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• • Vitamin A and its metabolites play diverse
roles in physiology, ranging from incorporation
into vision pigments to controlling
transcription of a host of important genes.
• • Health depends on maintaining vitamin A
levels within a normal range, as either too
little or too much of this vitamin lead to
serious disease
AETIOLOGY AND PATHOGENESIS
• Hypovitaminosis - A
• • Insufficient supply of the vitamin A in the ration (or) defective absorption from the
alimentary canal.
• Etiology
• • Primary Vitamin A deficiency
• o Major economic importance in groups of animals on pasture or fed diets deficient in the
Vitamin A or its precursors.
• o Ruminants on pasture or dry range pasture during periods of drought.
• o Maternal deficiency of Vitamin A can result in herd outbreak of congenital hypovitaminosis
A in calves.
• o Adequacy of supplements to diets not always be sufficient to prevent deficiency.
• • Secondary Vitamin A deficiency
• o Occur in cases of chronic disease of the liver or intestines because of lack of conversion of
carotene to Vitamin A occur in the intestinal epithelium and the liver is the main site of storage of
the vitamin.
• o Intake of inorganic P also affects Vitamin A storage.
• o Vitamin E and C help to prevent loss of Vitamin A in feed stuffs.
Pathogenesis
• • Night vision
• o Ability to see in dim light is reduced because of interference with
regeneration of visual purple.
• • CSF fluid pressure
• o Increase in CSF pressure is due to impaired absorption of the CSF
due to reduced tissue permeability of the arachnoid villi and thickening of
the connective tissue matrix of cerebral duramater.
• • Bone growth
• o Vitamin A is necessary to maintain normal position and activity of
osteoblasts and osteoclasts.
• o If deficiency occurs there is no retardation of endochondral bone
growth in that shaping, especially the finer molding of bones, does not
proceed normally.
• o Overcrowding of the cranial activity occur with resulting distortion
and herniation of the brain and an increase in CSF pressure upto 4-6 times
normal.
• • Epithelial tissues
• o Vitamin A deficiency leads to atrophy of all epithelial cells.
• o The secretory cells are gradually replaced by the stratified,
keratinizing epithelial cells common to non-secretary epithelial tissues.
• o This replacement of secretory epithelium by keratinized epithelium
occurs chiefly in the salivary glands, the urogenital tract the para-ocular
gland and teeth.
• • Embryological development
• o Vitamin A essential for organ formation during growth of the fetus.
• o Constriction of the optic canal with thickening of the duramater
results in ischemic necrosis of the optic nerve and optic disc edema
resulting in blindness.
• • Immune mechanisms
• o Vitamin A and β carotene afford protection against infection by
influencing both specific and non specific host defense mechanisms.
CLINICO-PATHOLOGICAL FINDINGS
• Clinical findings
• • Night blindness
• • Xerophthalmia -- thickening and clouding of the cornea in calf
• • Thin, serous mucoid discharge, corneal keratinization, clouding, ulceration and photophobia
in other animals.
• • Changes in the skin
• o A rough, dry coat with a shaggy appearance and splitting of the bristle tips in pigs.
• o Heavy deposits of bran like scales on the skin-cattle
• o Dry, scaly hooves – horse.
• • Body weight
• o Inappetance, weakness, stunted growth and emaciation.
• • Reproductive efficiency
• o In male – libido is retained but degeneration of the germinative epithelium of the
seminiferous tubules cause reduction in the number of motile, normal spermatozoa produced.
• o In female – placental degeneration leads to abortion the birth of dead or weak young one.
• Nervous system
• • Paralysis of skeletal muscle due to damage of peripheral nerve roots.
• • Encephalopathy
• • Blindness.
• • Convulsion -Common in beef calves at 6-8 months
• • Affected calves are usually not blind and the menace reflex may be
slightly impaired.
• • Some calves are hyper-aesthetic to touch or sound.
• • Blindness -- Usually occur up to 2-3 years of age. Both pupils are
widely dilated and fixed and will not respond to light.
• • Varying degrees of peripapillary retinal detachment, papillary and
peripapillary retinal hemorrhage and disruption of the retinal pigment
epithelium.
• • Menace reflex totally absent.
• • Palpebral and corneal reflex present.
• Congenital defects
• • In pigs
• Clinical pathology
• • Plasma Vitamin A
• o Cattle - 25-60 mg / dl
• o pigs - 23-29 mg/dl
• o Lambs - 45.1 mg/dl
• • Plasma retinol
• o Useful for horses - normal 16.5 mg/dl
• • Plasme carotene
• o Useful for cattle – normal 150 mg/dl
• • CSF
• o Vitamin A deficiency increases CSF pressure . In cattle :-Normal < 100 ; in
deficiency, it will rise to 200 mm
• o Pig -normal 80-145 mm it will rise above 200 mm
• o Sheep - normal 55-65 mm; it will rise to 70-150 mm.
