Hormone-Related Skin Diseases

Cortisone excess: Symmetric hair loss over trunk and body. Abdomen is pot bellied and pendulous. Seen with Cushing’s syndrome. In some cases, the dog is taking steroids.

Growth hormone-responsive alopecia: Bilaterally symmetric hair loss, mainly in male dogs. Begins around puberty. More prevalent in certain breeds, including Chow Chows, Keeshonds, Pomeranians, Miniature Poodles, Airedales, and Boxers.

Hyperestrogenism (estrogen excess): Occurs in females and males. Bilateral symmetric hair loss in perineum and around genitals. Enlarged vulva and clitoris; in males, pendulous prepuce.

Hypoestrogenism (estrogen deficiency): Occurs in older spayed females. Scanty hair growth and thinning coat, initially around vulva and later over entire body. Skin is smooth and soft, like a baby’s.

Hypothyroidism: Most common cause of bilaterally symmetric hair loss without itching. Coat is thin, scanty, and falls out easily. Involves the neck beneath the chin to the brisket, sides of body, backs of thighs, and top of tail.

Itchy Skin Diseases Of Dogs.

Canine atopy: Severe itching that occurs in young dogs and begins in late summer and fall. Caused by seasonal pollens. Occurs in mixed breeds as well as purebreds.Common. Tends to get worse each year. May start with face rubbing and foot chewing.

Chiggers: Itching and severe skin irritation between the toes and around the ears and mouth. Look for barely visible red, yellow, or orange chiggers.

Contact dermatitis: Red, itchy bumps and inflamed skin at the site of contact with a chemical, detergent, paint. or other irritant. Primarily affects feet and hairless parts of the body. Can also be caused by rubber or plastic food dishes, with hair loss on the nose.

Damp hay itch (pelodera): Red pimplelike bumps on skin. Severe itching. Occurs in dogs bedded on damp hay and similar grass. Caused by a parasite.

Flea allergy dermatitis: Red, itchy pimplelike bumps over the base of the tail, back of rear legs, and inner thighs. Scratching continues after fleas have been killed.

Fleas: Itching and scratching along the back, and around the tail and hindquarters. Look for fleas, or black and white gritty specks in hair (flea feces and eggs).

Fly-bite dermatitis: Painful bites at tips of erect ears and bent surfaces of floppy ears Bites become scabbed and crusty black, and bleed easily.

Food allergy dermatitis: Nonseasonal itching with reddened skin, papules, pustules and wheals. Found over the ears, rump, back of the legs, and undersurface of the body. Sometimes confined just to the ears with moist, weeping redness.

Grubs/Cuterebra: Inch-long fly larvae that form cystlike lumps beneath the skin with a hole in the center for the insect to breathe. Often found beneath the chin, by the ears, or along the abdomen.

Lice: Two-millimeter-long insects, or white grains of “sand” (nits) attached to the
hair. Not common. Found in dogs with matted coats. May have bare spots where hair has been rubbed off.

Lick granuloma (acral pruritic dermatitis): Red, shiny skin ulcer caused by continuous licking at wrist or ankle. Mainly in large, short-coated breeds.

Scabies (sarcoptic mange): Intense itching. Small red spots that look like insect bites on the skin of the ears, elbows, and hocks. Typical crusty ear tips.

Ticks: Large or very small insects attached to the skin. May swell up to the size of a pea. Found beneath the ear flaps and where hair is thin. May or may not induce itching.

Walking dandruff (cheyletiella mange): Occurs in puppies 2 to 12 weeks of age. Large amounts of dry, scaly, flaky skin over the neck and back. Itching is variable.

Maggots: Soft-bodied, legless fly larvae found in damp matted fur or wounds that aren’t kept clean.

Treatment trial for malassezia dermatitis.

Objective :

  • To do treatment trial for malassezia dermatitis on 6 animals with 2 different drug groups containing 3 animals each for a period of 1 to 2 weeks.
    • Group 1 – Ketoconazole
    • Group 2 – Ketoconazole+ vinegar..


