Alopecia Flashcards
- Where does the hair bulb sit?
- Glands associated with hairs?
- Muscle associated with hairs?
- 3 main stages of hair cycle?
- Deep in the dermis.
- Sweat and sebaceous glands.
- Erector pili muscles - helps hairs stand up on end.
- Anagen = active growth.
- Catagen = involution of the hair shaft.
- Telogen = no growth – hair retained until anagen initiated.
*Length of phases depends on breeds and adaptations.
- Anagen = active growth.
Hair growth basics.
Keratinocytes sit in matrix of hair bulb and form hair shafts.
Differentiation produces hair shaft and inner root shaft.
Process of epidermopoiesis and keratogenesis similar to surface epidermis.
Molecules collectively known as “morphogens” control development of hair follicle and are synthesised by:
- tissue cells adjacent to the follicle.
- cells elsewhere in the body.
– transported to the follicle.
–> e.g. sex hormones (such as oestrogen), thyroid hormones, glucocorticoids.
3 main mechanisms of alopecia.
- Destruction or distortion of normally growing hair follicles and shafts.
- Abnormalities of hair cycle (causing atrophy of hair follicles and regression of hair growth).
- Abnormalities of hair follicle and shaft development (causing structural defects, hair fragility and failure of normal growth of hair).
Causes of destruction or distortion of normally growing hair follicles and hair shafts.
Trauma - over-grooming, traction, collars.
Folliculitis - common.
- bacterial (staphylococci).
- dermatophytosis.
- demodicosis.
Inflammatory - bystander damage.
- vascular diseases.
- sebaceous adenitis.
- neoplasia.
- Causes of abnormalities of the hair growth cycle.
- Causes of abnormalities of hair follicle and hair shaft development.
- Endocrinopathies e.g. hypothyroidism, hyperadrenocorticism, hyperoestrogenism.
- Follicle dysplasia / dystrophy.
Can be associated w/ coat colour or type.
Bacterial folliculitis.
Common.
Secondary to an underlying disease process e.g. atopic dermatitis.
Pustules e.g. atopic dermatitis.
Small areas of alopecia - ‘moth-eaten coat’.
Dermatophytosis (ringworm).
Fungal infection.
Not commensal so finding abnormal, but can get carriage of them on the coat depending on lifestyle.
Highly contagious and zoonotic.
Most interested in Trichophytom mentagrophytes (can be caught by hunting rodents) and Microsporum canis species.
Dermatophytosis pathogenesis.
Fungal arthrospores need to adhere to skin (keratinocytes).
- microtrauma e.g. clipping, self trauma.
Invasion of superficial layers of the skin through production of enzymes such as proteases. - breakdown of keratinocytes.
Infection by contact with infected animals, contaminated hair and scale in the environment.
Incubation period may vary from 1-3w.
Dermatophytosis clinical signs.
“The great pretender” - so many potential kinds of presentation.
Alopecia and scale with central heating.
Pruritis varies.
More unusually: onychomycosis (rare), granulomas (rare), pustular form that resembles bacterial pyoderma or pemphigus foliaceus (rare).
Dermatophytosis in Persian cats.
Can see severe, chronic and generalised infections.
Do not mount sufficient immune response
- unsure as to why.
Can be difficult to treat
Trichophyton infection in terriers.
Lesions may be more inflammatory and pruritic. So can be harder to diagnose.
Dx of dermatophytosis.
Samples initially examined under microscope for identification of echothrix arthroconida spores.
Mainstay = culture of hair and scale.
- samples collected by:
– brushing affected areas (Mackenzie brush).
–> sterile brush, toothbrush or even carpet.
– plucking - can be uncomfortable.
– (scraping).
Fungal culture at a commercial lab. - may need to gently pat area clean with alcohol to reduce surface contamination (LA).
Skin biopsies - fungal culture and histopathology.
PCR quick but v sensitive - need to correlate with clinical signs and confirm w/ culture.
- can be useful to rule out.
Patient-side woods lamp exam.
- dark room, adjust eyes, use lamp for several mins to allow lesions to fluoresce, only useful for M. canis isolates, may help identify hairs for culture, ‘apple-green’.
In-clinic test medium - need to fully identify culture growth w/ microscopy!
- M. canis macronidoa and associated culture characteristics on Sabourad’s medium.
- False positives with colour change alone.
Therapy for dermatophytosis?
Self-limiting disease in healthy animals, but need treating as highly contagious and zoonotic.
Treatment helps to shorten the course of the disease, limiting spread.
Topical therapy reduces environmental contamination. - infection may spread up to 6cm from obvious lesions.
- reduces exposure risk to other animals.
- reduces risk of false positive culture when monitoring response to treatment.
Clipping controversial measure - may reduce environmental and host load but may spread disease on the affected animal.
Dermatophytosis - topical therapy.
Shampoos e.g. Malaseb (chlorhexidine and miconazole) - shown to help decontamination of environment w/ M. canis infection in cats.
Dips or rinses e.g. Enilconazole (Imaverol), lime sulphur (may be unpleasant).
Wash twice daily - needs 10 mins contact time before rinsing.
Dermatophytosis - systemic therapy.
Eliminates infection from within hair follicle.
Itraconazole - licensed in cats (Itrafungol), not dogs.
- treat 7d on, 7d off fir 2-3 cycles.
- suspension for kittens and cats.
- dose 5mg/kg/day, similar for dogs.
Ketoconazole licensed in dogs - more potential for adverse effects.
- 10mg/kg.
Itraconazole (non-compounded) and terbinafine are the most effective and safe treatments for dermatophytosis. - cascade!
