Dog Health by LowchensAustralia.com

2.1 General

2.1.1 Definitions

1. Immune-mediated diseases: a broad term encompassing those diseases whose etiopathogenesis involves tissue damage caused by the body's immune system. Synonyms include "allergy" and "hypersensitivity". Classically, four basic mechanisms of immune injury may be involved: type I (anaphylactic), type II (cytotoxic), type III (immune complex) and type IV (cell-mediated).
2. Autoimmune diseases: diseases whose etiopathogenesis involves the production of host antibodies and/or immunocompetent lymphocytes directed against "self" (host) antigens resulting in primary damage to the host's tissues. Autoimmunity should be demonstrable by in vitro and in vivo techniques.

2.2 . Diagnosis of immune-mediated diseases

2.2.1 Clinical presentation: 

1. History
2. General physical
3. Dermatological examination
4. Orthopedic examination

2.2.2 Laboratory tests - data base

1. Complete blood count (reticulocyte count, platelet count)
2. BUN, Creatinine
3. SGPT (ALT), SAP (ALA)
4. Urinalysis
5. Coomb's test
6. LE cell preparation
7. ANA titer
8. Routine dermatology procedures
   • a. Wood's light
   • b. dermatophyte culture
   • c. skin scraping
   • d. scotch tape test
9. Intradermal Skin testing
10. Radio Allergo Sorbant Test (RAST)
11. Transtracheal wash
12. Gastrointestinal biopsy

2.2.3 Histopathology

1. Demonstrate characteristic, often diagnostic lesions
2. Diagnostic lesions often hard to find
   • a. biopsy affected and non affected area whenever possible
   • b. multiple biopsies recommended
   • c. negative histopathology does not rule-out immune mediated disease
3. Histopathology requires formalin fixed tissue. Special immunological staining requires Michel's fixative.

2.2.4 Direct immunofluorescence of skin biopsies

1. Biopsy perilesional tissue - immunoglobulins and complement usually not detectable within the epidermis of blisters
2. Multiple biopsies
3. Preservation of tissue immunoglobulin
   • a. Freeze in isopentane (2-methyl butane) cooled in solid carbon dioxide or liquid nitrogen
   • b. Michel's fixative - preservation for up to one week (Most labs performing direct immunofluorescence will supply Michel's fixative
4. Evaluation of tissue for IgG, IgM, IgA and C3 optimum
5. Negative direct immunofluorescence does not rule-out immune mediated disease

2.2.5 Indirect immunofluorescence

1. For circulating autoantibody
2. Rarely positive in dogs and cats with autoimmune skin disease 

2.3 Immune-Mediated Disease

2.3.1 Atopy

2.3.1.1 General

1. Usually refers to allergy to inhaled antigens however allergens may be ingested or percutaneous
2. chronic and progressive
3. Increased incidence in females, dogs over 1 year of age and some breed predilection
4. hereditary disposition toward disease in some animals
5. seasonal manifestations initially
6. atopic animals sensitive to histamine

2.3.1.2 Etiology

1. inhaled allergen, IgE mediated hypersensitivity, type I
2. major allergens: food, pollens

2.3.1.3 Clinical features

1. pruritis, face rubbing, foot licking, otitis
2. urticaria, erythema, excoriations
3. secondary seborrhea, lichenified erythematous plaques with or without hyperpigmentation affecting periocular, axillary or inguinal skin
4. conjunctivitis, rhinitis, sneezing
5. lesions - non-specific may or may not be supportive of allergic disease - accumulation of fluid with mast cells, eosinophils, neutrophils, and plasma cells

2.3.1.4 Differential diagnoses

1. flea allergy
2. food allergy
3. scabies
4. seborrheic dermatitis
5. pelodera dermatitis
6. demodectic mange 

2.3.1.5 Diagnosis

1. physical examination and history
2. intradermal skin testing
3. RAST
4. skin scrapings
5. restrictive diet

2.3.1.6 Treatment

1. removal or avoidance of offending allergens
2. hyposensitization - 3 main techniques
   • 1) aqueous - 6 mos to 3 yrs for maximal response, requires a total of 96 injections
   • 2) propylene glycol or glycerine emulsions - 2-3 mos maximal response, requires a total of 4- 8 injections
   • 3) pyridine extracts of alum precipitates - 3-6 mos maximal response, requires 3-12 injections
3. steroid therapy
4. antihistamines