  • yeasts fitting the description of Malassezia have been recognized on human skin since 1846.
  • Their importance as members of the normal cutaneous biota and their role in disease continue to be prominent topics in human and veterinary medical literature.
  • It is now generally accepted that Malassezia yeasts are commensal organisms of mammals and may also be associated with various cutaneous diseases.
  • The predisposing factors and infectious properties of Malassezia are still a focus of research and debate.


  • Malassezia pachydermatis, lipophilic yeast is a commensal on canine skin. Malassezia were originally identified by the French scientist Louis-Charles Malassez in the late 19th century.
  • It becomes an opportunistic pathogen when normal cutaneous microclimate or host defence mechanisms are altered, favouring its growth to become pathogenic.
  • Malassezia produce many enzymes including lipases and proteases which can contribute to cutaneous inflammation through proteolysis, lipolysis and changes in cutaneous pH.
  • It has been implicated as a pathogen within the external ear canal but only recently it has been associated with dermatitis.
  • The yeast maintains a symbiotic relationship with cutaneous Staphylococci, producing both mutually beneficial growth factors and a favorable micro environment. Concurrent pyoderma frequently complicates Malassezia.


  • Due to their lipophilic nature, Malassezia species other than Malassezia pachydermatis

can be very challenging to culture. This difficulty may account for the initial confusion in classifying the organism (it was identified based on cytologic characteristics alone for over 50 years).

  • These yeasts, previously known as Pityrosporum, are now classified in the genus Malassezia. The genus Malassezia is taxonomically located in the family Cryptococcaceae. Based on the structure of the yeast cell wall (laminar with distinctive spiraling ridges).
  • Currently, seven species of Malassezia have been identified: pachydermatis, M.

furfur, M. sympodialis, M. globosa, M. obtusa, M. restricta, and M. slooffiae.

  • The species are defined by morphologic, physiologic, and molecular differences.
  1. pachydermatis is usually isolated from animals, particularly carnivores. It is rarely identified on human skin but has been associated with fungal septicemia.


  • Malassezia is a single cell yeast with a thick cell wall, individual cells areovoid to globular or cylindrical. Cells in the process of budding forms a charecteristic ‘Peanut’ to ‘Russian doll’ shaped.


  • Malassezia can be recovered from 3 day old puppies,suggesting there is a early transfer by licking, grooming or from vagina.
  • It is commenly found inear canals, anal sacs, interdigital skin & mucocutaneous junctions (lips, prepuce vagina, anus) of healthy animals.
  • Malassezia yeasts colonise the superficial layers of epidermal & infundibular stratum corneum.

Virulance factor:.

  • The virulence factors for Malassezia yeasts have not been well defined. Zymogens from the cell wall of Malassezia are capable of activating the complement system and liberating C5a anaphylatoxin.
  • Lipases and lipoxygenases produced by Malassezia can alter sebum and may help the yeasts utilize cutaneous lipids as nutrients. Malassezia produces an extracellular glycoprotein that may also contribute to virulence.
  • Yeast adherence to the stratum corneum may be an important factor in skin colonization and infection.
  • At this time, with the use of RNA sequencing, adherence assays, and electrophoretic protein profiles, there is no evidence that one strain of Malassezia is more pathogenic than another. These findings emphasize the opportunistic nature of Malassezia.

Host factor:

  • The lack of association with biological activity & virulance suggests that malassezia is an oppurtunistic pathogen able to estabish wherever there is a permissive environment.


  • Anatomical features (bodyfolds, pendulous lips, hairy feet),inflamation ,exudates and licking can create warm, moist microenvironment. .
  • keratinizatiom defects and endocrine disorders may increase humidity,and alter the quantity and quality of sebum, although the relationship between sebum production and malassezia growth is unclear. furthermore,disruption to the stratum corneum by self-trauma, keratinization or metabolic defects could also allow malasssezia to establish.

Breed susceptiblity:

  • Basset hounds
  • West highland
  • white terriers
  • Cocker spaniels
  • Shihtzus
  • Dachshunds
  • Miniature poodles
  • German shephered dogs
  • Australians silky terriers
  • English setters

Immune response:

  • Malassezia does not invade the staratum corneum even so immune response to this organisams can be detected healthy on affected dogs.
  • Atleast 14 different protien antigens have been identified.
  • Dogs with malassezia dermatitis tend to recognise more antigens than healthy dogs, but no association bettween the pattern of recogniyion and any particular malassezia strain are virulance has been demonstrated.
  • Affected dogs also have elevated serum lgA igG titres compared to healthy dogs but this does not appear to be protective.

