Avitaminosis
A,D,E,K
Rashid Hussain 48375 Group C
Vitamin A/Retinol
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Vitamin A is also called retinol. It was the first substance isolated in the group called vitamins.
Precursors of vitamin A exist in plants. They’re called carotenoids. These are fat soluble but nontoxic,
even in large quantities. The best-known carotenoid is beta-carotene. Both retinoids and carotenoids are
good antioxidants.
Vitamin A is part of the reproductive process. It helps with the growth of sperm. It also helps with the
growth of a baby in the womb. But high doses of vitamin A and synthetic retinols may lead to problems
with growth in the womb. It may also lead to birth defects. Vitamin A seems to help the growing tissues in
a baby in the womb. It also helps the placenta form during pregnancy.
Vitamin A is an important factor in growth throughout life. Vitamin A helps grow and maintain epithelial
tissues. These include mucous membranes, the lining of the gastrointestinal tract, lungs, bladder, urinary
tract, vagina, cornea, and skin. Vitamin A also helps the growth of bones and teeth.
Vitamin A prevents drying of the skin. This may protect the body from infectious diseases. It also helps
maintain the immune system.
Vitamin A is also needed for night vision. Retinol (a vitamin A metabolite) combines with opsin (a pigment
in the retina of the eye) to form rhodopsin. This is a chemical that helps with night vision.
Deficiency of Vitamin A
1.
2.
3.
4.
Two types of Vitamin Deficiency : 1st deficiency is where you have reduced intake and the second type is
where you have normal intake but have decreased absorption – e.g. in malabsorption syndrome.
Vitamin A is required by sheep and cattle for a variety of functions throughout multiple body systems.
Congenital defects are common in the offspring of deficient dams, with affected calves showing
blindness, nystagmus, weakness and incoordination.
Cattle can survive on stored Vitamin A for approximately six months before a deficiency results in clinical
signs, while adult sheep may be on a deficient diet for 18 months before their stores are depleted and the
disease becomes evident. Younger sheep generally become deficient after 5-8 months, but may not
show clinical signs for up to a year. Calves and lambs are born with low Vitamin A levels, and rely on
colostrum until Vitamin A is provided by the diet.
Deficiencies are generally primary deficiencies, arising from inadequate access to green feed, lack of
adequate supplementation, or the breakdown of Vitamin A additives in commercial feeds. Deficiency is
common in cattle and sheep during drought conditions, or in stock being full hand fed in conditions such
as feedlots
Signs and symptoms
1.
Dogs : Clinical signs include : Skin and coat problems, hairless patches, dry scaly skin
with bumps/lesions, dry itchy eyes and lung problems that have a tendency to develop
pneumonia when fighting a common cold. Dogs tend to be very weak and may have
deficiency related night blindless.
2.
Vitamin A deficiencies are especially hard on young dogs since retinol plays a crucial role
in bone growth and restructuring. This can translate into stunted growth and irregularities
of the bones in the inner ear, causing some dogs to become deaf or hard-of-hearing
3.
Cattle : The range of clinical signs observed included weakness, recumbency, weight loss,
ill thrift, eye infections, sudden deaths, poor coat condition, stillbirths, diarrhoea, seizures,
pneumonia and mastitis. In most cases, there were other contributing or primary
conditions, including deficiencies in calcium, magnesium and energy
Treatment
1.
Affected sheep and cattle should be injected with Vitamin A at a rate of 400
IU/Kg. Response to treatment is generally rapid, however animals that are
showing signs of eye damage may not recover and suffer permanent
blindness. Calves and lambs that are born with deformities due to deficiency
during fetal development cannot be treated with Vitamin A. Their survival will
depend on the level of damage and their ability to function.
2.
Cows that are already deficient in vitamin A have a reduced ability to store
vitamin A in the liver. Therefore it may be necessary to repeat the injection
monthly until adequate stores are achieved or sufficient oral supplementation
can be attained
Treatment
1.
It is also important to remember that cows and calves that are deficient in vitamin A are probably
deficient in other vitamins and minerals such as vitamin E, copper, manganese, selenium and zinc.
Thorough evaluation of vitamin and mineral status should be done routinely. Liver biopsies can be
performed on cows in mid to late gestation to assess and correct vitamin and mineral status prior to
calving.
