Virology Test 4 Flashcards

1
Q

What type of infections spread respiratory virus

A

Latent infections

persistent infections

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2
Q

What are the common small animal latent respiratory viruses

A

Alpha-herpes
FHV-1 in cats
CHV-1 in dogs

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3
Q

What are the common small animal persistent respiratory infections

A

FCV - calicivirus in Cats

Distemper - Morbillivirus in Dogs

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4
Q

What factors facilitate the spread of respiratory virus and expression of clinical signs

A
Stress - immunosuppressive
Poor Nutrition
Overcrowding
High turnover of animals (high exposure)
Weaning
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5
Q

What are the common feline upper respiratory viruses

A

FVR - feline viral rhinotrachtiious (FHV-1 herpes)

FCV - Feline calicivirus

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6
Q

What are the common bacterial respiratory infections

A

Chlamydophilia felis

Bordetella Bronchiseptica

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7
Q

What is the Alpha-Herpes Virus in Dogs

A

CHV-1

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8
Q

What is the Alpha-Herpes Virus in cattle

A

IBR - Infectious bovine rhinotracitious

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9
Q

What is the Alpha-Herpes Virus in equine

A

EHV-1 myelenocephalopathy

EHV4 - Rhinopneumonitis

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10
Q

What is the Alpha-Herpes Virus in chickens

A

Mareks Disease Galid HV-2

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11
Q

What is the Alpha-Herpes Virus in swine

A

Pseudorabies Suid HV-1

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12
Q

What is the Alpha-Herpes Virus in monkey

A

Macacine herpes B-virus

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13
Q

What is the Alpha-Herpes Virus in cats

A

FHV-1 feline viral rhinotracitious

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14
Q

What is the Alpha-Herpes Virus in humans

A

chicken poc Varicella zoster v

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15
Q

Which hepres virus has rapid replication, lyse the cell, and is latent in the sensory gangalia

A

ALPHA

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16
Q

which herpes virus replicate slowly, have continous shedding, and cells get large

A

BETA

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17
Q

which herpes virus are lymphtropic and latent in lymphocytes

A

GAMMA

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18
Q

What type of Virus are FVR, IBR, EHV-1&4, Markets, Pseudorabies, Macaque B

A

Alpha-herpes

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19
Q

What type of virus is porcine cytomegalovirus

A

Beta-herpes

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20
Q

what type of virus are MCF, BHV-4, EHV2&5

A

Gamma-herpes

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21
Q

What is the mode of transmission for Feline infectious Respiratory Dz

A

direct aerosol transmission

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22
Q

What cats are at greatest risk for feline infectious respiratory Dz

A

young kittens
vaccinated cats
high density groups

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23
Q

Where does the glycoprotein peplomer of FVR(FHV-1) bind

A

heprin sulfate proteglycan receptor on the host cell

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24
Q

FVR(FHV-1) replicates in the nucleus and causes what

A

intranuclear inclusion bodies

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25
Q

Who does FVR(FHV-1) infect

A

Felidae but domestic cat is the main host

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26
Q

Where does FVR(FHV-1) persist in the body

A

trigeminal ganglion
optic nerve
optic bulb
cornea

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27
Q

What is recurudesence

A

epsoides of virus shedding from stress, birth, lactation, or steriods

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28
Q

Where is FVR(FHV-1) shed

A

oronasal and conjunctival secretions

1 day post infection persist for 2-3 weeks

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29
Q

Where does viral replication of FVR(FHV-1) occur

A
lower body temperatures
epithelia muscosal cells of nasal septum
turbinates
nasopharynax
tonsils
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30
Q

T or F herpes are fragile and don’t survive well in the environment

A

TRUE

require close contact to spread

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31
Q

What clinical signs are seen with FVR(FHV-1)

A
sneezing
lacrimation
serous to mucopurlent discharge
cough
hypersalivation
fever
anorexia
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32
Q

T or F Alpha hereps only repliate in upper respiratory tract

A

TRUE

2nd bacterial infection.pneumonia RARE

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33
Q

If the FVR(FHV-1) infection gets in the cornea what is seen

A

keratitis

ocular ulcers

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34
Q

what can be seen with FVR(FHV-1) infections in pregant cats

A

abortion

general Dz in newborn kitten - encephalitis, necrotizing hepatitis

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35
Q

When FVR(FHV-1) viral replication permanently damages turbinates the cat is predisposed to what

A

chronic rhinitis and sinusitis

B. bronchiseptica

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36
Q

T or F FVR(FHV-1) vaccination will prevent infection

A

FALSE - just prevent clinical Dz can still get virus and even shed it

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37
Q

T of F FVR(FHV-1) is a core vaccine

A

TRUE

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38
Q

Why is MLV recommended for FVR(FHV-1)

