NON-PRURITIC ALOPECIA IN THE DOG- A CASE BASED REVIEW Alison Flynn-Lurie Miami Veterinary Specialists

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1 NON-PRURITIC ALOPECIA IN THE DOG- A CASE BASED REVIEW Alison Flynn-Lurie Miami Veterinary Specialists Alopecia is a common clinical finding in the dog. Alopecia is most commonly associated with pruritus due to allergic skin disease and bacterial/yeast folliculitis. Non-pruritic alopecia however, is a less common presentation. The history should help you to determine if the alopecia is congenital or acquired (was the pet born bald)? While your exam allows you to categorize the alopecia as multifocal, diffuse or symmetrical. The set of differential diagnoses will vary with each presentation- Acquired focal/multifocal: post traumatic vs folliculitis induced (bacteria, demodex, dermatophytosis) should be ruled out. If neither are the cause of the alopecia, skin biopsies are needed Acquired diffuse/symmetrical: post traumatic vs folliculitis induced (bacteria, demodex, dermatophytosis) should be ruled out. Does the pet have systemic signs of illness that may suggest an endocrinopath? If there are no constitutional signs present, skin biopsies are indicated, otherwise blood work, urinalysis and hormone analysis are indicated. CASE 1: 4 year old, male neutered, English Bulldog Presenting complaint: hair loss First noted 4 weeks ago Seemed abrupt Area involved is slowly enlarging Non-pruritic No recent admin of drug or vaccine No stressful events or illness Exam Bilaterally symmetric, annular alopecia of lateral TL region Borders of the alopecia are well demarcated Skin is hyper-pigmented but otherwise normal Dog is BARH with normal vitals Problems: 1. Non-pruritic alopecia 2. Hyperpigmentation

2 Differential diagnoses: Allergic: food allergy (approximately 10% of food allergic dogs present as recurring, non-pruritic bacterial folliculitis Infectious : bacterial folliculitis, Dermatophytosis, Malassezia, Leishmania Parasitic: demodex Misc: follicular dysplasia, pattern baldness, cyclic flank alopecia Endocrine: Hyperadrenocorticism, hypothyroidism, Alopecia X Immune mediated: sebaceous adenitis, pseudopalade, alopecia areata. Others are unlikelythese are associated with acrusts, ulceration etc and variable pruritus (pemphigus foliaceous, pemphigus vulgaris, systemic lupus erythematosus, Discoid lupus erythematosis, Iatrogenic: post clipping alopecia, anagen/telogen defluxion Neoplasia: unlikely The differential short list: Alopecia: Bacterial folliculitis Dermatophytosis Demodex Cyclic flank alopecia Endocrine: hyperadrenococrticism, hypothyroid, alopecia x Hyperpigmentation: Post inflammatory: allergic, parasitic (demodex), infectious, immune mediated Endocrine:hyperadre nococrticism, hypothyroid, alopecia X Diagnostic tests First line: Tape cytology Trichogram, DTM Deep skin scrape for Demodex Second line: Biopsy for histopathology: medusoid follicular morphology and follicular hyperkeratosis.

3 Third line?: ACTH stim: Tennesse panel (includes cortisol plus sex hormones) Thyroid panel: T4 by ED + TSH Answer: Seasonal or cyclic Flank Alopecia Key points: Also called Canine recurrent flank alopecia is a type of follicular dysplasia Seen most commonly in Boxers, English Bulldogs and Airedale terriers, is linked to photoperiod Lesions are well demarcated and hyperpigmented Most likely hair will re-grow in 3-8 months May fall out again in subsequent seasons- may or may not re-grow if recurs Cosmetic Unpredictable course, although spontaneous re-growth and later loss is typical Rx- Benign neglect, or oral melatonin 3-6 mg PO BID may be therapeutic and preventative Give before or shortly after onset of alopecia CASE 2 7 year old, MN, toy poodle Complaint: recent hair loss No recent vaccines or medications Non-pruritic, no prior history of skin problems Systemically healthy (no PU/PD/PP) now although was sick after boarding a couple of months ago (stress colitis) Exam Extensive patchy alopecia, mainly affecting the trunk Skin looks normal Hair epilates easily BAR, vitals within normal limits Diagnostic tests First line:

4 Tape cytology Trichogram, DTM Telogen hairs? Uniform shaft diameter Slightly clubbed, slightly tapered, non-pigmented root Minimal or absent pigmentation Deep skin scrape for demodex Second line: Biopsy for histopathology Third line: ACTH stim including sex hormones: U-Tennesse panel Thyroid panel: free T4 by ED, total T4 + TSH Answer à telogen defluxion Important facts about telogen defluxion: Cause: pregnancy, parturition, lactation, severe stress, systemic illness, febrile episodes, shock, surgery, various drugs Synchronous premature progression from anagen (growth) to telogen (rest) Specific therapy is not required, will re-grow What is the difference between telogen vs anagen defluxion? Telogen: Fever, pregnancy, shock, systemic illness, sx, anesthesia Loss w/in 1-3 months of initial insult Uniform, slightly clubbed hairs, non-pigmented root Hairs usually don t break Spontaneously resolves within 3-4 weeks when inciting cause removed Proposed pathophysiology: severe disease, post-partum, surgery etc trigger a sudden synchronisation of hair follicles in telogen phase. This results in an excessive shedding and alopecia. Shedding is also seen a few weeks later when normal hair growth reoccur (anagen).