Predisposing factors:

Factors, which appear to favor the growth of this yeast, include

  • Abnormal levels of ceruminous lipids (ear wax or saliva).
  • Excess sebum production/ reduced sebum quality
  • Summer months (high humidity and allergy season) – a seasonal increase in case number may be observed in geographical region where a noticeable change to warm, humid climatic condition is present.
  • Abnormal cell-mediated immunity due to allergies (atopy, food allergy, flea allergy, contact allergy), and disrupted epidermal surface and concurrent dermatitis eg. Pyoderma and endocrinopathy,
  • Alterations in normal microflora in the ear and skin due to concurrent antibiotic therapy
  • An alkaline/basic (rather than neutral or acidic) skin
  • Managemental conditions like frequent bathing, etc
  • In dogs the disease is most often seen at anatomic sites that create a relatively warm, moist skin environment. Thus the interdigital skin, ventral neck, lip region, ear canal, axilla, groin and folded areas are most often affected.

Zoonotic Potential:

  • Malassezia pachydermatis can transiently colonise humans.colonization of staff members hands from pet dogs was the likely cause of M.pachydermatis associated septicaemia, meiningitis and urinary tract infections in an intensive care nursery..
  • The yeast then persisted through patient-to-patient transmission.the elderly AIDS sufferers or patients undergoing chemotherapy may also be at risk.this underlies the need observe hygienic precautions when handling healthy animals as well as those affected by malassezia pachydermatis

Malassezia-associated diseases:

  • In dogs, Malassezia is also a common perpetuating factor of canine otitis externa and is characterized by pruritus and inflammation of the external ear canal and a yellow- brown waxy exudate.
  • It has been proposed that pachydermatis acts as an allergen in some dogs. Morris and colleagues demonstrated that atopic dogs with cytologic evidence of Malassezia dermatitis had stronger wheal and flare reactions to Malassezia antigen than atopic dogs without evidence of Malassezia dermatitis.

Clinical Signs:

5 most important cardinal signs to be looked in for the diagnosis of Malassezia dermatitis in a dog with pruritus and mal odour, in association in one or more of the following.

  • Erythema – redness, produced by capillary congestion
  • Scaling – visible flakes of abnormal or compacted epithelial cells
  • Greasy or waxy exudate
  • Hyperpigmentation – an increase in cutaneous pigmentation followed by chronic inflammation
  • Lichenification – thickening of skin with exaggeration of normal skin markings.


  • History
  • Clinical signs:
  • The diagnosis is based on clinical signs, presence of elevated number of yeast in lesional skin and a clinical and mycological response to antifungal therapy.
  • Laboratory examination of impression smear (cytology):

Cytology is quick, easy, cheap and non – invasive. Direct impression on to a glass slide is possible on accessible skin; it is helpful if the skin is very moist or waxy.

  • Moist cotton swabs can be rubbed over the lesion and then gently rolled over glass slide. The smear of suspected material is then air dried and heat fixed
  • Flood the slides with Loeffler’s alkaline Methylene blue and allowd to act for 2-4 minutes.
  • Wash in water, blot and dry.
  • Examine under oil immersion.

The yeast stains blue or purple. The individual yeast cells are ovoid to globular and in the process of budding forms the characteristic ‘peanut’ to ‘Russian doll’ shape.

Benchmark in diagnosis includes the following:

  • Five or more than 5 yeasts per high power magnification (x 100).
  • Presence of characteristic peanut shaped Malassezia yeast cells (rarely seen in healthy skin but are readily identified in specimen from affected individual).
  • Culture:
  • Malassezia will grow on Sabouraud’s medium / Modified Dixon’s agar. Plates should be kept in contact with the skin for 5-10 seconds, and then cultured at 32-370 C for 3-7 days. Colonies are small, cream to yellow, dome shaped, smooth to slightly wrinkled with a regular to slightly lobed edge. However, as Malassezia organisms are commensal, isolation is not necessarily significant.
  • Histopathology:
  • The histopathology of Malassezia dermatitis is characterized by acanthosis, hyperkeratosis, and a superficial inflammatory infiltrate.


