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Virology Final Flashcards

Tricias Equine, Swine, and Avian plus the 4 bovine

1
Q

What family is equine infectious anemia?

A

retroviridae

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2
Q

How is equine infectious anemia transmitted? 3 ways

A

blood feeding insects (stable fly and horse fly) - mechanical
iatrogenic
placenta and milk

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3
Q

Where does EIA persist in the horse for life?

A

leukocytes

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4
Q

What happens during the subacute form of EIA?

A

moderate fever, recovery from neutralizing Ab

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5
Q

What are the CS of chronic EIA?

A

mild, episodic fever, cachexia anemia, and ventral edema

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6
Q

What are the cells infected by EIA?

A

macrophages and lymphocytes

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7
Q

What can immune complexes cause in EIA?

A

vasculitis, glomerulonephritis

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8
Q

What can cause the reoccurant infection during EIA?

A

significant genomic variations

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9
Q

How is EIA diagnosed?

A

Serology - coggins, ELISA

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10
Q

What are characteristics of Arteriviridae?

A

RNA, enveloped

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11
Q

What diagnostic can be used to detect proviral DNA of EIA in foals and seropositive animals?

A

PCR

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12
Q

What are the 2 main CS of EVA?

A

respiratory dz and abortions

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13
Q

What kind of morbidity and mortality does EVA have?

A

high morbidity, low mortality

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14
Q

What is the rate of abortion in EVA and at what time of pregnancy do they occur?

A

50%, 5-10 months

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15
Q

What is atypical about the transmission of EVA?

A

can remain viable in the environment for long periods (but is enveloped)

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16
Q

What role do stallions play in transmitting EVA?

A

long term shedders, result in venereal spread

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17
Q

How else is EVA spread besides venereal?

A

fomites
fetal fluids of aborted fetus
transplacental

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18
Q

How does EVA become viremic?

A

alveolar macrophages –> lymph nodes –> viremia

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19
Q

Where does EVA replicate in the horse?

A

endothelial cells

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20
Q

What are some ddX for EVA?

A

equine herpesvirus, influenza, EIA

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21
Q

What is the diagnostic test of choice for EVA?

A

RT-PCR

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22
Q

Where are samples collected for diagnosing EVA?

A

nasopharyngeal swabs, blood, urine, aborted fetus

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23
Q

When should vaccines be given to mares before mating with a EVA stallion? Wen should mares NOT be vaccinated?

A

mating - at least 3 weeks in advance

dont vax during last 2 months of pregnancy

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24
Q

When should foals be vaccinated for EVA?

A

6-8 months

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25
Q

What family causes equine encephalitides?

A

togaviridae

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26
Q

What are the characteristics of togaviridae viruses?

A

RNA, enveloped, zoonotic, bird resevoirs

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27
Q

What are the CS associated with encephalitides?

A

neurologic signs, encephalitis, neurologic sequelae

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28
Q

What part of encephalitides pathogenesis is important for transmission and CNS invasion?

A

2nd viremia - high titer

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29
Q

What are the differential diagnosis for equine encephalitides?

A

rabies, equine herpes 1, west nile

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30
Q

What diagnostic tests are used for equine encephalitides?

A

IgM capture ELISA
confirmation - neutralization
postmortem RT-PCR from brain

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31
Q

What are the 2 control measures for equine encephalitides?

A

inactivated vax

mosquito control

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32
Q

What family is west nile encephalitis?

A

flavivirdae (RNA, enveloped, arbovirus, zoonotic)

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33
Q

What are the CS associated with west nile?

A

asymptomatic, neurologic, small proportion die

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34
Q

What are the diagnostic tests for west nile virus?

A

anything (sero or antigen)

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35
Q

What kind of vaccine is available for west nile?

A

recombinant vax

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36
Q

What is the agent that causes equine influenza?

A

orthomyxoviridae - influenza A

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37
Q

What clinical signs are present in equine influenza?

