Dermatologyvet

Allergic Skin Diseases-Practical Approach in India ( Atopy and Adverse food reaction)
K. G. Umesh, umeshkallahalli@gmail.com
Approach to pruritus - some key examples

A. History:
I. Age:
 Localized demodicosis – 3 to 6 months,
 Cheyletella/fungal – more than 4 months,
 Atopy – 6 months to 3 years,
 Food allergy – 4 months - 4 years.
II. Breed:
 Atopy – Terriers, Delmatian, GSD, Golden Retriver, Irish Setter,Boxer, Labrador, Lhasa Apso, etc.
 Idiopathic seborrhea-Cocker spaniel.
 Seboorrhea Sicca – Irish Setter, GSD, Doberman, Dachshund.
 Hypothyroidism – Bulldog, Boxer, Doberman, Daschung, etc.
 Superficial pyoderma – Doberman, Great Dane, Boxer, Bulldog, Dalmatian, Dachshund.
III. Sex:
Male – Sertoli cell tumour, feminizing syndrome
Female – Ovarian imbalance
IV. Hereditary: Atopy, iodiopathic seborrhea, demodicosis, etc.

V.Contagion: Sarcoptes, otodectes, fleas, fungus and other pets at home.
VI. Environment : Kennel, bedding material, plants, trees, shrubs, etc.
VII. Skin hygiene and flea control : Soap, shampoos, insecticide, etc.
VIII. Diet, drugs and previous treatment : collect detailed History.
B. Physical examination : Localised/generalized, Symmetric/asymmetric.
 Generalized pruritus: Sarcoptes, flea bite allergy, pelodera dermatitis, demodicosis, pyoderma,
food allergy, atopy – look for specific lesions and distribution.
 Facial pruritus : Sarcotes1, atopy1, food allergy, allergic contact dermatitis, fungal, bacterial
folliculitis, auto immune diseases (Pemphigus complex, SLE). Foreign bodies in ears and eyes, zinc
responsive dermatosis, idiopathic seborrhea and other rare diseases (dermatomyositis, solar, Vogt-
Koyanagi-Harada Syndrome, lethal acrodermatitis, juvenile cellulitis, necrolytic migratory erythema).
 Pinnal pruritus: Atropy1, food allergy, sarcoptes1, fly strike.

 Pedal pruritus: Atropy, food allergy, flea bite allergy, pyoderma1, autoimmune diseases, foreign
bodies.
 Facial/pedal: Atopy, Pyoderma.
 Lumbo sacral and tail head: Flea bite allergy1, atopy, food allergy, bacterial folliculitis.
 Axillary and inguinal: Flea bite allergy1, sarcoptes1, pyoderma, atopy, food allergy, contact
dermatitis.
 Steroid responsive: Atopy**, food allergy, flea bite allergy**, allergic contact dermatitis.
Kallahalli Umesh. Strictly for Internal education only – Not to be reproduced in any form 1
Downloaded from https://t.me/veterinaryinindia 1

 Steroid unresponsive (anti-inflammatory doses only): Parasitic – mites*, fleas, fungus*, hook
worm dermatitis*, Pelodera dermatitis, pediculosis, pyoderma*, food allergy cutaneous
neoplasia, autoimmune diseases, psychological (tail biting, acralick, flank sucking) and some
cases of flea bite allergy*.
Differential diagnosis of pruritus based on primary skin lesions

Pruritic pustular
 Infectious : Impetigo, folliculities – bacterial* fungal and demoectic
 Immune mediated: Pemphigus, contact dermatitis, drug erruption.
 Idiopathic: Juvenile pyoderma, subcorneal pustular dermatosis, eosinophilic pustulosis, sterile
furunculosis.
Pruritic dermatitis with plaques
 Infectious: Acute moist dermatitis*, seborrheic dermatitis, dermatophytes, bacterial
hypersensitivity.
 Immune mediated: Eosinophilic granuloma, SLE, drug erruption.
 Neoplastic: Mycosis fungoides, mast cell tumour.
Papular pruritus
 Infectious: Folliculitis* (bacterial fungal, demodex).
 Parasitic: Sarcoptes*, Cheyletiella, lice, fleas.
 Immune mediated: Allergic – flea allergy*, food allergy, contact dermatitis, atopy, drug
erruption.
 Auto immune: Pemphigus, lupus erythematosis.
 Idiopathic: Dalmatian bronzing syndrome.
Pruritic dermatitis
with erythema: Atopy, lupus erythematosis, systemic mastocytosis, drug erruption, staphylococcal
hypersensitivity, mycosis fungoides, contact dermatitis, Vogt-Koyonagi-Harada Syndrome.
Ulcerative pruritic: Lupus erythematosis, leukocytoclasic vasculitis, erythema multiforme, toxic
epidermal necrolysis, mycosis fungoides, epidermolysis bullosa complex, ermatomyositis, acute
contact dermatitis, Vogt-Koyonagi-Harada Syndrome.
Lichenoid dermatitis: Systemic lupus erythematosis (SLE), discoid lupus erythematosis,
bullous pemphigoid, pembhigoid complex, Vogt-Koyonagi-Harada Syndrome. Contact dermatitis,
toxic epidermal necrolysis, erythema multiforme, lichenold keratosis, idiopathic lichenoid
dermatitis.
PROPOSED DIAGNOSTIC PLAN FOR A PRURITIC DOG

1. Minimum data base – refer: Dermatology History and Examination Form.
a. Deep and superficial skin scraping.
b. KOH digest and concentration of scraping.
c. Dermatophyte and bacterial culture.
d. Response to reliable scabicide.
e. Response to antibiotics.
2. Rule out flea bite allergy – skin test, flea control.
3. Rule out atopy – history, physical examination, intradermal skin test.
4. Rule out food allergy – food allergy elimination diet.

