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Canine Miscellaneous Skin Diseases

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									Small and Large Animal Dermatology

    Miscellaneous Skin Diseases




                60
           Canine and Feline Miscellaneous Skin Diseases
                                  Dermatomyositis


   A. General Considerations:

       1. Dermatomyositis is a hereditary inflammatory disease of the skin and muscle.

       2. It is characterized by a scaring alopecia about the face and legs and atrophy of
          the muscles of mastigation.

                                  Important Facts

 Dermatomyositis is a hereditary inflammatory disease of the skin and muscle which is
   characterized by a scaring alopecia about the face and legs and atrophy of the muscles
   of mastigation.


   B. Cause and Pathogenesis:

       1. The etiopathogenesis of dermatomyositis is unknown.

       2. It is familial in Collies and Shetland sheepdogs and breeding studies in Collies
          support an autosomal dominant mode of inheritance with variable
          expressivity.

                                  Important Facts

 The pathogenesis is unknown.

 It is a genetic disorder of dogs transmitted as an autosomal dominant trait with
  variable expressivity.

   C. Clinical Signs:

       1. Breeds: most prevalent in Collies and Shelties, but has also been reported to
          occur in the Welsh corgi, Chow chow, German shepherd and Kuvasz.

       2. Age: lesions usually develop before 6 months of age but can occasionally
          develop in adults.




                                           61
       3. Distribution: face (especially the bridge of the nose, around the eyes and tip of
          the ears), carpal and tarsal areas, digitis and tip of the tail.

       4. Lesions: scaring alopecia, erythema, scaling and mild crusting are the most
          common findings. Vesicles, papules, pustules and ulcers may be found
          occasionally.

       5. The rate of development and progression of lesions is quite variable as they
          often wax and wane and may undergo spontaneous resolution.

       6. Muscle involvement occurs after the development of skin lesions and
          correlates with the severity of the skin lesions.

       7. Muscle involvement is often minimal and limited to temporal and masseter
          atrophy.

       8. Severely affected dogs have difficulty in eating, drinking, swallowing and
          may evidence growth retardation, megaesophagus, lameness, widespread
          muscle atrophy and infertility.

       9. Pruritus and pain are generally not features of the disease.



                                       Important Facts

 The disease is most prevalent in Collies and Shelties.

 Signs usually develop before 6 months of age.

 The most common lesions are alopecia, erythema, scales and crusting with vesicles,
   pustules and ulcers developing less frequently.

 Typical distribution involves the bridge of the nose, around eyes, tip of ears, carpal
   and tarsal areas, digits and tip of the tail.

 Lesions may spontaneously resolve.

 Muscle involvement occurs after the development of skin lesions and correlates with
   the severity of the skin lesions.

 Muscle involvement is often minimal and limited to temporal and masseter atrophy.

 Pruritus and pain are generally not features of the disease.


                                               62
   D. Diagnosis:

       1. Diagnosis is based on breed predilection, history, clinical signs, skin and
          muscle biopsies, and electromyograms (EMGs).

       2. Well-chosen skin biopsies may reveal an interface dermatitis at the
          dermoepidermal junction with vacuolated or necrotic basal cells; atrophic
          follicles are variably noted.

       3. Muscle biopsies tend to show a mixed-cell infiltration with muscle fiber
          degeneration, scarring, and atrophy.

       4. Electromyograms may display fibrillation potentials, positive sharp waves,
          and bizarre high-frequency discharges.

       5. Severely affected dogs may have a non-regenerative anemia, and serum
          creatine levels may be slightly elevated in dogs with myositis.

       6. Serum concentration of IgG and circulating immune complexes (CIC) usually
          are elevated in the face of normal IgA and IgM levels.

       7. Occasionally, Coombs’ and rheumatoid factor tests will be positive but results
          are inconsistent.

       8. Serum antibody titers to calicivirus and other viruses have been detected in
          affected dogs, suggesting the possibility that an infectious agent may
          contribute to the pathogenesis of dermatomyositis.



                                   Important Facts

 Diagnosis is based on history, clinical signs, skin and muscle biopsies and
   electromyograms.

 Anemia may develop in severe cases.

 Serum levels of IgG and immune complexes usually are elevated and the degree of
   elevation correlates positively with the severity of the disease.

 Coombs’ and rheumatoid factor tests are occasionally positive.




                                            63
   E. Treatment:

       1. As lesions of dermatomyositis can wax and wane it is difficult to determine
          the effectiveness of any particular treatment.

       2. No treatment may be needed for cases with minimal lesions as they may
          spontaneously resolve in many cases.

       3. Oral vitamin E (200 to 800 IU/day) or marine lipid supplements may provide
          some improvement for skin lesions but not muscle lesions.

       4. Prednisolone (1 mg/kg/day) have been used in more severe cases.

       5. Pentoxifylline (Trental) has been used for the management of severe cases. A
          dosage of 5 to 10 mg/kg,3 times a day, has been proposed. It must be given
          with food to prevent vomiting. There is a lag period of 1 to 2 months before
          clinical benefits are noted.

       6. Affected animals should not be used for breeding regardless of the severity of
          clinical signs.



                                   Important Facts

 Mild cases can resolve spontaneously.

 Therapy is only symptomatic and can include Vitamin E, marine lipid supplements,
   corticosteroids and pentoxifylline.

 The condition often follows its own course when the animal reaches maturity, with
   some animals getting progressively better and others getting progressively worse.

 Do not breed affected animals.




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                                       References

1. Nesbitt G.E. & Ackerman L.J. Miscellaneous Canine Skin Diseases. In: Canine and
   Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 314-353.




                                 Learning Objectives

1. Know! Dermatomyositis is a familial inflammatory condition involving the skin and
   muscle.

2. Know! It is most often seen in Collies and Shelties but it has also been described in
   Welsh corgi, Chow chow, German shepherd and Kuvasz.

3. Know! Breeding studies in Collies support an autosomal dominant mode of
   inheritance with variable expressivity.

4. Know! Signs usually occur before 6 months of age but, it has been reported in adult
   animals. Alopecia, erythema, scales and crusting are typically present on the bridge
   of the nose, around the eyes, tip of the ears, tarsal and carpal areas, digits and tip of
   the tail. Rarely, vesicles, pustules and ulcerations may also occur.

5. Remember! Muscle involvement occurs after the development of skin lesions and the
   severity of muscle lesions correlates positively with the severity of the skin lesions.
   Muscle lesions are usually limited to temporal and masseter atrophy.

6. Know! Severely affected dogs have difficulty in eating, drinking, swallowing and
   may evidence growth retardation, megaesophagus, lameness, widespread muscle
   atrophy and infertility.

7. Remember! Pruritus is usually not present.

8. How do you diagnose dermatomyositis? Would you consider including a Combs’
   test, rheumatoid factor test, serum IgG and immune complex concentrations in your
   diagnostic plan?

9. How do you manage dermatomyositis?




                                             65
                   Canine Miscellaneous Skin Diseases
                          Uveodermatologic Syndrome


   A. General Considerations:

       1. Canine uveodermatologic syndrome is a rare condition that is thought to
          represent an autoimmune attack against melanocytes.

       2. In humans, a cell-mediated hypersensitivity reaction against melanin has been
          demonstrated and similar mechanisms have been proposed for the dog.

       3. Heavily pigmented tissues such as the uveal tract, skin, and mucous
          membranes are primarily involved.

       4. Unlike the condition in people, auditory and meningeal abnormalities have not
          been documented in the dog.


                                  Important Facts

 Canine uveodermatologic syndrome is a rare condition that is thought to represent an
  autoimmune attack against melanocytes.

 Heavily pigmented tissues such as the uveal tract, skin, and mucous membranes are
  primarily involved.



   B. Clinical Signs:

       1. Breeds at increased risk include the Akita, Samoyed, Siberian husky, Alaskan
          malamute, and Chow chow. The condition has also been reported in the
          Shetland sheepdog, white Sherman shepherd, Irish setter, Ainu, and Shiba.

       2. Ocular signs usually precede skin lesions and consist initially of bilateral
          uveitis to severe, granulomatous panuveitis. Later retinal detachment,
          posterior synechiae with secondary glaucoma, and cataracts may develop.

       3. Skin and hair abnormalities consist of depigmentation that often involves the
          eyelids, nasal planum, lips, scrotum, vulva, and pads of the feet. Erythema,
          ulceration and crusting of the skin in the depigmented areas are also present
          signs.

       4. Pruritus may be present.



                                           66
       5. Lymphadenopathy is commonly seen.

       6. Initial onset of lesions has been noted in animals ranging from 13 months to 6
          years of age. Most affected animals are young adults.


                                   Important Facts

 Breeds at increased risk include the Akita, Samoyed, Siberian husky, Alaskan
  malamute, and Chow chow.

 Ocular signs usually precede skin lesions and consist initially of bilateral uveitis to
  severe, granulomatous panuveitis.

 Retinal detachment, posterior synechiae, glaucoma, cataracts and acute blindness
  may occur if the inflammatory process is not arrested.

 Depigmentation, erythema, ulceration and crusting involving the eyelids, nasal
  planum, lips, scrotum, vulva and footpads are the cutaneous signs.

 Pruritus is variable, but regional lymphadenopathy is common.

 Most affected animals are young adults.


   C. Diagnosis:

       1. Diagnosis is based on history, physical examination and skin biopsy findings.

       2. Histopathologic findings, early in the process, reveal a pronounced
          inflammatory reaction of histiocytic cells at the dermoepidermal junction and
          decreased epidermal melanin and melanocytes.


                                   Important Facts

 The diagnosis of uveodermatologic syndrome is based on history, physical
   examination and skin biopsy findings.

 Skin biopsy results reveal a pronounced inflammatory reaction of histiocytic cells at
   the dermoepidermal junction and decreased epidermal melanin and melanocytes.




                                            67
   D. Treatment:

       1. Topical or subconjunctival corticosteroids and topical cycloplegics are
          beneficial in patients with anterior uveitis.

       2. Oral prednisolone at the dose of 1 to 2 mg/kg daily is recommended until
          remission. Long term alternate day therapy is often needed to maintain
          remission.

       3. Azathioprine at the dose of 2.2 mg/kg q 24 h PO with tapering after clinical
          resolution to 0.5 mg/kg q 24h PO may allow for a reduction of the
          corticosteroid dose.

       4. In some patients it may be possible to discontinue the corticosteroids and rely
          on azathioprine alone.



                                     Important Facts

 Topical or subconjunctival corticosteroids and topical cycloplegics are beneficial in
   patients with anterior uveitis.

 Oral prednisolone and/or azathioprine will be required to treat the severe
   inflammatory process associated with this condition.

 Long term alternate day therapy is often needed to maintain remission.

 Some dogs can be maintained on azathioprine alone.




                                           68
                                      References


1. Nesbitt G.E. & Ackerman L.J. Canine Immune-Mediated Skin Diseases. In: Canine
   and Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 140-161.




                                Learning Objectives



1. Know! Canine uveodermatologic syndrome is rare and it is believed to be associated
   with an autoimmune attack against melanin and melanocytes. Therefore, it makes
   sense that the heavily pigmented tissues such as the uveal tract, skin, and mucous
   membranes are primarily involved.

2. Know! Akita, Samoyed, Siberian husky, Alaskan malamute, and Chow chow are the
   breeds at increased risk to develop the disease.

3. Know! Most animals are in young adulthood when first affected but, they can be as
   old as 6 years of age.

4. Know! Ocular signs are usually present first and include bilateral uveitis to severe,
   granulomatous panuveitis. Later retinal detachment, posterior synechiae with
   secondary glaucoma, and cataracts may develop. Acute blindness may develop if the
   inflammatory process is not arrested.

5. Know! The cutaneous signs are characterized by depigmentation, erythema,
   ulceration and crusting involving the eyelids, nasal planum, lips, scrotum, vulva and
   footpads.

6. Remember! Pruritus is rarely present but, lymphadenopathy is a common finding.

7. How do you diagnose this condition?

8. How do you manage this disease?




                                           69
                  Canine Miscellaneous Skin Diseases
             Idiopathic Sterile Granuloma and Pyogranuloma


   A. General Considerations:

      1. Idiopathic sterile pyogranuloma is a non-microbial pyogranulomatous process
         in dogs.

      2. It is presumed to be immune-mediated, based on histopathologic presentation
         and response to corticosteroid therapy.



                                  Important Facts

 Idiopathic sterile pyogranuloma is presumed to be immune-mediated, based on
   histopathologic presentation and response to corticosteroid therapy.


   B. Clinical Signs:

      1. Great Danes, St. Bernards, Newfoundlands, Boxers, Dachshunds, Golden
         retrievers, Chinese shar-peis, Pit bull terriers, and English bulldogs appear to
         be predisposed.

      2. No sex or age predilection has been reported.

      3. Lesions are usually multiple and typically affect the head (especially the
         bridge of the nose, the muzzle, and the periocular region), the pinnae and the
         paws.

      4. Lesions are characterized by firm, painless, nonpruritic, dermal plaques and
         nodules.

      5. The lesions may become alopecic, ulcerated, and secondarily infected,
         especially the ones on the paws.

      6. Animals are usually otherwise healthy.




                                           70
                                   Important Facts


 Firm, painless, nonpruritic, dermal plaques and nodules are usually multiple and
   typically affect the head, the pinnae and the paws.

 The lesions may become alopecic, ulcerated, and secondarily infected, especially the
   ones on the paws.

 Animals are usually otherwise healthy.


   C. Diagnosis:

       1. Diagnosis is based on history, clinical signs, cultures, and biopsy.

       2. The histopathologic findings reveal a nodular to diffuse pyogranulomatous
          dermatitis for which no cause can be determined.

       3. Cultures are best made from tissue taken by aseptic surgical biopsy techniques
          and they are negative.

       4. Differential diagnosis includes other granulomatous and pyogranulomatous
          (bacterial, mycotic, foreign body) and neoplastic disorders.


                                   Important Facts

 Diagnosis is based on history, clinical signs, cultures, and biopsy.

 Cultures are best made from tissue taken by aseptic surgical biopsy techniques and
   they are negative.


   D. Treatment:

       1. Therapy may consist of surgical excision of solitary lesions, if feasible, or of
          systemic corticosteroids if multiple lesions are present or surgery is
          impractical.

       2. Prednisone or prednisolone orally at the dose of 2.2 to 4.4 mg/kg q 24 until
          the lesions have regressed in 7 to 14 days.



                                            71
       3. About 60% of the dogs require prolonged alternate-morning glucocorticoid
          therapy.

       4. Azathioprine (2.2 mg/kg q 24h) may be needed for dogs that are unresponsive
          or become refractory to glucocorticoid therapy. After remission is achieve,
          resume alternate-day therapy.


                                   Important Facts

 Therapy consists of either resection of single lesions if feasible, or treatment with
  immunosuppressive doses of corticosteroids.

 Glucocorticoids often can be administered on alternate days once the condition is in
  complete remission.

 Relapses are common when therapy is interrupted.

 Azathioprine may be needed for dogs that are unresponsive or become refractory to
  glucocorticoid therapy.




                                            72
                                      References


1. Nesbitt G.E. & Ackerman L.J. Canine Immune-Mediated Skin Diseases. In: Canine
   and Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 140-161.

2. Scott, Miller & Griffin. Miscellaneous Skin Diseases. In: Small Animal
   Dermatology. W.B. Saunders, Philadelphia, 1995, pp 902-955.




                                Learning Objectives


1. Know! Idiopathic sterile pyogranuloma is a rare condition presumed to be immune-
   mediated, based on histopathologic presentation and response to corticosteroid
   therapy.

2. Know! Lesions are usually multiple and typically affect the head (especially the
   bridge of the nose, the muzzle, and the periocular region), the pinnae and the paws.
   Lesions are characterized by firm, red, painless, nonpruritic, dermal plaques and
   nodules. Rarely, the lesions can ulcerate and become secondarily infected.

