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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
Malignant Catarrhal Fever Virus • Natural host • Cattle
Natural host - Wildebeest - Sheep 2° host - Sheep - Cattle
26
Clinical signs assoc'd w/ Malignant Catarrhal Fever virus (Head &eye form)
* Purulent oculonasal discharge * mild keratitis -->corneal edema * Hyperemia of nose * Hypopyon * ulceration of oral cavity
27
Are animals protected after having MCF virus
* No good immunity following infection | * no Vx
28
How is African Swine Fever virus transmission?
Ticks (("only 'as far' as a tick can go" )) • vertical transmission in ticks Urine Feces Carcass
29
Pathogenesis of African Swine Fever
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
30
What could be ddx for African Swine Fever
1. Hog Cholera | 2. Salmonella
31
Asfarvi is a DNA virus, where does it replicate?
most DNA viruses use nucleus | • Asfarvi and Pox = CYTOPLASM
32
last case of smallpox
1977
32
last case of smallpox
1977
33
Variolation
intranasal inhalation of dried scabs
33
Variolation
intranasal inhalation of dried scabs
34
inoculation
injection of vesicle fluid into skin
34
inoculation
injection of vesicle fluid into skin
35
Vaccination
Vaccinia virus | • innoculation w/ cow pox
35
Vaccination
Vaccinia virus | • innoculation w/ cow pox
36
Eradication of Small pox
Cheap effective Vx 1. potent & stable freeze dried vx 2. bifurcated needle 3. surveillance & containment Virus factors 4. Single serotype 5. Single host 6. natural infection --> life-long immunity
36
Eradication of Small pox
Cheap effective Vx 1. potent & stable freeze dried vx 2. bifurcated needle 3. surveillance & containment Virus factors 4. Single serotype 5. Single host 6. natural infection --> life-long immunity
37
Why are vaccinia viruses used for vaccines?
1. easy to produce 2. high protein expression 3. Lg capacity for insert foreign DNA 4. Wide host range (ex Canary Pox)
37
Why are vaccinia viruses used for vaccines?
1. easy to produce 2. high protein expression 3. Lg capacity for insert foreign DNA 4. Wide host range (ex Canary Pox)
38
Dz names for Parapox-virus
* Contagious Ecthyma Virus (CEV) * Orf * Sore Mouth * Contagious Pustular Dermatitis
38
Dz names for Parapox-virus
* Contagious Ecthyma Virus (CEV) * Orf * Sore Mouth * Contagious Pustular Dermatitis
39
What are the lesions assoc'd with Parapox? Is it zoonotic?
Dermatotrophic (Goat /Sheep) • Lesions on Mouth • infected Lamb --> Ewe udder Zoonotic - hands & face
39
What are the lesions assoc'd with Parapox? Is it zoonotic?
Dermatotrophic (Goat /Sheep) • Lesions on Mouth • infected Lamb --> Ewe udder Zoonotic - hands & face
40
How do you vx for Parapox
Scarification + wt virus in groin area --> scabs fall off • isolate from non vx'd animals • 1 mo & 2-3mo later
40
How do you vx for Parapox
Scarification + wt virus in groin area --> scabs fall off • isolate from non vx'd animals • 1 mo & 2-3mo later
41
Orthopox
Monkey pox
41
Orthopox
Monkey pox
42
last case of smallpox
1977
43
Variolation
intranasal inhalation of dried scabs
44
inoculation
injection of vesicle fluid into skin
45
Vaccination
Vaccinia virus | • innoculation w/ cow pox
46
Eradication of Small pox
Cheap effective Vx 1. potent & stable freeze dried vx 2. bifurcated needle 3. surveillance & containment Virus factors 4. Single serotype 5. Single host 6. natural infection --> life-long immunity
47
Why are vaccinia viruses used for vaccines?
1. easy to produce 2. high protein expression 3. Lg capacity for insert foreign DNA 4. Wide host range (ex Canary Pox)
48
Dz names for Parapox-virus
* Contagious Ecthyma Virus (CEV) * Orf * Sore Mouth * Contagious Pustular Dermatitis
49
What are the lesions assoc'd with Parapox? Is it zoonotic?
