Morphologic and immunologic characterization of a canine isthmus mural folliculitis resembling pseudopelade of humans

The clinical, histopathologic and immunopathologic features of a novel form of isthmus mural folliculitis in dogs, which resembles pseudopelade in humans, were characterized. Clinically, dogs exhibited variably distributed foci of alopecia that persisted without treatment or did not respond to immunosuppressive therapy. Histopathologically, mixed mononuclear cell infiltrates, largely lymphocytes, infiltrated the follicular isthmus. Occasionally, inflammation extended above and below the follicular isthmus but did not involve the hair bulb or the epidermis. Severe follicular atrophy and variable atrophy of sebaceous glands occurred in all dogs. Folliculotropic lymphocytes exhibited most commonly CD3 and CD8 (cytotoxic T cells). Autoantibodies specific for the lower hair follicle were detected in the serum of affected patients. Western immunoblotting demonstrated binding of these antibodies to multiple follicular keratinocyte proteins, including hair keratins and trichohyalin. Lack of hair regrowth (in contrast to canine alopecia areata), as well as location of inflammation and extreme atrophy of adnexal units are similar to findings seen in human pseudopelade.     

Alopecia areata with lymphocytic mural folliculitis affecting the isthmus in a thoroughbred mare

A 13-year-old, thoroughbred mare was presented with an 8-year history of multifocal, generalized, noninflammatory alopecia and a 3-month history of alopecia, erythema and scaling of the white star on the forehead and muzzle. Histopathological examination of biopsy samples from multiple sites on the body (mane, neck, shoulder, flank and gluteal region) showed a subtle lymphocytic inflammatory infiltrate affecting and surrounding the anagen hair bulbs, consistent with a diagnosis of alopecia areata. The biopsy sample from the star on the forehead showed atrophic hair follicles with perifollicular and mural mononuclear folliculitis affecting the isthmus. Immunohistochemical staining with a CD3 marker confirmed the T-lymphocytic origin of the inflammatory infiltrate in all the samples. The concurrent presence of lymphocytic infiltration at the bulbar and isthmic level of the hair follicles in the same horse is unusual. This finding may represent a variation of the histological appearance of alopecia areata.     

Follicular dysplasia in two cows

The histological features of a follicular dysplasia with pigmentary changes is reported in two adult cows, one a black Brangus-cross and the other a black Angus. Adult onset of diffuse alopecia was present in both cows. Skin biopsies exhibited follicular distortion and atrophy, with melanin clumping in follicular epithelium, hair bulb matrix cells, hair shafts, and infundibular keratin. Both animals were clinically normal apart from the alopecia. This report confirms and expands on the infrequently reported syndrome of follicular dysplasia in cattle.     

An analysis of factors underlying hypotrichosis and alopecia in Irish Water Spaniels in the United Kingdom

A survey on the occurrence of dermatoses in the Irish Water spaniel (IWS) was carried out in the United Kingdom. A group of 20 dogs was selected and examined clinically. All dogs had a nonpruritic, noninflammatory, regionalized hair loss affecting the same areas of the body in males and females, although an initial cyclical pattern associated with the oestrus cycle was identified. Hormonal investigations showed features suggestive of an abnormality of steroidogenesis. Histopathology revealed features similar to canine recurrent flank alopecia (CRFA) and follicular dysplasia associated with abnormal melanization, as in colour dilution alopecia, although the clinical features did not correlate with those conditions. Dietary changes improved coat and skin quality in most of the cases in this series but the role of the diet was not investigated further. This study suggests that hair loss in IWS is influenced by dietary factors and sexual hormones. Abnormalities of the steroidogenic pathways may contribute to the severity of the condition.     

Severe bilaterally symmetrical alopecia in a horse

A 9-year-old Tennessee Walking Horse gelding was presented for diagnosis of the cause of extensive alopecia. Complete hair loss was noted over the head, neck, shoulder, thigh, and proximal limbs, but the trunk, distal limbs, pelvic area, mane, and tail were unaffected. The alopecic areas were visually noninflammatory with no exudate or crust except on the shoulder and along the back, where multifocal patchy areas of alopecia with scales and crust were evident. The horse was slightly pruritic. Microscopically, the hair bulbs, inner and outer root sheaths of inferior segments, and perifollicular regions were infiltrated by small to moderate numbers of small lymphocytes. Similar inflammation was occasionally evident in isthmus follicular walls as well as some apocrine glands. No sebaceous glands were affected. Immunohistochemistry confirmed that the small lymphocytes were CD3(+) T lymphocytes. The epidermis from the skin with scale and crusts along the horse's back exhibited mild to moderate hyperplasia, mild lymphocytic exocytosis, mild eosinophilic dermatitis, and diffuse parakeratosis with numerous budding yeasts, consistent with Malassezia spp. The final disease diagnosis was made as alopecia areata with Malassezia dermatitis. Alopecia areata could be a contributing underlying factor for Malassezia dermatitis.     