3. Know! Always perform culture and sensitivity to rule out infectious granulomatous
   dermatitis (bacterial, fungal). Collect samples for culture using a 2 mm punch biopsy.
   Cultures are invariably negative in this condition.

4. Know! The definitive diagnosis is based on negative culture results and
   histopathologic findings showing a pyogranulomatous inflammation without any
   infectious agents.

5. How do you manage this disease?




                                           73
                    Canine Miscellaneous Skin Diseases
                                       Panniculitis



   A. General Considerations:

       1. Panniculitis is inflammation of the subcutaneous fat tissue which may result
          from several different etiologies.

       2. It is characterized by deep-seated cutaneous nodules that often become
          ulcerated and develop draining tracts.


                                     Important Facts

 Panniculitis is inflammation of the subcutaneous fat tissue which may result from
   several different etiologies.


   B. Cause and Pathogenesis:

       1.    Lipocytes (fat cells) can be damaged by many factors resulting in the release
            of lipids which undergo hydrolysis to fatty acids which can incite further
            inflammation and granulomatous reactions.

       2.   Post-injection panniculitis:

            a. Occurs rarely.

            b. It has been associated with various vaccines and injection of other
               medications including antibiotics.

            c. It is postulated that the inflammation results from a combination of
               foreign body and hypersensitivity reactions.

       3. Traumatic panniculitis:

            a. Occurs when blunt trauma, chronic pressure, or decreased blood supply
               induces focal ischemia.

       4. Infectious panniculitis:



                                            74
           a. Occurs when bacteria or deep mycotic agents become established in the
              panniculus.

       5. Immune-mediated:

           a. Occurs with immune-mediated vascular diseases such as systemic lupus
              erythematosus and reactions occurring due to drugs, infectious agents, or
              visceral malignancy.

           b. Erythema nodosum-like panniculitis is a septal panniculitis associated
              with vascular damage due to systemic hypersensitivity reactions.

       6. Idiopathic panniculitis:

           a. Encompasses all of the sterile inflammatory diseases of the panniculus
              that have unknown etiologies.

           b. Example: idiopathic sterile nodular panniculitis and sterile pedal
              panniculitis of the German Shepherd dog.


                                     Important Facts

 Panniculitis is a multifactorial condition and possible etiologies include: post-
  injection, traumatic, infectious, immune-mediated and idiopathic.


   C. Clinical Signs:

       1. There is no age or sex predilection.

       2. Lesions associated with sterile nodular panniculits are most commonly located
          over the ventrolateral neck and trunk.

       3. Dachshunds and Collies appear to be predisposed to develop sterile nodular
          panniculitis.

       4. Animals with sterile nodular panniculitis are more likely to have multiple
          lesions.

       5. Some nodules are fluctuant and some rupture and drain an oily brown or
          blood-tinged exudate.

       6. There may be evidence of scarring in the area of the ruptured nodules, and a
          secondary staphylococcal infection may occur after rupture.



                                            75
       7. Fever, depression, lethargy, anorexia may be present in dogs with multiple
          lesions.

       8. Sterile pedal panniculitis of the German Shepherd dog appears as well-
          demarcated fistulous tracts that have slightly swollen erythematous borders.

       9. They are most frequently located to the footpads dorsal to the midline of the
          carpal or tarsal pads. Lesions have also been associated with other pads.


                                   Important Facts

 Signs will vary according to the etiology of the panniculitide.

 Animals with sterile nodular panniculitis are more likely to develop multiple lesions
  which are more frequently localized to the neck and trunk.

 Some nodules are fluctuant and some rupture and drain an oily brown or blood-
  tinged exudate.

 Ruptured nodules are likely to become secondarily infected.

 Fever, depression, lethargy, anorexia may be present in dogs with multiple lesions.

 Sterile pedal panniculitis of the German Shepherd dog appears as well-demarcated
  fistulous tracts that have slightly swollen erythematous borders.

 Sterile pedal panniculitis lesions are most frequently located to the footpads dorsal to
  the midline of the carpal or tarsal pads.


   D. Diagnosis:

       1. History and clinical signs are suggestive of panniculitis.

       2. The definitive diagnosis can be made only by biopsy, and excision biopsy is
          the recommended technique. Punch biopsies may not include the
          subcutaneous fat tissue in a large percentage of cases.

       3. Cutaneous biopsy reveals inflammation of the subcutaneous fat that may be
          pyogranulomatous or mononuclear. Ask for special stains to rule out
          infectious agents. Polarized light examination is indicated to rule out foreign
          bodies.

       4. A biochemical profile will help rule out systemic disease.



                                            76
       5. Bacterial cultures of unruptured nodules yield no growth, while
          Staphylococcus sp. may be cultured from draining nodules.

       6. Direct smear of exudate reveals more fat droplets than expected, foamy
          macrophages and/or neutrophils.



                                   Important Facts

 The definitive diagnosis can be made only by biopsy.

 Excision biopsy is the recommended technique. Punch biopsies may not include the
   subcutaneous fat tissue in a large percentage of cases.

 Cutaneous biopsy reveals inflammation of the subcutaneous fat that may be
   pyogranulomatous or mononuclear.

 Ask for special stains to rule out infectious agents.

 Polarized light examination is indicated to rule out foreign bodies.

 Bacterial cultures of unruptured nodules yield no growth, while Staphylococcus sp.
   may be cultured from draining nodules.

 Direct smear of exudate reveals more fat droplets than expected, foamy macrophages
   and/or neutrophils.


   E. Treatment:

       1. Solitary lesions may be removed surgically.

       2. If the panniculitis is due to infectious agents appropriate treatment for the
          specific agent should be instituted.

       3. Animals with multiple sterile lesions respond well to systemic corticosteroids
          (2.0 mg/kg q24h) until the lesions have regressed (3 to 8 weeks).

       4. Many animals will enter long-term or permanent remission.

       5. If lesions recur, long-term alternate dose corticosteroid therapy should be
          instituted.




                                            77
       6. In a few cases good results have been obtained with oral vitamin E at 400 IU
          q12h. It should be given at least 2 hours before or after food for maximum
          effectiveness.

                                 Important Facts

 Solitary lesions may be removed surgically.

 Sterile nodular panniculitis usually responds well to immune suppressive dosages of
   glucocorticoids.

 When lesions resolve (may take 3 to 8 weeks) try stopping the glucocrticoid therapy
   as many cases may undergo prolonged or permanent remission.

 Some cases will need long-term alternate dose glucocorticoid therapy.

 A few cases may benefit from vitamin E supplementation.




                                          78
                                      References



1. Nesbitt G.E. & Ackerman L.J. Miscellaneous Canine Skin Diseases. In: Canine and
   Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 314-353.

2. Scott, Miller & Griffin. Miscellaneous Skin Diseases. In: Small Animal
   Dermatology. W.B. Saunders, Philadelphia, 1995, pp 902-955.




                                Learning Objectives


1. Know! Panniculitis is a multifactorial inflammatory condition of the subcutaneous
   fat tissue. It is rare.

2. What are the causes of panniculitis?

3. Know! Clinical signs can vary depending on the etiology of the panniculitis. Sterile
   nodular panniculitis of unknown cause is more frequently seen in Dachshunds and
   Collies. It is characterized by multiple nodules more frequently localized to the trunk
   and neck. Some nodules can ulcerate and drain an oily brown to bloody exudate.
   Animals with multiple nodules can develop fever, depression, lethargy and anorexia.
   Ulcerated nodules can become secondarily infected.

4. Know! Skin biopsy is the only diagnostic method for panniculitis. Perform an
   excision biopsy instead of a punch biopsy. Punch biopsies of nodules, often do not
   include the subcutaneous fat tissue. Request special stains to rule out infectious
   agents. It is also a good idea to culture lesions to rule out any infectious agents.
   Avoid ulcerated nodules when collecting material for culture because they may be
   infected with Staphylococcus sp. Use a 2 mm punch biopsy to collect the sample for
   culture.

5. How do you manage pannicultis?




                                            79
                   Canine Miscellaneous Skin Diseases
                               Erythema Multiforme


   A. General Considerations:

       1. Erythema multiforme is an uncommon syndrome that presumably is immune-
          mediated.

       2. Most cases are idiopathic in origin but some cases are associated with adverse
          cutaneous drug reactions, infections, or internal disorders (e.g. connective
          tissue disease, neoplasia).

       3. The process is associated with keratinocyte cell death, known as apoptosis.

       4. It is postulated that T-helper cells (CD4+), stimulated by antigen-presenting
          Langerhans’ cells, become sensitized against keratinocytes and cause damage
          to the keratinocytes by releasing lymphokines, such as interferon-alpha and
          tumor necrosis factor-beta. Cytotoxic T-cells (CD8+) may also play a role in
          keratinocyte damage.


                                   Important Facts

 Erythema multiforme is an uncommon syndrome that presumably is immune-
   mediated.

 Most cases are idiopathic in origin but some cases are associated with adverse
   cutaneous drug reactions, infections, or internal disorders.


   B. Clinical Signs:

       1. The eruption is usually acute, and often involves the limbs, ventrum,
          mucocutaneous junctions, oral mucosa, axillae, and ears.

       2. Signs include erythematous macules, papules, urticarial plaques,
          vesicles/bullae, erosions, and ulcerations.

       3. Crusting, exudation, and the formation of epidermal collarettes are secondary
          manifestations.




                                            80
       4. Lesions often spread centrifugally, leaving a central clear area (“target”
          lesion) but also can be serpiginous or arciform.


                                   Important Facts

 The eruption is usually acute, and often involves the limbs, ventrum, mucocutaneous
   junctions, oral mucosa, axillae, and ears.

 Signs include erythematous macules, papules, urticarial plaques, vesicles/bullae,
   erosions, and ulcerations.

 Crusting, exudation, and the formation of epidermal collarettes are secondary
  manifestations.


   C. Diagnosis:

       1. Diagnosis is based on history, clinical signs and histopathologic findings.

       2. Preferred biopsy sites are erythematous papules or plaques without evidence
          of ulceration or crusting.

       3. Diagnostic findings are single cell necrosis of keratinocytes (apoptosis), and
          often vacuolar degeneration of the basal cell layer.

       4. The condition is usually difficult to differentiate from lupus erythematosus
          and ulcerative dermatosis.

       5. Try to identify underlying problems.

       6. The most common underlying causes are infections (e.g., staphylococcal
          folliculitis, and anal gland sacculitis, bacterial endocarditis), drugs (e.g.,
          chloramphenicol, cephalexin, diethylcarbamazine, thyroxine, trimethoprim-
          sulfonamides, etc.), and neoplasia (e.g., myeloproliferative disorders, splenic
          tumors).


                                   Important Facts

 Diagnosis is based on history, clinical signs and histopathologic findings.

 Try to identify underlying problems such as infections, drug therapy and neoplasia.



                                            81
   D. Treatment:

       1. Most cases in dogs have been secondary to bacterial folliculitis or reactions to
          drugs.

       2. If the causative insult can be treated, the condition can be expected to regress
          spontaneously.

       3. Antiinflammatory doses of prednisolone (0.5 to 1.0 mg/kg/day) may be given
          to decrease the inflammation and pruritus when present but are controversial
          because they can also exarcebate some cases.

       4. Pentoxifylline has been used anecdotally, at 5 to 10 mg/kg 3 times a day, with
          variable results in recurrent, non-drug associated cases.

       5. Azathioprine, sulfasalazine and cyclosporine have also been used as palliative
          treatments in resistant cases.


                                    Important Facts

 Look for underlying conditions! If the causative insult can be treated, the condition
   can be expected to regress spontaneously.

 Antiinflammatory doses of prednisolone may be given to decrease the inflammation
   and pruritus when present but are controversial because they can also exarcebate
   some cases.

 Pentoxifylline has been used anecdotally with variable results in recurrent, non-drug
   associated cases.

 Azathioprine, sulfasalazine and cyclosporine have also been used as palliative
   treatments in resistant cases.




                                            82
                                       References


1. Nesbitt G.E. & Ackerman L.J. Canine Immune-Mediated Skin Diseases. In: Canine
   and Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 140-161.




                                 Learning Objectives


1. Know! Erythema multiforme is a rare condition and believed to be immune-mediated.
   Keratinocytes are damaged by T-cells. Most cases are idiopathic but, some cases are
   associated with infectious diseases, drugs and neoplasia. Always look for an
   underlying condition when managing erythema multiforme!

2. What are the clinical signs associated with this disease?

3. Know! The diagnosis is based on history, clinical signs and skin biopsy. Consistent
   histopathologic findings are single cell necrosis of keratinocytes (apoptosis) and
   vacuolar degeneration of the basal keratinocytes. Again, try to identify an underlying
   disease.

4. How do you manage erythema multiforme?




                                            83
           Canine and Feline Miscellaneous Skin Diseases
                        Toxic Epidermal Necrolysis - Canine


   A. General Considerations:


       1. The pathogenesis is presumed Toxic epidermal necrolyis (TEN) is a life-
           threatening disease involving the mucosal and skin surfaces.to involve a
           lymphohistiocytic immunologic injury.

       2. It is often associated with an underlying infection, drug reaction, or metabolic
           disorder.

       3. It probably constitutes one extreme of a spectrum that ranges from drug
           eruption, through erythema multiforme, to TEN.



                                  Important Facts

 Toxic epidermal necrolyis (TEN) is a life-threatening disease involving the mucosal
   and skin surfaces.

 It is often associated with an underlying infection, drug reaction, or metabolic
   disorder.

 It probably constitutes one extreme of a spectrum that ranges from drug eruption,
   through erythema multiforme, to TEN.


   B. History and Clinical Signs:

       1. TEN is characterized by large, painful, ulcerative areas on any part of the
           body, but particularly on the head, footpads, and mucocutaneous junctions.

       2. The presentation can mimic a massive second-degree burn.

       3. A positive Nikolsky’s sign may be present. This means that lesions can be
          formed by applying lateral pressure on the skin adjacent to affected areas and
          indicates poor cellular cohesion.




                                           84
       4. In dogs, the disease is often associated with some predisposing conditions,
           such as staphylococcal infection, drug administration, or systemic neoplasia.

       5. Fever, anorexia, shock, and even death may be a consequence of TEN.


                                  Important Facts

 TEN is characterized by large, painful, ulcerative areas on any part of the body, but
  particularly on the head, footpads, and mucocutaneous junctions.

 In dogs, the disease is often associated with some predisposing conditions, such as
  staphylococcal infection, drug administration, or systemic neoplasia.

 Fever, anorexia, shock, and even death may be a consequence of TEN.


   C. Diagnosis:

       1. The diagnosis is based on history, clinical signs and skin biopsy.

       2. Biopsy of erythematous non-ulcerated areas reveals acute coagulation necrosis
          of the entire thickness of the epidermis and the formation of subepidermal
          vesicles.

       3. Additional data base to uncover internal manifestations of the disease should
          include a hemogram, serum chemistry profile and urinalysis.

       4. Common abnormalities include leukocytosis, electrolyte abnormalities,
          hypoproteinemia, and altered renal function.



                                  Important Facts

 The diagnosis is based on history, clinical signs and skin biopsy.

 . Biopsy of erythematous non-ulcerated areas reveals acute coagulation necrosis of
  the entire thickness of the epidermis and the formation of subepidermal vesicles.

 Additional data base to uncover internal manifestations of the disease should include
  a hemogram, serum chemistry profile and urinalysis.




                                           85
   D. Treatment:

       1. Supportive topical therapy with astringents, intravenous fluid therapy with
           electrolytes (perhaps with plasma replacement), and systemic antibiotics
           usually is indicated.

