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Viro Exam 2 > Overview cards > Flashcards

Overview cards Flashcards

1
Q

Bovine Herpes 1

A

5 forms
1 - Respiratory
= Infectious Bovine Rhinotracheitis Virus

2 - Genital
= Infectious pustualar vulvovaginitis/ balanoposthitis

3 - Neural

4 - Systemic
= Young calves (Liver necrosis –> abortion)

5 - Keratoconjunctivitis
= Pink eye

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2
Q

What farm management factors can cause BHV1?

A
  1. improper weaning
  2. mixing cattle
  3. long transport time
  4. dehydration
  5. poor nutrition
    - -> stress
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3
Q

The respiratory form of BHV1

A 
Infectious Bovine Rhinotrachitis
--> Ulcers in trachea --> bacterial infection -->
• Open mouth breathing
• salivation
• hemorrhage around muzzle
• ocular discharge
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4
Q

Describe immunity of BHV

A

Neutralizing Ab’s (IgA)

• immunity between forms

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5
Q

Other names for PHV1

A

Pseudorabies OR Aujeszky’s Dz

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6
Q

What are the dead end hosts of PHV1

A

Cattle & Sheep
Dog & Cat
Chicken
Raccoons, rabbits, rats, mice

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7
Q

How long does PHV survive in environment?

A

40-140 days

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8
Q

Pathogenesis of PHV

A

Tonsillar & pharyngeal tissue

  • -> CN 1, 5,9 = olfactory, trigeminal & glossopharyngeal
  • -> brain
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9
Q

Sow infection w/ PHV
• < 30 gestation
• > 30 gestation

A

• < 30 gestation
–> death & resorption
• > 30 gestation
–> Abortion/still birth of mummified fetus

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10
Q

Cattle infection with PHV

A
  • ↓ milk production
  • violent licking
  • frenzied
  • Death w/in 2 days of clinical signs
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11
Q

Immunity w/ PHV

A

Maternal Ab’s mask clinical signs NOT infection

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12
Q

Ab’s for EHV

A

EHV 1 & 4 = cross neutralizing Abs

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13
Q

Forms of EHV

A

EVH-1
–> Spontaneous Abortion
(widespread hemorrhage, edema & liver necrosis)

EHV-2 (throughout body)
–> Lumpy Bumpy –> chronic infection

EHV-3
–> Equine coital exanthema

EHV-4
–> Respiratory dz

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14
Q

Pathogenesis of EHV 1&4

A 
Ingestion/inhalation 
--> incubation 1-10d
--> @7-10d Shedding of virus 
& Ab production
--> cellular host defense --> latency

Stressor –> ↓ host defense –> reactivation of replication–>
• Fever 2-5 d
• Transient anorexia
• leukopenia (initial) –> leukocytosis
• inflamm / congestion / necrosis of Upper Resp Tract

Lymphocytes (infected w/ EHV1)
–> CNS –>
• hindlimb paralysis
• cauda equina neuritis –> gluteal atrophy

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15
Q

Canine Herpes (CHV)
• Puppies < 1wk
• Puppies >2wk
• adults

A 
• Puppies < 1wk
    - Macs infected 
      --> viremia 
      --> generalized infection 
      --> ENDOTHELIAL replication 
      --> fatal
• Puppies >2wk
      --> mild/subclinical
• Adults
      -->Nasal pharynx/ tonsil/ bronchial & retropharyngeal LNs         
      --> reactivation 
      --> virus shed in oronasal secretion

• Venereal dz
–> infertility
& abortion (multifocal placental necrosis)
w/ vesicular lesions

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16
Q

Where does FHV stay latent?

