Nutritional Diseases
A goat subject to deficiencies in dietary energy or protein can be expected to have a dry, sparse hair coat and dry, thin, scaly skin. These changes are non-specific because they occur with many chronic, wasting diseases.
Copper deficiency, which is discussed in Chapter 19, has been associated with depigmentation of the haircoat. Certain trace mineral or vitamin deficiencies cause changes in the skin that have been described in more detail. Alopecia, possibly related to liver damage, has been produced by experimental feeding of Aristolochia bracteata in goats in Sudan (Barakat et al. 1983).Zinc Deficiency
and Zinc-Responsive Dermatosis
It has been suggested that a practical level of dietary zinc in production diets is 45-75 parts per million (ppm; McDowell et al. 1991). The National Research Council (2007) now acknowledges that a previous recommendation of 10 ppm did not allow for poor absorbability, which can be estimated to be as low as 15%.
Etiology
Calcium excesses in the diet may contribute to a relative zinc deficiency. This might explain zinc-responsive dermatitis in non-lactating does or male goats receiving dairy rations or alfalfa. Zinc deficiency was recognized in two aged non-lactating does after their diet was switched to an alfalfa gruel to compensate for tooth loss (Singer et al. 2000). Other minerals that influence zinc absorption are selenium, copper, and cadmium (National Research Council 2007). Zinc is not stored in the body in an available form, so a daily dietary source is needed.
Some animals appear to have inadequate absorptive abilities (possibly genetically determined; Krametter- Froetscher et al. 2005), because dermatosis persists in the face of normal dietary concentrations of zinc and interfering minerals. Zinc-responsive dermatitis is relatively more common in Pygmy goats (Corke and Matthews 2018).
Second-generation goats on an experimental nickel- deficient diet developed zinc deficiency and associated par- akeratotic skin changes (Anke et al. 1977). This is unlikely to occur with ordinary diets.
Clinical Signs
Clinical signs observed in goats with zinc deficiency include hyperemia and pruritus (inconstant) of the skin; alopecia; thick fissured crusts on the back legs, escutcheon, face, and ears; and dandruff-like scales over the rest of the body (Neathery et al. 1973; Nelson et al. 1984; Scott 1988; Krametter-Froetscher et al. 2005). Crusts commonly encircle the nares, eyes, and mouth. The hair of zinc-deficient goats has been described as greasy and matted (Groppel and Hennig 1971). Fiber break with loss of mohair can have serious economic consequences in Angoras (Schulze and Ustdal 1975). Weight loss may occur; clinical aspects of zinc deficiency unrelated to the skin are discussed further in Chapter 19.
Diagnosis and Treatment
Skin biopsies are important for demonstration of hyperkeratosis and parakeratosis and for ruling out other conditions with similar signs (e.g., mange, dermatophilosis, psoriasiform dermatitis of Pygmy goats). The diagnosis of zinc deficiency by laboratory tests is difficult. It appears that some goats may have a zinc- responsive dermatitis, although plasma, liver, and even dietary zinc lev - els appear to be within normal ranges (Reuter et al. 1987; Hensel 2010). Serum levels less than 0.8 ppm might be associated with skin lesions. Lower serum zinc concentrations (0.54 ppm) have been recorded in goats from Florida herds with a history of seasonal dermatosis when compared with serum levels in other herds without such history (0.83 ppm; McDowell et al. 1991). An Austrian report gives the normal caprine serum zinc range as 0.57-0.63 ppm (Krametter-Froetscher et al. 2005). Blood for zinc testing should not be collected in tubes with ordinary rubber stoppers.
In many instances, the diagnosis is achieved by response to treatment (Scott 2018).