5. Rule out contact dermatitis and drug erruption – history environmental restriction and drug
withdrawal.
6. Rule out auto immune diseases – biopsy for histopathology, direct immunofluorescence, antinuclear
antibody test, consider electromylography (EMG) and muscle biopsy.
7. Assess response to anti-inflammatory doses of corticosteroids and review history and physical
examination.
Atopic dermatitis (Inhalant dermatitis)
Canine atopic dermatitis (AD) is a common skin disease. It is commonly associated with flea and food
hypersensitivities. It is beyond scope of this article to discuss immunopathogenesis of atopy and please
refer some reviews on IgE, TH2 cytokines and leukotrines involved ( Halliwell 2009,Deboer 2004,
Olivery et al 2005, 2009, Marsellaet al 2009, Nutall et al 2019). Presumably, like in human AD, the
background of the disease is multifactorial in origin including factors such as a changing environment
with increased exposure to allergens, less exposure to pathogens at young age, the role of the adaptive
immune system, the epidermal skin barrier and a genetic predisposition. Histamine is not a major
mediator of pruritus in canine atopy
1. Defective skin barrier allows microbial adherence, penetration of allergenic proteins, and initiation
of abnormal inflammatory and allergic responses - Decreased amounts of ceramides , fattay acids
and altered expression and distribution of filaggrin,
2. Stratum corneum- Decreased hydration, cellular cohesion , increased trasepidermal water loss
3. Increased seric enzymes -Stratum corneum chymotryptic enzyme (SCCE) and Stratum corneum
tryptic enzyme (SCTE)- increase PH
4. Alteration in skin antibacterial peptides
1. Loss-of-function filaggrin mutations are common in humans with atopic dermatitis and appear to be
involved in some, but not all, affected dog breeds- the gene for the TSLP receptor appears to be
involved in atopic dermatitis in dogs of all studied breeds
2. Immune response is dominated by TH2 cells and involves cytokines such as IL-4, IL-5, IL-6, IL-13, and
IL-31
3. Cytokines can trigger and perpetuate the clinical signs of itching, scratching and inflammation.
Pruritogenic and proinflammatory cytokines in skin disease: IL-2, IL-4, IL-6, IL-13 and IL-31
4. Mix of TH1, TH2, TH17, and TH22-cell mediators may be involved in chronic inflammation,
5. Dogs with atopic dermatitis are predisposed to recurrent Staphylococci and Malassezia organisms -
stimulate the release of pruritogenic and inflammatory cytokines from skin cells.
Canine atopic dermatitis : A genetically predisposed inflammatory and pruritic allergic skin disease with
characteristic clinical features associated with IgE antibodies most commonly directed against
environmental allergens.
Canine atopic-like dermatitis: An inflammatory and pruritic skin disease with clinical features identical
to those seen in canine atopic dermatitis in which an IgE response to environmental or other allergens
cannot be documented.
AD is caused by a combination of immediate and late-phase allergic reactions directed toward
environmental allergens such has house dust mites (Dermatophagoides sp.), molds, and various pollens.
The route of allergen penetration is now suspected to be principally epidermal. Atopic dermatitis is
accompanied also by cutaneous immunological abnormalities, increased prevalence of cutaneous
infections and possibly epidermal barrier defects.

The reported incidence of canine AD has ranged from a high of 15% of the general population to 8% of
referrals to a teaching hospital – which obviously is a selected and biased population.
The age of onset typically spans between 6 months and 6 years; however, more than 70% of AD dogs
develop clinical signs between 1 and 3 years of age. There is a breed predisposition that varies
geographically. There is no sex predisposition.
Acute lesions consist of erythematous macules, patches and papules that may be seen in poorly haired
ventral areas (abdomen, concave pinnae) and friction zones of the body (axillae, groin, flexural aspect of
the legs). As pruritus persists, most chronic lesions are self-induced. Allergic rhinitis may be the cause
of nasal pruritus. Allergic conjunctivitis is a common cause of periocular pruritus. Otic inflammation and
or infections are reportedly seen in two-thirds of the cases. Atopy also seems to predispose dogs to flea
allergy dermatitis and food allergy. Coexistent flea allergy dermatitis and/or food allergy will
dramatically impact the severity of pruritus seen in dogs with atopic dermatitis. In addition, the
presence of bacterial overgrowth, pyoderma, and Malassezia dermatitis also can severely increase the
pruritus seen with atopic dermatitis. Secondary infection can easily double the pruritus seen with
allergic skin diseases.
The diagnosis of AD is difficult because none of the typical signs or features are pathognomonic. A
diagnosis is based on suggestive clinical signs, history and excluding other pruritic skin diseases.
Intradermal testing and allergen-specific IgE serology (serum IgE test) should only be done if the owner
elects to pursue immunotherapy. These tests ARE NOT diagnostic tests for canine AD as they are often
positive in normal dogs.
Diagnosis of canine atopic dermatitis

Pruritus must be present and its absence rules out the diagnosis of AD. Secondary signs like
excoriations and self-induced alopecia and/or the signs of the secondary bacterial infection (papules,
pustules, crusts, erosions) and/or the symptoms of secondary yeast dermatitis (epidermal hyperplasia,
hyperpigmentation, lichenification) are usually observed as the consequences of the inflammation and
pruritus, Recurrent or chronic skin or ear infections are very frequently observed.
Favrot’s 2010 criteria for diagnosis of canine atopic dermatitis (Veterinary Dermatology 2010; 21: 23–31)
1. Onset of signs under 3 years of age

2. Dog living mostly indoors
3. Glucocorticoid-responsive pruritus, (Chronic or Recurrent yeast/pyoderma)
4. “pruritus sine material”(pruritus with no skin changes) at onset
5. Affected front feet ( flexural and Friction areas)
6. Affected ear pinnae
7. Non affected ear margins
8. Non affected dorso-lumbar area
A combination of five satisfied criteria has a sensitivity of 85% and a specificity of 79% to differentiate
dogs with AD from dogs with chronic or recurrent pruritus without AD. Adding a sixth fulfilled parameter
increases the specificity to 89% but decreases the sensitivity to 58%.
IDST and Serological tests : Refer standard dermatology textbooks for performing IDST and In-vitro
tests (ELISA/Heska corporation) and author may be contacted for selection of allergens-
recommended if immunotherapy is planned

Therapeutic approach to canine atopic dermatitis
Please refer the following article for complete management and guidelines on treatment of Atopy “
Treatment of canine atopic dermatitis: 2010 clinical practice guidelines from the International Task
Force on Canine Atopic Dermatitis” http://onlinelibrary.wiley.com/doi/10.1111/j.1365-
3164.2010.00889.x/pdf
Therapeutic options
1. Minimize allergen exposure
Excellent flea control, Good quality highly digestible diet/ rich in essential fatty acids, Allergen avoidance
if possible and allergens known, Frequent bathing
2. Control secondary infections

 Systemic antimicrobial therapy and treat yeast infection
 Routine bathing with topical anti-microbial agents-(benzyl peroxide, Chlorhexidine, ethyl lactate,
Triclosan) shampoos, soothing rinses, aqueous rinses, emmolient and moisturizing rinses,
antipruritic sprays/lotions/creams (Hydrocortisone, diphenydramine, Pramoxine, Colloidal oatmeal
etc) and
 Otic hygiene
3. Treatment of pruritus
Begin monotherapy or combination therapy , FLEA control
4. Immunotherapy
Specific allergen immunotherapy based on intradermal/ serological testing
Management of Acute flare

