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Virology > Virology Test 3 > Flashcards

Virology Test 3 Flashcards

1
Q

When Coronaviruses undergo rapid mutation how do they exist the cell

A

Quasispecies

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2
Q

Since Coronaviruses survive well in the environment at cool temperatures for weeks to months what type of transmission is important

A

Fomite Transmission

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3
Q

T or F Coronaviruses are acid stable and able to survive the gastric pH

A

TRUE

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4
Q

T or F Coronaviruses can withstand most disinfectants

A

FALSE - they are inactiviated

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5
Q

Coronaviruses have tissue tropism for what 2 tissues

A

Respiratory Epithelium

Enteric/Gastric Epithelium

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6
Q

The ability to infect different cell types and not be exclusively host-specific is known as what

A

tropism switching

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7
Q

What are the 5 most common veterinary Coronaviruses

A 
FIVP - Feline Infectious Peritonitis
TGE - Transmissible Gastro Enteritis
Novel Swine Enteric Coronavirus
CCV - Canine Coronavirus - scours in dogs
Bovine Coronavirus - scours in calves
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8
Q

What cells in the GI tract are effected by coronaviruses

A

Mature enterocytes in both the SI and the Proximal Intestine

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9
Q

What are the implications of antigenic drift of coronaviruses

A

Hard to develop Vaccines

Easy to have susceptible animals in population

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10
Q

Why does antigenic drift make it hard to develop vaccines

A

different isolates of field virus circulating

New pathogenic variants are arising all the time

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11
Q

Coronaviruses kill mature enterocytes on tips & sides of villi so the major lesion seen is

A

Villus Atrophy

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12
Q

What common disease is seen with Coronaviruses

A

malabsorption - scours

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13
Q

T or F Direct contact is required for Coronaviruses

A

FALSE - millions of virons are shed into environment in scours

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14
Q

What are the 4 swine Coronaviruses

A

Transmissible Gasterenteritis (TGE)
Hemagluttinating Encephalomyelitis (HEV)
Porcine Respiratory Coronavirus (PRCV)
Novel Swine Enteric Coronavirus (SECD)

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15
Q

What TGE virus protein binds to sialic acid receptor on upper respiratory and intestional epithelial cells

A

S - Spike Protein

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16
Q

Where does TGE viral replication occur

A

respiratory and enteric epithelium

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17
Q

the clinical effects of TGE are seen as a result to viral replication in what tissue

A

Small intestine epithelium

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18
Q

What is the results of viral replication of TGE in SI

A

villi slough
viral shed in feces
malabsorption and scours in piglets

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19
Q

Where is the TGE virus secreted in sow pigs

A

milk from mammary gland

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20
Q

TGE is a major cause of morbidity and mortality in piglets of what age

A

10-14 days

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21
Q

T or F Piglets over 5 weeks of age will expirence severe clinical signs of TGE

A

FALSE - mild clinical disease

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22
Q

TGE is a highly contagious disease that is transmitted by:

A

Oral

Inhalation

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23
Q

What is the epidemic form of TGE

A

when virus is first introduced to a navie herd usually winter

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24
Q

what is the endemic form of TGE

A

virus persists in partially-immune herd
large breeding herds
herds where finishing pigs are kept
herds that introduce new pigs

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25
Q

T or F Endemic TGE follows Epidemics of TGE

A

TRUE

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26
Q

What is the usual herd history for Epidemic TGE

A

1st introduction to navie herd
Explosive scours, vomit, dehydration, death in piglets under 10 days old (100% morbidity)
some adult scours but no death

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27
Q

How long do TGE epidemics usually last

A

3-5 weeks until herd immunity develops

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28
Q

What is the usual herd history in TGE endemics

A

Partially immune herd
scours in piglets 2-3 weeks age
outbreak at weaning bc lost IgA

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29
Q

What is diagnosis when Litters of piglets form new introduced sows have vomiting, scours, and high mortality

A

Endemic TGE

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30
Q

What is the major reservoir of TGE infections

A

weanling piglets - excrete in feces up to 100 days

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31
Q

What does an outbreak of clinical TGE usually follow

A

introduction of pigs into a herd

carrier pigs is source of infection

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32
Q

What are 2 management practices that lead to increased risk for TGE

A

continuous flow system of production

inadequate bio security practices

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33
Q

T or F Fomite transmission is important in TGE

A

TRUE - vehicles, boots, equipment

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34
Q

Who are the mechanical vectors for TGE

A

birds

insects - flies

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35
Q

What are the lesions of TGE (Small Intestine)

A

watery, yellow/green scours with milk clots
thin, translucent intestinal wall
NO chyle
stomach filled with gas

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36
Q

histopathic change with TGE

A

villus atrophy

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37
Q

The secretions of GIT affected what what part of the GI tract in TGE

A

jejunum

Ileum

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38
Q

WHat is lactogenic immunity for TGE

A

sows milk with have IgA in it which provides protection for intestinal epithelial cells

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39
Q

How does the sows GALT system work with TGE

A 
oral exposure to TGE
IgA precursor cell in intestine synthesized
migrate to mammary
become Aby - secreting plasma cells
Secret IgA into the milk
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40
Q

T or F sows will secrete IgA for TGE from vaccination

A

FALSE - TGE exposure must be oral route

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41
Q

T or F Pregnant sows who become infected with TGE will become immune

A

True - they do NOT shed but have protective IgA in their milk

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42
Q

T or F Vaccinating sows with a TGE vaccine provides piglets better immunity than natural infection

A

FALSE - feedback methods or natural exposure provides much better piglet protection