A

induces faster and better protection

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39
Q

Who is susceptible to FCV

A

all Feliadae

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40
Q

When is clinical Dz of FCV seen

A

kitten under 1

cheetahs

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41
Q

How long will a recovered cat shed FCV

A

30 days to a lifetime

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42
Q

T of F Caliciviruses are resistant in environment and can survive for days

A

TRUE

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43
Q

how is FCV transmitted

A

fomites

caretakers

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44
Q

What cells does FCV have affinity for

A

oropharyngeal epithelium
alveolar pneumocytes
cancasue pneumonia

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45
Q

FCV usually is seen as an acute oral and UPI with what signs

A

oral ulceration of tongue and palate
fever
sneezing
serous nasal discharge

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46
Q

IF FCV replicates in the oral cavity epithelium what is seen

A

vesicles and ulcers

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47
Q

if FCV replicates in alveolar epithelium what is seen

A

interstitial pneumonia

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48
Q

Some strains of FCV causes fever in acute synovitis that results in

A

limping kitten
lameness/joint swelling
immune complex driven

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49
Q

A highly virulent strain of FCV has been reported as acute, fatal septicemia due to

A

DIC, pancreatitis, hepatic and enteric necrosis

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50
Q

T or F FCV tends to be milder than FHV-1

A

TRUE

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51
Q

What tropism has the VS-FCV acquired

A

infects macrophages and endothelial cells in liver and pancreas

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52
Q

what signs are seen with VS-FCV

A
fever
SQ edema
ulcers on skin and paws
widespread hemmorrhages
thromboembolism
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53
Q

How is FCV diagnosed

A

clinical signs and history

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54
Q

Why is serology not useful to diagnosis FCV

A

most cats have high titer from vaccine or natural infection

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55
Q

What is the Gold standard test from FCV

A

Virus isolation from nasal or conjunctiva swab

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56
Q

IS RT-PCR used to Dx FHV-1 & FCV

A

not really you have to be cautious on a positive sample

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57
Q

Severe naso-ocular signs lead to what Dx in feline

A

FHV-1

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58
Q

corneal ulceration in feline is Dx for what

A

FHV-1

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59
Q

Oral ulceration and synovitis in cats is suggestive of what

A

FCV

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60
Q

T or F cats free of clinical symptoms of FCV & FHV-1 with good vaccination history can be subclinical shedders

A

TRUE

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61
Q

Canine infectious respiratory Dz (CIRD) is caused by what

A

Kennel cough

ITB

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62
Q

the complex syndrome that is caused by infection with a combination of bacterial and/or viral agents in dogs is called

A

kennel cough

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63
Q

what infectious agents are able to cause respiratory Dz in dogs by themselves

A

distemper

influenza

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64
Q

What are the common viral canine respiratory pathogens

A
parainfluenza
adeno-2
distemper
influenza
corona
hepres-1
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65
Q

what are the common bacterial pathogens that cause canine respiratory Dz

A

Bordetella Bronchiseptica
Streptoccous equi
mycoplasma spp

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66
Q

What are the most commonly isolated respiratory pathogens in dogs

A

parainfluenza
bordetella
adenovirus - 2

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67
Q

Signs of canine distemper

A

respiratory + GI + CNS

pneumonia, conjunctivitis, vomiting, scours, seizures

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68
Q

what are the canine flu viruses

A

H3N8

H3N2

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69
Q

What lesion is seen with distemper in dogs

A

interstitial pneumonia

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70
Q

T or F canine corna is usually a co-pathogen in canine respiratory Dz

A

TRUE

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71
Q

T or F Canine Respiratory Corona is Antigenically distinct from enteric corona

A

TRUE

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72
Q

T or F Bordetella is potentically zoonotic

A

TRUE

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73
Q

How is kennel cough transmitted

A

direct contact with aerosolized respiratory secretions

fomite

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74
Q

T or F kennel cough spread more in confined dogs with poor ventilation

A

TRUE

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75
Q

What is the primary target of kennel cough viruses

A

upper airway epithelium
necrosis
inflammation
dysfunction cilia

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76
Q

T or F kennel cough is owrse with exercise

A

TRUE

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77
Q

How can you elicite a cough when examining a dogs suspected of having kennel cough