 The identification and, if at all possible, the elimination of contact with, or ingestion of, such
allergens are important to prevent further worsening or recurrences of the flares
 Bacterial and yeast skin and ear infections are common causes of flares in dogs with AD.
 Oral prednisolone, prednisone or methylprednisolone at 0.5 to 1 mg/kg once to twice daily improve
clinical signs of dogs with severe or extensive AD.
 DO NOT use long acting steroids
 Oclacitinib (Apoquel, Zoetis) can be prescribed at 0.4–0.6 mg/kg orally twice daily for up to 14 days
 Cyclosporine and Fatty acids are helpful in Acute flares
Antihistamines
 Approximately 25 % of clients that gave oral antihistamines to their atopic dogs reported these to be
at least very effective in a retrospective survey
 Hydroxyzine and chlorpheniramine combination and dimetindene mildly improved pruritus and skin
lesions in dogs with AD

Topical therapy in acute flare
 Topical glucocorticoid sprays (Cortavance) are effective for treatment of flares of canine AD. Daily
for 1-2 weeks
 In the absence of availability of these formulations, other topical glucocorticoid formulations are
theoretically likely to be beneficial, Topical glucocorticoids are especially beneficial for localized skin
lesions and for short durations;
 Care must be taken to avoid the steroid-induced skin atrophy that will nearly always develop after
long-term daily application of the product at the same skin sites Treatment
 Emollient formulations containing either lipids, complex sugars and antiseptics (Allermyl, Virbac) or
phytosphingosine, raspberry oil and lipids (Douxo Calm, Ceva) have been shown to provide a modest
effect on skin lesions and pruritus in allergic dogs
 This benefit is likely highest in dogs with mild AD. The intensity and frequency of bathing may be the
most important factor in relieving pruritus .
 Other topical emollients have not been proven to consistently reduce signs of AD in dogs
Chronic ATOPY
 Flea control
 Food allergy- identify and treat
 No evidence of storage mites (Tyrophagus) in pet food but avoid storage of food in warm and humid
conditions
 House dust and storage mites and faeces are rarely present in commercial dry dog foods
 Bathing at least once weekly with a mild non-irritating shampoo and lukewarm water is likely to be
beneficial
 Allergen-specific intradermal testing (IDT) and/or IgE serologies are helpful to identify
hypersensitivity to environmental allergens ( NOT FOOD allergens) in dogs with AD.
 Topical steroids are beneficial when used on intermittent basis to avoid skin atrophy – plan must be
customized to each patient
 Tacrolimus has NO added benefit compare to Topical steroid except in AD dogs with skin atrophy
 Oral glucocorticoids, ciclosporin and oclacitinib are effective for treatment of chronic canine AD
 The concomitant use of allergen-specific immunotherapy, emollient shampoos, EFAs supplements or
enriched diets might allow for a further reduction in the dose and/or frequency of oral
glucocorticoids, ciclosporin (and perhaps even oclacitinib) required to maintain remission of clinical
signs of AD
1. Cyclosporine
(SandimmuneNeoral, Zymmune, Cyrin, imusporin 25, 50 100mg caps, 100mg/ml liquid)
 Cyclosporine is a calcineurin inhibitor, that inhibits T-cell activation- binds to cyclophilin and the
complex inhibits calcineurin, - (IL)-2, IL-4, interferon (IFN)-g, and tumor necrosis factor (TNF)-a. It
effects several cells in the skin, including T cells, dendritic cells, Langerhans cells, keratinocytes, mast
cells, and eosinophils.
 Side effects reported: (vomiting/diarrhea, Gingival hyperplasia, paillamatosis, bacteriuria,
pyoderma, anorexia, neuropathy, BM suppression, lymphoplasmacytic dermatosis
 After 4 to 6 weeks of CsA (5 mg/ kg once daily), a 40% decrease in skin lesions and at least a 30%
decrease in pruritus were noted.
 The percentage of dogs showing at least a 50% improvement in clinical signs increased from 20% to

60%, after 4 weeks of treatment and from 63% to 87% after 12 to 16 weeks of therapy
 In most of the evaluated studies, 40% to 50% of patients were able to have their dosage decreased
to every other day; In 20% to 26% of dogs the dosage could be decreased to twice weekly after 14 to
16 weeks. The remainder of dogs (approximately 25%) required once-daily treatment.
 Ciclosporin orally given at 5 mg/kg daily for 4 weeks, concurrently with prednisolone at 1 mg/kg
daily for 7 days followed by alternate day dosing for 14 days, led to a quicker improvement of skin
lesions and pruritus scores than when ciclosporin was given alone
 Recommendations - After satisfactory improvement (6-8 weeks), Increasing dosage intervals (e.g.
going from every day to every other day) or Decrease the daily dose by half. After reduction of
signs by 75%, Twice weekly or 75% reduction of the original daily dose
 Administration of CSA and KTZ concurrently at 2.5 mg⁄ kg each may be as effec ve as CSA alone at
5.0 mg⁄ kg for treatment of canine atopic derma s
Contraindications
 The safety and efficacy of CsA in dogs less than 6 months old or less than 1.8 kg are unknown.
 The drug is contraindicated for use in dogs with a history of malignant neoplasia and should not be
given to breeding dogs and pregnant or lactating bitches.
 The long-term concurrent use of CsA with glucocorticoids should be avoided to prevent the
development of potentially severe opportunistic infections.
 The manufacturer recommends the use of killed vaccines in patients receiving CsA, although it is
unclear on Ab titers to MLV vaccines
Side effects reported:

• Vomiting and diarrhoea is most common (freeze capsules or administer anti-emetics 2hours before)
- Gingival hyperplasia, paillamatosis, bacteriuria, pyoderma, anorexia, neuropathy, BM suppression,
lymphoplasmacytic dermatosis
When to use cyclosporine
• Onset 2-3 weeks, Broad spectrum, Effective in Chronic Atopy (Not acute), Otitis, Pododermatitis.
Can be combined with other Meds in short term, Long term safety is Good, Not for dogs and cats
less than 6 months of age ??
2. Oclacitinib (APOQUEL
 Selective inhibitor of the Janus kinase (JAK) 1 enzyme
 inhibit the function of JAK1-dependent cytokines involved in allergic inflammation (IL-2, IL-4, IL-6, IL-
13);
 Oclacitinib reduces IL-31-induced pruritus in dogs, likely because of its interference with the IL-31
receptor signal transduction.
 Minimal activity against JAK-2 dependent cytokines involved in hematopoiesis or those associated
with the innate immune response (ESVD-ECVD congress 2013).
 0.4 to 0.6 mg/kg ,orally, twice daily for up to 14 days, and then administered once daily for
maintenance therapy.
 In a trial of dogs with allergic dermatitis, treatment success, as defined by owner-assessed decrease
in pruritus, occurred in 67 percent of dogs treated with APOQUEL vs. 29 percent of dogs treated
with placebo after one week of treatment
 APOQUEL may be administered with or without food.
 Because of theoretical concerns for a potential dose-dependent drug-induced immunosuppression,
the concomitant use of oral glucocorticoids with oclacitinib is likely contraindicated, especially in

case of infections, though such combined use has not been evaluated
 This drug is not approved for dogs less than 12 months of age. The long-term administration of
oclacitinib administered once daily appears to be relatively safe. Not to be used in Neoplasia,
Demodicosis, cats and breeding animals
 oclacitinib had a faster onset of action and a lower frequency of gastrointestinal side effects
compared with ciclosporin.
 Both oclacitinib and prednisolone provided rapid, effective and safe control of pruritus associated
with allergic dermatitis, with substantial improvement in pruritus, reported by owners, and
dermatitis, reported by veterinarians (Gadeyne et al (2014). Vet Dermatol 25: 512–e86)
When to use oclacitinib

