Chapter 10 Diseases of the Integumentary System

Jerry R. Roberson, A.N. Baird, D.G. Pugh

We acknowledge and appreciate the original contributions of Drs. David E. Anderson and D. Michael Rings, whose work from the previous edition of this book has been incorporated into this chapter.

Dermatologic lesions, which tend to be more common among goats than among sheep, constitute a relatively major reason for examination of small ruminants. Although sheep and goat production has historically been an economic enterprise, an increasing number of owners keep these animals as pets. Diseases of the integumentary system include those that affect skin, hair, and wool. This chapter focuses on both presumptive and definitive diagnoses and conservative as well as optimal treatments.

Anatomy and Relevant Physiology

A complete discussion of the anatomy and physiology of the skin is beyond the scope of this chapter. This section reviews the unique anatomy and relevant physiology that is pertinent to veterinary management of small ruminant diseases and conditions.

The skin functions as a protective barrier to the environment. It also aids in thermoregulation, acts as a sensory organ, and communicates through the secretion of chemicals.^1,² Both sheep and goats have relatively thin skin, with an average thickness of 2.6 mm in sheep and 2.9 mm in goats.¹ Hair is important for thermoregulation. A short, thick hair coat is best for regulating body temperature during high environmental temperatures, whereas long, fine hair coats are most efficient at low environmental temperatures. Thus shearing sheep when environmental temperatures are still low is not without risk. Likewise, failure to complete shearing by the time hot weather arrives may predispose the animals to heat exhaustion. Secondary hairs make up a greater proportion of the hair coat compared with primary or guard hairs in goats and sheep. In Angora goats and sheep, three types of wool are recognized: true wool, Kemp fibers, and hair fibers. True wool fibers are fine and tightly crimped. Kemp fibers are coarse, relatively short, and poorly crimped. Hair fibers are somewhere in between wool and Kemp fibers in their morphologic characteristics. Guard hairs are undesirable in wool-bearing breeds, because the medulla makes the hair brittle and this hair type does not take up dye well. Small secondary hairs of goats are nonmedullated.

Hair grows in a cycle. The growing period is called anagen and the resting period is called telogen. The hair cycle is controlled by various influences, including photoperiod, temperature, nutrition, hormones, health status, and genetics, among other factors. Wool follicles constitute an exception in that no established cycle has been documented. Of interest, hair growth is most active during summer months, and during winter months nearly all primary hair follicles and approximately half of the secondary hair follicles are in the telogen phase. During periods of ill health or stress, the anagen phase may be considerably shorter, resulting in “hair break” or “wool break” (also known as telogen defluxion) secondary to growth stoppage. Hairs are more easily lost or pulled out during the telogen phase.

Specialized cells such as the sweat gland allow cooling.

The lanolin glands of sheep provide protection from drying out. The lanolin glands are located near the medial canthus of the eye, between the toes, and caudal to the udder in the inner flank.

The epidermis is composed of five layers—from outermost to innermost, stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. The stratum basale produces new cells that continuously move up to replace the sloughing cells of the stratum corneum. The melanocytes of the stratum basale and hair follicles are primarily responsible for the color of the hair coat. All melanins arise from a common metabolic pathway that is catalyzed by a copper-containing enzyme. One of the signs of copper deficiency, therefore, is a lighter-than-normal color of the hair coat. Besides the obvious physical barrier presented by the epidermis and hair or wool, chemical and microbial barriers to infection also are recognized: The secretion produced by the sweat and sebaceous glands has antimicrobial properties. Included within this secretion are fatty acids, inorganic salts, interferon, transferrin, complement, and immunoglobulins. Increased hydration of the skin greatly increases microbial populations. Normal skin flora can inhibit colonization of other potential pathogens. However, some skin pathogens also may be components of the normal flora. For example, dermatophytes and Staphylococcus aureus can be recovered from clinically normal mammals that do not develop clinical disease.

The dermis contains the arrector pili muscles, blood and lymph vessels, and nerves. The dermis functions as the major source of tensile strength and elasticity of the skin. Most of the dermal fibers are collagen. Collagen defects may arise in association with genetic disorders, vitamin C deficiency, iron deficiency, copper deficiency, and beta-aminopropionitrile poisoning.

In both hair and wool, follicles are divided into the innermost medulla, the cortex, and the outermost layer, the cuticle. The color of the hair is due primarily to pigment in the cortex. With simple follicle arrangements as in cattle and horses, each hair follicle is accompanied by sebaceous and sweat glands and an arrector pili muscle. Sheep and goats have a compound follicle arrangement, in which hair (or wool) follicles occur in clusters of two to five primary hairs surrounded by smaller secondary hairs. Each primary hair has associated sebaceous and sweat glands and an arrector pili muscle, whereas secondary hairs have associated sebaceous glands only. The wool of sheep becomes finer, with a higher secondary-to-primary hair ratio. In Merinos, known for fine wool, the ratio is 20:1, whereas that for the wool of meat breeds averages 5:1.

In goats, wattles may be present—typically along the ventral neck caudal to the angle of the mandible. Although the function of wattles is unknown, they contain extensive neurovascular structures and cartilage. The presence of wattles is controlled by an autosomal dominant gene.