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43
Q

What is the connection between TGE and PRCV

A

PRCV is a deletion mutant of TGE so it can’t effect an enterocyte only respiratory cells

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44
Q

What provides cross-protection immunity for TGE

A

PRCV

Immunize with PRCV 1st to prime immune system then follow with TGE - minimal environmental contamination

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45
Q

What are the economic losses with TGE

A 
dead pigs
downtime
increased labor cost
disturbance in breeding
reduced growth rate
curtailed performance in older piglets
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46
Q

TGE control methods

A

depopulation and replacement

Controlled, natural immunization, All in/out

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47
Q

what is a controlled natural immunization with TGE

A

partial depop - move piglets to finishing
plan exposure - confirm Dx, Feedback frozen dead piglet intestine for 3 days
Good biosecurity
All in/out system

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48
Q

How is TGE diagnosed

A

epidemiology and clinical signs

muscoal scraping

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49
Q

What test can distinguish TGE from PRCV

A

RT-PCR

competitive ELSIA

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50
Q

What test is used to measure level of TGE in a herd

A

ELSIA serologic test

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51
Q

What test do MU offer for TGE

A

PCR

serum neutralization

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52
Q

What are the 2 viruses cause swine enteric coronavirus diseases

A

Porcine Epidemic Diarrhea virus

Porcine Delta Coronavirus

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53
Q

T or F PEDV is report-able in the US

A

TRUE

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54
Q

When did PEDV enter the US

A

2013 - from china

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55
Q

When did Procine delta coronavirus enter the US

A

2014 - from china

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56
Q

Clinical signs of PEDV and PDCoV

A

vomiting & scours
high morbidity & mortality in suckling piglets
endemic and epidemic forms of PEDV

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57
Q

What is the control mechanism for PEDV

A

Feedback procedures to sows

conditional vaccine in 2014

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58
Q

What are PEDV lesions

A

SI - thin, dilated with fluid
villus atrophy
multi-nucleated syncytial epithelial cells

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59
Q

What is the vomiting and wasting diseases in piglets

A

Hemagluttinaning Encephalomyelitis Virus

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60
Q

Clinical signs of Hemagluttinaning Encephalomyelitis Virus

A 
vomiting
anorexia
thirst
CONSTIPATION
dehydration
emaciation
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61
Q

What age of pigs does Hemagluttinaning Encephalomyelitis Virus effect

A

suckling piglets up to 6 weeks of age

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62
Q

What clinical signs of HEV are seen in suckling piglets 4-7 days old

A

encephalitis
weakness
tremors
convulsions

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63
Q

T or F Hemagluttinaning Encephalomyelitis Virus is inapperant in adults

A

TRUE

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64
Q

Piglets that survive the acute phase of Hemagluttinaning Encephalomyelitis Virus can develop a chronic syndrome of

A

vomiting
wasting syndrome
stunting

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65
Q

T or F Hemagluttinaning Encephalomyelitis Virus is seen clinically very often

A

FALSE - seen in serology often but rarely seen clinically usually as an outbreak

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66
Q

How is Hemagluttinaning Encephalomyelitis Virus transmitted

A

Oral

Respiratory

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67
Q

What is the pathogensis of HEV

A

Ingestion of HEV
replication in nasal epi, tonsil, lung, SI
spread to peripheral nerves to CNS
infection of autonomic gangalia

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68
Q

What is responsible for vomiting and constipation in HEV

A

viral replication in autonomic ganglia

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69
Q

How is HEV diagnosed

A

virus isolation in tissure culture
IFA on tissue secretions
serologic tests include serum Nuet and HI

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70
Q

What lesions are seen with HEV

A

no specific lesions

non-suppurative encephalomyelitits in pigs if they have clinical neuro signs

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71
Q

What is the treatment for HEV

A

no treatment
no effective vaccine
feedback exposure to the sow

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72
Q

What is family and genus Infectious Bursal Disease

A

Birnaviridae
Genus - avibirnavirus
2 segmented non-env RNA virus

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73
Q

what serotype of Infectious Bursal Disease is pathogenic to chickens

A

Serotype 1

subgroup 1 - very virulent

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74
Q

Where does Infectious Bursal Disease replicate

A

dividing pre-B lymphocytes in the Bursa of Fabricius in chickens

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75
Q

Birds that have a sub-clincal infection of Bursal Disease have acquired what

A

permanent acquired B-Lymphocyte deficiency

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76
Q

WHat is the most common form of infectious Bursal disease

A

subclinical

chicks less than 3 weeks age don’t appear sick but they have permanent immune suppression (non functional B-lymphocyte)

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77
Q

Clinical infectious bursal disease (ruffled feathers, scours, depression) is seen ___

A

in chicks 3-6 weeks of age
Morbidity near 100%
Mortality near 50%

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78
Q

How is infectious bursal disease virus excreted

A

in feces usually scours

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79
Q

How is infectious bursal disease transmitted

A

direct

fecal oral

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80
Q

Lesions of Infectious bursal disease

A

Bursa - large, edematous, hyperemic
Lymphoid follicles are necrotic
swelling with edema then necrosis

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81
Q

what is the life long consequence of infectious bursal disease

A

life-long immune supression

absence of B-cells - more disease susceptible

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82
Q

how is infectious bursal disease controlled

A

vaccination programs to protect chick
oral MLV or inactivated
biosecurity

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83
Q

What type of virus is Rabbit Hemorrhagic Disease Virus

A

calicivirus
non-eneveloped RNA
cup-shaped depression “Calici or cup”

