Internal and technological diseases and deficiencies Flashcards
What is vent prolapse in birds?
lower part of the oviduct turns inside out and protrudes from the vent
Causes of vent prolapse in birds? (5)
o Too young birds start laying – underweight
o Jumbo eggs – excessive protein level in feed
o Overweight – especially in older birds
o Lack of calcium
o Reduction of the cloacal muscle tone, stretching of the cloacal muscles
o Constipation, diarrhea, parasites
Clinical signs of vent prolapse in birds?
- Lethargy, depression, reduced movement
- The feathers are ruffled, puffy
- Loss of appetite
- Breathing through the beak
- There may be no droppings in the cage
- Strained and painful defecation or laying
- Excessive grooming of the cloacal area
- Part of the oviduct has exited the cloaca
- Dirty cloacal feathers
- Infection – smell
Treatment of vent prolapse in birds?
❖ Isolation from the herd
❖ Thorough cleaning of the protruding part
❖ Manual repositioning of the oviduct
❖ Vitamins and minerals
❖ Analgesics, antibiotics
❖ Rest, monitoring
❖ Surgical installation possible in pet
birds
Or, slaughter/ put down.
How to prevent vent prolapse in birds?
Feed correction
o Extra calcium
o Prevention of obesity
o Feed must be balanced, not too rich in protein
Adjusting the light mode
o In young chickens
o About 16-18 weeks of age, depends on breed and line
o Body weight must be large enough
Uric acid poisoning/gout in poultry is caused by
Kidney damage -> high levels of uric acid in the blood and deposition of uric acid salts.
Other Causes:
Feeding-induced gout:
o Excessive calcium
o Lack of phosphorus, lack of the vitamin A
o Water shortage, excessive protein in the feed
- Toxicosis-induced gout: mycotoxins, antibiotics
- Infectious causes: Infectious Bronchitis Virus (IBRV), Avian Nephritis Virus (ANV) etc.
Forms of the gout in poultry (2)
visceral gout &
articular gout
Describe visceral gout in poultry.
Deposition of urates in serous membranes,
pericardium, liver, intramuscular fasciae etc.
Inadequacy of urate excretion, ureter obstruction, kidney damage, or fluid
deficiency.
Causes death of birds.
Describe articular gout in poultry.
Deposition of urates in joints and tissues surrounding the joints.
Detected at necropsy. Enlargement and deformation of joints.
Milky white articular fluid
Main cause is excess protein in the feed.
Clinical signs of gout in poultry.
Diagnostic challenge:
o Sick birds often look healthy
o No production losses
o Signs appear shortly before death: lameness, paresis, problems with walking and standing etc.
Treatment of gout in poultry.
No specific treatment, gross kidney damage.
o Special diets help some birds live
Ammonium chloride, ammonium sulfate, DL-methionine all Acidify urine, prevent kidney stones.
Prevention of gout in poultry.
Feeding
o Max. 1% calcium in chicks’ feed ration
o Enough phosphorus in feed
o Ca/P ratio balanced
o Enough water
o Feed testing
Control of infectious diseases: IBRV, ANV
o Regular testing
o Vaccination
Infectious Bronchitis Virus (IBRV),
Avian Nephritis Virus (ANV)
Describe Tibial dyschondroplasia in poultry.
Mostly in young chicks
o Rapid growth, the growth plates do not ossify
o Results in tendency toward fractures, infections, deformed bone development
Is The most common cause of lameness in the
broiler flock.
Reasons for Tibial dyschondroplasia in poultry.
Multiple reasons:
o Excessive phosphorus, imbalance of Ca/P
o Genetic factors
o Excessive Fusarium roseum toxins or tetramethylthiuram sulphate (fungicide) in grains
Clinical signs of tibial dyschrondroplasia in poultry.
Subclinical form – more common.
o Clinical symptoms appear when the condition is advanced
Clinical form
o Bilateral swelling of the knee area and bending of the leg
o Limping, abnormal gait
o Reduced and reluctant movement, frequent
resting
o Spontaneous bone fractures
Necropsy findings in tibial dyschrondroplasia in poultry.
o Abnormal amount of cartilage in the head of the tibia
o Enlargement of the proximal part of the tibiotarsal bone
o Bone fractures may occur below abnormal cartilage
o Microscopically: retention and accumulation of the prehypertrophic cartilage
Treatment and prevention of tibial dyschrondroplasia in poultry.