2.
Dogs : Fish-liver oil is commonly used as a concentrated source of vitamin A for supplementing the
diet as well as for medicinal treatment.. Feeds that are particularly valuable as sources of vitamin A in
the dog's diet are liver, green leaves of vegetables, and alfalfa leaf meal of good quality. The
Association of American Feed Control Officials (AAFCO) recommends that adult dog food provide
5000 IU of Vitamin A per kilogram of food.
Clinical Case
1.
A mob of 130 Charolais X Angus cows with calves at foot were
investigated for what the owner reported as "scruffy coats". 15 cows
were affected. They were generally in poor body condition, averaging
1.5-2/5 body condition score. They exhibited clinical signs of alopecia,
which was predominantly around the eyes, on the neck, backline and
between the hind legs. The lesions were not pruritic, and were
characterized by scaly skin and loose hair which was easily pulled out
in tufts. The cattle were being fed white cottonseed and rice straw,
with scant dry native pasture
The affected
mob, showing
generalized
poor body
condition
Alopecia on
the neck of
affected cow
Scaly skin and tufts of loose hair on the
dorsal midline of an affected cow
Clinical case
Examination of the skin for lice, ticks, and any evidence of contact with an irritant
such as a chemical was unrewarding. Skin scrapings were negative for mites.
Laboratory findings
1. Examination of skin scrapings at the NSW DPI State Veterinary Diagnostic
Laboratory for Dermatophilus was negative, and fungal culture was similarly
unrewarding.
2. Blood collected from three affected cows showed no significant abnormalities in
biochemistry. Vitamin A test results showed low levels in two of the three cows
tested (0.36, 0.18 and 0.20mg/L, normal range 0.26-0.6mg/L). There were no
clinical signs or abnormalities in the calves present in the mob, suggesting that the
deficiency had occurred recently, rather than throughout gestation.
1.
Vitamin D
1.
Vitamin D is obtained primarily from dietary sources in animals. Vitamin D is mostly thought
of with respect to calcium and phosphate status, however many cells contain vitamin D
receptors and vitamin D is needed for general metabolic and immune processes.
2.
Vitamin D can be obtained either through synthesis in the skin or from the consumption of
animal products that contain cholecalciferol (Vit D3). Dogs and cats have lost this ability,
therefore they appear to be dependent upon dietary sources of vitamin D. After the synthesis
or absorption it is stored in liver, muscle and adipose tissue as cholecalciferol (Vit D3), which
is the inactive form.
3.
Vitamin D is an important component in the homeostasis of the body’s calcium and
phosphorus pools by influencing their intestinal absorption and their deposition in the bone
tissue.
4.
The most common food sources of vitamin D for dogs are liver, fish and egg yolks, but it can
be found in beef and dairy as well. The Association of American Feed Control Officials
(AAFCO) recommends adult dog food provide a minimum of 500 international units (IU) of
vitamin D per kilogram of food, and no more than 3,000 IU per kilogram of food.
1.
There are two sources of vit D, cholecalciferol, known also as vit d3 and
ergocalciferol, also known as vit d2. Cholecalciferol occurs in animals, while
ergocalciferol occurs mostly in plants when exposed to UV lights. The
cholecalciferol is of greatest nutritional importance to omnivores and carnivores.
This form is either formed from 7-dehydrocholesterol when the skin is exposed to
UV lights
cholecalciferol (vitamin D3)
ergocalciferol (vitamin D2)
Deficiency of Vitamin D can
lead to
•
Dietary deficiency: A deficiency of vitamin D in the diet can result in rickets, skeletal abnormalities due
to abnormal physeal development. Dietary deficiency of phosphate can also result in rickets.
•
Genetic defects in the vitamin D receptor: This is called hereditary vitamin D-resistant rickets and can
result in similar skeletal abnormalities as that seen with vitamin D or phosphate deficiency.
•
Inflammation: Vitamin D (calcidiol) appears to be decreased in human patients with inflammation.
•
Renal disease: Low calcitriol concentrations can be seen in some dogs and cats with renal disease,
including acute kidney injury, protein-losing nephropathy and chronic renal disease.
