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VITAMINSοΏ½Unit-3

By: Dr Sonam Bhatt

Asstt Professor

Veterinary Medicine

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Vitamin B-Complex deficiency

  • Thiamine
  • Riboflavin
  • Pantothenic acid
  • Pyridoxine
  • Biotin &
  • Folic acid
  • B-Complex Synthesized by other means
  • Nicotinic acid

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INTRODUCTION

  • Source: A significant amount of readily fermentable carbohydrate causes increase synthesis of most of Vit B- complex
  • Degree of synthesis governed by the composition of the ration
  • Causes: Lack of ruminal activity – in young calf & lamb
  • Inadequate supply of this vitamins
  • Deprived from colostrum & milk- good source of water soluble vitamins ( Ewes milk are much richer than cow milk)
  • Prolong use of antibiotic & sulphonamide through oral route causes reduction of bacterial population, alter the synthesis of vitamin B-complex

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Thiamin Deficiency ( Vit. B1) ( Aneurin)οΏ½

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  • Causes: Microbial synthesis in alimentary canal but not sufficient to avoid the dietary supply
  • Thiamin is relatively unstable & easily destroyed by cooking
  • Coccidiostat amprolium is thiamine antagonist
  • It also occurs in pigs feeding bracken rhizomes
  • Also reported in horse when fed large quantity of turnips ( beta vulgaris ) without feeding adequate grain

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Thiaminase: Secondary thiamine deficiency recorded in horse when ingestion of excessive quantity of bracken fern ( pteridium aquilinum) & horse tail ( Equisetum arvense) causes nervous sign due to high content of thiaminase in these plants

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  • Thiamine act as co-carboxylase in the metabolism of fat, carbohydrate & protein and deficiency of this vitamin leads to accumulation of endogenous pyruvate (precursor of vitamin B1)
  • Polioencephalomalacia has been produced experimentally in pre-ruminant lamb on thiamin deficient diet
  • Deficiency causes decrease in erythrocyte prescursor & erythrocyte transketolase which is responsible for maintenance of alimentary & circulatory system.

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PATHOGENESIS

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HORSES

  • In-coordination in gait
  • Falling
  • Bradycardia due to cardiac irregularity
  • Weakness of cardiac muscle

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POULTRY

  • Anorexia, poor growth, ruffled feathers
  • Signs of polyneuritis – unsteady gait, generalised paralysis may occur

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  • Chicks – β€œSTARGAZING POSTURE”, convulsion with head retraction called polyneuritis & stargazing

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CLINICAL SIGNS

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Calves

  • Anorexia, weakness, in-coordination, convulsions, retraction of head, severe scouring, dehydration, somnolence, loss of condition & tetanic convulsions

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  • History of diet
  • Clinical sign
  • Clinical pathology:
  • Increase in concentration of pyruvate

(Normal = 2-3Β΅g/dl; Abnormal= 6-8 Β΅g/dl)

  • Thiamine conc. decreases in blood from normal 8-10 Β΅g/dl to 2.5-3Β΅g/dl; in severe cases = 0.5-1Β΅g/dl
  • ECG: evidence of myocardial insufficiency

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DIAGNOSIS

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  • Thiamin can be given orally for 10 days & dietary abnormalities should be corrected
  • Daily requirement of thiamine for monogastric animal is 30-60 ΞΌg/kg b.wt.

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TREATMENT

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Injection of Thiamine solution @ 5mg/kg b.wt. at every 6hrs interval give 3 inj then once in a day for 4-5days. Initially given I/V followed by I/M for 2-4 days

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Riboflavin deficiency/ Vitamin B2 deficiency/ hyporiboflavinosis

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  • Riboflavin is essential for cellular oxidative process in all animals
  • In natural condition deficiency is rare
  • Actively growing green plants & animal proteins ---good source
  • Synthesized in alimentary tract by microflora in all species
  • Present in the form of flavin mononucleotide

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  • On experimentation:
  • Pigs
  • Slow growth
  • Frequent scouring
  • Rough skin
  • Matting of the hair coat with heavy sebaceous exudates
  • Peculiar crippling of legs with inability to walk & marked ocular lesion including conjunctivitis, swollen eyelids & cataract
  • Still birth may be high