A

bronchopneumonia

prolonged fever –> abortion

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38
Q

What is the pathogenesis of equine infuenza? What are some of the secondary infections?

A

epithelial cells in respiratory –>inflammation –> nasal serous discharge
secondary infections –> conjuctivitis, bronchopneumonia, guttural pouch infections

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39
Q

What are the differential diagnosis for equine influenza virus?

A

herpes 1 and 4, adenovirus, rhinovirus

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40
Q

What samples can be used for equine influenza diagnosis?

A 
nasal mucus (early on)
lung material (necropsy)
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41
Q

What diagnostic tests are used for equine infuenza?

A

virus isolation in culture
hemagluttination inhibition –> strain
retrospective serologic testing

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42
Q

What is the agent that causes equine rhinopneumonitis?

A

EHV-4

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43
Q

What can be used to diagnose EHV-4 (equine rhinopneumonitis)?

A

almost anything - virus isolation

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44
Q

What are control measures for EHV-4?

A

vaccines

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45
Q

What are characteristics of the adenovirus family?

A

DNA, naked, intranuclear inclusion bodies

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46
Q

What are clinical signs of adenovirus pneumonia in horses?

A

most –>asymptomatic

mild upper and lower respiratory infection

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47
Q

What are the problems in arabian foals with SCID and have adenovirus pneumonia?

A

virus destroys cells in pancreas salivary glands, renal, bladder, intestinal epithelium

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48
Q

What can be used to diagnose adenovirus pneumonia? How is it controlled?

A

almost any test

nothing is done to control

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49
Q

What are the characteristics of coronaviridae?

A

RNA, enveloped

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50
Q

What are the clinical signs of coronavirus?

A

self limiting diarrhea in foals (not as common as rotavirus)

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51
Q

What is the agent that causes equine abortion virus?

A

EHV-1

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52
Q

When does abortion occur in horses when they have EHV-1?

A

last 4 months of pregnancy

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53
Q

What type of EHV-1 infection can result in fatal generalized disease in horses?

A

perinatal infection

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54
Q

What leads to ataxia, recumbency, limb paralysis and death in EHV-1 in horses?

A

encephalitis

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55
Q

What is the most common sign of EHV-1 in horses for virus myelopathy?

A

urinary incontinence

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56
Q

What is the pathogenesis of EHV-1?

A

antigen-antibody complexes –> vasculitis, ischemia, infarcts –> neurologic disease and abortion

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57
Q

What type of EHV-1 causes respiratory distress and high mortality?

A

pulmonary vasculotropic EHV1

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58
Q

What other clinical signs are present during EHV1 besides neurologic, respiratory, and abortion?

A

ocular disease

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59
Q

What tests are used to diagnose EHV-1?

A

anything - intranuclear bodies, virus isolation, PCR, immunoflourescence, paired serum

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60
Q

What is the causative agent of equine coital exanthema?

A

EHV-3

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61
Q

What are the general clinical signs of EHV-3?

A

acute, mild, pustules in genital area, on lips of foals, respiratory mucosa, NO ABORTION, decreased libido

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62
Q

How is EHV-3 diagnosed?

A

pigment loss on black skin in genital region

PCR, serology

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63
Q

What virus is suspected in causing equine sarcoid?

A

bovine papillomavrus

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64
Q

What equine sarcoid type are hairless areas of slightly thickened skin?

A

occult sarcoids

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65
Q

What type of equine sarcoid appears on head, neck, and groin and grows slowly?

A

verrucous sarcoids

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66
Q

What is the transmission of EHV-3?

A

direct, sexual, fomites

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67
Q

What lesions does equine papillomatosis cause??

A

small papillomas around lips, nose, regress in 1-9 months

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68
Q

How is vesicular stomatitis transmitted?

A

breaks in mucosa and skin

also by arthropods and fomites

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69
Q

What are some of the clinical signs of vesicular stomatitis?