•
Gastrointestinal disease: Decreased concentrations of vitamin D can occur due to inadequate
absorption from the gut, e.g. inflammatory bowel disease. This could be due to lack of vitamin D binding
proteins, fat malabsorption (vitamin D is a fat soluble enzyme), or intestinal inflammation.
•
Cancer: Low concentrations of calcidiol are seen in dogs and cats with various types of cancer, but
whether this is a cause or consequence of the disease is unknown. There was a higher risk of cancer in
dogs with lower vitamin D concentration (alternatively, the risk of low vitamin D could be associated with
cancer)
Symptoms
1.
In Dogs : Deficiency can show in lethargy, excessive thirst, excessive drooling, joint disease
and weight loss. A test must always be given as high dose can be dangerous. It is a hard
one to monitor as scientists can’t measure the important form of vitamin D, only its
precursor (25VitD) so we don't fully understand how it is utilized.
2.
In Dairy cows : Lameless in the legs and back – stiffness in the joints and limbs making it
difficult for them to walk or lie down. The knees hock and pastern joints become swollen,
tender and stiff. In severe cases the back becomes stiff and humped. Because of this lack
of minerals in the bones, the legs of the calf were usually crooked, giving the appearance of
rickets.
3.
Milk flow becomes lowered – Dairy cows have a rapid decrease in milk production and
whatever milk was produced, even under extreme vitamin-D deficiency, was entirely normal
in its content of calcium and phosphorus.
Symptoms
RICKETS IN PUPPY
OSTEOMALACIA IN GOAT
Treatment
1.
Treatment will depend on the underlying cause of the deficiency. Many efforts focus on
increasing the dietary vitamin D ingestion by feeding a high-quality dog food. The Association of
American Feed Control Officials (AAFCO) recommends that adult dog food provide 500 IU of
Vitamin D per kilogram of food. Food companies that follow these guidelines indicate that their
food is AAFCO compliant on the bag. Foods that are good sources of Vitamin D include fish
such as salmon, herring and mackerel, liver, egg yolks, beef, and dairy products.
2.
Disorders that cause vitamin D deficiency such as those that impair the absorption or metabolite
conversion will require different testing and treatments.
3.
Various sources of vitamin D can be used to cure or prevent a vitamin-D deficiency. Animals
suffering from a severe deficiency should be given 50,000 to 100,000 International Units of
vitamin D daily for a few days to a week or so and then given somewhat smaller amounts until
they recover.
Clinical case – rickets
1.
A female gazelle, 9 months old, was brought to the teaching hospital of the
Veterinary Faculty, Harran University. The owner reported that the animal was
raised in a closed stable, without direct sunlight from 1 month to 9 months old.
The animal was fed on straw and concentrated feed. It was unable to stand up
easily, its legs were bent and walking was difficult. The animal had an
abnormal posture. In addition, the hooves appeared dry and turned back. It
had difficulty walking and standing. It was very noticeable that the gazelle’s
weight was on the heels
2.
Blood samples were taken and normal values in healthy gazelles were
compared with levels obtained in this case
Some researchers reported that rickets caused a slight decrease in Ca,
marked decrease in P and a clear increase in ALP levels. Furthermore,
they reported that Ca and P were excreted easily without being
metabolized because of Vitamin D deficiency. Thus, the Ca/P ratio
(2/1) is impaired.
In this case, the serum Ca level was found to be within the minimum
normal limits and also the P level was markedly lower than normal. In
addition, serum ALP activity was clearly higher than normal levels. On
the other hand, the Ca/P ratio was calculated as 4.25/1. These results
resemble those of other studies on rickets.
Table shows marked decrease in P, slight decrease in
Ca, increase in ALP (3609).
Vitamin E
1.
Vitamin E is a term used to describe 8 different fat soluble tocopherols and
tocotrienols, alpha-tocopherol being the most biologically active. Four saturated named α, β-, 𝛾-, 𝛿-tocopherol. Vitamin E acts as an antioxidant, protecting cell membranes from
oxidative damage.
2.
• Plays a role for the immune system (increased dosages may reduce mastitis occurrence
in dairy cows)
3.
• Vitamin E is an enzyme activity regulator, e.g. by playing a role in deactivation of protein
kinase C to inhibit smooth muscle growth.
4.