Adjust the light mode
Adjust the feed ration
o Ca/P ratio
o Vitamin D3 additives
o Chloride level
o Acid/base balance
Genetic selection: lixiscope (fluoroscopic X-ray)
o From 2 weeks of age
o Evaluation of skeletal phenotype
o Denmark, USA, Germany
Describe Contact dermatitis in poultry.
Fast growing birds, pet birds
Any inflammatory or degenerative condition of the skin.
Different areas of the body:
o Soles, hocks, thighs, breast
Reasons:
o Unsuitable bedding
o Inappropriate/unbalanced feed
o Poor skin structure/integrity
etc.
Describe Pododermatitis in poultry.
Dark black scabs with sores underneath.
o Cellular debris, litter, bacteria
o Sole pads, toes, tibiotarsal-tarsometatarsal joints.
o Limping
o Secondary infections (e.g. Staphylococcus spp, Pseudomonas spp)
Prevention: litter management, ventilation, nipple drinkers.
Describe sternal bursitis in poultry.
Sternal slime bursae are in the proximity of the keel bone under the skin.
o Trauma or certain infections
o In layers uncommon, common in broilers.
o Spoils the appearance of the breast fillet.
o In transportation –> subcutaneous haemorrhages can arise from them.
More common in heavier meat birds.
Inflamed sternal bursa can grow up to 7 cm in length and 2 cm in width.
Also known as: breast blisters, keel lesions, keel cysts.
Possible pathogens to complicate sternal bursitis.
o Mycoplasma synoviae and other mycoplasmas
o Staphylococcus spp.
o Pasteurella spp.
o Viruses
o E. coli infection – treatment is successful when detected early, avoid fecal
contamination of the eggs.
Prevention of sternal bursitis.
Usually, there is no treatment.
Moist bedding increases the incidence of the disease.
Breed birds with less prominent keel and a fast-growing plumage.
The disease is very rare in birds with good health and normal body condition.
Equipment or feeding does not affect the occurrence of the disease.
Whats is unnatural appetite in fowl?
It’s when the bird eats anything and everything including hazards.
Common in chickens, turkeys and geese.
o Plastic, rubber, studs, glass, sawdust, matches, shiny objects etc.
o Coprophagia/eating manure is not included here.
* Mainly in hobby farms, rare in intensive
production.
Deficiencies in poultry: vitamin A
Avitaminosis of vitamin A:
o Chicks: visual disturbances, xerophthalmia, corneal detachment, growth retardation, weakness, bone deformities and movement impairment, ataxia, increased mortality.
o Adult birds: secretion from the nose and eyes, plaque formation, adhered eyelids,
paleness of the comb and wattles, decline in production, reduced hatchability.
Xerophthalmia = spectrum of ocular disease caused by Vit A deficiency.
What does an excess of vit A in poultry feed cause?
Excess: the effect of selenium and vitamin E, egg production and egg
quality are reduced
Where do poultry get vit A from?
Vitamin A – retinol, fat-soluble
o Animal-based feeds, is synthesized in the organism
o Provides normal metabolism and function of epithelial tissues
o The need increases with intestinal tract infections, stress
Necropsy findings for avitaminosis A
o Adhered and inflamed eyelids
o The kidneys and urethrae are filled
with urates
o Pustules in nasal passages, mouth,
esophagus and pharynx
o Hyperkeratosis of epithelial tissues
(picture)
Diagnosis of avitaminosis A
Clinical signs, necropsy findings, feed testing
- DDx: avian infectious coryza,
chronic fowl cholera,
trichomoniasis, candidiasis,
infectious sinusitis, etc., in the
presence of ataxia from encephalomalacia.
Where do poultry get vitamin D from?
Vitamins D – ergocalciferol (D2) and cholecalciferol (D3), fat soluble
o Produced in the organism
o Ensure a normal growth process
o Preserve the levels of calcium and phosphorus in the blood
o Bone mineralization regulation
When do poultry have an increased need for vitamin D?
Increased need: low and artificial lighting, feeding oats, dark plumage
Clinical signs of Rickets and osteomalacia.
o Beak curling, softening
o Softening of bones, deformation, thickening of joints
o Slowing down, stopping growth
o Deterioration of eggshell quality
o Suffocation
What is Exudative diathesis due to?
Lack of vitamin E/Se
o Poor quality/old feed
o Starvation
What age group is Exudative diathesis mostly seen in?
