Lecture 16: Poultry Diseases

Question 1

What is the etiology of cage layer fatigue?

Answer 1

-Metabolic disease of layer hens housed in conventional cages
-Due to a decrease in bone mineral density

Question 2

What are clinical signs of cage layer fatigue?

Answer 2

-Characterized by an inability to stand and fragile bones
-Mainly observed in young laying hens reared in conventional cages
-Affected birds lie down and stop eating
-Egg shells become thin and fragile
-Posterior paralysis (with legs extended) out behind her due to spinal cord compression as a result of fracture or collapse of the vertebrae, with or without a drop in egg production
-Deformed sternum and ribs
-Acute death: egg present in reproduction tract; shell partially or totally calcified (acute hypocalcemia)

Question 3

What is the pathogenesis of cage layer fatigue?

Answer 3

Osteoporosis: deficiency in the quantity of fully mineralized, structural bone
-Caused by a deficiency of ca, phosphorus or vit D3
-Lack of activity and load-bearing… related to housing

Deformed sternum and ribs
-Due to inadequate supply of ca and/or phosphorous during growth, and small fractures

Acute death
-Due to hypocalcemia

Note* Bone issues can come from using ca from bone since a deficiency in diet

Question 4

What is the impact on cage layer fatigue?

Answer 4

-Osteoporosis is a major welfare issue
-Legs and wings can be fractured during depopulation (removal from cage), loading or transport

Question 5

What are prevention and control measures for pullets to avoid cage layer fatigue?

Answer 5

-Flock uniformity in skeletal and reproductive development

-Important to achieve a good skeletal frame in the first 6 w of life

-Avoid excessive ca during rearing until the pre-lay period (~2w before lay) at which time the ca levels should be increased (if provided too early the birds metabolism may temporarily become refractory to Ca absorption when it is needed most)

-Water additives: vit D3 and Ca (ex Dical)

-Feed additives: oyster shell (slow release of Ca) is eaten with bedtime meal will get absorbed through the night

Newer housing systems: Enriched cages, non-cages system)

Feeding management: relating to dominant birds vs submissive birds (Dom eat first with little left over for sub. birds so if fed twice at night Dom will be too full to eat second time so sub can get full)

Question 6

What is the main role of the avian cecum?

Answer 6

-Water homeostasis

Question 7

What are the normal parts of the avian small intestine?

Answer 7

-Enterocytes are the “functional” absorptive cell in the gut
-Crypts (of Lieberkuhn)
-Lamina propria (below the enterocytes)

Question 8

What is the Etiology of Coccidiosis?

Answer 8

-A parasitic disease caused by species of the genus Eimeria
-Several species of importance in chickens and turkeys

Question 9

What are clinical signs of coccidiosis?

Answer 9

-Depression, ruffled feathers
-Diarrhea or soft mucoid feces (feces can be bloody depending on the species ex Eimeria tenella)
-Morbidity and mortality are variable depending on the species
-Poor growth with less pathogenic species

Question 10

Why is the coccidian life cycle and species of important in chickens?

Answer 10

-Certain stages do most damage
-Generally the second schizont stage is when the damage begins to the intestinal epithelium
-In immune birds, sporozoites were found to remain in the lamina proprietor rather than move to the crypt epithelium to continue their life cycle
-Short life cycle= lots of build up in barn
-inside and outside for schizont is the dangerous part

Question 11

What are the main parts in the life cycle of coccidian?

Answer 11

-unsporulated oocytes excreted in feces
-These sporulate outside the host within about 2 days. these are eaten by the chicken
-Sporocytes are released in intestine (infect enterocyte)
-Sporozoites are released and infect enterocytes and undergo asexual reproduction

Question 12

What are the different types of Coccidian parasites and how are they different?

Answer 12

Important because: Each species of coccidia has affinity for a different section of gut

Emieria acervulina
-Generally mild disease, low mortality but reduced production parameters (white striations are parasites in intestines)

Eimeria necatrix:
-May be severe and cause significant mortality plus decreased production parameters
-Not too common, mid portion of gut, rupture in lamina so can cause bloody feces

Eimeria maxima:
-May be severe and cause both mortality and decreased production parameters
-More common, mid gut, yellow material

Eimeria Tenella
-Caecal coccidiosis may causes high mortality
-Only affects caeca, may have hemorrhage, bad bc deals with water

Question 13

What is the impact on coccidiosis?