5 Anagen: Antimitotic drugs, infectious disease, endocrine, metabolic Sudden hair loss w/in days of insult Hairs are irregular with dysplastic changes Break easily, ragged points Spontaneously resolves when inciting cause removed CASE 3 1 yr, female intact Vizsla Exam: Complaint: Hair loss over head and limbs Non-pruritic No systemic illness, PU/PD/PP/ weight gain Annular areas of alopecia Bilaterally symmetrical Over the head and distal limbs Areas of alopecia are enlarging and some are coalescing Fine scale over head and trunk Problems and differentials: Non-pruritic alopecia Infectious: Staph, dermatophyte, leishmaniasis Endocrine: Hypothyroid, HAC, Hyperestrogenism, Hypogonadism in intact female Parasitic: Demodex Miscellaneous: Follicular dysplasia, Telogen defluxion, Pattern alopecia, Sebaceous adenitis Iatrogenic: Post clipping, Anagen defluxion Seborrhea Infectious: staph, dermatophytosis, lesihmania Keratinization disorder: Primary seborrhea, Ichthyosis Nutritional: Vit A responsive, Zn responsive Metabolic: Hepatocutaneous Endocrine: Hypothyroid, HAC

6 Diagnostic tests Cytology (+) for cocci, but minimal response to antibiotic therapy DTM: negative DSS :negative Trichogram: no significant findings Tennessee panel: hormone levels wnl for intact female Biopsy: Inflammation targeting the sebaceous glands Answer: sebaceous adenitis Therapy may improve coat quality but gland destruction is permanent Topical Anti-seborrheic shampoo Alpha Kerry oil baths or baby oil Propylene glycol spray Systemic Control secondary Staph and Malassezia infections Essential fatty acid s Synthetic retinoids Cyclosporine Spay or neuter genetic CASE 4 8 yr MN Yorkshire Terrier 6 month history of non-pruritic, progressive alopecia Hair loss began on the trunk and progressed to affect the whole dorsum and face Owner believes signs began a few weeks after adopting a stray DLH cat (no skin disease on cat) No signs of systemic illness, PU/PD/PP Heartgard Plus, Frontline plus monthly Prior treatment with prednisone no benefit Exam Regionally diffuse hyperpigmentation

7 Extensive alopecia- trunk, neck, face, sparing limbs Comedomes Problems, differentials 1. Hyperpigmentation: chronic inflammation vs endocrine 2. Alopecia: dermatophytosis (recent exposure to cats), demodex, bacterial folliculitis,hypothyroidism, hyperadrenocorticism, Alopecia X; color dilute alopecia 3. Comedomes: demodex, dermatophyte, staph, endocrine, actinic Diagnostic tests- first line: o Tape cytology: 2+ cocci o Deep skin scrape: negative o DTM: negative Second line: Biopsy: epidermal and follicular atrophy with follicular hyperkeratosisconsistent with endocrine; bacterial folliculitis Third line: Thyroid panel: total T4, free T4 (by equilibrium dialysis) and TSH: total T4 was slightly low but TSH and free T4 were within normal limits Adrenal panel: ACTH stimulation evaluating cortisol and sex hormones: elevated progesterone Answer: Atypical Cushing s syndrome Treatment 1. Antimicrobials for secondary bacterial folliculitis 2. Trilostane: competitive inhibitor of 3 beta-hydroxysteroid dehydrogenase, the enzyme that mediates the conversion of pregnenolone to progesterone and, hence, its end products (cortisol, aldosterone, and androstenedione) in the adrenals. Studies in dogs with hyperadrenoccorticism have shown that trilostane is an effective steroid inhibitor that is associated with minimal side effects. Although it s use for atypical Cushing s disease has been controversial, most dermatologists agree that it effectively controls the dermatological manifestations. Important points