A

profuse salivation, lameness, vesciles and ulcers on tongue

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70
Q

What allows for the rapid healing of vesicular stomatitis?

A

no viremic phase, only vesiculation and interstitial edema

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71
Q

What causes reinfections for vesicular stomatitis?

A

antibodies short lived, different serotypes

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72
Q

What virus family causes classical swine fever?

A

flaviviridae (rna, enveloped)

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73
Q

What is another name for classical swine fever?

A

hog cholera

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74
Q

What are some of the clinical signs associated with hog cholera?

A

conjuctivitis, GI signs, pneuomonia neurologic

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75
Q

What blood clinical sign indicates hog cholera?

A

leukopenia

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76
Q

What can happen in pregnant sows infected with hog cholera?

A

reabsorption, abortion, fetal mummification, still births, newborns die soon after birth

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77
Q

What causes the extended or intermittent clinical disease associated with classical swine fever?

A

strains of moderate virulence

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78
Q

Where does 2ry replication occur in the pathogenesis of hog cholera? What clinical signs does this lead to?

A

endothelial, lymphoid, BM

–>hemorrhages, leukopenia, thrombocytopenia

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79
Q

What cases of hog cholera may show no gross changes at necropsy?

A

peracute

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80
Q

What is the most prominent lesion at necropsy of acute hog cholera cases?

A

general exhaustion of the lymphoid system

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81
Q

What is the problem with live-born piglets infected in utero with hog cholera?

A

persistently infected, immunologically tolerant

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82
Q

What are the 2 most common diagnostic tests for hog cholera?

A

IF, antigen ELISA

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83
Q

How is classical swine fever transmitted?

A

direct/indirect

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84
Q

How is hog cholera controlled in US?

A

test and slaughter (vaccine available in endemic areas)

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85
Q

What virus family causes african swine fever?

A

asfaviridae

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86
Q

What are the characteristics of the asfaviridae family?

A

DNA, enveloped, paracrystalline arrays in the cytoplasm

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87
Q

What can transmit african swine fever and what is the resevoir species?

A

transmitted by soft ticks

asymptomatic in warthogs

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88
Q

What are the 2 distinct patterns of transmission in african swine fever?

A

sylvatic cycle and epidemic/endemic cycles of domestic swine

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89
Q

What are the clinical signs of african swine fever?

A

same as hog cholera

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90
Q

What lesions are present in acute cases of african swine fever?

A

lymphatic and vascular systems, petechia in cortex of kidney

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91
Q

What are the lesions associated with chronic cases of african swine fever?

A

cutaneous ulcers, pneumonia, pleuritis, arthritis

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92
Q

What diagnostic tests are used for african swine fever?

A

detect viral antigen, virus isolation

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93
Q

What are the big 5 problems in controlling african swine fever?

A

no vaccine, pork products, persistantly infected pigs, ticks, similar to CSF

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94
Q

What is the main source of virus to infect pigs with african swine fever?

A

direct contact, aerosols

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95
Q

Why is there a problem for developing an african swine fever vaccine?

A

pigs can’t make functional neutralizing antibodies

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96
Q

What viral family is pseudorabies?

A

herpesviridae

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97
Q

What is different about pseudorabies and the intranuclear inclusion bodies?

A

not always observed

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98
Q

Where is there a resevoir for pseudorabies in the states?

A

wild pigs in the south

99
Q

What are the secondary hosts of pseudorabies?

A

all domestic animals, not humans

100
Q

What clinical signs are present in weanlings infected with pseudorabies?

A

coughing, fever, GI signs, CNS signs (excess salivation)

101
Q

What clinical signs are present in mature swine that contract pseudorabies?

A

low mortality but weight loss and poor growth rates

102
Q

What is the major clinical sign in cattle that have pseudorabies?

A

pruritis, CNS involvement, death

103
Q

What are the clinical signs of pseudorabies in a dog? cat?