A

palpating trachea

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78
Q

How is CIRD Dx

A

clinical signs and history of exposure

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79
Q

What respiraoty vaccine are core

A

CpiV
CAV-2
CDV

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80
Q

When do you vaccinate for bordetella

A

high density

intranasal MLV

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81
Q

what does bordetella cause in humans

A

immune suppression

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82
Q

Why isnt virus isolation used to Dx CIRD

A

false negative if viron # low

slow turn around

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83
Q

why isn’t PCR used to Dx CIRD

A

no available for all virus
can detect MLV vaccine
False neg if sample degrades

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84
Q

what not use serology for Dx CIRD

A

natural exposure and previous vaccination cause problems

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85
Q

what is the primary control measure for CIRD

A

HYGIENE
reduce contact dog-dog
prevent indirect transmission

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86
Q

how can you reduce CIRD shedding to healthy dogs

A

isolation ward for coughing dogs

Tx as outpatients

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87
Q

How can you reduce stressor for CIRD

A

avoid high density confinement

good air quality

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88
Q

What type of viruses are influenza

A

Orthomyxoviridae
RNA enveloped
6-8 segments of genome

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89
Q

Who does Flu A effect

A

birds
horses
swine
humans

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90
Q

Who does flu B effect

A

Humans - common flu

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91
Q

who does flu C effect

A

humans and swine - no Dz

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92
Q

who does thogotovirus effect

A

tick-born, infects livestock

no Dz

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93
Q

who does isavirus effect

A

salmon anemia virus

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94
Q

What is flu nomenclature

A
virus type (ABC)
species
geographic orgin
strain no
year of isolation
H & N subtype
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95
Q

What is the viral receptor bind protein for flu

A

H - Hemagluttinin

17 subtypes

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96
Q

What is the flu protein that facilitates budding and cell to cell spread of virus

A

N - Neurminidase

10 subtypes

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97
Q

What protein identifies virus as an influenza strain

A

Matrix protein

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98
Q

What are the 2 steps in flu virus infection of a cell

A

1 - H on virus binds to sialic acid receptor

2 - Host cell protease cleaves viral H

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99
Q

T or F Flu host cell must be permissive to the flu virus can’t occur

A

True

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100
Q

What flu protein induces apoptosis in monocytes and macrophages

A

PB1-F2

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101
Q

which flu protein block IFN secretion by infected cells

A

NS-1

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102
Q

Why do chicken get multi-systemic disease from H5N1 and H5N2

A

cells in many organs are permissive for virons

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103
Q

why do aquatic waterfowl not expirence clinical Dz with the flu

A

only permissive cells are in the intestinal tract so the virus doesn’t spread systemically

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104
Q

What animals have sialic acid receptors for both avian and human influenza

A

Swine

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105
Q

Where does genetic re-assortment of human and avian flu occur

A

Swine

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106
Q

What is the only animal that can be infected with avian, human, and swine flu

A

Swine

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107
Q

human flu outbreak of global proportions from a new virus for which people have no immunity. spread easily from person-person

A

Pandemic Flu

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108
Q

seasonal flu virus that circulate through population. people have immunity from past infections and vaccinations.

A

Epidemic - usually type B

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109
Q

What happens when flu viruses kill humans via cytokin storm

A

over-reaction of the immune system causes a fatal acute inflammatory respiratory Dz
Mortality about 60-80%

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110
Q

Virion acquire new surface proteins
segmented viruses exchange genome segments
pandemic flu

A

Antigenic Shift

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111
Q

Virons have slight change in surface protein
point mutations
epidemic flu

A

antigenic drift

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112
Q

What are avian flus

A

Fly type A with H5 or H7 that infects poultry

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113
Q

T of F avian influenza is OIE notifiable

A

TRUE

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114
Q

Mild Dz in birds
no human threat
single Arginine at HA site
only respiratory and GI cells

A

Low Path AI

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115
Q

causes > 75% mortality in birds
several amino acids at HA site
tissue tropism
human threat

A

high path AI

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116
Q

how is AI transmitted

A

direct contact with respiratory droplets or feces
aerosol - close contact
fomities

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117
Q

What strains of AI are common in wild birds

A

low path - no clinical signs

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118
Q

what strains of AI are rare in US flocks

A

High Path

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119
Q

what are sigsn of High path AI

A
sudden death 
depression/ ruffled featehrs
swollen combs
scours
no shell, low egg prod
cough, sneez, discharge
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120
Q

high path AI lesions

A

comb swell

multifocal petechial hemorhages& infarcts

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121
Q

mortality of High path AI

A

75-100%

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122
Q

What is used to Dx AI

A

RT-PCR - sequence M then test for H5 or H7 genes
Virus isolation - tracheal or cloacal swabs from live bird
Serology - screen flocks

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123
Q

How is AI surveillance done

A

wildlife surveillanve
domestic bird surveillanve and diagnsotics
smuggling interdiction & trade ocmpliance

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124
Q

What type of survillence - USDA is testing Alaska birds in costal areas

A

wildlife survillence

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125
Q

what type of survelliance is NPIP and live market look outs

A

domestic bird

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126
Q

what type of surveillance is looking for smugglers

A

smuggling interdication and trade compliacne (SITC)

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127
Q

what are the 2 form of swine flu

A

acute - outbreak recover 4-6 days
100% morbidity
1% mortality
Andemic - subclin - bacterial pneumonia with PRRS

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128
Q

Lesions with sine influenza

A
demarcked purple to red lesion on lungs
atelectasis
consolidation of cardiac and apical obes
frothey exudate in ariway
edema in cervical and mediastinal mn
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129
Q

