Diagnostic Challenge in Veterinary Pathology: Alopecic Crusting Dermatitis in a Goat

Clinical History and Gross Findings

In April 2020, a 1-year-old castrated Nigerian dwarf goat presented with a 4-month history of skin lesions unresponsive to topical iodine and extra-label topical miconazole. The wether was bright, alert, and with normal appetite. The goat was the only affected animal in a mixed herd of 7 sheep and 4 goats aged from 6 months to 7 years. The animals were kept on a dry lot and fed strictly timothy and alfalfa hay with access to goat minerals (Purina®).

The goat had multifocal alopecia with fissures, erosions, crusting, and scaling that predominated on the ventrum (Fig. 1). The cutaneous lesions were nonpruritic, firm, raised, moderately demarcated, and nonpigmented.

Figure 1.

Skin, goat (ventrum, forelimbs at the top). Multifocal erosion, crusting, scale, and thickening that predominates on the ventrum.

Differential Diagnoses

Goats suffer from a multitude of skin diseases that have a similar gross appearance. ¹ Establishing the differential diagnosis should take into account the patient’s age, the breed, the season (eg, flies and lice), the geographic location (eg, endemic and foreign animal diseases), the distribution and macroscopic appearance of the lesions, the presence of pruritus or systemic signs, the response to treatments, diagnostic test results, and similar disease in conspecifics. ¹

The wether was the only affected animal, had no systemic signs, and the gross lesions were chronic, ¹ suggesting a long-standing primary dermatopathy. Despite the lack of convalescence with iodine and miconazole treatment, the appearance of the cutaneous lesions and the patient’s young age favored a presumptive diagnosis of dermatophytosis. Other considerations included bacterial dermatitis (Staphylococcus aureus, Dermatophilus congolensis), ectoparasites (lice, Chorioptes spp., Demodex spp., Sarcoptes spp.), verminous dermatitis (Stephanofilaria spp.), viral dermatitides (papillomavirus, herpesvirus), and noninfectious dermatopathies such as contact hypersensitivities or pemphigus foliaceus.

This young goat’s dermatopathy among a herd of unaffected small ruminants was suspicious of an infectious but poorly communicable cause. The lesions predominated on the ventrum and were dominated by nonpruritic alopecia, crusting, scaling, and erosion, features of nonspecific chronic skin disease. ¹ Alopecia and crusting without pruritus can occur with chronic fungal and bacterial infections, while ectoparasites tend to be pruritic, except for Demodex spp. and Chorioptes spp. ¹ And contrary to most viral dermatitides, cases of fungal or bacterial dermatitis typically lack systemic signs. ¹ Therefore, fungal or bacterial causes were favored in this case despite the nonconforming lesion distribution. Staphylococcus aureus is a frequent cause of caprine dermatitis that affects the legs, face, ears, udder, inguinal area, and perineum. ¹ Dermatophilus congolensis is also common, and infections involve the dorsum, face, ears, legs, and scrotum. ¹ Dermatophytosis caused by Trichophyton verrucosum, Trichophyton mentagrophytes, or Microsporum canis occur on occasion in goats and affect especially the head, ears, and neck. ¹ In immunocompetent goats, ringworm typically heals by 5 weeks of infection, which contrasts with this case. ¹ Because other small ruminants in the herd were unaffected, ectoparasites like Chorioptes spp. was deemed unlikely. Since the skin lesions were not verrucose nodules, papillomavirus was unlikely. ¹ The clinical signs and lesions ruled-out capripoxvirus, parapoxvirus (orf), and orbivirus (bluetongue), since these viruses do not cause alopecia, may cause systemic signs, may affect noncutaneous areas, and may target specific anatomic locations like the lips and muzzle in the case of orf. ¹ Pemphigus foliaceus, although uncommon in goats, was considered the most likely noninfectious etiology. ¹ This immune-mediated skin disease causes alopecia, crusting, variable pruritus, and may affect the ventrum. ¹ Histopathology is required for a definitive diagnosis. Therefore, to narrow the differential diagnosis and allow a diagnosis, skin samples were submitted for bacterial culture, fungal culture, and histopathology.

Laboratory and Microscopic Findings

Four 6-mm punch biopsies targeting the junction of affected and unaffected skin were taken. One punch biopsy was submitted for bacterial culture and fungal culture, and the other 3 biopsies were processed for routine histopathology. Aerobic and anaerobic culture yielded no significant growth, and mycology yielded growth of Curvularia lunata, Curvularia pallescens, Aspergillus niger, and Alternaria alternata. Dermatophytes, S. aureus, and D. congolensis were not supported by bacterial and fungal cultures.