A

dog - pruritis, jaw paralysis, no tendency to attack

cat - death

104
Q

What is unique about the pathogenesis of pseudorabies?

A

no viremia, no gross lesions, travels via axoplasm

105
Q

What is the diagnostic tests used for pseudorabies?

A

antibody ELISA

106
Q

What body fluids is pseudorabies spread?

A

saliva and nasal discharge

107
Q

What animal contributes to farm to farm transmission of pseudorabies?

108
Q

What is the etilogic agent of postweaning multisystemic wasting syndrome?

A

Circovirus 2

109
Q

What are the 3 forms of PMWS?

A

repro failure, resp dz, porcine dermatitis and nephropathy syndrome

110
Q

Where is the PMWS virus shed in?

111
Q

How long does passive immunity protect piglets from PMWS?

A

6 to 9 weeks

112
Q

What are the diagnostic tests used for PMWS?

A

intranuclear inclusion bodies

confirm by virus isolation or PCR

113
Q

What virus family causes encephalomyocarditis?

A

picornaviridae

114
Q

What are the natural hosts of encephalmyocarditis? What other species can it infect?

A

natural - rodents

others - humans, monkeys, horses, cattle, swine

115
Q

What are the CS of swine influenza?

A

explosive outbreak, respiratory distress, quick recovery

116
Q

What is the fatality rate of swine influenza? What causes the death?

A

less than 1%

bronchopneumonia

117
Q

What lesions are seen with swine influenza?

A

sharply demarcated lung lesions, consolidation, alveolar atelactasis, interstitial pneumonia, emphysema

118
Q

How is swine influenza diagnosed?

A

lab confirmation –> viral isolation, immunoflourescence

119
Q

What virus family causes porcine reproductive and respiratory syndrome?

A

arteriviridae

120
Q

What are the characteristics of arteriviridae?

A

RNA, enveloped

121
Q

What helps the PRRS virus persist in the environment?

A

low temperature

122
Q

How is PRRS transmitted?

A

airborne, sexual, persistantly infected healthy swine

123
Q

What are the CS of PRRS?

A

blue ears, snout and vulva
agalactia and late abortion
respiratory distress

124
Q

How is PRRS diagnosed?

A

moribund LIVE piglets –> viral isolation

125
Q

What virus uses the acronym SMEDI?

A

porcine parvo

126
Q

What are the clinical signs during infection of parvo when pig is less than 30 days pregnant?

A

resorption of fetuses

127
Q

What are the CS between 30 and 70 days of gestation of pigs with parvo?

128
Q

What are the CS after 70 days of gestation with pigs with parvo?

A

immune competence – developing lesions

129
Q

What can you see in a population of gilts infected with parvo?

A

return to estrus 3-8 weeks after breeding, sometimes remain endocrinologically pregnant

130
Q

What are other CS of parvo besides SMEDI?

A

leukopenia, low fertility of boars

131
Q

What is different about porcine parvo pathology than other parvo viruses?

A

persistant infection with chronic shedding

132
Q

How is porcine parvo diagnosed?

A

IF on fetal tissues, serology not helpful

133
Q

What is the problem with vaccinating for parvo virus?

A

brief window of time to immunize gilts

134
Q

What virus family causes transmissible gastroenteritis in pigs?

A

coronaviridae

135
Q

What are the 4 different disease patterns caused by coronavirus in swine?

A
  1. TGE
  2. vomiting and wasting
  3. porcine epidemic diarrhea
  4. respiratory dz
136
Q

What are the CS of coronavirus in swine?

A

vomiting and profuse yellow diarrhea in neonates

137
Q

What is the pathogenesis of coronavirus in swine?

A

small intestine - shortens villi

138
Q

How is coronavirus diagnosed in swine?

A

mucosal mpression smears –> IF
virus isolation
no time for serology

139
Q

How has control of TGE been achieved in swine?

A

giving virulent strains to pregnant sows

140
Q

What virus family causes swine vesicular dz?

