Herpesvirus Flashcards

(42 cards)

1
Q

Important facts on Herpes

A
• Every animal species has at least 1 type of herpesvirus
• dsDNA 
      --> mRNA and progeny genome
• Enveloped 
      -->  bind PM and Nucleocapsid migrates to cell nucleus for replication
• icosohedral capsid / helical
• Establish latency 
• no common Ag between species
• 3 main families 
       - Alphaherpesvirinae
       - Betaherpesvirinae
       - Gammaherpesvirinae
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2
Q

4 structural units of herpesvirus

A
  1. protein fibrillar spool wrapped around DNA core
  2. capsid composed of 12pentameric &150 hexametric capsomeres
  3. amorphous protein layer btwn capsid & protein
  4. enveloped
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3
Q

Alphaherpesvirinae family

A
  • Short replication pd (<24hr)
  • latency in neural cells

– Equine Herpesvirus

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4
Q

Betaherpesvirinae family

A
  • Long replication pd (>24hr)
  • marrow host range
  • slow destruction in cell culture
  • infected cells enlarge –> cytoplasmic/nuclear inclusions
  • Latent infection in Lymphoreticular & Secretory glands
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5
Q

Important viruses in Shipping fever

A
  • Bovine Herpesvirus 1
  • Bovine parainfluenza virus types 3
  • Bovine respiratory synciytial virus (BRSV)
  • Bovine viral diarrhea virus (BVDV)
  • Bovine cononavirus (BCV)
  • Bovine adenovirus (BAV)

Bacteria
- Pasteurella haemolytica

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6
Q

Pathogenesis of shipping fever

A

Viral infections –> ↑ colonization of lower lung by bacteria –> severe pneumonia

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7
Q

What proteins are assoc’d w/ attachment/penetration in bovine herpes virus

A

Glycoprotein B, C, & D

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8
Q

How is Bovine herpes transmitted?

A

Aerosol
Direct contact

    • 1° ruminants
    • 4-6 day incubation period
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9
Q

When does abortion occur w/ bovine herpesvirus?

A

First calf heifer
• any stage of gestation
• 14-90 days following infection

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10
Q

What forms are there of Bovine herpes?

A
1. Respiratory form (rhinotracheitis)
      • usually mild URI
2. Genital Dz
       • Infectious pustular vulvovaginitis (IPV) - cow
       • Infectious pustular balanoposthitis 
                 - bull glands/ prepuce
3. Neural form
        • meningoencephalitis (calves)
4. Systemic dz
        • Focal lesions in liver, forestomach, esophagus
        • young calves, generally fatal
5. Keratoconjunctivitis
        • Role in Pink Eye
        • profuse lacrimation
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11
Q

What is the immune response to Herpes virus?

A
  • Neutralizing Abs

* Secretory IgA & CMI

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12
Q

What is the virus assoc’d w/ Pseudorabies?

What is another name for it?

A

Porcine Herpesvirus 1

• Aujeszky’s Dz

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13
Q

What is a special characteristic assoc’d w/ PRV (pseudorabies) following passage in chick/bovine cell?

A

Spontaneous deletion of “Us” region of genome

• Us = Unique small

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14
Q

What is the main reason for Pseudorabies outbreak?

A

Change in management practice in swine industry
• Reservoir host = Swine
• Dead-end hosts = cattle, sheep, dog/cat, raccoons, rabbits, rodents, chickens

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15
Q

Important Ag proteins of pseudorabies?

A

gB, gC, gH, gD

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16
Q

Pathogenesis of Pseudorabies virus

A

Acute / latent infection of pig –> contact –> viremia –> tonsillar /pharyngeal tissue –> olfactory trigeminal n. & glossopharyngeal n –> brain

  • can replication in respiratory tract –> leukocyte infection
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17
Q

Transmission of Pseudorabies virus

A
  1. Nose-to- nose , licking, biting
  2. vertical transmission to piglet
  3. aerosol
  4. contaminated feed/facility –> cattle infection
  5. infected placenta –> other animals
18
Q

Where is pseudorabies infection most common?

A

Cold climates w/ extensive hog industries

• heat/direct sun/ dry –> inactivates virus

19
Q

What is the difference in clinical presentation btwn young/old/pregnant pigs, assoc’d w/ pseudorabies?

A

Young
• CNS dz
• die w/in 8 days after infection

Older
• respiratory dz

Sow
• Before 30 day gestation
      - abortion + resorption
• after 30 days of gestation
      - still birth & mummification
20
Q
Clinical signs of Pseduorabies in:
• cattle
• dog
• cat
• rabbits
A

Cattle
• ↓ milk
• frenzied, biting, gnawing at skin
• Die w/in 2 days

Dog
• pruritis
• excessive salivation, howling (like rabies infection)

Cat
• extremely fast progression of dz

Rabbit
• most vulnerable to infection

21
Q

Do maternal Ab’s prevent infection of pseduorabies?

