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Vitamin A is necessary for normal vision in animals, maintenance of healthy epithelial or surface tissues and normal bone development. The vitamin A deficiency signs observed in various species vary somewhat but most relate to changes in these tissues. Numerous studies have also demonstrated increased frequency and severity of infection in vitamin A-deficient animals. Lack of vitamin A results in decreased antibody production and impaired cell-mediated immune processes against infective agents (Davis and Sell, 1989). Clinical signs can be specific for vitamin A deficiency, or only general indications, including loss of appetite, loss of weight, unthrifty appearance, thick nasal discharge and reduced fertility. The normal epithelium in various locations throughout the body becomes replaced by a stratified, keratinized epithelium when vitamin A is deficient. This effect has been noted in the respiratory, alimentary, reproductive and genitourinary tracts, as well as in the eye. Dogs lacking vitamin A had increased infection with associated changes in the blood leukocyte differential count (NRC, 1985; Scott et al., 1995). Vitamin A-deficient cats had extensive infectious sequelae in the lung and occasionally in the conjunctiva and salivary glands (Gershoff et al., 1957a). For many species, keratinization lowers the resistance of the epithelial tissues to the entrance of infectious organisms. Thus, respiratory troubles, such as colds and sinus infections, tend to be more severe in vitamin A deficiency. In fact, death is often a consequence of pneumonia.
A number of criteria are available to evaluate the vitamin A status of animals, including production response, liver vitamin A stores, plasma vitamin A, and cerebrospinal fluid pressure. The blood maintains its level of vitamin A at the expense of liver stores. Thus, the blood level is not a reliable indication of vitamin A adequacy or deficiency. However, the vitamin A level in the liver can be a reliable indication of vitamin A adequacy or deficiency. Nevertheless, with a level of less than 40 µg of vitamin A per 100 ml of blood serum, a borderline deficiency of the vitamin would be expected. Nondetectable levels are the rule in severe deficiency. In severely vitamin A-deficient dogs, blood and liver concentrations of vitamin A were negligible (Ralston Purina, 1987). In histological exams of dogs, changes of squamous metaplasia in epithelial tissue are present, especially in the respiratory tract (Mellanby, 1950; Stewart, 1965) with liver depletion of the vitamin (< 10 µ/g) as conclusive evidence in support of the diagnosis.
A simple test for night blindness evaluation in dogs and cats can be made by darkening an unfamiliar room and observing the animals' movements in dim red light (Ralston Purina, 1987). More detailed analysis is possible with the electroretinogram in the anesthetized animal. Retinoid treatment of vitamin A deficiency in companion animals is presented in Illus. 1.
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Experimental vitamin A deficiency has been extensively studied in dogs, with the initial studies of this fat-soluble vitamin deficiency being made in dogs in the 1920s (Mellanby, 1950). Vitamin A deficiency is usually confined to young animals, and advanced deficiency is always associated with cessation of growth or even weight loss. Steenbock et al. (1921) reported that dogs deprived of fat-soluble vitamins developed an "ophthalmia." Signs of xeropthalmia (excessive dryness of the eye), night blindness, conjunctivitis, corneal opacity and ulceration, skin lesions and metaplasia of the bronchiolar were associated with rough haircoat, anorexia, growth depression and muscle weakness (Stimson and Hedley, 1933; Crimm and Short, 1937; Russell and Morris, 1939; Singh et al., 1965; Tighe and Brown, 1998). Respiratory infection in prolonged deficiency often resulted in death.
Deafness and facial paralysis occurred in puppies with severe chronic deficiency when bone growth of the skull was altered by inadequate remodeling and excessive periosteal growth to constrict cranial nerves. Blood and liver concentrations of vitamin A are negligible in these cases. Mellanby (1938) established that such damage to the cochlear and vestibular divisions of the eighth cranial nerve, plus a serious labyrinthitis, may induce deafness. Similar damage may also affect function of the optic nerve, although this only has been observed after prolonged experimental deficiency (NRC, 1985).
Vitamin A deficiency is generally a disease in growing pups, as adults seldom develop signs due to their extremely slow depletion of liver stores. In fact, several litters of pups have been produced while the dam was maintained on a deficient diet (Ralston Purina, 1987).
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Vitamin A deficiency signs in cats are characterized by lack of growth, loss of weight and poor appetite after two to three months of feeding a vitamin A-deficient diet. Muscle wasting was severe, while stored body fat may be nearly normal. Epithelial tissues and mucous glands forming the membrane lining of the alimentary, respiratory, urinary and reproductive tracts, as well as the membrane covering the eye and eyelids, were markedly impaired by vitamin A deficiency (Gershoff et al., 1957a). Follicular hyperkeratosis can be recognized as small reddish eruptions around the nose and eyebrows and is coupled with microscopic evidence of atrophy of epidermal adnexae. Acinar dysplasia of the pancreas has been described and marked hypoplasia of the seminiferous tubules, depletion of adrenal cortical lipid, and focal atrophy of the skin were also observed.
Night blindness can be detected early in vitamin A-deficient kittens. As the deficiency progresses, the pupillary reflex to light is delayed from 1 to 2 seconds in the normal state to 5 to 10 seconds in the deficient state. Irreversible degeneration occurs in the rods and cones (visual cells) of the retina. Unfortunately, assessment of night blindness in cats has not been adequately distinguished from retinal degeneration due to taurine deficiency (Knopf et al., 1978), since all experimental vitamin A-deficient diets to date have used casein as the source of protein, a procedure which depletes taurine in cats.
With vitamin A deficiency, bones become thickened and constrict the central nervous system. Ataxia, stiff gait and hydrocephalus in newborn kittens from deficient dams suggest an increased cerebrospinal fluid pressure, whereas the description of cleft palate suggests deranged intrauterine mitosis and cell differentiation (Ralston Purina, 1987).
Male cats become sterile from testicular hypoplasia; females in severe vitamin A deficiency do not ovulate. With a lesser degree of deficiency, queens conceive and implantation occurs, but resorption or abortion of the fetus results at approximately the 49th day of pregnancy (Gershoff et al., 1957a; Scott, 1965).
Bartsch et al. (1975) described ataxia, "star gazing," blindness, and intermittent convulsions in African lion cubs presumed to be vitamin A deficient. Severe thickening of the cranium, compression of the brain and partial herniation of the cerebellum also occurred.
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