       2. Corticosteroids use in the treatment of TEN is controversial.
          Antiinflammatory doses (1.1 mg/kg/day) can be tried in some cases.
          Decrease the initial high dose as soon as possible to the lowest possible dose
          and stop therapy if not helping.

       3. The underlying disease must be identified and treated concurrently if TEN is
           to resolve.


                                   Important Facts

 Supportive topical therapy with astringents, intravenous fluid therapy with
   electrolytes, and systemic antibiotics usually is indicated.

 Corticosteroids use in the treatment of TEN is controversial.

 The underlying disease must be identified and treated concurrently if TEN is to
   resolve.




                                            86
                                      References


1. Nesbitt G.E. & Ackerman L.J. Canine Immune-Mediated Skin Diseases. In: Canine
   and Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 140-161.




                                Learning Objectives


1. Know! Toxic epidermal necrolyis (TEN) is a life-threatening disease involving the
   mucosal and skin surfaces. Most cases in dogs are associated with an underlying
   condition such as infection, drug reaction, or metabolic disorder.

2. Know! TEN is characterized by large, painful, ulcerative areas on any part of the
   body, but particularly on the head, footpads, and mucocutaneous junctions.

3. Remember! In dogs, the disease is often associated with some predisposing
   conditions, such as staphylococcal infection, drug administration, or systemic
   neoplasia. Look for an underlying disease when managing TEN!

4. Know! Fever, anorexia, shock, and even death may be a consequence of TEN. It is a
   severe disease!

5. Do you understand what a Nikolsky’s sign is? If not ask Dr. Torres.

6. How do you diagnose TEN?

7. How do you manage TEN?




                                           87
           Canine and Feline Miscellaneous Skin Diseases
                      Drug Eruption – Canine and Feline


   A. General Considerations:

       1. Drug eruption is an immune-mediated reaction to medications administered
          orally, parentally or topically.

       2. Drug eruption can mimic any dermatosis.

       3. More extreme manifestations of drug reaction may include erythema
          multiforme or toxic epidermal necrolysis.


                                  Important Facts

 Drug eruption is an immune-mediated reaction to medications administered orally,
   parentally or topically. 2. Drug eruption can mimic any dermatosis.


   B. Clinical Signs:

       1. The clinical signs and distribution are variable and mimic many other
           dermatoses.

       2. Lesions involve the skin and/or mucus membranes.

       3. The following clinical signs have been described:

           a. Urticaria.

           b. Maculopapular eruptions: macules, papules, variable pruritus.

           c. Fixed drug eruption: focal to multifocal areas of sharply demarcated
              erythematous lesions. Upon rechallenge lesions recur in the same
              location.

           d. Erythroderma/exfoliative: diffuse erythema of the skin. It has been
              associated with topical or systemic medications. Not likely to be fatal.
              Main differentials are allergic dermatoses and Malassezia dermatitis.




                                           88
           e. Purpuric reactions: hemorrhage is present in the dermis. The condition
              has been associated with thrombocytopenia or vascular damage
              (vasculitis). It may be life-threatening.

           f. Vesicobullous reactions/vasculitis: mimic other immune-mediated skin
              diseases. It may be life-threatening.

           g. Lichenoid drug reaction: it presents as flat plaques composed of
              coalescing papules; many are self-limiting and asymptomatic.

           h. Superficial suppurative necrolytic dermatitis: observed primarily in
              Schnauzers after topical herbal or citrus or coal tar shampoos.
              Generalized erythematous papules coalescing to plaques over the body.
              The animals can present with fever, depression and pain. Three cases
              responded to antibiotics and supportive care and one case died.

           i. Injection site reactions: alopecia, crusting, ulceration and necrosis or
              subcutaneous nodules. The time from the injection to lesion development
              may be weeks or months. It may resolve over time or be surgically
              removed. In some cases the alopecia may be permanent.

           j. Erythema multiforme: macules, papules, plaques, wheals, bullae, ulcers,
              target lesions. Differentials include pemphigus vulgaris and systemic
              lupus erythematosus.

           k. Toxic epidermal necrolysis: progressive mucocutaneous junction and
              cutaneous erythema, vesiculation, epithelial necrosis and ulceration. The
              main differential is chemical burn.

       4. Drugs:

           a. Anything.

           b. Especially trimethoprim-potentiated sulfas, penicillins and
              cephalosporins.

                                  Important Facts

 The clinical signs and distribution are variable and mimic many other dermatoses.

 Lesions involve the skin and/or mucus membranes.

 The cutaneous lesions can manifest as urticaria, erythema, exfoliation, purpura,
   papules, lichenoid, erosive, ulcerative, vesiculopustular, and indurated.




                                            89
   C. Pathophysiology:

       1. Drug allergy:

           a. Requires previous exposure (sensitization).

           b. Signs may develop several days after first exposure to the drug.

           c. Minute quantities of drug required for signs to develop.

           d. Types I, II, III, and IV hypersensitivity have been implicated.

           e. The reaction observed is not related to the pharmacologic action of the
              drug.

       2. Drug eruption may occur secondary to drug administration by any route:

           a. Oral.

           b. Injectable. Intravenous administrations are more likely to induce
              anaphylactic reactions.

           c. Topical.



                                  Important Facts

 Previous exposure to the drug is required for sensitization to occur.


 Signs may develop several days after first exposure to the drug.

 Very small amounts of the drug is required for signs to develop.

 Types I, II, III, and IV hypersensitivity have been implicated.

 The reaction observed is not related to the pharmacologic action of the drug.

 Drug eruption may occur secondary to drug administration by any route.




                                           90
   D. Diagnosis:

       1. The history is the most important clue in diagnosing drug eruption.

       2. Do not forget to ask about vaccinations; topical shampoos; dips; ocular
          medications; diethylcarbamazine or vitamin-mineral supplements.

       3. Physical findings are not very helpful because drug eruption can mimic any
          dermatosis. It can look like anything!

       4. Histopathology findings are quite variable. Histopathology can be used to
          rule out other conditions.

       5. Response to withdrawal of drug:

           a. Usually occurs within 7 to 14 days.

           b. Occasionally, adverse reactions may persist weeks to months.

       6. Provocative exposure:

           a. Undesirable, dangerous, life-threatening.

           b. May need to do if no alternative drugs are available.

           c. Proceed cautiously: try prick test; then ID skin tests (start at 1:100,000
              dilution); then graded doses of the suspected drug. Oral route is the best.


                                  Important Facts

 The history is the most important clue in diagnosing drug eruption.

 Physical findings are not very helpful because drug eruption can mimic any
   dermatosis.

 Histopathologic findings are quite variable. They can be used to rule out other
   conditions.

 Resolution or improvement of clinical signs usually ocurs 7 to 14 days after
   discontinuing the drug.

 Occasionally, clinical signs may persist weeks to months.

 Provocative exposure is usually not recommended because it can be life-threatening.

                                           91
   E. Treatment:

       1. Discontinue and avoid further use of the suspected drug.

       2. Drugs of similar chemical structure to the suspected ones should be avoided
          because cross-reactivity can occur.

       3. Clinical signs are treated symptomatically.

       4. Corticosteroids (2 to 4 mg/kg/day) are indicated on a short-term basis to
          decrease the inflammation and pruritus.

       5. Do not use corticosteroids in cases with severe, extensive ulcerative lesions.
          Corticosteroids will predispose to bacterial sepsis in these cases.



                                  Important Facts

 Discontinue and avoid further use of the suspected drug or any drugs with similar
  chemical structure.

 Corticosteroids are indicated on a short-term basis to decrease the inflammation and
  pruritus, with the exception of severe ulcerative cases.

 Supportive treatment is given as needed.


   F. Prognosis:

       1. It depends on the severity of the eruption but it is generally good.




                                            92
                                        References


1. Nesbitt G.E. & Ackerman L.J. Canine Immune-Mediated Skin Diseases. In: Canine
   and Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 140-161.




                                  Learning Objectives


1. Remember! Drug eruption is an immune-mediated reaction to medications
   administered orally, parentally or topically. Drug eruption can mimic any
   dermatosis!

2. Know! Any drug can induce an allergic reaction. The ones more frequently reported
   in dogs are trimethoprim-potentiated sulfas, penicillins and cephalosporins.

3. Know! Several days may be necessary before sensitization to a drug occurs. Once
   the individual develops hypersensitivity to a medication very small amounts of this
   drug is necessary to elicit the clinical signs. All 4 types of hypersensitivity (types I,
   II, III, IV) have been implicated in drug eruption.

4. Know! The history is very important in diagnosing drug eruption. Physical findings
   are not very helpful because the clinical signs associated with drug reaction are quite
   variable and it can mimic any dermatosis. Skin biopsy can be performed to rule out
   other conditions. Generally, clinical signs resolve or improve within 7 to 14 days
   after discontinuation of the drug. However, in some cases it may take weeks to
   months before any improvement is observed.

5. Remember! Provocative exposure is not indicated because it is dangerous and it can
   be life-threatening.

6. How do you manage drug eruption?




                                              93
            Canine and Feline Miscellanous Skin Diseases
                           Juvenile Cellulitis - Canine



   A. General Considerations:

       1. Juvenile cellulitis, or puppy strangles, is an uncommon disease.

       2. The condition is presumed to be immune-mediated based on histopathologic
          features and response to immunosuppressive forms of therapy.

       3. A heritable nature has been suggested.


                                  Important Facts

 Juvenile cellulitis, or puppy strangles, is a rare disease presumed to be immune-
   mediated.

 A heritable nature has been suggested.


   B. Clinical Signs:

       1. Dachshunds, Golden retrievers, yellow Labrador retrievers, Gordon setters,
          Lhasa apsos, and Pointers are most commonly affected, but any other breed
          can have this disease.

       2. Most affected animals are less than 4 months old, but occasionally the
          disorder is reported in adults.

       3. Several puppies or only one in the litter may be affected.

       4. Signs are characterized by vesicles or pustules in the inner surface of the
          pinna, on the muzzle, lips, and eyelids which rapidly progresses to extensive
          facial swelling, abscessation and draining lesions.

       5. Submandibular lymphadenopathy occurs and occasionally lymph nodes will
          abscess and drain.

       6. A few cases will develop nodules over the trunk, preputial and perineal areas
          due to a pyogranulomatous panniculitis.


                                           94
       7. Puppies are usually febrile, depressed and anorexic.

       8. Permanent areas of alopecia and scarring may result if the lesions are
          extensive.


                                  Important Facts

 Most affected animals are less than 4 months old, but occasionally the disorder is
   reported in adults.

 Several puppies or only one in the litter may be affected.

 Papules, small nodules, vesicles or pustules are initially seen on the pinna, muzzle,
   lips and eyelids.

 Lesions rapidly progress to extensive swelling, abscessation and draining tracts.

 Submandibular lymphadenopathy occurs and occasionally lymph nodes will abscess
   and drain.

 Puppies are usually febrile, depressed and anorexic.

 Permanent areas of alopecia and scarring may result if the lesions are extensive.


   C. Diagnosis:

       1. Diagnosis is based on history, clinical signs, cytologic examination of
          draining exudate, skin biopsy and response to therapy.

       2. Skin scrapings should be performed to rule out demodicosis.

       3. Skin biopsies reveal a nodular to diffuse dermatitis and panniculitis composed
          of epithelioid histiocytes and neutrophils.

       4. Bacterial cultures sometimes reveal organisms, although they are secondary
          infection.

       5. Although juvenile cellulitis has many clinical similarities to pyoderma, it
          responds to corticosteroid therapy. Antibiotics are used to treat secondary
          infection.



                                           95
                                  Important Facts

 Diagnosis is based on history, clinical signs, cytologic examination of draining
  exudate, skin biopsy and response to therapy.

 Skin scrapings should be performed to rule out demodicosis.

 Although juvenile cellulitis has many clinical similarities to pyoderma, it responds to
  corticosteroid therapy.

 Antibiotics are used to treat secondary infection.


   D. Treatment:

       1. Treatment with a bactericidal antibiotic (cephalexin, cephadroxil) and
           immunosuppressive doses of corticosteroids (prednisolone, 1.1 mg/kg twice a
           day) is required for 2 to 3 weeks.

       2. Once lesions have resolved reduce the dose slowly to an alternate day
          schedule to prevent relapses.

       3. The condition usually responds completely, with little chance of recurrence.

       4. Owners should be prepared for scarring which may be permanent.


                                  Important Facts

 Treatment with a bactericidal antibiotic and immunosuppressive doses of
  corticosteroids is required for 2 to 3 weeks.

 The condition usually responds completely, with little chance of recurrence.




                                           96
                                      References


1. Nesbitt G.E. & Ackerman L.J. Canine Immune-Mediated Skin Diseases. In: Canine
   and Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 140-161.




                                Learning Objectives


1. Know! Juvenile cellulitis, also known as puppy strangles, is a rare condition usually
   seen in dogs less than 4 months of age. Occasionally, it can be diagnosed in adults.
   One or multiple puppies in the litter may be affected.

2. Know! Lesions are initially characterized by papules, small nodules, vesicles or
   pustules localized to the pinna, muzzle, lips and eyelids. Rapid and extensive facial
   swelling, abscessation, and draining lesions develop. Marked lymphadenopathy,
   fever, depression and anorexia are noted.

3. How do you diagnose juvenile cellulitis?

4. Remember! Always perform multiple skin scrapings to rule out demodicosis!

5. Know! Although juvenile cellulitis has many clinical similarities to pyoderma, it
   responds to corticosteroid therapy. Antibiotics are used to treat secondary infection.

6. How do you manage juvenile cellulitis.




                                            97
           Canine and Feline Miscellaneous Skin Diseases
                            Perianal Fistulas – Canine



   A. General Considerations:

       1. Perianal fistulas is also called anal furunculosis.

       2. The etiopathogenesis is unknown.

       3. There is very little evidence to support the contention that this is a primary
           bacterial disease.

       4. Researches have explored many possible etiologies, including overproduction
          by local secretory glands, poor ventilation associated with low tail carriage,
          anal sac disease, or hip dysplasia.

       5. To date, nothing conclusive has ever been demonstrated.


                                   Important Facts

 The etiopathogenesis of perianal fistulas or anal furunculosis is unknown.

 Possible etiologies include overproduction by local secretory glands, poor ventilation
  associated with low tail carriage, anal sac disease, or hip dysplasia.


   B. Clinical Signs:

       1. It is most common in German shepherd and Irish setter breeds. However, it
           has been seen in other breeds.

       2. Males outnumber females by 2 to 1.

       3. Most affected animals are 3 to 6 years of age.

       4. Clinical signs are characterized by multiple draining tracts and ulcers
          immediately surrounding the rectum.

       5. Animals may present tenesmus, dyschezia and constipation.




                                            98
       6. Affected area is usually very painful.

       7. An association between perianal fistulas and inflammatory bowel disease is
          suspected.


                                  Important Facts

 It is most common in German shepherd and Irish setter breeds.

 It occurs more frequently in males and most affected animals are 3 to 6 years of age.

 Clinical signs are characterized by multiple draining tracts and ulcers immediately
   surrounding the rectum.

 The affected area is painful and the animals may present tenesmus, dyschezia and
   constipation.

 An association between perianal fistulas and inflammatory bowel disease is
   suspected.




   C. Diagnosis:

       1. Diagnosis is based on history, physical findings and skin biopsy.

       2. Culture and sensitivity are recommended if antibiotic therapy is being
          considered as part of the treatment.

       3. The most common organisms recovered from culture include: E. coli,
           Staphylococcus aureus, beta-hemolytic Streptococcus, and Proteus mirabilis.

       4. Keep in mind that antibiotic therapy has very little impact on the clinical
          outcome.

       5. Evaluate every case for concurrent inflammatory bowel disease and adverse
          food reaction.




                                           99
                                  Important Facts

 Diagnosis is based on history, physical findings and skin biopsy.

 Culture and sensitivity are recommended if antibiotic therapy is being considered as
   part of the treatment.