Histopathology of skin biopsies identified the lesions as inflammatory. There was epidermal erosion and hyperplasia with spongiosis, parakeratosis, orthokeratosis, serocellular crusts, and multifocal transepidermal aggregates of neutrophils admixed with serum, cell debris, and keratinocyte death (Fig. 2). Follicular walls frequently had segmental or circumferential spongiosis with individual dead keratinocytes, cell debris, neutrophils, lymphocytes, histiocytes, and infrequent multinucleated giant cells with packed nuclei (Fig. 3). Follicular lumina were dilated with laminated keratin. Multiple arteries within the deep dermis were surrounded by histiocytes, lymphocytes, plasma cells, and fewer eosinophils and neutrophils. In the deep dermis of one section, a medium-sized artery had segmental fibrinoid degeneration with infiltrates of granulocytes and mononuclear inflammation (arteritis) rimmed by mixed inflammation and fibrovascular proliferation (Fig. 4). In a section stained with periodic acid–Schiff, there were no fungal hyphae within areas of follicular, dermal, or epidermal inflammation. One section had a fungal hypha at the hyperkeratotic surface that was considered secondary environmental contamination, because there was no deeper invasion or granulomatous inflammation.

Figures 2–7.

Skin, goat. Figure 2. The epidermis is irregularly hyperplastic, with parakeratosis and orthokeratosis, regional erosion and serocellular crusts containing neutrophils and other inflammatory cells. There is scattered individual keratinocyte death (inset), exocytosis of inflammatory cells, and dermal mononuclear cell infiltrates. Hematoxylin and eosin (HE). Figure 3. A follicular wall is disrupted by spongiosis, and resulting clefts contain neutrophils, mononuclear cells (mural folliculitis), and few multinucleated giant cells (arrow) with perifollicular mixed inflammation. HE. Figure 4. Deep dermal artery with segmental fibrinoid degeneration and transmural infiltration by eosinophils and fewer neutrophils, rimmed by fibrovascular proliferation and mixed inflammation. Figure 5. OvHV-2 ISH (in situ hybridization) labels nuclei of mononuclear cells within the epidermis and dermis and are admixed with other nonlabeled inflammatory cells (granulocytes). OvHV-2 probe. Figure 6. OvHV-2 ISH labels nuclei of mononuclear cells in the perifollicular dermis and the spongiotic follicular wall. A multinucleated giant cell has no signal (arrow). OvHV-2 probe. Figure 7. OvHV-2 ISH labels nuclei of mononuclear cells in the tunica intima and adventitia of the same artery as in figure 4. OvHV-2 probe.

Further Investigations and Diagnosis

The distribution and the type of inflammation without presence of intralesional organisms narrowed the differential diagnoses considerably. Because the inflammation was vasocentric and the lesions were similar to that of a previous report of OvHV-2 dermatitis in a goat, ³ OvHV-2 was a plausible cause.

Whole blood and an additional punch biopsy was submitted for multiplex real-time PCR (polymerase chain reaction) for five of the viruses that cause malignant catarrhal fever (MCF). ² The tissue sample, but not the blood, was positive for ovine herpesvirus-2 (OvHV-2) with a Ct value of 34.30. Samples were negative for alcelaphine herpesvirus-1, caprine herpesvirus-2, ibex MCF virus, and white-tailed deer MCF virus.

To understand the significance of the PCR result and to localize viral nucleic acid to the lesions, a nucleic acid probe to the ORF 25 and 50 of OvHV-2 was applied to 5-µm sections of the punch biopsies. ⁶ In situ hybridization (ISH) labeled the nuclei of mononuclear inflammatory cells that surrounded lesions of arteritis and that were transmigrating and surrounding follicles and within eroded epidermis (Figs. 5 –7). No virus was detected within multinucleated giant cells. The negative control had no positive ISH signal. The goat was diagnosed with OvHV-2-associated dermatitis.

Discussion

OvHV-2 infection does occur in goats, ^4,5,7 though cases of dermatitis are infrequently reported. ³ This case demonstrates that OvHV-2 can cause dermatitis in goats. Vasotropism, which is a classic lesion of OvHV-2 MCF in cattle, was a feature of the dermatitis in this goat. ^3,5 Because the gross presentation is not specific, OvHV-2-associated dermatitis in goats may be underdiagnosed, since it is not typically among the differential diagnoses of caprine dermatitis. ¹ However, if goats are known to be in close proximity to sheep, and if common dermatitides are ruled out, then testing for OvHV-2 should be considered.

More than a year since diagnosis, the patient’s skin lesions remain unchanged relative to the initial presentation. During that time, the patient received no treatment and has maintained normal appetite and growth. Other goats in close contact have not developed lesions.