Answer 13

-Important poultry disease worldwide
-Economic significance to the farmer bc of costs associated with prevention, reduced growth rates, and mortality

Question 14

What are risk factors for coccidiosis?

Answer 14

Host factors-age and immunity
-Younger and malnourished birds are generally more susceptible

Environmental factors
-Wet litter, poor barn conditions causing birds to be chilled, poor air quality

Question 15

How is coccidiosis spread?

Answer 15

-Oocytes in litter and droppings of broilers are at the highest numbers when the birds are b/w 3-5w of age
-Oocysts survive in the environment for several months
-Most common mode of transmission is by indirect (mechanical) transmission of oocytes by poultry workers contaminated clothing, equipment, or vehicles that move b/w barns or farms
-Strict host-specificity of the parasite eliminates wild birds as a source of infection

Question 16

How is coccidiosis prevented and controlled through management?

Answer 16

-Good biosecurity measures
-Remove litter b/w flocks and clean the barn thoroughly to reduce the number of oocytes (disinfectants do not kill oocytes)
-Good litter quality through proper ventilation (wet litter perpetuates parasite)
-Laying hens housed in conventional cages that separate the birds from their feces have fewer infections

Question 17

How is coccidiosis prevented and controlled through vaccinations?

Answer 17

-Species-specific immunity develops after natural infection or vaccination

-Objective of vaccination is to provide controlled, low-level exposure to oocytes of common pathogenic species to develop protective immunity against later challenge )proper vaccination and post-vaccination management in the barn should produce mild or no clinical signs

Note* by controlling # of oocytes and making sure its mild which doesn’t cause disease but does trigger response
-Want wet enough to grow to develop infection but not too wet that it will get out of control

-vaccine administation:
-Spray cabinet in the hatchery at 1d of age ex Coccivac-B
-Water vaccination on-farm up to 5 days of age

-Anticoccidial drugs (can become resistant so develop a plan)
-Rotation or shuttle programs to prevent the development of resistance to anticoccidials
-Shuttle: refers to the use of 2 or more products during the grow-out period of a flock
-Rotation: an informed decision is made to change the drug used at a given time in the future (ie every 4 m)

-Drug withdrawal time must be respected

Question 18

What is the Etiology of Necrotic Enteritis (NE)?

Answer 18

-Enteric disease of chickens and turkeys caused by a toxin produced by Clostridium perfingens Type A (most) and C (ubiquitous occurs everywhere)

-Necrotic enteritis has a world wide distribution and is most common in broiler chickens 2-5 woa but also occurs in young replacement broiler breeders, young meet turkeys, and layer chickens

-Gram stain: Gram + rods

Question 19

What are clinical sings of NE?

Answer 19

-Depression, dehydration, ruffled feathers, diarrhea, and sudden death (points towards NC vs coccidiosis)
-Subclinical sings include reduced growth rate, and impaired feed conversion

Question 20

What is the pathogenesis of NE?

Answer 20

-Initially there is overgrowth of clostridia in the intestinal lumen (bacteria living in intestines but starts with lumen)
-Under the anaerobic (without oxygen) conditions of the intestine, toxin is produced that causes severe necrosis (cell death) of contact enterocytes
-Enterocytes on scan: short, swollen, bacteria present everywhere
-Guts are initially think-walled and fluid-filled and then become thickened
-Dilated, thin-walled small intestine filled with gas
-Typical yellow pseudo-membrane (Turkish towel) completely non-functional
-Necrosis begins at villa tips and eventually the entire villous Is destroyed

Question 21

What is the impact of NE?

Answer 21

-One of the most economically important disease of commercial broiler chickens
-Flock mortality during an outbreak can be ~1% per day for several consecutive days (a lot of birds)
-Untreated disease can cause mortality of up to 50% in the infected flock
-Culling sick birds reduced growth rate of birds that survive and condemnation of carcass at proceeding due to secondary liver lesions

Question 22

What are risk factors for NE impacting the intestines?