• Necropsy
• o Squamous metaplasia of interlobular ducts
of parotid gland
• o Compression of optic nerve tracts and
spinal nerve root
• o Degeneration of testes
• Diagnosis
• The condidtions to be included in differential diagnosis are:
• • Cattle
• o Polioencephalomalacia
• o Hypo-magnesemic tetany
• o Lead poisoning
• o Rabies
• o Meningo-encephalitis.
• o Peripheral blindness due to bilateral opthalmitis.
• • Swine
• o Salt poisoning
• o Pseudo rabies
• o Viral encephalomyelitis
• o Spinal cord compression.
• Treatment
• • Vitamin A deficiency is treated immediately at a dose rate equivalent to 10-20 times the daily maintenance
• • 440 IU/kg b.wt.
• Control
• • Daily requirement – 40 IU/kg b.wt.
• • During pregnancy & Lactation ¬ by 50-75% of the requirements.
• • Supplementation method.
• • By parentral inj- I/m injection of Vitamin A at an interval of 50-60 days at the rate of 3000-6000 IU/kg b.wt.
• • Oral vitamin A- Single bolus of Vitamin A at a dose of 2.8 mg /Kg B.wt. in dry season.
• • To raise milk levels – adding 10g of powder to the drinking water.
VITAMIN D DEFICIENCY
• Diseases due to Vit. D deficiency
• • Rickets in calves.
• • Osteomalacia in adults.
• Vitamin D or its precursors enter the body by 3 routes
• • By solar radiation.
• • Vitamin D can be added to the milk or in milk replacers fed to calves
and in concentrates for adult cattle.
• • Ultra violet irradiation .
• Signs
• • Clinically the important effect of vitamin D deficiency is defective
growth and mineralization of bones.
• • Non specific signs include poor productivity, stunted growth and
lameness.
• • The joints enlarged and the growth plate thickens with uncalcified
cartilage.
RICKETS
• • A disease of growing animals.
• • Man, apes, birds and rats but not in swine .
• • It is due to failure of calcium salts to be deposited promptly in the
newly formed bone matrix.
• • Defective encdochondral mineralization of the zone of provisional
calcification of the long bones.
• • Miscellaneous group of Ca and P deficiency
• Causes
• • In adequate supply of Ca and/or P and / or vit D. For proper
mineralization of bones, osteoid requires ions of Ca & ionised P as HPO4 in
blood.
• • Low calcium absorption due to Gastroenteritis, lack of Vit.D and
formation of insoluble calcium salts.
• • Absorption of Ca is influenced by dietary Ca:P ratio.
• • Skeletal deformities due to other diseases eg. Canine distemper
• Clinical signs
• • G.I disorders.
• • Bronchitis.
• • Generalised tenderness.
• • Restlessness.
• • Emaciation.
• • Tiredness in puppies.
• • Occasional convulsion or tetany.
• • Walking in wrist than toes due to weakness of flexor tendons.
• • Recumbency.
• • Failure to grow.
• • Bone: Bowing of legs outward, , knobs on ribs (racketty rosary)
• • Body is too heavy to legs.
• • Epiphyses of long bones are swollen.
• • Long bones bend; Metacarpus – thin and crouching in goat.
• • Ribs – bend inwards – so on both the side of thorax, there is longitudinal shallow groove.
• • Pelvis – Acetabulum is pressed upwards & inwards by head of femur so, constriction of pelvis.
• • Vertebrae- various deformities. Hence, it is called Rachitis.
• • Scoliosis, kyphosis, lordosis or 2 or 3 antagonistic curves.
• • Skull: Thickening and deformity of Ramii of inferior maxillary region, difficulty in respiration, Asphyxia as
facial bone bulges.
• Differential diagnosis
• • Distemper: Nasal or ocular discharge if there is involvement of
G.I. tract
• • Muscular Rhematism: No enlargement in bones
• • Tumour: Individual bone only involved.
• Treatment
• • Ration containing Calcium 1.2% and Phosphorus 0.8%. (Ratio
1.5:1) with vitamin D supplement.
• • Add 0.5 gm Calcium carbonate for every 100 gm of meal fed.
• • Feed with organic meats like liver, kidney & heart
• • Give cod liver oil
• • Cortisone and Calcium supplements.
