, resp arrest, and death
  • harder to pin this down as rabies, tend to see this is larger animals ie cows and horses
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23
Q

laboratory diagnosis of rabies where require what

A
  • approved labs

- require whole brain

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24
Q

lab diagnostics of rabies tests

A
  • direct immunofluorescence (detect rabies antigen)

- RT-PCR (detect viral rna in brain)

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25
Q

prevention and control of rabies

A
  • animal control programs (cat, dog, ferret)

- vaccination (mandatory dogs, cats, domestic ferrets in nys)

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26
Q

post exposure rabies

A
  • for vac animals need rabies booster w/ in 5 days

- un vac animals: euthanasia or quarantine (6 months at owners expense)

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27
Q

protocol animal bite human

A
  • 10 day mandatory confinement/ observation of animal that bites human
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28
Q

prevention of rabies

A
  • avoid handling wild animals
  • screen windows to prevent bat access
  • vac at risk individuals
  • post exposure prophylaxis
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29
Q

post-exposure prophylaxis rabies

A
  • clean wound w/ soap/ water or iodine solution
  • seek medical attention
  • post exposure immune globulin
  • series of vac over course month
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30
Q

rabies virus type

A

rhabdoviruses

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31
Q

vesicular stomatitis virus virus type

A

rhabdoviruses

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32
Q

vesicular stomatitis virus causes what in who

A
  • vesicular dx
  • cow, horse, pig
  • rarely also in sheep and goats
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33
Q

vesicular stomatitis virus horse significance

A
  • if vesicular dx in horse its not foot and mouth its vsv
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34
Q

vesicular stomatitis virus serotypes

A

2

  • new jersey
  • indiana
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35
Q

vesicular stomatitis virus vs foot-and-mouth dx

A
  • clinically indistiguishable
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36
Q

vesicular stomatitis virus transmission

A
  • biting insects
  • fomites (via breaks in mucosa)
  • doesn’t transmit animal to animal
  • no viremia in domestic animals, dx not contagious
  • ZOONOTIC
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37
Q

vesicular stomatitis virus seen when

A

seasonal (bc insect vecor0

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38
Q

vesicular stomatitis virus in us

A
  • endemic in pt of southeaster US occasional outbreaks in south west
  • REPORTABLE
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39
Q

vesicular stomatitis virus economic impact

A
  • losses bc culling, dec milk, costs
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40
Q

clinical signs vesicular stomatitis virus

A
  • transient fever
  • lameness
  • vesicles and erosions (usually in mouth can -> inc salivation, teats, coronary band lesions)
  • horses: most severely affected, oral lesions, coronary band lesions
41
Q

diagnosis vesicular stomatitis virus clinically

A
  • can’t distinguish from other vesicular dxs unless in horses bc the dnt get foot and mouth
  • lesions generally restricted to one area of body
42
Q

lab diagnostics vesicular stomatitis virus

A
  • viral antigen (elisa)
  • virus neutralization
  • antibody (elisa, paired serum sample)
43
Q

differential diagnoses vesicular stomatitis virus

A
  • vesicular stomatitis virus
  • foot and mouth dx
  • swine vesicular dx
  • Seneca valley virus
44
Q

control vesicular stomatitis virus

A
  • control movement of animals
  • quarantine infected faciliies
  • separate healthy/ died animals
  • disinfect milking machines
  • milk affected animals last
  • control insects
  • vac available but not really used
  • REPORTABLE
45
Q

Rabies virus index of suspicion

A
  • maintain high index of suspicion bc you see rarely but its v bad to miss
46
Q

reoviridea general characteristics

A
  • nonenveloped
  • double or tripple layered capsid
  • segmented dsRNA genome
  • 5 genera of vet importance
47
Q

transmission orthoreoviruses and rotaviruses

A

fecal oral

48
Q

transmission oribiviruses (blue tongue and African horse sickness virus) and coltiviruses

A

biting insects

49
Q

transmission aquareoviruses

A

water

50
Q

orbiviruses include

A

blue tongue

African horse sickness virus

51
Q

orbivirus replciation

A

replicate in insects and mammals

- this means can overcome mammalian innate and adaptive immune system and insect innate immune system