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84
Q

IS Rabbit Hemorrhagic Disease Virus resistant to heat and detergents

A

YES but destroyed by acids

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85
Q

T or F Rabbit Hemorrhagic Disease Virus can be transmitted on Fomites

A

True

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86
Q

T or F Rabbit Hemorrhagic Disease Virus affects both wild and european rabbits

A

FALSE - only european rabbits

NOT wild rabbits

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87
Q

What is the signs of peracute Rabbit Hemorrhagic Disease Virus

A

found dead blood oozing from respiratory orifices

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88
Q

What are clinical signs reported with Rabbit Hemorrhagic Disease Virus

A

lethary
high fever
CNS signs

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89
Q

what are the gross lesions of Rabbit Hemorrhagic Disease Virus

A

pulmonary hemorrhages
deep vein thromboses
DIC

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90
Q

What is the primary lesion in Rabbit Hemorrhagic Disease Virus

A

Fulminant hepatic necrosis

bleeding from body orphesis

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91
Q

T or F Rabbit Hemorrhagic Disease Virus is reportable

A

TRUE

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92
Q

how is Rabbit Hemorrhagic Disease Virus diagnosed

A

RT-PCR

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93
Q

What is prevention of Rabbit Hemorrhagic Disease Virus

A

eradicaiton in the USA

Recombination vaccine in Europe

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94
Q

What are the 2 antigenically distinct paroviruses in dogs

A

CPV - 2

CPV -1 minute virus - not pathogenic really

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95
Q

Which parvo strain has been associated with canine abortions

A

CPV-1

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96
Q

What does CPV-2 cause in young dogs

A

hemorrhagic enteritis

viral diarrhea

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97
Q

What are variants of CPV-2

A

2
2a
2b -outbreaks in Us
2c - US 2006 MOST COMMON

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98
Q

Where did CPV-2 arise from

A

mutation in the feline panleukopenia virus that jumped species

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99
Q

T or F all canidae are susceptible to CPV-2

A

TRUE - dogs, foxes, wild dogs, coyotes, wolves

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100
Q

T or F some strains of CPV can infect domestic cats

A

TRUE - similar to panleuk

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101
Q

What is cross protection for CPV

A

feline panleuk vaccine

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102
Q

CPV routes of transmission

A

contact with feces

fomites

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103
Q

How long is CPV stable in environment

A

up to 5 months

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104
Q

T or F CPV is resistant to most disinfectants

A

TRUE

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105
Q

What age puppies are predilection for CPV

A

6 weeks to 6 months

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106
Q

Parthenogenesis of Parvo

A

replicate in nucleus of host cell

Require host cell functions

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107
Q

What are the clinical signs of CPV in older dogs

A

enteritis

leukopenia - loss of lymphocytes and enterocytes which divide fast

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108
Q

What is the incubation period of CPV-2

A

7-14 days

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109
Q

Where does replication CPV-2 begin

A

lymphoid tissue of the oropharynx

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110
Q

What happens after replication of CPV-2 occurs for 1-5 days

A

Primary Viremia occurs
virus disseminates to epi of SI, lymph, bone marrow
Older dogs CPV may spread to organs

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111
Q

What is the lesion of CPV-2

A

necrosis of crypt epithelium

blunting of villi

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112
Q

What causing leukopenia and lymphopenia in CPV-2

A

virus destorys mitotically active precursor cells of circulating leukocytes and lympthoid cells

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113
Q

Where is CPV shed

A

in feces for 7-10 days, shedding occurs before onset of scours

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114
Q

CPV-2 is associated with 2 major clinical syndromes in dogs

A

Enteritis

myocarditis

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115
Q

What does CPV-2 causes in pups newborn to 2 weeks old

A

generalized infection

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116
Q

What is enteritis in CPV dogs

A

rapidly progressive GI disease
fever, vomit, scours (hemorrhagic)
Luekopenia
Death within 2 days of onset

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117
Q

Where are CPV-2 lesions usually present

A

duodenum

Jejunum

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118
Q

What are enteric signs of CPV

A

thick discolored intestinal wall
bloody liquid in lumen
lymphoid necrosis in pyers pathc, mesenteric nodes thymus and spleen

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119
Q

What is seen with CPV myocarditis

A

young pups

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120
Q

What test is done for suspected parvo dog

A

ELSIA for CPV-2 antigen
detected virus for 10 days
gone day 5-7 of clinical illness

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121
Q

T or F dogs vaccinated for parvo will have a positive ELISA test

A

TRUE 5-12 days post MLV

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122
Q

T or F young puppies who recovery PCV have immunity

A

TRUE - IgG protects them for systemic spread of disease but IgA does not persits so they can be re-infected with mild clinical signs

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123
Q

T or F vaccination status of parvo is correlated to serum titer levels

A

TRUE

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124
Q

How is parvo controled

A

10 minutes of bleach solution

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125
Q

Can parvo be vaccianted

A

YES MLV or attenuated vaccines

BI, merck, merial, pfizer

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126
Q

Most common cause of vaccination failure for parvo is

A

interfering levels of maternal antibody to CPV-2 blocks the development of immune response in the puppy

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127
Q

What is parvo vaccination reccomendation

A

start at 6 weeks

redo every 3 to 4 weeks until 16 weeks

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128
Q

IS CPV zoonotic

A

NO

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129
Q

Where do coronaviruses replicate

A

cytoplasm

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130
Q

What is the incubation for coronavirus

A

1-4 days

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131
Q

Pathogenesis of coronavirus

A

CV infects mature epi cells of intestinal villus.
replicates in enterocytes
released by budding