A

picornaviridae

141
Q

What are the CS of swine vesicular dz?

A

lameness, vesicles b/w heel and coronary band, digits, sometimes mouth

142
Q

Where is swine vesicular dz most shed in?

143
Q

What are the diagnostic tests used for swine vesicular dz?

A

antigen ELISA, RT-PCR, virus isolation

144
Q

What are the problems with controlling swine vesicular dz?

A

resistant in environment

infected meat - months to years

145
Q

What virus family causes vesicular exanthema of swine?

A

caliciviridae

146
Q

Why do we need to know about vesicular exanthema of swine?

A

eradicated but in some marine mammals

147
Q

Why is vesicular exanthema of swine notifiable?

A

looks like FMD

148
Q

What virus family causes newcastle dz?

A

paramyxoviridae

149
Q

What are the characteristics of paramyxoviridae?

A

RNA, enveloped

150
Q

Which newcastle disease occurs outside the U.S.?

A

velogenic viscerotropic (exotic new castle)

151
Q

What are the clinical signs of new castle disease?

A

respiratory, circulatory, GI, nervous signs

152
Q

What is the DDX for newcastle dz?

A

avian influenza

153
Q

What are the gross lesions associated with newcastle virus?

A

hemorrhages in the respiratory and GI tracts

154
Q

What are the histo lesions associated with newcastle dz?

A

necrotic foci in intestinal and lymphatic tissue

155
Q

What are the 3 terms to indicated virulence of newcastle disease?

A

velogenic, mesogenic, lentogenic

156
Q

What antibody blocks viremia in chicks but does not prevent respiratory infection?

A

maternal IgY

157
Q

What diagnostic tests are used for newcastle disease? What is essential when diagnosing?

A

Virus isolation, IF

must determine virulence

158
Q

When can you use antibody detection for newcastle dz?

A

only diagnostic in unvaccinated flocks

159
Q

How is newcastle disease transmitted? How is it shed?

A

direct and indirect, surviving birds shed in all secretions and excretions for at least 4 weeks

160
Q

What is used for control for newcastle disease?

A

live vax w/ lentogenic strain an inactivated vax

laying hens revaccinated every 4 months

161
Q

What is the virus family that causes infectious bursal disease? What are it’s characteristics?

A

birnaviridae - RNA, segmented, naked

162
Q

What is another name for infectious bursal disease? What kind of infection does it cause?

A

gumboro disease

immunosuppression and mortality in young chickens

163
Q

Why is infectious bursal disease economically important?

A

increased susceptibility to other dzs and negative interference with effective vaccines

164
Q

How is IBD (infectious bursal disease) transmitted?

A

fecal oral route

165
Q

What is the mortality rate for IBD?

166
Q

What IBD infectious is in chickens less than 3 weeks of age and may not show clinical signs?

A

subclinical infection

167
Q

What are the clinical signs of acute IBD?

A

prostrated, debilitated, dehydrated, water diarrhea, recumbant, ruffed feathers

168
Q

Which IBD serotype causes disease in poultry?

A

serotype 1

169
Q

What is the importance of antigenic variants in IBD?

A

breaks thru high levels of maternal antibodies

170
Q

What virus family causes caprine arthritis-encephalitis?

A

retroviridae

171
Q

How is CAE transmitted?

A

through colostrum and milk

172
Q

What are the 2 syndromes of CAE? What ages do they occur at?

A

Leukoencephalomyelitis - in kids 2-4 months

arthritis - adults

173
Q

How is CAE diagnosed and controlled?

A

Diagnose - serology

control - no vax, separate kid at birth, give pasteurized colostrum

174
Q

How is scrapie diagnosed?

A

vacuoles in gray matter, histopath of brain, IHC, WB

175
Q

What virus family causes BVDV?

A

flaviviridae - pestivirus

176
Q

What is the resevoir for BVDV?

A

persistantly infected immunotolerant animals (happens in 2–4 months of pregnancy)

177
Q

How is IBR transmitted?