Since swine flu replicates in the bronchial epi cells what is prinicipal lesion

A

necrosis of airway epithelium - 2nd bacterial pneumonia

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130
Q

how do you Dx swine flu

A

nasophyaryngeal secretions on sacron swab
RT-PCR
IHC - formlin tissues
Serology - paired samples

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131
Q

why would serology Dx of flu not be helpful

A

if the herd was vaccinated it will show up

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132
Q

what are control measure form swine flu

A

vaccination

biosecurity

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133
Q

H7N7 & H3N8

A

Equine flu

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134
Q

T or F no clincal Dz has occurred from H7N7 in past 25 years

A

TRUE

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135
Q

What are the 2 lineages of H3N8

A

Euraisian & America - circulate world wide

multiple strains of each

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136
Q

what are animals are most suseptiable to flu

A

young

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137
Q

If a horses doesn’t have sufficienct levels of flu antibodies the duration of immuntiy is

A

short

months to a year

138
Q

what is causes problems with vaccine failure to protect agaisnt equine flu

A

antigenic drift

139
Q

What does natural flu infection generate

A

IgA

140
Q

how long does equine flu vaccine last

A

3-4 months
vaccine - IgG
poor CMI inducer

141
Q

What is teh most common and economically important viral respiratory Dz of horses

A

EIV

142
Q

why are equine flu outbreaks common

A

subclin shedders - partial immunity
vaccinated horses can shed with no signs of illness
congerating young horses

143
Q

epidemic horse respiratory Dz in young animals

A

fever, cough, discharge, anorexia
last up to 3 weeks
morb 100%
mort 0

144
Q

How is EIV usually acquired

A

direct contact

aerosols inhalation

145
Q

T or F fomites can spread equine flu

A

TRUE

traliers, vet equipment, clothing , buckets

146
Q

When do you vaccinate foals for EIV

A

after 6 months were maternal antibody is gone

147
Q

when do you vaccinate pregant mares for EIV

A

2-6 weeks before birth to boost passive transfer

148
Q

what is EIV vaccine protocol

A

initally a series of 3 then bi-annual or annual

149
Q

wheere did canince flue H3N8 first appear

A

racing greyhounds with hemmorrhagic pneumonia in 2004

150
Q

Where did H2N8 come from

A

Horses but transfer its entire genome

151
Q

Where was H3N2 isolated

A

Phillipines in 2007

152
Q

What flu is circulating in dogs in asia

A

H3N2

153
Q

Why is there concern about the close contact between humans and dogs

A

new flu pandemic strain

154
Q

what does canicne flu look like

A

kennel cough

80% URI

155
Q

how is canine influenza Dx

A

serology paired serum 4 fold increase

156
Q

Are PCR test available for canine flu

A

only A subtypes

157
Q

T or F canine flu is a core vaccine

A

FALSE

158
Q

T or F viral replication of herpes is required to establish latency

A

FALSE

159
Q

Lytic cycle of herpes

A

infection of epithelial cells
productive virus infection - virons
expression of viral proteins
infected cell lysed

160
Q

Latent cycle of herpes

A

infection of neuron or CD8T-lymphocytes
viral nucleic acid transcription and translation of viral genes
NO virons formed
host immune system does not detect virus

161
Q

What does re-activation of herpes involve

A

switch from latent to lytic infection

162
Q

What seen with herpes of the respiratory system

A

upper respiratory coughing

163
Q

what is seen with herpes of the ocular system

A

conjunctivites

corneal ulcers

164
Q

what is seen with herpes of the reproductive system

A

abortion

genitalia vesicles

165
Q

what is seen with generalized infection of herpes

A

necrosis in lungs and kidneys

166
Q

What are the equine alpha-herepes

A

1,3,4,6,8,9

167
Q

what are the equine gama-herpes

A

2 & 5

168
Q

what does EHV-1 cause

A

equine abortion
respiratroy disease
myeloencephalopathy
abortion and neonatal septicemia

169
Q

what does EHV-3 causes

A

equine coital exanthema

170
Q

what does EHV-4 causes

A

equine rhinopneumonitis

171
Q

what does EHV-6,8&9 cause

A

respiratory Dz in donkeys and zebras

172
Q

What does EHV-2 cause

A

pneumonia in foals and conjunctivities

cytomegalovirus

173
Q

what does EHV-5 cause

A

equine multinodular pulmonary fibrosis

174
Q

Are herpes susceptible to disinfectants

A

YES

175
Q

once latency of herpes is establish how long does it last

A

life - long

176
Q

What is the immunity of herpes

A

short term despite persistance of IgG in serum

177
Q

T or F horses can be re-infected with herpes multiple time in life

A

TRUE

178
Q

What cells are important in preventing systemic dissemenition of herpes

A

cytotoxic T-cells

179
Q

What is the common cause of respiratory Dz in young horses

A

EHV-4 endemic world wide

180
Q

How is EHV-4 transmitted

A

inhalation of infected droplets
nasal secretions/discharge
fomites

181
Q

Where does EHV-4 establish latency

A

trigeminal ganglion - intervates nasal mucosae

182
Q

Why is age a risk factor for EHV 4

A

foals get EHV-4 from mothers
more sever Dz
shed large # virons in nasal secretions
passive transfer only last about 6 months

