Diseases caused by mineral deficincies

DISEASES CAUSED BY DEFICIENCIES OF MINERAL NUTRIENTS : 

DISEASES CAUSED BY DEFICIENCIES OF MINERAL NUTRIENTS Prepared by Dr. Ghalib S. Ridha Visiting Assistant professor of Internal medicine & Infectious diseases. Dept. of Internal Medicine Faculty of Veterinary Medicine Al-Fateh university Tripoli, LIBYA E-mail: Dr.gsa56@Gmail.com Tuesday, June 22, 2010 Dr. Ghalib Lectures 1

Cobalt deficiency : 

Cobalt deficiency It is a disease of ruminants which characterized clinically by inapetence & loss of weight. It occurs when the animals fed on diet deficient of cobalt which is essential for synthesis of vitamin B12. Tuesday, June 22, 2010 2 Dr. Ghalib Lectures

Epidemiology : 

Epidemiology It affects sheep and cattle showing similar signs with cattle are slightly less susceptible than sheep, and lambs and calves are more seriously affected than adults. The disease occurs most commonly in ruminants at pasture in severely deficient areas, although sporadic cases may occur in stable feeding. Primary deficiency occurs only in soils which are deficient in cobalt. A specific liver dysfunction of sheep, called “white liver disease” because of grayish color of the liver, has been described in certain regions, manifested by photosensitization in acute cases and anemia and emaciation in chronic cases. Tuesday, June 22, 2010 3 Dr. Ghalib Lectures

Pathogenesis : 

Pathogenesis Cobalt is an essential trace element in ruminant nutrition and participate in synthesis of vitamin B12 (cyanocobalamin) which is important in ruminants. Vitamin B12 is required for the enzymatic activity which facilitates the production of glucose from propionic acid, so when deficient it results in loss of appetite and death from inanition. The pathogenesis of ovine white liver disease is unclear. Hepatic dysfunction occurs in affected sheep. Cobalt fertilization of deficient pasture results in an increase in vitamin B12 in lambs. Tuesday, June 22, 2010 4 Dr. Ghalib Lectures

Clinical findings : 

Clinical findings Signs of deficiency are not specific with only obvious signs is gradual decrease in appetite accompanied with weight loss and final emaciation and weakness. These signs are often observed in presence of abundant green feed. There is a sign of anemia with pallor mucous membranes and affected animal easily become tired. In advance cases of sheep, the most important signs is severe profuse lacrimation sufficient to mat the wool of the face. The disease in pregnant ewes can result in Decreased lambing percentage Increased percentage of stillbirths, and Increased neonatal mortality. Tuesday, June 22, 2010 5 Dr. Ghalib Lectures

Cobalt deficient lamb (top) compared to normal lamb (bottom) : 

Cobalt deficient lamb (top) compared to normal lamb (bottom) Tuesday, June 22, 2010 Dr. Ghalib Lectures 6

Slide 7: 

Tuesday, June 22, 2010 Dr. Ghalib Lectures 7 Lambs from deficient ewes are slow to start sucking with low serum immunoglobulins and vitamin B12. Signs may appear in affected animals after 6 mo of being grazing in deficient areas and death occurs in 3-12 mo after first appearance of illness. Sheep are more susceptible to cobalt deficiency than cattle, but the effects of severe deficiency are the same emaciation and eventual death. Sign of pica is likely to occur especially in cattle.

Slide 8: 

Tuesday, June 22, 2010 Dr. Ghalib Lectures 8 The sheep on the left has a cobalt deficiency; the one on the right is normal.