Alopecia areata in Eringer cows

Alopecia areata is a hair loss disorder in humans, dogs and horses with a suspected autoimmune aetiology targeting anagen hair follicles. Alopecia areata is only sporadically reported in cows. Recently, we observed several cases of suspected alopecia areata in Eringer cows. The aim of this study was to confirm the presumptive diagnosis of alopecia areata and to define the clinical phenotype and histopathological patterns, including characterization of the infiltrating inflammatory cells. Twenty Eringer cows with alopecia and 11 Eringer cows without skin problems were included in this study. Affected cows had either generalized or multifocal alopecia or hypotrichosis. The tail, forehead and distal extremities were usually spared. Punch biopsies were obtained from the centre and margin of alopecic lesions and normal haired skin. Histological examination revealed several alterations in anagen hair bulbs. These included peri‐ and intrabulbar lymphocytic infiltration, peribulbar fibrosis, degenerate matrix cells with clumped melanosomes and pigmentary incontinence. Mild lymphocytic infiltrative mural folliculitis was seen in the inferior segment and isthmus of the hair follicles. Hair shafts were often unpigmented and dysplastic. The large majority of infiltrating lymphocytes were CD3⁺ T cells, whereas only occasional CD20⁺ lymphocytes were present in the peribulbar infiltrate. Our findings confirm the diagnosis of T‐cell‐mediated alopecia areata in these cows. Alopecia areata appears to occur with increased frequency in the Eringer breed, but distinct predisposing factors could not be identified.     

Follicular dysplasia in five Weimaraners

This study evaluated the clinical and histopathological features and results of light and electron scanning microscopy assessments of follicular dysplasia in five Weimar Pointers. The data were compared with those obtained in three normal Weimaraners. In our study, this dermatosis affected young adults that showed progressive alopecia of the trunk (head and limbs were spared) associated with recurrent folliculitis/furunculosis. Exclusion of other dermatoses and the presence of histopathological lesions and hair shafts abnormalities seen in light and/or scanning electron microscopy similar to colour dilution alopecia led to the diagnosis of follicular dysplasia. The lesions we observed are the same as those described previously in colour dilution alopecia, but they were less pronounced in all our samples.     

Alopecia and dermatopathy of the lower back following pelvic fractures in three cats

Abstract   An alopecia and dermatopathy following pelvic fractures associated with vehicular trauma is reported in three cats. The animals presented 3–4 weeks post injury with acute hair loss, glistening appearance of the skin and erosions involving the lower back. Histological examination revealed atrophy of the hair follicles and adnexal structures and follicular telogenization, dermal fibroplasia and mild lymphocytic infiltrate, fibroplasia and inflammation in the panniculus. Vascular damage secondary to the external trauma to blood vessels supplying the skin over the lumbar region and subsequent ischaemia may represent the pathomechanism of this type of alopecia. Focal permanent hair loss can be expected.     

Alopecia areata (pelade) in a cow

A case of alopecia areata (pelade) is described in a cow. Alopecia areata is a rare idiopathic dermatosis of cattle. It is characterized by asymptomatic, solitary or multiple, annular areas of noninflammatory alopecia. Scrapings and cultures are negative, and the diagnosis is confirmed by skin biopsies taken from early lesions, which reveal accumulations of lymphocytes around the bulbs of anagen hair follicles. There is no known effective and practical treatment for affected cattle. The dermatitis is a cosmetic problem, but does not seem to affect general health and production, and spontaneous remission may occur.     