Rapid action, Effective in Acute Atopy , Not chronic, Semi Broad spectrum ,Can be combined with
Steroids, Avoid with Cyclsosporine ??? Long term safety Unknown. Not for dogs less than one year of
age
3. LOKIVETmab (Cytopoint –Zoetis)- Monoclonal ab against IL-31

 Once a month Injection
 2mg/Kg, SC, every 4-8 weeks
 80% success by 3rd day
 Lokivetmab at a minimum monthly dose of 1 mg/kg provided quick onset (within one day) of a
lasting effect in reducing pruritus and skin lesions with a good safety profile.
When to use LokiVETmab

Very rapid, Narrow spectrum, Effective in Acute Atopy, Not chronic, Can be combined with other Meds
in short term, Long term safety not known
How to reduce Itching quickly

 Oral prednisolone at 1 mg/kg once daily for 7 day then every other day for 14 days - Rapid reduction
in pruritus and a higher perception of good-to-excellent response by the owner
 Concurrent administration of cyclosporine and oclacitinib (at their approved dosages) was safe for
21 days.
4. Fatty acids
 Fatty acids influence superficial skin lipids and improve the gloss and quality of the coat.
 Oral EFAs might also provide some small benefit in reducing clinical signs of AD in dogs,
 In general, EFA-enriched diets provide higher amounts of EFAs than oral administration of EFA
supplements
 No evidence of superiority for any particular EFA combination, dosage, ratio or formulation
 The benefit of EFAs, if any, might not be seen before two months of supplementation.
 The benefit of topical EFA containing formulations is likely minimal in dogs already fed EFA-rich diets
or EFA supplements
5. Recombinant canine interferon-gamma (Interdog, Toray Industries),

 given subcutaneously at 5,000–10,000 units/kg three times weekly for 4 weeks, then once weekly, is

effective for treatment of canine AD
 Recombinant feline interferon-omega (Virbagen omega, Virbac), administered subcutaneously or
orally, has been shown to provide some inconsistent reduction of skin lesions and pruritus in dogs
with AD
6. Topical Ceramides
• Pseudoceramide-containing physiologic lipid mixture and topical steroids
• TEWL, hydration, skin fold thickness, TNF-E, INF-F, and IL4 CRAMP
• Eosinophils -↓ inflammatory infiltrate, S. aureus binding - ↓ bacterial adhesion
• ↓ 50% of pruritus within 24 hours in 25% of treated dogs, ↑ Efficacy when used in a whirlpool
7. Topical Phyotosphingosines
• Plant-derived sphingosines (serine plus palmitoyl CoA)
• Fungicidal - Inhibit amino acid uptake, cell membrane distruption, and inducing apoptosis, Inhibit
protein kinase C > regulation of cell growth, Inhibit IL-1 release after UVB exposure, Antibacterial :
0.04% inhibits S. aureus, P. acnes, P. aeruginosa, E. coli, and C. albicans, 4 weekly chlorhexidine–
phytosphingosine baths, ↓ bacterial count on kera nocytes of atopic dogs No significant difference
with the vehicle.
• Allerderm©,applied twice weekly to predisposed and affected areas- This study could not confirm
significant clinical improvement when using the product compared to the placebo, although its use
was not associated with adverse effects.( Hobi et al ( 2017) Vet Dermatol 28: 369–e84)
• Ribes pet Ultra emulsion, Twice daily for 90 days- The emulsion had some transient beneficial
clinical effects. However, it was not effective in controlling pruritus as monotherapy (Morsella et al
(2017) Vet Dermatol ; 28: 577–e140)
8. Topical steroids
Mometasone 0.1%, Prednicarbate 0.1%, ↑ stability and affinity for GC receptors, ↑ An -inflammatory
effects, ↑ Penetra on of stratum corneum, ↑ Metabolism in dermis, ↓ Effects on hair follicles,
fibroblasts and vessels, ↓ Interac on with adrenal axis and IDT
Hydrocortisone aceponate 0.058% (Nuttall et al 2009; Nuttall et al 2011; Lourenco-Martins et al 2012)

Q24 for 28d EOD or twice weekly, ↓ CADESI and pruritus score, ↓ 86% CADESI-03 and 65% pruritus .
Maintenance 14% Q24, 33% EOD, 28% twice weekly, 24% required additional therapy, No adverse
effects, Equivalent to CsA, Long term weekly
Nam et al 2012 study -Q24 to the lesions for 14 days, Clinical assessment and changes in skin barrier
function. At the 14th day, 54% CAD severity, 65% pruritus scores, 70% TEWL
Budesonide
• 0.025% budesonide leave-on-conditioner weekly for 3 weeks- CADESI-03, pruritus and QoL-
CADESI-03 ↓ 51% on treatment and ↑ 150% on placebo, Pruritus decreased significantly, QoL
improved significantly
9. Topical Calcineurin inhibitors

Tacrolimus and pimecrolimus- Comparable to glucocorticoids, ↓ itch and nocturnal scratching,
Rapid action and long-lasting effect, Safe for long-term use, Short- and long-term treatment. Side
effect- Transient skin burning, pruritus, erythema- 5% lidocaine gel 20 minutes before the
application

Marsella et al 2004; Bensignor et al 2005 study - 0.1% Tacrolimus ointment is safe and minimally
absorbed. Well tolerated and effective, Clinical score ↓ 58% : 24% generalized : 60% localized,
Adverse drug events : Minor irritation
10. Others
• Essential oils and unsaturated fatty formulation- Dermoscent Essential 6® spot-on weekly,
Dermoscent Atop 7® spray daily - 8 weeks trial, ↓CADESI score,
Spot on: 40%, Spray: 79%. ↓ pruritus Spot-on: 32% Spray: 43%, ↑ TEWL (Tre er et al. 2011)
 Plant extracts, including glycyrrhetinic acid and Vitis Vinifera (Atopiclair Galderma S.A., Lausanne,
Switzerland)
 Coal tar, menthol, capsaicin, doxepin, and endo-cannabinoids Chinese herbal/ Phytopica
• PDE inhibitors- Increase cyclic AMP : Papveine 150-300 mg.dog q 12 h po, Arofylline 1mg/kg q 12 h
po, Pentoxyfylline 10mg/kg q 12 h PO ( Rx Flextal, Flopent, trental 400mg tabs)
 Leukotrine inhibitors: Misoprostal PG E1 analogue 3-6 ug/kg q 8h PO significant reduction in
pruritus
11. Immunotherapy ( refer publications or books)

