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Virology Spring 2017 > Retroviridae-Birnaviridae (exam 2) > Flashcards

Retroviridae-Birnaviridae (exam 2) Flashcards

1
Q

T/F: Retroviridae may exist as a stable component in the host genome

A

True

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2
Q

T/F: Reverse transcriptase is an RNA-dependent DNA polymerase

A

True

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3
Q

What is essential for retroviruses to replicate?

A

reverse transcriptase

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4
Q

What are the 2 subfamilies within retroviridae?

A

Orthoretrovirinae and spumaretrovirinae

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5
Q

How do retroviruses acquire their envelope?

A

By budding from the cell membrane of the cell they replicate from.

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6
Q

T/F: Retroviruses have a diploid genome with 2 copies of single stranded, negative sense RNA.

A

False. It is positive sense RNA (everything else is true).

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7
Q

How do retroviruses integrate into the host genome?

A

by using an enzyme called integrase.

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8
Q

What is found within the nucleocapsid of retroviruses?

A

2 single strands of viral RNA, reverse transcriptase, integrase, and protease.

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9
Q

T/F: retroviridae virions are not resistant to UV or x-rays

A

False.

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10
Q

How are retroviridae virions inactivated?

A

lipid solvents or detergents and by heating.

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11
Q

What does the gag gene encode?

A

capsid, nucleocapsid, and matrix.

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12
Q

What does the pol gene encode?

A

reverse transcriptase and integrase

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13
Q

Alpharetroviruses are within which family and subfamily?

A

Family: retroviridae Subfamily: orthoretrovirinae.

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14
Q

What two diseases represent alpharetroviruses?

A

avian leukosis and sarcoma virus (ALSV)

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15
Q

How are exogenous retroviruses transmitted?

A

horizontally.

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16
Q

What are endogenous retroviruses and how are they transmitted?

A

Viruses included in the genome of most, if not all, animals. Vertically as part of the host genome (passed on from generation to generation).

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17
Q

Who are the members of the alpharetrovirus genus?

A

avian leucosis virus, avian sarcoma virus, avian myeloblastosis virus, Rous sarcoma virus.

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18
Q

What virus is representative of betaretroviruses?

A

Mouse mammary tumor virus.

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19
Q

What does the sag gene in MMTV code for?

A

superantigen.

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20
Q

Feline leukemia virus belongs to what genus?

A

Gammaretroviruses.

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21
Q

T/F: gammaretroviruses affect mammals and reptiles.

A

True

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22
Q

What is special about the deltaretroviruses genome?

A

they contain regulatory genes rex and tax that are expressed from an alternatively spliced mRNA.

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23
Q

T/F: deltaretroviruses are endogenous and exogenous.

A

False. Only exogenous.

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24
Q

What is the prototype of epsilonretroviruses?

A

Walleye dermal sarcoma virus.

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25
Q

T/F: epsilonretroviruses are the only exogenous retroviruses found in fish and reptiles.

A

False. Only endogenous retroviruses in fish and reptiles.

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26
Q

HIV, caprine arthritis-encephalitis virus and meadi-visna virus are important members of what genus?

A

Lentiviruses

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27
Q

What is the purpose of the nef gene and what genus is it found in?

A

it encodes for the nef protein which is essential for replication in target hosts but not in vitro. It can also downregulate the expression of CD4 molecule and alter the activation status of target cells. It is found in lentiviruses.

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28
Q

T/F: Spumaviruses are zoonotic.

A

True.

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29
Q

What viruses (genus) are considered complex viruses?

A

Spumaviruses, lentiviruses, epsilonretroviruses, and deltaretroviruses.

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30
Q

What virus exemplifies spumaviruses?

A

human foamy virus

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31
Q

What is necessary for retroviruses to enter a cell?

A

interaction between a cell surface molecule (receptor) and the envelope proteins on the virion surface.

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32
Q

What receptor is present for cat, dog, and primate gammaretroviruses?

A

GLVR1

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33
Q

What receptors are present for FeLV gammartroviruses?

A

FeLIX and Pit

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34
Q

What is the core receptor for lentiviruses?

A

CD4 found on T helper cells.

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35
Q

What are some outcomes of retroviruses?

A

acute disease due to cell death, latent infection, chronic infection.

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36
Q

What do retroviruses that lead to acute transformations contain?

A

viral oncogenes

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37
Q

p27 in FeLV is encoded by what gene and what is it’s purpose?

A

encoded by the gag gene and it is used in ELISA tests.

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38
Q

Do we have to worry about FeLV transmission via fomites? Why or why not?

A

No, because the virus is readily destroyed by disinfectants, soap, heating and drying.

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39
Q

How is FeLV shed?

A

in saliva, nasal secretions, feces, and milk.

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40
Q

T/F: FeLV can be transmitted through mutual grooming

A

True.

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41
Q

T/F: FeLV can be transmitted via individual mammary glands.

A

True

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42
Q

What is the main determinant of pathogenicity in FeLV?

A

SU protein.

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43
Q

Tropism to lymphoid tissue is seen with FeLV. What can this lead to?

A

Immunosuppression, which can lead to secondary infection.

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44
Q

T/F: there is low or no humoral immunity with FeLV.

A

False. There is low or no cellular immunity.

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45
Q

What role does p15e play in FeLV?

A

blocks T cell reactivity to IL-1 and IL-12 and blocks production of hematopoietic cells, which leads to anemia.

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46
Q

What immunoglobulin levels are normal in an FeLV infection?

A

IgG

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47
Q

What are some clinical signs seen with FIV?

A

dehydration, stomatitis, fever, along with bite wounds and other changes in the oral cavity.

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48
Q

T/F: FeLV can cause lymphoma and leukemia in chronic infections.

A

True.

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49
Q

What is the diagnostic of choice for FeLV?

A

p27 ELISA.

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50
Q

T/F: FeLV vaccine prevents infection and provides complete protection.

A

False.

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51
Q

What interleukin’s production is reduced by FIV? Which is increased?

A

IL-2 is decreased, IL-10 is increased (leading to immunosuppression).

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52
Q

How does FIV deepen immunosuppression?

A

by activating CD4+/CD25+ Treg

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53
Q

Who discovered FIV?

A

Janet Yamamoto and Niels Pederson.

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54
Q

Who is more likely to get FIV, male or female felines?

A

Males.

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55
Q

How is FIV spread?

A

Deep bite wounds and scratches. Saliva must enter bloodstream.

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56
Q

T/F: FIV cannot be transmitted in utero or via mother’s milk.

A

False. It can be, although it is rare.