• • Avoid Continuous yeast or Liquid paraffin.
OSTEOMALACIA
• • Horses, cattle and pigs are affected.
• • Pregnant and lactating animals are more prone.
• • Lameness and pathological fracture are common clinical findings.
• Etiology
• • Horse - dietetic: wide Ca:P ratio 1 : 2 .
• • Cattle: It is primary not secondary; Vit D is not having much role.;Mostly
animals kept in stall.
• Pathogenesis
• • Softening of mature bone due to extensive resorption and failure of
mineralization of newly formed matrix.
• • There are no enlargement at the ends of long bones but spontaneous
fracture.
• • Osteodystrophia fibrosa: - excessive resorption of bones and replacement by
connective tissue.
• • Secondary hyperthyroidism resulting in swelling of mandible, maxilla &
frontal bone (Big Head) and spontaneous fracture of long bones & ribs.
• Physical changes
• • Cattle: Epiphysitis, vertebral exostosis usually T2 and T12 , L2 – L3.
• • Old bulls which will have more pressure during breeding – Fusing of
vertebrae (spondylitis) occurs.
• • Horse also fusing of vertebrae degeneration of intra vertebral disc.
• Symptoms
• Cattle
• • First licking the soil , faeces and urine then formation of body deformities.
• • Stunted, head is bigger, perverted appetite, crooked legs, cracking sound in
points.
• • Lack of growth and production, stiff Limb and swollen joints and easy
fracture in hip and ribs.
• • Tail will become soft and it can be coiled like rope, sterility, peculiar gait,
arched back in lumbar vertebrae, recumbent due to pain or due to fracture of
pelvic bones.
• Horse
• • Head larger.
• • Roof of the mouth bulging in oral cavity not able to
close, look like maxillary paralysis difficult mastication,
some time Blood stain in the tongue. Narrowing of Nasal
passage – snoring asphyxia.
• Diagnosis
• • X-ray – Horse Extreme porosity of entire skeleton.
• • Blood chemistry: Ca:P normal for long time in severe
cases alkaline phosphatase increased. serum inorganic P
1.3 to 1.6 mmol/L to 0.48 to 1.13 mmol/L.
• • Histopathology of bone biopsy.
• Treatment
• • Dicalcium Po4 @ 3-4 times the daily
requirement for 6 days, orally. The slow
reduction until 10th day with vit D @ 10,000
I.U / kg b.wt.
• •
vit A.pptx
vit A.pptx
vit A.pptx
vit A.pptx
vit A.pptx
vit A.pptx

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vit A.pptx

  • 1.
  • 2. • • Vitamin A and its metabolites play diverse roles in physiology, ranging from incorporation into vision pigments to controlling transcription of a host of important genes. • • Health depends on maintaining vitamin A levels within a normal range, as either too little or too much of this vitamin lead to serious disease
  • 3. AETIOLOGY AND PATHOGENESIS • Hypovitaminosis - A • • Insufficient supply of the vitamin A in the ration (or) defective absorption from the alimentary canal. • Etiology • • Primary Vitamin A deficiency • o Major economic importance in groups of animals on pasture or fed diets deficient in the Vitamin A or its precursors. • o Ruminants on pasture or dry range pasture during periods of drought. • o Maternal deficiency of Vitamin A can result in herd outbreak of congenital hypovitaminosis A in calves. • o Adequacy of supplements to diets not always be sufficient to prevent deficiency. • • Secondary Vitamin A deficiency • o Occur in cases of chronic disease of the liver or intestines because of lack of conversion of carotene to Vitamin A occur in the intestinal epithelium and the liver is the main site of storage of the vitamin. • o Intake of inorganic P also affects Vitamin A storage. • o Vitamin E and C help to prevent loss of Vitamin A in feed stuffs.
  • 4. Pathogenesis • • Night vision • o Ability to see in dim light is reduced because of interference with regeneration of visual purple. • • CSF fluid pressure • o Increase in CSF pressure is due to impaired absorption of the CSF due to reduced tissue permeability of the arachnoid villi and thickening of the connective tissue matrix of cerebral duramater. • • Bone growth • o Vitamin A is necessary to maintain normal position and activity of osteoblasts and osteoclasts. • o If deficiency occurs there is no retardation of endochondral bone growth in that shaping, especially the finer molding of bones, does not proceed normally. • o Overcrowding of the cranial activity occur with resulting distortion and herniation of the brain and an increase in CSF pressure upto 4-6 times normal.