2.3.2 Contact Dermatitis

2.3.2.1 General

Incudes two types - primary irritant and allergic forms

2.3.2.2 Primary irritant contact dermatitis

2.3.2.2.1 General

• 1) dog and cat - not uncommon
• 2) probably the only form of contact dermatitis in the cat
• 3) no breed, sex or age predilections

2.3.2.2.2 Etiology

• 1) non-allergic
• 2) caused by cutaneous contact with substances that would cause irritation to all individuals
• 3) examples: soap, detergent, acids, alkalis, fertilizer, salt, petroleum, topical medications
• 4) cats are irritated by numerous topical medications - coal tar, flea collars, selenium and neomycin

2.3.2.2.3 Clinical features

• 1) acute onset
• 2) distribution - anywhere, but often the normal contact areas (feet and ventrum)
• 3) lesions (variable) - erythema leading to necrosis and ulceration

2.3.2.2.4 Diagnosis - history and physical examination

2.3.2.2.5 Treatment

• 1) remove or wash off offending irritant
• 2) symptomatic - soaks, steroid topical preparations, etc

2.3.2.3 Allergic Contact dermatitis

2.3.2.3.1 General

• 1) dog - not uncommon; any breed age or sex
• 2) cat - does not occur?

2.3.2.3.2 Etiology

• 1) delayed type hypersensitivity (type IV)
• 2) examples: wool, synthetic carpets (especially indoor- outdoor carpets), poison ivy-oak, topical medications. Often there is a history of these items as being new to the environment

2.3.2.3.3 Clinical features

• 1) onset 12-72 hours after re-exposure in a sensitized individual
• 2) distribution
  • a) primarily hairless areas (particularly those that contact surfaces)
  • b) interdigital, axilla, inguinal areas; genitalia; under the tail; muzzle and ears
• 3) lesions (milder that irritant form)
  • a) acute - erythema, papules, crusts, excoriations, rarely vesicles
  • b) chronic - lichenification, hyperpigmentation, alopecia
• 4) varying degrees of pruritis

2.3.2.3.4 Differential diagnoses

• 1) irritant contact dermatitis
• 2) acute moist dermatitis
• 3) neurodermatitis
• 4) pelodera dermatitis

2.3.2.3.5 Diagnosis

• 1) detailed history and physical examination
• 2) patch testing
  • a) poor result in animals
  • b) apply suspect materials to shaved area for 72 hours the look for reactions
• 3) isolation and provocative exposure
  • a) hospitalize or otherwise confine to a benign surface (e.g. concrete floor) for five days; signs should resolve
  • b) then reintroduce animal to suspect contact allergens, one at a time (e.g. one carpet or rug at a time)
• 4) treatment
• a) avoidance is the most effective treatment
• b) glucocorticoids - systemic and topical; variable effectiveness if animal continues to be exposed to allergen 

2.3.2.4 Flea Collar dermatitis

2.3.2.4.1 General

• 1) dogs and cats - uncommon, no breed, age or sex predilections
• 2) experimental studies in cats have demonstrated both contact dermatitis and systemic toxicity

2.3.2.4.2 Etiology

• 1) skin disease - primary irritant contact dermatitis to organophosphate or components of plastic flea collar
• 2) systemic disease - chronic organophosphate toxicity or delayed type hypersensitivity

2.3.2.4.3 Clinical features

• 1) reaction graded as to severity (experimentally)
  • a) grade I - mild erythema, pruritus - skin beneath collar
  • b) grade II - erythema, edema, alopecia, excoriations, pruritis
  • c) grade III - grade II plus pyoderma
  • d) grade IV - generalized skin disease plus signs systemic (anorexia, depression, ataxia, fever); occasionally death

2.3.2.4.4 Diagnosis

History and physical examination

2.3.2.4.5 Treatment

• 1) remove collar
• 2) clip and clean
• 3) soaks - antiseptics or astringents 10 minutes twice or three times a day
• 4) topical and systemic glucocorticoids
• 5) antibiotics if pyoderma is present

2.3.2.4.6 Prognosis

• 1) good - skin lesions heal slowly
• 2) grade III and IV patients take months to recover

2.3.2.4.7 Prevention

• 1) keep collar loose around neck to minimize skin contact (2 fingers under the collar)
• 2) cut off extra length
• 3) do not use canine collars on cats
• 4) do not use other organophosphates or carbamates at the same time
• 5) do not use on sick, debilitated, pregnant, lactating or juvenile (less than 4 months of age) animals
• 6) let the collar "air out" 1-2 days before using