Degenerative mucinotic mural folliculitis in cats

A novel form of mural folliculitis is described in seven cats. Clinically, all cats exhibited generalized alopecia with scaling or crusting that was more pronounced over the head, neck, and shoulders. The face and muzzle of all cats was unusually thickened. Six of seven cats were progressively lethargic but did not demonstrate any other consistent systemic abnormalities. Histologically, there was severe mixed inflammation of the wall of the follicular isthmus in all cats, accompanied by some follicular destruction in five cats. Sebaceous glands were not affected. All cats had variable, but often striking, follicular mucin deposition, as well as epidermal hyperkeratosis and crusting. The cause of the severe mural folliculitis was not identified, and all cats responded poorly to immunomodulating therapy. Follicular mucinosis may be a nonspecific finding, likely reflective of the follicular lymphocytic milieu, and does not always herald follicular lymphoma.     

Alopecia in the horse – an overview

Dr Stannard explains different forms of alopecia in the horse with emphasis on the hair follicle and its function in the production of hairs. Both normal and abnormal patterns of hair growth and shedding in the horse are reviewed. Overviews of several specific hair follicle abnormalities, both inflammatory and noninflammatory, are discussed in detail with their clinical relevance. Some of the clinical entities covered in this section (linear alopecia and alopecia areata) are caused by immunological attack against normal structures and could have been placed in Immunologic diseases. However, because the clinical presentation for these entities is alopecia, Dr Stannard chose to include them in his notes on alopecia. Other inclusions in this section include cutaneous bacterial infections (e.g. pastern folliculitis and dermatophilosis) as well as fungal infections of the hair (dermatophytosis).     

Bald thigh syndrome of Greyhound dogs: gross and microscopic findings

Bald thigh syndrome (BTS) is a disease limited to Greyhound dogs. It is characterized clinically and grossly by bilateral hair loss on the lateral and caudal thighs. The cause of BTS is unknown but may be associated with hypothyroidism or hyperadrenocorticism. Samples of skin, thyroid glands, and adrenal glands from 43 Greyhound dogs with BTS were examined microscopically. Microscopic changes were characterized by dilatation of follicular infundibula, presence of catagen follicles and epidermal hyperplasia. Changes in the skin from these Greyhound dogs suggest an endocrinopathy as the cause; however, we were unable to confirm which one.     

Congenital anemia, dyskeratosis, and progressive alopecia in Polled Hereford calves

A new syndrome of anemia, alopecia, and dyskeratosis was identified in Polled Hereford calves in this study. Cutaneous changes included hyperkeratosis and hair loss around the muzzle and ear margins, which progressed to a generalized alopecia and hyperkeratotic dermatitis. Histologically, orthokeratotic hyperkeratosis with dyskeratosis of epidermal and follicular keratinocytes was present. Alopecia was correlated with dyskeratosis of Huxley's layer and an increasing proportion of follicles in the telogen phase of the hair cycle. Dermatitis was characterized by a mild dermal mononuclear cell infiltrate and mild lymphocytic perivascular dermatitis. The anemia present at birth was nonprogressive and was classified as normochromic and normocytic to macrocytic. Reticulocytosis was absent, but bone marrow was markedly hyperplastic. Nuclear cytoplasmic asynchrony of the rubricyte and metarubricyte stages occurred in the bone marrow. Abnormal rubricyte nuclei and maturation arrest at the late rubricyte stage were common. Cytologic features of the erythroid series are similar to those of type I congenital dyserythropoietic anemia of human beings. Genealogic features suggest that this is a primary hereditary defect. The mode of inheritance, however, remains to be determined.     

Mutually-induced traumatic alopecia responsive to husbandry modification in two cohabiting donkeys

Cutaneous expression of behavioural processes remains unexplored in donkeys. This case report describes a case of traumatic alopecia in two donkeys secondary to mutual hair plucking behaviour. Two genetically unrelated, male castrated, 4-year-old Cotentin donkeys living together were presented for a 2-year history of alopecic, mainly nummular, nonpruritic lesions developing on the back, loin and croup. The general physical examination and behavioural assessment were unremarkable. Trichoscopy, scrapings and cytology were performed. Superficial bacterial infection was diagnosed but a 2-week course of antibacterial treatment showed no improvement. Histopathological examination showed features compatible with traumatic alopecia and consistent with several behavioural causes of alopecia resembling human trichotillomania or acute traction alopecia, canine traction alopecia, feline self-induced alopecia and murine barbering. Separation of the donkeys led to complete long-term remission. Clinical and histopathological findings in our case share lots of similar features with the different mechanical traumatic alopecic disorders mentioned above, making it impossible to simply classify the described affection. Whether alopecic lesions resulted from an exclusive behavioural process (either abnormal excessive mutual grooming or other social interactions) or were associated with underlying causes of pruritus is uncertain. Mechanical alopecia secondary to a behavioural process should therefore be suspected in cases of permanent patchy alopecic nummular lesions on donkeys living in groups.     

