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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Alopecia is characterized by an absolute decrease in the number of hairs per given area of body surface or hairs that are shorter than normal even though their number is within normal limits. Simply stated, it is a loss or lack of the hair from skin areas where it is normally present
  • Alopecia may be congenital or acquired
  • Congenital alopecia is rare in horses and represents changes in hair follicle quantity or quality
  • Common etiologies of acquired alopecia are adnexal destruction or atrophy secondary to infection, physical trauma, immune-mediated reactions, nutritional supplements and deficiencies, toxicities, physiologic stressors, hypersensitivities, neoplasia, and various miscellaneous causes. Acquired alopecia can be subdivided into infectious and noninfectious causes

Pathophysiology!!navigator!!

  • Acquired alopecia represents a disruption in the growth of the hair follicle with or without damage to the hair bulb, follicular wall, and/or hair shaft. The animal is born with a normal hair coat, has or had normal hair follicles at one time, and is or was capable of producing structurally normal hairs
  • Congenital alopecia is the result of abnormal morphogenesis or lack of adnexal structures (therefore hair) in regions of the body where they normally are expected. Animals with congenital hypotrichosis may be born with varying degrees of hypotrichosis or a complete haircoat; however, if born with a complete haircoat a rapid onset of progressive permanent alopecia within the first few months of life ensues

Systems Affected!!navigator!!

Skin/exocrine

Genetics!!navigator!!

Congenital alopecia does not necessarily imply a genetic basis, although in most cases the disease is based on genetic abnormalities and thus is hereditary. The exact mode of inheritance is unknown.

Incidence/Prevalence!!navigator!!

True incidence is unknown.

Geographic Distribution!!navigator!!

Presumably worldwide.

Signalment!!navigator!!

  • Congenital hypotrichosis has been documented in certain Arabian lines and a blue roan Percheron
  • Appaloosas with foundation bloodlines have hair dystrophy/thinning of the long mane and tail hair
  • Acquired alopecia can occur in all breeds
  • Appaloosas and Quarter Horses are predisposed to alopecia areata
  • Both sexes are affected equally

Signs!!navigator!!

General Comments

  • May be an acute onset or slowly progressive
  • Multifocal patches of circular alopecia are most commonly associated with bacterial folliculitis, dermatophytosis, or dermatophilosis
  • Large diffuse areas of alopecia may indicate an immune-mediated etiology or congenital abnormality
  • Congenital hypotrichosis may be regional, multifocal, or generalized. It might become clinically apparent only weeks after birth and usually does not continually progress with age

Causes!!navigator!!

  • Noncicatricial alopecia (nonscarring causes)
    • Mild to moderate inflammation of the hair follicle (folliculitis and furunculosis)
    • Defects in the hair shaft
    • Hair follicle dystrophies
    • Altered hair follicle function
    • Trauma (self-induced from pruritus)
  • Cicatricial alopecia (scarring causes)
    • Physical, chemical, or thermal injury
    • Severe furunculosis
    • Neoplasia
    • Severe inflammatory disease such as in cutaneous onchocerciasis

Congenital Causes

  • Congenital hypothyroidism may be a cause of congenital hypotrichosis and alopecia
  • Trichorrhexis nodosa is a hair shaft defect that may be hereditary or acquired
  • Congenital hypotrichosis
  • Epidermolysis bullosa
  • Mane and tail dystrophy
  • Follicular dysgenesis

Acquired Causes

Infectious

  • Bacterial
    • The most common bacterial infection is dermatophilosis. Folliculitis and furunculosis due to Staphylococcus spp. (common) and Corynebacterium pseudotuberculosis (uncommon). Other bacterial causes are abscesses due to Fusiformis and Streptococcus spp.
  • Fungal
    • Dermatophytosis due to Microsporum gypseum, M. equinum or M. canis or Trichophyton equinum var. equinum cause alopecia. Other fungal causes are mycetoma and subcutaneous mycosis such as phycomycosis and pythiosis
    • Brittle tail syndrome caused by the contagious, keratolytic fungus Equicapillimyces hongkongensis is a newly described condition causing weakening and breakage only of the tail hairs
    • Piedra is a rare fungal infection caused by Trichosporon beigelii that causes white nodules on the hair shafts that cause breakage of the shafts. The mane, tail, and distal limbs are most commonly affected
  • Parasitic
    • Follicular parasitic infections of the follicle that result in alopecia are rare and include Demodex equi and Pelodera strongyloides. Other more common parasitic infections that cause alopecia are Culicoides, onchocerciasis, lice, ticks, oxyuriasis and mites (Sarcoptes spp., Chorioptes spp., Psoroptes spp., and Trombiculidae)
  • Viral
    • Viral papillomas—congenital, cutaneous, or pinnal