• Vitamin E can also affect gene expression, e.g. by downregulation of the expression of
the CD36 scavenger receptor gene and modulate the expression of connective tissue
growth factor.
Source of Vitamin E
1.
Horses : Naturally, horses obtain sufficient amounts of vitamin E through lush green
pasture. However, this is not a realistic option for all horse owners. Another option to
increase vitamin E levels in a deficient animal is through supplementation. Most vitamin E
supplements consist of alpha-tocopherol because alpha-tocopherol is the most
biologically available and well researched isoform of vitamin E
2.
Dogs : Most dogs receive vitamin E in their commercially bought dog food. However, a
dog eating a homemade or specially formulated diet may be getting varying amounts.
According to the Association of American Feed Control Officials, adult dogs should be
consuming no less than 50 IU of vitamin E (33.5 mg d-alpha-tocopherol or 45 mg of dlalpha-tocopherol) daily
3.
Normally vitamins such as E and A are obtained by cattle from their diet. These vitamins
are usually abundant in fresh forage. Alfalfa meal contains a high percent of alphatocopherol. Green leafy forages and whole grains are sources of vitamin E. Much of the
vitamin E is in the oil of the seed
Vitamin E deficiency
Dogs :
1.
Vitamin E deficiency in dogs can develop anorexia, reproductive failure,
skeletal and endocardial muscle degeneration, retinal degeneration,
dermatitis, and subcutaneous edema
Cats:
1. Clinical signs of vitamin E deficiency in cats and kittens include anorexia,
depression, myopathy, and pansteatitis
Vitamin E deficiency
Horses :
1. Nutritional myodegeneration Nutritional myodegeneration (NMD), also referred to as white
muscle disease, affects skeletal or cardiac muscle of rapidly growing, active foals and is
primarily due to a dietary deficiency of selenium beginning in the uterus. In some, but not all
cases, there may also be a vitamin E deficiency. Clinical signs include : Muscle weakness,
difficulty rising, trembling of the limbs, and unable to stand, stiffness and firm painful muscles,
pneumonia, difficulty breathing, foamy nasal discharge, depression, Rapid heart rate, Sudden
death.
2.
Neuroaxonal Dystrophy / Equine Degenerative Myeloencephalopathy : Although the
pathophysiology is not completely defined, there is strong evidence of a genetic component
that is highly influenced by alpha-tocopherol deficiency during the first year of life. Low serum
alpha-tocopherol has been described in most, but not all, of affected foals. Clinical signs may
include: ataxia, an abnormal base-wide stance while resting, below normal or lack of skin
twitch reflexes occur in the neck, face and chest in addition to an absent laryngeal reflex.
Other diseases include : Vitamin E responsive myopathy and Equine Motor Neuron Disease
Pigs
1. Diseases associated with vitamin e deficiency include : mulberry heart disease,
hepatosis dietetica (HD) and white muscle disease.
2.
Mulberry heart disease. MHD usually occurs when vitamin E is low but is also seen in
adequate levels of vitamin E in tissue or serum. MHD is manifested by sudden death in
pigs from a few weeks to four months of age that were believed to be in excellent health.
The condition was named after the mottled appearance of the heart muscle in affected
pigs. Supplementation with vitamin E - orally, will prevent deaths from this disease.
3.
Hepatosis dietetica (HD) is a much more rarely encountered presentation of vitamin E
and/or selenium deficiency - HD presents as sudden deaths with few or no preceding
signs. This syndrome was named on the basis of hepatic lesions and the belief that they
are related to the pig’s diet. Vitamin E and/or selenium deficiency is much more common
in lambs, calves and chickens rather than swine. Skeletal muscle pallor or streaks of
white, gritty mineralization are observed, particularly in the longissimus dorsi muscle
Treatment
1.
Horses : Current National Research Council (NRC) daily recommendations for vitamin E
in horses are 1 -2 IU/kg body weight, however, these NRC recommendations do not
discriminate between natural or synthetic sources. The NRC has set the upper safe diet
concentration at 20 IU/kg BW based on biopotency of synthetic vitamin E (10,000 IU/500
kg horse).
2.
Pigs : pigs can be injected with vitamin E and/or selenium and tissue levels will be
increased rapidly. Also, prevention is possible through supplementation of feed or drinking
water.
3.
