Under-performance in poultry Flashcards
1
Q
Describe a poultry pyramid
A
TOP:
Pure line genetic flock - genetic companies
Great grandparents - genetic companies
Grandparents - Integrator/genetic companies
Parent flocks - Integrator companies
Broilers or layers - Integrators/ farmers
BOTTOM OF PYRAMID
2
Q
Where does crop sit (crop, proventriculus or gizzard)?
A
Gizzard
3
Q
How much of the market do free range eggs make up?
A
43%
4
Q
Describe enriched cages
A
potential to nest potential to roost potential to scratch potential to stretch 15 birds/pen produces cleaner eggs
5
Q
Name 3 laying systems
A
free range: access to fields and barn
enriched colony cage - 750cm2/bird
barns - 11 hens per m2
6
Q
Describe hen lifecycle
A
- 0-16 w birds are reared in bars on pullet rearing farm (20 vaccines in this time, most in water)
- pullet moved to laying farm
- 18-20 w pullet starts to lay (very small eggs to start)
- pullet becomes a ‘layer’ and lives until 72 w (aim to increase to 100d)
7
Q
Outline diagnostics in poultry
A
FLOCK LEVEL!
- serology (Ab titres, 10% flock)
- swabs (PCR/bacteriology culture and sensitivity)
- virus isolation
- FEC, cocci oocyst counts
- PME
8
Q
How is mycoplasma tested for?
A
PCR
9
Q
Main cause - under-performance in layers
A
Poor management
10
Q
CS - poor management in layers
A
- egg production drop
- change in egg shell quality
- change in egg size
- mortality
- water/feed intake reduction
11
Q
List some dz affecting layers
A
- infectious bronchitis (IB)
- mycoplasma
- peritonitis
- endoparasites and ectoparasites
- POOR MANAGEMENT
12
Q
What is IB?
A
- common virus
- coronavirus
- virus mutates readily –> many shells (>100 strains)
13
Q
CS - IB
A
- snicking
- watery eyes/nose
- head shaking
- ‘wrinkly egg’s
14
Q
Pathogenesis - IB
A
- IB damages cilia in respiratory tract –> infected birds cannot remove mucus containing these bugs out of lower respiratory system –> allows bacteria and viruses better access to the air sacs than in healthy birds
- once in the air sacs bacteria (e.g. Pasteurella, E.coli) can cause air sacculitis and even cross the thin air sac wall into abdomen to cause peritonitis and death
15
Q
Dx and prevention of IB
A
- PCR swabs (cloacal, 10 samples), 1st point of call
- paired serology (£600 so commercial flocks only)
- ensure good vaccination technique (rear)
- ensure correct vaccines are used at correct time (q6-8 weeks during lay)
16
Q
Describe mycoplasma infection
A
- bigger than a virus, smaller than a bacteria
- 23 different types with M.gallisepticum most prevalent
- once infected birds remain infected for life
17
Q
CS - mycoplasma
A
- swollen head
- swollen tissue around eye
- bubbles in corner of eye
- wrinkly white eggs
- affects flying ability?
18
Q
Transmission - mycoplasma
A
- adult to chick through egg/semen
- bird to bird: sneezing, coughing, directly or through water system
- incubation period is 6-10d
- infected birds on farm boundary to neighbouring farms
- from wild bird population
19
Q
Describe peritonitis
A
- most common dx in adults, secondary to almost all dz
- stress and coming into lay
- oviduct and tracheal similarities
- primary/secondary
- many types of E.coli involed
- tx included AB based on C+S (4 types with 0d egg withdrawal, 2 work = Denigrad and tylan. You can’t use baytril in layers as specifically contraindicated on the datasheet)
- Vaccines - 2 types - 1 commerical, covers many E.coli strains, other is specific autogenous vaccine to farm based on farm E.coli type
20
Q
Outline worm tx
A
- Fubenvet in feed licensed fro 7d
- Solubenol in water licensed for 7d
- Fimabo in water licensed for 7 days
- Panacure Aquasol licensed for 5 days (expensive, commercial only)
21
Q
What are the different worm types?
A
- Ascaridia galli (round worm, intestinal)
- Capillaria (hair worm, crop)
- Heterakis gallinarum (caecum, carries Blackhead - not good, causes sudden death, hobnail liver lesions, caecal ulcers)
- Syngamus trachea = gape worm
- PPP vary 14-21 days
22
Q
Describe red mite
A
- v common
- nocturnal
- vampires of poultry world
- think fleas!
- you may not know the birds have an infestation
- visible to naked eye
- life cycle can be as short as 10d in warm weather
- can liver 2 y w/o eating
- tx is a powder, organic, causes outer skin of mite to be scratched out –> dehydration
23
Q
CS - underperformance in broilers
A
- underweight
- reduced water consumption
- reduced feed intake
- CS - enteritis, diarrhoea
24
Q
Describe broiler life cycle
A
- chick placed weigh 40-50g
- kept until 30-65d then slaughtered
- birds remain on same farm until cleared
- standards kept in barns whole life, max crop 100,000
- free range kept in barns until 21d of age then allowed out until clearing, 10,000 birds maximum
- organic kept in small sheds allowed out from 21 days, max crop size 5000
25
How can prevalence of pododermatitis be reduced?
lifting nipple feeders higher as birds grow/ get older
26
Name diseases in BROILERS
- IB
- Infectious Bursal Disease = IBD (Gumboro)
* coccidiosis
- enteritis/ dysbacteriosis
27
Outline IBD
= Infectious bursal disease
- bursa is the bird immune system HQ
- aka Gumboro dz
- affects B cells in bursa of fabricius
- birnavirus
- NOT zoonotic
- damages immune system --> other conditions
- vaccinated at 18, 24 and 28 d in some cases
28
Outline coccidioss in BROILERS
- Eimeria acervulina at 14d : won't kill birds but they slow in growth and become uneven
- E. tenella (blood) at 25d : kills birds
- sometimes secondary necrotic enteritis
- 8 spp of cocci affect layers and 5 spp of cocci affect broilers (d/t lifespan)
29
Outline cocci control
- coccidiostats ionophores
- chemical cocci tx (Baycox/Ampolium, virkon useless)
- cleaning of houses with chemicals that kill oocysts
- burning of barn floors (most effective)
30
Outline enteritis/ dysbacteritis
- bacterial scour (usually clostridia)
- variable causes (secondary to lots of things)
- difficult to tx (Amoxicillin)
- next stage is necrotic enteritis
- cholangiohepatitis
31
Outline neteritis
- Clostridia perfingens type C
- spike in mortality
- penicillin sensitive
- associated with coccidia
- possibly low mortality followed by secondary cholangiohepatitis