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132
Q

What are clinical signs of coronavirus

A

suddon onset of scours in young puppies

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133
Q

WHat is recovery for coronavirus

A

8-10 days

mortality low without complications

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134
Q

How is coronavirus diagnosed

A

RT-PCR
electron microscopy
SN or ELISA

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135
Q

How is coronavirus prevented

A

inactivated and MLV

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136
Q

T or F Coronavirus is a core vaccine for dogs

A

FALSE - only in some kennels

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137
Q

T or F Rotavirus can be controlled with a vaccine

A

FALSE

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138
Q

T or F many dogs are positive for Herpes 1

A

TRUE but clinical Dz is rare

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139
Q

How is CHV-1 maintained in nature

A

latent infection in sensory gangalia

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140
Q

T or F CHV-1 are stable in environment

A

FALSE - they are destroyed by heat and disinfectants

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141
Q

What are the main ways of transmission for CHV-1

A

Oral -nasal
genital - vaginal secretions
in utero - possible abortion, sillbirth, infertile

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142
Q

What age puppies does CHV-1 affect

A

under 4 weeks of age - usually fatal

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143
Q

What is the incubation period of CHV-1

A

3-8 days

signs last 1-2 days

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144
Q

What clinical disease does CHV-1 cause

A

Genital Dz

respiratory like kennel cough

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145
Q

Pathogensis of CHV-1

A

replication in nasal mucosa, pharynx, tonsils
viremia often fatal
hypothermic

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146
Q

What is the best temperature for CHV-1 replication

A

33C

genital and upper respiratory tract

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147
Q

Lesions of CHV-1

A

multifocal necrosis hemorrhage

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148
Q

T or F intranuclear inclusions occur with CHV-1

A

True

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149
Q

How is CHV-1 diagnosed

A

gross or histopath lesions

PCR on tissue or swabs

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150
Q

T or F there is a good vaccine for CHV-1

A

FALSE

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151
Q

Prevention of CHV-1

A

Materal Ab
C-section
Rear pups in incubator at 35C

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152
Q

Where does Canine hepatitis CAV cause inclusion bodies

A

hepatocytes

endothelia cells

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153
Q

What does each strain of CAV cause

A

CAV-1 infectious hepatitis

CAV-2 respiratory disease

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154
Q

What type of adeno infectio happens in wild dogs

A

CAV-1 - subclinical

155
Q

WHat does CAV-1 cause in dogs

A 
acute fulimiant hepatitis
chronic hepatitis
ocular and respiratory disease
encephalitis
glomerulonephritis
156
Q

What does CAV-1 cause in foxes

A

encephalitis

157
Q

What is the epidemiology of CAV

A

world-wide

clinical Dz - less than 1 year

158
Q

How is transmission of CAV

A

direct contact with fluids
fomites
Oral, nasopharyngeal, conjuctival

159
Q

What does the CAV preferentially damage

A

hepatocytes

vascular endothelial cells

160
Q

What are the primary organs for CAV

A

Liver and kidney

161
Q

Where is the CAV shed

A

renal tubular epithelia cells are PI and shed virons for most post infection

162
Q

WHat is the peracute stage of CAV

A

death in hours from massive hepatic necrosis

163
Q

what is the acute stage of CAV

A

hepatic necrosis often fatal

164
Q

What is the chronic Dz stage of CAV

A

chronic active hepatitis or chronic renal Dz 2nd to immune complex glomerulonephrtis

165
Q

What is the mild Dz stage of CAV

A

transient corneal opacities

166
Q

What is the inapparent stage of CAV

A

healthy - no signs illness

167
Q

WHat is the ocular lesion “blue eye” from CAV

A

diffuse corneal edema

168
Q

How is CAV diagnosed

A

virus isolation in cell culture
IFA on frozen sections
IHC on fixed tissue
PCR

169
Q

What is the control of CAV

A

CAV-1 vaccination control using CAV-2 vaccine bc CAV-1 has adverse rx

170
Q

what type of virus is BVD

A

pestivirus

RNA virus

171
Q

WHat are the 2 biotypes of BVD

A

cytopathic

non-cytopathic 95%

172
Q

Which type of BVD crosses the placenta and invades the fetus to establish a PI and spread the virus

A

Non- cytopathic

173
Q

Which type of BVD is associated with mucosal disease

A

cytopathic

174
Q

What are genotypes of BVD

A

1 & 2

both in cytopathic and non-cyto

175
Q

What are the host for BVD

A

CATTLE

sheep, goats, antelope, deer, bison, camelids

176
Q

T or F WT deer can be BVD PI carriers

A

TRUE

177
Q

What is the seroprevlence of BVD in teh US

A

60-90%

178
Q

WHat is the rate of PI BVD calves

A

2-30%

179
Q

What age cattle is clinical Dz of BVD seen

A

6 months and 2 years

180
Q

How is BVD transmitted

A

Direct contact
Transplacental to fetus
Indirect - fomites, OB sleeves, needles

181
Q

What is the major source of BVD infection

A

PI viremic animals

182
Q

T or F BVD can be transmitted by AI

A

TRUE

183
Q

What are the clinical symptoms of BVD PI cattle

A

normal but can be poor doers

184
Q

What 4 things determine transmission of BVD

A

1 - PI calves
2 - animal to animal contact
3- Virulence of the virus
4 - susceptibility of cattle

185
Q

Explain the PI of BVD

A

non-cyto infection 1st 1/2 gestation (125d) viral replication and shedding occurs for life