Sebaceous glands (holocrine glands) produce an oily secretion that keeps the skin soft and pliable and promotes retention of moisture, thereby helping to maintain hydration. This oily substance also covers the hair, yielding a glossy hair coat. In times of stress or illness, the hair coat may appear dull and dry, due in part to inadequate sebaceous gland function. The dull hair coat may be a consequence of involution of the sebaceous glands caused by estrogen and glucocorticoids. Sebaceous glands increase in size in intact male goats at the beginning of rut. Sebaceous scent glands are located in tissue caudal and medial to the base of the horn in goats. In male goats, these glands produce a pungent odor. Surgical procedures to remove the scent glands of goats (descenting) involve excising the sebaceous glands caudal and medial to the horn base. This procedure is easily done in young buck kids at the time of dehorning. In sheep, scent glands are present rostral and medial to the eye and may produce a pungent odor in rams.

Sweat glands are present in both sheep and goats. Although sweat production increases in response to a hot environment, sweat glands are not thought to constitute an important means of thermoregulation in these species.

Approach to Diagnosis

The approach to diagnosis will certainly vary from clinician to clinician, depending on past experience, knowledge of herd or flock disease history and economics, and availability of diagnostic centers. With experience, many veterinarians will be able to diagnose the disease with reasonable accuracy on the basis of history and reported clinical signs alone. Veterinarian confidence and competence will be enhanced with opportunities for definitive confirmation of this diagnosis early in the practitioner’s career. The diagnosis of skin disease is accomplished in the same way as that for diseases affecting other body systems: analysis of complete historical data, including environment and commingling risk assessment; detailed assessment of clinical signs; findings on a thorough physical examination; and results of diagnostic testing directed by the most likely possibilities in the differential diagnosis. Specific diagnostic tests may be performed when diseases fail to respond to seemingly appropriate therapy or when animals are scheduled for sale or show activities.

Historical data should include the signalment of the animal: species, breed, age, gender, weight, and color. Some breeds have a higher likelihood of developing specific disease conditions (Table 10-1). Therefore breed information is useful to assess for susceptibility. The clinician should note details concerning the origin of the animal and exposure risks. Origin includes whether the animal was born and raised on the farm, purchased by farm contracts, purchased through sale barns, or imported from another state or country. Exposure risks include transportation to another farm; commingling in sales, shows, or fairs; farm tours involving children or livestock owners; and diseases that are endemic to the particular farm. In the last case, the clinician also should note when the last outbreak occurred. Chronologic data are important in making a differential diagnosis. The date of the first observation of clinical signs should be determined, the duration of clinical signs should be evaluated, and details regarding the progression of the disease within the affected animals should be described. The region of the body affected and the spread of disease to other regions of the body also are important. Often the presenting disease state is so severe that the point of origin cannot be determined by physical examination. Assessment of whether the disease has spread from one animal to another within the flock or herd is particularly important. Finally, the veterinarian may assemble a detailed chronology of any treatments applied, the dosage and route used for administration, and the duration of treatment.

TABLE 10-1 Breed Predilections for Skin Diseases in Sheep and Goats

Disease	Breed(s) With Recognized Predilection
Cutaneous asthenia	Border Leicester-Southdown cross sheep Finnish crossbred sheep Merino sheep Norwegian Dala sheep Romney sheep
Congenitohereditary photosensitivity	Corriedale sheep Southdown sheep
Viable hypotrichosis	Dorset sheep
Hereditary goiter	Merino sheep Saanen dwarf–cross goat
Epidermolysis bullosa	Scottish blackface sheep Southdown sheep Suffolk sheep
Scrapie	Suffolk sheep

Modified from Scott DW: Large animal dermatology, Philadelphia, 1988, WB Saunders.

Clinical signs are important in the development of a differential diagnosis. They can vary widely and depend on the tissues involved in the disease process. Possibilities in the differential diagnosis are most easily determined early in the course of disease, when the primary lesions are abundant (Table 10-2). As the disease progresses, secondary lesions such as infection, thickening, crusting, and hair loss may overwhelm the primary disease and make assessment of skin disease extremely difficult. Therefore animals with newly emerging disease should be selected for examination.

TABLE 10-2 Typical Distribution of Lesions Associated With Selected Diseases of the Skin