Noninfectious

  • Immune mediated
    • Cell-mediated autoimmune disease directed toward the hair follicle and adnexa
      • Alopecia areata
      • Hair follicle dystrophy—possible variant of alopecia areata
      • Sebaceous adenitis—rare, case reports in 2006 and 2013
    • Drug eruptions
    • Pemphigus foliaceus
    • Systemic lupus erythematosus
    • Sarcoidosis
  • Physical
    • Burns from chemicals, hot, cold, or ropes
    • Scalding from exudate, urine, or feces
    • Tail and mane rubbing as stable vice
  • Neoplasia
    • Sarcoids
    • Squamous cell carcinoma
  • Miscellaneous
    • Symmetrical atrophy of hair follicles secondary to endocrine disorders is extremely rare to nonexistent
    • Anagen and telogen effluvium
    • Anhidrosis
    • Iodism
    • Selenium, mimosine, or mercury toxicities
    • Copper deficiency

Risk Factors!!navigator!!

N/A

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Accurate diagnosis of alopecia requires a careful history and physical examination
  • Key points in the history include recognition of breed predispositions for congenital alopecia; the duration and progression of lesions; the presence or absence of pruritus or evidence of contagion
  • On physical examination, the distribution of lesions should be noted (focal, multifocal, generalized, or symmetrical), and the hairs examined to determine if they are being shed from the hair follicle or broken off. Signs of secondary infections or ectoparasites should be noted. The degree of crusts, scale, and exudate help prioritize the differentials
  • Patchy, localized to multifocal
    • Bacterial folliculitis and furunculosis
    • Dermatophytosis
    • Dermatophilosis
    • Linear alopecia
    • Alopecia areata—results from selective and reversible damage to anagen hair follicles. Initial lesions may be focal or multifocal, well-circumscribed alopecia that progresses to diffuse alopecia. The mane, tail, and face are often involved and hoof dystrophies can occur. The alopecic skin has minimal or no visible inflammation. Prognosis varies, some cases spontaneously resolve, some respond to immunosuppressive doses of steroids, while others have no hair regrowth
  • Generalized, symmetrical, and large patchy multifocal
    • Normal shed—“physiologic telogen effluvium”
    • Telogen effluvium—a reaction pattern characterized by widespread alopecia in response to severe metabolic stress. Serious illness, high fever, pregnancy, and adverse reaction to supplements are all potential inducers of telogen effluvium. Rapid premature cessation of anagen growth leads to abrupt synchronization of the follicular cycle such that hair follicles proceed in unison through catagen and telogen. This leads to hair loss of variable severity when old telogen hairs are forced out by new, synchronous anagen hairs. Hair loss usually occurs within 3–4 weeks after the insult but may occur up to 2 months later. Alopecia resolves spontaneously if the initiating factor is no longer present, and new anagen hairs grow
    • Anagen effluvium—a reaction pattern characterized by shedding during anagen arrest. Severe stresses such as high-dose cytotoxic therapy or infectious or metabolic disease halt anagen hair growth and result in hair loss within days to weeks of the insult. The hairs are lost due to structural weakness or dysplastic changes damaging the hair shaft

CBC/Biochemistry/Urinalysis!!navigator!!

Useful to rule out metabolic causes.

Other Laboratory Tests!!navigator!!

N/A

Imaging!!navigator!!

N/A

Other Diagnostic Procedures!!navigator!!

  • Cytology should be obtained from pustules, papules, erosions, or ulcers. Neutrophilic exudate with intra- and/or extracellular cocci representative of a secondary folliculitis are easily identified if cytology is sampled from ruptured pustules or impression smears made from the underside of crusts or a fresh erosion or ulcer. Impression smears from the surface of lesions often do not show bacteria, but rather numbers of shed keratinocytes
  • Direct hair examination (trichography)—hairs will have either anagen or telogen roots. Telogen hairs have uniform shaft diameters and slightly rough-surfaced, tapered, spear-shaped angular non-pigmented roots. Anagen hairs have rounded, smooth pigmented bulbs that bend. Distal ends of hair shafts may appear fractured from self-induced trauma. No normal animal should have all of its hairs in telogen but rather should have an admixture of anagen and telogen. Anagen defluxion reveals fragmented hair shafts with the absence of roots. Animals with alopecia areata may have short hairs with fractured distal ends and shafts that taper towards the proximal end (exclamation point hairs)
  • Perform skin scrapings to rule out ectoparasites
  • Perform bacterial and dermatophyte test medium cultures to determine bacterial species and susceptibility and/or dermatophyte infections
  • Perform skin biopsies if the tests listed above do not identify or suggest an underlying cause. A biopsy evaluates hair follicles, adnexal structures, inflammation, and anagen/telogen ratios. Biopsies may reveal evidence for bacterial, parasitic, or fungal causes of alopecia but should not be considered as the definitive test for determination of alopecia caused by infectious agents. If cytologic identification reveals evidence of folliculitis, treat the patient with appropriate antimicrobials, parasiticides, or antifungals for a minimum of 3 weeks. If no improvement in the degree of alopecia is noted, obtain a biopsy for histopathology, preferably while the patient is still receiving treatment. Often biopsies submitted from patients with moderate to severe bacterial folliculitis make it difficult to determine and may mask the primary cause of alopecia. Submit biopsies from affected and nonaffected sites
  • Definitive diagnosis of alopecia areata requires histologic confirmation. Multiple biopsies need to be collected as pathognomonic lesions can be sparse. Biopsy from newly developed areas of alopecia, rather than older lesions

Pathologic Findings!!navigator!!