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57
Q

FIV’s oral clinical signs resemble what other virus?

A

Calicivirus.

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58
Q

Does FIV cause abortions?

A

Yes, but indirectly. It is the high fever which is thought to be the reason for abortions.

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59
Q

What is the most common and reliable method of diagnosis for FIV?

A

ELISA.

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60
Q

T/F: cats affected with FIV cannot live long, happy lives.

A

False. They can and should not be condemned.

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61
Q

Retroviruses that cause disease in birds belong to what groups?

A

Alpharetroviruses and gammaretroviruses.

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62
Q

What is the most common form of avian leukosis caused by retroviruses?

A

Lymphoid leukosis.

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63
Q

What can lead to tumor formation in avian retroviruses?

A

overexpression of the c-myc oncogene.

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64
Q

What is “thick leg syndrome” and what is it caused by?

A

osteoporosis, caused by a replication defective avian retrovirus.

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65
Q

What is one example of cellular transformation of oncogenic viruses? What organs may you see swollen due to this?

A

erythroblastosis, liver and kidneys may be swollen.

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66
Q

Why is equine infectious anemia virus (swamp fever) typically not reported?

A

Because animals are usually asymptomatic.

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67
Q

How is swamp fever transmitted?

A

mainly by biting insects.

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68
Q

What is special about the fly’s ability of transmitting equine infectious anemia virus?

A

It will not transmit the virus if it is able to feed uninterrupted.

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69
Q

Where does swamp fever replicate and how does it get there?

A

In macrophages. It infects monocytes initially and begins to replicate once monocytes become macrophages.

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70
Q

What are the clinical signs you look for in equine infectious anemia virus?

A

petechial hemorrhages and edema. Asymptomatic carriers have a decrease in performance.

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71
Q

What is the test of choice for swamp fever?

A

Coggin’s test, AKA agar gel immunodiffusion.

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72
Q

Paramyxoviruses belong to what order?

A

Mononegavirales

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73
Q

What genus of paramyxoviruses are of concern?

A

Henipavirus

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74
Q

What family does Newcastle disease now belong to?

A

Avulavirus.

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75
Q

What is bovine respiratory syncytial virus used for?

A

as a model to study the human virus.

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76
Q

T/F: Paramyxoviruses virions are pleomorphic

A

True

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77
Q

T/F: the paramyxovirus genome is linear, single stranded, negative sense RNA.

A

True

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78
Q

What are the attachment proteins in paramyxovirus?

A

HN or G.

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79
Q

How do the antibodies directed against glycoproteins HN, H, or G protect against paramycovirus infection?

A

They are neutralizing antibodies.

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80
Q

Where do paramyxoviruses replicate?

A

Cytoplasm of infected cells.

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81
Q

What is the F protein responsible for?

A

F protein mediates fusion of the viral envelope lipid membrane with the target cell membrane.

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82
Q

What is a distinctive feature of paramyxoviruses that express the H or HN protein?

A

Hemoadsorption.

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83
Q

T/F: Inclusion bodies are always produced when paramyxoviruses replicate.

A

True

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84
Q

New Castle Disease is in what genus? What serotype has it been designated?

A

Avulavirus APMV-1

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85
Q

Does New Castle disease affect turkeys?

A

Yes, but infection is usually mild.

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86
Q

Who can transmit New Castle disease subclinically?

A

Wild birds and waterfowl

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87
Q

Is New Castle disease zoonotic?

A

Yes! Causes mild disease characterized by excessive lacrimation, oedema of the eyelids, conjunctivitis, and sub-conjunctival hemorrhage.

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88
Q

How is New Castle disease transmitted?

A

Direct contact with secretions of infected birds (ingestion or inhalation), and via fomites.

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89
Q

Where are lentogenic strains of NDV found?

A

Worldwide.

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90
Q

Can you diagnose NDV by looking at clinical signs alone/

A

No.

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91
Q

What do you typically see with lentogenic strains of NDV?

A

subclinical disease with mild respiratory symptoms.

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92
Q

In which strains is mortality low for NDV?

A

Mesogenic and lentogenic

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93
Q

Which strain of New Castle Disease cause greenish or white diarrhea, dyspnoea, inflammation of the head and neck, and cyanotic discoloration?

A

Velogenic Strain

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94
Q

Which strain of NDV has high mortality?

A

Velogenic strain

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95
Q

How do you diagnose velogenic strains of NDV?

A

tentative dx determined by examining several birds. Final DX determined by virus isolation.

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96
Q

T/F: Velogenic and Mesogenic strains cause significant gross lesions.

A

False. Only Velogenic strains do.

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97
Q

Is NDV a reportable disease?

A

Yes.

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98
Q

What is the best way to dx NDV?

A

Isolating the virus.

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99
Q

Is there a vaccine available for NDV?

A

Yes, there are 2 groups of vaccines: lentogenic and mesogenic vaccines.

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100
Q

Is there treatment or paramyxovirus 1?

A

No.

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101
Q

Is the Nipah virus zoonotic?

A

Yes, it is an emerging zoonosis causing severe disease in animals AND humans.

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102
Q

What does the Nipah virus typically cause?

A

encephalitis and respiratory illness.

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103
Q

What genus does Nipah virus belong to?

A

Henipavirus.

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104
Q

What does Nipah virus cause in pigs? And in humans?

A

severe, respiratory disease in pigs and rapidly progressive encephalitis in humans.

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105
Q

What animals carry the Nipah virus and where is it found?

A

Flying foxes (aka fruit bats). They carry it in their urine and potentially saliva.

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106
Q

Is Nipah virus stable in the environment? What is it susceptible to?

A

Yes, especially in bat urine and contaminate fruit juice. Susceptible to common soaps and disinfectants.

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107
Q

What clinical signs are typically seen in young swine 1-6 months old with Nipah virus?

A

acute fever, labored breathing, nasal discharge, and loud, nonproductive cough. Neurologic signs can be seen.

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108
Q

What clinical signs are typically seen in swine greater than 6 months with Nipah virus?

A

acute fever, marked neurologic signs, respiratory signs, and first trimester abortions.

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109
Q

This virus is in the genus Henipavirus and is classified as a BSL4 agent.

A

Nipah virus

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110
Q

What are 3 ways to ID Nipah virus? What is the preferred method of ID?

A

Virus isolation and characterisation, virus neutralisation, and immunohistochemistry.

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111
Q

What do you do if a pig tests positive for Nipah virus?

A

Cull them.

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112
Q

T/F: Nipah virus is a biological weapon and can be used in bioterrorism.

A

True.

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113
Q

What genus does the canine distemper virus belong to?