Cats : The Association of American Feed Control Officials (AAFCO) recommends that
adult cat food provide 30 IU of Vitamin E per kilogram of food.
4.
Dogs : The Association of American Feed Control Officials (AAFCO) recommends that
adult dog food provide 50 IU of Vitamin E per kilogram of food
Vitamin K
Vitamin K, a fat-soluble vitamin, is a group of naphthoquinone compounds that have
characteristic antihemorrhagic effects
Vitamin K extracted from plant material was named phylloquinone or vitamin K1
Vitamin K extracted from bacterial fermentation were named menaquinones or vitamin K2
A synthetic form named menadione (K3)-simplest form of vitamin K, is water soluble
Vitamin K1 (phylloquinone))
Vitamin K2 (menaquinone)
Vitamin K3 (menadione)
SYNTHETIC
Function
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The liver is the main repository of vitamin K.
Vitamin K is required for the hepatic post-synthetic transformation of several
protein clotting factors
It is essential for the post-translational processing of the prothrombin group of
coagulation factors (Factors II, VII, IX, and X).
Used as an antidote in poisoning by dicoumarol or warfarin.
A role in bone metabolism, as well as in the renal reabsorption of Ca++.
Ruminants make this through rumen microbial biosynthesis and absorbed in
the small intestine
Horses generally receive sufficient vitamin K from pasture, hay, and intestinal
bacteria to meet their needs.
Dogs receive both K1 and K2 in their diets, and cats derive their quinones from
eating meat.
Etiology
1.
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3.
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5.
Deficiencies may result from inadequate vitamin K in the diet, disruption of microbial
synthesis within the gut, inadequate absorption from the intestine, ingestion of vitamin K
antagonists (substances that counteract the effect of vitamin K), or the inability of the liver
to utilize available vitamin K.
Neonates are prone to vitamin K deficiency because the placenta transmits lipids and
vitamin K relatively poorly, the neonatal liver is immature with respect to prothrombin
synthesis. The neonatal gut is sterile during the first few days of life.
In adults, vitamin K deficiency can result from fat malabsorption (for example, due to biliary
obstruction, malabsorption disorders, cystic fibrosis, or resection of the small intestine).
Certain antibiotics (particularly some cephalosporins and other broad-spectrum antibiotics),
salicylates, mega-doses of vitamin E, and hepatic insufficiency increase risk of bleeding in
patients with vitamin K deficiency.
Inadequate intake of vitamin K is unlikely to cause symptoms.
Ruminants
1. Seen only in the presence of a metabolic antagonist, such as dicumarol from moldy sweet clover.
2. Death from hemorrhage following a minor injury or from a spontaneous bleeding
3. Accidental poisoning of animals with warfarin (a synthetic coumarin used as a rodent poison)
4. Initial clinical signs may be stiffness and lameness from bleeding into muscles and articulations.
5. Hematomas, epistaxis (nose bleed), or gastrointestinal bleeding
6. Death may occur suddenly, with little preliminary evidence of disease, and is caused by spontaneous
massive hemorrhage or bleeding after injury, surgery, or parturition
DOGS AND CATS:
1. Accidental intake of dicumarol types of rat poison, such as warfarin and diphenadione (vitamin K
antagonist), will result in a hemorrhagic condition in dogs
2. Clinical signs in dogs include paleness and evidence of slow but persistent bleeding from a number of
sites, including gums, bowel, and several injection punctures
Swine:
1. Increased prothrombin and blood-clotting time, internal hemorrhage, and anemia due to blood loss
2. Newborn pigs may be pale with loss of blood from the umbilical cord
Differential diagnosis
Vitamin K Absorption Defects
Intrahepatic cholestasis
Biliary obstruction
Chronic oral antibiotic
administration
Infiltrative bowel disease
Dietary vitamin K deficiency
Vitamin K Recycling Defects
Anticoagulant rodenticide toxicity
Dicoumarol (moldy feed) poisoning
Coumadin therapy
Neonatal vitamin K deficiency
Hereditary hepatic recycling enzyme defects (epoxide
reductase or carboxylase defects)
Treatment:
Vit. K1 @1- 2 mg/kg administered intramuscularly /SC (especially in
Dicumarol poisoning)
Blood transfusion@10ml/Kg BW