52
Q

orbivirus transmission

A
  • blood eating insects

- non-contagious

53
Q

orbivirus infect what

A
  • prolonged cell associated viremia

- infect and damage endothelial cells -> damage

54
Q

blue tongue dx spread

A
  • spread by biting midges (no seeums)
55
Q

blue tongue virus affects who and infects who

A
  • infects ruminants but clinical dx = severe in sheep
56
Q

blue tongue dx control

A
  • hard to control bc variety of serotypes around

- serotype in Europe = more severe dx than serotype currently in us

57
Q

economic importance blue tongue us and europe

A
  • us: low virulence serotype blue tongue, greatest impact on cattle industry -> lost money bc loss trade and cost animal testing
  • europe- sigificant emergence blue tongue virus -8 in Northern Europe
58
Q

sheep susceptibility to blue tongue virus + morbidity and mortality

A
  • dx severity varies with serotype and strain of virus
  • morbidity = up to 100%
  • mortality = up to 50%
59
Q

cattle and goats blue tongue virus morbidity/ mortality/ dx

A
  • low morbidity - 5%

- clinical dx = rare

60
Q

deer, antelope, pronghorn blue tongue virus morbidity/ mortality/ dx

A
  • severe dx
  • morbidity up to 100%
  • mortality 90-100%
61
Q

Blue tongue virus transmission

A
  • midges (gnats)
  • ticks, sheep keds (mechanical)
  • mechanical
  • general (in semen but unlikely route of transmission)
62
Q

blue tongue virus lifecycle

A
  • adult female feeds, virus replicates inside insect 4-20 days, then infected adult bites again and if bites susceptible host infects suceptible host, susceptible hosts viremic 2-4 days
  • other modes transmission possible but this one via biting midge = most common
63
Q

blue tongue virus epidemiology

A
  • dx occurs late summer when vector = most numerous
  • geo distribution mirror that of insect vector (tropical, subtropical, and temperate zones across the world; if in tropics virus persists year round if there is winter dx disappears in winter then reappears)
64
Q

blue tongue virus overwintering theories

A
  • prolonged viremia (viremia late fall to spring so infectious for insects in spring)
  • transplacental transmission
  • persistent infeciton ys T cells
65
Q

blue tongue virus pathogeneiss

A
  • saliva of biting midge
  • local spred
  • viral réplication in regional lns
  • viremia
  • virus réplication in hematopoietic cells and endothelial cells (endothelial ell infection -> clinical signs) ->
    1. endothelial damage ->
    1a. vascular occlusion -> tissue edema or epithelial sloughing bc loss microvasculature
    1b. hemorrhage
    2. cell associated viremia (prolonged) -> new vectors become infected by feeding on viremic animal
66
Q

blue tongue clinical signs

A
  • fever, face, feet
  • weight loss
  • edema*****
  • hyperemia muzzle, face, neck
  • rarely cyanotic mucosa (ie blue tongue)
  • salivation
  • resp (heavy breathing / panting)
  • sores tongue, mouth, nostrils
  • lamness (if on hard surface)
  • aborption, congenital abnormalities (repro)
67
Q

blue tongue pathology

A
  • edema and hyperemia of mucosa
  • petechial hemorrhages
  • abrasions or ulcers lips, dental pad, tongue, cheeks
  • hemorrhage tunica bee of luminary artery
  • pathoneumonoc for blue tongue but see this rarely
68
Q

blue tongue in us

A

REPORTABLE

69
Q

blue tongue immunity

A
  • systemic antibody response -> lifelong protection against infectiong serotype
  • lambs born to immun ewes= partially protect by colostral immunoglobulins
  • vac (use in rare cases when outbreak hard to keep up bc virus evolves quickly and mult serotypes)
70
Q

blue tongue control

A
  • vectors control (get rid of place insects breed)
  • housing (covered buildings
  • > dec insects)
  • move to higher altitudes during insect season
71
Q

blue tongue virus type

A

reoviruses

72
Q

African horse sickness virus virus type

A

reoviruses

73
Q

African horse sickness virus affects who where

A
  • serious dx horses
  • affects donkeys and mules but not as much as horses
  • zebras = natural resrvious but are asymptomatic carriers
  • not in us
  • sub-saharan, central, east, south, africa
74
Q