A

Morbilivirus.

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114
Q

Which lineage of canine distemper virus is circulating in dogs in north america?

A

None.

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115
Q

Which lineage of canine distemper virus is circulating in raccoons in the USA?

A

America 1

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116
Q

What percentage of distemper infections are subclinical or mild?

A

50%

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117
Q

What is a key sign of distemper?

A

nasal discharge that starts as serous and quickly becomes mucopurulent.

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118
Q

What is typically seen in dogs with canine distemper that have CNS signs?

A

seizures, paraparesis, tetraparesis, and hyperkeratosis on footpads and nose.

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119
Q

T/F: canine distemper virus is stable in the environment.

A

False.

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120
Q

Who is most susceptible to canine distemper?

A

young dogs, 4-6 months of age.

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121
Q

In what cells does the canine distemper virus replicate?

A

Upper respiratory tract macrophages.

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122
Q

T/F: Canine distemper virus infects all cells expressing CD150

A

True

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123
Q

What is the best way to diagnose canine distemper?

A

virus isolation, by adding the virus to lymphocytes. If the cells become shiny, you know the virus is present.

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124
Q

When do you vaccinate puppies against canine distemper?

A

Only after maternal antibodies have gone down.

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125
Q

When was the high pathogenicity avian influenza virus isolated?

A

in 1961

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126
Q

What disease do orthomyxoviruses cause?

A

Influenza

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127
Q

How are influenza viruses classified?

A

based on the type of hemagglutinin and neuraminidase

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128
Q

Which strain of influenza was the first high pathogenicity avian influenza virus of the H5 subtype?

A

H5N1

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129
Q

T/F: orthomyxoviruses are pleomorphic with a segmented genome

A

True.

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130
Q

Which influenza genus lacks neuraminidase?

A

Influenza C.

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131
Q

What are the functions of the surface HA?

A

receptor binding, membrane fusion, and receptor cleavage.

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132
Q

What protein is important in the diagnosis of the influenza virus?

A

M1- matrix protein.

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133
Q

What causes influenza viruses to be sensitive to heat, acidic pH and lipid solvents?

A

their lipid envelope.

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134
Q

Are influenza viruses negative or positive sense?

A

Negative sense.

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135
Q

Where in the cell do orthomyxoviruses replicate?

A

In the nucleus.

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136
Q

What orthomyxovirus is transmitted by ticks and replicates both in the tick and in mammals?

A

Thogotoviruses.

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137
Q

Changes in antigenic setup due to point mutations is known as what?

A

Genetic drift.

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138
Q

Changes in antigenic set up due to reassortment of genetic segments is known as what?

A

Genetic shift

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139
Q

What is the most important viral respiratory disease of horses?

A

Equine influenza viruses

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140
Q

T/F: equine influenza virus is zoonotic.

A

False.

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141
Q

T/F: It is the immune response that makes equine influenza virus worse on the horse, the initial damage of the virus is actually minimal.

A

True.

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142
Q

When is equine influenza likely to end up as bronchopneumonia or chronic respiratory disease?

A

When the virus is not taken care of rapidly and secondary infections occur.

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143
Q

What is the normal temperature of a newborn horse? Adult horse?

A

99.5-102.1 (37.5-38.9) and 99.1-101 (37.2-38.3)

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144
Q

T/F: equine influenza can lead to abortion.

A

True. Prolonged fever due to the virus can cause abortion.

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145
Q

How long do animals remain infectious with equine influenza virus?

A

5 days after clinical signs have disappeared.

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146
Q

T/F: equids are not the only source of equine influenza viruses.

A

False. They are the only source.

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147
Q

What is the diagnostic test of choice for equine influenza?

A

RT-PCR (it is also quick)

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148
Q

Is there a vaccine for equine influenza virus?

A

Yes, there are inactivated vaccines or live vectored vaccines.

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149
Q

Who was the person that isolated swine influenza?

A

Richard Shope

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150
Q

Is swine influenza zoonotic?

A

yes.

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151
Q

T/F: pigs can become infected with avian and human strains of influenza viruses.

A

True. This causes them to be known as “mixing vessels”

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152
Q

How is swine influenza transmitted?

A

through aerosols.

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153
Q

Where does swine influenza replicate?

A

In the upper respiratory tract.

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154
Q

T/F: swine influenza has a long incubation period.

A

False.

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155
Q

T/F: you have to cull all pigs diagnosed with swine influenza, despite their ability to recover.

A

True

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156
Q

What is the preferred method to diagnose swine influenza?

A

hemagglutination inhibition test. Can indicate whether or not there is an active infection.

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157
Q

Why are swine influenza viruses economically important?

A

because of the losses caused due to culling the piggies.

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158
Q

Are there vaccines available for swine influenza?

A

Yes, but they do not provide cross-protection against new subtypes.

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159
Q

What virus is known as the “fowl plague”?

A

Avian influenza virus.

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160
Q

T/F: you have to cull birds affected with avian influenza, thus bringing about economic losses.

A

True.

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161
Q

This virus is notifiable, affects poultry, and is divided into highly pathogenic and low pathogenicity.

A

Avian influenza virus

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162
Q

Where does the avian influenza virus replicate in birds?

A

In the intestinal and respiratory tracts, which causes very high viremia.

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163
Q

Which subtype of avian influenza may kill birds with no clinical signs?

A

Highly pathogenic avian influenza

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164
Q

What is a typical clinical sign of both avian influenza viruses?

A

cessation/decrease in egg production.

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165
Q

How is avian influenza diagnosed?

A

by RT-PCR to detect the matrix protein gene.

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166
Q

How do you know which subtype of avian influenza is present?

A

Analyzing the H gene (if H5 or H7) to determine the cleavage site. If the cleavage site is arginine, it is LPAI, if it is basic amino acids it is HPAI.

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167
Q

Is there a vaccine available to control HPAI?

A

No.

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168
Q

T/F: there is limited person to person spread of swine influenza

A

True.

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169
Q

T/F: all flaviviruses are transmitted by vectors.

A

True.

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170
Q

Who recognized flavivirus as a filterable agent?

A

Walter Reed and James Carrol

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171
Q

Are flaviviruses positie or negative sense? Are they enveloped?

A

positive, yes.

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172
Q

T/F: flaviviruses have an infectious RNA.

A

True.

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173
Q

Where does flavivirus replication take place?

A

In the cytoplasm.

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174
Q

What are flaviviruses susceptible to?

A

heat, common disinfectants, and lipid solvents.

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175
Q

Which is the only flavivirus resistant to heat?

