Metabolic Disorders of poultriews Flashcards
Most important metabolism,sleep troubles in poultries
- Early mortality of day-old chicks
- Acute death syndrome: M
- Malabsorption syndrome: M
- Ascites syndrome: M
- skeletal disorders: M
- Rickets (juvenile osteomalatia)
- perosis (chondrodystrophy)
- torsion of the tibia
- dyschondroplasia
- cage layer fatigue L - Fatty liver haemorrhagic syndrome
Meat birds are at greater risk of developing metabolic diseases because of their rapid growth rate and allometric growth of some organs
Early mortality of day-old chicks
- nutritional cause: due to inadequate micro element and vitamin supply of the parents’ generation -0> yolk low in this elements
- management causes (tº, humidity, stock density, etc)
- infections diseases (E.coli, Salmonella)
Acute death syndrome (=flip-over disease; dead in good condition)
- birds show no signs
- usually 3-4 weeks old birds flip over and die on their back
- short convulsions (wing-beating) can be seen before death
- broiler chicken, turkey hybrids
- 60-80% are males - higher BW
- cause of death: breakdown of heat function —> collapse of the blood circulation
- usually stress triggers this condition —> cardiac arrhythmias —> predisposition to death from ventricular fibrillation
- predisposition: genetics (hybrids) + intensive feeding
- BW develops much faster than heart
- prevalence: 0,5-4%
- prevention: feed restriction around day 20, diet texture (mash) (there wont be effect on final BW because of compensatory growth)
Malabsorption syndrome (=stunting syndrome = helicopter disease = “pale bird syndrome”
- symptoms (day 4-7): not specific: growth depression, uneven growth; lack of pigmentation in skin, leg weakness, higher early mortality, diarrhea, undigested feed in feces
- symptoms (week 3-4): incomplete feathers (helicopter appearance)
- broiler chicken, turkey hybrids
- possible causes: nutrition: anti nutritive factors, mycotoxins; heat stress; viral infections (?)
- consequences: enteritis, insufficient enzyme activity —> malabsorption, slow development of an active immunity
- treatments: check quality of diet, extra vitamin supply in water
Ascites syndrome (=pulmonary hypertension syndrome, waterbelly)
- symptoms: serum-containing liquid; loose abdominal wall; cyanosis; frequently die on their backs
- broiler chicken (mainly males on 3-4 week of life) with genetic predisposition to pulmonary hypertension
- cause: increased vascular pressure in the venous system which is most commonly caused by right ventricular failure
- allometric growth of the lungs —> tissues are poorly oxygenated —> heart pumps more blood to meet the demand —> pulmonary hypertension —> congestive heart failure —> ascites
- predisposition factors: high growth rate —> higher oxygen demand comparing to small lung capacity; intensive feeding; poor air quality
- treatment: if symptoms developed, no way to treat
- prevention: less intensive feeding (mash), better ventilation
Skeletal disorders in birds
- rickets (juvenile osteomalatia)
- perosis (chondrodystrophy)
- torsion of the tibia
- dyschondroplasia
- cage layer fatigue
Predisposing factors to skeletal diseases in poultries
- genotype (hybrids for intensive production)
- intensive feeding
- deficiency of minerals and vitamins!
- anti nutritive factors, mycotoxins
DD of non-infectious skeletal disorders
Infectious skeletal disorders:
- Mycoplasma synovial
- E.coli
- Staphylococci
Rickets (juvenile osteomalatia)
- chicks develop rubbery bones that can’t support their BW
- deficiency of Ca and vit D, vit K def
- inadequate Ca : P ratio
- inadequate nutrition or intestinal disease with malabsorption
- abnormal ossification with a failure of mineralization
Perosis (chondrodystrophy)
- deficiency of other deficiencies (choline, biotin, folic acid, etc …)
- retarded growth of long bones, widening of the tibia metatarsal joint, slipping of the gastrocnemius muscle tendon from its condyles (usually 1 leg is affected)
Torsion of the tibia
- turkeys!
- I balance newer BW increase and bone maturation
- most of the in both legs
Tibial dyschondroplasia
- abnormal cartilage development, mainly in the proximal end of the tibia
- failure of chondrocyte differentiation
- various degrees of severity
- dyschondroplastic lesions are masses of avasculat cartilage extending from the growth plate into the metaphysis
- focal thickening of the growth plate and is most commonly seen in the proximal tibiotasus but also can be in other bones as well
- influencing factors: rapid growth rate, intensive feeding, CA : P ratio, metabolic acidosis (excess chloride in the feed), copper deficient diet
Cage layer fatigue (osteparalysis)
- laying hens
- Ca metabolism disorder
- death occurs from starvation and dehydration (birds can’t move)
- spontaneous bone fractures, thin eggshells
- amount of eggs produced is the same
- blood Ca is unchanged because Ca is mobilised from bones reserves
- predisposing factors: battery keeping of young layers, peak of egg production, Ca deficient diet
- stress increases vit C demand and vit C is needed for formation of collagen
- treatment: Ca and vit D, vit C supplementation
Fatty liver haemorrhagic syndrome
- high producing laying hens
- disturbance in fat metabolism
- symptoms: significant drop (30-40%) in egg production, fat accumulation in hepatocytes and in the abdomen
- subcupsular haemorrhages and sudden death
- cause: intensified de novo lipid synthesis of the liver
- predisposing factors: CHs rich diet —> elevated insulin —> intensive lipid synthesis
- also high level of egg production —> elevated blood oestrogen conc -> increase of lipid synthesis
- birds kept in cages —> inhibition of catabolic hormones
- treatment: reduction of dietary starch level, replacemt by vegetable oils