Mostly in 1-3 week old chicks
Clinical signs of Exudative diathesis
o Accumulation of blood plasma in tissues
(swelling), bleeding
- Tissues are fluid-filled, jelly-like
- Ventral part of the trachea, stomach,
lower jaw, legs
o Cyanosis of the skin of the breast area
Encephalomalacia is due to
Lack of vitamin E
o Predisposing factors: rapid growth, broiler
o breed and line, gender
Clinical signs of Encephalomalacia in poultry.
impaired movement
o Rotation of the neck, head and neck retraction
o Ataxia, falling on the back, torticollis, opisthotonus
o Drooped wings
o Paralysis
At necropsy: petechiae in cerebellum
(pictured)
Muscular dystrophy is due to
Lack of vitamin E, S-containing amino acids
(especially cystine)
o Fast growth, broiler breed and line, gender
Clinical signs of Muscular dystrophy in poultry?
o Sluggishness, listlessness
o Lameness, scudding with legs
o Falling sideways
Necropsy findings: liver failure, necrosis of
muscles, especially pectoral and thigh
muscles.
Deficiencies: vitamin B1 causes?
polyneuritis
o Promoted by: coccidiostatics, mycotoxins
o Short-term deficiency: birds are easily excited and fly around
o Long-term deficiency: mainly in chicks, degeneration of peripheral nerves
Clinical signs of B1 deficiency in poultry?
decreased appetite, diarrhea, limping, lethargy, head tremors, stargazing, opisthotonus, ataxia, convulsions
Alt. name for vit. B2 and function + source for poultry?
Vitamin B2 - riboflavin, water soluble
o Respiratory enzymes, growth factor
o Sources: feed yeast and grass meal
- Carbohydrates reduce the need
- Fats increase the need
Vit. B2, riboflavin deficiency causes what in poultry?
o Unbalanced feeding
o Signs of B2 deficiency are the first to appear
o Effect on the nervous system
* Nervus ischiadicus: curled toe paralysis
Describe Curled toe paralysis in chicks.
Chicks: symptoms develop gradually over 2-3
weeks.
o Slow growth, weakness, diarrhea
o Chicks do not want to move, feet muscle atrophy.
o Toes bend inwards
o Head and tail are kept lower than usual
o Dry and tough skin
o With advanced riboflavin deficiency, chicks sleep with stretched legs
o High mortality at 3 weeks
o Three stages of difficulty
Clinical signs of pellagra in adults and chicks?
pellagra = vit B3/niacin deficiency
Chicks: curling of legs, poor plumage, dermatitis
Adults: loss of appetite, weakness, indigestion
DDx: Other diseases causing skeletal deformities, dermatitis and digestive problems
Clinical signs of perosis.
This is Mn and Zn deficiency + Vitamin B deficiency.
Leg-deforming weakness:
o Young chickens (especially broilers), ducks and turkeys
o Tendons soften and thicken
o Displacement of the communal hock tendon (pictured) → outward misalignment
of distal part of limb
o One or both legs
Difficulties in rising up, leg bending
The bird can’t correct the position itself!
Technological issues in poultry husbandry
- Lack of feed/starvation
- Obesity (Fatty liver disease)
- Lack of water
Lack of feed may be used to trigger
molting
o Reducing feed quantity
o Removal of feed
o Change in feed ration – less energy, lower nutrient content, and no additives.
o Additionally, water deprivation can be used.
Purposeful lack of feed for triggering molt or other purpose, may be used in what chickens at what stage?
Used in 2nd- and 3rd-cycle chickens
(layers, breeders)
o Improvement of productivity
o Improvement of egg quality
Fatty liver disease (FLD) is also known as what in poultry?
Also known as fatty liver hemorrhagic disease (FLHD).
What type of bird is FLD seen in?
In young chickens with high production capacity.
o Overfeeding
o Energy surplus –> obesity
In large farms
Sudden deaths
- Birds with a larger than average body weight, body cavity organs are covered with a thick layer of fat.
- General disease symptoms are not observed -> FLD is a post mortem diagnosis.
Necropsy findings when FLD.
Pale comb and wattles
Significant obesity of the internal organs
- Large, brittle, yellowish liver (pictured)
- The liver tissue may have petechiae and ecchymoses under the lining.
- Liver rupture can have occurred (looks like a fissure in the parenchyma) and bleeding.
- As an additional finding, softening of the skeleton might be detected.