Area Involved	Disease	Primary Lesion Type
Head and neck	Dermatophytosis	Papulocrustous
	Dermatophilosis	Pustulocrustous
	Demodicosis	Papulonodular
	Elaeophoriasis	Ulcerative
	Fly bites	Papulocrustous
	Actinobacillosis	Nodular
	Clostridiosis	Edematous
	Sarcoptic mange	Papulocrustous
	Contagious viral pustular dermatitis	Pustulocrustous
	Ovine viral ulcerative dermatitis	Ulcerative
	Goat pox	Pustulocrustous
	Sheep pox	Pustulocrustous
	Pemphigus foliaceus	Vesiculopustular, crusts
	Zinc deficiency	Crusts
	Contact dermatitis	Variable
	Viral papillomatosis	Papulonodular
	Squamous cell carcinoma	Nodular, ulcerative
Ears	Dermatophytosis	Papulocrustous
	Dermatophilosis	Pustulocrustous
	Sarcoptic mange	Papulocrustous
	Fly bites	Papulocrustous
	Pemphigus foliaceus	Vesiculopustular, crusts
	Ergotism	Necrotizing
	Fescue toxicosis	Necrotizing
	Frostbite	Necrotizing
	Photodermatitis	Edematous, necroulcerative
	Squamous cell carcinoma	Nodular, ulcerative
Mucocutaneous	Contagious viral pustular dermatitis	Pustulocrustous
	Goat pox	Pustulocrustous
	Sheep pox	Pustulocrustous
	Bluetongue	Erythema, edema
	Zinc deficiency	Crusts
	Bullous pemphigus	Vesiculoulcerative
	Pemphigus foliaceus	Vesiculopustular, crusts
	Dermatophytosis	Papulocrustous
	Dermatophilosis	Pustulocrustous
	Squamous cell carcinoma	Nodular, ulcerative
Dorsum	Dermatophilosis	Pustulocrustous
	Fly bites	Papulocrustous
	Psoroptic mange	Papulocrustous
	Contact dermatitis	Variable
Ventrum	Dermatophilosis	Pustulocrustous
	Fly bites	Papulocrustous
	Sarcoptic mange	Papulocrustous
	Contact dermatitis	Variable
	Goat pox	Pustulocrustous
	Sheep pox	Pustulocrustous
	Contagious viral pustular dermatitis	Pustulocrustous
	Zinc deficiency	Crusts
	Corynebacterium pseudotuberculosis infection	Abscesses
Trunk	Dermatophytosis	Papulocrustous
	Dermatophilosis	Pustulocrustous
	Psoroptic mange	Papulocrustous
	Psorergatic mange	Alopecia, pruritus
	Keds	Alopecia, pruritus
	Ovine fleece rot	Moist dermatitis
	Pemphigus foliaceus	Vesiculopustular, crusts
	Demodicosis	Papulonodular
	Caprine viral dermatitis	Papulonodular
	Scrapie	Excoriation, pruritus
	Vitamin A deficiency	Hyperkeratosis
	Iodine deficiency	Alopecia, scaling
	Biotin, niacin, riboflavin, pantothenic acid deficiency	Alopecia, scaling, crusts
	Vitamin C–responsive dermatosis	Alopecia, erythema, purpurea
	Copper deficiency	Depigmentation
Hindquarters	Dermatophilosis	Pustulocrustous
Hindquarters	Chorioptic mange	Papulocrustous
Legs and feet	Dermatophytosis	Papulocrustous
	Dermatophilosis	Pustulocrustous
	Chorioptic mange	Papulocrustous
	Contact dermatitis	Variable
	Elaeophoriasis	Necroulcerative
	Clostridiosis	Edema
	Sarcoptic mange	Papulocrustous
	Zinc deficiency	Crusts
	Vitamin C–responsive dermatosis	Alopecia, erythema, purpurea
	Ovine viral ulcerative dermatitis	Ulcerative
	Pemphigus foliaceus	Vesiculopustular, crusts
Tail	Psoroptic mange	Scales, pruritus
Tail	Selenosis	Alopecia
Coronary band	Pemphigus foliaceus	Vesiculopustular, crusts
	Bluetongue	Erythema
	Contagious viral pustular dermatitis	Pustulocrustous
	Ergotism	Edema
	Fescue toxicosis	Edema
	Dermatophilosis	Pustulocrustous
	Zinc deficiency	Crusts

Modified from Scott DW: Large animal dermatology, Philadelphia, 1988, WB Saunders.

Erythema refers to reddening of the skin. It is not a disease-specific change but usually indicates the presence of inflammation. Papules are solid masses, small in diameter (less than 1 cm), that are reddened, raised from the surface of the skin, and may be painful to palpation. They are consistent with infection, allergic reaction, and ectoparasites. When the papule is centered on a hair follicle, bacterial or fungal folliculitis and ectoparasites such as the agent of demodectic mange should be suspected. When papules occur independent from hair follicles, allergic skin reactions and ectoparasites such as scabies mites should be suspected.

Vesicles are similar in size and shape to papules, but these masses are filled with a serous fluid and are fluctuant. Vesicle formation may be preceded by a papule. Vesicles most often are associated with viral skin diseases such as poxvirus infections, contact allergy, and autoimmune diseases such as pemphigus. Pustules are similar to vesicles but are purulent in nature. Purulent exudate is formed as a result of migration of neutrophils either in response to infection or as part of an autoimmune disease process. Vesicles and pustules are ruptured by abrasion or spontaneous disruption of the overlying membrane. The fluids accumulated on the skin surface form crusts, and the underlying skin becomes thickened in response to the injury. Crusts are firm, adherent amalgamations of serum, pus, blood, cellular debris, and associated organisms. The presence of crusts indicates an exudative process but is not disease-specific. Microscopic examination of crusts may reveal infectious organisms such as fungi, bacteria, or cells. The term scale simply refers to desquamated stratum corneum and also is not disease-specific. Thickening of the skin (specifically, thickening of the stratum corneum) often is referred to as hyperkeratosis. The term orthokeratosis is used to describe hyperkeratosis without the presence of nuclei. Parakeratosis is hyperkeratosis with nuclei present in the keratinized skin. Unfortunately, these findings are consistent with chronic dermatopathy and are not disease-specific. The distribution of lesions may be more important than the actual histopathologic description in this scenario.

Alopecia is hair loss. It may be associated with disease or other stressors, producing a stress-induced telogen phase. This “stress break” in the hair shaft may result in generalized hair loss. Stress alopecia usually is associated with normal skin and normally growing hair elsewhere on the body. Systemic disease causing prolonged pyrexia also can disrupt normal hair and fiber growth, potentially resulting in easily epilated hair. In sheep, this latter condition is referred to as wool break. Nutritional deficiencies in zinc, selenium, and vitamin E may cause hair loss.

Scratching typically is occasioned by the itching or similar discomfort, other than pain, associated with skin disease, termed pruritus. Assessment of the severity of pruritus can aid in the formulation of an accurate differential diagnosis. Severe pruritus typically is associated with ectoparasitism. Mild pruritus more often is associated with nutritional deficiency, allergic skin disease, bacterial or fungal skin disease, or autoimmune disease. It is a common clinical symptom associated with scrapie that also occurs with pseudorabies virus and rabies virus infections.