8 Do not treat with trilostane or mitotane for purely cosmetic alopecia Do treat if recurrent bacterial folliculitis, demodex or systemic signs of illness are present Trilostane is preferred to mitotane in dogs that are not polyphagic, because it is challenging for owners to monitor for signs of mitotante toxicity at home without baseline polyphagia. CASE 5 5 yr old long haired Dachsund At 6 months of age hair loss began on caudal aspects of both ears and thighs Over the last 3 years there has been gradual, progressive alopecia of the dorsum Non-pruritic, non-seasonal No other pets in home Owner does not have lesions No recent stress or systemic illness Receives Advantage Multi once a month Prior therapy: fatty acids, steroids, antibiotics- none helped Exam Symmetrical, patchy alopecia- dorsal trunk, neck Symmetrical, complete alopecia- backs of the ears, thighs Diagnostic tests First line: Tape cytology: negative Biopsy for histopathology: mild to moderate epidermal melanosis, orthokeratotic hyperkeratosis, cystic hair follicles and follicular keratosis, variable follicular atrophy and hair dystrophy, prominent clumping of melanin both within and around hair follicles with many melanophages surrounding the base of the follicles and aggregates of melanin in the hair cortex and medulla. Alopecia can be explained, thus, by hypoactive follicles, blockage of follicular orifices and breakage of hair shafts at the site of melanin aggregates. Answer: Color mutant alopecia and suspected pattern baldness Treatment Melatonin 3 mg PO BID, owner thought that there was hair regrowth of the light brown hairs

9 overlying the dorsum after 2 months of therapy. Melatonin non-specifically promotes anagen phase Important points- Pattern baldness Pattern baldness is a non-congenital alopecia has been reported mainly in Dachshunds, but is seen in Chihuahuas, Boston Terriers, greyhounds, miniature pinschers and others. Commonly affected areas include: caudal auricular area, ventral neck, chest, abdomen and caudal thighs Clinical signs begin as early as 6 months when the normal puppy coat is replaced with thinner than normal adult hairs in the affected regions. Those hairs are slowly lost with increasing age. There is no treatment although some claims that melatonin (0.5 mg/kg ql2h) may improve hair growth. Important Points- Color mutant alopecia It is a hereditary tardive alopecia seen in the blue and fawn mutants of Doberman pinschers, miniature pinschers, Irish setters, Dachshunds, chow-chows, poodles, great Danes, whippets, Yorkshire terriers, Chihuahuas and Italian greyhounds. Black hair follicular dysplasia has been reported in bearded collies, Dachshunds, Schipperke, basset hounds, Papillon spaniels, Cocker spaniels, pointers, Gordon setters and mon Clinical signs usually begin to appear a few months after birth and only affectsthe diluted colour areas. The alopecia is typically partial and the hair looks dry and dull. Secondary seborrhoea sicca and bacterial folliculitis are common. Black hair follicular dysplasia affects only the black hair coat areas of partially black dogs. Diagnosis of both conditions is made by assessment of history, physical examination and histopathology which showsthe genetic factors of both diseases are not known but might be identical, since CMA does not seem to be linked to the d allele. The dd genotype could increase the incidence of the disease. Topical antiseborrhoeic therapy is partially effective. Retinoids (acitretin, lmg/kg/day) could be useful. CASE 6 6 month, FS Shetland sheepdog Began having patches of hair loss on the face, elbows and hocks Non-pruritic Gradually progressive No signs of systemic illness although she has been taking longer to finish her food Vaccinated 2 weeks before clinical signs began

10 2 cats, 1 other dog in home, no signs of skin disease in these pets Exam Patchy alopecia face, ears, paws, elbows, hocks The alopeciac areas have a small amount of crust and scale The skin is not erythematous Very slight temporal muscle atrophy Diagnostic tests Tape cytology: 2+ cocci Deep skin scrape: negative for demodex DTM: negative Second line diagnostic tests Biopsy skin and temporal muscle for histopathology: follicular atrophy, perifolliculitis and perifollicular fibrosis, hydropic degeneration of epidermal basal cells with some Civatte bodies and dermo-epidermal clefting. Answer: Dermatomyositis/Ischaemic Dermatopathy Treatment Systemic prednisolone is indicated during acute phases of the disease but it s use should be minimized because the side effects exacerbate the muscle weakness and skin fragility seen in the disease Sunlight-avoidance Oral vitamin E (100 to 400 mg per day) Pentoxifylline (Trental, mg/kg TID) Fatty acid supplementation Key Points about Dermatomyositis This is a hereditary inflammatory skin and muscle disease, seen in Collies, Shetlands, and Beaucerons (and possibly other breeds as well). The mode of inheritance is believed to be autosomal dominant. Transient papules and vesicles may be seen. Erosions, ulcers and crusting are much more common. Alopecia is an early sign of the disease which can begin at 6 months of age. Face, bony prominences, ear pinnae, limbs, fingers, tail tip and pawpads are involved. Muscle lesions (lymphocytic myositis) are discrete with mainly temporal and masseter muscles atrophy. There is marked variation in disease severity and in the degree of muscle involvement

11 Treatment is not necessary in mild cases, the lesions may quickly heal without specific therapy and the disease does not necessarily progress Most cases have progressed (or not) by 1 yr of age Muscle involvement can be debilitating