5. Plastic, Vinyl, Rubber dish syndromes

General

• 1) dog - uncommon; no age, sex or breed predilection

Etiology

• 1) delayed type hypersensitivity
• 2) percutaneous contact with plastic vinyl, and synthetic rubber (the latter contains accelerators and antioxidants which are allergenic); usually associated with feeding dishes

Clinical features

• 1) distribution - lips and nose
• 2) lesions - depigmentation (leukoderma) plus erythema and alopecia

Diagnosis

History and physical examination

Treatment

• 1) remove dish
• 2) glucocorticoids

f. Prognosis - pigment rarely returns

2.3.3 Food Allergy

2.3.3.1 General

1. dogs and cats - uncommon; no age, sex or breed predilections
2. true incidence unknown - dogs (1-40% of allergic skin diseases)

2.3.3.2 Etiology

a. unknown - types I, II, and IV hypersensitivity have all been implicated; most are probably type I

b. changes in diet often associated with condition, but can occur after long term consumption of the same diet

2.3.3.3 Clinical features - variable

• a. Canine syndromes
  • 1) atopy-like
  • 2) flea allergy-like
  • 3) generalized pruritic follicles
  • 4) seborrheic dermatitis-like
  • 5) pruritis without lesions
  • 6) urticaria-angioedema
• b. Feline syndromes
  • 1) miliary eczema-like
  • 2)pruritic, ulcerative dermatitis of head, neck and axillae
  • 3) pruritis without lesions
  • 4) pruritic urticaria-angioedema
• c. May occur suddenly, anytime in life
• d. Concurrent GI signs (diarrhea) common (50%) in dogs; rare in cats

2.3.3.4 Differential diagnoses

1. Flea allergy dermatitis
2. Seborrheic dermatitis
3. Parasitic dermatitis
4. GI signs differentiate from other causes of gastroenteritis

2.3.3.5 Diagnosis

1. history and physical examination
2. elimination and provocative exposure
   • 1) elimination
     • a) hospitalize - give laxative and enema; no food, just water for 3 days; pruritis and inflammatory skin changes usually improve in 1-2 days
     • b) hypoallergenic diet - 10 days at home on diet of long- grained rice (gluten-free)

2.3.3.6 Bacterial hypersensitivity

2.3.3.6.1 General

1. controversial areas - existence, incident and pathogenesis
2. dog - common?, no breed, age or sex predilections; cat rare
3. superficial pyoderma

2.3.3.6.2 Etiology

1. unknown - possibly type II or IV hypersensitivity to staphylococcus aureus antigens (cell wall, enzymes, or exotoxins)
2. often secondary to some other dermatosis, e.g. seborrhea, hypothyroidism, atopy, food allergy

2.3.3.6.3 Clinical features

• a. Canine syndromes
  • 1) all forms - moderate to intense pruritis
  • 2) erythematous pustule form
    • a) distribution - especially ventrum (inguinal, belly, chest, and axillary areas), the medial extremities and feet (pododermatitis)
• b) lesions - pustules surrounded by a halo of erythema; these lesions are easily ruptured, after rupturing the lesion crusts over and form annular seborrheic dermatitis lesions
• c) most common form
  • 3) seborrheic dermatitis form
  • 4) hemorrhagic bulla form - red, red-purple, fluctuant "blood- blister"-like lesions, 1-3 cm in diameter
  • 5) pododermatitis
  • 6) generalized folliculitis
  • 7) deep pyoderma
• b. Feline syndrome
  • 1) "miliary dermatitis-like"

2.3.3.6.4 Diagnosis

1. history and physical examination
2. intradermal skin testing: using staphylococcus bacterin or commercial antigens (diluted 50:50 with sterile saline); inject 0.1 ml mixture intradermally; all dogs have immediate wheal reactions (15-30 minutes); positive reaction at 24 to 72 hours with large (9 to 75 mm in diameter) erythematous, indurated, oozing, reddish purple nodules which occasionally necrose and slough
3. bacterial culture and sensitivity is almost always coagulase positive staphylococcus
4. skin biopsy