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Clinical signs

  • Calves
  • Anorexia
  • Poor growth
  • Scour
  • Excessive salivation
  • Lacrimation
  • Alopecia
  • Hyperemia at oral commissures on the edges of the lips & around navel
  • No ocular lesion

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Birds

  • Curled toe paralysis
  • Poor growth
  • Weakness, emaciation
  • Leg muscles- atrophied
  • Decrease in egg production
  • Poor hatchability
  • Dead embryo have clubbed down feathers

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Nicotinic acid deficiency/ Niacin/ deficiency/ Vitamin B3 deficiency/ hyponiacinosis

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  • Essential for normal carbohydrate metabolism, reduction & oxidation process
  • Deficiency is important in pigs ----- feeding with corn rich diet
  • Pigs feeding ration high in corn -- low content of niacin & its precursor tryptophan (precursor of niacin)
  • A low feeding of protein with maize feeding also lead to niacin deficiency

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  • Nicotinic acid is a derivatives of pyridine & is interchangeable with its amide nicotinamide
  • Both forms are equally active

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  • Nicotinamide is a component of coenzyme NAD (Nicotinamide adenine dinucleotide) and NADP is its phosphate
  • Nicotinic acid is essential in diet but also formed in small amount in the body from the essential amino acid

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Deficiency of niacin produces:

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  • Black tongue in poultry
  • Black tongue in dogs with ulcerative stomatitis
  • Pellagra (dementia, diarrhoea, & dermatitis – the 3Ds) in humans, pigs & cats

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Pigs

  • Inappetence
  • Severe diarrhea
  • Dirty yellow skin with severe scabby dermatitis & alopecia
  • Posterior paralysis

Chicks

  • Retarded growth
  • Hock disorder (perosis), swollen hock & bowed legs, lameness

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Clinical signs

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  • Daily requirement for mature pigs are 0.1-0.4mg/kg BW
  • Growing pigs required 0.6-1 mg/kg BW for optimum growth
  • Oral therapeutic dose rate of nicotinic acid in pigs is 100-200 mg once in a day
  • Prophylactic dose: 10-20 gm/tone of feed (All ages)
  • In dogs: 0.5-0.8mg/pup; 0.25-0.4mg/dog
  • Chicks : 27mg/kg of feed
  • Growers: 11mg/kg of feed
  • Layers : 10mg/kg of feed

Treatment

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Pyridoxine Deficiency (VitAMIN B6)

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  • Deficiency in pigs characterized by
  • Periodic epileptiform convulsions
  • In necropsy: generalized hemosiderosis with microcytic anemia
  • Hyperplasia of the bone marrow & fatty infiltration of the liver
  • Calves: anorexia, poor growth apathy, dull coat & alopecia
  • A severe fatal epileptiform seizure occurs in some animal
  • Anemia with poikilocytosis is characteristic of this deficiency in cows & calves

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  • Treatment

Daily requirement of pyridoxine in the pig is 100 microgram/kg b.wt. or 1 mg/kg of solid food

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Pantothenic Acid Deficiency / VITAMIN B3

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  • Synthesized in rumen of the ruminant
  • Deficiency recorded mainly in pigs on ration based on corn
  • Clinical Signs
  • Pigs: Decreased weight gain due to anorexia and inefficient food utilization.
  • Dermatitis with dark brown exudates collecting around eyes
  • Patchy alopecia
  • Diarrhea, ulcerative colitis
  • Spastic goose-stepping gait
  • Degeneration of myelin

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In experimental deficiency manifestation by

  • Rough coat
  • Dermatitis under the lower jaw
  • Excessive nasal mucous
  • Anorexia & reduced growth rate & eventually fatal

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Treatment

  • Ca Pantothenate @ 500 micro gram/kg b.wt. is effective in treatment & prevention
  • As feed additive 10-12 g/tone is adequate

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Biotin Deficiency / vitamin H

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  • Several biochemical function
  • Cofactor in several enzyme system involved in carbohydrate metabolism, fatty acid synthesis, purine synthesis & nucleic acid metabolism
  • Biotin is present in almost all plants & animal material
  • Required in small amount
  • Unlikely to be deficient under natural condition except in pigs due to its large requirements (300-500Β΅g/kg BW)

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  • Important for differentiation of epidermal cells which required for normal production of keratin, hoof horn & tissue
  • Act as cofactor of carboxylase enzyme ------- important for gluconeogenesis and fatty acid synthesis
  • Biotin elevates plasma glucose & lowers nonesterified fatty acid (involved in hepatic gluconeogenesis)