  • Biopsies of telogen effluvium are misleading, as they will demonstrate most follicles in the active growing (anagen) phase. Often the hair cycle has returned to normal by the time the decision to biopsy has been made
  • Anagen effluvium findings include apoptosis and fragmented cell nuclei in the keratinocytes of the hair matrix of anagen follicles, as well as eosinophilic dysplastic hair shafts within the pilar canal
  • Alopecia areata has 2 major histologic features. The first is hair follicle miniaturization and the second feature is lymphocytic bulbitis. The lymphocytic bulbitis involves anagen follicles and is best found in recently developed areas of alopecia. A lymphocytic mural folliculitis affecting the follicular isthmus is possible. The bulbitis may be very difficult to demonstrate especially in chronic lesions where the inflammation may be nonexistent. Chronic lesions only exhibit small telogen follicles lacking hair shafts that may be somewhat atrophic
  • Histologic findings of alopecia secondary to infectious organisms are covered in the appropriate dermatology sections

Treatment ⬆ ⬇

Outline

TREATMENT

The clinical approach to alopecia is to identify the cause and, if the etiology is something that may benefit from pharmaceutical treatment, then therapy may resolve the clinical signs.

Appropriate Health Care!!navigator!!

Relevance equated to etiology; most require outpatient medical management.

Nursing Care!!navigator!!

Relevance equated to etiology.

Activity!!navigator!!

Patients with multifocal to generalized hypotrichosis may be more susceptible to hypothermia and solar dermatoses.

Diet!!navigator!!

Telogen effluvium has been associated with the administration of a feed supplement.

Client Education!!navigator!!

Relevance equated to etiology.

Surgical Considerations!!navigator!!

N/A

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Varies with cause
  • Dermatophytosis—lime sulfur or enilconazole, miconazole/chlorhexidine rinses; systemic griseofulvin
  • Dermatophilosis—topical antimicrobial therapy
  • Bacterial folliculitis—systemic and topical antimicrobial therapy
  • Pemphigus foliaceus—immunosuppressive therapy
  • There are no hair growth-promoting pharmaceuticals for horses

Contraindications!!navigator!!

N/A

Precautions!!navigator!!

N/A

Possible Interactions!!navigator!!

None

Alternative Drugs!!navigator!!

None

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Varies with cause.

Prevention/Avoidance!!navigator!!

  • Varies with cause
  • Patients with documented congenital alopecia and their parents should not be used for breeding

Possible Complications!!navigator!!

N/A

Expected Course and Prognosis!!navigator!!

  • Prognosis is based on whether the alopecia is classified as noncicatricial or cicatricial
  • Cicatricial alopecia is characterized by permanent destruction of the hair follicles and regrowth of hair will not occur
  • In noncicatricial alopecia, future hair growth will occur if the causative factors are eliminated or corrected
  • Telogen and post-anagen effluvium resolve upon identification and elimination of cause

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

N/A

Age-Related Factors!!navigator!!

N/A

Zoonotic Potential!!navigator!!

Dermatophytosis and dermatophilosis are zoonotic.

Pregnancy/Fertility/Breeding!!navigator!!

  • Postpartum telogen effluvium is thought to be due to the physiologic stress of pregnancy and lactation
  • Avoid the use of griseofulvin to treat dermatophytosis in pregnant mares
  • Mares that receive iodine-deficient diets give birth to weak or dead foals with no haircoat

Synonyms!!navigator!!

  • Alopecia = hypotrichosis
  • Anagen effluvium = anagen defluxion or defluvium
  • Telogen effluvium = telogen defluxion or defluvium

Suggested Reading ⬆ ⬇

Pascoe RRR, Knottenbelt DC. Manual of Equine Dermatology. London, UKWB Saunders, 1999:68.

Rosychuk R. Noninflammatory, nonpruritic alopecia of horses. Vet Clin North Am Equine Pract 2013;29:629–641.

von Tscharner C, Kunkle GA, Yager JA. Stannard's illustrated equine dermatology notes. Alopecia in the horse—an overview. Vet Dermatol 2000;11:191–203.

Author(s) ⬆

Author: David Senter

Consulting Editor: Gwendolen Lorch

Acknowledgment: The author acknowledges the prior contribution of Gwendolen Lorch.