African horse sickness transmisison

A
  • very high mortality
75
Q

African hrose sickness concern

A
  • that dx will spread with inc range vector
76
Q

african horse sickness forms

A
  • peracute dx

- subacute edematous form

77
Q

African horse sickness peracute dx signs

A
  • acute fever
  • sudden onset resp distress
  • terminally spasmodic c+and frothy nasal exudate
  • rapid death (30 min - 1-2 hrs)
78
Q

African horse sickness subacute edematous form

A
  • fever 3-6 days
  • edema (supraorbital fossa and eyelids)
  • colic
  • petechiae under tongue and on conjunctivae
79
Q

African horse sickness diagnosis

A
  • clinical signs and hx
  • lab tests: viral isolation and id, serology, necropsy
  • REPORTABLE
  • no tx
80
Q

rotavirus virus type

A

reoviruses

81
Q

rotavirus affects who and causes what

A
  • infects all domestic animals

- d+ in intensively reared young animals (neonatal scours)

82
Q

rotavirus transmission and stablity

A
  • fecal oral transmission

- v stable in environment

83
Q

rotavirus pathogenesis

A
  • infects mature enterocytes and enteroendocrine cells in proximal ileum, crypt cells = spared
  • mature enterocytes = infected at tip; kill apical enterocyte villi which become blunted and loose ability to absorb and get inc fluid and electrolyte loss
  • enteroendocrine cells = infected (along with enterocytes) then produce serotonin -> inc mobility and peristalsis of gut
  • virus release its own toxin -> secretion cl- ions -> water loss
  • epithelial cells stop secreting disaccharide like lactase -> change osmotic conditions -> bacteria overgrowth
  • NOT leakage dx bc gut enterocyte tigh junctions remain tight
84
Q

rota virus clinical features

A
  • affects young animals (1-8 weeks)
  • recover rapidly
  • stress can worsen dx
85
Q

rotavirus clinical signs

A
  • white scours or milk scours
  • feces may be mucoid
  • depression but eating
86
Q

rota virus tx

A
  • supportive tx
87
Q

rota virus immunity

A
  • mucosal immunity = protective- IgA
  • colostrum = protective for short time
  • vac: give to preg cows (modified live) or vac new calf give to unvaccinated dam or that didn’t get colostrum
88
Q

rota virus control

A
  • housing
  • separate dxed and healthy
  • hygiene
89
Q

birnaviridae general characteristics

A
  • non enveloped
  • ds rna
  • two segments
90
Q

infectious bursal dx virus what type of virus

A

birnaviridae

91
Q

infectious bursal dx virus alt name

A

gumboro dx

92
Q

infectious bursal dx virus affects who where

A
  • chickens

- worldwide

93
Q

infectious bursal dx virus important

A
  • economically important
94
Q

infectious bursal dx virus infects what

A
  • primarily bursa of Fabricius (pre-b lymphocytes -> acquired B lymphocyte deficiency)
95
Q

infectious bursal dx virus isolates

A
  • isolates in us = low virulence

- v virulent isolates can -> mortality rates > 50%

96
Q

infectious bursal dx virus transmission

A
  • fecal oral
  • v stable and highly contagious also spread by fomites and insects
  • hard to disinfect
97
Q

infectious bursal dx virus pathogenesis

A
  • infects pre-b cells in bursa of rabricius
  • clinical d in chicks 2-6 weeks
  • loss b-lymphocytes -> permanent immunosuppression
  • most severe immunosuprsson in chicks infected closer to hatch
98
Q

clinical signs infectious bursal dx virus

A
  • feather ruffling
  • trembling/ dehydration
  • watery d+
  • recovered birds = permeant immunosuppression (inc susceptibility to other viral infections and poor response to vac)
99
Q

infectious bursal dx virus control

A
  • difficult
  • can give oral live attenuated vac to breeders; passive transfer immunity to hatching chick; not fully affective plus possibility of vaccine reversion
  • newer vac antibody-coupled ibdv give at 1 day
  • once chicks > 8 weeks virus not that big a deal

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