12. Sublingual Immunotherapy (SLIT)
Allows specific antigens placed under the tongue to induce immunologic tolerance.
Muting of immediate and delayed allergic responses, Tolerance of mucosally -delivered allergens. 30 ml
multidose bottle of allergenic extract preserved in 50% glycerin, enhancing absorption through mucosa
14-21 week supply Up to 22 allergens included for each major aerobiological region Standardized
extracts selected based on geographic region, allergenicity, and cross-reactivity Includes dust mites and
pollens (grass, tree, and weed) + 2 mold spores Daily oral administration is favored by many pet parents
over injections
Client education on atopy

 Likely Lifelong treatment
• Aim is to control clinical symptoms, not to cure
• There is no single panacea for all cases of AD
• May take time to find best treatment option
• Relapses are likely to occur
• Give honest opinion of your expectations : be confident and positive about treatment plan
• Do not prejudge the owners willingness to treat the dog

Summary for Atopy
Topical Steroid cyclosporine Oclacitinib Lokivetmab

steroids
Spectrum Broad Broad broad semi Narrow
Cost ++ + +++ ++++ +++++
Onset of action Rapid Very Rapid 2-3 weeks Rapid Rapid
Acute effective effective Less effective effective effective
Chronic effective effective effective Less effective Less effective
Otitis effective effective effective Less effective Less effective

&Pododermatitis
Adverse effects Rare common Common Com to Uncommon

uncom
Long term safety Moderate Poor Good Unknown Unknown
Monitoring clinical Clinical, Clinical and Clinical, Clinical

Biochem UA Biochem
CBC, UA CBC, UA
Combine with yes Short term Yes Yes- short Yes
steroids term
Adverse Food Reactions : Basics
Adverse Food reaction (AFR, Dietary Sensitivity) : It is defined as clinically abnormal response to food
and /or additives. Traditionally, allergies are thought to occur as a reaction primarily to a protein in the
diet. However, non-Immunologic reactions can occur to anything the dog ingests, whether it is a protein,
carbohydrate, food additive, etc. AFR encompass both immune mediated (Food hypersensitivities) and
non immune mediated (food intolerances) reactions to components of the animal's diet.Therefore, it is
likely that of these group of diseases may be over /under diagnosed and the term “Food allergy” is
misused in the practice. They manifest as dermatological and /or gastrointestinal with or without
respiratory signs.
1. Immunologic food reactions can be
 IgE mediated ( Immediate or anaphylaxis) or Intermediate Type 1hypersensitivity : occurs with in

minutes, Local and systemic signs
 Non IgE Mediated – Intermediate (type III) occurs with in hours and Delayed Hypersensitivity (type
IV)- CMI mediated- hours to days

II. Non Immunologic food reactions further classified as
1. Food intolerance – classified as

a) Food poisoning : Botulism , Salmonella etc
b) Pharmacological reactions : Caffeine, Histamine( eg.,fish ) etc
c) Metabolic reactions : Carbohydrate malabsobtion, Fat metabolism by bacteria
d) Food idiosyncrasy----- Anaphylactic reactions- preservatives, colouring agents etc
2. Dietary Indiscretions – classified as

a) Gluttony
b) Ingestion of Garbage
c) Pica
Proposed pathophysiological mechanisms of Food Hypersensitivity

 Mucosal barrier is not impervious to macromolecules - The GI barrier consists of several anatomic,
physiologic, and immunologic components. Almost all of absorbed proteins enters enterocyte by
endocytosis and is released to lamina propria by exocytosis : A malfunctioning gastrointestinal
defence can be situated at four different levels: mucosal barrier, regulation of immune response,
elimination and tolerance of the antigens reaching the mucosa.
 The rate of entry in jejunum is 2-4ug/hour/cm 2
 Oral tolerance : High-dose tolerance results from lymphocyte anergy, and low-dose tolerance is
mediated by Regulatory T cells. Abnormalities in the development of low-dose tolerance are
thought to be an important cause of AFR in people. microbiota and the genetics may influence oral
tolerance
 The exact mechanism leading to AFR in dogs is unknown, and type I (immediate), III, and IV
(delayed) hypersensitivities have been postulated to occur
 Approximately 0.02% of daily dietary protein intake is absorbed intact and Most allergens are water-
soluble glycoproteins that are 10 to 70 kDa in size andrelatively stable to heat, acid, and proteases.
 Allergy is consequence of increased mucosal permeability?
 Incomplete digestion, Decreased IgA,
 Deranged CMI/GALT, Portosystemic shunts etc
 Inflammation in gastrointestinal tract-
 The International Task Force on Canine Atopic Dermatitis to suggest that some cases of
Cutaneous AFR may trigger flares of atopic dermatitis (as many AFR signs mimick those of atopic
dermatitis)
It is also proposed that cutaneous AFR (CAFR) plays a role in canine atopic dermatitis. The concept that
food allergens might trigger flares of AD in some dogs has been discussed in the literature. The
International Task Force on Canine Atopic Dermatitis supports the concept that CAFR might manifest as
AD in some canine patients. However, dogs with CAFR may also experience clinical signs that are not
typically associated with AD, such as GI signs. It has recently been suggested that AD be divided into
food-induced atopic dermatitis (FIAD) and non–food-induced atopic dermatitis (NFIAD) or canine
atopic dermatitis sensu stricto for cases that are not responsive to an elimination diet. A recent large
multicenter prospective study of dogs with AD reports a GI signs prevalence of 26.3% among dogs with
FIAD, whereas it was only 10.5% in dogs with NFIAD. It should be noted that, in addition to clinical signs
typical of AD, CAFR could also manifest as other syndromes, such as urticarial or pruritus without lesions
or with lesions at unusual sites