A

Classical swine fever

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176
Q

Which West Nile Virus lineage is seen in North and South America and is also enzootic in Australia?

A

WNV-1

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177
Q

T/F: Humans and horses are main hosts of WNV

A

False. They are accidental, dead end hosts.

178
Q

T/F: Ticks and mosquitoes are both vectors of WNV

A

True. Ticks mainly transmit it in cases of dogs.

179
Q

In what species does WNV cause the most concern in?

A

Horses.

180
Q

What are some clinical signs of WNV in horses?

A

fever, abnormal gait, weakness, and recumbence

181
Q

High viremia is seen in which animals affected by WNV?

A

Birds.

182
Q

What immunoglobulin is used to detect acute infection and when do you test for it?

A

IgM, ~5 days after noticing clinical signs.

183
Q

Are there vaccines for WNV?

A

Yes, and they can prevent disease.

184
Q

T/F: immunity is developed in animals after they have been infected with WNV

A

True.

185
Q

Which BVDV group causes persistent infection?

A

Non-cytopathic viruses.

186
Q

T/F: BVDV can be transmitted vertically.

A

True

187
Q

T/F: acutely infected animals transmit BVDV more efficiently than persistently infected animals.

A

False. Persistently infected animals are more efficient at transmitting the virus.

188
Q

How is bovine viral diarrhea transmitted from herd to herd?

A

via contaminated feed and fomites that are contaminaed with urine, oral, and nasal secretions from persistently infected animals.

189
Q

What are the 3 disease patterns arising from BVDV infection?

A
  1. postnatal infection in non-pregnant cattle (most common in young animals and mild disease).
  2. Infection in pregnant cows
  3. Persistent infection in calves and mucosal disease.
190
Q

What is commonly seen in postnatal infection of non-pregnant cattle with BVDV?

A

mild disease, biphasic fever, diarrhea, ulcerations on lip, muzzle, and oral cavity, as well as decreased milk production.

191
Q

When is BVDV likely to cause embryonic death?

A

When a cow is infected in early pregnancy.

192
Q

When is weak calf syndrome usually seen? What else may be seen in these calves?

A

When the cow is infected with BVDV before there is immunological competence in the fetus. If calf survives they can carry the virus and be seronegative (due to immunotolerance).

193
Q

Persistent infection is caused by what strain of BVDV?

A

non-cytopathic virus.

194
Q

When is mucosal disease often developed?

A

When a cow has both cytopathic and non-cytopathic strains.

195
Q

What is the main manifestation of mucosal disease?

A

Profuse watery diarrhea, fever, and anorexia, as well as nasal discharge.

196
Q

Where does BVDV replicate in a post-natal infection?

A

nasal mucosa and tonsils, before moving to lymph nodes and intestines.

197
Q

Where does BVDV replicate in prenatal and persistent infections?

A

in the fetus (which can lead to autolysis and abortion). If fetus is born, euthanize because they’re gonna die anyways.

198
Q

Where does BVDV replicate in mucosal disease?

A

throughout the GI tract and lymph nodes. This causes acute mucosal disease .

199
Q

In what form of BVDV is hyperkeratosis typically seen?

A

Chronic mucosal disease. Seen on the head, neck, shoulders, and distal extremities.

200
Q

What specimens are collected to diagnose BVDV?

A

nasal exudates, blood, tissue at necropsy, and aborted fetuses.

201
Q

How is BVDV diagnosed?

A

via detection of viral antigen in ear notch samples.

202
Q

What is the best form of control of bovine viral diarrhea ?

A

ID and cull persistently infected animals. Can also vaccinate.

203
Q

What is another name for classical swine fever virus? Where is it not found?

A

Hog Cholera. Not found in N.A.

204
Q

T/F: classical swine fever virus is not a reportable disease because it has been eradicated in North America, Austrailia, New Zealand, Ireland, the UK, and Scandinavia.

A

False. It is 100% reportable.

205
Q

What is the primary site of replication for classical swine fever virus? The secondary site?

A

Tonsils, then lymphoid tissue.

206
Q

Aside from tonsils and lymphoid tissue, what other tissue can classical swine fever virus move to?

A

vascular endothelium, mononuclear phagocytes, and other cells of the immune system.

207
Q

How is classical swine fever transmitted?

A

direct contact (oronasal route) or through fomites.

208
Q

What clinical signs are seen with classical swine fever?

A

very high fever, diffuse hyperemia on the abdomen and ears, depression, anorexia, and conjunctivitis.

209
Q

How long is the incubation period of hog cholera?

A

2-4 days

210
Q

What strain can cause a chronic or sub-acute infection with classical swine fever?

A

a moderately virulent strain.

211
Q

T/F: a pig can be infected with classical swine fever and have no visible clinical signs.

A

True. This would mean they’re infected with a low virulence strain.

212
Q

What is the outcome of a pregnant sow becoming infected with classical swine fever?

A

fetal infection, embryonic death, abortion, fetal mummification, or still births.

213
Q

T/F: tissue specimens collected when classical swine fever is suspected do not need to be sent to reference laboratories.

A

False.

214
Q

Are there vaccines available for CSF? If so, what types?

A

Yes, both live attenuated and live virus vaccines.

215
Q

What do you do if animals are infected with classical swine fever?

A

cull them

216
Q

What order does arteviridae belong to? How many genuses does it have?

A

Order: Nidovirales, 1 genus (arterivirus).

217
Q

Is Arterivirus an enveloped virus? Does it have positive or negative sense RNA?

A

Yes. Positive sense.

218
Q

What is the major glycoprotein present in arteriviruses and what is it responsible for?

A

GP5, responsible for induction of neutralizing antibodies.

219
Q

Where do arteriviruses replicate?

A

Mainly in macrophages.

220
Q

What glycoproteins are responsible for cell tropism and receptor binding?

A

GP2, 3, and 4.

221
Q

What does equine arteritis virus (EAV) cause in horses?

A

Equine viral arteritis (EVA)

222
Q

How is equine arteritis spread, and who does it affect?

A

mainly spread by asymptomatically infected stallions. Only affects horses and donkeys.

223
Q

T/F: most infections of EAV have distinct clinical signs.

A

False. Most are asymptomatic.

224
Q

How is EAV transmitted?

A

Via aerosol or venereal routes.

225
Q

What are some clinical signs of EAV?

A

excessive lacrimation, conjunctivitis, fever at onset of disease, and nasal discharges.

226
Q

What disease that belongs to the genus arterivirus causes edema over the eyes, which then progresses backwards towards the abdomen, prepuce, scrotum, and mammary glands?

A

Equine arteritis virus.