183
Q

Pathogensis of EHV-4

A

virus inhaled
binds to and replicates in UR epi causing necrosis
virus spreads down into deeper parts of respiratory tract and lympoid tissue
leukocyte associated viremia
latency in trigeminal ganglion

184
Q

what are the signs of EHV-4

A
fever
cough
rhinitis
conjunvtivitis 2-20 days
recovery 2-5 days
cough last up to 3 weeks
185
Q

what are the 4 syndromes caused by EHV-1

A

respiratory
myceloencephalopathy
abortion
neonatal secretions

186
Q

T or F EHV-1 is endemic in horses

A

True

187
Q

what 3 organ systems are involved in EHV-1 infections

A

respiratory tract
uterus & placenta
CNS

188
Q

Final common pathway for tissue injury of EHV-1 is

A

damage to vascular endothelium

vasulities necrosis thrombosis and ichemia

189
Q

Pathogenesis of EHV-1

A

infection of endothelium causes cell death
inflammation and activation of clotting factors
ischemia & necrosis

190
Q

WHat causes abortions with EHV-1

A

vaculitis in placenta, endometrium or fetus

191
Q

What causes myeloencephalopathy with EHV-1

A

vasculitis and not by direct viral infection of neural tissue

192
Q

T or F humoral immunity is protective against EHV-1

A

FALSE

its cell-ass during viremia not free in plasma

193
Q

T or F Mares will abort many times with EHV1

A

FALSE usually only once but can still shed virus

194
Q

What causes CNS disease with EHV1

A

point mutation from G to A within ORF gene

195
Q

pathogensis of neurotropic EHV varients

A

replicate to very high titer
increased leukocyte-ass viremia
infection and necrosis of eno cells in CNS
vasculitis

196
Q

what lesions is seen with neurotropic EHV-1

A

mutlifocal distrubtion

197
Q

T or F neurotropic EHV1 sheds short period of time

A

FALSE - longer 21 days instead of 7-20

198
Q

T or F horses with myeloencephalopathy are especially contagious

A

True

199
Q

signs of EHV-1 myeloencephalopathy

A

fever by 24-72 hours
rapid neuro signs stabilize 1-2 days
spinal white matter involvment

200
Q

Clinical signs of EHV-1 myeloencephalopathy

A
ataxia & paresis
toe dragging, stumbling
hindlimbs
hypotonia of tail and anus
fecal and urinary incontinence
crainal nerve deficits
201
Q

when does EHV-1 abortion occurs

A

last trimester

28% of pregant mares

202
Q

What is the gold standard EHV test

A

Virus isolation but it takes 5-7 days

203
Q

RT- PCR of EHV is helpful for what

A

distinguishing latent from active infection

204
Q

Dx test for the presence of EHV

A

IFA and IHC on aborted fetus tissues

205
Q

T or F most horses are seropositive to EHV 1 &4

A

TRUE natural infection or vaccine

206
Q

what can distinguish between EHV 1 and EHV 4

A

ELSIA detecting IgG

207
Q

what is a complement fixation test for EHV

A

detects IgM
levels decay >30 days PI
4 fold increase on paried samples =recent infection

208
Q

What is a viral neutrilization test

A

dectects IgG levels
persist for > 9 months
not useful for acute infections only retrospective

209
Q

T or F inactivated EHV 1 & 4 vaccines produce sterilizing immunity

A

FALSE but they do lessen clinical Dz

210
Q

T or F inactivated EHV vaccines make claim on label to prevent abortion

A

TRUE

211
Q

T or F new ts-MLV intranasal vaccine show good efficacy against respiratory Dz and abortion

A

TRUE

212
Q

T or F there are many vaccines to protect horses from EHV myeloencephalopathy

A

FALSE

213
Q

EHV control measures

A
reduce new arrivals and fomite transfer
isolate new arrivals for 21 days
do not add new horses to groups of mares
reduce stress
quarentine sick animals
sanitation
214
Q

what are control measure for EHV-1 abortions

A

rapid diagnosis - necropsy fetus
prevent spreading
vaccinate prego mares routinely

215
Q

control measures for EHV CNS in MO

A
report to state vet
isolation and quarentine
confirm Dx
no mov't on off farms for 28 days
monitior signs of EHV
Do not vaccinate
216
Q

Signs of EHV-2

A

purlent nasal discharge
fever
lymphadenopathy and conjunctivitis - in foals
foals recover 7 days