Changes in skin and hair pigmentation are uncommon in most ruminant diseases. Exceptions include the hair pigment lightening seen in cattle with chronic copper deficiency and molybdenosis and the black wool pigment that develops in blackfaced sheep after skin injury (abrasions, laceration, chronic irritation). The development of dark pigmentation also has been observed in Saanen goats exposed to excessive sunlight.

Lesion location can be useful in establishing a differential diagnosis (see Table 10-2). Regions commonly affected in the early stages of skin disease include the face, ears, feet, udder, and perineal region. Fungal skin infections more commonly occur on the face, neck, and ears, whereas bacterial skin diseases also affect the feet, udder, and perineum. Nutritional deficiencies typically involve all regions to various degrees. Photosensitization is more severe in areas that receive little protection by the hair coat and those with slight or no pigmentation. Ectoparasite lesions are most severe on the feet, face, and ears.

Diagnostic Tests

Although many skin diseases are diagnosed on the basis of clinical signs and the intuition of an experienced veterinarian’s sense of the significance of these and other findings, specific diagnosis requires confirmation by laboratory tests (Table 10-3).

TABLE 10-3 Tests Used for Diagnosis of Skin Disease

Cause of Skin Disease	Tests Used
Parasites	Acetate tape Skin scraping Fecal flotation
Fungi	Potassium hydroxide Mineral oil mount Wood’s lamp examination Fungal culture Cytology
Bacteria	Direct smear Bacterial culture
Viruses	Viral isolation Electron microscopy Serologic studies
Allergy	Intradermal skin tests
Miscellaneous pathologic conditions	Histopathologic techniques—examination of biopsy sections, immunofluorescence tests, antinuclear antibody tests, use of special stains

Modified from Scott DW: Large animal dermatology, Philadelphia, 1988, WB Saunders.

Skin Scraping

Cytologic evaluation of skin scrapings is easily performed under field conditions and may be diagnostic of certain diseases. Observation of bacteria on cytologic preparations is not diagnostic because bacteria are ubiquitous on the surface of the skin. Bacteria observed in pustule fluid are more diagnostic. The contents of skin pustules or abscesses may be aspirated and cultured for identification. A direct smear with Gram staining will permit immediate identification of infectious bacteria. The presence of phagocytized bacteria supports a diagnosis of bacterial infection. In the absence of neutrophils or macrophages, however, such bacteria are likely to be contaminants rather than the cause of disease.

Description of the morphology of groups of bacteria may be helpful. For example, Dermatophilus congolensis is a gram-positive filamentous branching bacterium that forms colonies. Scales and crusts also can be examined under a microscope. Direct examination usually is not rewarding, but softening the material with sodium nitrate solution may allow visualization of ectoparasites or fungal hyphae. These organisms often float to the top of the solution; placing a slide on top of the solution will aid in identification, because mites often are carried with the water adhesion onto the slide.

Skin scrapings can be frustrating to interpret. The scraping should be done firmly and deeply into the skin surface. The presence of blood at the site of scraping indicates that the depth is adequate to collect any infesting ectoparasites. Careful microscopic examination of the debris is useful to identify mites or their eggs. Potassium hydroxide solution may be used to clear the sample for examination.

Microbial Culture

Bacterial and fungal cultures can be used to determine the presence of pathogenic organisms. Culture results may be challenging to interpret, because some cultured microbes may be part of the normal resident flora of the skin of sheep and goats (Table 10-4). Bacterial cultures may be obtained by aspirating pustules, abscesses, and other nodules. If a skin biopsy is to be performed, material for bacterial culture may be obtained from a sample of skin tissue. The clinician cleanses the desired sample area with alcohol and obtains a hair sample from the periphery of an active lesion. Cultures for dermatomycotic agents must be set up on special media. Fungal cultures may require weeks in a favorable environment before a positive or negative result can be reported.

TABLE 10-4 Normal Microbial Inhabitants of the Skin in Sheep and Goats

Species	Bacteria	Fungi
Goat	Staphylococcus aureus	Aspergillus
	Coagulase-negative staphylococci	Mucor
Sheep	Bacillus
	Escherichia coli
	Micrococcus
	S. aureus
	S. epidermidis
	Streptococcus

Modified from Scott DW: Large animal dermatology, Philadelphia, 1988, WB Saunders.

Impression Smear

Impression smears may be of some (albeit limited) value, particularly in the diagnosis of very exudative or very dry lesions. A moist lesion or an area from which a scab has just been removed is selected. A clean glass microscope slide is carefully pressed against the lesion and is allowed to air dry or is fixed. The slide is then suitably stained and the cytologic evaluation is performed.