Answer 22

Predictable disease, occurring at ~3woa at the time when
-Feed is changed from starter to grower (high to low protein and low to higher energy)
-Food size from crumble or mash to pellet
-Coccidiostats are changed on rotation program

-A lot hitting the intestines at once these all affect intestinal motility and/or mucous production

Question 23

What are the risk factors for NE impacting host/environment?

Answer 23

Host factors- age, immunity, strain
Environmental factors:
-Coccidiosis is a predisposing factor (coc. parasite causes damage and NE takes advantage)
-Housing conditions (high stocking density, wet litter)
-Farm history (build-up of the bacteria)
-Feed ingredients and nutrients content (high fat content, wheat and barley) western CA feed more wheat vs ON feed corn so can have more incidence out west

Question 24

What is are preventive and control measures for NE?

Answer 24

-Antimicrobial use for disease prevention is becoming increasingly restricted in livestock
-Vaccination or medication to control coccidiosis
-Reduce stress in barn by providing proper ventilation, littler quality, stocking density, lighting (wood shavings might be preferable to straw bc more absorptive)
-Thorough cleaning b/w flocks (eliminate bacteria and coc. oocytes, research suggests that dry cleaning rather than disinfection, decreases the risk of C. perfringens)

Question 25

What is the Etiology of infectious bronchitis (IB)?

Answer 25

-IB an acute, highly contagious respiratory disease of chickens caused by infectious bronchitis virus (IBV) which is a coronavirus (not zoonotic)
-Worldwide distribution
-Several variants exist, and variations in virulence have been reported

Question 26

What is an important IBV genotype in Ca?

Answer 26

-The highly virulent Delmarva (DMV) strain has been circulating in CA since 2016
-DMV has the most clinical signs
-# of different types with different strains

Question 27

What are the general IB clinical signs?

Answer 27

-Can vary and depend on the age of the birds, host immune status, and virulence of the virus
-Disease can vary from asymptomatic to involvement of the respiratory renal, and reproduction organs

Question 28

What are IB clinical signs in chicks?

Answer 28

-Early signs include depression, ruffled feathers, and huddling near heat sources
-Within 24h, signs of respiratory disease can be observed, including coughing sneezing, nasal discharge and gasping (inflammation in airways)
-Conjunctivitis, ocular discharge, tearing, swollen sinuses
-Reduced feed intake and poor weight gain might be observed
-Gasping and respiratory distress (will have to be euth)

Question 29

What are IB clinical signs in older birds?

Answer 29

-In flocks > 6woa, signs are similar but may be less severe and may be so subtle that they are only observant at night when the birds are normally quiet (before walk in listen)
-In laying hens, eggs production may drop by up to 50%
-Ocular and nasal discharge

Question 30

What are IB clinical signs from eggs?

Answer 30

-When IBV replicates in the reproductive tract of laying hens, normal ca reposition in the eggshells may be disrupted, resulting in soft-shelled or shell-less, abnormally shaped eggs
-Egg colour and texture can be affected
-Internal quality of the egg is often poor, albumin may be think and watery and the separation b/w the thick and thin albumen may be absent (determine through candling)

Question 31

What are IB clinical signs from renal?

Answer 31

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

Question 32

How is IB spread?

Answer 32

-Virus is shed in the nasal excretions and feces of infected birds
-Virus spreads quickly from 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 (intestinal tract and shed when stressor), carriers increase the possibility of flock-flock spread via contaminated personnel

Question 33

What is the impact of IB?

Answer 33

-Laying hens: economically the most important aspects are the affects on egg production and quality (when recover never fully reaches peak production)
-Defective eggshells, abnormal albumen, hens that recover from the infection may never return to pre-infection egg laying levels

-Broiler chickens: economically the most important aspects are the effects on production performance
-Initial respiratory infection frequency exacerbated by secondary infection (never make it before slaughter)

-Morbidity can be very high, for most strains its low unless complicated by secondary bacterial infections (4/91 and DMV strains have caused high mortality)

-Pullets <2woa may suffer permanent damage to the oviduct, resulting in poor to no egg production capacity later in life (false layers)

Question 34

What are risk factors of IB?