A

Trigeminal gangion

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17
Q

FHV pathogenesis

A

Oronasal & conjuctival secretion

  • -> nasal septum, turbinates, tonsils, nasopharynx
  • -> incubation 2-6d
  • -> Shed 1-13d
  • -> 2-3 wks clinically healthy & no shedding

• Stress/ glucocorticoids

  • -> 4-11 d lag
  • -> virus shedding
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18
Q

Clinical signs of FHV

A

• Respiratory Tract
& ulcerative/ interstitial keratitis

–> encrusted nares & eyes
(serous –> mucopurulent)
–> sneezing
–> lethargy

  • Osteolytic change in turbinates
  • generalized dz in neonates
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19
Q

Maternal Abs for FHV

A
  • -> subclinical infection –> latency

* neutralizing & CMI

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20
Q

Avian infectious laryngotracheitis virus

A

Mainly chickens
• Peracute form = 50% mortality
• Subacute = 10-30% mortality
• Chronic – will eventually die of hypoxia

–> difficulty breathing / Upper Respiratory hemmorhage

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21
Q

Marek’s Disease

A

Avian herpes
(household flocks, not vx @ day old)

3 forms
1 - oncogenic
2 - non-oncogenic
3 - Turkey herpes

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22
Q

How is Marek’s dz spread

A

Virus shed Feather follicles

  • -> 4-14d incubation
  • -> Latent in LYMPHS
  • -> transformation in Tcells
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23
Q

Clinical signs assoc’d w/ Mareks dz

A
  • 4 - 20 wk chicks
  • limb paralysis (nerve plexus enlargement
  • enlarged feather follicles
  • malignant lymphoma
  • Pale Iris –> lymphotoid infiltrate
  • Bursa atrophy –> immunosupressed
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24
Q

What are ddx that could be thought with Mareks dz

A
  1. Vit E/Se Deficits
  2. Botulism
  3. 3-nitrophenylarsonic acid tox
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25
Q

Malignant Catarrhal Fever Virus
• Natural host
• Cattle

A

Natural host

  • Wildebeest
  • Sheep

2° host

  • Sheep
  • Cattle
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26
Q

Clinical signs assoc’d w/ Malignant Catarrhal Fever virus (Head &eye form)

A
  • Purulent oculonasal discharge
  • mild keratitis –>corneal edema
  • Hyperemia of nose
  • Hypopyon
  • ulceration of oral cavity
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27
Q

Are animals protected after having MCF virus

A
  • No good immunity following infection

* no Vx

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28
Q

How is African Swine Fever virus transmission?

A

Ticks ((“only ‘as far’ as a tick can go” ))
• vertical transmission in ticks

Urine
Feces
Carcass

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29
Q

Pathogenesis of African Swine Fever

A

Transmitted by tick

  • -> 5-15d incubation (tonsils/dorsal pharygeal mucosa)
  • -> reticular cells, monocytes, Macs
  • -> blood spleen lungs LNs–>
  • Cynosis
  • Organ hemorrhage
  • Tremors
  • lacrymal discharge
  • bloody diarrhea
  • Gall Bladder EDEMA
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30
Q

What could be ddx for African Swine Fever

A
  1. Hog Cholera

2. Salmonella

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31
Q

Asfarvi is a DNA virus, where does it replicate?

A

most DNA viruses use nucleus

• Asfarvi and Pox = CYTOPLASM

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32
Q

last case of smallpox

A

1977

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32
Q

last case of smallpox

A

1977

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33
Q

Variolation

A

intranasal inhalation of dried scabs

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33
Q

Variolation

A

intranasal inhalation of dried scabs

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34
Q

inoculation

A

injection of vesicle fluid into skin

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34
Q

inoculation

A

injection of vesicle fluid into skin

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35
Q

Vaccination

A

Vaccinia virus

• innoculation w/ cow pox

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35
Q

Vaccination

A

Vaccinia virus

• innoculation w/ cow pox

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36
Q

Eradication of Small pox

A

Cheap effective Vx

  1. potent & stable freeze dried vx
  2. bifurcated needle
  3. surveillance & containment

Virus factors

  1. Single serotype
  2. Single host
  3. natural infection –> life-long immunity
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36
Q

Eradication of Small pox

A

Cheap effective Vx

  1. potent & stable freeze dried vx
  2. bifurcated needle
  3. surveillance & containment

Virus factors

  1. Single serotype
  2. Single host
  3. natural infection –> life-long immunity
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37
Q

Why are vaccinia viruses used for vaccines?

