Lecture 18: Avian Viruses 2 Flashcards
Type of virus causing avian pox virus
Avian Pox virus
* dsDNA
- narrow spectrum of hosts
What is the pathogenesis and histologic features of avian pox
Pathogenesis
* target skin epithelium
* make it hyperplastic
* cause ballooning degeneration
* borrel bodies - intracytoplasmic inclusion bodies
- target unfeather areas: comb, wattle
Compare the 2 types of poxvirus and how they are transmitted and their mortality
- 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
Compare the 2 types of poxvirus and the clinical signs
- 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
How is avian poxvirus diagnosed in a labratory
- 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
How is avian pox controlled in chickens and pigeons, as well as turkeys
o chicken/pigeon: wing-web method (dip needle in vaccine and puncture wing)
o turkey: drumstick stab method at 2-3 months old
What are the features of avian pox vaccine? how does this affect other viruses? How does this effect its implementation and efficacy?
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
what type of chickens aren’t vaccinated for avian pox?
o broiler not vaccinated unless in endemic area
How do you monitor vaccine efficacy of avian pox virus
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
What are the virus features of Infectious bursal disease/Gumboro disease
Infectious bursal disease/Gumboro disease
* birnaviridae, non-enveloped, segmented
* Genus: Avibirnanirus
What are the features of the subtypes of IBD
- 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
What are the gross lesions associated with IBD
- Hemorrhagic and swollen/englarged/edematous/gelatinous bursa
- Dehydration
- Severe urate accumulation
What are the histologic lesions associated with IBD
- 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
What other disease causes similar histologic lesions as IBD and why
- *mareks disease can also deplete B cells
What is the pathogenesis of IBD
- Inflammation of bursa followed by B cell necrosis and apoptosis then acquired B cell deficiency = atrophy
What are the clinical signs of IBD
- Anorexia
- Depression
- Ruffled feathers
- Diarrhea (stained vent feathers – feces and urates)
How is IBD dx
- Acute = disease lasts 7 – 10d
- Virus isolation – RT-PCR of bursa
- Serologic testing + increasing Ig titres using virus neutralization = confirm serotype and strain
What is the vx strategy for IBD
- Vaccine
o Broiler: in ovo (ED18) or 1d then 2-3 weeks
o Layer: 2 – 3 weeks
Why might a vaccine fail
- 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
What is the route of admin of live vs inactivated vx
o Live attenuated = spray or water
o Inactivated = injection
How is maternal immunity passed to chicks
o Usually birds are vaccinated before laying period – inactivated vx
o Maternal Ig transmitted to chicks and persist for 6 weeks
Describe 2 ways to overcome maternal immunity when vaccinating chicks
- 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)
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
C
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
B
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
C
D -avian leukosis dz
Chicken anemia virus infection is immunosuppressive. Explain (3 marks).
- infects hemocytoblasts = causes apoptosis
- all downstream cells would be reduced (erythrocyte/heterophil/thrombocytes)
- reduced innate immunity - infects hemocytoblasts = causes apoptosis
- reduce cytotoxic T cell function
- reduced adaptive immunity - reduced T cells reduced the T cell help for B cell activation
- reduced adaptive immunity
What are the viral features of the virus causing chicken anemia virus
Circovirus
* ssDNA, non-envelopes
* Genus: Gyrovirus
* 1 serotype
* Very resistant
Geography: common globally
What animals does chicken anemia virus target and how does this impact disease manifestation
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)
List 3 viruses with segmented genomes
- orthomyxovirus
- reovirus
- birnavirus
What is the pathogenic mechanism o chicken anemia virus
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
What are the 3 primary indicators that point to chicken anemia virus
- Poor performance/increased mortality in broiler (normal mortality = 2%)
- Secondary infection increased
- vaccine failure (any other vaccines administered because immunosuppressed)
What is the timeline of clinical signs in chicken anemia virus
- 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
How is chicken anemia virus transmitted
- vertical transmission (also avian leukosis virus) = infect eggs
- horizontal transmission = in birds will lowered immunity between chicks
What is the primary species affected by chicken anemia virus
Host: chickens (can be found in turkey/quail but not clinically significant)
What are the gross lesions associated with chicken anemia virus
Gross: thymic atrophy
* wing hemorrhage
* gangrenous dermatitis (blue wing dz) – due to secondary infection
* subcutaneous hemorrhage
* bone marrow atrophy + ‘watery’ blood = pale carcass
What is the vaccination protocol for chicken anemia virus
- 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
What are the virus features of reoviral arthritis
Reovirus
* non enveloped, segmented genome
* common in NA
What are the clinical signs of reoviral arthritis and what animal does it occur in
Clinically:
* lameness + hockey stick legs – swollen tendons/hocks/joints/shanks
* ruptured gastrocnemius tendon (40d broiler)
broilers
How is reoviral arthritis controlled
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