2.3.3.6.5 Treatment

1. systemic antibiotics for 4-6 weeks (2 weeks past resolution of all active lesions)
2. antimicrobial baths
3. biologics (hyposensitization)
   • 1) mechanism of action unknown
   • 2)staphylococcal antigens introduced into system at increasing doses to "hyposensitize" patient or otherwise decrease patient susceptibility to infection
   • 3) several forms
     • a) autogenous staph. bacterin
     • b) staphylococcal phage lysate (SPL)
     • c) commercial bacterin
   • 4) successful 50-80%
   • 5) frequently require indefinite boostering
   • 6) prognosis - guarded

2.3.3.7 Flea Allergy dermatitis

2.3.3.7.1 General

1. mediated by type I and type IV hypersentivities
2. seasonal cother arthropod bites may lead to cutaneous or anaphylactic reactions

2.3.3.7.2 Etiology

1. allergen is the saliva of the flea
2. only takes one flea that may not be present at time of examination

2.3.3.7.3 Clinical signs

1. acute - intense pruritis, erythema, papules, pustules, crusts, acute moist dermatitis
2. chronic - alopecia, hyperkeratosis, hyperpigmentation, secondary seborrhea
3. distribution of lesions
   • 1) dog - lumbosacral region and base of tail
   • 2) cat - head and neck area involved
4. lesion - early mast cell hyperplasia and edema

2.3.3.7.4 Differential diagnoses

1. pyoderma
2. inhalant allergies
3. food allergy
4. drug reaction
5. contact dermatitis
6. cutaneous neoplasia and mast cell tumors

2.3.3.7.5 Diagnosis

1. response to short-term cortico steroid therapy
2. hemogram
3. biopsies
4. evaluation of animal habits and environment

2.3.3.7.6 Treatment

1. avoidance and treatment of arthropod (fleas)
2. short-term steroid or antihistamine therapy
3. flea control
4. hyposensitization

2.3.3.8 Drug Eruption

2.3.3.8.1 General

1. dogs - uncommon, no age, sex or breed predilections;
2. cats - rare

2.3.3.8.2 Etiology

1. any medication given orally, by injection or topically
2. mechanisms of eruptions unknown; probably variable and may include all four types of hypersensitivity plus primary irritant phenomena

2.3.3.8.3 Clinical features

1. may mimic any skin disorder
2. distribution - cutaneous or mucocutaneous
3. no characteristic lesions

2.3.3.8.4 Diagnosis

1. history and physical examination
2. drug withdrawal with improvement of lesions
3. purposeful read ministration (dangerous)
4. CBC, and other appropriate laboratory tests

2.3.3.8.5 Treatment

1. discontinue drugs - usually improvement seen by 7 to 14 days; signs may persist for several months
2. corticosteroids
3. antihistamines and epinephrine -for urticaria/angioedema or anaphylaxis
4. avoid chemically related drugs

2.3.3.9 Intestinal parasitism

2.3.3.9.1 General

1. Dogs - not uncommon, any age (especially puppies), no sex or breed predilection
2. cats - rare

2.3.3.9.2 Etiology

1. all intestinal parasites
2. stimulation of production of skin-sensitizing IgE?

2.3.3.9.3 Clinical features

1. Canine syndromes
   • 1) pruritis without gross lesions
   • 2) erythema/eruptions especially lumbosacral, flanks, ventral abdomen plus pruritis
   • 3) seborrhea sicca plus pruritus
2. Feline syndromes
   • 1) "miliary dermatitis-like" plus pruritis
   • 2) pruritis without gross lesions
   • 3) seborrhea sicca plus pruritus
3. Gastrointestinal signs may coexist

2.3.3.9.4 Diagnosis

1. history and physical examination
2. fecal flotation
3. response to therapy

2.3.3.9.5 Treatment

1. anthelmintics
2. symptomatic - corticosteroids 

2.3.3.10 Hormonal Hypersensitivity

2.3.3.10.1 General

1. more common in females
2. females are often atopic
3. estrus cycle abnormalities seen

2.3.3.10.2 Etiology

1. associated with endogenous progesterone, estrogen or androgen
2. Type IV hypersensitivity

2.3.3.10.3 Clinical signs

1. pruritis, papules, crusts
2. lesions seen in perineal and genital regions and progress forward
3. associated with estrus or pseudopregnancy

2.3.3.10.4 Differential diagnoses

1. ovarian imbalance
2. seborrheic dermatitis
3. contact dermatitis
4. flea allergy dermatitis
5. atopy
6. superficial pyoderma