186
Q

WHat happens with transplacental transmission of BVD late in festation

A

abortion
congenital malformations
sero+ calves

187
Q

Pathogenesis of BVD in non-preg immunocompetent cow

A

sub-clin infection
elminate virus
life-long immunity

188
Q

what happens when susceptible cattle are infected with cyto BVD

A

outbreak of scours
thrombocytopenia bloody scours
immune suppression

189
Q

WHat is the pathogensis of immunocompetent preg cattle with BVD

A

infertility and abortion
PI calves
congenital defects
effective immune response and clear the virus

190
Q

What happens with PI calves who have non-cyto that turns into cytopathic BVD

A 
mucosal Dz
low morbidity
high mortality
depressed febrile scours, oral ulcers, lameness
death 5-7 days
191
Q

What lesions are seen with BVD

A

Ulcers and erosions pm muzzle, mouth, pharynx

192
Q

what is the histopathology of BVD

A

necrosis of epi cells and lymphoid tissues in GIT

193
Q

T or F specific lesions are seen in BVD aborted fetus

A

FALSE

194
Q

Why is lab diagnosis required for BVD conformation

A

similar to rinderpest and malignant catarrhal fever

195
Q

BVD PI calves will be sero-positive

A

FALSE they are negative

196
Q

What is the standard serologic test for BVD

A

Serum neutrilization with 4-fold increase

197
Q

What is the goal of BVD contol programs

A 
prevent fatal infections
decrease transient infection
remove PI calves
vaccinate
enhance bio-security
198
Q

WHat is biosecurity for BVD

A

prevent new cattle into

quarantine and test new cattle & embroys, semen, bulls

199
Q

T or F MLV of BVD can cross the placental and infect fetus

A

TRUE

200
Q

WHat is the problem with inactivated BVD vaccines

A

lack of infectivity but safe for pregnant cows

201
Q

WHen should you vaccinate cows for BVD

A

before breeding

duration is only 140 days

202
Q

If calves are vaccinated for BVD before 6 months of age do they need a booster

A

YES

203
Q

What does BVD in camelids look like

A 
similar to cattle
abortions, early preg loss
stillbirth
PI crias
scours
respiratory Dz
ill thrift
204
Q

What does BVd in goats look like

A

infection and abortion

205
Q

what does BVD in white tail deer look like

A

infection

Persistent infections

206
Q

What does BVD look like in sheep

A

similar to border disease
reduced fertility
abortion
congenital defects

207
Q

T or F BVD is zoonotic

A

FALSE - humans not susceptible

208
Q

How many of the 25 serotypes of Blue tongue occur in the US

A

5 of them
genetic drift within serotypes
immunity is strain specific

209
Q

An infectious, arthropod-borne Dz of wild and domestic ruminants

A

Blue Tongue

210
Q

T or F most infections of BT are subclinical

A

TRUE

211
Q

Severe BT disease is seen in domestic sheep like

A

pronghorn
bighron
white-tailed deer

212
Q

Where is BT endemic

A

Southwestern US

213
Q

Who is the host of BT

A

clinical Dz in sheep but all ruminants are possible

214
Q

Who are the reservoir and amplifying host of BT

A

Cattle - high titer viremia

215
Q

What is the BT mortality and morbidity in sheep

A

Morbidity - 50-75%
Mortality 50%
US mortality is 0-14%

216
Q

How is BT transmistted

A

Culocodies - biting midge
dam to fetus
in semen
iatrogenic - contaminated needles

217
Q

What is effective at killing BT

A

iodophors and acid disinfectants

218
Q

Pathogensis of BT

A

transmitted by Culicoides
replication in lymph nodes
dissemination in macrophages to vascular endo cells
vascular necrosis thrombosis hemorrhage

219
Q

What does BT inoculation occur

A

site of exposed skin
Peracute - 7-9 days
Chronic 3-5 weeks

220
Q

Where does viral replication of BT occur

A

hematopoietic cell

endothelial cells

221
Q

After BT incubates for about a week what do sheep develop

A

fever
nasal discharge
edema - face, lips, gums, dental pad tongue
red vertical line coronary band - vasculitis
oral ulceration
swelling and cyanosis of tongue

222
Q

WHat is the pathogensis of BT in goats

A

mild disease
moderate fever
hyperemia mucous membranes

223
Q

What is the pathogensis of BT in cattle

A

inapparetnt

come clinical Dz similar to cattle

224
Q

What serotype of BT is causing death in European cattle

A

8

225
Q

How is BT diagnosised

A

PCR
virus isolation
salivary gland and blood

226
Q

What serologic test used to determine herd infection status

A

AGID

ELISA - more sensitive

227
Q

WHat is BT control methods

A

vector control
polyvalent non-replicating vaccines to reduce cases in endemic areas
annual vaccine 1 month prior to vector activity

228
Q

What is the problem with BT MLV

A

genetic reassortment causing emergence of new pathogenic strain

229
Q

How are the host of Epizootic hemorrhagic disease

A

White-tail deer and mule deer

cattle, deer, buffalo can show mild clinical Dz

230
Q

What is the epidemiology of Epizootic Hemorrhagic disease

A

occurs 5-10 Year intervals

2012 was huge

231
Q

what is the mode of transmission for epizootic Hemorrhagic disease

A

Culocodies - biting midge

232
Q

What age deer are susceptible to Epizootic hemorrhagic disease

A

any age

morbidity and mortality - HIGH

233
Q

WHat is the pathogensis of Epizootic Dz

A

infects endothelia cells and signs and lesions are like BT in sheep

234
Q

What is the peracute form of epizootic hemorrhagic disease

A

sever edema of the head and neck

pulmonary edema

235
Q

If a deer lives through epizootic Dz what occurs

A

hemorrhages in heart, rumen, and intestine and oral ulcers

236
Q

How is epizootic Dz diagnosed

A

PCR
virus isolation - conformation
FA - on frozen sections
AGID - detect serum Ab