217
Q

where does EHV-2 establish latency

A

lymphocytes and mononuclear leukocytes draining infected lymphatic tissue

218
Q

What is signs of EHV 3

A

veneral Dz of papular pustular and ulcer lesions on vaginal mucosa, penis, prepuce

219
Q

Where does EHV-3 latency occur

A

sciatic ganglion

220
Q

what is incubation of EHV-3

A

2-10 days
outbreak at 14 days
lesions on mouth of foals

221
Q

How do you control for EHV3

A

Artificial insemination

222
Q

what are the 2 common types of adenovirus in foals

A

Eadv-1

Eadv-2

223
Q

what does adeno virus cause in horses

A

inapparent Dz or mild upper respiratory or mild scours

224
Q

What does adeno cause in arabian foals with SCID mutation

A

fatal pneumonia

225
Q

Where are equine rhinitis virus shed

A

nasal secretions and trasmitted via aersol inhalation

226
Q

Where is equine rhinitis virus A shed long term

A

urine

227
Q

T or F equine rhinitis A is zoonotic

A

TRUE
fever and pharyngitis in humans
inactivated vaccine cond license

228
Q

Inclusion body rhinitis caused by suid herpes -2 causes what

A

cytomegalovirus - forms large basophillic intranuclear inclusion bodies in mucous glands of the nasal turbinates

229
Q

how is suid herpes 2 transmitted

A

direct
aersol
transplacental
urine

230
Q

What age pigs is suid herepes 2 seen in

A

3-5 week old

fever, sneezing discharge eyes

231
Q

T or F Endemic herd infections of suid herpes leads to accelerated atrophic rhinitis

A

TRUE

232
Q

What is seen with generalized infection of suid herpes in piglets less than 3 weeks

A

outbreak of sudden death and anemia

intrauterine exposure

233
Q

how is inclusion body rhinitis Dx

A

histopath on turbinates
PCR - nasal scraping
IFA or ELISA serology

234
Q

Viral pneumonia in cattle cause

A

damage to respiratory epi
decreased alveolar macrophages
immunosupression

235
Q

When does diagnostic and treatment interventions occur with bovine pneumonia

A

stage of bronchopneumonia

difficult to detect viral pathogens at this stage

236
Q

What are the 4 viral pathogens in cattle

A

IBR
PI3
BRSV
BVD

237
Q

how do viral pathogens pre-dispose cattle to bacterial pneumonia

A

reducing normal defense mechanisms

238
Q

pasturella is a virulent bacteria that produces a potent virulence factor

A

leukotoxin that binds and kills ruminant macrophages and neutrophils

239
Q

What can be seen with late stages of bronchopneumonia

A

pulmonary abcesses

bronchiectasis

240
Q

What does histophilus somni produce

A

suppuritive and fibrinous bronchopneumonia

241
Q

IBR BHV-1 is associated with what 2 diseases

A

respiratory and genital

242
Q

BHV5 is associated with what rare disease

A

encephalitis

243
Q

T or F IBR BHV-1 has been found in deer across North America and europe

A

True

244
Q

T or F goats and sheep can be latently infected and reactive IBR BHV-1

A

True

245
Q

T or F Cattle are immune to other ruminant herepes virus and only can get BHV

A

FALSE - can be infected by elk heres

246
Q

What is the most common respiratory disease of feedlot and unvaccinated cattle

A

IBR BHV-1

247
Q

what is the most common age for outbreaks of IBR BHV-1

A

cattle over 6 months being stressed

248
Q

Where does the primary infection of IBR BHV-1 occur

A

respiratory tract
conjunctiva
reproductive tract

249
Q

Where does IBR BHV-1 establish latency

A

sensory ganglia neurons - for life of animal

250
Q

There is local replication of IBR BHV-1 but it can spread to the eyes and lacrimal ducts and even to the

A

trigeminal ganglion

251
Q

what is different about BHV5 than BHV1

A

it can spread beyond the brain trigeminal ganglion and cause non-suppurative encephalitis

252
Q

T or F IBR BHV-1 can cause abortion

A

True - usually follows respiratoy illness in herd or vaccination with MLV
6-8 months of gestation