Dermatotrophic (Goat /Sheep) • Lesions on Mouth • infected Lamb --> Ewe udder Zoonotic - hands & face
50
How do you vx for Parapox
Scarification + wt virus in groin area --> scabs fall off • isolate from non vx'd animals • 1 mo & 2-3mo later
51
Orthopox
Monkey pox
52
last case of smallpox
1977
53
Variolation
intranasal inhalation of dried scabs
54
inoculation
injection of vesicle fluid into skin
55
Vaccination
Vaccinia virus | • innoculation w/ cow pox
56
Eradication of Small pox
Cheap effective Vx 1. potent & stable freeze dried vx 2. bifurcated needle 3. surveillance & containment Virus factors 4. Single serotype 5. Single host 6. natural infection --> life-long immunity
57
Why are vaccinia viruses used for vaccines?
1. easy to produce 2. high protein expression 3. Lg capacity for insert foreign DNA 4. Wide host range (ex Canary Pox)
58
Dz names for Parapox-virus
* Contagious Ecthyma Virus (CEV) * Orf * Sore Mouth * Contagious Pustular Dermatitis
59
What are the lesions assoc'd with Parapox? Is it zoonotic?
Dermatotrophic (Goat /Sheep) • Lesions on Mouth • infected Lamb --> Ewe udder Zoonotic - hands & face
60
How do you vx for Parapox
Scarification + wt virus in groin area --> scabs fall off • isolate from non vx'd animals • 1 mo & 2-3mo later
71
Orthopox
Monkey pox
72
Reservoir for Monkey pox
African rodents -- > zoonotic • flu-like w/ pustules
73
Serotypes of FMD
Type O, A, C, Asia1, STAT 1,2,3
74
What dz is caused by Aphthovirus
Foot & Mouth Dz | • cloven-hoofed animals
75
What countries are FMD-free
North america Australia New Zealand UK
76
Clinical dz seen with Apthovirus
``` FMD • Systemic dz w/ - high fever - vesicles on epithelial surface - salivation - Adults = not fatal --> economic loss - Young ---> myocarditis --> fatal = Tiger Heart ```
77
What host are: • Maintenance • sentinel • amplifying
• Maintenance - Sheep - Mild dz -->spread thru flocks undetected • Sentinel - cattle - highly sensitive to respiratory infection • amplifying - Pig - Shed high amts of virus
78
Pathogenesis of FMD
< 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
When is virus shed in FMD process
1-4 days before clinical signs
80
What causes rapid spread of FMD
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
Acute test for FMD
CHEKIT Foot&Mouth Dz 3ABC
82
What dz is caused by Entrovirus?
Swine Vesicular Disease Virus | - Portugal & Italy
83
How is Swinve Vesicular Dz Virus spread?
* Contaminated garbage ingestion * Pig-to-Pig contact * Non-heat treated meat --> zoonotic
84
Clinical signs of SVDV in pig/humans
Pig - vesicles at coronary band & interdigital space & mouth/snout --> rupture --> ulcers & lameness - Immune to re-infection Human - flu-like
85
Vesicular dz's
1. FMD 2. Vesicular Stomatitis 3. Vesicular Exathema 4. Swine Vesicular Dz virus
86
What dz does vesivirus cause?
Feline Calicivirus - prevalent in colonies - persists in tonsilar/oropharyngeal tissue - FIV ---> potentiates FCV shedding
87
Clinical signs assoc'd w/ FCV
- Stomatitis - Oral ulcers - Lameness (Macs in synovial membrane) - Oculonasal discharge
88
What does the Feline calicivirus prevent
Acute oral & upper respiratory infection -- NOT protection against infection or shedding
89
Vesicular Exanthema of Swine virus
Calicivirus of Sea Lion & Pigs - uncooked garbage to pigs - -> 12-24hr incubation pd NO vx!
90
What is the Dz assoc'd w/ Pestivirus
(Flaviviridae) 1. Bovine Viral Diarrhea virus 2. Classical swine Fever (Hog Cholera)
91
Cytopathic vs Non-cytopathic strains of BVDV
Cytopathic strain = NS3 gene Non-cytopathic = NS 2-3
92
Infection of Pregnant cow w/ BVDV
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
Infection of BVDV transplacentally
``` • fetus death • fetus mummification • weak calf syndrome • clinically normal • congenital anomalies - < 100 d = Peidmontese calf - 100 -150 d = Cerebellar hypoplasia & retinal dyscrasia ```
94
Teratogenic
causes embryologic malformations | • BVDV
95
Clinical signs of Hog cholera
``` 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
What dz does Flavivirus cause?