Biopsy

Skin biopsy is most useful to identify lesions consistent with ectoparasites and allergic and autoimmune disease. Skin biopsy is indicated when a lesion is unusual in appearance or location, has failed to respond to treatment, is suspected to be neoplastic, or is persistently ulcerative or exudative. It also can be used to rule out various pathologic conditions in the differential diagnosis. Biopsy specimens should be obtained from primary lesions and ideally should include the junction of normal and abnormal skin. Commercial skin biopsy instruments (with internal diameters of 4 to 8 mm) provide the best-quality samples for pathologists. Areas with minimal skin tension should be chosen. A needle and scalpel blade can be used to harvest a skin sample, or the entire lesion may be submitted if surgical excision has been performed. Full-thickness skin biopsy is recommended to allow examination of all layers of the epidermis and dermis. Sedation or tranquilization of the patient may be required. The clinician may clip the hair surrounding the area of skin biopsy; however, hair emerging from the skin sample is desirable to enhance the pathologist’s evaluation. Therefore only minimal clipping should be performed, and a razor blade should not be used. A small amount of lidocaine hydrochloride 2% is deposited in the subcutaneous tissue deep within the specimen. This should be done carefully and immediately before biopsy, because the side effects of lidocaine include vascular dilatation and edema, both of which may confuse histologic evaluation. Many pathologists prefer that skin specimens be preserved attached to a wooden plank such as a piece of a tongue depressor. Fixatives for skin samples include 10% neutral buffered formalin for routine light microscopy and glutaraldehyde for electron microscopy. Skin biopsy specimens may be fixed with Michel’s fixative or fresh-frozen without fixative if immunohistochemistry analysis or other such testing is desired. In one study, shrinkage was similar for formalin-fixed and for fresh-frozen specimens (approximately 20%).³ Skin biopsy specimens should be submitted to a veterinary pathologist experienced in the interpretation of histopathologic findings in skin. Because skin histology varies dramatically among species, a pathologist experienced in evaluation of the skin of sheep and goats is preferable. If preferred by the clinician or the owner, the biopsy site can be closed (using a simple interrupted or cruciate suturing pattern) with either absorbable or nonabsorbable material.

References

1. Scott D.W. Large animal dermatology. Philadelphia: WB Saunders; 1988.

2. Smith M.C., Sherman D.M. Skin. Goat medicine, ed 2. Ames, Iowa: Wiley-Blackwell, 2009.

3. Steinhagen O., Bredenhann A.E.J. The effect of histological processing on sheep skin samples,. S Afr J Anim Sci. 1987;17:151.

Viral Diseases

Contagious Ecthyma (Sore Mouth/Orf/Contagious Pustular Dermatitis)

Contagious ecthyma—also called “sore mouth,” orf, and contagious pustular dermatitis—is a unique viral skin disease caused by a parapoxvirus. It is seen primarily in sheep and goats but also has been reported in other wild and domestic ruminants and in humans. The morbidity in naive herds or flocks will approach 100%, but mortality rates rarely exceed 1%. Death, if it occurs, usually is due not to the infection itself but rather to secondary complications such as pneumonia or starvation. The causative virus can persist in the soil for years and has survived in a laboratory environment at room temperature for 20 years.¹ A conflicting report indicated that the virus was undetectable in scabs shed naturally from healed lesions.² Nevertheless, once on the farm, it is considered to be on the farm forever. Outbreaks tend to occur around lambing or kidding time, when newly susceptible offspring are present. Transmission may be through direct contact with clinically affected animals or on fomites contaminated by the clinically affected, or may occur indirectly by contact with virus-contaminated soil or shed scabs, and some evidence points to the possibility of spread by nonclinical carriers.³ Transmission by nonclinical carriers has been disputed, however: “[Orf virus] does not cause latent infections in animals that recover from clinical disease, but clinically healthy animals that are moved from infected to noninfected premises or transported in contaminated vehicles can act as mechanical carriers.”⁴ The virus typically finds entry through a break in the skin. Thus the disease tends to be most prevalent in young animals, sometimes in association with tooth eruption.⁵ The incubation period is 3 to 14 days. It is one of the more significant zoonotic skin diseases of sheep and goats and is considered to be extremely painful for affected humans. Veterinarians and producers should take precautions to avoid exposure by wearing disposable gloves for treatment or examination in suspected cases.

Clinical Signs

The clinical presentation is relatively unique, with scab-like lesions appearing most often on the lips and muzzle and in the oral cavity (Figure 10-1). Lesions appear as crusty proliferations at mucocutaneous junctions, similar to fever blisters. Initial lesions appear as papules, followed by vesicles and pustules and scab formation. Scabs heal over and drop off in 1 to 4 weeks. A typical mild course of the disease in 10- to 21-day-old lambs has been reported, with resolution occurring beginning at 7 days.⁵ Lesions also may develop on the teats and udders of nursing dams, often as a result of suckling of affected lambs or kids. Udder and teat lesions appear to be more painful, leading to refusal of the affected dam to nurse her offspring. This feeding hiatus in turn may result in neonatal starvation. Lesions also have been reported on the ears, face, periorbital region, poll, scrotum, perianal region, and distal extremities. Rare cases of body (trunk and flanks) lesions have been reported in both sheep and goats.^6,⁷ More severe forms, described as malignant, persistent, or chronic, have been reported. In rare cases, extension of lesions down the respiratory tract may predispose the affected animal to pneumonia, and extension down the alimentary tract may lead to gastroenteritis. A mortality rate of 10% was reported among 550 5-month-old lambs, in which severe facial edema and extensive proliferative necrotic lesions developed in the anterior two thirds of the buccal cavity, including the tongue.⁸ The stress of transportation may have increased the clinical severity of the disease in the aforementioned report.

Figure 10-1 Contagious ecthyma. The lesions can be seen to follow the contour of the lips and extend to the nasal mucosa. In this instance, the disease was endemic in a milking sheep flock, where the lambs were removed from the dams shortly after birth and then bottle- or bucket-fed. Nearly 100% of the lambs were clinically affected.

Diagnosis

Diagnosis most commonly is based on clinical signs. In many countries, diseases with a clinical appearance and history similar to those of contagious ecthyma (typically a mild disease with high morbidity rates) are rare; other considerations in the differential diagnosis include bluetongue, ulcerative dermatosis, sheep pox, capripox, and foot and mouth disease. A skin biopsy and histopathologic examination can be confirmatory. Histopathologic findings include ballooning and degeneration of keratinocytes and eosinophilic intracytoplasmic viral inclusions. Electron microscopy has been used to detect the virus in scabs. More viral particles are present in early scabs than in aged scabs, so “fresh” scabs should be submitted for examination. Samples for diagnosis can be submitted refrigerated or at room temperature but should be packaged to prevent human contact. One drawback to electron microscopy is that all parapoxviruses (e.g., the agents of bovine papular stomatitis and pseudocowpox) are morphologically indistinguishable. Serologic testing can be used to determine exposure status and gives presumptive evidence for the disease. Polymerase chain reaction (PCR) tests have been developed and may become the preferred method of diagnosis.