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AVIDIN

  • Inhibitor of biotin

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  • Eating raw eggs ----deficiency of biotin ( egg white contains a basic protein --- avidin)

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CLINICAL SIGNS:

Pigs

  • Alopecia dermatitis & painful cracking of the soles & walls of hooves
  • Arching of back & haunched stance with hindlegs positioned forward. This posture is known as Kangaroo sitting posture
  • Birds :
  • Congenital deformities like chondrodystrophy, micromelia, parrot beak
  • Growing birds: broken flight feathers (feather loss), bending of metatarsal, dermatitis

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Treatment

  • Basic diet for gilt contain 35-50ΞΌg/kg & addition of 350-500 ΞΌg/kg is recommended. This provide a daily intake of 4.0-5.0 mg/sow/day

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  • Horses: 10-30mg/day for 6-9 months ---- treatment of weak hoof

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FOLIC ACID DEFICIENCY

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  • A dietary source is necessary to all species & an adequate intake is provided by pasture
  • Horses in training may require additional folic acid on daily basis by oral route

Treatment

  • Folic acid @ 1mg /kg b.wt. orally daily for 2 weeks was used successfully for the treatment of acquired alopecia in 3 weeks old calf but spontaneous recovery was possible

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Cyanocobalamin deficiency/ VITAMIN B12

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  • Naturally not occurs because microbial synthesis in rumen in presence of adequate cobalt & in intestine of other herbivores such as horse
  • Only in primary dietary deficiency of cobalt
  • It is dietary essential for pig & young calf
  • Animal protein is a good source.
  • Deficiency syndrome produced in young calves on a synthetic ration.

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  • Clinical signs are anorexia, cessation of growth, loss of condition & muscular weakness
  • The daily requirement in this condition is 20-40 ΞΌg/kg of vitamin B12.
  • For pig 10-50nmg/tonn of feed is considered to be adequate
  • The vitamin is used empirically in racing horse to alleviate parasitic and dietetic anemia in these animals at dose rate of 2 ΞΌg/kg b. wt.

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ASCORBIC ACID deficiency/ VITAMIN C DEFICIENCY

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  • Source: Fruits, Vegetables
  • Synthesized in tissues of alimentary tract of all species
  • Essential for maintaining the health of connective tissue & integrity of cell wall
  • It is necessary for the synthesis of collagen
  • Scurvy
  • Dermatoses in young calf, heavy dandruff followed by waxy crust
  • Treatment: Single dose of ascorbic acid @ 3g in young calves is effective for dermatosis
  • Daily oral administration of 4.5 g or 20 g ascorbic acid results in significant increase in plasma concentration
  • Curative dose is 1-2g I/V or S/C for cow & 2g S/C for horse

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FAT SOLUBLE VITAMIN

  • A
  • D
  • E
  • K

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  • Dietary deficiency or defective absorbtion from alimetary canal
  • Two forms:-

Alcoholic form- Present in carotene, does not pass placental barrier

Ester form- Present in fish liver oil, crosses placental barrier & Vit A content in foetal liver

  • Regeneration of visual purple ---- dim light vision
  • Bone growth
  • Maintenance of normal epithelial tissues

VITAMIN A DEFICIENCY

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Etiology

  • Primary deficiency --- absolute deficiency of vitamin A or its precursor carotene in diet
  • Secondary deficiency --- Chronic disease of liver- Storage in liver

Diseases of Intestine- Conversion of Carotene to Vit A

  • Poisoning with highly chlorinated napthalene --- interrupts with conversion of carotene to vitamin A
  • Long term ingestion of mineral oil

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Pathogenesis

  • Night Blindness: Vit A ---- stored as retinol in liver……..converted into pigment rhodopsin by rod cells …. Responsible for Dim light vision
  • Oedema, keratinization & ulceration of cornea and ultimate blindness
  • Increase in CSF/intracranial pressure --- convulsion and syncope in calves
  • Deficiency of osteoblast cell --- bending of bones
  • Atrophy of epithelial cells ---Salivary glands, urogenital tract, Skin (Scale formation & pityriasis), placental degeneration, corneal opacity, exophthalmia
  • Congenital defects

