Disease review

Question 1

Cage Layer Fatigue - who gets it? what is it? signs?

Answer 1

 A metabolic disease of laying hens housed in
conventional cages
 Due to a decrease in bone mineral density
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 Characterized by an inability to stand and fragile bones
 Mainly observed in young laying hens reared in
conventional cages during peak production
 Affected birds lie down and stop eating
 Egg shells become thin and fragile
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 Posterior paralysis (with legs extended) due to spinal cord compression as a result of fracture or collapse of the vertebrae
 Deformed sternum and ribs
 Acute death: egg present in shell gland; shell partially or totally calcified

Question 2

Cage Layer Fatigue – PM lesions

Answer 2

 Fragile bones, thin cortices, +/- fractures
 Deformed sternum, characteristic in-folding of ribs at
costochondral junctions

Question 3

Cage Layer Fatigue – Pathogenesis

Answer 3

 Osteoporosis (deficiency in the quantity of fully
mineralized, structural bone)
> Caused by a deficiency of calcium, phosphorous, or vitamin D3
> Lack of activity and load-bearing… related to housing
 Deformed sternum and ribs
> Due to inadequate supply of calcium and/or phosphorous during growth, and small fractures
 Acute death
> Due to hypocalcemia
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- calcium absorbed from intestine and mobilized from medullary bone > egg shell formation
> enough calcium and/or phosphorus not absorbed from the intestine for the remineralization of medullary bone > medullary bone becomes depleted of calcium
> breakdown of the trabecula and cortical bone to provide calcium for the formation of egg shell and remineralization of medullary bone
> decrease in cortical and trabecula bone volume (osteoporosis)
> bones become light, fragile, brittle, and break easily

Question 4

Cage Layer Fatigue – Pullet Management

Answer 4

• Flock uniformity in skeletal and reproductive
  development
• Important to achieve a good skeletal frame in the first
  6 weeks of life
• Avoid excessive calcium during rearing until the pre-
  lay period (~2 weeks before lay), at which time the
  calcium levels should be increased
  > If provided too early, the bird’s metabolism may
  temporarily become refractory to Ca2+ absorption when it is needed most

Question 5

Cage Layer Fatigue – Layer Management

Answer 5

 Water additives: Vit. D3 and Ca2+ (e.g. Dical)
 Feed additives: oyster shell (slow release of Ca2+)
 Newer housing systems (enriched cages, non-cage
systems)
 Feeding management (eg. 2 phase)

Question 6

Cage Layer Fatigue – Impact

Answer 6

Osteoporosis is a major welfare issue
 Legs and wings can be fractured during depopulation
(removal from cage), loading, or transport
 Keel fractures can still be an issue in alternative housing systems

Question 7

M. gallisepticum causes what diseases?

Answer 7

• Chronic respiratory disease (CRD); MG
  > Airsacculitis, fibrinous pericarditis/perihepatitis.
  Occasionally synovitis or salpingitis
• Infectious sinusitis
  > Uni- or bilateral infraorbital sinusitis +/- lower resp dz, airsacculitis, pericarditis, perihepatitis

Question 8

M. synoviae causes what disease?

Answer 8

Infectious synovitis
> Infection of synovial lining of joints and tendon sheaths, resulting in swollen joints

Question 9

M. meleagridis causes what disease?

Answer 9

MM infection
> Subclinical venereal infection of turkeys. Causes airsacculitis in embryos & poults

Question 10

Mycoplasma gallisepticum
 MG, Chronic Respiratory Disease (CRD)
- who is affected?
- general clinical signs?

Answer 10

 Species affected: 1˚ chickens & turkeys (others also)
 General clinical signs:
 Characteristic of many avian respiratory diseases - coughing, sneezing, snicking, rales, ocular and nasal discharge
 Severity can vary with changes in weather
 Usually develop slowly within flock
 Can persist for weeks or months
 Poor condition and weight loss suggest chronic disease

Question 11

Mycoplasma gallisepticum
 MG, Chronic Respiratory Disease (CRD)
- additional clinical signs for layers, broilers, turkeys?

Answer 11

• Layers: decreased feed consumption and egg production, unthriftiness, low mortality
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• Broilers: Signs more pronounced and dz more severe than in adult chickens, variable mortality (high if poor husbandry)
• Decreased feed intake and growth rate
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• Turkeys: Swelling of infraorbital sinus(es) +/- nasal exudate (often noted on wing)
• High mortality from pneumonia and airsacculitis if air sacs and lungs affected (even if few swollen sinuses)

Question 12

Mycoplasma gallisepticum - significance of the existence of variants

Answer 12

• variable pathogenicity, immunogenicity,
  harder to isolate

Question 13

one of the main issues with MG - what is CRD?

Answer 13

• it predisposes other pathogens, such as E. coli.
• The term Chronic Respiratory Disease (CRD) is used to
  describe this complicated situation. CRD can cause serious losses from high condemnations at processing.
• CRD is historical term, not used much anymore.