 Keep in mind that antibiotic therapy has very little impact on the clinical outcome.

 Evaluate every case for concurrent inflammatory bowel disease and adverse food
   reaction.


   D. Treatment:

       1. Management of these cases is often disappointing because they do not
          respond consistently to antibiotics, corticosteroids and surgery.

       2. Keep the affected area clean by clipping the hair and flushing the lesions with
          chlorhexidine or povidone iodine.

       3. Immunosuppressive therapy is helpful in those dogs in which eosinophilic
          infiltration is most profound.

       4. Prednisolone at 1.1 mg/kg twice a day for 14 days, then weaning, is usually
          adequate but, add azathioprine in cases that did not respond well to
          prednisolone.

       5. Recently, cyclosporine has been reported to be very effective at 5 mg/kg b.i.d.
          during an average treatment duration of 16 weeks.

       6. Preliminary successes with isotretinoin (Accutane) at 1.0 mg/kg daily suggest
          that this disorder may share some similarities with acne.

       7. Surgery is recommended for those animals that fail to respond to medical
          therapy.

       8. The best surgical approach to date has been cryosurgery, with multiple
          freezes.

       9. Removing part of the tail musculature, neutering and extirpation of the anal
          sacs, or chemical cauterization may be indicated.




                                          100
        10. Post-operative complications include fistulae recurrence, anal strictures,
           fecal incontinence, tenesmus, and dyschezia.


                                   Important Facts

 Perianal fistulas is a challenging condition to manage.

 Many treatment modalities have been used to mange this disease including:
  immunosuppressive doses of corticosteroids alone or in association with azathioprine;
  cyclosporine; isotretinoin and surgery.

 Antibiotic therapy is usually administered to treat the secondary bacterial infection.




                                           101
                                      References


1. Nesbitt G.E. & Ackerman L.J. Miscellaneous Canine Skin Diseases. In: Canine and
   Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 314-353.

2. Mathews KA et al. Cyclosporine treatment of perianal fistulas in dogs. Canadian Vet
   Journal 38(1):39-41, 1997.




                                Learning Objectives
1. Remember, but don’t get discouraged! Perianal fistulas is a very difficult disease to
   manage.

2. Know! The etiopathogenesis is unknown. Possible etiologies include: overproduction
   by local secretory glands, poor ventilation associated with low tail carriage, anal sac
   disease, or hip dysplasia. Bacterial infection is always present but, it is considered a
   secondary problem.

3. Know! The disease occurs most frequently in German shepherd and Irish setter
   breeds. Males are predisposed and most affected dogs are 3 to 6 years old. Clinical
   signs are characterized by multiple draining tracts and ulcers immediately
   surrounding the rectum. The lesions are very painful and the dogs present with
   tenesmus, dyschezia and constipation.

4. How do you diagnose perianal fistulas?

5. Keep in mind that antibiotic therapy has very little impact on the clinical outcome!
   Be sure to perform culture and sensitivity tests if you are considering antibiotic
   therapy.

6. Remember! Evaluate every case for concurrent inflammatory bowel disease and
   adverse food reaction.

7. How do you manage this challenging condition?




                                           102
           Canine and Feline Miscellaneous Skin Diseases
                            Anal Sac Disorders – Canine


   A. General Considerations:

        1. Anal sac disorders occur with relatively high frequency.

        2. Predisposing factors to anal sac disease include large quantities of thick
           secretions, an abnormally small duct system, anal irritation, changes in
           muscle tone or fecal form, and as a sequelae following diarrhea or estrus.

        3. Several bacteria are associated with anal sac disease including Staphylococcus
           fecalis, Echerichia coli, Clostridium welchii, Proteus sp., micrococci,
           Staphylococcus sp., and diptheroids.

        4. The pathogenesis of anal sac disease and associated clinical signs are not fully
           understood. It is generally accepted that an initial anal sac impaction occurs
           followed by bacterial fermentation of the incarcerated material.


                                    Important Facts

 Predisposing factors to anal sac disease include large quantities of thick secretions, an
  abnormally small duct system, anal irritation, changes in muscle tone or fecal form,
  and as a sequelae following diarrhea or estrus.

 It is generally accepted that the pathogenesis of anal sac disorders involves an initial
  anal sac impaction which is followed by bacterial fermentation of the incarcerated
  material.


   B. Clinical Signs:

        1. Primary anal sac disease is divided into 4 clinical entities:

           a. Impaction.

           b. Infection.

           c. Abscessation.

           d. Neoplasia.


                                             103
        2. Distended anal sacs can be palpated on either side of the anal canal at about 4
           and 8 o’clock positions.

        3. Normal anal sac fluid is described as pale yellow or straw-colored, serous,
           clear to translucent, slightly viscous, and granular with a pungent odor, often
           with small brownish flecks.

        4. Abnormal fluid color varies from greenish yellow (pus) to red to brown to clay
           to black.

        5. Infected anal sacs often are associated with an opaque, thick, red or greenish-
           colored fluid having a fetid odor.

        6. Impacted anal sacs are characterized by clay-or black-colored contents that
           are dry or pasty and have minimal odor.

        7. An abscessed anal sac ruptures and drain cutaneously and is often associated
           with cellulitis of the surrounding tissue.

        8. Anal sac tumors are rare. They occur more often in old females of any breed.
           Perianal swelling with or without ulceration is the primary complaint.

        9. Hypercalcemia and hypophosphatemia may be present and metastasis to the
           regional lymph nodes occurs frequently.

        10. Anal sac disorders are more frequent in small breeds.


                                   Important Facts

 Primary anal sac disease is divided into 4 clinical entities: impaction, infection,
  abscessation and neoplasia.

 Abnormally distended anal sacs can be palpated on either side of the anal canal at
  about 4 and 8 o’clock positions.

 Normal anal sac fluid is described as pale yellow or straw-colored, serous, clear to
  translucent, slightly viscous, and granular with a pungent odor, often with small
  brownish flecks.

 Abnormal fluid color varies from greenish yellow (pus) to red to brown to clay to
  black.

 Anal sac tumors are rare and more often seen in old females of any breed. Anal sac
  disorders are more frequent in small breeds.


                                            104
   C. Diagnosis:

       1. Diagnosis is based on history and clinical signs.

       2. Manual expression and characterization of the anal sac content are very
          important.

       3. Evaluation of the anal sac disease should include bacterial culture and
          sensitivity, direct microscopic evaluation of the anal sac content and, rarely,
          biopsy.

       4. Cytologic exam of normal anal sac content reveals cellular debris and a few
          leukocytes.

       5. Cytologic exam of diseased anal sacs reveals a large number of leukocytes
          and numerous bacteria.

       6. Bacterial culture and sensitivity should be performed in chronic,
          nonresponsive, or recurrent infections.

       7. Biopsy should be performed if suspecting of neoplasia. Abdominal
          radiographs also are indicated in suspected anal sac neoplasia.

       8. Look for concomitant dermatoses and treat them appropriately.


                                   Important Facts

 Diagnosis is based on history and clinical signs.

 Evaluation of the anal sac disease should include manual expression and
   characterization of the anal sac content, bacterial culture and sensitivity, direct
   microscopic evaluation of the anal sac content and, rarely, biopsy.

 Bacterial culture and sensitivity should be performed in chronic, nonresponsive, or
   recurrent infections.

 Biopsy and abdominal radiographs should be performed if suspecting of neoplasia.




                                            105
D. Treatment:

   1. Impaction:

      a. Gentle expression of sacs either cutaneously or per rectum.

      b. If the contents are thick and inspissated, a softening or ceruminolytic
         agent, such as hexamethyltetracosane or mineral oil, can be instilled in to
         the sacs using a blunt needle or lacrimal cannula.

      c. It will usually recur periodically especially in toy breeds.

      d. Surgical removal if frequent recurrences.

   2. Infection:

      a. Express anal sacs and flush (may require anesthesia) with 0.5%
         chlorhexidine or 10% povidone iodine solution.

      b. Instill antibiotics into sacs, such as chloramphenicol cream, nitrofurazone
         lotion, or corticosteroid-antibiotic ointment.

      c. Systemic antibiotic should be given in conjunction with topical therapy.

   3. Abscess:

      a. If abscess is not ruptured, a hot pack several times a day should be applied
         until the abscess is ready for drainage.

      b. The abscess then is lanced and the contents are expressed.

      c. The anal sac duct must be opened, often requiring cannulation.

      d. When the abscess has ruptured or has been surgically opened, it should be
         flushed with 10% povidone iodine and/or hydrogen peroxide daily until
         closed.

      e. Systemic antibiotics should be administered.

      f. Hot packs should be applied until the inflammation resolves.

   4. Neoplasia:

      a. Resect sac along with tumor and surrounding margins.



                                      106
        5. Surgical excision of the anal sacs is indicated in recurrent episodes of severe
           impaction or infection and abscesses of anal sacs; in chronic anal sac disease;
           neoplastic anal sac glands; adjunctive surgical treatment for perianal fistula.


                                   Important Facts

 Gentle expression of the sacs via rectal palpation is indicated in all cases of anal sac
  disease.

 . In some cases of anal sac impaction a softening or ceruminolytic agent will be
  instilled in the sacs to allow adequate content removal.

 Antiseptic flush, topical and systemic antibiotics are required in cases of infection.

 Surgical excision is indicated in cases of neoplasia.




                                            107
                                       References


1. Nesbitt G.E. & Ackerman L.J. Miscellaneous Canine Skin Diseases. In: Canine and
   Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 314-353.


                                 Learning Objectives


1. Know! Several bacteria are associated with anal sac disease including Staphylococcus
   fecalis, Echerichia coli, Clostridium welchii, Proteus sp., micrococci, Staphylococcus
   sp., and diptheroids. Therefore, bacterial culture and sensitivity should be performed
   on cases associated with infection.

2. Know! Anal sac disorders are primarily associated with one of 4 conditions:
   impaction, infection, abscessation or neoplasia. Abnormally distended anal sacs can
   be palpated on either side of the anal canal at about 4 and 8 o’clock positions.

3. What is the characteristic of a normal anal sac content?

4. What is the characteristic of the anal sac content in cases of impaction or infection?

5. Know! Abscessed sacs will often rupture and drain cutaneously.

6. Know! Anal sac tumors are rare but carcinomas of the apocrine glands do occur. Old
   females are predisposed and they may present with paraneoplastic hypercalcemia.
   Metastases to regional lymph nodes occur frequently. Clinically a large, firm mass
   with or without ulceration will be present at the area of the anal sacs (4 and 8 o’clock
   positions).

7. Know! Evaluation of the anal sac disease should include manual expression and
   characterization of the anal sac content, bacterial culture and sensitivity, direct
   microscopic evaluation of the anal sac content and, rarely, biopsy. Bacterial culture
   and sensitivity should be performed in chronic, nonresponsive, or recurrent
   infections.

8. Know! Surgical excision of the anal sacs is indicated in recurrent episodes of severe
   impaction or infection and abscesses of anal sacs; in chronic anal sac disease;
   neoplastic anal sac glands; adjunctive surgical treatment for perianal fistula.

9. How do you manage anal sac disorders?


                                            108
           Canine and Feline Miscellaneous Skin Diseases
                          Acral Lick Dermatitis – Canine


   A. General Considerations:

        1. Acral lick dermatitis, lick granuloma, or acral pruritic nodule is a single or
           multiple lesion on one or more extremities resulting from excessive and
           persistent licking.

        2. The exact cause is not known.


                                    Important Facts

 Acral lick dermatitis is a single or multiple lesion on one or more extremities
  resulting from excessive and persistent licking.


   B. Etiologic Factors:

        1. Many factors have been suggested to predispose to or cause acral lick
           dermatitis, including allergy (atopic dermatitis, food), psychogenic cases,
           boredom, bacterial folliculitis, foreign bodies, neuropathy, local trauma, and
           joint or bone diseases.

        2. Independent of the precipitating factor, once the lesion has developed it will
            contribute to the perpetuation of the compulsive licking behavior.


                                    Important Facts

 Many factors have been suggested to predispose to or cause acral lick dermatitis,
   including allergy (atopic dermatitis, food), psychogenic cases, boredom, bacterial
   folliculitis, foreign bodies, neuropathy, local trauma, and joint or bone diseases.

 The acral lick lesion will always perpetuate the compulsive licking behavior.




                                            109
   C. Clinical Signs:

        1. The most frequently affected site is the anterior carpal or metacarpal region.
            However, it can also develop on the tarsus or metatarsus area.

        2. Lesions are usually single but they can be multiple.

        3. Large breeds are predisposed (Doberman pincher, Labrador retriever,
            Dalmation, Irish setter, Weimaraner, German shepherd, Great dane).

        4. Onset of lesions can occur at any age, but it is more common in dogs more
           than 5 years of age.

        5. Lesions tend to be recurrent, either at the same or different sites.

        6. There is often a history of poor or partial response to many therapeutic
            regimens.

        7. Lesions are created and maintained by constant licking or chewing.

        8. Clinically the lesion is characterized by alopecic, erythematous, eroded or
           ulcerated, firm, nodular plaque(s).


                                    Important Facts

 Lesions are created and maintained by constant licking or chewing .

 Alopecic, erythematous, firm, eroded or ulcerated nodular plaques develop often on
   the carpus or metacarpus area.

 Lesions are usually single but they can be multiple.

 Large breeds are predisposed.

 Lesions tend to be recurrent, either at the same or different sites.

 Onset of lesions can occur at any age, but it is more common in dogs more than 5
   years of age.




                                             110
   D. Diagnosis:

        1. Diagnosis of acral lick dermatitis is based on history, clinical signs, and
           elimination of other primary causes.

        2. The minimum data base should include skin scrapings, impression smear
           cytology, and fungal culture (to rule out dermatophytosis).

        3. Biopsy of the lesion is helpful to rule out neoplasia.

        4. If joint or bone involvement is suspected, radiographs should be taken.

        5. If there is a history of generalized pruritus (either seasonal or nonseasonal) an
           allergy workup should be performed.

        6. Differentials include: stress or conflict behaviors, neoplasia (e.g. mast cell
           tumor), parasitism (e.g. demodocosis), mycotic infections (e.g.
           dermatophytosis, sporotrichosis), trauma (e.g. fracture, neural injury, prior
           wound, foreign body), focal allergic manifestation (e.g. contact eruption,
           atopic dermatitis, food allergy), and acral mutilation sysndrome.



                                   Important Facts

 Diagnosis of acral lick dermatitis is based on history, clinical signs, and elimination
  of other primary causes.

 The minimum data base should include skin scrapings, impression smear cytology,
  and fungal culture.

 Biopsy of the lesion is helpful to rule out neoplasia.

 If joint or bone involvement is suspected, radiographs should be taken.


   E. Treatment:

        1. In most cases a fair to guarded prognosis is given to dogs with acral lick
            dermatitis.

        2. If the underlying condition can be determined, the prognosis improves
             dramatically.




                                            111
3. Approximately 65% of the cases can be satisfactorily controlled with medical
    and/or behavior management.

4. Even if an underlying problem has been identified and treated, concurrent
    treatment of the skin condition is essential.

5. It is important to treat the frequently associated secondary bacterial infection
     with appropriate long-term (6 to 8 weeks) antibiotics.

6. Treat the lesion:

   a. Stop the lick cycle by recommending a device to prevent licking:
      elizabethan collar, bandaging, bad tasting topicals, basquet muzzle.

   b. Synotic is the best antiinflammatory agent for this condition because it
      contains DMSO and a fluorinated steroid. The DMSO will help the
      fluorinated steroid to penetrate the extensively fibrotic lesion.
      Recommend applying Synotic at least 3 times daily.

