Difference between revisions of "Alopecia and Hypotrichosis"
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==Introduction== | ==Introduction== | ||
− | Hair growth follows an intrinsic rhythm and is regulated by multiple growth factors, cytokines and local mediators. It is modified by systemic factors and | + | Hair growth follows an intrinsic rhythm and is regulated by multiple growth factors, cytokines and local mediators. It is modified by systemic factors and pineal, pituitary, thyroidal, adrenal and reproductive hormones. |
There is also a seasonal regulation in colour, thickness and length. | There is also a seasonal regulation in colour, thickness and length. | ||
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Its main form is '''acquired''', and the main mechanisms for alopecia are presented below. | Its main form is '''acquired''', and the main mechanisms for alopecia are presented below. | ||
− | ==Traumatic/ | + | ==Traumatic/pruritic alopecia== |
Any pruritic dermatosis will cause alopecia due to the behaviour of the animal who will '''scratch, rub itself on objects, overgroom or bite off hair'''. | Any pruritic dermatosis will cause alopecia due to the behaviour of the animal who will '''scratch, rub itself on objects, overgroom or bite off hair'''. | ||
This is a common cause of bilaterally '''symmetrical alopecia in cats'''. | This is a common cause of bilaterally '''symmetrical alopecia in cats'''. | ||
− | ==Non- | + | ==Non-traumatic== |
− | ===Secondary | + | ===Secondary inflammatory=== |
− | Any marked epidermal or dermal inflammatory disease which does not selectively target the hair follicles can still '''damage adjacent hair follicles''' and lead to alopecia. Examples include | + | Any marked epidermal or dermal inflammatory disease which does not selectively target the hair follicles can still '''damage adjacent hair follicles''' and lead to alopecia. Examples include leishmaniasis or dermal neoplasia. |
Scarring can also lead to alopecia through follicular destruction or displacement. | Scarring can also lead to alopecia through follicular destruction or displacement. | ||
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'''Follicular infections''' include: | '''Follicular infections''' include: | ||
− | '''Parasites''': '' | + | '''Parasites''': ''Demodex'', ''Straelensia'', ''Pelodera'' |
'''Viruses''' | '''Viruses''' | ||
− | '''Bacteria''': ''Staphylococcal'' pyoderma, '' | + | '''Bacteria''': ''Staphylococcal'' pyoderma, ''Dermatophilus congolensis'' |
− | '''Fungi''': | + | '''Fungi''': dermatophitosis (''Microsporum canis, Trichophyton mentagrophytes'') |
− | '''Sterile folliculitis''' includes cases of: | + | '''Sterile folliculitis''' includes cases of: sebaceous adenitis, alopecia areata, idiopathic lymphocytic mural folliculitis, linear alopecia |
===Non-inflammatory=== | ===Non-inflammatory=== | ||
− | These diseases tend to slow of inhibit follicular growth | + | These diseases tend to slow of inhibit follicular growth. |
− | + | On histopathology, there is telogen and catagen growth with very few hairs in anagen. | |
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− | + | There is possible atrophy of the follicular epithelium and adnexae and varying degrees of surface and follicular hyperkeratosis. | |
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− | + | =====Coat colour-linked===== | |
− | + | Colour-dilution alopecia, black hair dysplasia, follicular lipidosis | |
− | + | =====Endocrine-related hair cycle problems===== | |
− | + | Hypothyroidism, hyperadrenocorticism, testicular cell tumours | |
− | + | =====Miscellaneous hair cycle problems===== | |
− | + | Post-clipping alopecia, traction alopecia, pattern alopecia, cyclic flank alopecia, alopecia X, mane and tail dystrophy | |
− | + | =====Ischaemic/atrophic===== | |
− | + | Post-rabies vaccine, dermatomyositis, topical glucocorticoid-induced, paraneoplastic syndrome | |
− | ==Clinical | + | =====Neoplastic===== |
+ | Epitheliotropic lymphoma | ||
+ | |||
+ | =====Nutritional/metabolic/debilitation/toxicosis===== | ||
+ | Iodism, plant toxicoses, selenium, anhidrosis, starvation, chronic hepatic/renal disease | ||
+ | |||
+ | ==Clinical signs== | ||
The signs can be '''obvious or subtle''', depending on the disease. Congenital hair loss is often symmetrical and not accompanied by any inflammatory changes. | The signs can be '''obvious or subtle''', depending on the disease. Congenital hair loss is often symmetrical and not accompanied by any inflammatory changes. | ||
In acquired alopecia, the clinical signs are influenced by the cause. The alopecia can be '''localised, multifocal, symmetric or generalised'''. | In acquired alopecia, the clinical signs are influenced by the cause. The alopecia can be '''localised, multifocal, symmetric or generalised'''. | ||
− | Inflammatory changes such as: '''lichenification, hyperpigmentation, erythema, scaling and pruritus''' are common. Some causes of alopecia predispose animals to developing '''secondary skin diseases''' such as bacterial pyoderma or | + | Inflammatory changes such as: '''lichenification, hyperpigmentation, erythema, scaling and pruritus''' are common. Some causes of alopecia predispose animals to developing '''secondary skin diseases''' such as bacterial pyoderma or seborrhoea. |
In '''endocrine disorders''', the pattern of loss is symmetrical, often in wear areas first, and pruritus is not generally present. | In '''endocrine disorders''', the pattern of loss is symmetrical, often in wear areas first, and pruritus is not generally present. | ||
− | == | + | ==Diagnostic tests== |
A thorough history and physical examination are very important. | A thorough history and physical examination are very important. | ||
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Diagnostic tests: | Diagnostic tests: | ||
− | + | ||
− | + | '''Skin scrapings''': for ectoparasites (especially ''Demodex'') | |
− | + | ||
− | + | '''Hair brushings''': for fleas, mites, lice | |
− | + | ||
− | + | '''Tape strips''' for bacterial or yeast infections | |
+ | |||
+ | '''Fungal culture''' for evidence of ringworm | ||
+ | |||
+ | '''Skin biopsy''': if the other tests are normal. The hair follicles and structures can be examined and any inflammatory patterns can be noted. | ||
+ | |||
+ | '''Haematology and biochemistry''' are helpful in the diagnosis of endocrinopathies, and specific '''endocrine function tests''' should be performed if such a disease is suspected. | ||
==Treatment== | ==Treatment== | ||
This will depend on the underlying cause of the alopecia. | This will depend on the underlying cause of the alopecia. | ||
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==References== | ==References== | ||
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Kahn, C. (2005) '''Merck Veterinary Manual''' ''Merck and Co'' | Kahn, C. (2005) '''Merck Veterinary Manual''' ''Merck and Co'' | ||
+ | [[Category:To Do - Helen]] | ||
+ | [[Category:To Do - Review]] | ||
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[[Category:Integumentary System - Developmental Pathology]] | [[Category:Integumentary System - Developmental Pathology]] |
Revision as of 07:18, 28 July 2011
Introduction
Hair growth follows an intrinsic rhythm and is regulated by multiple growth factors, cytokines and local mediators. It is modified by systemic factors and pineal, pituitary, thyroidal, adrenal and reproductive hormones.