237
Q

Is there a vaccine for Epizootic hemorrhages Dz

A

a killed one that only includes a few strains

238
Q

How many serotypes of Border dz are there

A

4

1 is similar to BVD

239
Q

T or F Border Dz is common in sheep and goats

A

FALSE -
common - sheep
Rare - goats

240
Q

Epidemiology of border Dz

A

exists world wide in sheep

241
Q

What are the clinical signs of border Dz

A

abortion prior to 45d gestation
Persistent infection - lambs before 72 days gestation (low birth weight, tremors, hairy coat)
sub-clinical - have recovered

242
Q

what are the lesions for border Dz

A

abnormal wool coat
congenital abnormalities
hypo-myelinogensis in CNS

243
Q

how is border Dz diagnosised

A

Viral antigen with IFA, IHC, PCR

viral neutrilization to detect Ab

244
Q

What is the major obstacle to elimination border Dz

A

Persistently infected sheep

245
Q

What should be done to replacement ewes before they intro to herd to prevent border Dz

A

serologic testing - need to be negative

246
Q

T or F inactivated BVD vaccine is used in sheep for protection from Border Dz

A

TRUE but effectiveness not proven

247
Q

What are the 2 feline coronaviruses

A

Feline Infectious Peritonitis (FIP)

Feline Enteric Coronaviruses (FEC)

248
Q

Wat is a high progressive and always fatal Dz in cats

A

FIP - deadliest Dz in cats known

249
Q

No definitive diagnostic test
no effective treatments
no reliable vaccine

A

FIP

250
Q

What is the clinical form of FIP

A

consequence of the cats immune reaction to the virus NOT the actual action of the virons on the cells

251
Q

Where did FIp arises from

A

mutations of Spike gene & ORF 3c accessory gene in harmless enteric FECV

252
Q

What is the defining event n FIP infections

A

infection of monocytes to macrophages

FECV to FIPV

253
Q

Where does massive amounts of replication of FECV occur

A

in the gut with shedding in the feces

environmental contamination

254
Q

What are the primary sources of infection with FIP

A

Litter Box

Queen to kitten early in life

255
Q

Parthogenesis of FIP

A

Ingestion of FECV
infection and replication in enterocuytes and marcophages
FECV mutates to FIP
Infection of marchophage and monocyte
Inflammation
Vasculitis, polyserositits, polygranuloma

256
Q

What groups of cats have the highest prevalence of Coronavirus

A

confinfed crowed grup housing cats

257
Q

What 2 types of cats have genetic susceptibility

A

cheetahs

persian cats

258
Q

T or F most cats who get FCoV get very sick

A

false 90-95% remain healthy

259
Q

How many FCoV cats become life long shedders

A

15%

260
Q

How many cats with FCoV will develop FIP

A

10-12%

261
Q

What are cats at most risk for developing FIP

A

6-18 months after initial infection

262
Q

FECV replicates in mature enterocytes but is excreted where

A

in feces of apperently healthy cats

263
Q

What are importatn sources of transmission for FECV

A

little box with dried up feces
fomites
fur contaminated with dust or liter

264
Q

what is the primary mode of transmission for FECV

A

Fecal-oral

Saliva from Queen

265
Q

What are the 2 main clinical signs of FIP

A

Pyogranulomatous vasculitis

Polyserositis

266
Q

What is the most importatn immunity in preventing clinical disease from FIP

A

CMI

267
Q

FIP cats with a strong T-cell immunity but weak antibody will have what clinical signs

A

healthy NO Dz

268
Q

FIP cats with failure of T-cells response and strong antibody response will have what clinical signs

A

Wet FIP

269
Q

FIP cats with a weak/poor T-cell response but a strong antibody response will have what clinical signs

A

DRY FIP

270
Q

T or F Humoral immunity makes FIP worse

A

TRUE

271
Q

Explain Type 3 hypersensitivity with FIP

A

antigen-antibody complexes deposit around vessels, fix C causes vasculitis and fibrinous polyserositis

272
Q

Explain Antibody-dependent enchancement with FIP

A

Ab complexes with FIP and taken up by macrophages
increased replication & lysis of macrophage
increased necrosis & inflammation
FIP accelerated

273
Q

Why have attempts to develop FIP vaccines failef

A

generating systemic Ab usually accelerate clinical Dz

274
Q

What is the most common form of FCoV infections in adult cats

A

Subclinical

275
Q

What symptoms does enteric FCoV cause

A

transient scours

vomiting

276
Q

What are the 2 forms of FIP

A

Effusive - WET

Non-effusive - DRY

277
Q

What is effusive FIP

A 
slow ascities with fluid wave
no pain
thoracic & pericardial effusion
low fever
anorexia & lethargy
Acute clinically
278
Q

Describe the ascities in Wet FIP

A 
clear, viscous, straw yellow or golden
total protein >3.5
>50% globulin
low cell counts
pyogranulomatous
neutrophils or macrophages
279
Q

