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VETM 422 Virology > Lecture 18: Avian Viruses 2 > Flashcards

Lecture 18: Avian Viruses 2 Flashcards

1
Q

Type of virus causing avian pox virus

A

Avian Pox virus
* dsDNA

  • narrow spectrum of hosts
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2
Q

What is the pathogenesis and histologic features of avian pox

A

Pathogenesis
* target skin epithelium
* make it hyperplastic
* cause ballooning degeneration
* borrel bodies - intracytoplasmic inclusion bodies

  • target unfeather areas: comb, wattle
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3
Q

Compare the 2 types of poxvirus and how they are transmitted and their mortality

A
  • cutaneous/dry form
    o transmit: skin abrasions/mosquito/cannibalism (skin damage)
    o low mortality
  • wet/dipthirtic form
    o low mortality
    o transmit via respiratory aerosols
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4
Q

Compare the 2 types of poxvirus and the clinical signs

A
  • cutaneous/dry form
    o severe follicular multifocal and follicular epithelial hyperplasia and folliculitis
  • wet/dipthirtic form
    o severe multifocal to coalescing mucosal hyperplasia
    o diffuse necrosuppurative tracheitis with extensively diptheretic membrane
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5
Q

How is avian poxvirus diagnosed in a labratory

A
  • laboratory: use chorioallantoic membrane of 9 – 11d old (poxvirus and infectious laryngotracheitis virus)
    o if positive = multifocal hyperplasia (pox lesions) in 6 days
  • identify virus in lesion/scab
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6
Q

How is avian pox controlled in chickens and pigeons, as well as turkeys

A

o chicken/pigeon: wing-web method (dip needle in vaccine and puncture wing)
o turkey: drumstick stab method at 2-3 months old

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7
Q

What are the features of avian pox vaccine? how does this affect other viruses? How does this effect its implementation and efficacy?

A

o fowlpox vectored infectious laryngotracheitis, Newcastle disease vaccine = in ovo or 1d after hatch
 fowlpox is ‘backbone’ of vaccine – remove fowlpox genes and insert desired genes
 give immunity against fowl pox and inserted gene pathogen
 if used in a fowlpox endemic area – it can cause vaccine failure (because there is existing ig/adaptive immune stimulation)
 can also use poxvirus as a backbone for vaccine production

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8
Q

what type of chickens aren’t vaccinated for avian pox?

A

o broiler not vaccinated unless in endemic area

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9
Q

How do you monitor vaccine efficacy of avian pox virus

A

o monitor: 8-10d after vaccine, examine 10% of birds
 lift wing and look for proliferative lesions (scab formation) where the vaccine was administered – if present = vaccine take is good/vaccine is working

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10
Q

What are the virus features of Infectious bursal disease/Gumboro disease

A

Infectious bursal disease/Gumboro disease
* birnaviridae, non-enveloped, segmented
* Genus: Avibirnanirus

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11
Q

What are the features of the subtypes of IBD

A
  • 2 serotypes
    1. Type 1: with 3 subtypes
    a. Classic/standard = 10 -50% mortality
    b. Variant (no mortality) immunosuppression
    c. Very virulent (50-100% mortalitty
    2. Type 2; non pathogeneic
    a. 3-6 weeks
    b. Acute/contagious
    c. As long as chickens have functioning burssa of fabricus (<16wk) can have clinical dz
    3. Turkey/duck = subclinical
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12
Q

What are the gross lesions associated with IBD

A
  • Hemorrhagic and swollen/englarged/edematous/gelatinous bursa
  • Dehydration
  • Severe urate accumulation
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13
Q

What are the histologic lesions associated with IBD

A
  • Infiltration of B cells in bursa – as a tropism for dividing pre-B cells in bursa
  • Interfollicular areas become thickened due to depletion of b cells
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14
Q

What other disease causes similar histologic lesions as IBD and why

A
  • *mareks disease can also deplete B cells
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15
Q

What is the pathogenesis of IBD

A
  • Inflammation of bursa followed by B cell necrosis and apoptosis then acquired B cell deficiency = atrophy
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16
Q

What are the clinical signs of IBD

A
  • Anorexia
  • Depression
  • Ruffled feathers
  • Diarrhea (stained vent feathers – feces and urates)
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17
Q

How is IBD dx

A
  • Acute = disease lasts 7 – 10d
  • Virus isolation – RT-PCR of bursa
  • Serologic testing + increasing Ig titres using virus neutralization = confirm serotype and strain
18
Q

What is the vx strategy for IBD

A
  • Vaccine
    o Broiler: in ovo (ED18) or 1d then 2-3 weeks
    o Layer: 2 – 3 weeks
19
Q

Why might a vaccine fail

A
  • Vaccine failure due to:
    o Uneven vaccine administration (if in water or spray)
    o Improper storage
    o Route of administration
    o Evolution of virus
    o Maternal Ig interference
20
Q

What is the route of admin of live vs inactivated vx

A

o Live attenuated = spray or water
o Inactivated = injection

21
Q

How is maternal immunity passed to chicks

A

o Usually birds are vaccinated before laying period – inactivated vx
o Maternal Ig transmitted to chicks and persist for 6 weeks