7. Treat the mind if you believe the problem is psychogenic in nature.

   a. Anxiolytic drugs:

       1. Phenobarbital 2.2 – 6.6 mg/kg BID.

       2. Diazepam (Valium) 0.2 mg/kg BID.

       3. Hydroxyzine (Atarax) 2.2 mg/kg TID.

   b. Tricyclic antidepressants:

       1. Amitriptyline (Elavil) 1-3 mg/kg BID.

       2. Imipramine (Tofranil) 2-4 mg/kg SID.

       3. Clomipramine (Anafranil) 1-3 mg/kg SID.

   c. Serotonin re-uptake inhibitor:

       1. Fluoxetine (Prozac) 1 mg/kg SID (expensive).

   d. Endorphin blockers:

       1. Naltrexone (Trexan) 2.2 mg/kg SID.

   e. Endorphin substitution:



                                    112
               1. Hydrocodone (Hycodan) 0.25 mg TID.

       8. Avoid surgical excision: dehiscence is common.


                                     Important Facts

 If the underlying condition can be determined, the prognosis improves dramatically.

 Approximately 65% of the cases can be satisfactorily controlled with medical and/or
  behavior management.

 Even if an underlying problem has been identified and treated, concurrent treatment
   of the acral lick lesion is essential.




                                            113
                                       References


1. Nesbitt G.E. & Ackerman L.J. Miscellaneous Canine Skin Diseases. In: Canine and
   Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 314-353.




                                 Learning Objectives


1. Know! The pathogenesis of acral lick dermatitis is unknown and it is one of the most
   frustrating dermatologic conditions to manage. Most cases recur at the same site or
   different sites.

2. Know! Many factors have been suggested to predispose to or cause acral lick
   dermatitis, including allergy (atopic dermatitis, food), psychogenic, boredom,
   bacterial folliculitis, foreign bodies, neuropathy, local trauma, and joint or bone
   diseases. Always look for an underlying condition when managing this disease!

3. Know! Lesions are usually single but multiple lesions can be present. Lesions
   generally develop on the carpus or metacarpus area and are characterized by alopecic,
   erythematous, eroded or ulcerated, firm nodular plaques. Large breeds are
   predisposed.

4. Know! Diagnosis is based on history, clinical signs and elimination of other primary
   causes. The minimum data base should include skin scrapings (to rule out demodex
   mange), impression smear cytology (to look for bacteria or fungal organisms), and
   fungal culture (to rule out dermatophytosis). Perform a biopsy if you suspect of
   neoplasia. If joint or bone involvement is suspected, radiographs should be taken.

5. How do you manage acral lick dermatitis?

6. Remember! The lesion(s) is induced by the animal and contribute to the perpetuation
   of the compulsive licking behavior. Stop the licking!




                                            114
           Canine and Feline Miscellaneous Skin Diseases
                   Cutaneous Asthenia – Canine and Feline



   A. General Considerations:

       1. Cutaneous asthenia, also known as Ehlers-Danlos syndrome and
          dermatoparaxis, is a rare hereditary group of conditions characterized by
          abnormal collagen development.

       2. Several forms of cutaneous asthenia based on clinical, genetic, and
           biochemical differentiation have been recognized in man, dogs, cats, cattle
           and sheep.

       3. All these forms have a common basis in that they are accompanied by
          connective tissue weakness due to abnormalities in biosynthesis or post-
          translational modifications of collagen.


                                  Important Facts

 Cutaneous asthenia, also known as Ehlers-Danlos syndrome and dermatoparaxis, is a
   rare hereditary group of conditions characterized by abnormal collagen development.

 Several forms of cutaneous asthenia based on clinical, genetic, and biochemical
   differentiation have been recognized in man, dogs, cats, cattle and sheep.


   B. Pathogenesis:

       1. In dogs, cutaneous asthenia is usually an autosomal dominant condition.

       2. It is associated with collagen packing defect characterized by focal or diffuse
           areas of severely disorganized fibers with many abnormally large fibrils.

       3. The loss of rigidity and tensile strength associated with the collagen packing
           defect predisposes the affected skin to excessive tearing.




                                           115
       4. Two forms of cutaneous asthenia have been reported in the cat: a dominant
           form similar to the collagen packing defect of dogs and a recessive form
           characterized by a deficiency on N-procollagen peptidase enzyme which
           results in collagen that is in the form of twisted ribbons instead of cylindric
           fibrils and fibers.


                                   Important Facts

 In dogs, cutaneous asthenia is usually an autosomal dominant condition associated
   with collagen packing defect.

 Two forms of cutaneous asthenia have been reported in the cat: a dominant form
   similar to the collagen packing defect of dogs and a recessive form characterized by a
   deficiency on N-procollagen peptidase enzyme which results in collagen that is in the
   form of twisted ribbons instead of cylindric fibrils and fibers.


   C. Clinical Signs:

       1. Cutaneous asthenia has been reported in the Beagle, Boxer, English setter,
          English springer spaniel, German shepherd, Greyhound, Irish setter,
          Keeshond, Saint Bernard and mixed breed dogs.

       2. In cats, cutaneous asthenia has been documented in domestic short-haired cat,
           and the Himalayan cat.

       3. Fragility of the skin since birth is the most characteristic clinical sign.
           However, it may not be recognized by the owner very early in life.

       4. Clinically, animals will have multiple scars or tears in the skin.

       5. There is minimal hemorrhage associated with skin lacerations.

       6. Some animals will also have hyperextensibility of the skin and/or joint laxity.

       7. Cats may develop fragile skin due to naturally occurring or iatrogenic
          hyperadrenocorticism, diabetes mellitus, or with excessive use of megestrol
          acetate.




                                            116
                                   Important Facts

 Fragility of the skin since birth is the most characteristic clinical sign. However, it
   may not be recognized by the owner very early in life.

 Clinically, animals will have multiple scars or tears in the skin with minimum
   hemorrhage.

 Some animals will also have hyperextensibility of the skin and/or joint laxity.

 Cats may develop fragile skin due to naturally occurring or iatrogenic
   hyperadrenocorticism, diabetes mellitus, or with excessive use of megestrol acetate.


   D. Diagnosis:

        1. History and clinical signs are usually sufficient to make a diagnosis of
           cutaneous asthenia.

        2. Histopathologic findings are variable. The collagenous fibers in the affected
           skin are small and sparse compared with control sections.

        3. Electron microscopic and biochemical analysis of the dermal collagen are
            needed for definitive diagnosis.


                                   Important Facts

 History and clinical signs are usually sufficient to make a diagnosis of cutaneous
  asthenia.

 Electron microscopic and biochemical analysis of the dermal collagen are needed for
  definitive diagnosis.


   E. Treatment:

        1. There is no specific treatment for cutaneous asthenia.

        2. Lacerations must be sutured using tension patterns.

        3. The animal should be protected from any minor or major trauma.




                                            117
       4. Cats should declawed to prevent wounding during grooming or scratching.



                                  Important Facts

 There is no specific treatment for cutaneous asthenia.

 Lacerations must be sutured using tension patterns.

 The animal should be protected from any minor or major trauma.




                                          118
                                      References



1. Nesbitt G.E. & Ackerman L.J. Miscellaneous Canine Skin Diseases. In: Canine and
   Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 314-353.

2. Scott, Miller & Griffin. Congenital and Hereditary Defects. In: Small Animal
   Dermatology. W.B. Saunders, Philadelphia, 1995, pp 736-805.




                                Learning Objectives



1. Know! Cutaneous asthenia, also known as Ehlers-Danlos syndrome and
   dermatoparaxis, is a rare hereditary group of conditions characterized by abnormal
   collagen development.

2. Know! A dominant form of the disease has been documented in dogs and it is
   associated with abnormal collagen packing resulting in decreased skin tensile
   strength. In cats, a dominant and a recessive form have bee reported. The recessive
   form is associated with a deficiency of N-procollagen peptidase enzyme and the
   dominant form is similar to the one described in dogs.

3. Know! Signs are present at birth but they are not always recognized by the owner
   early in life. The skin may present with multiple scars and will lacerate easily with
   minor trauma. Minimum blood is usually associated with the skin laceration. Some
   animals will also have hyperextensibility of the skin and or joint laxity.

4. Remember! Cats may develop fragile skin due to naturally occurring or iatrogenic
   hyperadrenocorticism, diabetes mellitus, or with excessive use of megestrol acetate.

5. Know! Diagnosis can usually be done based on history and clinical signs.
   Remember, there are other conditions that can cause skin fragility in cats. The
   definitive diagnosis requires electron microscopy and biochemical analysis of the
   dermal collagen.

6. How do you manage cutaneous asthenia?



                                           119
           Canine and Feline Miscellaneous Skin Diseases
                        Tail Gland Hyperplasia – Canine


   A. General Considerations:

       1. It is a hyperplasia of the glands present on the dorsal surface of the tail which
          results in an area of alopecia and thickening of the skin.


                                   Important Facts

 Tail gland hyperplasia is a hyperplasia of the glands present on the dorsal surface of
  the tail which results in an area of alopecia and thickening of the skin.



   B. Etiology and Pathogenesis:
       1. Dogs have a focal oval area on the dorsum of the tail about 2.5 to 5 cm distal
          to the anus that has simple hair follicles with large numbers of sebaceous
          glands and occasional perianal (hepatoid) glands.

       2. In some animals for unknown reasons, these glands become hyperplastic.

       3. Foreign body reaction may occur if there is rupture of hair follicles or
          sebaceous glands.


                                   Important Facts

 Dogs have a focal oval area on the dorsum of the tail about 2.5 to 5 cm distal to the
  anus that has simple hair follicles with large numbers of sebaceous glands and
  occasional perianal glands.

 In some animals for unknown reasons, these glands become hyperplastic and if the
  hair follicles or sebaceous glands rupture, a foreign body reaction will develop.


   C. Clinical Signs:

       1. Signs are characterized by an oval area of alopecia and thickening of the skin
          on the dorsal surface of the tail about one fourth of distance from the tail
          base.




                                           120
        2. Skin overlying the affected area may be normal, hyperpigmented, greasy,
           scaling or evidence comedones.

        3. Papules, nodules, hemorrhagic bullae, and draining tracts may develop due to
           foreign body reactions caused by ruptured hair follicles or sebaceous glands
           and may predispose to secondary infection.

        4. Pruritus is usually not present.

                                     Important Facts

 Signs are characterized by an oval area of alopecia and thickening of the skin on the
  dorsal surface of the tail about one fourth of distance from the tail base.

 Skin overlying the affected area may be normal, hyperpigmented, greasy, scaling or
  evidence comedones.

 Draining tracts will be formed if hair follicles rupture and a foreign body reaction
  occurs.

 Pruritus is usually not present.


   D. Diagnosis:

        1. Diagnosis is based on history, clinical signs and skin biopsy (rarely
           performed).

        2. Differentials include: neoplasia, staphylococcal furunculosis, arthropod-bite
           granuloma.


                                     Important Facts

         Diagnosis is based on history, clinical signs and skin biopsy.




   E. Treatment:

        1. Treatment is usually not necessary as the condition is, in most cases, a non -
           progressive cosmetic disorder.

        2. If the area is greasy, bathing it with a benzoyl peroxide shampoo every 2 to 5
           days may be helpful.


                                              121
       3. Oral glucocorticoids for 5 to 10 days would be appropriated if there is a
          foreign body reaction and systemic antibiotics for at least 14 days if there is a
          secondary bacterial infection.

       4. Neutering of male dogs may result in some decrease in size of the lesion.

       5. Twice a day application of a solution containing flucinolone acetonide in
          dimethyl sulfoxide (Synotic) may be helpful in cases associated with severe
          inflammation.


                                  Important Facts

 Treatment is usually not necessary as the condition is, in most cases, a non -
  progressive cosmetic disorder.

 Degreasing shampoos can be used if the area is very greasy.

 Systemic and/or topical glucocorticoids should be prescribed if there is severe
  inflammation.

 Systemic antibiotics should be prescribed for secondary bacterial infections.




                                           122
                                      References


1. Scott, Miller & Griffin. Keratinization Defects. In: Small Animal Dermatology.
   W.B. Saunders, Philadelphia, 1995, p 824-844.



                                Learning Objectives


1. Know! Dogs have a focal oval area on the dorsum of the tail about 2.5 to 5 cm distal
   to the anus that has simple hair follicles with large numbers of sebaceous glands and
   occasional perianal (hepatoid) glands. In some dogs for unknown reasons these
   glands become hyperplastic.

2. Know! Clinical signs are characterized by an oval, bulging, hairless area on the tail.
   The overlying skin may be normal, scaly, greasy, hyperpigmented, or some
   combination thereof. Comedones can also be seen at this area. If hair follicles or
   sebaceous glands rupture, a foreign body reaction develops which is characterized by
   the presence of draining tracts. Secondary bacterial infection is rare but can occur.

3. Know! Diagnosis is based on history and clinical signs. Biopsies can be performed
   to rule out neoplasia or arthropod-bite granuloma.

4. How do you manage tail gland hyperplasia?




                                           123
           Canine and Feline Miscellaneous Skin Diseases
                         Tail Gland Hyperplasia – Feline


   A. General Considerations:

       1. Cats have the same tail gland area as dogs, but it is located in a line along the
          dorsal aspect of the tail and is commonly called the supracaudal organ.

       2. As in dogs, this area is rich in sebaceous and apocrine glands, and a waxy
          secretion accumulates on the surface.

       3. These glands are most active in intact cats; however, tail gland hyperplasia
          does occur in neutered males or females.


                                   Important Facts

 Cats have the same tail gland area as dogs, but it is located in a line along the dorsal
  aspect of the tail and is commonly called the supracaudal organ.

 These glands are most active in intact cats; however, tail gland hyperplasia does occur
  in neutered males or females.


   B. Clinical Signs:

       1. The affected area is characterized by accumulation of a waxy secretion on the
          surface, which leads to matting of the hair, formation of scales and crusts,
          thinning of the hair, and sometimes hyperpigmentation.

       2. Occasionally, there will be a secondary bacterial folliculitis and/or
          furunculosis.


                                   Important Facts

 The affected area is characterized by accumulation of a waxy secretion on the surface,
  which leads to matting of the hair, formation of scales and crusts, thinning of the hair,
  and sometimes hyperpigmentation.




                                            124
   C. Diagnosis:

       1. Diagnosis is based on history and clinical signs.


   D. Treatment:

       1. Treatment consists of clipping the affected area and bathing with
          antiseborrheic shampoos such as benzoyl peroxide.

       2. This treatment should be followed by daily cleaning with alcohol or a milder
          antiseborrheic shampoo such as sulfur-salicylic acid.

       3. Retinoids have not been used in this condition but they may be of some value
          in recalcitrant cases.

       4. If the cat fails to groom the affected area, the owner must carefully and
          frequently comb and groom the area to prevent recurrences.

       5. Treat secondary bacterial infections with appropriate antibiotics.

       6. Castration does not resolve the condition but may help stop its progression.


                                  Important Facts

 Treatment consists of clipping the affected area and bathing with antiseborrheic
  shampoos such as benzoyl peroxide.

 Frequent grooming and combing of the area may be needed for chronic cases.

 Castration does not resolve the condition but may help stop its progression.




                                           125
                                      References


1. Scott, Miller & Griffin. Keratinization Defects. In: Small Animal Dermatology.
   W.B. Saunders, Philadelphia, 1995, p 824-844.




                                Learning Objectives


1. Know! In cats, as in dogs, there is an increased concentration of sebaceous and
   apocrine glands along the dorsal tail. In cats this area is more extensive and occupies
   a line along the dorsal aspect of the tail and it is called supracaudal organ.

2. Know! Hyperplasia of these glands is clinically characterized by accumulation of a
   waxy secretion on the surface, which leads to matting of the hair, formation of scales
   and crusts, thinning of the hair, and sometimes hyperpigmentation. Occasionally, a
   secondary bacterial folliculitis and furunculosis may develop.