Answer 34

Host factors
-Species (only affects chickens) young chicks (more severe disease) old birds (more severe reproduction lesions)

Environmental factors
-concurrent infection with other respiratory pathogens or immunosuppressive viruses, especially if stocking density is high chilling in brooding chicks, poor ventilation, high ammonia levels

Renal strains: breed, high protein diet

Question 35

What are prevention and control methods for IB?

Answer 35

-Difficult with common sanitary and biosecurity measures because IBV is highly infectious
-Through C&D with adequate down-time might help to prevent recurrent infections on problem farms
-Farm complexes with multiple ages of laying hens, always move from young to older flocks, or have personnel dedicated to specific barns
-Attenuated live vaccines delivered in drinking water or by spray for broilers and for the initial cavitation 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 bc vaccines against one serotype do not cross-protect against a different serotype (ex strain 4/91)

Question 36

What re reportable diseases?

Answer 36

-Defined in the Health of Animals Act and Reportable Diseases Regulations
-Diseases that have significant importance to human or animal health or to the Canadian economy-can affect trade
-Responsability:

Question 37

What re reportable diseases?

Answer 37

-Defined in the Health of Animals Act and Reportable Diseases Regulations
-Diseases that have significant importance to human or animal health or to the Canadian economy-can affect trade
-Responsibility to: animal owners, vets, laboratories are required to immediately report the presence of an animal that is contaminated, or suspected of being contaminated with a reportable disease to a Canadian Food Inspection Agency (CFIA) district vet
-Control (ex quarantine) or eradication measures will be applied immediately

Question 38

What are Fowl Typhoid and Pullorum disease?

Answer 38

Fowl Typhoid: Salmonella Gallinarum (bacteria)
-Clinical disease is usually seen in grower or adult birds
-Affects chickens, turkeys, and minor poultry types

-Pullorum Disease: Salmonella Pullorum
-Clinical disease is primary seen only in young chicks
-Bacterial disease causing high mortality in affected flocks with additional economic losses due to chronic disease (loss of condition, drop in egg production)

BOTH
-Can be passed from parent to offspring through the egg
-Ca has monitoring program (al breeder flocks tested and fluff samples are collected at hatchery and tested)
-Free since 1982

Question 39

What is Newcastle disease?

Answer 39

-Caused by avian paramyxovirus
-Viral disease that cases high mortality following respiratory and nervous signs, or hemorrhage in the intestine tract
-Zoonotic potential- cases conjunctivitis
-There are 5 forms (velogenic (most pathogenic) forms are the most virulent and are reportable, Ca is free of the disease)

Question 40

What are clinical sings of Newcastle?

Answer 40

-Swelling of the eyelids (almond shape) ocular discharge and conjunctivitis
-Neurological sings, such as twisting of the head and neck
-Zoonotic- hemorrhagic conjunctivitis

Question 41

What is avian Influenza?

Answer 41

-Caused by an orthomyxovirus, type “A” influenza virus
-Characterized by respiratory and nervous signs, or sudden death- mortality rate can be close to 100%
-Zoonotic potential (mostly poultry workers not indirect/occasional contact)
-All highly pathogenic avian influenza and low pathogenicity H5 and H7 avian influenza viruses are notifiable (CA has had 6 outbreaks since 2007)

Question 42

What are the clinical signs of Avian Influenza?

Answer 42

-Respiratory distress, and swelling and hemorrhage of the comb and wattles

Question 43

Where is Avian Influenza transmitted?

Answer 43

-Waterfowl are natural reservoirs of the virus (usually low pathogenic types but these have the potential to mutate into highly pathogenic types)
-Wild birds, primarily waterfowl and shorebirds, are through to be the main source for into of the virus onto a poultry farm
-There is no vaccination in CA (conflicts with checking for virus, if bird was positive wouldn’t know if they have virus or just vaccinated)
-Prevention is though tight biosecurity and coordination federal control during an outbreak