Alopecia in a black Labrador retriever associated with focal sub‐follicular panniculitis and sebaceous adenitis

A 6‐year‐old entire male black Labrador retriever was presented with nonpruritic multicentric, well‐demarcated alopecia of 12‐weeks duration. Skin biopsies from the margins of alopecic regions showed sebaceous adenitis and sub‐follicular panniculitis. Biopsies from alopecic areas showed severe follicular atrophy with residual fibrous tracts, loss of sebaceous glands and lymphohistiocytic panniculitis beneath individual atrophic hair follicle groups. These features differed from previous reports of pilosebaceous diseases of dogs and appeared to extend the spectrum of inflammatory patterns in presumed immune‐mediated adnexal diseases of this species. During the 12‐month follow‐up, there was partial hair regrowth without treatment but alopecia was permanent in the centre of larger lesions.     

Vaccine-induced ischemic dermatopathy in the dog

Post-rabies vaccination alopecia associated with concurrent multifocal ischemic dermatopathy was identified in three unrelated dogs. All dogs received subcutaneous rabies vaccine dorsally between the scapulae several months prior to observation of the initial area of alopecia at the vaccination site. All three dogs developed multifocal cutaneous disease within 1–5 months after the appearance of the initial skin lesion. Cutaneous lesions were characterized clinically by variable alopecia, crusting, hyperpigmentation, erosions, and ulcers on the pinnal margins, periocular areas, skin overlying boney prominences, tip of the tail, and paw pads. Lingual erosions and ulcers were observed in two dogs. Histopathologic examination of the skin revealed moderate to severe follicular atrophy, hyalinization of collagen, vasculopathy, and cell-poor interface dermatitis and mural folliculitis. Hypovascularity was demonstrated by diminished Factor VIII staining of blood vessels. Nodular accumulations of lymphocytes, plasma cells, and histiocytes in the deep dermis and panniculus also were noted at the rabies vaccination site. An atrophic, ischemic myopathy paralleling the onset of skin disease was identified in two dogs. Histological examination of muscle biopsy specimens demonstrated perifascicular atrophy, perimysial fibrosis, and complement (C) _5b-9 (membrane attack complex) deposition in the microvasculature of both dogs with myopathy. Marked improvement of the skin disease was obtained with oral pentoxifylline and vitamin E.     

FC‐10 Adult‐onset hair loss in Chesapeake Bay retrievers: a clinical and histological study

Hair loss in Chesapeake Bay retrievers has been increasingly recognized by breeders in recent years. Anecdotal reports suggest an endocrine disorder or follicular dysplasia as the underlying cause, but no scientific study has been done to investigate the underlying problem. A prospective study was carried out in collaboration with the American Chesapeake Club. Affected dogs were recruited into the study. Routine dermatological and hormonal (blood and urine) tests, and skin biopsies were performed. Ten dogs (age 1.5–10 years), seven females (two spayed) and three males (two neutered), were included in the study. All dogs had mild or severe hair loss affecting the lateral ventral chest, flanks, rump and thighs. Affected dogs were clinically healthy. Hormonal tests revealed normal thyroid hormone panels, insulin‐like growth factor‐1 levels, and urinary cortisol:creatinine ratios in samples collected for ten consecutive days. In six of 10 dogs, an adrenal hormone panel showed slight or moderate increased values pre‐ and/or post‐ACTH stimulation of cortisol (three of six), 17‐hydroxyprogesterone (five of six), androstenedione (three of six), estradiol (two of six) and progesterone (six of six). The major histopathologic changes resembled canine flank alopecia and follicular dysplasia with pronounced infundibular hyperkeratosis, mild follicular atrophy, and occasional melanin clumping with dystrophic hair shafts. Chesapeake Bay retrievers suffer from a type of hair loss that is likely related to an abnormal production of adrenal sex hormone. Further studies are currently underway to determine if there is a heritable basis for this disease and to evaluate therapeutic options. Funding: University of Pennsylvania.     