227
Q

Why do we care about EAV if most infections are subclinical/asymptomatic?

A

Because abortion is characteristic in mares infected with certain strains of EAV.

228
Q

Where is the virus seen during persistent infection?

A

To the reproductive tract.

229
Q

Where does EAV replicate initially?

A

in alveolar macrophages and endothelial cells.

230
Q

Spread of EAV to what tissues cause abortion?

A

mesothelium and smooth muscles of the media of arteries and uterine wall.

231
Q

T/F: the cytokine storm caused by EAV is mainly responsible for the vascular damage seen.

A

False. Most damage is actually caused by the immune system response.

232
Q

What is the preferred form of diagnosis of EAV?

A

RT-PCR. Quick!

233
Q

What are some ways to prevent EAV?

A

ID carrier stallions and remove them from the herd, as well as vaccinating mares a few weeks before pregnancy. Can also vaccinate breeding stock and colts.

234
Q

Porcine reporoductive and respiratory syndrome virus (PRRSV) is part of what genus?

A

Arterivirus.

235
Q

Where is PRRSV typically seen?

A

Worldwide in swine breeding countries.

236
Q

Who typically suffers from reproductive failure caused by PRRSV?

A

gilts or sows. Not very frequent in boars.

237
Q

What secretions is PRRSV present in?

A

urine, nasal secretions, semen****, and mammary gland secretions.

238
Q

T/F: PRRSV has mosquitoes and house flies serving as fomites.

A

True.

239
Q

What age groups are the most susceptible to PRRSV?

A

Gilts.

240
Q

What are one of the first signs seen in young animals suffering from PRRSV?

A

respiratory distress. Will also see cyanosis of the ears, abdomen, and vulva.

241
Q

What does PRRSV do to a boar’s semen?

A

decreases the quality of it.

242
Q

When are mummies and stillbirths typically seen during a PRRSV infection?

A

When the infection occurs in the third trimester.

243
Q

Where does PRRSV primarily replicate?

A

in lymphoid tissue, particularly pulmonary alveolar and intravascular macrophages.

244
Q

When is PRRSV likely to cross the placenta and replicate in umbilical vessels of the fetuses?

A

in late gestation (72 days), which can kill all or non of the fetuses.

245
Q

What is the most accurate way to detect PRRSV?

A

fluorescent antibody test.

246
Q

What are the best tissues used for virus detection of PRRSV?

A

BAL, serum, lung lymph nodes, tonsils, and spleen.

247
Q

T/F: vaccines are an efficient way to control PRRSV.

A

False. There is too much virus variation for vaccines to be the solution. There is no single successful control measure.

248
Q

What is the best way to achieve stabilization of the virus in large herds?

A

Intentional whole herd infection. Important to select appropriate strains because some animals can die.

249
Q

When should pigs be vaccinated against PRRSV?

A

Before the breeding season.

250
Q

What viruses are considered arboviruses?

A

Orthobunyavirus, Phelbovirus, and Nairovirus.

251
Q

What family of viruses have a lipid envelope with glycoprotein spikes, has 3 segments of negative sense, single stranded RNA, with each segment designated as L,M, and S?

A

Bunyaviridae.

252
Q

Which protein is responsible for cell receptor binding in bunyaviruses?

A

Gn protein.

253
Q

Bunyaviruses are sensitive to what?

A

sensitive to heat and acid conditions, detergents, lipid solvents, and common disinfectants.

254
Q

Where does replication of Bunyaviruses take place?

A

the cytoplasm

255
Q

The Akabane virus belongs to what genus?

A

Orthobunyavirus.

256
Q

Where is Akabane virus found and what does it cause?

A

Found in Africa, Asia, Australia, and Japan. It causes fetus death and abortion or deformation hydraencephaly or arthrogryposis.

257
Q

Who is the most susceptible to Akabane virus?

A

Pregnant cow and ewes.

258
Q

Where does the Akabane virus replicate when it infects the fetus?

A

In the nervous system and muscles.

259
Q

What is the best way to diagnose Akabane virus?

A

gross pathological examination and isolation of the virus from the placenta, fetal brain, and muscles.

260
Q

Is there a vaccine available for the Akabane virus?

A

Yes.

261
Q

Rift Valley fever virus belongs to what genus?

A

Phlebovirus

262
Q

Who does the rift valley fever virus affect and how is it transmitted?

A

sheep, goats, and cattle. Transmitted by mosquitoes (aedes spp.).

263
Q

What is the incubation period of the rift valley fever virus?

A

3 days (short)

264
Q

What are the clinical signs of rift valley fever virus?

A

fever, inappetence, mucopurulent nasal discharges, and nasal diarrhea.

265
Q

T/F: although abortion can occur in pregnant ewes affected with RVFV, it is not a common occurrence.

A

False. Abortion occurs in 90-100% of pregnant ewes.

266
Q

Where does the rift valley fever virus replicate?

A

In liver parenchyma and lymphoreticuloorgans.

267
Q

What is usually the cause of death in animals affected by RVFV?

A

hepatic necrosis or renal failure.

268
Q

This virus is an overlap select agent, it is zoonotic, and considered a BSL3 agent.

A

Rift Valley Fever virus.

269
Q

What is the best way to control RVFV?

A

Mosquito control.

270
Q

Bornaviridae belongs to what order?

A

Mononegavirales

271
Q

What is the G protein in bornaviridae responsible for?

A

induction of neutralizing antibodies.

272
Q

Where do bornaviruses replicate?

A

In the nucleus.

273
Q

what mediates endocytosis of the virus into the host cell?

A

attachment of the viral g glycoproteins to host receptors.

274
Q

T/F: Bornaviruses are cytolytic and do not cause persistent infections.

A

False. They are non-cytolitic and DO cause persistent infections.

275
Q

What virus within the bornavirus family is a natural infection in horses and sheep?

A

Borna disease virus

276
Q

T/F: Borna disease virus is zoonotic.

A

True.

277
Q

T/F: Borna disease causes a neurological disease that can be fatal

A

True, although it is rare.

278
Q

How is borna disease virus transmitted?

A

oronasally.

279
Q

What are some clinical signs of borna disease virus?

A

chewing motion without food intake, excessive salivation, fever, neurologic disturbance

280
Q

T/F: borna disease virus can cause blindness and headpressing

A

True

281
Q

What virus is implicated in neuropsychiatric disease in humans?

A

Borna disease virus

282
Q

T/F: Borna disease virus elicits protective immune response.

A

False.

283
Q

What are some pathological processes caused by Borna disease virus?

A

extensive perivascular cuffing with T cells, macrophages, and plasma cells.