There is also a seasonal regulation in colour, thickness and length.
Alopecia refers to the absence of hair where it is normally present, or the loss of hair.
Hypotrichosis is a congenital alopecia, such as that seen in certain breeds with a hairless trait: Mexican Hairless and Chinese Crested dog and Sphinx cat.
Alopecia can be congenital, such as those breeds and cases of ectodermal dysplasia and hair shaft defects.
Its main form is acquired, and the main mechanisms for alopecia are presented below.
Traumatic/pruritic alopecia
Any pruritic dermatosis will cause alopecia due to the behaviour of the animal who will scratch, rub itself on objects, overgroom or bite off hair.
This is a common cause of bilaterally symmetrical alopecia in cats.
Non-traumatic
Secondary inflammatory
Any marked epidermal or dermal inflammatory disease which does not selectively target the hair follicles can still damage adjacent hair follicles and lead to alopecia. Examples include leishmaniasis or dermal neoplasia.
Scarring can also lead to alopecia through follicular destruction or displacement.
Folliculitis
Inflammation targeting the hair follicle will lead to destruction or damage of the hair shaft.
Follicular infections include:
Parasites: Demodex, Straelensia, Pelodera
Viruses
Bacteria: Staphylococcal pyoderma, Dermatophilus congolensis
Fungi: dermatophitosis (Microsporum canis, Trichophyton mentagrophytes)
Sterile folliculitis includes cases of: sebaceous adenitis, alopecia areata, idiopathic lymphocytic mural folliculitis, linear alopecia
Non-inflammatory
These diseases tend to slow of inhibit follicular growth.
On histopathology, there is telogen and catagen growth with very few hairs in anagen.
There is possible atrophy of the follicular epithelium and adnexae and varying degrees of surface and follicular hyperkeratosis.
Coat colour-linked
Colour-dilution alopecia, black hair dysplasia, follicular lipidosis
Hypothyroidism, hyperadrenocorticism, testicular cell tumours
Miscellaneous hair cycle problems
Post-clipping alopecia, traction alopecia, pattern alopecia, cyclic flank alopecia, alopecia X, mane and tail dystrophy
Ischaemic/atrophic
Post-rabies vaccine, dermatomyositis, topical glucocorticoid-induced, paraneoplastic syndrome
Neoplastic
Epitheliotropic lymphoma
Nutritional/metabolic/debilitation/toxicosis
Iodism, plant toxicoses, selenium, anhidrosis, starvation, chronic hepatic/renal disease
Clinical signs
The signs can be obvious or subtle, depending on the disease. Congenital hair loss is often symmetrical and not accompanied by any inflammatory changes.
In acquired alopecia, the clinical signs are influenced by the cause. The alopecia can be localised, multifocal, symmetric or generalised.
Inflammatory changes such as: lichenification, hyperpigmentation, erythema, scaling and pruritus are common. Some causes of alopecia predispose animals to developing secondary skin diseases such as bacterial pyoderma or seborrhoea.
In endocrine disorders, the pattern of loss is symmetrical, often in wear areas first, and pruritus is not generally present.
Diagnostic tests
A thorough history and physical examination are very important.
Key points in the history: breed (any congenital predispositions), duration and progression of lesions, presence of pruritus, evidence of contagion, other non-dermatological problems.
On physical examination: the type and distribution of lesions should be noted.
Hairs should be examined to determine if they are being shed from the follicle or broken off, which suggests pruritus.
Diagnostic tests:
Skin scrapings: for ectoparasites (especially Demodex)
Hair brushings: for fleas, mites, lice
Tape strips for bacterial or yeast infections
Fungal culture for evidence of ringworm
Skin biopsy: if the other tests are normal. The hair follicles and structures can be examined and any inflammatory patterns can be noted.
Haematology and biochemistry are helpful in the diagnosis of endocrinopathies, and specific endocrine function tests should be performed if such a disease is suspected.
Treatment
This will depend on the underlying cause of the alopecia.
References
Gross, T. (2005) Skin diseases of the dog and cat: a clinical and histopathological diagnosis Wiley-Blackwell
Mecklenburg, L. (2009) Hair loss disorders in domestic animals John Wiley and Sons
Kahn, C. (2005) Merck Veterinary Manual Merck and Co