  • 5. • • Epithelial tissues • o Vitamin A deficiency leads to atrophy of all epithelial cells. • o The secretory cells are gradually replaced by the stratified, keratinizing epithelial cells common to non-secretary epithelial tissues. • o This replacement of secretory epithelium by keratinized epithelium occurs chiefly in the salivary glands, the urogenital tract the para-ocular gland and teeth. • • Embryological development • o Vitamin A essential for organ formation during growth of the fetus. • o Constriction of the optic canal with thickening of the duramater results in ischemic necrosis of the optic nerve and optic disc edema resulting in blindness. • • Immune mechanisms • o Vitamin A and β carotene afford protection against infection by influencing both specific and non specific host defense mechanisms.
  • 6. CLINICO-PATHOLOGICAL FINDINGS • Clinical findings • • Night blindness • • Xerophthalmia -- thickening and clouding of the cornea in calf • • Thin, serous mucoid discharge, corneal keratinization, clouding, ulceration and photophobia in other animals. • • Changes in the skin • o A rough, dry coat with a shaggy appearance and splitting of the bristle tips in pigs. • o Heavy deposits of bran like scales on the skin-cattle • o Dry, scaly hooves – horse. • • Body weight • o Inappetance, weakness, stunted growth and emaciation. • • Reproductive efficiency • o In male – libido is retained but degeneration of the germinative epithelium of the seminiferous tubules cause reduction in the number of motile, normal spermatozoa produced. • o In female – placental degeneration leads to abortion the birth of dead or weak young one.
  • 7. • Nervous system • • Paralysis of skeletal muscle due to damage of peripheral nerve roots. • • Encephalopathy • • Blindness. • • Convulsion -Common in beef calves at 6-8 months • • Affected calves are usually not blind and the menace reflex may be slightly impaired. • • Some calves are hyper-aesthetic to touch or sound. • • Blindness -- Usually occur up to 2-3 years of age. Both pupils are widely dilated and fixed and will not respond to light. • • Varying degrees of peripapillary retinal detachment, papillary and peripapillary retinal hemorrhage and disruption of the retinal pigment epithelium. • • Menace reflex totally absent. • • Palpebral and corneal reflex present.
  • 8. • Congenital defects • • In pigs • Clinical pathology • • Plasma Vitamin A • o Cattle - 25-60 mg / dl • o pigs - 23-29 mg/dl • o Lambs - 45.1 mg/dl • • Plasma retinol • o Useful for horses - normal 16.5 mg/dl • • Plasme carotene • o Useful for cattle – normal 150 mg/dl • • CSF • o Vitamin A deficiency increases CSF pressure . In cattle :-Normal < 100 ; in deficiency, it will rise to 200 mm • o Pig -normal 80-145 mm it will rise above 200 mm • o Sheep - normal 55-65 mm; it will rise to 70-150 mm.
  • 9. • Necropsy • o Squamous metaplasia of interlobular ducts of parotid gland • o Compression of optic nerve tracts and spinal nerve root • o Degeneration of testes
  • 10. • Diagnosis • The condidtions to be included in differential diagnosis are: • • Cattle • o Polioencephalomalacia • o Hypo-magnesemic tetany • o Lead poisoning • o Rabies • o Meningo-encephalitis. • o Peripheral blindness due to bilateral opthalmitis. • • Swine • o Salt poisoning • o Pseudo rabies • o Viral encephalomyelitis • o Spinal cord compression. • Treatment • • Vitamin A deficiency is treated immediately at a dose rate equivalent to 10-20 times the daily maintenance • • 440 IU/kg b.wt. • Control • • Daily requirement – 40 IU/kg b.wt. • • During pregnancy & Lactation ¬ by 50-75% of the requirements. • • Supplementation method. • • By parentral inj- I/m injection of Vitamin A at an interval of 50-60 days at the rate of 3000-6000 IU/kg b.wt. • • Oral vitamin A- Single bolus of Vitamin A at a dose of 2.8 mg /Kg B.wt. in dry season. • • To raise milk levels – adding 10g of powder to the drinking water.
  • 11. VITAMIN D DEFICIENCY • Diseases due to Vit. D deficiency • • Rickets in calves. • • Osteomalacia in adults. • Vitamin D or its precursors enter the body by 3 routes • • By solar radiation. • • Vitamin D can be added to the milk or in milk replacers fed to calves and in concentrates for adult cattle. • • Ultra violet irradiation . • Signs • • Clinically the important effect of vitamin D deficiency is defective growth and mineralization of bones. • • Non specific signs include poor productivity, stunted growth and lameness. • • The joints enlarged and the growth plate thickens with uncalcified cartilage.