284
Q

Does Borna disease virus have pathognomonic lesions? If so, what are they?

A

Yes, eosinophilic intranuclear inclusion bodies in neurons called “Joest-Degen” bodies.

285
Q

What is the best way to dx BDV?

A

Post-mortem immunohistochemistry in brain sections.

286
Q

What disease causes proventricular dilatation disease of psittacine birds?

A

Avian bornavirus

287
Q

This virus family is the cause of fatal disease only in birds and is second only to rotaviruses in causing diarrhea?

A

Astroviridae.

288
Q

What are the 2 genera within the family Astroviridae, and which do we care about?

A

Avastrovirus and mamastrovirus. We care more about avastrovirus.

289
Q

T/F: Astroviridae are enveloped viruses

A

False.

290
Q

Where does astroviridae replicate? Is its RNA infectious?

A

cytoplasm, yes.

291
Q

Do all strains of turkey astrovirus kill the birds?

A

No. Only some strains do.

292
Q

What is the main clinical sign of turkey astrovirus?

A

diarrhea

293
Q

What pathology does turkey astrovirus cause?

A

intesines (particularly the ceca) are dilated and filled with fluid.

294
Q

What is a characteristic of all prion diseases?

A

spongiform degeneration of the gray matter of the brain. They are responsible for transmissible spongiform encephalopathies.

295
Q

What are prions?

A

normal cellular proteins that have undergone conformational changes and have become pathogenic.

296
Q

What is the abnormal cell protein called?

A

PrPsc

297
Q

T/F: amino acid sequence of PfPc and PrPsc in a given host are different, making the easily distinguishable.

A

False. They are identical.

298
Q

What breeds of sheep are susceptible to Scrapies?

A

Suffol and Hampshire sheep breeds

299
Q

T/F: Goats are also primary hosts of Scrapies

A

False. They are incidental hosts.

300
Q

What is the main mode of transmission of scrapies?

A

Unknown, but oral route is suspected, via infected feed.

301
Q

What is the incubation period of scrapies?

A

2-5 years

302
Q

What are the clinical signs of scrapies?

A

intense pruritus (leading to loss of wool), tremors seen initially, ataxia.

303
Q

T/F: neuronal vacuolation and degeneration, astrocytic hypertrophy and hyperplasia, and an inflammatory reaction are all pathological processes seen with scrapies.

A

False. No inflammatory reaction is seen.

304
Q

What prion disease causes “mad cow disease”?

A

Bovine spongiform encephalopathy.

305
Q

How is BSE transmitted?

A

Through meat-and-bone meal derived from ruminant meat or offal (oral route)

306
Q

What are some clinical signs of BSE?

A

progressive apprehensive behavior, hind limb ataxia, reduced milk yield, tremors.

307
Q

What are some pathologies seen with BSE?

A

neuronal vacuolation, astrocytic hypertrophy and hyperplasia, degeneration and loss of neurons.

308
Q

T/F: diagnosis is based solely on clinical signs.

A

True.

309
Q

What is used to demonstrate PrPsc?

A

Immunohistochemistry.

310
Q

What is the viral genome of reoviruses composed of?

A

segmented, double stranded RNA.

311
Q

Where in the cell do reoviruses replicate?

A

in the cytoplasm.

312
Q

What two subfamilies are found within the Reoviridae family?

A

Sedoreovirinae and Spinareovirinae.

313
Q

Blue Tongue disease is a member of what genus?

A

Orbivirus.

314
Q

T/F: Blue tongue disease affects both sheep and deer.

A

True. White tailed deer are most susceptible to BTV.

315
Q

Who is the primary reservoir and amplifying host of BTV?

A

Cattle.

316
Q

T/F: Blue Tongue disease is a list B disease of OIE and is notifiable.

A

False. It is a list A disease.

317
Q

T/F: Blue tongue virus is a very expensive disease.

A

True.

318
Q

What 2 viral proteins make up the outer shell of blue tongue?

A

VP2 and VP5

319
Q

What species of biting midges are the vectors in Southeast US? In the rest of the US?

A

Culicoides insignis and culicoides variipennis (respectively)

320
Q

Can blue tongue virus be transmitted transplacentally and venereally?

A

Yes, but its less common.

321
Q

T/F: Blue tongue virus causes abortion.

A

True, in enzootic areas.

322
Q

What are some of the main clinical signs of BTV in sheep?

A

cyanosis and necrotic ulceration of the tongue (hence the name). Severe fever initially.

323
Q

What are some clinical signs of BTV seen in cattle?

A

Hemorrhage and congestion of muzzle, serous to mucopurulent nasal discharge, coronitis and lameness, abortion.

324
Q

What is the best way to dx blue tongue virus?

A

Blue tongue is a major way. Competitive ELISA is the ideal test, followed by the AGID test.

325
Q

T/F: blue tongue vaccines are not typically serotype specific.

A

False.

326
Q

T/F: dogs are often also affected by African Horse sickness, if they are in close contact with horses, donkeys, or mules.

A

False. They can contract AHS but it is rare and they have to eat infected carcass material.

327
Q

T/F: AHS and BTV are both regarded as List A diseases by the OIE

A

True

328
Q

Who is the primary vector of African Horse Sickness?

A

Culicoides imicola. C. bolitinos is also a vector, just not primary.

329
Q

What animal is an inapparent carrier of AHS?

A

Zebras. They serve as a reservoir.

330
Q

What are some clinical findings in horses affected with AHS?

A

profuse nasal discharge of serous fluid and froth, pulmonary edema, frothy fluid in lungs and trachea, among others. Seen in Dunkop (acute version of disease).

331
Q

What is another name for the sub-acute horse sickness? What clinical signs are seen with this form?

A

Dikkop. Hydroperitoneum, edema of the mucosa of the colon, numerous petechiae in serosa of large intestine.

332
Q

Is African horse sickness a notifiable disease?

A

Yes.

333
Q

What is the recommended course of action for animals infected with African Horse Sickness?

A

Slaughter.

334
Q

Which rotavirus is the most common cause of viral diarrhea in young humans and animals/birds?

A

RVAs (Group A rotaviruses)

335
Q

What 2 viral proteins of rotaviruses are used as the basis for rotavirus vaccines?

A

VP7 and VP4

336
Q

What is the most likely route of rotavirus spread?

A

Fecal-oral. Very stable virus present in large amounts in infected stool.

337
Q

What is the main site of replication of rotaviruses?

A

mature enterocytes on the villi of upper small intestine.

338
Q

What is the main clinical sign of rotavirus?

A

profuse diarrhea, watery to pasty in consistency, often pale yellow in color, sometimes with blood flecks.