A rather arbitrary dose of 1 g zinc sulfate orally per day has been used with good success, while others suggest 10 mg/kg (Hensel 2010); if marked improvement has not occurred after two weeks of therapy, other diagnoses should be pursued more vigorously. There is a published report of a single goat with skin lesions of lateral truncal alopecia and scaling improving in 7-10 days with institution of 14 g zinc sulfate orally per day for six weeks. Signs rea.p- peared two to three weeks after cessation of therapy (McDowell et al. 1991). In the Austrian report, two adult goats with onset of clinical signs during pregnancy responded to 1 g zinc sulfate per day, whereas the response to 50-200 mg zinc oxide per day was less complete (Krametter-Froetscher et al. 2005). Although the efficacy of dietary zinc methionine for alleviating signs in goats has not been documented experimentally, a multispecies zinc methionine supplement (TruCare Z/M, ZinPro, Eden Prairie, MN, USA), is commonly used in the United States to diagnose and treat zinc-responsive dermatitis in goats. A mineral supplement that includes zinc should be offered routinely, with additional zinc for animals with a suspected hereditary basis for the dermatosis. A slow-release bolus containing zinc, cobalt, and selenium is available in the United Kingdom (Matthews 2016; Corke and Matthews 2018). Dietary excesses of calcium should be corrected.Iodine Deficiency
Diseases of the thyroid gland are discussed in detail in Chapter 3, and the role of iodine in caprine nutrition is discussed in Chapter 19.
Etiology
Certain soils (such as that found in much of the northern United States and the Himalayas) are deficient in iodine. Goitrogens (such as members of the Cruciferae family and Leucaena; see Chapter 3) may interfere with uptake of iodine by the thyroid gland. Additionally, inherited abnormalities of thyroid function have been recognized in inbred Dutch goats.
Clinical Signs
Adult goats with goiter caused by iodine deficiency generally show no skin changes (Kalkus 1920; Dutt and Kehar 1959).
Likewise, clinical signs of hair loss or skin abnormalities were absent in one outbreak of goiter and cretinism in Angora kids ascribed to consumption of goitrogens during pregnancy (Bath et al. 1979). In iodine deficiency severe enough to cause stillbirth, however, newborn kids sometimes had a normal hair coat, but often were hairless or covered with very fine hair (Kalkus 1920). Severe alopecia and colloid goiter were observed in an adult goat in Brazil after long-term consumption of the fodder shrub Leucaena (Peixoto et al. 2008). Skin lesions have been reported in experimental hypothyroidism produced by administration of thiourea to kids. A rough hair coat and subcutaneous edema were noted clinically. Histologic changes included hyperkeratosis and plugging of hair follicles (Sreekumaran and Rajan 1977). Kids with hereditary goiters were similar to thiourea-treated animals, in that they were sluggish and grew poorly. Again, the hair coat was sparse and the skin thick and scaly (Rijnberk 1977). It appears that goats with goiter may or may not have accompanying skin lesions, but that iodine deficiency should not be suspected as the cause of skin disease in the absence of goiters.Treatment and Prevention
Iodine deficiency can usually be prevented by supplying an iodized salt or salt and mineral product (as the only source of supplemental salt). Excessive feeding of goitrogens should be avoided. Weekly application of an iodine- containing solution (such as 1 mL of tincture of iodine) to the skin will also meet the needs of the animal (Kalkus 1920).
Vitamin A Deficiency
Vitamin A is necessary for normal function of epithelial tissues, including the skin. Neurologic manifestations of deficiency are discussed in Chapter 5 and ocular manifestations in Chapter 6.
Etiology
Because beta-carotene, which is abundant in green-leaved plants, is converted into vitamin A after ingestion, deficiencies are unlikely when goats are fed good pasture or green hay.
Grains (except yellow corn and green peas), roots (except carrots and sweet potatoes), and old or weathered hays are low in carotene. Cases of vitamin A deficiency in goats are most likely to occur in semi-arid environments (during the dry season or periods of drought) or when the diet consists of poor, old hay and grain other than corn. Experimental aflatoxicosis in goats has caused a gradual decrease in serum vitamin A levels (Maryamma and Sivadas 1973).Colostrum is rich in vitamin A and usually supplies the needs of the kid until forage consumption begins. Colostrum-deprived kids can be expected to be deficient in vitamin A.