A

NO, prevents signs of dz, but not infection

22
Q

Equine herpesvirus 1 (EHV1)

A
  • Young animals – Upper respiratory
  • Induce abortion (@ 8-11month)
    * Usually only once
  • Respiratory dz – intranuclear inclusion
  • Induced neurologic dz
    * Virus spreads from respiratory tract to CNS via Leukocytes
23
Q

EHV-2

A

Chronic throat infection (Lumpy dumpies)

• life long carrier

24
Q

EHV-3

A
Equine coital exanthema
• Small, raised, red papules --> pustules --> ulcerations
• recovery ~2wks
• mild genital infection  
     - No abortion
25
EHV4
• Upper respiratory infection -- eosinophilic intra-nuclear inclusion • fever lasting 2-5 days • recovery ~1 wks
26
Gammaherpesvirinae
Vericellovirus | --Canine herpesvirus
27
Canine Herpesvirus transmission
1. Oronasal exposure - secretion from infected dam 2. In utero infection -- infect while passing thru birth canal 3. contact w/ infected puppy 4. fomites
28
What lesions would you see in puppies less than 1 week infected with CHV
Fatal generalized infection • Viral replication in epithelial cells & mucosa of nasopharynx --viremia via Macrophage infection • progressive multifocal necrosis & hemorrhage • generalized lympadenopathy • DIC • Menigoencephalitis ``` Clincal signs • hypothermia • yellow-green feces • persistant cry • hemorrhagic nasal discharge • seizures • muli-focal necrotizing lesions in placenta ```
29
What lesions would you see in puppies >2weeks?
Mild to subclinical infections
30
Where does the Canine herpes virus replicate?
1. Nasopharynx 2. Tonsil 3. Retropharyngeal LN 4. Bronchial LN 5. Lungs 6. Genital tract
31
If a mother has CHV what clinical signs will you see?
* infertility * Abortion of mummified / dead fetus * still births * weak pups - not apparent clinical signs - maternal Ab or immune lymphocyte thru colostrum
32
Most common transmission of feline herpesvirus Incubation pd
Oronasal & conjunctival exposure w/ oronasal secretions or fomites 2-6 days
33
How does stress affect feline herpes virus shedding?
reactivation --> lag period of ~1 wk -->virus excretion for 1-2 wks
34
Initial replication of FHV
nasal septum, turbinates, tonsils, nasopharynx Mostly localized to respiratory tract --> initially serous discharge--> mucopurulent --> encrusted nares & eyelids chronic - ->multifocal epithelial necrosis w/ neutrophilic infiltration - -> osteolytic changes in nasal turbinates
35
Pathogens of feline respiratory infections
1. FHV 2. Feline calicivirus 3. Feline reovirus 4. Bordetella bronchiseptica 5. chlamydia psittaci 6. Mycoplasmas
36
Immunity in FHV
kittens become sub clinically infected - -in the presence of maternal Abs - -> Latent carrier Important for protection • Neutalizing Ab • CMI repsonse
37
What is the herpesvirus of Chickens?
Marek's Disease (alphaherpesvirus) • virus-induced neoplasic dz • paralysis & lymphosarcoma of peripheral nerves & internal organs • problem in household flocks which were not vx at 1 day old 3 sero-types • 1 = oncogenic • 2 = non-oncogenic • 3 = Turkey herpesvirus
38
How is Marek's Dz spread?
Virus shed in FEATHER FOLLICLES (dander) --> air currents --> oronasal route • 4-12 wk incubation pd
39
What are the 3 types of Virus-Cell interations assoc'd w/ Marek's dz
• Productive - virus particles produced in feather follicle • Latent - virus resides in lymphocytes - w/o virus production • Transformation - only T-lymphocytes Serotype 1 induces neoplastic transformation of T cell genome - viral Ag's expressed
40
what is the standard method of protection from Marek's dz
• vx chicks at 1 day
41
What are the natural hosts for Malignant catarrhal fever virus (MCF)
Blue wildebeest & black wildebeest - natural host --inapparent infection Sheep -natural / 2° hosts Cattle & buffalo - 2° host - acute & generalized dz Direct contact transmission • nasal discharge • 2-4 day incubation
42
Forms of MCF (malignant catarrhal fever)
1. Per-acute (1-3days) • severe inflame of oronasl mucosa • hemorrhagiic gastroenteritis ``` 2. Intestinal form (4-9 days) • pyrexia • diarrhea • hyperemia of ochulonasal mucosa • nasal & ocular discharge • LN enlargement ``` ``` 3. Head & eye form = typical (7-14 days) • 2-7day pyrexia • oculonasal discharge -serous to mucoid to purulent • dyspnea due to mucoid blockage • oral mucosa hypermia w/ diffuse superficial necrosis ``` 4. Mild form • experimental infection w/ modified virus --> recovery