Transfer of soil cobalt into fetus in form of vitamin B12 : 

Transfer of soil cobalt into fetus in form of vitamin B12 Tuesday, June 22, 2010 Dr. Ghalib Lectures 9

Diagnosis : 

Diagnosis The most valuable diagnostic test is estimation of cobalt & vitamin B12 content of the liver. Measurement of cobalt and vitamin B12 levels in sheep plasma is valuable aid for diagnosis. The concentration of formiminoglutamic acid (FIGLU) in urine considered to be reliable indicator of cobalt status in lamb. In subclinical cases the test is not useful for diagnosis because affected animals produce low level acid in the urine. The determination of methylmalonic acid (MMA) in plasma and urine is diagnostic and prognostic indicator. This biochemical test is able to distinguish between subclinical and clinical cases. PM findings show extreme emaciation and heavy deposit of hemosiderin in the spleen and also in the liver. Tuesday, June 22, 2010 10 Dr. Ghalib Lectures

Differential diagnosis : 

Differential diagnosis It is difficult to differentiate the disease from other causes of “illthrift” particularly in young animals which often encountered nutritional deficiencies of copper, selenium and vitamin D and, the most important cause, the internal parasitism. Cobalt-deficient animals are more susceptible to parasitism and the presence of a heavy parasite load should not rule out the diagnosis of primary cobalt deficiency. It is also common for parasitic disease and cobalt deficiency to occur together in the one animal. It is important to differentiate the disease from John’s disease. And other diseases cause anemia. Tuesday, June 22, 2010 11 Dr. Ghalib Lectures

Treatment : 

Treatment Deficient animal respond well to oral dosing with cobalt or IM injection of vitamin B12. Oral dosing with cobalt sulphate (1mg cobalt/day in sheep) & can be given in accumulated dose at the end of each wk. the response to dosing is very quick, significant elevation of serum vitamin B12 levels being evident within 24 hr. Vitamin B12 should be given in 100-300 mcg doses for lambs and sheep at weekly intervals. One injection of 1 mg provides protection to lambs for 14 wk and for weaners protection for up to 40 wk. Tuesday, June 22, 2010 12 Dr. Ghalib Lectures

Control : 

Control Calves reared on cobalt deficient pastures require cobalt or vitamin B12 supplementation prior to weaning. Top-dressing of affected pasture with cobalt salts can prevent cobalt deficiency in grazing animals. The response to this method is slow. Cobalt can also be supplied to cattle in their drinking water. The use of pellet in the form of a bolus orally (5g in sheep, 20g for cattle), gives off cobalt continuously in very small and adequate amounts. Tuesday, June 22, 2010 13 Dr. Ghalib Lectures

Iodine deficiency (IDD) : 

Iodine deficiency (IDD) The most serious thyroid disorder of farm animals is congenital goitre caused by iodine deficiency. A goitre can be detected as a swelling in the neck starting just below the throat. In severe cases the enlargement can actually be seen as a swelling in the neck. Congenital goitre occurs most commonly in lambs, less frequently in calves and very occasionally in foals. Goat kids are particularly susceptible. Lambs may be stillborn or weak at birth because of IDD yet show no visible enlargement of their thyroid gland. A mild deficiency of iodine, causing minimal outward signs of goitre, could be a major contributing cause of young lamb deaths. Tuesday, June 22, 2010 14 Dr. Ghalib Lectures

Etiology : 

Etiology Primary deficiency occurs due to deficient intake or secondarily (conditioned iodine deficiency) by high intake of calcium, diet consisting largely of Brassica forages Such as kale, rape and turnips. or gross bacterial pollution of feedstuffs or drinking water. Certain plants contain goitrogens that inhibit the use of iodine and increase its requirement.Continuous intake of white clover (cyanogenetic glycosides) is commonly associated with high incidence of goitrous offspring. Ewes fed linseed meal during pregnancy result in goitrous newborn lambs. Rapeseed meal are also goitrogenic. Feeding on certain grass with low iodine and high cyanogenetic glucoside contents is also recorded as a cause of goiter in lambs. Tuesday, June 22, 2010 Dr. Ghalib Lectures 15

Pathogenesis : 

Pathogenesis In ruminants, around 80% of the total iodine is concentrated in the thyroid gland which acts as iodine reserves. Iodine is used in the manufacture of thyroid hormones, which have a crucial role in energy metabolism. Energy production is vital for maintaining body temperature and vigor in newborn animals. IDD is likely to result in higher neonatal death rates, as affected newborns have a reduced ability to regulate body temperature or suckle from the mother. Tuesday, June 22, 2010 16 Dr. Ghalib Lectures