  • 12. RICKETS • • A disease of growing animals. • • Man, apes, birds and rats but not in swine . • • It is due to failure of calcium salts to be deposited promptly in the newly formed bone matrix. • • Defective encdochondral mineralization of the zone of provisional calcification of the long bones. • • Miscellaneous group of Ca and P deficiency • Causes • • In adequate supply of Ca and/or P and / or vit D. For proper mineralization of bones, osteoid requires ions of Ca & ionised P as HPO4 in blood. • • Low calcium absorption due to Gastroenteritis, lack of Vit.D and formation of insoluble calcium salts. • • Absorption of Ca is influenced by dietary Ca:P ratio. • • Skeletal deformities due to other diseases eg. Canine distemper
  • 13. • Clinical signs • • G.I disorders. • • Bronchitis. • • Generalised tenderness. • • Restlessness. • • Emaciation. • • Tiredness in puppies. • • Occasional convulsion or tetany. • • Walking in wrist than toes due to weakness of flexor tendons. • • Recumbency. • • Failure to grow. • • Bone: Bowing of legs outward, , knobs on ribs (racketty rosary) • • Body is too heavy to legs. • • Epiphyses of long bones are swollen. • • Long bones bend; Metacarpus – thin and crouching in goat. • • Ribs – bend inwards – so on both the side of thorax, there is longitudinal shallow groove. • • Pelvis – Acetabulum is pressed upwards & inwards by head of femur so, constriction of pelvis. • • Vertebrae- various deformities. Hence, it is called Rachitis. • • Scoliosis, kyphosis, lordosis or 2 or 3 antagonistic curves. • • Skull: Thickening and deformity of Ramii of inferior maxillary region, difficulty in respiration, Asphyxia as facial bone bulges.
  • 14. • Differential diagnosis • • Distemper: Nasal or ocular discharge if there is involvement of G.I. tract • • Muscular Rhematism: No enlargement in bones • • Tumour: Individual bone only involved. • Treatment • • Ration containing Calcium 1.2% and Phosphorus 0.8%. (Ratio 1.5:1) with vitamin D supplement. • • Add 0.5 gm Calcium carbonate for every 100 gm of meal fed. • • Feed with organic meats like liver, kidney & heart • • Give cod liver oil • • Cortisone and Calcium supplements. • • Avoid Continuous yeast or Liquid paraffin.
  • 15. OSTEOMALACIA • • Horses, cattle and pigs are affected. • • Pregnant and lactating animals are more prone. • • Lameness and pathological fracture are common clinical findings. • Etiology • • Horse - dietetic: wide Ca:P ratio 1 : 2 . • • Cattle: It is primary not secondary; Vit D is not having much role.;Mostly animals kept in stall. • Pathogenesis • • Softening of mature bone due to extensive resorption and failure of mineralization of newly formed matrix. • • There are no enlargement at the ends of long bones but spontaneous fracture. • • Osteodystrophia fibrosa: - excessive resorption of bones and replacement by connective tissue. • • Secondary hyperthyroidism resulting in swelling of mandible, maxilla & frontal bone (Big Head) and spontaneous fracture of long bones & ribs.
  • 16. • Physical changes • • Cattle: Epiphysitis, vertebral exostosis usually T2 and T12 , L2 – L3. • • Old bulls which will have more pressure during breeding – Fusing of vertebrae (spondylitis) occurs. • • Horse also fusing of vertebrae degeneration of intra vertebral disc. • Symptoms • Cattle • • First licking the soil , faeces and urine then formation of body deformities. • • Stunted, head is bigger, perverted appetite, crooked legs, cracking sound in points. • • Lack of growth and production, stiff Limb and swollen joints and easy fracture in hip and ribs. • • Tail will become soft and it can be coiled like rope, sterility, peculiar gait, arched back in lumbar vertebrae, recumbent due to pain or due to fracture of pelvic bones.
  • 17. • Horse • • Head larger. • • Roof of the mouth bulging in oral cavity not able to close, look like maxillary paralysis difficult mastication, some time Blood stain in the tongue. Narrowing of Nasal passage – snoring asphyxia. • Diagnosis • • X-ray – Horse Extreme porosity of entire skeleton. • • Blood chemistry: Ca:P normal for long time in severe cases alkaline phosphatase increased. serum inorganic P 1.3 to 1.6 mmol/L to 0.48 to 1.13 mmol/L. • • Histopathology of bone biopsy.
  • 18. • Treatment • • Dicalcium Po4 @ 3-4 times the daily requirement for 6 days, orally. The slow reduction until 10th day with vit D @ 10,000 I.U / kg b.wt. • •