Treatment

Treatment of contagious ecthyma is seldom attempted because the disease is self-limiting and should resolve within 3 weeks. At that time, the scab will fall off, thereby contaminating the environment. The disease is of little clinical consequence in weaned and older animals, but neonates may need supplemental feedings. Secondary bacterial infection may occur and if suspected can be treated with topical or systemic antibiotics (see Appendix 1). In some parts of the world, blowfly strike can complicate contagious ecthyma, so affected animals should be observed for this disease and treatment instituted as necessary. Animals with greater economic or sentimental value in which the disease results in anorexia secondary to painful oral lesions may be treated with electrocautery and débridement after spray cryotherapy, with good results.⁹ Use of ointments and astringent lotions may actually delay healing.¹⁰

Prevention

Prevention is best achieved by preventing the disease from entering the farm through quarantine and physical examination of stock entering the farm and by purchasing new stock from contagious ecthyma–free herds or flocks. Special efforts should be made to prevent contact with suspect animals at livestock shows and sales and to avoid use of common feed, water, and grooming equipment. In an outbreak situation, the affected stock should be isolated and the remainder vaccinated. This method should help limit production losses through control of the location of the disease.

Once the disease is on the farm, vaccines are available that can help in its control. Vaccines are live and should not be used unless the disease is known to be present in a herd or flock. Most commercial vaccines are labeled for sheep but not goats. Although use of these vaccines in goats has at times appeared anecdotally efficacious, research has indicated that sheep vaccines were not effective in protecting goats from the wild-type contagious ecthyma virus found in goats.¹¹ More recently, a goat strain vaccine for contagious ecthyma was found to be protective against experimental challenge.¹²

Vaccines typically are placed on scarified skin of the medial thigh. Other sites should be used, such as inside the ear pinna or under the tail, for vaccinating lactating females. Formation of scabs should occur by 3 to 4 days if the vaccination is successful. If vaccination is used, its use should be tailored to optimal management for a particular herd or flock. One approach to vaccine use is to begin with vaccination of all animals that have not been previously exposed and then vaccinate only new naive stock (from new births and new additions) annually. Immunity is reported to be acquired by 3 weeks after vaccination but is not considered to be lifelong.¹³ Naturally exposed animals that have recovered usually are solidly immune for 2 to 3 years.¹⁰ It has been stated that colostrum immunity does not occur, because antibodies do not appear to be passed in the colostrum.^1,¹⁰ A study by Perez, however, demonstrated that lesions did not develop in kids of vaccinated does when challenged before 45 days of age, whereas lesions did appear in kids older than 45 days of age.¹⁴ On some farms in which the disease is endemic, producers may choose to simply live with the disease. The disease has a shorter course and is less severe in reinfected animals.

Malignant Contagious Ecthyma

A persistent form of contagious ecthyma known as malignant contagious ecthyma has been recognized in a limited number of sheep within infected flocks. Proliferative lesions develop, especially on the distal legs and feet and, less commonly, on the head. Unlike with ordinary contagious ecthyma, however, the lesions fail to regress and may continually enlarge. Secondary bacterial infections, fly strike, and hemorrhage are major complications. Although a poxvirus morphologically similar to the contagious ecthyma virus has been identified by electron microscopy in typical lesions, the disease has a different course.

Affected sheep do not pass the infection to commingling animals. Preliminary studies of the cellular immune system in affected sheep have failed to demonstrate any deviation from normal.

Ulcerative Dermatosis

Ulcerative dermatosis is a disease of sheep caused by a virus similar to but distinct from the contagious ecthyma parapoxvirus. Infection typically follows a break in the skin such as from shearing injuries and breeding-related injuries. The virus may be spread through physical contact during breeding season, perhaps accounting for the highest prevalence of disease in the fall and winter. The incubation period is 2 to 7 days. Healing of lesions occurs in 2 to 6 weeks. In the United States, the disease is most common in western regions, and the morbidity rate usually is 15% to 20% but may be as high as 60%.

Sheep Pox and Goat Pox

The agents of sheep pox and goat pox are closely related viruses of the Capripox genus in the family Poxviridae. Although the viruses tend to be species-specific, cross-species infection has been reported. Mortality is low in endemic regions but may be high when naive sheep or goats are exposed. Transmission (thought to occur by aerosol and contact with lesions) increases with close contact with infected herds or flocks. These diseases currently are endemic in northern Africa, the Middle East, and southeastern Asia, with occasional outbreaks in southeastern Europe. One case of goat pox in the United States has been reported,¹⁶ but a U.S. Department of Agriculture–Animal and Plant Health Inspection Service (USDA-APHIS) website states that neither disease has occurred in the United States. Contagious ecthyma is the primary consideration in the differential diagnosis for sheep pox and goat pox. However, sheep and goat pox lesions tend to occur over the entire skin surface. The two viral agents (of contagious ecthyma and of sheep or goat pox) are easily differentiated by electron microscopy. A recent review of sheep pox has been published.¹⁷

Scrapie

A discussion of scrapie is beyond the scope of this chapter (see Chapter 13). As a consequence of the intense associated pruritus, however, scrapie-infected sheep or goats (although pruritus is much less common in goats than in sheep) may present with hair or wool loss secondary to mechanical excoriation. Scrapie does not directly affect the skin; skin lesions are simply a result of the intense pruritus and subsequent aggressive scratching.