  • Several topical and systemic treatment options are available to treat Malassezia
  • Topical therapy

The yeast is located in stratum corneum and thus topical therapy alone can be successful when potent antifungal agents are promptly applied. Topical therapy avoids the expense and potential toxicity of systemic azole drugs and is considered as the most cost effective and safe treatment of dogs.

Miconazole 2%,  Chlorhexidine 2% shampoo Excellent antibacterial and antifungal; residual activity
Selenium sulfide (1 %) shampoo Good antifungal and keratolytic agent
Chlorhexidine scrubs (1-4 %) Good antibacterial and antifungal; residual activity
Enilconazole rinse Good antifungal agent

As on date the best treatment for yeast and Staphylococcal infections is to alter the pH of the dog skin to make it more acidic.

A solution of equal parts of white vinegar and water (with a pinch of Boric acid), an inexpensive acidifying topical agent shall be applied to the skin of dogs and should be allowed to dry for good results. This can be repeated daily for a week period followed by shampoo bath (Antifungal and Antibacterial) at weekly interval.

  • Systemic Therapy

When topical therapy is impractical or ineffective, systemic triazole antifungals can be used.

Drugs for systemic therapy of Malassezia  infection in dogs

Drug Dose (mg/kg) Route Interval (hrs) Duration

( weeks)

Ketoconazole 5-10 PO 12-24 2-4 Tab. Petoral – K 200 mg

Tab. Ketopet 200 mg

Itraconazole ( daily therapy)

Itraconazole (Pulse treatment)

5-10 PO 24 2-4 Cap. Sporanox 100 mg
10 PO First two days of each week for 2 – 4 weeks.

Clinical improvement should be obvious after 7-14 days after treatment although treatment should be continued for another 7-14 days beyond clinical cure. Maintenance doses two to three times weekly may be necessary in certain cases. Itraconazole is better tolerated than Ketoconazole.

Performa for Malassezia Dermatitis                    

Case number:                                                                                      Date:

Animal details Owner details
Species: Name    :
Breed  : Address:
Age      :
Sex       :
Color    : Phone no:


Dermatology history

Onset of Problem first noticed:                  Sudden/Slow

Is it a year round:                                        Yes/No

If seasonal influence:                                   Summer/Winter

Where did problem begin:

Does animal Scratch:-                                  Yes/No

  • Frequency: Constant/Sporadic/Night

Are other animals or people affected:        Yes/No

Animal’s environment :                               Outside (  %)/Inside (  %)

Animal’s diet:                                                Veg/Non-Veg

Previous treatment, if any:

Other illness of animal:

Dandruff:                                                       Yes/No

Frequency of bathing:                                              shampoo used:

Dermatology examination

Distribution of lesions:-                              Dorsal        /      Ventral

Lesions noticed:-

Primary lesions: Bulla/macule/nodule/papule/patch/plaque/pustule/tumour/vesicle/wheal

Secondary lesions:  abcess/alopecia/callus/comedone/crest/cyst/epidermal collaratte/erosion/erythema/excoriation/fissure/hyperkeratosis/hyperpigmentation/hypopigmentation/lichenification/scale/scar/ulcer

Quality of hair coat:  Dry/brittle/dull/oily

Diagnostic tests:-

  • Cytology (impression smear): +/-
  • of org./field:
  • Presence of dumb bell shaped organisms:

Differential diagnosis:

Treatment trial:-

          Ketoconazole     Ketoconazole+Vinegar

Treatment Trial:


Group 1 (Ketoconazole)

Drug Dose (mg/kg) Route Interval (hrs) Duration

( weeks)

Ketoconazole 5-10 PO 12-24 2-4 Tab. Petoral – K 200 mg

Tab. Ketopet 200 mg


  • Clinical improvement should be obvious after 7-14 days after treatment although treatment should be continued for another 7-14 days beyond clinical cure. Maintenance doses two to three times weekly may be necessary in certain cases.
  • Absorption of Ketoconazole is improved when taken with meal or an acidic diet. Further antacids and H2 blockers should strictly be avoided.
Case no Species Breed Sex Age Colour SGPT/ALT  SGOT/AST
  4519 Canine Pug Male 3months Fawn   40 IU/L      22 IU/L
  6876 Canine Pug Female 1.5years Fawn   65 IU/L      37 IU/L
  2580 Canine Mongrel Male  6years White   48 IU/L      24 IU/ L
  • Adverse effects include anorexia, nausea, vomiting, diarrhea and elevated serum liver enzyme activities and hence Serum biochemistry to be monitored during therapy. Ketoconazole can also be teratogenic.