2.3.3.10.5 Diagnosis

1. intradermal skin test

2.3.3.10.6 Treatment

1. ovariohysterectomy
2. castration
3. improvement should be seen in 5-10 days 

2.3.3.11 Experimental Allergic Asthma

2.3.3.11.1 General

1. dog has been the model (natural disease is rare)
2. beta adrenergic theory of atopic disease thought to occur in experimental allergic asthma
3. imbalance in the alpha adrenergic and beta adrenergic tone with insensitivity to beta adrenergic stimulation

2.3.3.11.2 Etiology

1. nebulized pollen allergens to atopic dogs
2. nebulized Ascaris antigen to dogs infected with Toxocara canis
3. airway responsiveness dependent upon the level of IgE antibody and degree of airway sensitivity to mediator

2.3.3.11.3 Clinical signs

1. dyspnea
2. urticaria
3. insensitive to antihistamine
4. dermatitis on repeated exposure to antigen
5. cough

2.3.3.11.4 Diagnosis

1. positive skin test to nebulized antigen
2. rare spontaneous disease due to the low numbers of mast cells in the pulmonary tract of the dog

2.3.3.11.5 Treatment

1. hyposensitization
2. corticosteroids

2.3.3.12 Canine Allergic Tracheobronchitis

2.3.3.12.1 General

1. differs from asthma because bronchospasm is not a feature

2.3.3.12.2 Etiology

1. no specific allergic etiology seen
2. anesthetic incriminated in one case

2.3.3.12.3 Clinical signs

1. peripheral eosinophilia
2. dyspnea
3. increased lung sounds
4. cough

2.3.3.12.4 Diagnosis

1. physical examination and history?
2. radiographic evidence of pulmonary alveolar and peribronchial infiltrates
3. response to corticosteroids

2.3.3.12.5 Treatment - prednisolone 

2.3.3.13 Pulmonary Infiltrates with Eosinophilia (PIE)

2.3.3.13.1 General

1. eosinophilic lung infiltration associated with multiple diseases
2. criteria for diagnosis - infiltrative lung disease with either pulmonary or peripheral eosinophilia
3. considered a manifestation of a number of diseases

2.3.3.13.2 Etiology

1. multiple etiologies
2. once diagnosed etiology should be sought for vigorously
3. dirofilariasis in endemic heartworm areas
4. pathogenesis related to circulating microfilaria

2.3.3.13.3 Clinical signs

1. exercise intolerance
2. cough
3. dyspnea
4. anorexia
5. acute or chronic onset

2.3.3.13.4 Diagnosis

1. physical examination and history
2. Knotts test
3. Occult heartworm test
4. Complete blood count
5. Radiographs
6. Transtracheal wash

2.3.3.13.5 Treatment

1. corticosteroids
2. remove etiology
3. aspirin

2.3.3.14 Feline Asthma

2.3.3.14.1 General

1. seasonal or non seasonal disease
2. persistent or intermittent
3. acute or chronic onset
4. cats may progress from mild to severe forms or may remain at a particular stage

2.3.3.14.2 Etiology

Ragweed pollen

2.3.3.14.3 Clinical signs

• a. five stages of increasing severity are recognized
  • 1) stage 1 - cat only affected intermittently with periodic bouts of lower respiratory signs
  • 2) stage 2 - cat is symptomatic for longer periods and clinical presentation of coughing, gagging and mild hyperventilation, wheezing and increased bronchovesicular sounds are auscultated
  • 3) stage 3 - cat shows marked hyperventilation, coughing, gagging, open-mouth breathing especially during stress, there is severe airway obstruction and respiratory alkalosis
  • 4) stage 4 - cat is hypoxemic, there is continuous open-mouth breathing and a marked expiratory effort, percussion reveals hyperresonance as a result of air entrapment, animal develops a barrel-shaped thorax

2.3.3.14.4 Diagnosis

1. physical examination and history
2. radiographic signs vary and may be non-diagnostic
3. pathognomonic radiographic signs - areas of radiolucency and an increased thorax size with a flattened diaphragm
4. bronchial washings

2.3.3.14.5 Treatment

1. bronchodilators - isoproterenol, terbutaline
2. intravenous corticosteroids
3. long-term management pursue allergic cause, appropriate avoidance and hyposensitization