253
Q

venereal forms of IBR BHV-1 cause

A

pustular vulvovaginitis and balanoposthitis

erosions and ulcers in the vagina and penis

254
Q

T or F in many cases of IBR BHV-1 fibrinopurulent exudate is seen

A

TRUE

255
Q

What are gross lesions in abort fetus IBR BHV-1

A
multifocal necrosis (liver, lungs)
IHC can detect viral antigen
256
Q

what samples are used for PCR testing of IBR BHV-1

A

nasal secretions
tissues
semen
blood

257
Q

What test is used to recent IBR BHV-1 infections

A

IgM - ELISA

4 fold increase in titer

258
Q

T or F both intransal and IM vaccines for IBR BHV-1 stimulate humoral antibody

A

TRUE

259
Q

T or F intranasal and IM vaccines for IBR BHV-1 both stimulate local IgA

A

FALSE

only intranasal

260
Q

what vaccines will be useful in IBR BHV-1 eradication

A

BHV subunit vaccines

able to distinguish it from wild type virus

261
Q

What countires have eridacted IBR BHV-1

A
austria
denmark
finland
sweden
italy
switerzland
norway
262
Q

Who is the host for BRSV

A

cattle but it can infect sheep and goats

263
Q

T or F matenal antibodies provide good protection from BRSV

A

FALSE

264
Q

How is BRSV transmitted

A

aersol

direct contact

265
Q

what does BRSV cause

A

rhinitis
tracheitis
intersitital pneumonia

266
Q

primary infection of BRSV is usually seen as sudden outbreak of

A

acute respiratory Dz
most recovery in 1 week
some die of fatal pneumonia

267
Q

lesions seen with BRSV

A

lungs that fail to collapse and emphysema

large multinucleated syncytial cells

268
Q

How is BRSV disagnosied

A

PCR
virus isolation
IHC on tissues
IFA on cells from transtrachela aspirate

269
Q

who are the host for PI3

A

cattle and sheep

270
Q

pathogensis of PI3

A

transient clinical Dz 3-4 days

formation of syncytial cells and intracytoplasmic inclusions

271
Q

What are the porcine respiratory viruses

A

Influenza
PRRSV
Circovirus

272
Q

Viral causes of abortion in swine

A
parvo
entero
PRRS
Pseudorabies
classical swine fever
273
Q

PRRS subtypes provide cross protection to one another

A

FALSE

274
Q

T or F PRRS can establish persistent infection

A

True can cause severe Dz

275
Q

PRRS can survie for days inwater and feezing as well

A

true

276
Q

Where did PRRS come from

A

1987 prolly from mutations in mouse arterivirus

277
Q

What is death and Dz of PRRS associated with

A

secondary pathogens

278
Q

How is PRRS transmitted horozontal

A

direct contact with nasal discharge, semen, saliva, urine, or feces
shedding for up to 15 weeks
airborn possible

279
Q

How does PRRS transmit vertically

A

in utero - PI piglets

280
Q

Pathogensis of PRRS

A

Spread and replication in many organs

REplicates in macrophages, esp pulmonary compromises thier function and pre-disposes them to bacterial infections

281
Q

T or F PRRS respiratory and reproductive Dz may occur in the same herd

A

TRUE - milf fever, blue ears, labored breathing, late term abortions, weak un-thrifty pigs

282
Q

What age piglets does PRRS respiratory Dz affect

A

any age
mainly nursey and weaned pigs
respiratory signs
conjunctivitis and scours

283
Q

what test is used to analyza tissues and screen boar semen for PRRS

A

PCR

284
Q

Why can virus isolation be a problems to detect PRRS

A

neutralizing antibody may inhibit virus isolation

285
Q

T or F sometimes antibodies enhance the replication of PRRS in macrophages

A

TRUE

materal antibodies do provide protection

286
Q

What is the control of PRRS

A

eradication - depop
move nursey off-site sanitize
move gilts off site
close herd

287
Q

What is vaccine control of PRRS

A

inactivated and MLV are used

MLV - stronger

288
Q

Why have PRRS MLV been a problem

A

induce clinical Dz in pregnant sows

289
Q

Why does PRRS MLV not protect against heterologus strains

A

they have resulted from virus evolution

290
Q

T or F use of vaccines have been a great controlled method for PRRS in the US

A

FALSE

management has been better

291
Q

What 2 proteins does circovirus nucleic acid encodes 2 proteins what are they

A

replicase

capsid

292
Q

What species does circo infect

A

pigs dogs

birds - parrots, pigeons, chickens, ducks

293
Q

Which PCV is associated with Dz

A

PCV-2

294
Q

what disease is OCV-2 associated with

A

postwean multisystemic wasting

Procine dermatitis and nephtopathy

295
Q

What kind of infections does PCV-2 predispose pigs to

A

congential tremors
neonate cardiomyopathy
repro failures
porcine respiratory disease

296
Q

T or F PCV-2 is very stable

A

True - resistant to heat, humidity and common disinfectants

297
Q

T or F the European strain of PCV is more virulent

A

TRUE - more disease

298
Q

How is PCV-2 transmitted

A

in secretions
fecal-oral
persist for long time

299
Q

What are facts about PCV-2 pathogenesis

A

macrophages important
co-infections important
Dual infection may increase replication
genetics can be factor

300
Q

Pathogensis of PCV-2

A

destruction of lymphocytes
inflammation in LN, spleen, tonsil, kidney
large viral replication decreased immune function

301
Q

What is the major clinical sign of piglets wtih PCV-2 PMWS (nursing)