  • SGPT & SGOT levels are taken before starting the treatment.
  • Oral administration of ketoconazole alone gave a good respone im these 3 dogs, but taken upto 10 days or above to show the clinical improvement.

Group 2 (Ketoconazole+vinegar)

  • As on date the best treatment for yeast and Staphylococcal infections is to alter the pH of the dog skin to make it more acidic.
  • A solution of equal parts of white vinegar and water (with a pinch of Boric acid), an inexpensive acidifying topical agent shall be applied to the skin of dogs and should be allowed to dry for good results. This can be repeated daily for a week period followed by shampoo bath (Antifungal and Antibacterial) at weekly interval.


Case no Species Breed Sex Age Colour SGPT/ALT SGOT/AST
842 Canine Labrador Retriever Male 4years  black   44 IU/L    24 IU/L
7470 Canine Labrador Retriever Female 2years  Fawn   20 IU/L    137 IU/L
654 Canine Labrador Retriever Female 6years  Fawn   70 IU/L    80 IU/L



  • Oral administration of ketoconazole combined with external application of vinegar gave best results, clinical improvements can be seen within a week.



  • In the above treatment trial with Group1 (ketoconazole) & Group2 (Ketoconazole+vinegar).
  • Group2 (Ketoconazole+vinegar) gave good results, the reasons are as follows
    • Vinegar alters the pH of the skin, so it acts against both bacteria (Staphylococcus sp.) & fungi (Malassezia sp.) present on the skin surface.
    • Vinegar directly acts on the organism present on the body surface. whereas ketoconazole is absorbed in the body via digestive tract, then acts on the organism.

Atopic Dermatitis


  • Genetically predisposed inflammatory and pruritic skin disease associated with allergies.
  • Common in dogs ( 6 months to 6 years ) and uncommon in cats.
  • Second most common allergic skin disease in dogs.
  • Hypersensitivity reaction to inhaled or cutaneously absorbed environmental antigens in genetically predisposed individuals.
  • It is frequently associated with elevated serum IgE levels.


  • Early onset is often associated with a family history  of skin allergies
  • This may lead the dog to become susceptible to allergens such as

Animal danders

Airborne pollens (grasses ,weeds, trees )

Mold spores(indoor and outdoor)

Dust mites

Why does a dog develop atopic dermatitis

  • A combination of factors predisposes dogs to atopic dermatitis
  • Both their genetic make-up and environment may interact to allow atopic dermatitis to develop
  • Caused by an inappropriate immune reaction rather than by the allergens themselves

How are dogs exposed to allergens

  • Many allergens are airborne and are found nearly everywhere
  • Pollens are found at high levels only at some times during the year
  • Skin is an important barrier to allergens
  • When the barrier function of the skin is impaired due to genetics or self trauma , allergens can penetrate the skin and trigger allergies

Examples of breeds predisposed to atopic dermatitis (breed predisposition may vary from region to region)

Boxer, Belgian Tervuren, Boston Terrier, Cairn Terrier, Scottish Terrier, West Highland, White Terrier, Wire haired Fox Terrier, American Cocker Spaniel, Chinese Shar Pei, Dalmatian, English Bulldog, English Setter, Irish Setter, Golden Retriever, Labrador Retriever, Newfoundland, German Shepherd, Lhasa Apso, Shih Tzu, Miniature Schnauzer, Pug, Miniature Poodle, Shiba Inu.


The definition of classical canine AD implies a pivotal role for IgE in the pathogenesis which may well be the case. However in fact the pathogenesis of AD is exceedingly complex, and can be categorized under three headings

Defects in innate immunity

Defects in barrier function

Defects in acquired immunity.