3. How do you manage feline tail gland hyperplasia?




                                           126
       Canine and Feline Miscellaneous Skin Diseases
            Psychogenic Alopecia and Dermatitis –Feline


A. General Considerations:

   1. Psychogenic alopecia or dermatitis is an alopecia or a chronic skin
      inflammation produced by constant licking.

   2. When dermatitis is not present, the complaint may be of excessive grooming.

   3. The dermatitis results from more severe grooming.


                               Important Facts

  Psychogenic alopecia or dermatitis is a self-inflicted alopecia or
   dermatitis.


B. Cause and Pathogenesis:

   1. Psychogenic alopecia or dermatitis is believed to be a stereotypic behavior
      disorder (anxiety neurosis) manifested by self-licking, hair pulling, and
      incessant overgrooming.

   2. There is a probable relationship between stressful stimuli and the release of
      adrenocorticotropin hormone and alpha-melanocyte-stimulating hormone
      (alpha-MSH) which then causes increased endorphin production .

   3. The endorphins protect the animal from abnormalities associated with chronic
      stress. However, their narcotic, addictive-like effect may act to reinforce the
      abnormal grooming behavior.

   4. Many predisposing factors have been associated with the development of
      stress-related anxiety activities.

   5. Some cats are temperamentally predisposed, with the predilections reported
      for Siamese and Abyssinian cats.

   6. Lifestyles of the cats may predispose to territorial or psychologic stress.

   7. The introduction of new pets, a baby, or visitors into the cat’s environment
      may trigger a psychogenic dermatosis.


                                       127
       8. Displacement factors, such as moving to a new home or boarding of the
          animal, may result in excessive grooming.

       9. In some of these cases, the initial pruritic stimulus may no longer be present
          and identifiable, but overgrooming has become self-reinforcing.


                                  Important Facts

 Psychogenic alopecia or dermatitis is believed to be a stereotypic behavior disorder
  manifested by self-licking, hair pulling, and incessant overgrooming.

 Many predisposing factors have been associated with the development of stress-
  related anxiety activities such as: breeds, the introduction of new pets, a baby, or
  visitors into the cat’s environment, moving to a new home or boarding of the animal.

 A thorough history is very important to identify and modify or remove these factors.


   C. Clinical Signs:
       1. Psychogenic alopecia or dermatitis can be expressed in many ways.

       2. Some cats lick vigorously at a particular area until the sharp barbs on the
          tongue produce alopecia, abrasion, ulceration, and secondary infection.
          Eosinophilic plaque may develop in these cases.

       3. Other cats lick and chew more gently or over a more widespread area, so
          alopecia is the predominant lesion.

       4. Some cats actually chew at their hair or skin, whereas others chew and pull
          their hair out.

       5. Areas that the cat can lick easily are the most common sites: medial forelegs,
          the inside of the thigh, the caudal abdomen, and the inguinal region.

       6. Less commonly, the dorsal lumbar, sacral, or tail regions may be involved.

       7. Symmetric bilateral alopecia is common.

       8. The course is long and progresses slowly, sometimes remaining static for
          months.




                                           128
       9. In the Siamese cat, color changes in the coat are observed. The hair may
          become dark due to activation of the temperature-labile enzymes that convert
          melanin precursors to melanin.

                                   Important Facts

 Psychogenic alopecia or dermatitis can be expressed in many ways such as: self-
  licking or gentle chewing, hair pulling, and incessant overgrooming.

 An inflammation of the skin may or may not be present depending on how aggressive
  the cat is when performing the stereotypic behavior.

 Eosinophilic plaques may develop if the animals lick aggressively and constantly one
  focal area of the skin.

 Areas that the cat can lick easily are the most commonly affected sites.

 The course is long and progresses slowly, sometimes remaining static for months.


   D. Diagnosis:

       1. The diagnosis of psychogenic alopecia is difficult.

       2. One must be aggressive in ruling out a primary pruritic dermatitis, which
          would include allergies (flea, food, atopy), external parasites (fleas,
          Cheyletiella, Otodectes), and dermatophytosis.

       3. Because feline psychogenic alopecia is diagnosed primarilly by ruling out
          other differential diagnoses, an accurate diagnosis involves a complete work-
          up.

       4. Skin scrapings, fungal cultures, biopsies (which should show normal skin in
          nondermatitic areas), and a CBC constitute the minimal data base that should
          be obtained.

       5. If an eosinophilia is present or the biopsy reveals an inflammatory or
          endocrine appearance, the diagnosis of psychogenic alopecia is not warranted.

       6. Further tests should include hypoallergenic diet trials, trial ectoparasite
          therapy for Cheyletiella, and Otodectes, intradermal skin testing, and
          endocrine function testing.

       7. An initial alternative to the endocrine function test may be a 30-day trial with
          an Elizabethan collar. Cats that have hormone imbalances (very rare) do not
          regrow their hair when grooming is prevented.


                                            129
       8. If there is any question about the self-inflicted nature of the alopecia, one
          should perform a trichogram (microscopic examination of hairs) to
          demonstrate broken hair shafts.

                                   Important Facts

 The diagnosis of psychogenic alopecia is difficult.

 Because feline psychogenic alopecia is diagnosed primarilly by ruling out other
  differential diagnoses, an accurate diagnosis involves a complete work-up which
  should include: skin scrapings, fungal cultures, biopsies, CBCs, food elimination trial,
  intradermal skin testing, trial ectoparasite therapy, and endocrine function testing.


   E. Treatment:

       1. The goal of the treatment is to remove the cat’s desire to obsessively lick
          himself, thus reducing self-trauma.

       2. The two approaches to achieve this are:

           a. Identify and modify or remove the initiating stress factors.

           b. Use medical therapy to reduce the cat’s response to the stress.

               1. The identification and modification of stress factors requires
                  counseling and education of the client. It is frequently impossible to
                  avoid the predisposing stress factor.

               2. Many of the medications used for psychogenic alopecia have potential
                  side-effects, require frequent administration and are expensive:

                  a. Tricyclic antidepressants (serotonin reuptake inhibitors):

                      1. Amitriptyline (Elavil): 1 to 2 mg/kg BID.

                      2. Clomipramine (Anafranil): 1 to 3 mg/kg q 24h.

                          a.   Serotonin reuptake inhibitor:

                      3. Fluoxetine (Prozac): 1 mg/kg q 24h (20 mg cap).

                          a. Valium: ¼ of 5 mg tab 2 to 3 times daily.



                                            130
       3. Again, the side effects of these drugs can be striking so, one must weight the
          severity of the disease against the possible drug toxicities.


                                   Important Facts

 The goal of the treatment is to remove the cat’s desire to obsessively lick himself,
  thus reducing self-trauma.

 The two approaches to achieve this are: identify and modify or remove the initiating
  stress factors which is not always easy; and use medical therapy to reduce the cat’s
  response to the stress (medications have potential side effects, have to be given
  frequently and are expensive).




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                                       References


1. Scott, Miller & Griffin. Psychogenic Skin Diseases. In: Small Animal Dermatology.
   W.B. Saunders, Philadelphia, 1995, p 845-858.


                                 Learning Objectives

1. Know! Psychogenic alopecia or dermatitis is an alopecia or a chronic skin
   inflammation produced by licking, chewing, hair pulling or overgrooming. The
   presence or absence of skin inflammation will depend on how aggressive the animals
   are when performing the obsessive behavior.

2. Know! Psychogenic alopecia or dermatitis is believed to be a stereotypic behavior
   disorder. It is believed that endorphins are released during the stress situations
   associated with the obsessive grooming behavior and that endorphins play and
   additive reinforcement role, maintaining the stereotypic behavior response.

3. Know! Many predisposing factors have been associated with the development of
   stress-related anxiety activities such as: breeds, the introduction of new pets, a baby,
   or visitors into the cat’s environment, moving to a new home or boarding of the
   animal. So, a thorough history is very important to identify and modify or remove
   these factors.

4. Know! Psychogenic alopecia or dermatitis can be expressed in many ways such as:
   self-licking or gentle chewing, hair pulling, and incessant overgrooming. An
   inflammation will be present if the animal licks at his skin constantly and
   aggressively. Eosinophilic plaques can develop if the cat is obsessive about a specific
   area of the skin.

5. Know! Areas that the cat can lick easily are the most commonly affected sites: medial
   forelegs, the inside of the thigh, the caudal abdomen, and the inguinal region. Less
   commonly, the dorsal lumbar, sacral, or tail regions may be involved. Symmetrical
   bilateral alopecia is common.

6. Know! The diagnosis of psychogenic alopecia is difficult and frustrating. Because
   feline psychogenic alopecia is diagnosed primarilly by ruling out other differential
   diagnoses, an accurate diagnosis involves a complete work-up which should include:
   skin scrapings, fungal cultures, biopsies, CBCs, food elimination trial, intradermal
   skin testing, trial ectoparasite therapy, and endocrine function testing. If a biopsy of
   a nodermatitic area shows inflammation, the diagnose of purely psychogenic alopecia
   is not warranted. However, some cats may have an allergic and psychogenic
   components contributing to their problems.

7. How do you mange this challenging skin condition?


                                            132
           Canine and Feline Miscellaneous Skin Diseases
                   Feline Eosinophilic Granuloma Complex

   A. General Considerations:

       1. The eosinophilic granuloma complex include a group of lesions that affect the
          skin, mucocutaneous junctions and oral cavity of cats.

       2. Depending on the type of lesion and body location, the disease can have a
          variable history and clinical presentation.

       3. It is important to realize that the eosinophilic granuloma complex is nothing
          more than a skin reaction pattern in cats, not a specific disease.

       4. Three lesions have been recognized:

           a. The indolent ulcer.

           b. The eosinophilic plaque.

           c. The eosinophilic granuloma.

              1. These occur frequently, and are most commonly seen in cats with
                 allergies to inhalants, foods, or insects, especially to fleas and
                 mosquitoes.

              2. Bacterial involvement may occasionally be a factor, because antibiotic
                 therapy resolves or markedly improves some lesions.

              3. When no hypersensitivity disorders can be identified, a heritable form
                 of the disease should be considered.

                                    Important Facts
 The eosinophilic granuloma complex include a group of lesions that affect the skin,
  mucocutaneous junctions and oral cavity of cats.

 Depending on the type of lesion and body location, the disease can have a variable
  history and clinical presentation.

 Three lesions have been recognized: the eosinophilic ulcer, the eosinophilic plaque
  and the eosinophilic granuloma.

 The etiology is unknown but, some cases are associated with allergic conditions,
  bacterial infections and genetic factors.




                                          133
I. Feline Indolent Ulcer

   A. General Considerations:

       1. Indolent ulcer, also called eosinophilic ulcer or rodent ulcer, is a common
          cutaneous, mucocutaneous, and oral mucosal lesion of cats.

                                  Important Facts

 Indolent ulcer, also called eosinophilic ulcer or rodent ulcer, is a common cutaneous,
  mucocutaneous, and oral mucosal lesion of cats.


   B. Etiology:

       1. The etiology of indolent ulcers is unknown.

       2. There are reports of cats with indolent ulcers having positive intradermal skin
          tests and subsequent response to hyposensitization therapy, suggesting an
          allergic etiology.

       3. A genetic predisposition has been suggested based on studies in a SPF cat
          colony in which there was a high incidence of indolent ulcers without
          identification of allergy or parasites.


                                  Important Facts

 The etiology of indolent ulcers is unknown.

 However, some cases may be associated with allergies or genetic factors.


   C. Clinical Signs:

       1. There are no age or breed predilection, but females may be predisposed.

       2. The lesions are well-demarcated with raised margins and a central granular
          and glistening ulcerated area. The size is quite variable.

       3. Most indolent ulcers occur unilaterally on the upper lip. However, lesions can
          be bilateral and also occur in the oral cavity or in other areas of the skin.

       4. Pruritus and pain are rare, and peripheral lymphadenopathy may be present.


                                          134
       5. They recur frequently and, occasionally they will be refractory to treatment.

       6. Nodular or ulcerative lesions in the oral cavity or on the lateral lips are usually
          eosinophilic granulomas.

       7. Rarely, an indolent ulcer will transform into a squamous cell carcinoma.


                                   Important Facts

 There are no age or breed predilection, but females may be predisposed.

 The lesions have variable sizes and are well-demarcated with raised margins and a
  central granular and glistening ulcerated area.

 Most indolent ulcers occur unilaterally on the upper lip. However, lesions can be
  bilateral and also occur in the oral cavity or in other areas of the skin.

 Lesions recur frequently and, occasionally they will be refractory to treatment.

 Rarely, an indolent ulcer will transform into a squamous cell carcinoma.


   D. Diagnosis:

       1. The history and clinical signs are usually diagnostic of indolent ulcers.

       2. It is important to try to identify any underlying conditions such as food allergy
          and atopy while also maintaining a good flea control.

       3. Differentials include: neoplasia (squamous cell carcinoma or mast cell tumor)
          or infectious granulomas (bacterial, fungal, FeLV-associated). Skin biopsies
          are necessary to rule out these other dermatoses.

       4. The histopathologic findings are variable and non-diagnostic.




                                            135
                                   Important Facts

 The history and clinical signs are usually diagnostic of indolent ulcers.

 It is important to try to identify any underlying conditions such as food allergy and
  atopy while also maintaining a good flea control.

 Biopsies are necessary to rule out neoplasia and infectious granulomas but, the
  histopathologic findings of indolent ulcer are non-diagnostic.

   E. Treatment:

       1. Look for an underlying condition and try to resolve it, if feasible, or to
          control it.

       2. Corticosteroids are often needed to control the lesions.

       3. Methylprednisolone acetate (Depo-Medrol) at the dose of 4 mg/kg IM
          (minimum of 20 mg/cat) every 2 weeks as an initial therapy is usually
          satisfactory.

       4. Before the lesions resolve, 2 or 3 injections may be necessary.

       5. If the problem recurs, the residual corticosteroid injections may need to be
          administered every 2 months (never more frequently than every 2 months).

       6. Oral prednisolone (4 to 5 mg/kg every 24 hours) may be satisfactory. If long-
          term maintenance is needed, 2 mg/kg every 48 hours is suggested.

       7. Chlorambucil (Leukoran-Glaxo Wellcome) 0.1 to 0.2 mg/kg orally every 24
          to 48 hours may be used in conjunction with the corticosteroids to decrease
          steroid dosage.

       8. Triamcinolone acetonide (0.5 to 0.75 mg/kg orally every 24 hours) as the
          initial dosage then tapered to every 48 to 72 hours is another alternative
          therapy.

       9. If there is a poor response to corticosteroids, gold salts (aurothioglucose;
          Solganal-Schering) are an option. It is administered at the dose of 1 mg/kg
          every 7 days. There is a lag phase of 6 to 12 weeks before clinical response is
          observed.

       10. Steroids can be used in conjunction with gold salts.

       11. Cats being treated with gold salts should be monitored for bone marrow
           suppression, proteinuria and cutaneous or oral cavity drug eruption.


                                           136
       12. Some cases will completely respond to antibiotic therapy, others will show
           significant improvement. Appropriate antibiotics include: trimethoprim-
           sulfadiazine (30 mg/kg every 12 hours), cefadroxil (22 mg/kg every 12 hours),
           and amoxicillin-clavulanate acid (12.5 mg/kg every 12 hours).

       13. Megestrol acetate has resulted in satisfactory resolution of lesions, but is
           generally not recommended because of the many long-term side effects.


                                    Important Facts

 Look for an underlying condition and try to resolve it if feasible, or to control it.

 Injectable or oral glucocortocoids are often needed to control the lesions.

 Lesions often recur and animals may need to be maintained on long-term alternate
  schedule of oral glucocorticoids or periodic injectable glucocorticoids.

 Chlorambucil may be used in conjunction with the corticosteroids to decrease steroid
  dosage.

