Environmental Insults
The skin may be damaged by excessive exposure to light, cold, or irritants such as urine. Bites by poisonous snakes and spiders undoubtedly affect goats occasionally, but are poorly documented in the literature.
In one case series of rattlesnake bites in dairy goats, pitting edema and sometimes skin necrosis were observed at the site of puncture wounds, in addition to systemic signs (Smith et al. 2015). If available, early antivenin therapy might be beneficial.Sunburn
Exposure to sunlight is associated with the development of skin tumors in white goats, as discussed below. Lightskinned animals exposed to bright sunlight (ultraviolet light, 290-320 nm; Scott 1988) after a winter stabling period are also susceptible to sunburn, especially of the muzzle, perineum, and teats. Signs include erythema, edema, vesicles, ulceration, and crusts (Scott 2018). Prevention involves gradually increasing times of exposure to sunlight and applying sunblocking ointments or iodine teat dips after milking. Treatment is by temporary removal from the sun and use of soothing burn ointments. Contamination of milk should be avoided.
Burns Induced by Fire
Goats exposed to wildfires or bush fires and those trapped in burning buildings may experience serious skin burns, in addition to damage to the eyes or respiratory tract. First- degree burns involve the superficial epidermis, second- degree burns involve the entire epidermis, while third-degree burns include the epidermis, dermis, and appendages (Scott 1988). Necrosis and ulceration occur, and third-degree burns are treated by thorough cleaning repeated daily, debridement if necessary, and topical antibiotics. Silver sulfadiazine ointment is often used (although off label) and analgesics such as meloxicam are indicated. One retrospective study of small ruminants injured in wildfires found that the eyes, ears, nose, mouth, hooves, perineum, and ventral abdomen were most commonly injured in severely burned goats (Chigerwe et al.
2020). Soft food or feeding by rumenostomy may be necessary if burns to the head interfere with eating. Sheep in this same study were euthanized because of laminitis and devitalization of the distal limbs.Photosensitization
In photosensitization, superficial layers of lightly pigmented skin are sensitized to ultraviolet light (320-400 nm) of wavelengths longer than those causing simple sunburn.
Etiology
There are several mechanisms by which a photodynamic agent may reach the skin and cause dermatitis if exposed to light (Galitzer and Oehme 1978). Certain toxins are ingested preformed, and are said to cause primary photosensitization. Examples include phenothiazine, fagopyrin (from buckwheat, Fagopyrum esculentum), hypericin (from Hypericum spp.; Bale 1978), and furocoumarins (from Ammi majus and Thamnosma texana; Ivie 1978; Scott 1988, 2018). Primary photosensitization due to an unknown toxin in Froelichia humboldtiana has been reported in dairy goats in Brazil (Santos et al. 2017). Secondary, or hepatogenous, photosensitization (sometimes referred to as type III photosensitivity) occurs when the normal end product of chlorophyll degradation in the rumen, phylloerythrin, accumulates because of faulty liver excretion. Any severe liver disease could conceivably lead to photosensitization in goats consuming chlorophyll and exposed to sunlight, but toxic plants are most frequently incriminated. These include Lantana (Pass 1986), Agave lecheguilla (Mathews 1938; Burrows and Stair 1990), Nolina texana (Mathews 1940), Panicum coloratum (Muchiri et al. 1980) and Tribulus terrestris possibly in association with the saprophytic fungus Pithomyces chartarum (Glastonbury and Boal 1985; Jacob and Peet 1987). Additional hepatotoxic plants are listed in Chapter 11. An inherited congenital porphyria has been reported in other species, but apparently not in goats.
Clinical Signs
The clinical signs in goats with photosensitization vary, depending on the protection afforded the skin by long hair or pigmentation and whether liver disease is present.
The head, udder, and vulva of white breeds exposed to sunlight initially develop erythema, edema, and intense pruritus. Photophobia is observed and the goats seek shade. Acutely there may be dyspnea or dysphagia. Eventually necrosis and sloughing of lips or teats may occur. Pigmented skin is unaffected. The entire dorsum may be involved in recently shorn animals. Liver function tests help to differentiate primary from secondary photosensitization.Exudation of yellow, serous fluid from the skin surface (Glastonbury and Boal 1985) and intense icterus of the entire carcass are reported in goats with hepatogenous photosensitization from T terrestris. This condition is called geeldikkop, which means “yellow thick head.” Similar lesions have been produced experimentally by oral dosing of goats with sporidesmin. Feral and Angora cross goats were more resistant than Saanens, which in turn required two to four times as much sporidesmin as sheep to produce comparable liver lesions and clinical signs (Smith and Embling 1991).
Therapy and Prevention
Affected goats should be removed from the sun, and additional ingestion of hepatotoxic plants or toxins avoided. This may require moving or supplementing range animals. Laxatives might be helpful if ingestion has occurred recently, and antihistamines and antibiotics are given if much skin is destroyed. Affected skin is sprayed with methylene blue and fly repellents if housing is not possible. Selection for skin pigmentation will decrease the prevalence of photosensitization, but losses resulting from liver disease will continue unabated unless exposure to hepato- toxins is prevented.