Abnormal sebaceous gland differentiation in 10 kittens ('sebaceous gland dysplasia') associated with generalized hypotrichosis and scaling

A rare congenital dermatosis, characterized by progressive hypotrichosis with variable scaling and crusting, occurred in 10 short-haired kittens in North America and Europe. Lesions appeared at between 4 and 12 weeks of age, commencing on the head and becoming generalized. The tail was spared in two kittens. Generalized scaling was mild to moderate, often with prominent follicular casts. Periocular, perioral, pinnal and ear canal crusting was occasionally severe. The skin was thick and wrinkled in two kittens. Histologically, the main lesion was abnormal sebaceous gland morphology. Instead of regular differentiation from basal cells to mature sebocytes, the glands were composed of a haphazard collection of undifferentiated basaloid cells, some partly vacuolated and a few containing eosinophilic globules. Mitotic figures and apoptotic cells were present in an irregularly thickened follicular isthmus. Lymphocytic mural folliculitis and mild sebaceous adenitis were rare. Orthokeratotic hyperkeratosis and follicular casts were present. Hair follicles were of normal density and were mostly in anagen, but some contained malacic hair shafts. Perforating folliculitis, leading to dermal trichogranuloma formation, occurred occasionally. Further biopsy samples taken at 2 years and at 3 and 4 years, respectively, from two kittens revealed similar but often more severe sebaceous gland lesions. Hair follicles were smaller, with many in telogen. The young age of onset suggests a genetic defect interfering with sebaceous and, possibly, follicular development. These lesions are discussed with reference to studies of mouse mutants in which genetic defects in sebaceous differentiation cause a similar phenotype of hyperkeratosis and progressive alopecia.     

Black-hair follicular dysplasia in a New Zealand Huntaway dog

CASE HISTORY: A 6-year-old intact male New Zealand Huntaway dog had slowly progressive alopecia that was first observed at 12 weeks of age.

CLINICAL FINDINGS: Patchy alopecia was confined to the black-haired areas of the body, and was most evident on the head and dorsum of the body; tan-haired areas of skin appeared normal. Histological examination of black-haired skin revealed distended melanocytes and large aggregates of melanin within, and surrounding, the hair follicles and the epidermis. Macrophages distended with melanin were also visible within the perifollicular and superficial dermis, and follicular lumina were often plugged by keratin that contained aggregates of melanin. The follicles were dysplastic and few hair shafts were visible emerging from follicular infundibula within the sections.

DIAGNOSIS: The clinical and histological findings were consistent with black-hair follicular dysplasia (BHFD).

CLINICAL RELEVANCE: This is the first report of BHFD in a dog in New Zealand, and is the first report in a Huntaway. The most significant effect of BHFD is a predisposition to follicular plugging and secondary bacterial skin infections. Due to the hereditary nature of the follicular dysplasias, breeding from affected dogs should be discouraged. Histological examination of the skin is required to differentiate between the different follicular dysplasias as well as differentiating between follicular dysplasia and follicular atrophy due to endocrinopathy.     

Black hair follicular dysplasia in Large Münsterländer dogs: clinical, histological and ultrastructural features

Four Large Münsterländer cross‐bred dogs affected with black hair follicular dysplasia (BHFD) and one unaffected control littermate were observed, and skin was sampled weekly over the first 19 weeks of life. Affected dogs were born with silvery grey hair, a consequence of melanin clumping in the hair shafts. Hair bulb melanocytes were densely pigmented, and contained abundant stage IV melanosomes but adjacent matrix keratinocytes lacked melanosomes. Melanin clumping was not prominent in epidermal melanocytes in the haired skin but occurred in the foot pads. Follicular changes progressed from bulbar clumping, clumping in the isthmus/infundibulum and finally to dysplastic hair shafts. Alopecia developed progressively in pigmented areas. Silver‐grey hair, melanin clumping, accumulation of stage IV melanosomes within melanocytes and insufficient melanin transfer to adjacent keratinocytes are also classic features of human Griscelli syndrome. The underlying cause in Griscelli syndrome is a defect of melanocytic intracellular transport proteins leading to inadequate and disorganized melanosome transfer to keratinocytes with resultant melanin clumping. In view of the correlation in the phenotype, histology and ultrastructure between both disorders, a defect in intracellular melanosome transport is postulated as the pathogenic mechanism in BHFD.