Slide 17: 

Iodine has a vital role in the growth and development of the foetus in general and specific organs (e.g. heart, lungs and brain), in particular. A severe IDD with hypothyroidism in pregnant ewes causes reduction in fetal brain ( mental retardation) and body weight and absence of wool growth and delayed skeletal maturation near parturition. Lack of iodine can also lower fertility of breeding stock, as well as reduce milk and wool production. Tuesday, June 22, 2010 17 Dr. Ghalib Lectures

Clinical findings : 

Clinical findings The most common manifestations of IDD is a high incidence of stillbirths and weakness of newborn animals. Other signs which occur with varying degree in different animal species is partial or complete alopecia & palpable enlargement of thyroid gland (goitre). At birth, foals are unable to stand without support, too weak to suck milk and show a normal hair coat with little thyroid enlargement. While in adult horses thyroid enlargement is more common in affected areas. Excessive flexion of the lower part of forelimbs and extension of lower hind limbs has also been observed in affected foals. Tuesday, June 22, 2010 18 Dr. Ghalib Lectures

Iodine deficient foal : 

Iodine deficient foal Tuesday, June 22, 2010 Dr. Ghalib Lectures 19

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Adult sheep are clinically normal but cases with thyroid enlargement may show high incidence. New born lambs manifest weakness, extensive alopecia and palpable enlargement of the thyroid glands. Goats show similar signs but signs are more severe than in lambs. Kids are goitrous and alopecic which varies from complete absence of hair to very fine hair or the hair is almost normal. Recovered animals may show partial persistence of the goiter. Auscultation and palpation of the jugular furrow may reveal the presence of a murmur & thrill, “thyroid thrill” due to the arterial blood supply of the glands. Tuesday, June 22, 2010 20 Dr. Ghalib Lectures

Lambs born dead with sign of goiter : 

Lambs born dead with sign of goiter Tuesday, June 22, 2010 Dr. Ghalib Lectures 21

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In cattle, the incidence of enlargement is much less than in horses. While thyroid enlargement and weakness are the cardinal signs in newborn calves. In some cases, thyroid gland is sufficiently large to cause obstruction to respiration. Manifestations of hypothyroidism in cattle are, Failure to express estrus in the cow and A high incidence of aborted, stillborn or weak calves and Loss of libido in the bull. While in mare and ewes prolonged gestation is reported Tuesday, June 22, 2010 22 Dr. Ghalib Lectures

Calf with severe goiter : 

Calf with severe goiter Tuesday, June 22, 2010 Dr. Ghalib Lectures 23

Diagnosis : 

Diagnosis It easily to diagnose IDD if there is thyroid gland enlargement and stillbirths but it be confusing if stillbirths occur without obvious goiter. In these circumstances, abortion due to infectious diseases in sheep and cattle should be considered. In stillbirths due to IDD, gestation is usually prolonged beyond the normal period. A reliable indicator of thyroxin status is estimation of iodine levels in blood and milk of the animal. Estimation of thyroxin level in the blood to measure thyroid gland sufficiency in animals has not been much used because of the variety of factors which affect thyroxin level. Tuesday, June 22, 2010 24 Dr. Ghalib Lectures

Cow with a newborn calf showing the enlarged thyroid : 

Cow with a newborn calf showing the enlarged thyroid Tuesday, June 22, 2010 25 Dr. Ghalib Lectures

Slide 26: 

PM findings of goitre, alopecia and myxedema may be evident, and the weights of thyroid glands have diagnostic value. There is retardation of brain development and delayed skeletal maturation and absence of wool growth of lambs born of pregnant ewes with severe dietary IDD. On histopathological examination of the gland, there is evidence of hyperplasia. Tuesday, June 22, 2010 26 Dr. Ghalib Lectures

Treatment : 