West Nile virus • mosquito • bird • horse / human = incidental host
97
Pathogenesis of WNV
Langerhan DC's --> LN --> replication --> viremia --> peripheral organs • TNF alpha --> ↑ BBB permeability --> CNS neurons
98
Ornithophilic ticks
1. pipiens 2. restuans 3. meanura
99
Opportunisitic ticks
1. salinarius 2. albopictus 3. veans 4. ferox
100
mammalophilic ticks
1. canadensis 2. cantator 3. triseriatus 4. trivittatus 5. punctipennis
101
What is a sentinel? | What is used for a sentinel in WNV?
indicator of dz presence | • mammals
102
Clinical signs of WNV in Birds
``` hrs --> 6 d • circling • Muscle tremors • Abnormal head posture • recumbency • convulsion • Cerebral hemorrhage • myocarditis • splenomegaly • intestinal diphtheritic ```
103
Clinical signs of WNV in Horse
``` • Ataxia • recumbency • Depression • muscle tremors • SubAcute NonSuppurative Encephalomyelitis (Pons, Medulla, Spinal cord) ```
104
Can horses recover from WNV?
Yes, w/ deficits • Gait • Behavior change • Neuro deficits -- 33% mortality
105
Togavirus
EEE/WEE/VEE
106
EEE
90% mortality (30% in humans) - Horse / pigeon/pheasant / humans - vector = culiseta melanura - Muscle & CNS
107
WEE
20-40% mortality (10% humans) - Horse/ human - Vector = Culex tarsalis / Culiseta melanrua - Muscle, brown fat, choroid plexus/ependyma, neurons * last human case 1999
108
Clinical signs of WEE/EEE
- Fever - Seizure - myalgia - irritability - sweating - Menigismus - -nuchal rigidity - -photophobia - -headache - extensor rigidity
109
VEE
Not fatal - Epizootic ~ 10 yr intervals - Upper respiratory tract - lymphatics, liver, pancreas - CNS
110
Where is the virus found in an EEE infected bird / mosquito?
Feather follicles - Young birds --> virus amplification --> mosquitos (4-10d in midgut to salivary gland)
111
What is the significance of Canine Coronavirus?
Puppies more susceptible - -> replication in enterocytes - -> shorten villi (spares crypts) * If concurrent infection with Parvo --> Severe dz * Short lived IgA protection
112
Porcine Respiratory Coronavirus (PRCV)
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
Transmissible Gastroenteritis Virus pathogenesis
``` • 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
TGE transmission
ORONASAL cat, dog, fox starling house fly
115
TGE depending on age • 3d • >3wk • grower/finisher
• 3d - Severe villus atrophy - high mortality • >3wk - regenerate epithelium - unthrifty • grower/finisher - mortality low
116
TGE maternal Ab's
Not absorbed | • passive intestinal immunity
117
Important Ag's on TGE virus
1 - Peplomer glycoprotein 2 - Integral membrane protein 3 - Nucleocapsid protein
118
What part of FIP virus induces Ab's?
Peplomer --> neutralizing Ab
119
How do recombinants occur in FIP
Canine Coronavirus
120
Pathogenesis of FIP
``` 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
Strong response to FIP
--> Recovery / carrier
122
Deficient CMI response to FIP
--> 2° viremia --> circulating immune complexes --> Perivascular inflamm • NO CMI --> EFFUSIVE • Partial CMI --> non-effusive
123
Pre-existing Anti-FIP IgG (ex. vx)
>> 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
Porcine Epidemic Diarrhea (PED)
Coronaviridae - Multifunctional virulence factor (spike structural gene) - Similar signs to TGE - slower spread - Acute Back Muscle necrosis - 100% morbidity
125
Tx for PED
Most recover w/o Tx unless 2° infection | • control = All-in All-out
126
Arterivirus | • Main dz forms
1. Equine Arteritis virus (EAV) 2. Porcine Reproductive & Respiratory Syndrome (PRRS) * Respiratory * Venereal (abortion)
127
EAV
- 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
``` PRRS • young • older • sows • boars ```
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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