School of Veterinary Science, University of Queensland, Stafford, QLD, Australia
When an animal first presents the causes of alopecia can be differentiated into 2 broad categories:
Either there is excessive loss (mostly inflammatory causes) or there is inadequate production (noninflammatory causes). The first step is to decide which path of investigation to.
Excessive Loss (Inflammatory)
The cause of the alopecia in these cases is loss, faster than the follicle is able to replace it. There is nothing fundamentally wrong with the follicular unit, either in the signaling for the production of a new shaft or in the production of the shaft.
The hair is being lost due to traumatic removal, via any of the manifestations of itch; i.e., biting, rubbing, rolling, licking, biting, gnawing, etc. In many cases the clients are unaware or unwilling to believe that the animal is traumatizing itself. The easiest method of identifying self-trauma is via a trichogram demonstrating damage to the hair tips.
The types of allergies that may lead to generalised alopecia are
1.1.1. Insect bite hypersensitivity
1.1.3. Food adverse reactions
Whilst most cases of pyoderma present with the classic clinical signs; i.e., papules, pustules, epidermal collarettes, target lesions, some cases will show as a "moth-eaten" patchy alopecia. This is particularly so in the short-coated breeds, many of which will not be particularly itchy.
1.3. Malassezia Dermatitis
Overgrowth with excessive number of Malassezia can lead to an increase in pruritus that leads to traumatic loss of the hair as the animal attempts to relieve the irritation. In addition, some may develop a hypersensitivity to the Malassezia so that even relatively low organism counts may lead to severe pruritus.
Whilst dermatophytes may cause inflammation they should be considered in any cases of annular alopecia. In most instances the hair loss is localised rather than generalised, but more widespread loss may occasionally occur. Investigation may be done via Wood's lamp examination (positive only for Microsporum canis, and then only in up to 50% of cases), trichogram and examination for arthrospores, fungal culture or biopsy.
Skin scrapes should be performed in any area of alopecia. It is a simple technique that will quickly rule the presence of the mites in or out. With a few exceptions, demodicosis is readily identified with a deep skin scrape, performed in areas once the skin has been firmly squeezed and scraped until there is capillary oozing present. There are 3 species identified on the dog: Demodex canis, short-bodied (may be a morphological variant of D. canis) and D. injai (long-bodied). Whilst Demodex (D. canis) infection is traditionally not pruritic, it may become so with secondary bacterial infection. I have found infection with the short-bodied variant to be commonly pruritic and these seem to be controlled quicker and easier than the D. canis.
Infestation is quite pruritic and hair loss is due to traumatic removal.
Inadequate Production (Noninflammatory)
The cause of the alopecia in these cases is inadequate production of a new hair, either because there are abnormalities in morphogenesis (production of a new follicular shaft) or in follicular cycling (signaling for the production of a new shaft).
Hair growth is divided into 4 phases:
Anagen: Active growth where there is an intact inner root sheath (IRS)
Catagen: Still actively growing but the IRS is being actively replaced by tricholemmal cornification
Telogen: IRS completely replaced by tricholemmal cornification. Resting phase of the hair cycle
Exogen: The old telogen shaft is shed and a new anagen hair replaces it.
Noninflammatory alopecia develops because of either an abnormality in the formation of the hair shaft (dysplasia) or a failure of the follicle to continuously cycle.
Dysplasia is a proliferative process that result in a defect in the quantity or quality of the structural proteins (and or lipids) that form a hair shaft. The resultant shaft is abnormal and fragile so that growth is impossible.
It is associated with the following features:
It is a proliferative process, so becomes apparent during anagen not telogen.
Dysplasias are associated with abnormalities of the shaft (so any alopecic disease lacking this is not a dysplasia).
Although dysplasias may become atrophic, atrophic diseases do not become dysplastic (Dunstan 2009).
Alopecia due to hair cycle abnormalities may be caused by anagen inhibition, catagen induction and or prolongation of telogen.
The alopecia is characterized by three basic morphological features that may be present singly or in combination.
Miniaturisation of the hair shafts increase/persistence in haired telogen follicles increase in hairless telogen follicles (Dunstan 2009).
As no new hair growth is occurring, the hair is gradually lost as a result of frictional forces, leading to the characteristic but often nonspecific clinical appearance which characterizes these forms of alopecia.