339
Q

How is rotavirus diagnosed?

A

PAGE, ELISA, PCR, FAT, among others.

340
Q

T/F: there are rotavirus vaccines available that are highly efficacious and recommended for control of the virus.

A

False. Vaccines are available but efficacy is questionable.

341
Q

Is rotavirus zoonotic?

A

Yes.

342
Q

How are reoviruses spread and who is most susceptible to them?

A

Fecal oral route, broiler chickens being the predominant host.

343
Q

What is a major clinical sign of avian reovirus?

A

lameness/leg weakness.

344
Q

Pale bird syndrome is seen with which virus?

A

Avian Reovirus

345
Q

Are there vaccines available for avian reovirus?

A

Yes.

346
Q

What is the difference between the nucleocapsid in the genus coronavirus vs. genus torovirus?

A

coronavirus has a helically coiled nucleocapsid, whereas torovirus has a tubular nucleocapsid that looks like a donut.

347
Q

How does coronaviridae acquire its envelope?

A

By buddin off of the endoplasmic reticulum.

348
Q

This disease is caused by the genus corona virus and is a highly infectious viral disease of pigs characterized with vomiting, diarrhea, and high mortality in piglets. It is a List B OIE disease.

A

Transmissible gastroenteritis (TGE)

349
Q

Which form of TGE is less severe, becomes a respiratory virus due to a mutation and has a significantly lower mortality/morbidity?

A

The endemic form. Often seen in partially immune herds.

350
Q

Where is the epidemic form of TGE usually seen?

A

In farms where TGE has not been before (naive herds)

351
Q

T/F: TGE can be spread by the fecal oral route and aerosol transmission.

A

True.

352
Q

How are piglets most commonly infected with TGE?

A

By coming into direct contact with subclinically infected adults.

353
Q

What does the virus infection of TGE do to the intestinal villi and how does this lead to diarrhea?

A

It causes blunting and fusion of intestinal villi, leading to malabsorption and diarrhea

354
Q

What are the clinical signs of TGE? What is the incubation period?

A

incubation: 24-48 hrs. Will typically see: profuse diarrhea, vomiting, severe depression and dehydration, watery, yellow-green stool, feces with undigested milk.

355
Q

T/F: bloated intestines are not part of the pathogenicity of TGE.

A

False.

356
Q

How do you prevent piglets from acquiring a TGE infection?

A

All in, all out management system. keeping piglets separated from adult pigs.

357
Q

What group of coronavirus causes porcine epidemic diarrhea?

A

group 1b (1a causes TGE)

358
Q

T/F: PED does not have a high mortality rate and it is not an important viral pathogen in N.A.

A

False. mortality is almost 100% and it is important in the US, causing big economic losses.

359
Q

what does porcine hemagglutinating encephalomyelitis do to RBCs? What is another name for this disease?

A

can agglutinate RBCs. AKA vomiting and wasting disease in pigs.

360
Q

T/F: acute encephalomyelitis caused by PHE is non-suppurative and often affects piglets <2 weeks of age.

A

True.

361
Q

What clinical signs are often seen with the vomiting and wasting disease form of PHE?

A

repeated retching and vomiting, rapid emaciation, anterior abdomen distended from impaired emptying and accumulation of gas. Neonates can become dehydrated, cyanotic, and die.

362
Q

When is bovine coronavirus infection in calves usually most common?

A

During the winter months.

363
Q

What is the main finding of bovine coronavirus infection in calves? what is a minor clinical finding of this disease.

A

Main: diarrhea. Minor: respiratory symptoms.

364
Q

How is bovine coronavirus infection in calves transmitted?

A

fecal oral, potentially aerosol.

365
Q

How do you treat bovine coronavirus infection?

A

IV fluid therapy!

366
Q

T/F: there is no vax for bovine coronavirus infection.

A

False. There is a vaccine and it is administered to pregnant mommas to give passive immunity to calves.

367
Q

T/F: winter dysentery causes mild disease in case of calves.

A

True. Disease occurs in mature cattle. esp recently calved lactating cows.

368
Q

What are the clinical signs of dysentery in cows?

A

explosive outbreak of diarrhea, dark green to black colored feces, presence of blood flecks in poop, dehydration, decline in mil production and coughing.

369
Q

T/F: Winter dysentery is a self limiting disease.

A

True.

370
Q

What is the main form of transmission of FIP?

A

Fecal-oral transmission. However, can also be inhaled and transplacentally transmitted.

371
Q

What percentage of cats are affected by FIP? How many are persistent carriers? How many have a transient infection?

A

1-3%; 5-10%; 70%

372
Q

T/F: most mutations of feline coronavirus result in avirulent/less virulent variants.

A

True.

373
Q

FIPV is dependent on what type of immunity?

A

cell mediated immunity. If the response is strong, FIPV can be prevented.

374
Q

T/F: FCoV has no affinity for macrophages and don’t replicate efficiently there.

A

True. FIP mutations are the ones that efficiently replicate in macrophages/have increased affinity there.

375
Q

How do FIPV infected macrophages diminish the CMI?

A

production of IL-10 which skews the immune response to a Th2 cell response, diminishing the cell mediated immunity.

376
Q

How does FIP enter the macrophage?

A

Via a CD13 receptor.

377
Q

What are common clinical signs of FIP effusive form?

A

ascitis (distended abdomen), diffuse fibrinous peritonitis, ascites, and pyogranulomas. Will also see serofibrinous pleuritis and thoracic effusion.

378
Q

What are common clinical signs of the non-effusive form of FIP?

A

ganulomatous inflammation and enlarged mesenteric lymph nodes, pyogranulomatous lesions and meningoencephalitis, granulomatous uveitis and leratic precipitates on the inner cornea.

379
Q

How is FIP diagnosed?

A

Rivalta test, if the drop of abdominal effusion disappears, negative for FIP.

380
Q

T/F: you can tell the difference between FCoV and FIP using ELISA, IFA, and virus neutralization tests.

A

False. You can only test for the presence of antibodies.

381
Q

What causes avian infectious bronchitis?

A

coronavirus infectious bronchitis virus.

382
Q

T/F: avian infectious bronchitis can cause respiratory, nephrotropic, and uterotropic disease.

A

True.

383
Q

What is the most common presentation of IBV?

A

respirator disease.

384
Q

How is IBV transmitted?

A

aerosol/inhalation, direct contact, and contact with contaminated poultry, litter, food, water, equipment, or other fomites.

385
Q

T/F: mycoplasma or E.coli can enhance the severity of IBV

A

True.