FIP effusive lesions

A

Fibrinous polyserositis

Pyogranulomas

280
Q

non effusive FIP

A

multifocial pyogranulomas
necrotizing vasculities in organs
weeks to months

281
Q

Clinical signs of Non-effusive

A 
mild fever, wt loss, dull, 
Enlarged LN
nodules on kidney or viscera
ocular lesions
neuro signs
282
Q

what are the ocular lesions seen with DRY FIP

A

brown iris
aquesous flare
couldy anterior chamber
cuffing retinal vessels

283
Q

What are the neuro signs seen with Dry FIP

A

ataxia
nystagmus
seizures common

284
Q

hwat neuro signs is highly suggestive of non-effusive FIP

A

hydrocephalus

285
Q

what are the lesions of non-effusion FIP

A

multifocal pyogranulomatous nephritis
lesions follow vasculature
pyogranulomatous splenitis
hydocephalus

286
Q

What is the Dx test for FIP

A

NONE - clinical skills, blood work

287
Q

what is the gold standard test for FIP

A

histopath with IHC on the section but biopsy is not always an option

288
Q

What does a + serology FIP test tell you

A

exposure to FCoV

289
Q

what does a negative FIP serology test tell you

A

healthy kitten - may still have Dz

290
Q

What is the limitation of RT-PCR for FIP

A

cant distinguish FIP from FECV bc antigen shift

291
Q

How do you control FIP/FECV

A 
good hygine with multi-cats
early weaning (5-6wks) kittens
292
Q

What is the vaccine for FIP

A

Primucell MLV
ts-mutatn of Type2 corona
intranasal

293
Q

T or F FIP vaccine is licensed for kittens

A

FALSE

294
Q

T or F FIP vaccine is a core vaccination

A

FALSE

295
Q

T or F if a kitten is negative for FCoV then vaccine may provide protection

A

TRUE

296
Q

What occurs with panleuk replication in nucleus of dividing cells

A

wait for mitosis s pahse
forms intra-nuclear inclusions
hemagluttinate RBC

297
Q

What are important Parvo Dz in Cats, Dogs, Swine

A

Cats - panluekopenia
Dogs - parvo 2
Swine - Porcine virus

298
Q

parvovirus infection in fetus or neonate

A

widespread many cell populations are mitotic

299
Q

parvo infections in adults

A

infections of active tissues

lymoh, hematopoietic bone marrow, epithelial crypt cells

300
Q

Intracellular effects of parvo

A

DNA genome enters at nucleus
S phase - transscript/translate
G2-M checkpt arrest - genome replication-protein synthesis
virons released via necrosis & apoptosis

301
Q

How does parvo survive so long in enviroment

A

persistence rather than viral shedding for almost 1 year

302
Q

what is the most common mode of transmission for parvo

A

indirect contact with contaminated premises (intranasal or oral)

303
Q

T or F inutero tranmission can occur with parvo

A

TRUE

304
Q

What genera do feline panleuk, CPV 1&2, porcine parvo and aleutian Dz belong to

A

Protoparvovirus

305
Q

what genera do adeno-associated viruses belong too

A

dependoparvovirus - require helper virus to replicate

306
Q

what are the host for FPV

A

Felidae
raccoon
ferrets
mink

307
Q

How long is FPV shed in feces

A

up to 6 weeks

308
Q

T or F FPV is resistant to most disinfectatns

A

TRUE but bleach will kill it

309
Q

what virus is thought to have originated as FPV

A

CPV-2 AA mutations to jump species

310
Q

When FPV causes predilection of rapidly dividing cells in of the intestinal crypt epithelium what happens

A

scours

enteritis

311
Q

When FPV causes predilection of rapidly dividing cells in bone marrow, hematopoietic what happens

A

anemia

panleukopenia

312
Q

When FPV causes predilection of rapidly dividing cells in lymphoid tissure what happens

A

secondary infections
thyic atrophy
lymphopenia

313
Q

When FPV causes predilection of rapidly dividing cells in fetus

A

death

cerebellar hypoplasia

314
Q

FPV pathogensis in early fetus gestation

A

infertility
fetal death
reabsoption

315
Q

FPV pathogensis in mid to late gestation

A

abort

mummified fetuses

316
Q

FPV in late gestation

A 
lymphoid tissue
bone marrow
CNS
cerebellar hypoplasia
hydrancencephaly
optic never atrophy
317
Q