A
  1. easy to produce
  2. high protein expression
  3. Lg capacity for insert foreign DNA
  4. Wide host range

(ex Canary Pox)

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37
Q

Why are vaccinia viruses used for vaccines?

A
  1. easy to produce
  2. high protein expression
  3. Lg capacity for insert foreign DNA
  4. Wide host range

(ex Canary Pox)

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38
Q

Dz names for Parapox-virus

A
  • Contagious Ecthyma Virus (CEV)
  • Orf
  • Sore Mouth
  • Contagious Pustular Dermatitis
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38
Q

Dz names for Parapox-virus

A
  • Contagious Ecthyma Virus (CEV)
  • Orf
  • Sore Mouth
  • Contagious Pustular Dermatitis
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39
Q

What are the lesions assoc’d with Parapox? Is it zoonotic?

A

Dermatotrophic (Goat /Sheep)
• Lesions on Mouth
• infected Lamb –> Ewe udder

Zoonotic - hands & face

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39
Q

What are the lesions assoc’d with Parapox? Is it zoonotic?

A

Dermatotrophic (Goat /Sheep)
• Lesions on Mouth
• infected Lamb –> Ewe udder

Zoonotic - hands & face

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40
Q

How do you vx for Parapox

A

Scarification + wt virus in groin area –> scabs fall off
• isolate from non vx’d animals
• 1 mo & 2-3mo later

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40
Q

How do you vx for Parapox

A

Scarification + wt virus in groin area –> scabs fall off
• isolate from non vx’d animals
• 1 mo & 2-3mo later

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41
Q

Orthopox

A

Monkey pox

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41
Q

Orthopox

A

Monkey pox

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42
Q

last case of smallpox

A

1977

43
Q

Variolation

A

intranasal inhalation of dried scabs

44
Q

inoculation

A

injection of vesicle fluid into skin

45
Q

Vaccination

A

Vaccinia virus

• innoculation w/ cow pox

46
Q

Eradication of Small pox

A

Cheap effective Vx

  1. potent & stable freeze dried vx
  2. bifurcated needle
  3. surveillance & containment

Virus factors

  1. Single serotype
  2. Single host
  3. natural infection –> life-long immunity
47
Q

Why are vaccinia viruses used for vaccines?

A
  1. easy to produce
  2. high protein expression
  3. Lg capacity for insert foreign DNA
  4. Wide host range

(ex Canary Pox)

48
Q

Dz names for Parapox-virus

A
  • Contagious Ecthyma Virus (CEV)
  • Orf
  • Sore Mouth
  • Contagious Pustular Dermatitis
49
Q

What are the lesions assoc’d with Parapox? Is it zoonotic?

A

Dermatotrophic (Goat /Sheep)
• Lesions on Mouth
• infected Lamb –> Ewe udder

Zoonotic - hands & face

50
Q

How do you vx for Parapox

A

Scarification + wt virus in groin area –> scabs fall off
• isolate from non vx’d animals
• 1 mo & 2-3mo later

51
Q

Orthopox

A

Monkey pox

52
Q

last case of smallpox

A

1977

53
Q

Variolation

A

intranasal inhalation of dried scabs

54
Q

inoculation

A

injection of vesicle fluid into skin

55
Q

Vaccination

A

Vaccinia virus

• innoculation w/ cow pox

56
Q

Eradication of Small pox

A

Cheap effective Vx

  1. potent & stable freeze dried vx
  2. bifurcated needle
  3. surveillance & containment

Virus factors

  1. Single serotype
  2. Single host
  3. natural infection –> life-long immunity
57
Q

Why are vaccinia viruses used for vaccines?