The prevalence of adverse food reactions (AFR) and food allergy is not precisely determined. Dietary
indiscretion is much more common in dogs than other types. There is no sex, age or breed
predisposition. About one per cent of all dermatological diseases and 10 per cent of all allergic
dermatoses are reportedly attributable to food allergy. How ever It does seem to be less common in
practice than other allergic diseases like atopy and flea allergy. Studies reported that between 25 and 36
percent of the dogs that were diagnosed with food allergies had additional allergies. Most animals have
been eating the same food for years when they start having problems. Approximately 25 percent of the
dogs discussed in the dermatological literature have concurrent GI complaints. It is speculated that
activated T cells home to different target organs may be possible cause why some dogs and cats with
AFR develop cutaneous signs, whereas others show GI signs or a combination of both. Dogs that
respond to an elimination trial but do not relapse after provocation with their original diet or
components thereof do not have true AFR, such as food intolerance or AFR. It is likely that these animals
have mild to moderate enteritis, colitis, or enterocolitis as a result of other causes and benefit from
other advantageous properties of the special diet ( Gaschen and Mercheant 2011) Food processing can
influence the allergenicity of foods. Sensitisation to an antigen usually follows a long refractory period,
up to two years or more, before clinical manifestations become evident. These ingredients include meat
(beef, chicken, pork, horse, lamb, fish), egg, milk, rice and other cereals but could be any protein or
allergenic proteins in a single food (eg., 2S in soy). Like wise there can be cross reactions between food
ingredients
Canine AFRs were considered responsible for only 1 to 5% of all canine skin disease (Walton 1967,
Carlotti and others 1990, Denis and Paradis 1994, Scott and others 2001, Wilhelm and Favrot 2005) and
10 to 15% of all canine allergic dermatoses (Carlotti and others 1990, Scott and others2001). The
prevalence of AFR among dogs presented to a dermatology center with cutaneous signs is estimated
between 7.6% and 12%. Among allergic dogs, 9% to 36% are diagnosed with Cutaneous AFR ( Gaschen
and Merchant 2011)
1. Dermatological manifestations
 1-5 % of all dermatoses and 10-15 % of all allergic skin diseases?
 11% of feline miliary dermatitis ?
 10% of non-seasonal dermatitis/Pruritus (10-23%) ?
2. Gastrointestinal manifestations - scant data

3. Respiratory and Neurological Manifestations - Very rare
4. Food allergens and GIT
Disorder Role of food allergens Treatment(s)
IBD May contribute to Elimination diet + Immun
Inflammation osuppressive drugs
Gluten sensitive enteropathy Abnormal response to Gliadin Gluten free diet- Rare in pets
Protein Losing Enteropathy in Food allergy leading to Elimination diet +
Soft Coated Wheaten Enteritis PLE and Immunosuppressive drugs
Terriers

Mueller and Olivry BMC Veterinary Research (2018) 14:341 - GIT hypersensitivity signs reported
Vomiting ( 5-21.9%), Diarrhoea (70-89%) , Idiopathic IBD ??? increased frequency ( 6%), Tenesmus
(2%), liquid diarrhoea, mucus or fresh blood in faeces, Weight loss (gluten sensitive enteropathy),
Inappetence, Abdominal discomfort
Refer Mueller and Olivry series of articles on Critically appraised topic on adverse food reactions of
companion animals- seven parts in BMC Veterinary Research
The clinical signs of food hypersensitivity/AFR can be quite variable, involving both the gastrointestinal
tract, respiratory and the skin. Common signs are listed below
 In a published case series, the ear region was involved in 80% of the cases of AFR; paws in 61%;
inguinal region in 53%; and axillary, anterior foreleg, and periorbital regions in 31% to 37% of cases
 Pruritus is the most well recognised symptom. Although, common in head and neck, pedal or Peri-
anal, the pattern of pruritus may mimic atopy or flea allergy! Pruritus is non-seasonal in most
cases. Perianal pruritus or Otitis extrerna may be seen alone
 Recurrent skin infections (Staphylococcus pseudointermedius (formerly S. intermedius), or
Malassezia) may be the presenting complaint in dogs. These may or may not be associated with
pruritus.
 The patient may have symptoms of inflammatory bowel disease with diarrhoea, vomiting,
flatulence, or increased frequency of defecation.
 History of recurrent otitis externa occurs in majority of cases and may be in about 80 –85 % cases.
Yeast otitis or bacterial otitis may be seen
 Cats may have pruritus similar to canine patients, but they may also present with head & neck
pruritus, miliary dermatitis, fur pulling, or eosinophilic plaques.
 Only small percentage of dogs may respond to anti inflammatory doses of steroids
 Other Clinical signs of AFR include vasculitis food induced urticaria, and even food-induced
erythema multiforme vomiting. Diarrhoea, constipation, pododermatitis, asthma, upper resp
inflammation etc ??
 No breed predisposition but Cutaneous AFR seems to occur frequently in American cocker spaniel,
English springer spaniel, Labrador retriever, collie, miniature schnauzer, Chinese shar-pei, poodle,
West Highland white terrier, boxer, dachshund, dalmatian, Lhasa apso, German shepherd, and
golden retriever
Diagnosis
1. Elimination and provocative test : Diagnosis is obtained by use of a restrictive diet consisting of
ingredients not previously eaten by the animal. It is important to rule out other pruritic skin conditions
such as flea allergic dermatitis, sarcoptic and Atopy prior to initiating an elimination diet trial. You have
to keep infection and infestation under control throughout the trial.
Basically, one protein and one starch source that the animal has not been fed in the past are used ( for
eg., Lamb /Chicken/Venison/Rabbit/Rice etc). Food Trials require a compliant client! Food trials can only
be accomplished when the clients have complete control of what their pet is eating. Family motivation
can be improved by asking the clients to keep a log and making this a family project. Snacks, treats or
Supplements containing proteins must be avoided.
A home made diet may be preferable, although owners may elect to use commercially available hypo-
allergenic ( hydrolysate proteins ? ) diets. Home-cooked diets can be unbalanced and may be
inadequate unless formulated by vet nutritionist. Only a few studies have tested hydrolysed diets in
dogs where the food antigen was identified. The commercially available hydrolysate diets (Royal canin)

may tolerated by most, but not all, of the dogs sensitized to the intact proteins. The Hydrolysate-
containing diets were probably best used in dogs with no suspected hypersensitivity to the original
source of hydrolyzed peptides. In addition to novel protein sources and additive-free formulae, the
ideal elimination or test diet should avoid protein excess, contain a reduced number of protein-
containing ingredients, have high protein digestibility and be nutritionally adequate for the intended
species and life stage. The length of the dietary trial is controversial, in most cases 8 -10 weeks is
sufficient. Most dogs (~60%) with food allergy/AFR respond with in first 4 weeks. Confirmation of AFR is
made if pruritus and otitis disappear during the dietary trial and resume immediately following
reintroduction of the offending foods. The Task Force on Canine Atopic Dermatitis recognizes that, in
the absence of gastrointestinal signs, some food allergies may manifest as the atopic phenotype and be
fully or partially responsive to food trials. Some dogs with AD will exhibit flares when exposed to foods,
but not all dogs. The Task Force strongly supports one or more dietary restriction–provocation
challenges in dogs with non seasonal signs.
Prognosis is good if the offending ingredients have been identified and removed.
II. In-vitro tests : Intra dermal skin testing and in-vitro testing using RAST or ELISA are not conclusive and
lack both specificity and sensitivity.
Limitations of In-vitro
 Not all food allergy is IgE mediated and these tests are looking for IgE.
 These tests utilized ground up and solubilized raw ingredients and these may not contain the
antigens that are present after cooking and digestion.
 Animals may develop antibody reactions to food stuff that are not clinically important (false
positives).
 perinuclear antineutrophil cytoplasmic antibodies (pANCA) – Marker for food responsive chronic
enteropathy ?
 Some food reactions are not immune-mediated at all!
III. Other tests studied but not validated:

 Differential Sugar absorption tests using Lactulose and rhamnose for permeability/Mucosal barrier
function
 Gastroscopic and Colonoscopic Allergen provocation test (COLAP)
 Biopsy
 Mast cell Degranulation products Assay
 CMI function / Patch tests
 Basophil Histamine Assay
References are available upon request

Pyoderma- antibiotics Guidelines (Hiller et al (2014) Veterinary Dermatology, 25, 163–e43. Summers et
al (2012) Vet Dermatol ; 23: 305–327)
Classification of pyoderma
 Surface Pyoderma
• Acute moist dermatitis (pyotraumatic dermatitis, “hot spots”)
• Skin fold pyoderma (intertrigo)
 Superficial pyoderma
• Impetigo (“puppy pyoderma”)*
• Superficial spreading pyoderma
• Superficial folliculitis
• Mucocutaneous pyoderma*
• Dermatophilosis*
 Deep pyoderma
• Muzzle folliculitis and furunculosis “canine acne”)*
• Pyotraumatic folliculitis and furunculosis
• Localised deep pyoderma (nasal, pedal, pressure point and acral lick
pyoderma,)*
• Generalised deep pyoderma*
• Bacterial granuloma*
*Not associated with Allergy diseases
A good level of evidence - High efficacy

 Superficial pyoderma -Subcutaneously injected cefovecin
 Deep pyoderma- oral amoxicillin–clavulanic acid
A fair level of evidence -Moderate to High efficacy

 Superficial Pyoderma-oral amoxicillin–clavulanic acid, clindamycin, cefadroxil, trimethoprim–
sulphamethoxazole and sulfadimethoxine–ormetoprim in
 Deep Pyoderma- oral pradofloxacin, oral Cefadroxil and subcutaneously injected cefovecin
First tier Primary choice empirical therapy of known or suspected SBF
 Clindamycin or lincomycin, First generation cephalosporins (e.g. cefalexin, cefadroxil), Amoxicillin–
clavulanate
Additional choices only if local regional susceptibility of Staphylococcus pseudintermedius is known
 Trimethoprim- and ormetoprim-potentiated sulphonamides
First or second Tier antibiotics

• Third generation cephalosporins (cefovecin, cefpodoxime).
• There is insufficient evidence for this working group to reach consensus on categorization of these
agents as first or second tier drugs
Second Tier Antibiotics

When empirical selection of first tier systemic AMD and topical therapy are not appropriate and when
cultures indicate susceptibility
• Doxycycline or minocycline Chloramphenicol

• Fluoroquinolones (such as enrofloxacin, marbofloxacin, orbifloxacin,pradofloxacin and ciprofloxacin)
(should only be used when other feasible options are not available)
• Rifampicin. Commonly used in combination
• Aminoglycosides, including gentamicin and Amikacin.
• First tier AMD (clindamycin, lincomycin and potentiated sulphonamides) may also be considered
when cultures indicate susceptibility
Extensive or generalized disease
• Shampoos, lotions, rinses, sprays, conditioners
• Antiseptics, including chlorhexidine (also with miconazole) and benzoyl peroxide, are preferred,
• Ethyl lactate, povidone iodine and triclosan may also be helpful
Two or three times weekly. Shampoos or conditioners: 10 min contact time prior to rinsing
Focal and localized infections

• Gels, creams, ointments, lotions and wipes
• Antiseptics, including hydroxyl acids (e.g. acetic, lactic and malic acids), benzoyl peroxide and silver
sulfadiazine.
• Antimicrobial drugs, including novobiocin, pristinamycin, bacitracin, fusidic acid and mupirocin
• Use one or two times daily
•
Recurrent Pyoderma management
 Deficiencies in the defense mechanisms of the skin--cutaneous, metabolic or immunologic
abnormality are the classic examples ( Scott and Muller Text book)
 Immunodeficiency syndromes, while chic, are really quite rare.
 Most common causes were Atopy(60%), Food allergy (7%), Flea allergy (7%), Hypothyroidism
(7%), Hyperestrogenism (4%), Demodicosis (4%), and Zinc-responsive dermatosis (4%).
 Treatment Options
1. antibacterial topical agents
2. Bbacterial vaccines:
• Staphage Lysate
• Immunoregulin
3. intermittent (“pulse”) antibiotic therapy
 Nisin Wipes—nisin is an antimicrobial peptide that is commonly used in some areas of the world
as a disinfectant teat wipe for dairy cattle and is even used as a food preservative.
 Preliminary studies in dogs demonstrated that use of these wipes twice daily could limit
bacterial colonization and slightly accelerate healing of existing pyoderma.
 Very dilute sodium hypochlorite solutions (“bleach baths”) has become very popular in human
atopic dermatitis, studies are lacking in dogs
 Peroxide is an excellent oxidizing disinfectant. The most recently popular products contain
“accelerated hydrogen peroxide,” which is simply hydrogen peroxide with added stabilizers and
surfactants to enhance its efficacy.

Yeast Infection ( Malseezia)
Systemic therapy with Fatty meal :
• Check Liver enzymes and bilirubin every 2 weeks
• Ketoconazole/Itraconazole : 5 - 10 mg/kg q24h, 2-4 wks
• Itracanazole -better tissue penetration and a longer half-life than ketoconazole
• Flucanzole 2.5-5 mg/kg q24h, Terbinafine 20-30 mg/kg q24h,
Pulse therapy :
• Itraconazole 5 mg/kg PO q 24 hrs for 2 consecutive days per week.
• Terbinafine - 30 mg/kg PO q 24 hrs for 2 consecutive days per week
• Evidence study publication (2009) - Only one topical treatment of Malassezia dermatitis (2%
miconazole nitrate +2% chlorhexidine, twice a week for 3 weeks) and with fair evidence the use of
two systemic treatments with azole derivatives (ketoconazole, 10 mg/ kg/ day and itraconazole, 5
mg /kg/day for 3 weeks).
Topicals
• Nystatin, Amphotericin B 3%, Miconazole 2%, Ketoconazole,
• Enilconazole 0.2%, Chlorhexidine 3-4%, Lime sulfur 2%, Acetic acid/boric acid Acetic acid 2.5%
Oral flea control tabs