Clinical Signs and Diagnosis
Clinical signs relative to the skin include a rough, dry hair coat, patchy alopecia, and a generally unhealthy appearance (Majumdar and Gupta 1960; Caldas 1961; Dutt and Majumdar 1969). Hyperkeratosis (identified histologically; Scott 1988) and plasma vitamin A levels less than 13 μg∕dL, at least in sheep (Ghanem and Farid 1982), support the diagnosis, as do low levels of vitamin A in the liver (except for precolostral neonates).
Treatment and Prevention
Dietary supplementation, as discussed in the nutrition chapter, is preferable to injectable vitamin A. An excellent source is leafy alfalfa or alfalfa meal. Intramuscular or subcutaneous injection of vitamin A (3000-6000 IU∕kg every two months) is appropriate for individual unthrifty goats or when daily oral supplementation is not possible. A single oral dose of 600 000 IU has proven effective in lambs for 34 weeks, and it is recommended that this be given two months after the start of the dry season (Ghanem and Farid 1982).
Massive overdose of vitamin A, as has been achieved in experimental feeding trials, results in a moderate hyperplasia of the dermis and seborrhea of the ventral abdominal and inguinal skin (Frier et al. 1974).
Vitamin E and Selenium-Responsive Dermatosis
A non-pruritic dermatosis characterized by a dry, thin hair coat, general seborrhea and scales, and periorbital alopecia has been observed in kids and adult goats (Smith 1981).
In some instances, dietary selenium deficiency has been documented, and the response to injectable vitamin E/ selenium has been dramatic. In other goats, diagnosis was based on negative skin scrapings and response to both injectable E/selenium and oral vitamin E (400 IU) given with vegetable oil daily for one month. Dietary supplementation with black oil sunflower seeds or wheatgerm oil might be helpful because of vitamin E and fat content (Konnersman 2005b). Controlled therapeutic trials have not been conducted, and criteria for positively diagnosing the condition have not been established.
Zinc deficiency is an important differential. Skin biopsy results of goats with vitamin E and selenium-responsive dermatosis have revealed orthokeratotic hyperkeratosis, whereas zinc-responsive disease is characterized by par- akeratotic hyperkeratosis (Scott 1988, 2018).
Selenium Toxicosis
Hair loss in goats consuming Astragalus spp., especially involving the beard and flank region, has been linked to possible selenium excess (Reko 1928). This seems plausible, because selenium toxicity from a variety of selenium- concentrating plants or from contaminated water causes loss of mane and tail hairs in horses. In another herd outbreak ascribed to consumption of a seleniferous (500 ppm) Astragalus spp., the only reported skin change in goats that died was a rough hair coat (Hosseinion et al. 1972). Selenium may substitute for sulfur in sulfur-containing amino acids in the hair and hoof (Scott 1988). This leads to alopecia and lameness, with cracks and deformities developing in horns and hooves (Gupta et al. 1982), as discussed in Chapter 4.
Sulfur Deficiency
A condition of severe fleece eating in cashmere-producing goats and of sheep in one valley (Haizi area) in China has been ascribed to sulfur deficiency, possibly compounded by calcium and copper deficiency. Affected goats repeatedly bite bits of fleece off themselves or other animals in the flock, concentrating on the fiber over the hips, abdomen, and shoulder. Some animals are left with almost naked skin and may die of exposure. Skin is keratinized and hair follicles are reduced in size and number. Signs are alleviated by moving to another valley or by the arrival of lush spring grass. The sulfur content of the fiber in affected animals was low (2.4%) compared with a normal content of 4%. Medicated pellets containing aluminum sulfate prevented or treated the skin condition, although muscle atrophy and kidney lesions were not reversed (Youde 2001, 2002; Youde and Huaitao 2001). The effects of sulfur deficiency on the performance of fiber-producing goats and methods of supplementation have been reviewed (Qi et al. 1994).
Rule-outs for such a herd problem include external parasites, lack of dietary fiber, boredom, and accidental deposition of concentrates into the fleece during distribution of feed.