A
  1. easy to produce
  2. high protein expression
  3. Lg capacity for insert foreign DNA
  4. Wide host range

(ex Canary Pox)

58
Q

Dz names for Parapox-virus

A
  • Contagious Ecthyma Virus (CEV)
  • Orf
  • Sore Mouth
  • Contagious Pustular Dermatitis
59
Q

What are the lesions assoc’d with Parapox? Is it zoonotic?

A

Dermatotrophic (Goat /Sheep)
• Lesions on Mouth
• infected Lamb –> Ewe udder

Zoonotic - hands & face

60
Q

How do you vx for Parapox

A

Scarification + wt virus in groin area –> scabs fall off
• isolate from non vx’d animals
• 1 mo & 2-3mo later

71
Q

Orthopox

A

Monkey pox

72
Q

Reservoir for Monkey pox

A

African rodents
– > zoonotic
• flu-like w/ pustules

73
Q

Serotypes of FMD

A

Type O, A, C, Asia1, STAT 1,2,3

74
Q

What dz is caused by Aphthovirus

A

Foot & Mouth Dz

• cloven-hoofed animals

75
Q

What countries are FMD-free

A

North america
Australia
New Zealand
UK

76
Q

Clinical dz seen with Apthovirus

A 
FMD
• Systemic dz w/ 
    - high fever
    - vesicles on epithelial surface
    - salivation
    - Adults = not fatal --> economic loss
    - Young ---> myocarditis --> fatal
         = Tiger Heart
77
Q

What host are:
• Maintenance
• sentinel
• amplifying

A

• Maintenance

 - Sheep 
 - Mild dz -->spread thru flocks undetected

• Sentinel

- cattle
- highly sensitive to respiratory infection

• amplifying

 - Pig
 - Shed high amts of virus
78
Q

Pathogenesis of FMD

A

< 10 particles inhaled ingested AI

  • -> 3-10d incubation pd
  • -> Binds heprin sulfate + integrin receptor (epithelial cells)
  • -> virus uncoats
  • -> sheds VP4 capsid protein
  • -> RNA enters cell thru pores
  • -> replication in cytoplasm (RNAdepRNApol)
  • -> viral assembly –> cell lysis –> virus release
  • -> Regional LN infection –> viremia
  • -> 2° site –> ↑ viral load
    • collects in cornified epithelium
    • foot, mouth/tongue, mammary glad
79
Q

When is virus shed in FMD process

A

1-4 days before clinical signs

80
Q

What causes rapid spread of FMD

A
  1. Ag Variation btwn serotypes
  2. Lg host range
  3. Low infectious dose
  4. Virus shed before clinically ill (no signs in sheep)
  5. Persistent infection in some
  6. Hardy/ easily transmitted
  7. Vx only short term immunity
81
Q

Acute test for FMD

A

CHEKIT Foot&Mouth Dz 3ABC

82
Q

What dz is caused by Entrovirus?

A

Swine Vesicular Disease Virus

- Portugal & Italy

83
Q

How is Swinve Vesicular Dz Virus spread?

A
  • Contaminated garbage ingestion
  • Pig-to-Pig contact
  • Non-heat treated meat –> zoonotic
84
Q

Clinical signs of SVDV in pig/humans

A

Pig

  • vesicles at coronary band & interdigital space & mouth/snout –> rupture –> ulcers & lameness
  • Immune to re-infection

Human
- flu-like

85
Q

Vesicular dz’s

A
  1. FMD
  2. Vesicular Stomatitis
  3. Vesicular Exathema
  4. Swine Vesicular Dz virus
86
Q

What dz does vesivirus cause?

A

Feline Calicivirus

  • prevalent in colonies
  • persists in tonsilar/oropharyngeal tissue
  • FIV —> potentiates FCV shedding
87
Q

Clinical signs assoc’d w/ FCV

A
  • Stomatitis
  • Oral ulcers
  • Lameness (Macs in synovial membrane)
  • Oculonasal discharge
88
Q

What does the Feline calicivirus prevent

A

Acute oral & upper respiratory infection

– NOT protection against infection or shedding

89
Q

Vesicular Exanthema of Swine virus

A

Calicivirus of Sea Lion & Pigs

  • uncooked garbage to pigs
  • -> 12-24hr incubation pd

NO vx!