Pathogensis of FPV postnatal up to 2 weeks

A

cerebellar hypoplasia

318
Q

pathogensis of FPV postnatal with adequate titer

A

no disease

319
Q

What are the clinical signs of subclinical Dz in cats

A

common in health adults

no signs of illness

320
Q

what is signs of FPV in generalized infection

A

in kittens

fever, depression, vomit, scours, dehydration

321
Q

what are signs of FPV perinatal infection of neonates up to 2 weeks

A

cerebellar hypoplasisa

322
Q

what are the results of in utero infection of FPV

A

embryonic resorption
abortion
still birth

323
Q

what is the lesion seen with FPV

A

lymphocytosis in thymus, GALT, nodes , spleen

324
Q

T or F dehydration is seen as sunken eyes in FPV cases

A

TRUE

325
Q

T or F FPV can cuase gelatinous bone marrow

A

TRUE - leukopenia & anemia

326
Q

What are the histopath lesions seen with FPV

A

villus atrophy of crypt epithelim

327
Q

What test is used for Dx of FPV

A

CPV-2 antigen test but only detectable for 24-48 hours post infection

328
Q

T or F FPV is a core vaccine

A

TRUE
MLV
killed
detection of Ab titres not useful

329
Q

Mature columnar cells that line intestine and have microvilli

A

enterocytes

330
Q

What is the function of enterocytes

A

nutrient digestion & absorption

NOT mitotic

331
Q

What gut cells have receptors for IgA and IgM

A

crypt cells

332
Q

what is the enterocyte turnover rate

A

3 to 7 days

333
Q

M cells form a dome over GALT but what is the function

A

uptake of antigens in the GIT

334
Q

Ostomtic movement of fluid into the lumen

incomplete digestion, disaccharidase deficiency

A

Ostomtic scours

335
Q

inflammation and necrosis increase fluid production in the intestine

A

Exudative Diarrhea

salmonellosis BVD

336
Q

Diarrhea caused by enteroteoxigenic E. Coli

A

secretory-absorptive imbalance

337
Q

Diarrhea caused by stress, convulsions with increased peristalysis

A

Intestinal hypermotility

338
Q

Sites where viruses have been shown to destory intestinal cells

A

mature enterocyte at tip of villus
crypt epithelium
M cell over GALT

339
Q

THese viruses have trophism for mature epithelium enterocytes on the sides and tips of villus

A

Rota
Corona
Calici
Toro

340
Q

This virus has a tropism for crypt epithelium cells and lymphocytes in GALT, virus arrives via 2nd virema

A

Parvo

341
Q

Has tropism for M-cell and lymphocytes in GALT virus arrives by 2nd viremia

A

Pesti

342
Q

What are the Pesti viruses that cause necrosis over M cells and peyers patch

A

Cattle - BVD & Rinderpest
Dogs - Parvo -2
Cats - Panleukopenia

343
Q

T or F Viruses that effect mature enterocytes but not mitotic crypt cells cause milder disease with lower mortality

A

TRUE

animals recovery with fluids

344
Q

T or F Viruses that destory crypt epi and or GALT tend to produce very bad Dz with high mortality

A

TRUE
healing takes long time
2nd bacteria problem
aggressive treatment

345
Q

What do adenviruses cause in calves

A

necrosis & hemorrhages from rumen to colon. Muscoal necrosis from infarts, colitis occurs

346
Q

T or F Animals with mixed infections will have less clinical signs

A

FALSE - usually more severe

347
Q

Where does Rota affect in the GI

A

upper SI

jejunum & Ileum

348
Q

where does corna effect

A

SI - epi necrosis in procimal colon

349
Q

Why is the source of infection for neonates with viral scours

A

MOTHEr

350
Q

What influence does milk have on viralvirus as it trasverse the stomach

A

milk buffers and coats the virus to protect it from gastric acid

351
Q

Why are young animals suceptible to scours

A

IgA is provided in milk while nursing and provdies protection but when it declines they become susceptibile

352
Q

What age does IgA in the milk start to decline

A

first week up to 3-4 weeks

353
Q

T or F Single viral infections are more common than mixed infections

A

False

354
Q

What are the common causes of scours in bovine

A

rota

corona

355
Q

what are the less common causes of scours in bovine

A

adeno
parvo
toro

356
Q

what are the common causes of scours in equine

A

rota

357
Q

what are the less common causes of scours in equine

A

adeno

358
Q

what are the common causes of viral scours in pigs

A

rota

3 corona

359
Q

what is the less common viral scours in pigs

A

toro

360
Q

what is the common cause of viral scours in goats and sheep

A

rota

361
Q

what is the less common viral cause of scours in sheep and goats

A

adeno

362
Q

T or F Rotavirus Enteritis secretes entertoxins

A

True

363
Q

Group A rota causes scours in which animals

A

Large

364
Q

Groups C & E rota causes scours in which animals

A

swine

365
Q

Groups D & F rota causes scours in which animals

A

birds

366
Q

Why are rota viruses so named

A

spikes on a wheel

367
Q

What is the major cause of scours in intensivily housed animals

A

Rota

368
Q

what are the 2 ways rota causes severe scours

A

lyses enterocytes at tips of villi - osmotic scours

NSP4 entertoxin - secretory scours

369
Q

What does equine rota infection look like

A

adults - subclinical

foals - watery scours

370
Q

How is rota transmitted in equine

A

fecal - oral

feces and fomites

371
Q

T or F there is a vaccine for equine rota

A

TRUE it is inactivated vaccine with conditional approval from USDA

372
Q

What is the biggest risk factor for equine rota

A

overcrowding - foal hygiene is essential

373
Q

WHat are the 2 most common causes of scours in calves

A

ROTA

Corna

374
Q

when do outbreaks of scours occur in calves

A

5-14 days

up to 3-4 weeks

375
Q

T or F adeno and parvo cause severe damage to the GI tract of young calves

A

TRUE

376
Q

WHat cells does corona infect

A

mature enterocytes

377
Q

Why is corons considered a winter disease

A

it survives well in cool moist enviroments

378
Q

Why is bovine corona pnemotropic

A

it can also replicate in respiratoy tract

379
Q

T or F humans can be infected with bovine corona

A

TRUE

380
Q

What is the common cause of sporadic scours in calves 1-8 week old and in feedlot cattle

A

adeno

381
Q

What are the 3 corona virus of pigs

A

TGE - vomit Scours
procine epidemic scours - milder
procine hemaggulating encephalomy - vomit & wasting

382
Q

How do we control viral scours

A

reduce infection pressure - clean & less animals
ensure colostrum intake
vaccinate dam to ensue lactogenic immunity

383
Q

T or F most viral enteric virus can withstand gastric pH

A

True

384
Q

What is the effect of the large number of replication from enteric virus

A

cytolysis large # virons released

contamination of enviroment in large volumes

Virology (4 decks)

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