The likely sequence of events

Impaired barrier function facilitates the percutaneous absorption of allergen. Allergen is captured by Langerhans’ cells armed with IgE antibody. In the resultant immune response to the allergen, the genetic features of the atopic trait favour the development of an IgE response which is largely elaborated in the local lymph node. Exposure of mast cells armed with IgE antibody initiates release of preformed and newly generated mediators, which aids the influx of inflammatory cells. In turn, these release other pro-inflammatory mediators. Particularly in the chronic phase, a concomitant Th1 response occurs with γIFN prominent Secondary infection compounds the problem, leading to further Th1 responses. A failure of immune regulation allows the continuation of the immune responses and resultant inflammation.


  • Skin erythema
  • Pruritus  (licking, chewing, scratching, rubbing)
  • The distribution of the pruritus usually involves the feet, flanks, groin, axillae, face, and ears.
  • Erythema of pinnae
  • Self-trauma often results in secondary skin lesions, including salivary staining, alopecia, excoriations, scales, crusts, hyper pigmentation, and lichenification.

Prélaud et al proposed a list of five major criteria

The presence of 3/5 criteria resulted in the diagnosis of CAD with a specificity and a sensitivity of 80%.

The five “Prelaud’s criteria” are:

– Corticosteroid-sensitive pruritus

– Erythema of pinnae

– Bilateral cranial erythematous podo dermatitis

– Cheilitis

– First clinical signs reported between the age of  6 months and 3 years

More recently, Favrot et al have reviewed the symptoms and propose the following criteria:

– Age at onset < 3 years

– Mostly indoor dog

– Corticosteroid-sensitive pruritus

– Chronic or recurrent yeasts infections

– Affected front feet

– Affected ear pinnae

– NON-affected ear margins

– NON-affected dorso-lumbar area

Five criteria provide a 85% sensitivity and a 79% specificity for a diagnosis of CAD.


The clinical manifestations of canine AD reflect a multi factorial disorder, which can be complicated by self-trauma or secondary infection. It cannot be over-emphasised that allergy tests are never a substitute for meticulous history, thorough physical examination and careful elimination of other diagnoses.Seasonal foot licking is the most unique and typical symptom of atopy. If year-round allergens (house dust mites) are causing the allergy, the foot licking may be non seasonal.

                                        Intradermal testing

  • Small amount of test allergens(60 allergens) are injected in the skin on one side of trunk after hair has been clipped and wheal (a red bump) response is measured , may also be used to identify the cause of pet’s allergic reaction…
  • Positive reactions to grass, weed, tree, mould, insect, dander, or indoor environmental allergens are seen. False-negative and false-positive reactions may occur.
  • This test requires sedation
  • This test is often referred as ‘golden standard’ for this condition
  • 100% reliable

Allergy tests

  • The term is poorly chosen because:
  • These tests do not allow to distinct allergic dogs from normal dogs
  • Clinically normal dogs can have a positive « allergy test »
  • Atopic dogs can have negative « allergy test »
  • These tests are only interesting in order to elaborate the composition of a possible specific “immunotherapy” Correlation between IDST and “blood test” is difficult to analyze.
  • Actually, it is impossible to determine which of IDST or “blood test” is the most appropriate.
  • May be the best solution would be to perform both tests

Allergen-specific IgE serological tests

  • These tests significantly varies from one laboratory to an other and only little standardization and quality control data is available.
  • The “human technique” can never be used in the dog (specificity of canine IgE, determination of the Cut-off values).
  • Because of the cross reactivity of IgE antibodies against IgE and subclasses of Ig G,
  • it is important to use one or more IgE specific monoclocal antibodies in blood tests in dogs (or a more specific reagent, using the IgE receptor alpha-subunit: FceRIa ).
  • Only few vet labs can offer guarantee for a good quality technique.
  • In the same way as the IDST, a blood test for the diagnosis of adverse reactions to food is not recommended (very poor sensitivity and specificity).