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  • Ocular signs: congenital xerosis, bitot’s spot, conjuctival & corneal xerosis, night blindness, xeropthalmia corneal scar
  • Changes in skin: rough & dry coat with shaggy appearance, keratinization, heavy deposits of bran like scales on the skin; scaly hooves with vertical cracks are seen in horses
  • Nervous sign: convulsion --- encephalopathy associated with inc. in CSF pressure – common in calves at 6-8mon of age ; blindness; ocular form of hypovitaminosis A occurs usually in yearling cattle (12-18mon)
  • Congenital defects: piglets & calves – blindness, encephalopathy; Piglets- anopthalmos or micropthalmos, presence of cleft palate

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Clinical signs

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  • Clinical signs
  • Clinical pathology :
  • Plasma level 20Β΅g/dl is minimal conc. of vit A
  • Plasma carotene: in cattle: 150Β΅g/dl are optimum (clinical sign develops when level falls to 9Β΅g/dl)
  • Increase in CSF pressure

DIAGNOSIS

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Differential diagnosis

  • Hypomagnesemic tetany
  • Polioencephalomalacia
  • Lead poisoning
  • Rabies
  • Pseudorabies
  • Organic arsenic poisoning

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TREATMENT

  • Parentral injection of vitamin A @ 440IU/kg/BW, IM
  • CONTROL : 40IU/KG BW in feed

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  • Vit D --- anti-rachitic factor
  • Caused by insufficient solar irradiation of animals or their feed.
  • Clinically characterised by poor appetite & growth and in advanced cases -- osteodystrophy

Etiology :

  • Lack of solar irradiation of skin
  • Indoor keeping of animals, excess carotene in diet, dark skin, long fleece

VITAMIN D DEFICIENCY

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  • Variety of vit D……D2 & D3 have physiological function
  • D2 – Ergosterol; D3– Cholecalciferol
  • Vit D2 --- present in sun cured hay & is produced by UV irradiation of plant sterols
  • Vitamin D2 is formed into D3 under the influence of Uv rays
  • Vitamin D3 is synthesized from 7-dehydrocholesterol known as provitamin D3
  • Provitamin ---- in gut from cholesterol
  • Epidermal cells of skin --- large quantity of provitamin ---- converted into vit D3--- presence of light

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Pathogenesis

VITAMIN D

Ingestion

Skin

Transported & stored

KIDNEY

1,25- dihydrocholecalciferol(1,25, DHCC)

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24, 25- dihydrocholecalciferol(1,25, DHCC)

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25- hydroxy cholecalciferol

LIVER

Transported & stored

MOST ACTIVE

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  • Amount of 1, 25- DHCC produced by kidney is controlled by PARATHYROID HORMONE

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Clinical findings

  • Stiffness
  • Lameness
  • Joint enlargement
  • Rachitic rosary
  • Rickets

TREATMENT

  • Calciferol @ 11,000IU/kg BW in cattle

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Source:

  • Plant
  • Synthesis by microbial activity in alimentary canal
  • Normally no deficiency

Cause: Impaired Bile Flow- reduces digestion, absorption of fat soluble vitamin

Characterized by- hypersensitivity, anemia, anorexia, weakness & marked increased prothrombin time

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VITAMIN K DEFICIENCY

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  • Clinical sign: Hemorrhagic disease - in recently weaned pig (6-15 weeks of age)
  • Excessive fatal hemorrhage occurs in pigs of 30-40 days of age during castration
  • S/C massive hemorrhage is more common in pigs at 40-70 days of age
  • At necropsy extensive hemorrhage in the muscle of the hind limbs, forelimbs & axillar & mandibular region
  • Prothrombin time & activated partial prothrombin time are prolonged along with decreased level of vitamin K dependent factors II, VII, IX & X

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Treatment:

  • Minimum requirement for new born pigs is 5 ΞΌg/kg b.wt. & curative dose is four times larger
  • Vit K or K2 @ 3 mg/kg b.wt. I/M single dose is effective for blood coagulation defect
  • Vitamin K3 should be added in feed @ 25 mg/kg for 4 days is effective
  • Vit. K is used in sweet clover poisoning where toxic quantities of coumarin severely depress thrombin level of blood & interfere the clotting mechanism
  • Industrial poisons used for rodent control contains anticoagulant as coumarin type eg. Warfarin causes fatal hypo thrombinemia & Vit K is effective antidote

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