Bluetongue

A discussion of bluetongue is beyond the scope of this chapter (see Chapters 4 and 14). However, skin lesions suggestive of bluetongue include coronitis, ulcerations of the oral mucosa, and muzzle edema. Goats are relatively resistant to clinical bluetongue.

Vesicular Stomatitis

Vesicular stomatitis is a viral disease that creates ulcerations of the oral mucosa in cattle, swine, and horses. Although both goats and sheep may be experimentally infected with the causative virus, natural clinical disease is quite rare, and no case reports documenting clinical disease are found in the literature.

Sheep and goats never show clinical signs of vesicular stomatitis.¹⁸ A 1995 outbreak of the disease in the western United States did not identify a single sheep or goat seropositive for the virus.¹⁸ Unpublished reports of vesicular stomatitis in goats, however, indicated that vesicles may occur at the commissures of the lips.¹⁹

References

1. Scott D.W. Large animal dermatology. Philadelphia: WB Saunders; 1988.

2. Romero-Mercado C.H., et al. Virus particles and antigens in experimental orf scabs. Arch Gesamte Virusforsch. 1973;40:152.

3. Nettleton P.F., et al. Natural transmission of orf virus from clinically normal ewes to orf-naive sheep. Vet Rec. 1996;139:364.

4. de la Concha-Bermejillo A. Orf/contagious ecthyma. In: Haskell S.R.R., editor. Blackwell’s Five-minute veterinary consultant. Singapore: Wiley-Blackwell, 2008.

5. McElroy M.C., Bassett H.F. The development of oral lesions in lambs naturally infected with orf virus. Vet J. 2007;174:663.

6. Coates J.W., Hoff S. Contagious ecthyma: an unusual distribution of lesions in goats. Can Vet J. 1990;31:209.

7. Sargison N.D., Scott P.R., Rhind S.M. Unusual outbreak of orf affecting the body of sheep associated with plunge dipping. Vet Rec. 2007;160:372.

8. Gumbrell R.C., McGregor D.A. Outbreak of severe fatal orf in lambs. Vet Rec. 1997;141:150.

9. Meynink S.E., Jackson P.G.G., Platt D. Treatment of intraoral orf lesions in lambs using diathermy and cryosurgery. Vet Rec. 1987;121:594.

10. Blood D.C., Radostits O.M., Henderson J.A., et al. Veterinary medicine. London: Baillière Tindall; 1983.

11. de la Concha-Bermejillo A, Ermel RW, Zhang MZ: Contagious ecthyma (ORF) virulence factors and vaccine failure, Proceedings of the One Hundred and Third Annual Meeting of the United States Animal Health Association, San Diego, Calif, 1999.

12. Musser J.M.B., et al. Development of a contagious ecthyma vaccine for goats. Am J Vet Res. 2008;69:1366.

13. Mullowney P.C. Skin diseases of sheep. Vet Clin North Am Large Anim Pract 6. 1984:131.

14. Perez JLT: Kids immunity to contagious ecthyma (orf virus), presented at the Goat Diseases and Production 2nd International Colloquium, Niort, France, June 26 to 29, 1989 (Abstract p 24).

15. Renshaw H.W., Dodd A.G. Serologic and cross-immunity studies with contagious ecthyma and goat pox virus isolates from the western United States. Arch Virol. 1978;56:201.

16. Animal Health Monitoring and Surveillance: Status of reportable diseases in the United States, USDA-APHIS (website): http://www.aphis.usda.gov/vs/nahss/disease_status.htm#sheep, Accessed November 12, 2008.

17. Bhanuprakash V., et al. The current status of sheep pox disease. Comp Immunol Microbiol Infect Dis. 2006;29:27.

18. Kitching P. Notifiable viral diseases and spongiform encephalopathies of cattle, sheep and goats. In Practice. 1997;19:51.

19. Bridges V.E., et al. Review of the 1995 vesicular stomatitis outbreak in the western United States. J Am Vet Med Assoc. 1997;211:556.

20. Smith M.C., Sherman D.M. Skin. Goat medicine, ed 2. Ames, Iowa: Wiley-Blackwell, 2009.

Bacterial Diseases

Dermatophilosis (Streptothricosis, Lumpy Wool Disease, Rain Scald, Rain Rot)

Dermatophilosis (streptothricosis, lumpy wool disease, rain scald, rain rot) is a disease of all ruminants caused by the gram-positive filamentous bacterium Dermatophilus congolensis. This bacterium appears to be maintained within herds or flocks by carrier animals. The organism is considered an obligate parasite of ruminant skin and was not thought to survive for very long in the soil, but later research indicates that it may survive for several months, especially within cast-off crusts.^1,² Predisposing factors for clinical disease include skin damage (as from biting insects or physical abrasion), excessive moisture (hence the common name “rain rot”), and concurrent diseases and stresses that compromise the host immune system. The loss of the sebaceous film layer on skin is thought to predispose the animal to development of the disease. Excessively rainy conditions without appropriate shelter can lead to dilution of this sebaceous layer, thereby increasing the chance of clinical disease.