Hair Cycling Abnormalities
It is known as the "great imitator" due to the wide variety of clinical signs that may be manifested, alopecia is just one of these and is generally manifested as: bilaterally symmetric truncal alopecia (spares extremities) - hypotrichosis in frictional areas first; large/giant breeds lose it on lateral surface of extremities; in advanced cases, a loss of all but head and distal extremities; dull, dry, brittle, easily removed haircoat; fails to regrow post clipping.
Hypothyroid dogs normally present with a gamut of clinical signs and because of this and the fact no one test is definitive, a range of tests may be necessary, including haemogram, serum biochemistry, thyroid hormone testing and functional studies.
Cause and Pathogenesis
Iatrogenic, pituitary-dependent hyperadrenocorticoidism (PDH) or adrenal tumour
There are a range of clinical signs affecting different organ systems, but the coat changes include
Coat early, becomes dull, more difficult to groom later hairs lost - hypotrichosis/alopecia. symmetric of trunk, with sparing the head and extremities
Short-coated breeds may appear moth eaten
Failure to regrow shaved area
Tips - due to sun bleaching because hairs not shed
Entire shaft - appears to be mediated by sex hormones
2.3. Sex Hormone Dermatoses
The direct relationship between excessive sex hormones and skin and coat changes are well understood and documented in the overproduction syndromes. In males these include Sertoli cell tumour, Leydig (interstitial cell tumour), and in females granulosa cell tumour and ovarian cysts. These conditions generally respond to desexing. However, in castration responsive dermatosis, oestrogen and testosterone responsive dermatoses and congenital adrenal hyperplasia; the cause and effect relationship is much less clear and remains controversial. It may be that the problem lies not with the serum level of hormone but rather the sensitivity of follicle receptors or may be due to some inherent follicular abnormality.
An oestrogen receptor pathway has been shown to regulate the anagen-telogen transition in mice. Oestradiol inhibits anagen initiation, shortens the anagen period, promotes catagen, and lengthens the duration of the resting phase (Frank 2009).
Hyperandrogenism is not generally associated with alopecia in dogs, intact males do not develop hair growth in the presence of testosterone nor do they lose it in response to testosterone secretion. It has been shown that the hair follicles of dogs lack the ability to convert testosterone to dihydrotesterone (DHT) which is a mechanism by which hair loss occurs in sensitive human males (Frank 2009).
2.4. Nonhormonal Alopecia
3 syndromes recognised:
2.4.1. Pinnal alopecia dachshunds
Male and rarely female dachshunds
Slowly lose hair form pinnae 6–9 m, progresses to complete loss by 8–9 y
Other parts of coat are normal, exposed skin hyperpigments
2.4.2. American water spaniels and Portuguese water dogs
Hair loss noted at ~ 6 m restricted to ventral neck, caudomedial thighs and tail
2.4.3. Primarily dachshunds, also recognized in Boston terriers, Chihuahua, whippets, Manchester terriers, greyhounds
Almost exclusively in females
6 m, hair loss from postauricular area, along ventral neck and entire ventrum, caudomedial thighs
Close inspection - multiple fine hairs still present
(DDx oestrogen responsive - this develops later 2–4 y and leaves no residual hairs)
1. Colour dilution (mutant) alopecia
2. Cyclic flank alopecia
3. Follicular dysplasia of Siberian Husky and other breeds
4. Black hair follicular dysplasia
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2. Feldman EC, Nelson RW. Canine and Feline Endocrinology and Reproduction. 2nd ed. Philadelphia, PA: WB Saunders; 1996.
3. Frank L. Of hormones and hair - hormonal mechanisms of canine alopecia. In: 24th Proceeding from the North American Veterinary Dermatology Forum; 2009; Savannah, GA.
4. Scott, Miller, Griffin, eds. Muller and Kirk's Small Animal Dermatology. 5th ed. Philadelphia, PA: WB Saunders; 1995.
5. Schmitzel LP, Lothrop CD, Rosenkrantz WS. Congenital adrenal hyperplasia like syndrome. In: Kirk's Current Veterinary Therapy XIII. Philadelphia, PA: WB Saunders; 1995:600–604.