 If there is a poor response to corticosteroids, gold salts are an option.

 Some cases will completely respond to antibiotic therapy, others will show significant
  improvement. Therefore, antibiotics should be always tried.




                                            137
II. Feline Eosinophilic Plaque


   A. General Considerations:
       1. Eosinophilic plaque is a common cutaneous lesion of cats.

       2. The etiology is unknown. However, the eosinophilic plaque is thought to be a
          hypersensitivity reaction to fleas, food, or environmental allergens.


                                  Important Facts

 The etiology of eosinophilic plaque is unknown. However, the eosinophilic plaque is
  thought to be a hypersensitivity reaction to fleas, food, or environmental allergens


   B. Clinical Signs:

       1. Most eosinophilic plaques occur on the ventral abdomen and medial thighs.

       2. Lesions may be single or multiple, and they may occur on mucocutaneous
          junctions or in other areas of the skin.

       3. Eosinophilic plaques are well circumscribed, raised but flat, round to oval,
          red, oozing, often eroded and sometimes ulcerated. Size varies from 0.5 to
          7 cm in diameter.

       4. Pruritus is usually severe.

       5. Most plaques occur in allergic patients.

       6. Peripheral lymphadenopathy may be present.

       7. There are no age or breed predilection but, females may be predisposed.




                                          138
                                   Important Facts

 Most eosinophilic plaques occur on the ventral abdomen and medial thighs.

 Lesions may be single or multiple, and they may occur on mucocutaneous junctions
  or in other areas of the skin.

 Lesions often will have an eroded or ulcerated surface and have variable sizes.

 Pruritus is usually severe.

 Most plaques occur in allergic patients.


   C. Diagnosis:

       1. Diagnosis is based on history and clinical signs.

       2. Skin biopsy is important to rule out infectious granulomas (bacterial, fungal)
          and neoplasia (mast cell tumor, lymphoma).

       3. Biopsy results are variable and non-diagnostic.

       4. It is necessary to try to identify an underlying allergic condition (flea control,
          food elimination trial, and /or intradermal skin testing).


                                   Important Facts

 Diagnosis is based on history and clinical signs.

 Skin biopsy is important to rule out infectious granulomas (bacterial, fungal) and
  neoplasia (mast cell tumor, lymphoma).

 It is necessary to try to identify an underlying allergic condition (flea control, food
  elimination trial, and /or intradermal skin testing).


   D. Treatment:

       1. Treatment methods are as described for feline indolent ulcer.

       2. Treat appropriately any identified underlying allergic condition.


                                             139
                                   Important Facts

 Treat appropriately any identified underlying allergic condition.

 All aspects of treatment are similar to the ones already described for indolent ulcer.




                                           140
III. Eosinophilic Granuloma

   A. General Considerations:

       1. Feline eosinophilic granuloma is a common cutaneous, mucocutaneous and
          oral mucosal lesion of cats.

       2. The pathogenesis and etiology of eosinophilic granulomas are unknown.

       3. In some cats, an allergic etiology has been reported.

       4. In other cats, an allergic etiology was not identified despite a comprehensive
          evaluation.

       5. There are a limited number of reports of a hereditable basis for the
          development of lesions.

                                  Important Facts

 Feline eosinophilic granuloma is a common cutaneous, mucocutaneous and oral
  mucosal lesion of cats.

 The pathogenesis and etiology of eosinophilic granulomas are unknown but, in some
  cases an allergic etiology has been reported.

 Genetic factors may also play a role in the pathogenesis of this condition.


   B. Clinical Signs:

       1. Eosinophilic granulomas are raised, pink, alopecic lesions that may feel coarse
          or gritty.

       2. The lesions may ulcerate.

       3. The distribution is variable.

       4. The linear granuloma, often occurring in cats less than 2 years of age, is
          characterized as a raised linear orientation on the caudal or medial aspects of
          the thigh. They are usually firm and have a yellow or pink color.

       5. Linear granulomas are often discovered by accident because they are not
          pruritic lesions.



                                           141
6. Occasionally, linear granulomas can be observed on the lateral trunk, neck,
   thorax, and forelimbs.

7. Lesions of linear granuloma may spontaneously resolve.

8. A second presentation of eosinophilic granuloma is individual or grouped
   nodular and/or ulcerated lesions. These have a diverse distribution including
   the footpads and trunk.

9. The pad lesions manifest with crusting and ulceration as well as interdigital
   alopecia and erythema.

10. Lesions on the footpads are usually associated with lameness.

11. Firm plaques or nodules may be seen on the pinnae.

12. The lip margins and chin often show marked edema (pouting).

13. Eosinophilic granuloma is the most common cause of lower lip swelling and
    nodules and asymptomatic swollen chins (fat-chinned cats) in the cat.

14. Nodules are observed in the oral cavity, especially the tongue and hard palate,
    and may become ulcerated.

15. Cats with oral lesions may be anorexic, have hypersalivation, problems with
    prehension of food, and halitosis.

16. Some cats with severe eosinophilic granuloma lesions have peripheral
    eosinophilia and eosinophilic lymphadenopathy.




                                    142
                                   Important Facts

 The clinical presentation varies according to the location of the lesion.

 Lesions are raised, alopecic, yellow or pink in color.

 Depending on the location, the lesions may ulcerate and may have a linear or nodular
  configuration.

 Linear lesions are more frequently seen on the caudal or medial aspects of the thighs
  and they are asymptomatic and can spontaneously regress.

 Lesions on the feet and oral cavity are nodular, usually ulcerated and will cause
  discomfort to the animals to walk or eat.

 Eosinophilic granuloma is the most common cause of lower lip swelling and nodules
  and asymptomatic swollen chins (fat-chinned cats) in the cat.

 Some cats with severe eosinophilic granuloma lesions have peripheral eosinophilia
  and eosinophilic lymphadenopathy.


   C. Diagnosis:

       1. The history and clinical signs are very suggestive of eosinophilic granuloma.

       2. All allergic causes, including fleas, food, and atopy, should be ruled out.

       3. Surface impression smears of eroded or ulcerated lesions will reveal
          eosinophils and their granules.

       4. Differentials for feet lesions are an abscess and plasma cell pododermatitis.

       5. Differentials for oral lesions include: neoplasia, inflammatory nodules, and
          foreign body reactions.

       6. Biopsies are indicated to rule out the various differential diagnoses.

       7. The key histopathologic findings are eosinophilic infiltration with
          degranulation and collagen degeneration.




                                           143
                                   Important Facts

 The history and clinical signs are very suggestive of eosinophilic granuloma.

 All allergic causes, including fleas, food, and atopy, should be ruled out.

 Biopsies are indicated to rule out the various differential diagnoses.


   D. Treatment:

       1. Any specific hypersensitivity reaction should be identified and controlled
          (flea, food, atopy).

       2. Linear granulomas are usually asymptomatic and do not need to be treated.
          Most cases have spontaneous resolution.

       3. All other aspects of therapy are as described for indolent ulcer.


                                   Important Facts

 Any specific hypersensitivity reaction should be identified and controlled (flea, food,
  atopy).

 Linear granulomas are usually asymptomatic and do not need to be treated. Most
  cases have spontaneous resolution.

 All other aspects of therapy are as described for indolent ulcer.




                                           144
                                       References


1. Scott, Miller & Griffin. Miscellaneous Skin Diseases. In: Small Animal
   Dermatology. W.B. Saunders, Philadelphia, 1995, p 902-955.

2. Nesbitt G.E. & Ackerman L.J. Miscellaneous Feline Dermatosis. In: Canine and
   Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 471-490.



                                 Learning Objectives


1. Know! The eosinophilic granuloma complex constitutes a group of lesions, not a
   specific disease. Lesions can be present on different skin sites, mucocutaneous
   junctions and oral cavity. Clinical presentation vary depending on the location of the
   lesion and type of the lesion. Three patterns of lesions have been recognized: the
   eosinophilic ulcer, the eosinophilic plaque and the eosinophilic granuloma.

2. Know! The etiology of the three lesion patterns is unknown but, some cases are
   associated with allergic conditions, bacterial infections and genetic factors.

3. Know! All 3 lesion patterns have the characteristic of being recurrent. Some lesions
   can eventually become refractory to treatment.

4. Know! Most indolent ulcers occur unilaterally on the upper lip. However, lesions
   can be bilateral and also occur in the oral cavity or in other areas of the skin. Females
   seen to be predisposed. Some cases of eosinophilic ulcer can transform into a
   squamous cell carcinoma.

5. Know! Most eosinophilic plaques occur on the ventral abdomen and medial thighs.
   Lesions may be single or multiple, and they may occur on mucocutaneous junctions
   or in the other areas of the skin. Lesions often will have an eroded or ulcerated
   surface and have variable sizes. Many cats with eosinophilic plaques have allergies
   (flea, food or atopy). Puritus is a common sign and it is usually severe.




                                            145
6. Know! Eosinophilic granuloma can develop on the skin, oral mucosa and
   mucocutaneous junctions. The clinical presentation varies depending on the site
   involved. The linear granuloma, occurs often in cats less than 2 years of age and is
   characterized as a raised linear orientation on the caudal or medial aspects of the
   thigh. They are usually firm and have a yellow or pink color. They are asymptomatic
   and can spontaneously resolve. Linear granulomas can also occur on the neck,
   thorax, lateral trunk and forearms. A second presentation of eosinophilic granuloma is
   individual or grouped nodular and/or ulcerated lesions. These have a diverse
   distribution including the footpads and trunk. Footpad lesions can become eroded
   and ulcerated and can cause lameness. Lesions of eosinophilic granuloma can
   develop in the oral mucosa and can be associated with anorexia, hypersalivation,
   problems with prehension of food, and halitosis. Eosinophilic granuloma is the most
   common cause of lower lip swelling and nodules and asymptomatic swollen chins
   (fat-chinned cats) in the cat.

7. Know! The diagnosis of the eosinophilic granuloma complex is based on history and
   clinical signs. It is very important to always look for underlying allergic conditions
   which are more often associated with the eosinophilic plaque. Skin biopsies are
   necessary to rule out neoplasia (squamous cell carcinoma, mast cell tumor,
   lymphoma) and infectious granulomas. However, the histopathologic findings
   associated with the eosinophilic granuloma complex are variable and non-diagnostic.

8. How do you manage these interesting group of lesions? Remember! The linear
   granuloma lesions are usually asymptomatic and most cases resolve spontaneously.




                                           146
           Feline and Canine Miscellaneous Skin Diseases
                                 Miliary Dermatitis




   A. General Considerations:

       1. Miliary dermatitis is a multifactorial cutaneous reaction pattern, and most
          cases are associated with flea allergies.

       2. All other causes of feline allergy including food allergy, atopy, and drug
          reactions must be considered as differential diagnoses.

       3. Other immunologic disorders which may have miliary-like lesions are
          pemphigus foliaceus and the hypereosinophilic syndrome.

       4. Parasitic disorders that may manifest as miliary dermatitis include:
          cheyletiellosis, otodectic acariasis, mosquito-bite hypersensitivity,
          pediculosis, demodicosis, and trombiculidiasis.

       5. Infectious agents causing this cutaneous reaction pattern include
          dermatophytosis, bacterial folliculitis, and Malassezia dermatitis.

       6. Making a long history short, almost every feline dermatosis can manifest
          clinically as miliary dermatitis.

                                  Important Facts

 Miliary dermatitis is a multifactorial cutaneous reaction pattern, and most cases are
  associated with flea allergies.

 Almost every feline dermatosis can manifest as miliary dermatitis.


   B. Clinical Signs:

       1. The gross lesions of miliary dermatitis consist of multiple, small, crusted
          erythematous papules.

       2. In areas where the haircoat is intact, the papules are more easily palpated
          rather than observed and are variably distributed depending on the primary
          cause.



                                           147
       3. Patchy alopecia secondary to self-trauma is common.


                                   Important Facts

 The gross lesions of miliary dermatitis consist of multiple, small, crusted
  erythematous papules.

 In areas where the haircoat is intact, the papules are more easily palpated rather than
  observed and are variably distributed depending on the primary cause.


   C. Diagnosis:

       1. It is not difficult to recognize clinically miliary dermatitis. However, the
          challenging part is to diagnose the primary dermatosis.

       2. The history and distribution of lesions may be supportive of a specific cause
          of miliary dermatitis, especially in the case of flea infestations.

       3. A thorough evaluation to rule out potential causes is necessary.

       4. This may include skin scrapings, flea combing, cytology, food trials,
          intradermal skin testing or ELISA tests for atopy, and fungal cultures.

       5. Biopsy findings are supportive of miliary dermatitis, but seldom will yield a
          definitive etiology.

       6. The predominant cells in the perivascular and interstitial dermal infiltrate are
          eosinophils and mast cells. Spongiotic eosinophilic pustules may be seen in
          the dermis. Eosinophilic folliculitis and furunculosis are observed in some
          severe miliary dermatitis lesions.



                                   Important Facts

 It is not difficult to clinically recognize miliary dermatitis. However, the challenging
  part is to diagnose the primary dermatosis.

 The history and distribution of lesions may be supportive of a specific cause of
  miliary dermatitis.

 A thorough evaluation to rule out potential causes is necessary.




                                           148
   D. Treatment:

       1. The successful management of miliary dermatitis is dependent upon
          identifying and controlling the primary causes.

       2. Supplementation with evening primrose oil alone or with a combination of
          evening primrose and fish oil may be used as adjunctive therapy.


                                 Important Facts

 The successful management of miliary dermatitis is dependent upon identifying and
  controlling the primary causes.




                                         149
                                      References


1. Nesbitt G.E. & Ackerman L.J. Miscellaneous Feline Dermatosis. In: Canine and
   Feline Dermatology: Diagnosis and Treatment. Veterinary Learning Systems,
   Trenton, New Jersey, 1998, p 471-490.




                                Learning Objectives

1. Know! Feline miliary dermatitis is not a disease entity but a cutaneous reaction
   pattern associated with almost every feline dermatosis. The most common clinical
   presention of flea bite hypersensitivity in cats is miliary dermatitis.

2. Know! The gross lesions of miliary dermatitis consist of multiple, small, crusted
   erythematous papules. If alopecia is not present, the lesions can be diagnosed
   through palpation. The distribution of the lesions will correspond to the primary
   cause. Pruritus may or may not be present depending on the primary disease.

3. Know! It is not difficult to diagnose the miliary dermatitis lesions but, it can be
   challenging to diagnose the dermatosis causing miliary dermatitis. A thorough
   evaluation to rule out potential causes is necessary and may include skin scrapings,
   flea combing, cytology, food trials, intradermal skin testing or ELISA tests for atopy,
   and fungal cultures. Biopsy findings are supportive of miliary dermatitis, but seldom
   will yield a definitive etiology.

4. How do you manage feline miliary dermatitis?




                                           150
              Large Animal Miscellaneous Skin Diseases
                            Equine Pastern Dermatitis



   A. General Considerations:

       1. Equine pastern dermatitis, so-called grease-heel is not a specific disease. It is
          a cutaneous reaction pattern of the horse.

       2. It is very important to remember that greasy heel is a multifactorial dermatitis
          having many potential causes.


                                   Important Facts

 Equine pastern dermatitis or greasy heel is a general term to describe a dermatitis
  localized to the pasterns that can be caused by many dermatoses.


   B. Clinical Signs:

       1. This dermatitis typically affects the caudal aspect of the pasterns.

       2. The hind limbs are most commonly involved, and the condition is almost
          always bilaterally symmetric.

       3. Initially, there is erythema and edema, which progresses to exudation and
          crusting.

       4. Secondary bacterial infection is a frequent complication.

       5. The dermatitis can spread cranially and proximally on the limbs.

       6. Pain and pruritus are variable.

       7. In chronic cases, thickening of the skin, fissures, exuberant granulation tissue,
          and severe edema of the limbs may be seen.