Treatment Several supplemental sources of iodine are relatively available to ruminants such as potassium iodide, sodium iodide and calcium iodate, but these will leach and evaporate from salt blocks under humid, hot tropical conditions. The EDDI (ethylenediamine dihydroiodide) source of iodine is organic iodide compound that is used for treatment of footrot, lumpy jaw and other conditions, is often given in daily doses of 50-200 mg/ cow for prevention and therapy of these conditions. Painting the teats of ewes, goats and cows with tincture of iodine or an iodophor teat dip once each day for a fortnight, will allow the suckling young to obtain enough iodine to limit development of most goitres. Other method of providing iodine to animals is through IM injection of iodized oil which proven to be effective in both human and livestock Tuesday, June 22, 2010 27 Dr. Ghalib Lectures

Control : 

Control Iodine Dosing Dosing ewes with iodine compounds in the 4th and 5th months of pregnancy with 280 mg potassium iodide prevents goitre in their lambs. The iodine compounds can be given directly or mixed with worm drenches. Oily preparation of iodine can be injected IM 7-9 wk before lambing is sufficient to prevent severe goitre and neonatal mortality Salt licks Salt licks containing potassium iodide are likely to lose much of the iodine by evaporation and leaching. Sodium iodate is more stable in salt mixtures but, as with all licks, not all animals in a herd or flock will use them. Tuesday, June 22, 2010 28 Dr. Ghalib Lectures

Slide 29: 

Skin Application For individual animals, such as goats and for small numbers of ewes, tincture of iodine will prevent goitre in the newborn. It should be painted weekly (4 ml in cattle, 2 ml in sheep) on the soft skin of the inner thigh during the final six weeks of pregnancy. Tuesday, June 22, 2010 29 Dr. Ghalib Lectures

Zinc deficiency : 

Zinc deficiency It occurs in sheep, cattle, goats and pigs and result in parakeratosis, alopecia, wool-eating, abnormal hoof growth, lameness, and unthriftiness. Tuesday, June 22, 2010 30 Dr. Ghalib Lectures

Etiology : 

Etiology The cause is not simple zinc deficiency. Its availability in the plant is adversely affected by the presence of phytic acid as in soybean meal. In ruminants primary deficiency may occur but is rare. Zinc deficiency is influenced by many factors and the risk increases when soil pH rises above 6.5 and using nitrogen and phosphorus fertilizers. Secondary zinc deficiency occurs due to several factors which affect the availability of zinc including the following: Consumption of immature grass which affect digestability The feeding of late-cut hay which may be poorly digestable and Presence of excessive dietary sulfur. Tuesday, June 22, 2010 Dr. Ghalib Lectures 31

Epidemiology : 

Epidemiology Naturally occurring cases in cattle, sheep and goats have been recorded. Inherited disease is common in certain cattle families with increased dietary requirements for zinc have been recorded in Friesian & Black Pied cattle calves (4-8 wk of age), and is known as lethal trait A46. Outbreaks of the disease have been occurred in Sudanese desert ewes and their lambs fed on deficient diet. Marginal zinc deficiency been reported in sheep with signs of poor growth and low fertility as the only signs. Tuesday, June 22, 2010 Dr. Ghalib Lectures 32

Pathogenesis : 

Pathogenesis Zinc is a component of carbolic anhydrase enzyme which play important role in CO2 transport and HCl secretion by gastric mucosa. It is also associated with RNA function and related to insulin, glucagon and other hormones. It has a role in keratinization, calcification, wound healing and somatic and sexual development. Failure of keratinization resulting in parakeratosis, and loss and failure of growth of wool and hair. Zinc deficiency may adversely affect the cell-mediated immune system because of its role in nucleic acid and protein metabolism. Tuesday, June 22, 2010 Dr. Ghalib Lectures 33

Clinical findings : 

Clinical findings In ruminants, the growth is stunted and the lesions of parakeratosis and alopecia occurs mostly on muzzle, vulva, tail-head, ears, backs of the hind limbs, kneefolds, flank and neck. Clinical signs in calves and lambs appear within 2wk of being feeding on deficient diet. In goats, there is extensive alopecia, a kyphotic stance, extensive areas of parakeratosis, abnormal hoof growth and flaky painful coronary bands. Growth rate and spermatogenesis are reduced. In sheep, the earliest signs noticed in lamb is wool eating. Other signs of loss of wool and development of thick, wrinkled skin have been reported in natural disease. The most common effects in ram lambs is impaired testicular growth and complete cessation of spermatogenesis. Tuesday, June 22, 2010 Dr. Ghalib Lectures 34

