Lecture 16: Poultry Diseases Flashcards
(43 cards)
What is the etiology of cage layer fatigue?
-Metabolic disease of layer hens housed in conventional cages
-Due to a decrease in bone mineral density
What are clinical signs of cage layer fatigue?
-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)
What is the pathogenesis of cage layer fatigue?
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
What is the impact on cage layer fatigue?
-Osteoporosis is a major welfare issue
-Legs and wings can be fractured during depopulation (removal from cage), loading or transport
What are prevention and control measures for pullets to avoid cage layer fatigue?
-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)
What is the main role of the avian cecum?
-Water homeostasis
What are the normal parts of the avian small intestine?
-Enterocytes are the “functional” absorptive cell in the gut
-Crypts (of Lieberkuhn)
-Lamina propria (below the enterocytes)
What is the Etiology of Coccidiosis?
-A parasitic disease caused by species of the genus Eimeria
-Several species of importance in chickens and turkeys
What are clinical signs of coccidiosis?
-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
Why is the coccidian life cycle and species of important in chickens?
-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
What are the main parts in the life cycle of coccidian?
-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
What are the different types of Coccidian parasites and how are they different?
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
What is the impact on coccidiosis?
-Important poultry disease worldwide
-Economic significance to the farmer bc of costs associated with prevention, reduced growth rates, and mortality
What are risk factors for coccidiosis?
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
How is coccidiosis spread?
-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
How is coccidiosis prevented and controlled through management?
-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
How is coccidiosis prevented and controlled through vaccinations?
-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
What is the Etiology of Necrotic Enteritis (NE)?
-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
What are clinical sings of NE?
-Depression, dehydration, ruffled feathers, diarrhea, and sudden death (points towards NC vs coccidiosis)
-Subclinical sings include reduced growth rate, and impaired feed conversion
What is the pathogenesis of NE?
-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
What is the impact of NE?
-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
What are risk factors for NE impacting the intestines?
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
What are the risk factors for NE impacting host/environment?
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
What is are preventive and control measures for NE?
-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)