A

failure to thrive
weight loss
respiratory

302
Q

what is the major clinical signs of piglets with PDNS PCV-2

A

end of nursey start of grower

skin lesions on hindlimbs, perineum, kidney

303
Q

WHat are the gross lesions seen with PCV-2

A
wasting
pulmonary edema
gastric ulceration
enlarged kidney
ascites
plueral/pericardical effusions
304
Q

What are the histopath lesions seen with PCV-2

A

granulomatous inflammation with multinucleated giant cells and basophilic inclusions
intersticial pneumonia

305
Q

Test and tissue used for PCV Dx

A

PCR or IHC - blood or tissue

Tonsil or lymph nodes

306
Q

where is there limited value to serology testing of PCV

A

most pigs are infected when young so they will be seropositive

307
Q

WHat are control measures for PCV-2

A

reduce crowding

all in all out

308
Q

are there vaccines available for PCV

A

chimeric PCV-1 Europe
inactivated PCV-2 Europe
US some eff in reducing Dz
vaccinate 3 weeks and 6 weeks

309
Q

What does porcine parvo cause

A

repro failure

endemic in many herds

310
Q

T or F if a gilt is exposed to natural PPV they will become diseased

A

FALSE

311
Q

What happens when gilts are exposed to PPV in first 1/2 gestation

A

transplacental infection

aborted or mummified

312
Q

T or F fetuses affected with PPV after 70 days gestation will be born alive

A

True but will shed PPV early postnatal

313
Q

When are losses most severe with PPV

A

when PPV is introduced into seronegative herds during pregancy

314
Q

transmission of PPV

A

direct contact
ingestion of secretions
vertical to fetus
boar semen

315
Q

what is the primary reservior of virus on farms with PPV

A

contaminated enviroment

316
Q

what is the first sign of PPV infection in a herd

A

increase in open gilts returning to heat 3-8 weeks after breeding

317
Q

T or F all fetus in a liter will be affected by PPV

A

FALSE

some will be born alive some will be born mummified

318
Q

Dx test for PPV

A

IFA on frozen tissue of fetus

serology limited bc widespread infection

319
Q

Prevention and control of PPV

A

vaccination with inactive vaccine 2 weeks apart before breeding

320
Q

T or F pseudorabies has been eradicated from the US

A

TRUE

2007 all state free status

321
Q

T or F pseudorabies remains present in feral pigs in the Us

A

TRUE - concern for transmisson to commerical herds

322
Q

T or F pseudorabies is reportable

A

yes to state and federal

323
Q

T or F pigs that recover from pseudorabies are latent carriers for life

A

TRUE - alpha herepes sets up latent infection in sensory ganglia
reactivation during stress

324
Q

T or F pseudorabies is stable in environment

A

FALSE - survive for 2 weeks but easily destroyed by disinfectants

325
Q

Who is the host for pseudorabies

A

swine natural host and reservoir

accidental host - dogs cats cattle sheep goats

326
Q

what type of Dz does accidental host of pseudorabies develop

A

acute sever Dz

327
Q

How is pseudorabies transmitted to ruminants and horses

A

close contact with swine usually ingestion of pig meat

328
Q

What are the 5 ways pseudorabies is transmitted

A
direct oral-nasal contact
airborn from sneezing
contaminated food water (14d)
veneral transmission
transplacental transmission
329
Q

Pathogenesis of Pseudorabies

A

oral or intranasal infection
PHV-1 replicates in the oropharynx
24 hrs goes to brain via cranial nerves
encephalitis occurs
PHV-1 pantropic disseminates many tissues
presits in tonsils and trigeminal ganglion

330
Q

what are the clinical signs of psedurabies in a navie swine herd

A

infection of respiratory, nervous, and reproductive system

331
Q

what signs does suckling piglets with pseudorabies show

A

CNS signs
incoordination, tremors, paddling, convuslsions, vomit, scours
mortality 100%

332
Q

what signs do grower pigs with pseudorabies show

A

5% mortality
fever, respitory signs
trembling, incoordination, seizures

333
Q

what signs do sows with pseudorabies show

A

early gestation -abort

late gestation - mummifed fetus

334
Q

what are the signs of pseudorabies in accidental host

A

intestn local puritis violent licking, chewing rubbing
self-mutilation
neurologic signs
death within hours

335
Q

Dx test for pesudorabies

A

PCR
virus isolation
IF
nasal cavity and tonsil

336
Q

What is the standard herd test for pseudorabies

A

SN

337
Q

what test can distingush a vaccinated pseudorabies pig for a natural infection

A

ELSIA

338
Q

How is pseudorabies infection identified in accidental host

A

IFA on brain
virus isolation
PCR

339
Q

When was the US eradication program for pseudorabies

A

1989 - depop

2005 domestic swine free

340
Q

What is the control metod used in countires with endemic pseudorabies

A

vaccination with ML gene deletion vaccines

341
Q

T or F pseudorabies is zoonotic

A

FALSE