2.3.3.15 Feline PIE

2.3.3.15.1 General

1. incidence low
2. majority of all cases are parasitic in origin

2.3.3.15.2 Etiology

1. aberrant dirofilariasis
2. microfilaremia rare
3. adult worms are few in number

2.3.3.15.3 Clinical signs

1. coughing
2. intermittent dyspnea
3. chronic onset
4. sudden death in some cases

2.3.3.15.4 Diagnosis

1. physical examination and history
2. radiographs
3. Knotts test (usually negative), occult heartworm test detecting antigen or antibody (must be appropriately adapted for the cat) 

2.4 Autoimmune Diseases

2.4.1 Pemphigus Complex

2.4.1.1 Disease involve in skin membrane

1. A group of chronic, relapsing, bullous diseases involving the skin or mucous membranes. Autoantibody directed against intercellular cement substance and possibly the epidermal cell wall. The cytotoxic damage may or may not involve activation of the complement system. Direct immunofluorescence testing reveals IgG in most cases with IgA, IgM, and C3 found uncommonly.

2.4.1.2 Four variants have been described in small animals

1. P. vulgaris
2. P. foliaceus
3. P. erythematosus
4. P. vegetans

2.4.1.3 Pemphigus vulgaris (P.V.)

2.4.1.3.1 General

• 1) dog - no breed or sex predilection, age usually middle aged or older, uncommon
• 2) cat - rare

2.4.1.3.2 Clinical features

• 1) distribution of lesions: oral mucosa and mucocutaneous junctions
• 2) lesions: usually erosions, ulcerations and crusts; bullae are rare
• 3) secondary bacterial infection common
• 4) +/- pain and pruritus
• 5) acute form associated with fever and systemic signs
• 6) chronic form more insidious no systemic signs
• 7) feline PV is primarily oral lesions

2.4.1.3.3 Diagnosis

• 1) histopathology - acantholysis with intra-epidermal cleft formation in the suprabasilar area
• 2) direct immunofluorescence of skin: deposits of immunoglobulin within the intercellular area of the epidermis
• 3) indirect immunofluorescence - rarely positive immunoglobulin within the intercellular area of the epidermis
• 4) indirect immunofluorescence - rarely positive

2.4.1.4 Pemphigus foliaceus (P.F.)

2.4.1.4.1 General

• 1) dog - uncommon; no age, sex or breed predilections
• 2) cat - rare

2.4.1.4.2 Clinical features

• 1) distribution primarily the skin, often initially around the head and ears, but then frequently will generalize; mucocutaneous and oral involvement - rare
• 2) lesions erythema, erosions, oozing serum and exudate, scaling ( epithelial collarettes), crusts, large areas of epidermis may exfoliate. Bullae are rare
• 3) secondary bacterial infection +/-
• 4) pain and pruritus +/-
• 5) fever and systemic signs rare

2.4.1.4.3 . Diagnosis

• 1) must distinguish from subcorneal pustular dermatosis
• 2) histopathology: subcorneal bullae - often full of inflammatory cells (PMNs)
• 3) direct immunofluorescence: identical to PV
• 4) indirect immunofluorescence: rarely positive
• 5. Pemphigus erythematosus (P.E.)

2.4.1.5 Pemphigus erythematosus (P.E.) 

2.4.1.5.1 General

• 1) dog - uncommon
• 2) cat - rare
• 3) has features common to PF and lupus erythematosus
• 4) may be an important cause of "collie nose"
• 5) exacerbated by sunlight

2.4.1.5.2 Clinical features

• 1) similar to PF but confined to the head
• 2) distribution: nose, periocular skin and ears
• 3) lesions: depigmentation is the earliest sign; progresses to erythema, erosions, exudation and ulceration
• 4) insidious start and progression
• 5) secondary bacterial infection +/-
• 6) systemic signs rare

2.4.1.5.3 Diagnosis

• 1) Histopathology: identical to PF
• 2) Direct immunofluorescence: immunoglobulin deposits in the intercellular spaces of the epidermis and at the dermoepidermal junction
• 3) ANA titer +/-

2.4.1.6 Pemphigus vegetans

2.4.1.6.1 General

• 1) Dog - very rare
  • b. Clinical features
• 1) Distribution: generalized cutaneous involvement, sparing the mucous membranes
• 2) Lesions: erythema, exudate, alopecia, crusts, pustules, verrucous vegetations and papillomatous proliferations
• 3) Systemic signs may or may not be present