A

direct contact (herpes)

178
Q

How is IBR controlled?

A

combo vax reduce incidence and severity, does not prevent infection

179
Q

What herpes causes IBR?

A

bovine herpesvirus 1

180
Q

What does the IBD virus destroy after it is ingested?

A

lympoid follicles in bursa of fabricus and B-cells in 2ry lymphoid tissues

181
Q

Where do very virulent strains of IBD deplete cells from?

A

thymus, spleen, bone marrow

182
Q

What is the common cause of mortality in IBD infection?

A

kidney failure -enlarged kidneys, accumulation of urates due to immune complexes

183
Q

What age is clinical disease of IBD seen?

A

between 3 and 6 weeks of age

184
Q

What will be seen in necropsy of chickens with IBD?

A

changes in bursa - swelling, edema, hemorrhage, transudate and eventually bursal atrophy. Also hemorrhages seen in muscle, intestines, kidney and spleen

185
Q

What 4 tests are used for diagnoses of IBD?

A

IF or IHC, RT-PCR, Viral isolation

186
Q

How long do maternal antibodies protect chicks from IBD? What do you do if their antibody levels are low?

A

4-7 weeks, breeder flocks immunized

vaccinate with attenuated virus at 1-2 weeks of age

187
Q

What virus family causes Marek’s dz?

A

herpes (DNA, enveloped)

188
Q

Where can free mareks disease virus be found?

A

dander in the feather follicles (atypical)

189
Q

What are the 4 overlapping syndromes associated with Marek’s disease?

A

Neurolymphomatosis - classic, asymetrical paralysis, wing drooping
Acute Mareks - explosive outbreak
Ocular lymphomatosis - graying of iris
Cutaneous mareks - nodular lesions at follicles

190
Q

What causes immunosuppression in mareks disease?

A

infection of lymphoid cells in thymus, bursa, BM, spleen

191
Q

What happens after the viremic stage of mareks dz?

A

T lymphoblastoid cell proliferation -> lesions result from transformation of T cells by oncogene

192
Q

What is the most constant gross finding in Mareks dz?

A

enlargement of peripheral nerve trunks unilaterally

193
Q

What lesions of Mareks disease are indistinguishable from avian leukosis?

A

lymphomatous lesions - small diffuse and translucent nodules

194
Q

How is mareks disease transmitted?

A

adults are life long shedders but NOT transmitted in ovo

195
Q

Which chicken disease affects birds of all ages? Mareks or leukosis?

196
Q

How is mareks disease diagnosed?

A

antigen or serology

197
Q

How is virus isolation done for mareks disease?

A

inoculated egg with buffy coat

198
Q

What does the vaccine for marek’s prevent?

A

prevent tumors but still have neurologic dz at reduced numbers, doesnt prevent transmission

199
Q

What may help control mareks dz besides vaccination in ovo?

A

genetics - found a gene resistant to mareks

200
Q

What virus family causes avian leukosis?

A

retroviridae (RNA, enveloped)

201
Q

How can chicks get a congential infection of avian leukosis?

A

hen transmits whole virus in cytoplasm, chick has immune tolerance

202
Q

How can chicks get a genetic transmission of avian leukosis?

A

viral DNA integrated into genome, chick gets no viremia, no leukemia

203
Q

What is the main differential for avian leukosis?

A

mareks disease

204
Q

What causes heavy environmental contamination in avian leukosis?

A

virus shed in meconium at hatching

205
Q

How is avian leukosis controlled?

A

some genetic resistance

vaccines with limited success

206
Q

Which type of avian influenza undergoes antigenic shift and drift?

207
Q

What is the main resevoir for avian influenza?

208
Q

What are highly pathogenic strains of avian influenza called? What are the signs?

A

“fowl plague” sudden death with no prodromal signs

209
Q

What part of the avian influenza virus is important in determining virulence? Why?