Question 14

CRD classic lesions

Answer 14

fibrinous pericarditis, perihepatitis, and peritonitis

Question 15

Mycoplasma gallisepticum epidemiology, associations, environmental survival

Answer 15

 Often associated with other pathogens (IBV, NDV, E.
coli, Pasteurella multocida, Haemophilus paragallinarum)
 In chickens, disease often triggered by stress (e.g.
changes in housing, management, nutrition, weather,
vaccination) or increased dust or ammonia
 Carrier birds are essential for survival (only lives a few
days outside host)

Question 16

Mycoplasma gallisepticum transmission

Answer 16

 Vertical (transovarian) - via eggs by carrier birds
 Horizontal
> Infected progeny spread bacteria through aerosols
(coughing) and contamination of feed, water, and the
environment
> Other domestic or wild birds
 Mechanical
> Via footwear, clothing, other

Question 17

Mycoplasma gallisepticum management

Answer 17

 Depopulation, C&D, down-time, strict biosecurity
 Ontario Hatchery and Supply Flock Policy
> Routine testing of breeder flocks
> Ensures chicks and poults are free from MG
 Reduce dust, ammonia, stressors
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 Vaccination of breeder pullets
> Killed oil-adjuvanted (bacterins) – protect against egg
production losses but do not prevent infection
> Live – via eye drop or spray

Question 18

Infectious bronchitis
- agent
- geography
- species
- variants

Answer 18

 Acute, highly contagious respiratory disease caused by infectious bronchitis virus (IBV), which is a coronavirus
 Worldwide distribution
 Species affected: chickens
 Several variants exist, and variations in virulence have
been reported

Question 19

IBV strain to watch out for

Answer 19

The highly virulent Delmarva (DMV) strain has been circulating in Canada since 2016

Question 20

IB – Clinical Signs - General, what signs depends on and range, systems affected

Answer 20

 Clinical signs vary and depend on the age of the bird, host immune status, and virulence of the virus
 The disease can vary from asymptomatic to involvement of the respiratory, renal, and reproductive organs

Question 21

IB – Clinical Signs – Chicks

Answer 21

 Early signs include depression, ruffled feathers, and
huddling near heat sources
 Within 24 hours, signs of respiratory disease can be
observed, including coughing, sneezing, nasal discharge, and gasping
 Conjunctivitis, ocular discharge, tearing, and swollen
sinuses are common
 Reduced feed intake and poor weight gain might be
observed

Question 22

IB – Clinical Signs – Older Birds, layers

Answer 22

 In flocks > 6 weeks of age, signs are similar but may be less severe and may be so subtle that they are only
observed at night when the birds are normally quiet
> Ocular and nasal discharge
 In laying hens, egg production may drop by up to 50%

Question 23

IB – Clinical Signs – Eggs

Answer 23

 When IBV replicates in the reproductive tract of laying
hens, normal calcium deposition in the egg shells may be disrupted, resulting in soft-shelled or shell-less,
abnormally-shaped eggs
 Egg color and texture can be affected
 Internal quality of the egg is often poor

Question 24

IB – Clinical Signs – Renal

Answer 24

 Some strains of IBV can affect the kidneys
 Birds generally recover from early respiratory signs then later develop diarrhea and inflammation of the kidneys (which produces an increased amount of urates in the droppings), sometimes with fatal blockage of the urinary system

Question 25

IB – Spread

Answer 25

 Virus is shed in the nasal excretions and feces
 Virus spreads quickly from bird to bird, via direct and indirect contact with contaminated feed, water,
equipment, and other infected birds
 In some birds, internal organs become persistently
infected, resulting in intermittent shedding of the virus
> Carriers increase the possibility of flock-to-flock spread via contaminated personnel

Question 26

IB – Impact for layers and broilers

Answer 26

Laying hens: economically, the most important aspects
are the effects on egg production and quality
 Pullets < 2 weeks of age may suffer permanent damage to the oviduct, resulting in poor to no egg production capacity later in life (false layers)
 Hens that recover from the infection may never return to pre-infection egg laying levels
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Broiler chickens: economically, the most important
aspects are the effects on production performance

Question 27

IB – Prevention and Control

Answer 27

 Difficult using common sanitary and biosecurity
measures because IBV is highly infectious
 Thorough C&D with adequate down-time might help to prevent recurrent infections on problem farms
 For farm complexes with multiple ages of laying hens,
always move from younger flocks to older ones, or have personnel dedicated to specific barns
 Attenuated live vaccines delivered in the drinking
water or by spray for broilers and for the initial
vaccination of laying birds
 Inactivated oil-emulsion vaccines administered by intramuscular or subcutaneous injection for breeders and layers before the beginning of the production cycle
 Despite vaccination efforts, outbreaks of IB occur
frequently because vaccines against one serotype do
not cross-protect against a different

Question 28

Inclusion Body Hepatitis (IBH)
- type of virus, persistence

Answer 28

• Aviadenoviruses
• DNA virus , 70-90 nm in diameter
• Characteristically produces IN inclusion bodies
• Relatively resistant virus (pH, alcohol , phenol)

Question 29

Inclusion body hepatitis groups, serotypes

Answer 29

(avian adenovirus group I)
* Five group 1 species of adenovirus
A – E (based on Restriction Enzyme Fragmentation
Patterns)
* Within these species there are 12 serotypes recognized
* In Canada, serotypes 2, 8, and 11 are
most commonly associated with outbreaks of IBH

Question 30

IBH transmission

Answer 30

• Vertical transmission is important
• Peak virus excretion is around 4-6 wks of age, but we have seen mortality in birds as young as 1 week of age and peaking by 2 weeks of age
• Horizontal transmission occurs once the virus is established in the flock (feces, nasal secretions, kidneys etc.)

Question 31

IBH classic PM lesions

Answer 31

• Hepatic necrosis and typical IN inclusion bodies
• Glomerulitis associated with IBH

Question 32

IBH prevalence in ontario, mortality

Answer 32

• Prevaelnce: 1.9% of all broiler chicks
• Mortality: increase of 3.1% in affected flocks