90
Q

What is the Dz assoc’d w/ Pestivirus

A

(Flaviviridae)

  1. Bovine Viral Diarrhea virus
  2. Classical swine Fever (Hog Cholera)
91
Q

Cytopathic vs Non-cytopathic strains of BVDV

A

Cytopathic strain
= NS3 gene

Non-cytopathic
= NS 2-3

92
Q

Infection of Pregnant cow w/ BVDV

A

infected w/ non-cytolytic strain –> passive immunity –> tolerance +virus remains –> mutations in virus –> cytopathic form –> infect others w/ cytopathic form

  • Infection before immune competent –> persistent infection & ↑ ↑ ↑ shedding
  • Mucosal dz
93
Q

Infection of BVDV transplacentally

A 
• fetus death
• fetus mummification
• weak calf syndrome
• clinically normal 
• congenital anomalies
     - < 100 d = Peidmontese calf
     - 100 -150 d = Cerebellar hypoplasia & retinal dyscrasia
94
Q

Teratogenic

A

causes embryologic malformations

• BVDV

95
Q

Clinical signs of Hog cholera

A 
incubation 2-4 d
• diffuse hyperemia
• organ hemorrhage
• Goose Stepping
• Diarrhea 
• Button ulcers in colon
• Weak --> ↑ Sitting
• Sleep close together (act cold)
• Cerebellar Hypoplasia
• Splenic Infarct
96
Q

What dz does Flavivirus cause?

A

West Nile virus
• mosquito
• bird
• horse / human = incidental host

97
Q

Pathogenesis of WNV

A

Langerhan DC’s –> LN –> replication –> viremia –> peripheral organs

• TNF alpha –> ↑ BBB permeability –> CNS neurons

98
Q

Ornithophilic ticks

A
  1. pipiens
  2. restuans
  3. meanura
99
Q

Opportunisitic ticks

A
  1. salinarius
  2. albopictus
  3. veans
  4. ferox
100
Q

mammalophilic ticks

A
  1. canadensis
  2. cantator
  3. triseriatus
  4. trivittatus
  5. punctipennis
101
Q

What is a sentinel?

What is used for a sentinel in WNV?

A

indicator of dz presence

• mammals

102
Q

Clinical signs of WNV in Birds

A 
hrs --> 6 d
• circling
• Muscle tremors
• Abnormal head posture
• recumbency
• convulsion
• Cerebral hemorrhage
• myocarditis
• splenomegaly
• intestinal diphtheritic
103
Q

Clinical signs of WNV in Horse

A 
• Ataxia 
• recumbency
• Depression
• muscle tremors
• SubAcute NonSuppurative Encephalomyelitis
 (Pons, Medulla, Spinal cord)
104
Q

Can horses recover from WNV?

A

Yes, w/ deficits
• Gait
• Behavior change
• Neuro deficits

– 33% mortality

105
Q

Togavirus

A

EEE/WEE/VEE

106
Q

EEE

A

90% mortality (30% in humans)

  • Horse / pigeon/pheasant / humans
  • vector = culiseta melanura
  • Muscle & CNS
107
Q

WEE

A

20-40% mortality (10% humans)

  • Horse/ human
  • Vector = Culex tarsalis / Culiseta melanrua
  • Muscle, brown fat, choroid plexus/ependyma, neurons
  • last human case 1999
108
Q

Clinical signs of WEE/EEE

A
  • Fever
  • Seizure
  • myalgia
  • irritability
  • sweating
  • Menigismus
    - -nuchal rigidity
    - -photophobia
    - -headache
  • extensor rigidity
109
Q

VEE

A

Not fatal

  • Epizootic ~ 10 yr intervals
  • Upper respiratory tract
  • lymphatics, liver, pancreas
  • CNS
110
Q

Where is the virus found in an EEE infected bird / mosquito?