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Tuesday, June 22, 2010 Dr. Ghalib Lectures 35

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Tuesday, June 22, 2010 Dr. Ghalib Lectures 36

Zinc deficiency in ewe : 

Zinc deficiency in ewe Tuesday, June 22, 2010 Dr. Ghalib Lectures 37

Diagnosis : 

Diagnosis Serum zinc levels may have good diagnostic value. Normal levels are 80-120 mcg/dl in sheep and cattle. Histological examination of skin biopsy sections will confirm the diagnosis of parakeratosis. Skin scrapings show negative results. Sarcoptic mange may resemble parakeratosis but is accompanied by much itching and rubbing. Tuesday, June 22, 2010 Dr. Ghalib Lectures 38

Treatment : 

Treatment IM injection of zinc oxide in olive oil at a dose of 200 mg of zinc for adult sheep and 50 mg for lambs will result in clinical cure within 2 mo. Zinc sulphate administered orally in a dose of 250 mg daily for 4wk resulted in a clinical cure in goats in 12-14 wk. Tuesday, June 22, 2010 Dr. Ghalib Lectures 39

Control : 

Control It is recommended to add 200 g of zinc carbonate or sulphate to each tonne of animal feed. As an emergency measure, feeding 2-4 g of zinc sulphate daily is recommended. Intraruminal pellets have been applied in sheep as an alternative to dietary supplementation for ruminants, but it was effective for 7 wk only. Tuesday, June 22, 2010 Dr. Ghalib Lectures 40

Manganese deficiency : 

Manganese deficiency The diseases cause infertility in cattle & sheep and skeletal deformities in calf & lambs. Tuesday, June 22, 2010 Dr. Ghalib Lectures 41

Etiology : 

Etiology The disease has been enzootically reported in some areas with geological deficiency as a primary manganese deficiency. There is other factors which depress the availability of ingested manganese in the adult cattle and calves, e.g diet with excess of calcium and /or phosphorus. A secondary soil deficiency (conditioned manganese deficiency) and reduction of availability of manganese in the soil to plants is due to high soil alkalinity. Pathogenesis The element play an important role in, The synthesis of chondroitin sulphate content of cartilage Bone matrix formation and Maintenance the rigidity of connective tissue. So Skeletal abnormalities in manganese deficiency are attributed to defects mentioned above Tuesday, June 22, 2010 Dr. Ghalib Lectures 42

Clinical findings : 

Clinical findings The common sign in cattle is infertility manifested by, Anestrus or delayed estrus Reduction in conception rate Subnormal size of one or both ovaries production of poor quality semen by bull Calves show signs of poor growth, dry coat and loss of coat color. Congenital deformities may be evident in affected calves, including; Knuckling over at the fetlock Enlarged joints and possibly Twisting of the legs. The bone of affected lambs may be shorter & weaker with signs of joint pain, hopping gait and reluctance to move. Tuesday, June 22, 2010 Dr. Ghalib Lectures 43

Diagnosis : 

Diagnosis The manganese concentration in the diet provides the most useful means of detecting deficiency in animals. The level of manganese in the blood of normal cow is 18-19 mcg dl. In cases of infertility the content of the hair of affected animal may drop from 12 mg/dl to less than 8 mg/dl. However there is no simple single diagnostic test for detection of manganese deficiency in animals. Treatment Affected cattle show a good response in their fertility with supplementation of the feed with manganese sulphate at 4 g/cow, 2 g/heifer or 1 g/calf, daily will prevent manganese deficiency. Tuesday, June 22, 2010 Dr. Ghalib Lectures 44

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Tuesday, June 22, 2010 Dr. Ghalib Lectures 45