22
Q

Describe 2 ways to overcome maternal immunity when vaccinating chicks

A
  • 2 strategies to overcome maternal Ig interference
    o Must vaccine before it declines below minimum protection level
     If at 3 weeks – high maternal Ig = need more virulent vaccine
  • If give avirulent vaccine = neutralized by maternal Ig
     3 – 6 weeks = intermediate virulent vaccine
     >6 weeks = avirulent vaccine
    o Or use immune complex vaccine
     If coat virus in serum with virus specific Ig
     Virus Ig bind maternal Ig (form complex) and prevent neutralization
     Over time the complexes will decay and it will reveal the vaccine virus
  • Virus released once the maternal Ig removed
     Not found in any other animal species
     Either given in ovo or 1d (with high maternal Ig)
23
Q

You are asked to vaccinate a flock of chickens to prevent pox viral infection. You administer the vaccine via
a
In ovo route
b
Intramuscular
c
Wing web
d
Drinking water
e
Aerosols

A

C

24
Q

In ovo immune complex vaccines against infectious bursal disease (IBD)
a
Consist of T cells and the vaccine virus in one formula
b
Prevent maternal antibody interference
c
Provide passive as well as active immunity
d
Provide passive immunity only when maternal antibody levels are low
e
Used for stimulating innate immune responses rather than antibody-mediated immune responses

A

B

25
Q

Which of the following gross lesion is found consistently in 4 weeks old broiler chickens infected with a field strain of infectious bursal disease virus?
a
Petechial hemorrhage in the brain
b
Atrophy of skeletal muscles
c
Inflamed swollen bursa of Fabricius with hemorrhages
d
Nodular lesions in the bursa of Fabricius
e
Congestion and edema of the lung

A

C

D -avian leukosis dz

26
Q

Chicken anemia virus infection is immunosuppressive. Explain (3 marks).

A
  1. infects hemocytoblasts = causes apoptosis
    - all downstream cells would be reduced (erythrocyte/heterophil/thrombocytes)
    - reduced innate immunity
  2. infects hemocytoblasts = causes apoptosis
    - reduce cytotoxic T cell function
    - reduced adaptive immunity
  3. reduced T cells reduced the T cell help for B cell activation
    - reduced adaptive immunity
27
Q

What are the viral features of the virus causing chicken anemia virus

A

Circovirus
* ssDNA, non-envelopes
* Genus: Gyrovirus
* 1 serotype
* Very resistant

Geography: common globally

28
Q

What animals does chicken anemia virus target and how does this impact disease manifestation

A

Target: young (2-3 weeks old) chicks but can infect all ages (only chicks will develop clinical signs)
* Mortality/morbidity depends on age
* Develop resistance > 2 -3 weeks (can still be infected)

29
Q

List 3 viruses with segmented genomes

A
  • orthomyxovirus
  • reovirus
  • birnavirus
30
Q

What is the pathogenic mechanism o chicken anemia virus

A

Path: target T cells (thymus degradation) = immunosuppression
* Target the hemocytoblast cells (progenitor cell for RBC/heterophil/thrombocyte) and T lymphocyte precursor = cause apoptosis
* Reduced T cells will also reduce the activation of B cells
* Virus found mainly in most organs (brain/liver/spleen/bursa of fabricus/bone marrow/serum/repro organs) – no seroconversion until the birds come into production
* Long incubation period

31
Q

What are the 3 primary indicators that point to chicken anemia virus

A
  • Poor performance/increased mortality in broiler (normal mortality = 2%)
  • Secondary infection increased
  • vaccine failure (any other vaccines administered because immunosuppressed)
32
Q

What is the timeline of clinical signs in chicken anemia virus

A
  • 8d after infection - anemia/thrombocytopenia (increased bleeding)/heterocytopenia (immunosuppression/increased infection)
  • 28 – 36 d after infection – blood parameters become normal again
  • Enhances impact of other immunosuppressive agents
33
Q

How is chicken anemia virus transmitted

A
  • vertical transmission (also avian leukosis virus) = infect eggs
  • horizontal transmission = in birds will lowered immunity between chicks
34
Q

What is the primary species affected by chicken anemia virus

A

Host: chickens (can be found in turkey/quail but not clinically significant)

35
Q

What are the gross lesions associated with chicken anemia virus

A

Gross: thymic atrophy
* wing hemorrhage
* gangrenous dermatitis (blue wing dz) – due to secondary infection
* subcutaneous hemorrhage
* bone marrow atrophy + ‘watery’ blood = pale carcass

36
Q

What is the vaccination protocol for chicken anemia virus

A
  • vaccinate breeder flocks (not commercial flocks)
    o live modified vaccine – mass vaccination (SC or IM)
    o vaccinate between 8 -16 weeks
  • maternal Ig will protect – higher levels of maternal Ig = longer protection
    o if you vaccinate the breeders = effective at protecting progeny
    o vaccinating breeders will generate high homogenous levels of maternal Ig
    o if you have more maternal Ig then your neutralizing titre will be low
37
Q

What are the virus features of reoviral arthritis

A

Reovirus
* non enveloped, segmented genome
* common in NA

38
Q

What are the clinical signs of reoviral arthritis and what animal does it occur in

A

Clinically:
* lameness + hockey stick legs – swollen tendons/hocks/joints/shanks
* ruptured gastrocnemius tendon (40d broiler)

broilers

39
Q

How is reoviral arthritis controlled

A

Control
* 4 strains included in the vaccine (S1133, 1722, 2408, 2177)
* vaccine strains don’t protects against disease from variants
* preventing viral arthritis = detect variants and make custom-made vaccines

40
Q
A

VETM 422 Virology (19 decks)

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