A 
viral hemagglutinin (HA)
epithelial cells of respiratory and GI cleave HA to activate, in viral strains, HA cleaved in other tissues -->death
210
Q

What are the gross lesions associated with avian influenza?

A

petechial hemorrhages and serous exudates in respiratory, digestive, and cardiac tissues

211
Q

How is the virus isolated in avian influenza?

A

cloacal swabs injected into allantoic sac of eggs

212
Q

How is virulence determined for avian influenza in 1 to 6 day old chicks?

A

intracerebral and intravenous pathogenecitiy

213
Q

How is avian influenza shed and transmitted?

A

shed in feces, lasts long in water at low temp

214
Q

What are the control measures for avian influenza?

A

notifiable under OIE, quarantine, prevent intro from wild birds

215
Q

What virus family causes avian infectious bronchitis?

A

coronaviridae (RNA, enveloped)

216
Q

What are the clinical signs of infectious bronchitis in chicks 1 -4 weeks

A

gasping, coughing, rales, lasting 5-7 days

217
Q

When can high mortality occur during infectious bronchitis in chickens?

A

broilers - due to 2ry infection with e coli or mycoplasma

218
Q

What are the CS of egg laying chickens infected with infectious bronchitis?

A

respiratory signs plus involvement of repro tract, pasting

219
Q

What are the gross lesions associated with avian infectious bronchitis?

A

mucosal thickening, yellow casts block bronchi in chicks

220
Q

What antibodies are produced during avian infectious bronchitis?

A

IgM, IgY, IgA

221
Q

What diagnostic test is used for infectious bronchitis?

A

direct IF of tracheal smears early on

222
Q

How is avian IB transmitted?

A

aerosols and feces, fomites in cold climates

223
Q

What is used to control avian infectious bronchitis?

A

attenuated vaccine in eggs, control difficult because of vaccination outbreaks of antigenic strains and persistantly infected chickens

224
Q

What virus family causes avian infectious laringotracheitis?

225
Q

What age of chickens is infected with laringotracheitis?

A

4-18 months old

226
Q

What are the CS of laringotracheitis?

A

respiratory signs, depression, expectoration of bloody mucus or blood

227
Q

What is the term used for head shaking with cough in laringotracheitis?

A

pump handle respiration

228
Q

What are the diagnostic tests for laringotracheitis?

A

IF of smears and virus isolation in eggs, serology

229
Q

What are the ddx for laringotracheitis?

A

fowl pox (diphteric form) and other respiratory dzs

230
Q

How is laringotracheitis transmitted?

A

droplet inhalation, less commonly ingestion

231
Q

How is laringotracheitis controlled?

A

attenuated vax -> doesnt protect against infection

232
Q

What are characteristics of reo viruses?

A

RNA, segmented, naked

233
Q

What are the CS of avian reovirus dz?

A

ranges from inapparant to fatal, arthritis is main sign

234
Q

How is avian reovirus transmitted?

A

fecal-oral

235
Q

How is avian reovirus diagnosed?

A

IF and virus isolation

236
Q

How is fowlpox transmitted?

A

mosquitos mechanically

237
Q

What are the 2 forms of fowlpox?

A

Cutaneous - low mortality

Dipthteric - high

238
Q

Why is fowlpox hard to control?

A

persist in environment in scabs, hard to dessicate, transmitted by alot of things

239
Q

How is fowlpox controlled?

240
Q

What virus family causes chicken anemia? What kind of disease does it cause?

A

circoviridae (naked, DNA)

acute immunosuppressive dz in young chickens

241
Q

How is chicken anemia transmitted?

A

horizontal and vertical (viremia)

242
Q

What do chicks show at 3 weeks when infected with chicken anemia?

A

lethargy, anorexia, depression, PALE

243
Q

Where might hemorrhages occur in chicken anemia?

A

subcutaneous and intramuscular

244
Q

How is chicken anemia controlled?

A

live vaccines

Virology (10 decks)

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