Kaalsiekte
The South African bitter bush or bitterkaroo Chrysocoma ciliata (Chrysocoma tenuifolia) produces skin disease in young kids and lambs if their dams consume large quantities of the plant pre partum. The toxin is excreted in milk, causing hair shedding and diarrhea (Steyn 1934). Kids develop pruritus when exposed to sunlight and lick off large patches of hair.
Sequelae include death from exposure, a crusty dermatitis from sunburn, and abomasal hairballs. Supportive treatment (protection from sunburn and wind, laxatives to remove hairballs) should continue until hair returns. Keeping the does and ewes off the infested veld from one month before until one month after parturition will prevent the condition (Kellerman et al. 2005).Frostbite
Special attention should be given to drying of the ears when kids are born in cold environments. Otherwise it is common for the ear tips to develop frostbite. If the initial edematous stage is not treated, the affected skin becomes necrotic and eventually sloughs. The ear tips are rounded and alopecic and the remaining pinna is of variable length. The feet of neonates and teats and scrotum of adults are also at risk of frostbite under extreme environmental conditions.
Immediate first aid involves rapid thawing in warm water 106-111 °F (41-44 °C) (Scott 1988) or with a hair dryer on low. Avoid rubbing the injured tissue. Beef calf producers report that freezing of the ear tips can be prevented by using stockinette or duct tape to keep the ears closely apposed to the warmer head during the first days.
Ergotism
Ergot toxicosis (a mycotoxicosis caused by alkaloids produced by Claviceps and Epichloe fungi) causes sloughing of the extremities in cattle, similar to frostbite, and is potentiated by exposure to cold (Klotz 2015). There is a single report of lameness and gangrenous necrosis with sloughing just above the coronary band in goat kids grazing on fescue parasitized by the fungus (Hibbs and Wolf 1982). Abdominal fat necrosis has been reported in one goat exposed to ergot alkaloids on pasture (Smith et al. 2004).
Urine Scald
During the breeding season bucks urinate on their face, beard, and front legs whenever sexually aroused. Although this habit heightens the doe-attracting aroma of the breeding male, it can lead to dermatitis in the areas that are continuously wet with urine.
Clipping of long hair allows for faster drying of the skin. Skin lesions can be washed with a mild soap or vinegar solution (5 mL in 500 mL water; Konnersman 2005a) and then liberally coated with petroleum jelly, zinc oxide, or other water-repellent ointment daily, until the end of the breeding season.Similar skin care year-round may be required for intersexes or males after urethrostomy or bladder marsupialization if the perineum or inside of the thighs becomes wet during urination. Males on a high-protein diet may develop posthitis and moist infections of the skin of the prepuce. In addition to general wound care, the ration should be corrected, as described in Chapters 12 and 19.
Other Contact Dermatitis Conditions
Caustic agents that cause stomatitis (see Chapter 10) may be expected to cause dermatitis as well, if applied to the external skin. There are various anecdotal reports of occasional skin irritation and hair loss following topical application of numerous parasiticides. If this occurs, the animal should be washed with warm water and a mild detergent to remove residual product.
Dehorning Paste
An alkaline paste is sometimes used by producers to disbud young kids. The paste eats through and destroys the skin from which horns would grow. Clipping hair and applying a ring of petroleum jelly may help contain the paste to the horn bud. Rubbing against other animals and pawing with a hind foot in response to local pain spread the paste and cause skin necrosis elsewhere on the body of the disbudded kid or other pen mates. Paste dehorning should be discouraged.
Milk
Some kids develop alopecia or even raw skin lesions (due to rubbing) on the lips and face where contact with milk or milk replacer has occurred, as from pan feeding. The condition has been termed “labial dermatitis” and can be prevented by washing or wiping the kid's face after each feeding (King 1984).
Decubital Sores
Emaciated or recumbent animals commonly develop fullthickness skin necrosis over bony prominences such as elbows, hocks, and sternum.
Deep, clean, dry bedding and frequent turning of the animal help prevent such lesions. Even with daily cleansing and drying of the sores, healing occurs very slowly, and only if underlying debilitating conditions are corrected. Sternal abscesses are discussed in Chapter 3.Embedded Plant Material
The barbed seeds of numerous plants, especially grass awns, can penetrate the skin and migrate in the subcutaneous or deeper tissues. Nodules, abscesses, or draining tracts may develop (Scott 2018). In one herd outbreak, an extensive discussion of potentially damaging plants in southern Africa (Kellerman et al. 2005) does not mention goats, but there is no reason to believe that they would not be affected.
In one herd outbreak in Boer goats, ulceration, proliferative tissue, and thick crusts large enough to impede breathing developed in the nostrils of goats fed a hay containing much brown knapweed (Centaurea juncea). Biopsies demonstrated plant material in the lesions, which cleared during the summer grazing season, but recurred the following winter when hay feeding resumed (Scott 2018).