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Hypovitaminosis A

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one of important nutritional deficiency diseases in animals

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(A, D, E,& K)

        Dr. Ghalib's Lectures   Friday, April 02, 2010   1
            Prepared by
        Dr. Ghalib S. Ridha
 Visiting Assistant Professor of
Internal Medicine and Infectious
    Dept of Internal Medicine,
 Faculty of Veterinary Medicine,
 University of Al-Fateh, Tripoli,
                    Dr. Ghalib's Lectures   Friday, April 02, 2010   2
   Vitamin A or Retinol
    is the immediate
    precursor to two
    important active
    metabolites: retinal,
    which plays a
    critical role in
    vision, and retinoic
    acid, which serves
    as an intracellular
    messenger that
    affects transcription
    of a number of

                            Dr. Ghalib's Lectures   Friday, April 02, 2010   3
•Vitamin A is present in many animal tissues, and is
readily absorbed from such dietary sources in the
terminal small intestine. Liver is clearly the richest dietary
source of vitamin A.

•Plantsdo not contain vitamin A, but many dark-green or
dark-yellow plants (including carrot) contain carotenoids
such as beta-carotene that serve as provitamin because
they are converted within the intestinal mucosa to retinol
during absorption.

•Vitamin  A is stored in the liver as retinyl esters and,
when needed, exported into blood, where it is carried by
retinol binding protein for delivery to other tissues.

                                    Dr. Ghalib's Lectures   Friday, April 02, 2010   4
Dr. Ghalib's Lectures   Friday, April 02, 2010   5
Some of the well characterized effects of vitamin A
 Vision: vitamin A (Retinol) is a necessary structural
component of rhodopsin or visual purple, the light
sensitive pigment within rod and cone cells of the retina.
If inadequate quantities of vitamin A are present, vision
is impaired and causes night blindness. This can lead to
blue cloudiness of the eye followed by ulcer formation.

 Resistance to infectious disease: In almost every
infectious disease studied, vitamin A deficiency has been
shown to increase the frequency and severity of disease..
This is due, in part, to the necessity for vitamin A in
normal immune responses. Additionally, inflammatory
reactions lead to reduced synthesis of retinol-binding
protein and thus, reduced circulating levels of retinol.
                                  Dr. Ghalib's Lectures   Friday, April 02, 2010   6
  Epithelial cell "integrity": Many epithelial cells appear
to require vitamin A for proper differentiation and
maintenance. Lack of vitamin A leads to dysfunction of
many epithelia - the skin becomes keratinized and scaly
(pityriasis), and mucus secretion is suppressed. It seems
likely that many of these effects are due to impaired
transcriptional regulation (transcription of a number of

 Bone remodeling: Normal functioning of osteoblasts
and osteoclasts is dependent upon vitamin A.

 Reproduction: Normal levels of vitamin A are required
for sperm production. Similarly, normal reproductive
cycles in females require adequate availability of vitamin

                                    Dr. Ghalib's Lectures   Friday, April 02, 2010   7
 Vitamin A deficiency usually results from malnutrition,
but can also be due to abnormalities in intestinal
absorption of retinol or carotenoids.

 Diets consisting of aged feed material, all grain diets
that have not been supplemented with vitamin A, diets in
which vitamin A may have been destroyed by heat, or diets
completely devoid of green forage can lead to natural
outbreaks of vitamin A deficiency.

 In herbivores such as cattle, vitamin A deficiency is
usually due to lack of green feed, such as in animals
coming off of dry summer pastures or those fed poor
quality hay. Because the liver stores rather large amounts
of retinol, deficiency states typically take several months,
mostly at late winter to develop.
                                    Dr. Ghalib's Lectures   Friday, April 02, 2010   8
Dr. Ghalib's Lectures   Friday, April 02, 2010   9
    Vitamin E and vitamin C are help to prevent
    vitamin A loss.

    High nitrate and high temp increase vitamin A

    A continued ingestion of mineral oil decreased
    vitamin A in the plasma.

                                 Dr. Ghalib's Lectures   Friday, April 02, 2010   10
Some of the more serious manifestations of vitamin A
deficiency include:
 Blindness due to inability to synthesize adequate
quantities of rhodopsin. Moderate deficiency leads to
deficits in vision under conditions of low light
(Nyctalopia or "night blindness"), while severe deficiency
can result in severe dryness and opacity of the cornea

 Increased risk of mortality from infectious disease has
been best studied in malnourished children, but also is
seen in animals. In such cases, supplementation with
vitamin A has been shown to substantially reduce
mortality from diseases such as measles and
gastrointestinal infections.
                                  Dr. Ghalib's Lectures   Friday, April 02, 2010   11
Dr. Ghalib's Lectures   Friday, April 02, 2010   12
Abnormal  function of many epithelial cells, manifest
by such diverse conditions as
   dry, scaly skin, inadequate secretion from mucosal surfaces,
   infertility,
   decreased synthesis of thyroid hormones and
   elevated cerebrospinal fluid pressure due to inadequate
    absorption in meninges.

Abnormal   bone growth in vitamin A-deficient animals
can result in malformations and, when the skull is
affected, disorders of the central nervous system and
optic nerve.

                                        Dr. Ghalib's Lectures   Friday, April 02, 2010   13
Poor growth, blindness, inappetence, dermatitis,
diarrhea, xerophthalmia, and pneumonia have been
observed in young dairy cattle experimentally deprived
of vitamin A

Neurologic signs, in both experimental and natural
outbreaks, include blindness, seizures (convulsion),
circling, disorientation, opisthotonous, depression, and
elevated head carriage.

                                  Dr. Ghalib's Lectures   Friday, April 02, 2010   14
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The   finding of optic disc edema (associated retinal
edema and hemorrhages) in a group of animals showing
signs of blindness with abnormal pupillary light
responses and other neurologic signs is pathognomonic
for vitamin A deficiency.

 Rations and blood from affected animals should be
assessed for vitamin A or carotene levels. Normal values
for vitamin A in serum range from 25 to 60 g/dl. The
severity of clinical signs is inversely proportional to the
level of vitamin A when serum levels decrease to 20 g/dl.

 Histopathology in active cases in growing animals
reveals optic nerve degeneration resulting from dural
fibrosis within the optic canal, squamous metaplasia of
parotid salivary ducts, and many other changes.
                                    Dr. Ghalib's Lectures   Friday, April 02, 2010   16
 Normally vitamin A deficiency is prevented by feeding
green forage or a diet supplemented with vitamin A.

 However, if the disease occurs, all animals in the group
should receive 440 IU/kg body weight of vitamin A by

This  may be repeated, and dietary supplementation
should begin immediately with sufficient levels of vitamin
A in the diet to provide 40 IU/kg body weight/day for the

                                   Dr. Ghalib's Lectures   Friday, April 02, 2010   17

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