       8. Lameness may be present.




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                                   Important Facts

 This dermatitis typically affects the caudal aspect of the pasterns, with the hind legs
  being more often involved. The dermatitis can spread cranially and proximally on the
  limbs.

 Initially, there is erythema and edema, which progresses to exudation and crusting.

 Secondary bacterial infection is a frequent complication.

 In chronic cases, thickening of the skin, fissures, exuberant granulation tissue, and
  severe edema of the limbs may be seen.

 Lameness may be present.


   C. Diagnosis:

       1. Differentials include many dermatoses: staphylococcal folliculitis,
          dermatophilosis, dermatophytosis, horsepox, chorioptic mange,
          trombiculidiasis, primary contact irritant dermatitis, contact hypersensitivity,
          photosensitization, vasculitis and pemphigus foliaceus.

       2. Diagnosis of the primary condition is based on a thorough history, clinical
          signs and extensive work up to rule out or rule in the various dermatoses that
          can potentially cause pastern dermatitis.

       3. The minimum data base should include skin scrapings, cytologic examination
          of exudate, fungal and bacterial cultures and skin biopsies.

       4. In chronic cases, the etiology may be indeterminable.


                                   Important Facts

 Differential diagnosis include many dermatoses.

 Diagnosis of the primary condition is based on a thorough history, clinical signs and
  extensive work up to rule out or rule in the various dermatoses that can potentially
  cause pastern dermatitis.

 The minimum data base should include skin scrapings, cytologic examination of
  exudate, fungal and bacterial cultures and skin biopsies.



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   D. Treatment:

       1. Therapy is most successful when administered specifically and early.

       2. General symptomatic care includes: gentle clipping and cleasing; topical
          application of astringent and antiseptic soaks (if moist) or emollient creams
          and ointments (if dry and thickened); systemic antibiotic if needed; systemic
          glucocorticoids or nonsteroidal anti-inflammatory agents, and environmental
          hygiene.

       3. Chronic cases with exuberant granulation tissue may require surgical excision
          or cryosurgery.


                                  Important Facts

 Therapy is most successful when administered specifically and early.

 General symptomatic care should be instituted in association with the specific
  therapy.

 Chronic cases with exuberant granulation tissue may require surgical excision or
  cryosurgery.




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                                      References


1. Scott W.D. Miscellaneous Dermatoses. In: Large Animal Dermatology. W.B.
   Saunders, Philadelphia, 1988, p. 399-410.




                                Learning Objectives


1. Know! Pastern dermatitis is not a specific disease but, a term used to describe a
   cutaneous inflammation of the pastern region which can be caused by various
   dermatoses.

2. Know! The caudal aspects of the pasterns of both hind legs are more often affected.
   The lesion can progress cranially and proximally on the limbs. Initially, there is
   erythema and edema which progresses to exudation and crusting. Secondary bacterial
   infection is a common complication. In chronic cases, thickening of the skin, fissures,
   exuberant granulation tissue, and severe edema of the limbs may be seen. Lameness
   can be a problem in some cases.

3. Know! The list of conditions that can cause pastern dermatitis are lengthy and
   include: staphylococcal folliculitis, dermatophilosis, dermatophytosis, horsepox,
   chorioptic mange, trombiculidiasis, primary contact irritant dermatitis, contact
   hypersensitivity, photosensitization, vasculitis and pemphigus foliaceus. To
   determine the primary cause a thorough history and physical examination and an
   extensive work up including skin scrapings, fungal and bacterial cultures, cytologic
   exam of exudate and skin biopsies are needed. In chronic cases, the etiology may be
   indeterminable.

4. How do you manage equine pastern dermatitis?




                                           154
              Large Animal Miscellaneous Skin Diseases
                               Aural Plaque – Equine


   A. General Considerations:

       1. Aural plaque is a common skin disease of horses that occurs throughout the
          United States.

       2. Although it is rare or nonexistent in horses less than one year of age, it is
          common in all other age groups.

       3. The disease occurs in all breeds of horses, with no sex predilection.


                                   Important Facts

 Aural plaque is a common skin disease of horses that occurs throughout the United
  States.

 There is no sex, breed or age predilection.


   B. Etiology and Pathogenesis:

       1. Aural plaques are caused by a papilloma virus.

       2. Black flies (Simulium spp.) may serve as a mechanical vector.


                                   Important Facts

 Aural plaques are caused by a papilloma virus and black flies may serve as a
  mechanical vector.


   C. Clinical Signs:

       1. The lesions consist of one to several gray or white plaques involving the inner
          surface of the pinna.

       2. The individual plaques are sharply demarcated and vary from less than 1 mm
          to more than 2 cm in diameter.



                                            155
       3. When large numbers of plaques are present, they tend to coalesce; in severe
          cases, up to 50% of the inner surface of the pinna may be involved.

       4. The superficial portion of the plaques is composed of a keratinous crust that
          can be dislodged, revealing a pink nonulcerated base.

       5. The plaques appear to cause the horse no discomfort. If the horse’s ear itches,
          look for another problem!

       6. Once they occur, the lesions usually persist indefinitely.

       7. Identical lesions have occasionally occured around the anus and vulva.

                                  Important Facts

 The lesions consist of one to several gray or white plaques involving the inner surface
  of the pinna.

 The superficial portion of the plaques is composed of a keratinous crust that can be
  dislodged, revealing a pink nonulcerated base.

 The plaques appear to be asymptomatic.

 If the horse’s ear itches, look for another problem!

 Lesions tend to persist indefinitely.

 Identical lesions have occasionally occured around the anus and vulva.


   D. Diagnosis:

       1. The disease has a characteristic clinical appearance that should not be
          confused with any other disease.

       2. In horses with aural plaques that are showing signs such as pruritus or head
          shaking, should be thoroughly searched for other causes of ear irritation such
          as ear ticks, foreign bodies, psoroptes otitis.




                                           156
                                   Important Facts

 Diagnosis is based on the classic appearance of the lesions.

 In horses with aural plaques that are showing signs such as pruritus or head shaking,
  should be thoroughly searched for other causes of ear irritation such as ear ticks,
  foreign bodies, psoroptes otitis.


   E. Treatment:

       1. Aside from the unsightly appearance of this condition, it is of little
          consequence.

       2. A variety of topical medications have been used without success.

       3. There is one case report of 2 horses that responded to topical 0.05% tretinoin.
          Discontinuation of therapy resulted in recurrence of lesions.

       4. Can conceal with dyes or black markers for show horses.



                                   Important Facts

 Aural plaque is completely asymptomatic to the animal, however it can be
  cosmetically unpleasant.

 A variety of topical medications have been used without success.

 Topical tretinoin has temporarily resolved 2 cases.

 Can conceal with dyes or black markers for show horses.




                                           157
                                       References


1. Scott W.D. Neoplastic Diseases. In: Large Animal Dermatology. W.B. Saunders,
   Philadelphia, 1988, p. 419-467.


                                 Learning Objectives


1. Know! Aural plaque is a common equine disorder throughout the U.S.. There is no
   sex, breed or age predilection but it is rarely seen in horses less than one year old.

2. Know! Aural plaque is caused by a papilloma virus and, it is believed that black flies
   may serve as a mechanical vector.

3. Know! Lesions occur bilateral on the inner surface of the pinna and are characterized
   by one to several gray or white plaques of variable sizes. When the keratinous
   material covering the plaque is dislodged, an erythematous, non-erosive surface is
   present. Lesions do not bother the animal. If a horse with aural plaque shows signs
   of pruritus or head shaking, look for another condition! Lesions persist indefinitely.

4. Know! Diagnosis is based on clinical signs which are very typical. Again, in horses
   with aural plaques that are showing signs such as pruritus or head shaking, should be
   thoroughly searched for other causes of ear irritation such as ear ticks, foreign bodies,
   psoroptes otitis.

5. How do you manage equine aural plaque?




                                            158
              Large Animal Miscellaneous Skin Diseases
                          Exuberant Granulation Tissue


   A. General Considerations:

       1. The horse is notorious for the formation of exuberation granulation tissue
          (proud flesh) in wounds, especially those on the distal extremities.

       2. The cause of the condition is unknown.

       3. Exuberant granulation tissue differs from hypertrophic scar and keloid in that
          it lacks an epithelial covering and forms earlier in the healing process.


                                   Important Facts

 The horse is notorious for the formation of exuberation granulation tissue in wounds,
  especially those on the distal extremities.


   B. Clinical Signs:

       1. Equine exuberant granulation tissue is characterized clinically by a
          proliferation of hemorrhagic granulation tissue that fails to heal and
          epithelialize.


                                   Important Facts

 Equine exuberant granulation tissue is characterized clinically by a proliferation of
  hemorrhagic granulation tissue that fails to heal and epithelialize.


   C. Diagnosis:

       1. Differentials include: equine sarcoid, squamous cell carcinoma,
          habronemiasis, and infectious granulomas (e.g. pythiosis, botryomycosis).

       2. The diagnosis is based on biopsy findings.




                                           159
                                  Important Facts

 The diagnosis is based on biopsy findings.

 The differential diagnosis include: equine sarcoid, squamous cell carcinoma,
  habronemiasis, and infectious granulomas (e.g. pythiosis, botryomycosis).


   D. Treatment:

       1. Surgical excision of the exuberant tissue.




                                          160
                                      References


1. Scott W.D. Neoplastic Diseases. In: Large Animal Dermatology. W.B. Saunders,
   Philadelphia, 1988, p. 419-467.

2. Fretz P.B. et al. Treatment of exuberant granulation tissue in the horse: Evaluation of
   four methods. Vet. Surg. 12:137, 1983.

3. Jacobs K.A. et al. Comparative aspects of the healing of excisional wounds on the
   leg and body of horses. Vet Surg. 13:83, 1984.


                                Learning Objectives


1. Know! The horse is notorious for the formation of exuberation granulation tissue
   (proud flesh) in wounds, especially those on the distal extremities. The cause of this
   condition is unknown!

2. Know! Clinically it is characterized by a proliferation of hemorrhagic granulation
   tissue that fails to heal and lacks an epithelial covering. The exuberant granulation
   tissue usually forms early in the healing process.

3. Know! The diagnosis is based on the histopathologic findings. Differentials should
   include: equine sarcoid, squamous cell carcinoma, habronemiasis, and infectious
   granulomas (e.g. pythiosis, botryomycosis).

4. How do you manage exuberant granulation tissue?




                                           161
              Large Animal Miscellaneous Skin Diseases
                      Collagenolytic Granuloma – Equine


   A. General Considerations:

       1. Also called equine eosinophilic granuloma with collagen degeneration.

       2. It is probably the most common nodular skin disease of the horse.


                                   Important Facts

 Collagenolytic granuloma is also called equine eosinophilic granuloma with collagen
  degeneration.

 It is the most common nodular skin disease of the horse.


   B. Etiology and Pathogenesis:

       1. The etiology and pathogenesis are unknown.

       2. However, a hypersensitivity reaction to insect bites has been suspected. It is
          most likely a type IV hypersensitivity.

       3. Other possible causes are migrating parasites, trauma and an aberrant reaction
          to free hair in the dermis. It has been suggested that the collagen degeneration
          is secondary to the release of toxic eosinophilic contents such as major basic
          protein.




                                   Important Facts

 The etiology and pathogenesis are unknown.

 Because the lesions often begin in warmer months, a hypersensitivity reaction to
  insect bites have been suspected.

 It is most likely a type IV hypersensitivity.




                                           162
   C. Clinical Signs:

       1. The disease usually occurs during the warmer months of the year. However,
          it has also been reported in the winter.

       2. There is no apparent breed, age, or sex predilections.

       3. The lesions consist of one to several firm nodules situated in the dermis.

       4. A generalized form with lesions localized to the face, neck, and thorax occurs
          in Arabs. The lesions are pea-sized and number in the 100’s.

       5. The overlying skin and hair coat are usually normal in appearance. The
          surface may occasionally ulcerate, and drain.

       6. Some lesions may be cystic or plaque-like, with a centermost caseous or
          calcified cove.

       7. The nodules usually occur on the sides of the neck, withers, and back.

       8. There is no pruritus or pain associated with the disease.


                                    Important Facts

 The disease usually occurs during the warmer months of the year. However, it has
  also been reported in the winter.

 There is no apparent breed, age, or sex predilections.

 Single or multiple lesions from 2 to 10 cm in diameter most commonly affect the
  neck, withers, and back.

 The lesions are usually rounded, well-circumscribed, firm, nonalopecic,
  nonulcerative, nonpainful, nonpruritic.


   D. Diagnosis:
       1. Differentials include: bacterial folliculitis/furunculosis, tick reaction,
          neoplasia, hypoderma, and amyloid.

       2. Biopsy (total excision) of a lesion for histopathology is necessary to make a
          definitive diagnosis.




                                            163
3. The histopathologic findings reveal multifocal areas of collagen degeneration
   followed by granulomatous inflammation containing eosinophils. Older and
   larger lesions exhibit marked dystrophic mineralization and may be
   misdiagnosed as calcinosis circumscripta or tumoral calcinosis.

4. Skin test to insects?




                                   164
                                    Important Facts

 Differentials include: bacterial folliculitis/furunculosis, tick reaction, neoplasia,
  hypoderma, and amyloid.

 Biopsy (total excision) of a lesion for histopathology is necessary to make a definitive
  diagnosis.

   E. Treatment:
       1. The lesions may spontaneously regress with time.

       2. If there are only a few lesions, sublesional triamcinolone acetonide is probably
          the treatment of choice. Use 5 mg/lesion 2 to 3 times at 10 day intervals.

       3. It has been recommended that no more than 20 mg of triamcinolone acetonide
          be administered sublesionally, at once, to any horse because of the potential
          for laminitis.

       4. Horses with multiple lesions may be treated with oral prednisolone or
          prednisone given at the dose of 1.1 mg/kg once daily for two to three weeks.

       5. Mineralized lesions will not disappear completely with steroid therapy.

       6. Single lesions respond to surgical excision.

       7. Strict insect control is recommended.

                                    Important Facts

 The lesions may spontaneously regress with time.

 If only a few lesions are present, they can be treated with sublesional injections of
  triamcinolone acetonide.

 It has been recommended that no more than 20 mg of triamcinolone acetonide be
  administered sublesionally, at once, to any horse because of the potential for
  laminitis.

 Horses with multiple lesions may be treated with oral prednisolone or prednisone
  given at the dose of 1.1 mg/kg once daily for two to three weeks.

 Single lesions respond to surgical excision.

 Strict insect control is recommended.


                                             165
                                        References



1. Scott W.D. Miscellaneous Dermatoses. In: Large Animal Dermatology. W.B.
   Saunders, Philadelphia, 1988, p. 399-410.




                                 Learning Objectives


1. Know! Also called equine eosinophilic granuloma with collagen degeneration. It is
   probably the most common equine nodular skin disease.

2. Know! The etiology and pathogenesis are unknown but, because the lesions often
   begin in warmer months, a hypersensitivity reaction to insect bites has been
   suspected. A type IV hypersensitivity reaction is likely involved.

3. Know! The disease usually occurs during the warmer months of the year. However,
   it has also been reported in the winter. There is no apparent breed, age, or sex
   predilections. Single or multiple lesions from 2 to 10 cm in diameter most commonly
   affect the neck, withers, and back. The lesions are usually rounded, well-
   circumscribed, firm, nonalopecic, nonulcerative, nonpainful, nonpruritic. Lesions
   may spontaneously regress.

4. Know! The diagnosis is based on the histopathologic findings. Sample a whole
   lesion. Differentials should include: bacterial folliculitis/furunculosis, tick reaction,
   neoplasia, hypoderma, and amyloid.

5. How do you manage equine collagenolytic granuloma?




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