Role of the inflammatory mediators in the skin

  • Histamine: it is obvious that histamine plays a role in CAD but further studies are needed to define the precise role of this mediator.
  • Serotonine: this mediator, released by mast cell degranulation , also seems to play a significant role in allergic reactions in humans.
  • The role of serotonine in CAD remains unknown. The use of serotonine antagonists in the management of CAD has a low efficacy (even if all these drugs also have an antihistaminic effect: cyproheptadine, amitriptyline, hydroxyzine, doxepin, fluoxepin).
  • Leukotrienes: LTB4 are elevated in lesional skin of humans with AD. The importance of this mediator in CAD is suggested by the beneficial effect observed after essential fatty acids complementation in dogs (reduction of the LTB4 production, a pro inflammatory product). The efficacy of this complementation remains quite low (not so far than a placebo effect).
  • Cytokines: in the dog, IL-4 and IL-5 are more commonly detected in atopic skin biopsies. IL-2 is more often found in normal skin.

Differential diagnosis

  • Food allergy
  • Scabies
  • Malassezia dermatitis
  • Bacterial pyoderma
  • Hypersensitivities (flea bite, contact)
  • Parasites (cheyletiellosis, pediculosis), and folliculitis (dermatophyte, Demodex).

How to manage CAD

Treatment of CAD includes a combination of management techniques focusing on different elements constituting the severity of the symptoms: allergen avoidance, antiinflammatory treatments, anti-microbial treatments , allergen-specific immunotherapy.

It seems essential to control, as soon as possible, the gravity of the disease in order to avoid a self-inducing mechanism that could lead to a chronic stage where no more treatments could be effective.

  1. Antimicrobial therapy
  • any secondary pyoderma, otitis externa and Malassezia dermatitis should be treated with appropriate therapies. Controlling and preventing secondary infection is an essential component of managing atopic dogs.
  • Bathing every 3 to 7 days and treating the ears after every bath help to wash off pollens and disinfect the skin and ear canals, preventing secondary infections from recurring.
  1. Symptomatic therapy (itch control)
  • Topical therapy with antimicrobial shampoos and anti-itch conditioners, and sprays (i.e., those containing oatmeal, pramoxine, antihistamines, or glucocorticoids) applied every 2 to 7 days or as needed may help reduce clinical symptoms.
  • Systemic antihistamine therapy reduces clinical symptoms in many cases Antihistamines can be used alone or in combination with glucocorticoids or essential fatty acids for a synergistic effect.
  • One- to 2-week-long therapeutic trials with different antihistamines may be required to determine which is most effective.
  • Chlorpheniramine 0.2–3 mg/kg PO q 8–12 hours
  • Diphenhydramine 1–4 mg/kg PO q 8 hours
  • Dextromethorphan, an opioid antagonist, may be a useful adjunct in managing the licking, chewing, and biting behaviors associated with allergic dermatitis in dogs. Dextromethorphan 2 mg/kg PO should be administered every 12 hours. A beneficial effect should be seen within 2 weeks.
  • Injectable short-acting steroids (dexamethasone sodium phosphate 0.5–1 mg/kg or prednisolone acetate 0.1–1 mg/kg) are effective at providing relief and may last 2 to 3 weeks if no concurrent secondary infection occurs.
  • Temaril-P (trimeprazine and prednisolone combination) is a unique drug that provides significant antipruritic effects at a relatively lower dose of the prednisolone. One tablet per 10 to 20 kg should be administered every 24 to 48 hours. The dosage should be tapered to the lowest possible dose and frequency.
  1. Allergy treatment (immune modulation)
  • Cyclosporine (Atopica) helps control pruritus in 75% of atopic dogs. A dose of 5 mg/kg PO should be administered every 24 hours until beneficial effects are seen (approximately 4–6 weeks). Then, dosage frequency should be tapered down to every 48 to 72 hours.


  • The prognosis is good
  • although lifelong therapy for control is needed in most dogs
  • Relapses (pruritic flare-ups with/without secondary infections) are common, so individualized treatment adjustments to meet patient needs may be required periodically.
  • In dogs that become poorly controlled, one should rule out secondary infection (e.g., that caused by bacteria or Malassezia); sarcoptic mange; demodicosis; and concurrent food, flea bite, and recently acquired hypersensitivity to additional environmental allergens.
  • Because a strong genetic component is present, the breeding of any male or female dog with clinical signs of atopic dermatitis should be discouraged.