A

Feather follicles
- Young birds –> virus amplification

–> mosquitos (4-10d in midgut to salivary gland)

111
Q

What is the significance of Canine Coronavirus?

A

Puppies more susceptible

  • -> replication in enterocytes
  • -> shorten villi (spares crypts)
  • If concurrent infection with Parvo –> Severe dz
  • Short lived IgA protection
112
Q

Porcine Respiratory Coronavirus (PRCV)

A

Antigenically indistinguishable from TGEV
• Winter / Spring

• Replicates in respiratory epithelium

  • -> subclinical infection
  • -> Incomplete immunity to TGE
  • -> Rapid 2° immune response if exposed to TGE
113
Q

Transmissible Gastroenteritis Virus pathogenesis

A 
• NOT in winter
• incubation 18h - 3d
--> destroy villous epithelium 
--> ↓ enzymatic activity
--> ↓ digestion & absorption
--> Undigested lactose
--> osmotic pull into lumen 
--> Diarrhea, dehydration, acidosis, cardiac dysfxn
114
Q

TGE transmission

A

ORONASAL
cat, dog, fox
starling
house fly

115
Q

TGE depending on age
• 3d
• >3wk
• grower/finisher

A

• 3d

- Severe villus atrophy
- high mortality

• >3wk

- regenerate epithelium
- unthrifty

• grower/finisher
- mortality low

116
Q

TGE maternal Ab’s

A

Not absorbed

• passive intestinal immunity

117
Q

Important Ag’s on TGE virus

A

1 - Peplomer glycoprotein
2 - Integral membrane protein
3 - Nucleocapsid protein

118
Q

What part of FIP virus induces Ab’s?

A

Peplomer –> neutralizing Ab

119
Q

How do recombinants occur in FIP

A

Canine Coronavirus

120
Q

Pathogenesis of FIP

A 
LARGE inoculum of virus
--> enterocyte replication (2-3m)
--> Virus shed (1-10d PI)
--> Macs --> LNs
--> 1° targets (LIVER, LN, SPLEEN)
--> results depend on immune response
• Strong immunity
• deficient CMI Response

• Usually assoc’d w/ FIV, FPV, FeLV

121
Q

Strong response to FIP

A

–> Recovery / carrier

122
Q

Deficient CMI response to FIP

A

–> 2° viremia
–> circulating immune complexes
–> Perivascular inflamm
• NO CMI –> EFFUSIVE
• Partial CMI –> non-effusive

123
Q

Pre-existing Anti-FIP IgG (ex. vx)

A

> > opsonization

  • -> ↑ Macrophage uptake
  • -> ↑ immune complex deposition
  • -> complement activation in vascular endothelium

Ab dependent enhancement
• Vx cats –> faster & higher rate of mortality
• Ab facilitates uptake by Mac

124
Q

Porcine Epidemic Diarrhea (PED)

A

Coronaviridae

  • Multifunctional virulence factor (spike structural gene)
  • Similar signs to TGE
    - slower spread
    - Acute Back Muscle necrosis
  • 100% morbidity
125
Q

Tx for PED

A

Most recover w/o Tx unless 2° infection

• control = All-in All-out

126
Q

Arterivirus

• Main dz forms

A
  1. Equine Arteritis virus (EAV)
  2. Porcine Reproductive & Respiratory Syndrome (PRRS)
  • Respiratory
  • Venereal (abortion)
127
Q

EAV

A
  • highly infectious
  • young animals most susceptible
  • virulent & avirulent strains
Other clinical signs
• edema of limbs & genitals 
• necrosis of small arteries (tiny bumps)
• conjunctivits
• Epiphora
128
Q 
PRRS
• young
• older
• sows
• boars
A

Young pigs = severe respiratory signs (interstitial pneumonia)

Older pigs = rolling inappetence, bluish discoloration

Sows = abortion

Boars –> virus in semen

Viro Exam 2 (8 decks)

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