The incubation period averages 2 weeks. The infective form of the organism is the motile zoospore (Figure 10-2), which germinates, penetrates the epidermis, and invades hair or wool follicles. Neutrophils migrate to the affected areas, resulting in accumulation of a serous exudate that seeps to the epidermal surface. The older epidermal skin deteriorates while a new layer of epidermis forms below. This new layer also becomes infected with hyphal branches. Eventually, thick scabs are formed. Early clinical manifestations include small, raised, and circumscribed crusts of epidermal cells and serous exudates with embedded hairs or wool. The disease follows a similar pattern in sheep, but the serous exudates may not be adherent to the epidermis. It also is responsible for “strawberry footrot” of sheep, which appears as dry scabs on the lower legs. Removal of the dry scabs leaves a mass of granulation tissue that has the appearance of a strawberry (hence the name). Although it can be spread from acutely infected animals, outbreaks are rare but have been reported.³ Young goats appear to be more susceptible than adults to development of clinical disease.^3,⁴ Likewise, young sheep are more susceptible than adult sheep.⁵

Figure 10-2 Dermatophilus congolensis showing zoospores. A diagnostic slide can be easily and reliably made in field conditions by pressing the slide against the underside of the scab, allowing the slide to air dry, and then staining with Wright’s stain.

(Courtesy Dr. Mike Fry. University of Tn, Knoxville, Tn)

Clinical Signs

Follicular and nonfollicular papules and pustules develop and rapidly coalesce and rupture, with consequent matting of groups of hairs or clumps of wool. These are classically described as “paintbrush lesions” in haired ruminants. Lesions may be painful but are not pruritic. In sheep, crusts occurring at the coronary band (i.e., strawberry footrot) also may extend to the carpi or tarsi. Lesions also may be present on other parts of the body. In goat kids, lesions tend to be on the ears and tails; in adults, lesions tend to be on the muzzle, in the dorsal midline, or on the scrotum or distal legs.⁴ Lesions have been reported in the ears of kids at 5 days of age.⁶ Although the condition is relatively rare, it may be fatal in livestock debilitated by other diseases and poor nutrition.

Diagnosis

Staining (Gram stain or methylene blue) of direct smears of lesions should reveal branching hyphae with cuboidal packets of coccoid cells arranged in parallel rows (resembling railroad tracks) within the filaments (see Figure 10-2). Skin biopsy and histopathologic examination also may be helpful. Culture can be confirmatory, although possible subsequent infestation by other bacterial and fungal organisms may complicate the diagnosis in chronic cases.⁷

Treatment

Agents for topical treatment include iodophors, 2% to 5% lime sulfur, 0.2% copper sulfate, 0.5% zinc sulfate, and 1% potassium aluminum sulfate. These agents may be applied as total body washes, sprays, or dips for 3 to 5 consecutive days and then weekly until healing has occurred. Systemic antibiotics such as procaine penicillin G (5000-10000 IU/kg twice a day for 4 to 5 days), oxytetracycline (one or two doses of 20 mg/kg during a 72-hour interval), or ceftiofur (2 ml/100 lb once daily for 4 to 5 days) may be effective. The organism is reported to be resistant to polymyxin B, bacitracin, and sulfonamides. Lesions in kids tend to heal without treatment within 2 to 3 months.⁸ Dermatophilus is potentially zoonotic to humans.

Prevention

In areas in which the disease is prevalent, removal and disposal of crusts, keeping stock dry (providing shelter from wet weather), providing good-quality nutrition, and control of ectoparasites may limit the number of clinical cases. Vaccines have been studied but do not appear to offer significant protection.⁵

Fleece Rot (Water Rot, Weather Stain)

Fleece rot is an exudative bacterial dermatitis of sheep that is characterized by a greenish-discolored, matted wool. This disease reduces the quality of the wool but is most important as a predisposing factor for fly strike. Although other fleece bacteria may play a significant role in the disease, Pseudomonas aeruginosa is considered the primary etiologic agent.⁹ The disease was first recognized in Australia in the latter part of the 1800s.⁵ Bacteria cultured from the skin of affected sheep, when applied to unaffected sheep, resulted in the disease.¹⁰

The necessity of moisture for development of disease symptoms was noted in 1929 by Seddon and McGrath.¹¹ Both wool traits and body conformation traits are predisposing factors for fleece rot in sheep, and this susceptibility is reportedly heritable.¹¹ The disease appears to be most prevalent in Australia, with reported prevalence rates averaging 24%.⁵ The disease does not appear to be of clinical or economic significance in the United States but has been reported.¹² The reason for the increased susceptibility of young sheep compared with older stock is not known, but causative or contributing factors may include maturity of wool and skin characteristics and development of a certain level of immunity after exposure.⁵ Fleece rot predisposes affected sheep to blowfly strike.

Clinical Signs

The most characteristic clinical sign is the greenish discoloration of wool. A copious serous exudate also may be evident and probably is the attraction for flying insects that leads to associated fly strike. The inflammatory reaction can result in a grayish matted wool. Pruritus also has been reported, but not all affected sheep demonstrate evidence of this symptom.¹³ Lesions are most common on the back and withers.

Diagnosis

Culture of samples from involved skin and wool is the definitive method to diagnose fleece rot (and would be especially definitive for greenish-discolored wool). Pseudomonas aeruginosa may be found in pure culture. It produces the green pigment pyocyanin.¹⁴ Fleece rot may be distinguished from dermatophilosis in that no scab formation is associated with the former.

Treatment

Antibiotics may be helpful, but studies have shown P. aeruginosa to be quite resistant to many antibiotics.^15,¹⁶ In clinical practice, shearing to allow the involved skin to dry is the most effective means of treatment.

Prevention

Vaccines are under development, but efficacy to date has been disappointing.⁵ Some prevention is afforded by producing more resistant sheep by breeding for characteristics of wool and body conformation that are less predisposing to the condition. Perhaps the most practicable control measure is to shear the sheep before the onset of the rainy season.