2.4.1.6.3 Diagnosis

• 1) Histopathology: intraepidermal abscesses (usually deep layers of the epidermis) containing acantholytic cells, neutrophils and other inflammatory cells
• 2) Direct immunofluorescence: similar to PV and PF

2.4.2 Bullous pemphigoid

2.4.2.1 General

1. dog - uncommon
2. cat - rare
3. possibly due to autoantibodies directed against antigens in the basement membrane zone

2.4.2.2 Clinical features

1. slow insidious and acute, fulminating forms
2. acute fulminating cases are clinically indistinguishable from PV and result in fever and other systemic signs
3. chronic cases - often more generalized, especially severe ventrally, no systemic illness seen
4. lesions - occasionally bullae (persist longer than pemphigus complex), usually erosions, ulcers and crusts

2.4.2.3 Diagnosis

1. Histopathology: subepidermal bullae - often full of inflammatory cells
2. Direct immunofluorescence - linear deposits of immunoglobulin (IgA - 2/3 of the cases, IgG 1/2, IgM 1/3) in the basement membrane zone
3. Indirect immunofluorescence - rarely positive

2.4.3 Therapy for autoimmune bullous disease

2.4.3.1 Systemic immunosuppressive therapy

• a. Indication: severe, generalized disease
  • 1) PV, PF, PV
  • 2) bullous pemphigoid
  • b. Remissions often difficult to obtain and maintain
• c. Induction protocols
  • 1) prednisolone/prednisone
  • 2) prednisolone/prednisone plus cyclophosphamide
  • 3) prednisolone/prednisone plus azathioprine
  • 4) Chrysotherapy - aurothioglucose
• d. Following remission the therapy is gradually tapered, but this may frequently result in relapses
• e. Antibiotics - if secondary bacterial infection is present

2.4.3.2 Local therapy

1. PE
2. Protocol
   • 1) topical glucocorticoids - frequently not effective
   • 2) sunscreen
   • 3) reduce exposure to ultraviolet light
   • 4) tatoo
   • 5) systemic immunosuppressive therapy

2.4.4 Systemic lupus erythematosus (SLE)

2.4.4.1 General

1. polysystemic disease characterized by the formation of numerous autoantibodies and immune complexes.
2. cutaneous lesions are probably due to a deposition of immune complexes in the skin
3. dogs - uncommon, increased incidence in females, no age or breed predilection
4. cats - rare

2.4.4.2 Clinical features

• a. dogs
  • 1) cutaneous lesions variable may have a mucocutaneous distribution with a predilection for the nose, head and ears
  • 2) sunlight may cause exacerbation of the skin lesions
  • 3) other clinical manifestations: Coomb's positive hemolytic anemia, immune-mediated thrombocytopenia, leukopenia or leukocytosis, glomerulonephritis, polyarthritis, polymyositis, fever, CNS signs (rare), pleuritis (rare) 
• b. Cats
  • 1) generalized chronic dermatitis: erythema, vesicles, paronychia, mucocutaneous ulcers of nostrils and lips, and pruritus
  • 2) systemic signs - depression anorexia, weight loss, fever, peripheral lymphadenopathy

2.4.4.3 Diagnosis

1. LE cell preparation +
2. ANA titer +
3. Histopathology: hydropic degeneration of the basal cell layer of the epidermis, edema of the dermis, fibrinoid deposits around collagen, hyperkeratosis with keratotic plugging and patchy lymphoid infiltrates around the appendages
4. Direct immunofluorescence - (lupus band test) positive test reveals immunoglobulin deposited at the dermoepidermal junction

2.4.4.4 Treatment

1. Systemic immunosuppressive therapy
2. Plasmapheresis
3. Monitor clinical signs and ANA titer to determine course of therapy and withdrawal of therapy

2.4.5 . Discoid lupus erythematosus (DLE)

2.4.5.1 General

1. disease limited to the skin
2. many cases of "collie nose" may actually be DLE

2.4.5.2 Clinical features

1. distribution: primarily the bridge of the nose
2. lesions: depigmentation, erythema, ulceration crusting and scarring
3. may be exacerbated by sunlight

2.4.5.3 Diagnosis

1. histopathology of skin lesions are per SLE
2. Direct immunofluorescence : + lupus band test in affected skin only
3. usually ANA, LE cell prep, negative

2.4.5.4 Treatment

1. as per P. erythematosus

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