386
Q

How is IBV controlled?

A

proper hygiene and vaccination. Live vax is given to prime meat type chickens, and inactivated vax is given 13-18 weeks post priming.

387
Q

How are toroviruses transmitted? What do they cause and who do they affect?

A

transmitted by fecal oral route, cause gastroenteritis in mammals, primarily in cattle.

388
Q

What are the 2 serotypes of bovine torovirus? What is another name for this virus?

A

serotypes 1 and 2. AKA Breda virus.

389
Q

Where do alphaviruses replicate?

A

in the cytoplasm.

390
Q

The rural cycle (aka epizootoic cycle) involves what animals?

A

Domestic animals and vectors. Domestic animals are the amplifying hosts.

391
Q

What is another name for the enzootic cycle? What animals does it involve?

A

sylvatic cycle. vector and vertebrate host.

392
Q

The epidemic cycle is also known as ____.

A

The urban cycle.

393
Q

Which equine encephalitis virus is the most severe?

A

Eastern equine encephalitis.

394
Q

Which EEEV group is the most virulent to humans and horses?

A

group I

395
Q

Who is the main vector for the EEEV enzootic cycle? When is this typically seen?

A

C. melanura, primary summetime.

396
Q

T/F: humans and horses are primary hosts of EEEV.

A

False. They are dead end hosts and cannot transmit the virus.

397
Q

Who serves as the primary and amplifying host of EEEV?

A

passerine birds/marsh birds.

398
Q

Where does EEEV replicate?

A

myocytes, fibroblasts,reticuloendothelial cells, lymphoid cells, and osteoblasts. Will replicate in organs after this.

399
Q

T/F: EEEV will present with colic, blindly walking into objects (head pressing), involuntary muscle movement, and then paralysis

A

True.

400
Q

T/F: many humans suffer from severe disease when affected with EEEV.

A

False. Mainly they get the mild/subclinical forms of the disease.

401
Q

T/F: birds usually suffer from severe disease when affected with EEEV

A

False. asymptomatic, considered reservoir hosts.

402
Q

Which strains of western equine encephalitis virus are more virulent?

A

epizootic strains found in north america.

403
Q

T/F: sporadic individual cases of WEEV are more common than epidemics.

A

True.

404
Q

Who is the main vector for the primary cycle of WEEV?

A

Culex spp. (mosquitoes) reservoir hosts is birds still.

405
Q

In what cycle do lagomorphs and rodents serve as amplification hosts?

A

Secondary cycle, epizootic. (Aedes is the mosquito vector species)

406
Q

T/F: WEEV is clinically different from EEEV

A

False. clinically indistinguishable.

407
Q

How long is the incubation period of WEEV in humans?

A

5-10 days.

408
Q

Which subtypes of VEEV are highly virulent for equines?

A

I-A, I-B, I-C (epizootic/epidemic cycle.

409
Q

Who is the amplification host in the enzootic cycle of VEEV? Who is the primary vector?

A

Rodents, Culex species of mosquito.

410
Q

Who is the amplification host in the epizootic cycle of VEEV? Vector?

A

Horses. Vector is mosquito, multiple species.

411
Q

Can in-utero infections occur in horses affected with VEEV?

A

Yes.

412
Q

How does VEEV normally present in humans?

A

acute, mild, systemic disease, usually. Can cause congenital disease in pregnant women, along with fetal encephalitis, abortions, or stillbirth.

413
Q

What is the best way to control and prevent equine encephalitis?

A

Control of mosquito population.

414
Q

T/F: there are vaccines for EEV in both humans and horses.

A

False. Only authorized vaccines for horses.

415
Q

What is the genome of caliciviridae like?

A

linear, single stranded, positive sense.

416
Q

Where does calicivirus replicate?

A

in the cytoplasm.

417
Q

What does the virulence of virus depend on?

A

The genetic makeup of the virus.

418
Q

What genus does Calicivirus belong to?

A

Vesivirus.

419
Q

What causes limping syndrome?

A

Feline calicivirus. This happens occasionally.

420
Q

T/F: calicivirus can be fatal.

A

True. This is new, due to newly emerged highly virulent forms of the virus.

421
Q

How is FCV transmitted?

A

shed in oral, nasal, and conj. secretions. Largely transmitted by direct contact (inhaled, ingested, or via conj).

422
Q

What is the most common lesion seen with FCV? What else is seen?

A

ulcers on tongue. rhinitis, pneumonia in complications.

423
Q

Do vaccines protect against FCV-associated virulent systemic disease?

A

No, vaccinated cats have been affected

424
Q

What is seen with FCV-VSD?

A

ulceration of tongue, mild hyperemia to sloughing of the foot pad, bronchointestinal pneumonia and necrosis of the liver, spleen and pancreas.

425
Q

Should you vaccinate cats that have been affected by FCV?

A

Yes. They are likely not protected for life or from different strains.

426
Q

What other diseases is vesicular exanthema of swine?

A

foot-and-mouth disease, vesicular stomatitis, and swine vesicular disease.

427
Q

Is VES reportable?

A

Yes.

428
Q

VES is antigenically related to what other virus?

A

San miguel sea lion virus.

429
Q

Is birnaviridae enveloped? is the RNA single or double stranded?

A

non-enveloped, double stranded

430
Q

Where does birnaviridae replicate?

A

in the cytoplasm

431
Q

What is another name for infectious bursal disease?

A

Gumboro Disease.

432
Q

What is the primary target of infectious bursal disease?

A

lymphoid tissue, with special predilection for bursa of fabricious

433
Q

Which IBD serotype is pathogenic to chickens?

A

Serotype 1.

434
Q

How is IBD transmitted?

A

fecal-oral transmission.

435
Q

How do you control IBD?

A

Hard to, it is very stable against cleaning and disinfectants. Detected in water and feed after 52 days.

436
Q

What leads to immunosuppression during infection with IBD?

A

severe depletion in B cell production (due to necrosis and apoptosis).

437
Q

T/F: If birds recover, they can live normally, and their immune system recovers.

A

False. Antibody response is diminished and they are susceptible to secondary infections.

438
Q

What clinical signs are seen with IBD?

A

distress, depression, ruffled feathers, diarrhea, anorexia, swollen bursa fabricious with hemorrhages.

439
Q

How do you diagnose IBD?

A

clinical signs and post mortem exam.

440
Q

Why is it not recommended to vaccinate a bird with the mild form of the vaccine before they are 4 weeks of age?

A

Because the maternal antibodies can neutralize the vaccine, and immunity doesn’t form. Would give intermediate or hot vax.

Virology Spring 2017 (1 decks)

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