 Nitenpyram (Capstar) tabs : Novartis, > 4 wks of age
 Milbemycin+ lufenuron (Sentinel) tabs-Novartis, > 6 wks of age
 milbemycin oxime/lufenuron/praziquantel (Sentinel spectrum)
 Spinosad, 30mg/Kg ( Comfortis/Trefexis) oral tabs Eli lilly > 14 wks
 Lufenuron (Programme tabs, Ciba, > 12 weks of age
 Spinosad + milbemycin oxime (Trifexis)from Elanco, >8 wks of age
 Fluralaner (Bravecto) from Merck (intervet) tab for fleas and ticks- Once in 3 months, 6 months
and above
 Afoxolaner (Nexgard), dogs > 8 wks of age
 Sarolaner (Simpirica from zoetis), dog, > 6months
 Lotilaner (Credelio) elanco , 8 weeks, dogs only
 Imidacloprid (Advantus) tabs, 8 weeks, dog
Spot- on
 Fluralaner (Bravecto) topical for Cats and Dogs, 12 weeks
 Imidacloprid + Permethrin (K9advantix) Bayer, 7 weeks
 Imidocloprid + Ivermectin ( advantage duo) Bayer, 7 weeks
 Imidacloprid + Milbemycin /Moxidectin(Advantage multi) Bayer, > 7 wks of age, 9 wks for cats
 Selamectin 6 mg/Kg (Revolution) Pfizer, 6 wks dogs, 8 wks cats
 Fipronil + (S) Methoprene (Frontline plus,) Merial, 8 weeks dogs and cats
 Fipronil + Pyriproxyfen (Effipro, effipro plus)Virbac, 8 weeks cats
 Fipronil + Permenthrin ( Effitix) Virbac, 8 wks Not for cats
 Dinotefuran, Permethrin, and Pyriproxyfen (Vectra3D ) also for mosquitoes (summit vet
pharma) 8 wks only dogs
 Pyriprole - like fipronil, (Prac-Tic from Novartis , 8 weeks, dogs only
 Flumethrin4.5%,Imidocloprid10% (Seresto from Bayer), 8 weeks
 Methaflumizone/amitraz (Promeris Duo Fort dodge – 8 weeks, fleas and ticks in dogs

 Fipronil/cyphenothrin (Parastar® Plus ) Elanco, 8 weeks , dogs
 4% Fipronil, 5.8% (S)-Methoprene, and 7.6% Amitraz (Certifect from Merial) 8 weeks, Only dogs
 Indoxacarb (Activyl) from Merck animal health) 8 weeks dogs and cats Activyl plus + permethrin
for ticks, dogs only

Demodicosis in dogs - An update
Kallahalli Umesh, Scientific communications Manager, Mars Inc
Demodicosis is one of the ten most common skin diseases seen in small animal practice. Canine
demodicosis is one of the most common inflammatory parasitic skin diseases, characterized by an
excessive proliferation of Demodex mites in hair follicles and skin surfaces. Canine demodicosis is probably
the best and most important example of overgrowth-induced disease. Dogs have three recognized
species of Demodex mites. Clinically, the most common is Demodex canis.
Demodex mites are part of the normal fauna of the dog, and mites are present in the hair follicles of
healthy dogs and genetically preprogrammed immunological defect is responsible for the exaggerated
replication of mites in demodicosis. This mite is limited to the hair follicle and, rarely, the sebaceous
gland. Demodex mites were found in the skin of 5.4% of healthy dogs (Gaafar et al.1958) but using
trichoscopy, could not detect Demodex canis mites in any of 78 dogs examined but a single Demodex injai
one dog (Fondati et al.2010). However, Using a real-time PCR technique, Demodex mites, albeit in very
low numbers, were found to be normal inhabitants of haired areas of the skin of healthy dogs (Ravera et
2013)
Demodex canis is the canine commensal follicular mite and is found in most dogs soon after birth. The
D. canis mite develops through four life stages: a fusiform egg, a six-legged larva, an eight-legge nymph,
and an eight-legged adult. The mite considered to be commensal organism of skin in al mammalian skin
and spends entire life cycle on the host, residing in hair follicle, feeding on cellular debris. Puppies and
kitten acquire the mites during nursing in first 72 hours after birth. Except for this short period, the mites
are not considered to be contagious. The life cycle probably takes 20-35 days. Transmission of mites
between canine hosts takes place soon after birth while the pups are feeding from the dam. Initially, mites
are found on the head and fore limbs of newly infected It is generally accepted that mites are not
transmissible between adult dogs under normal circumstance ( Mason et al 1996). If a puppy is stillborn,
delivered by caesarean section or not nursed, no mites are found, therefore there can be no transmission
in utero (Greve and Gaafar, 1966).
Thermostatic zone of D.canis is between 16 and 41 C. Movement of mites ceases at env.temp below 15
C. In artificial and laboratory condition, mites reported to live as long as 37 days away from dogs. Mites
can be killed by desiccation in 45-60 min at 20 C. and RH at 40%.( Scott et al 2001)
A long bodied species was first reported in 1997 and was named Demodex injai. Demodex injai, the large-
bodied Demodex species mite, is larger in all life stages than D. canis Histologic examination shows that
these mites tend to reside within the sebaceous glands. Cases of D. injai infection are associated primarily
with a dorsal seborrheic dermatitis. This mite infests hairfollicles and sebaceous glands primarily in the
trunk region. With a body length of 306-451 (361 µm) it is twice the length of D. canis ( Desch2003,
Bensigno et al 2006, Hiller et al 2003).
A newly identified short-bodied Demodex species mite has tentatively been named Demodex cornei.
Unlike the other canine Demodex species mites, D. cornei can reside in the most superficial layer of the
epidermis. It is 50% shorter than the adult form of D. canis and about half the length (148 µm) of D. canis.
Compared to their long bodied counterparts, they have a short opisthosoma with a varying length

between 90-148 µm in the dog, 80-90 µm for the short form of cat mite- Demodex gatoi (Chesney et al
1999,Tamura et al 2001).
Recently using mitochondrial rDNA assay, D. cornei is found to be a morphological variant of D. canis,
while D. injai appeared to be closer to D. folliculorum than to D. canis (Sastre et al 2012)
Cats - Demodex cati is manor mite about 200 μm in length The ova are more oval than the eggs of D. canis.
Another commonly found mite in cats is Demodex gatoi, which is the short-bodied Demodex mite of cats
There is evidence of hereditary predisposition in certain breeds but genetic transmission is not known.
However, the mode of inheritance and the precise genetic defect or mutation remain to be elucidated.
There was significant association between the phenotype ‘generalized juvenile demodicosis’ and certain
microsatellite markers or DLA haplotypes (FH2202, FH2975 and FH2054). Despite this, Breeding of such
dogs are not recommended.
One North American study found the Generalized demodicosis to common in breeds like Shar Pei, West
Highland White Terrier, Scottish Terrier, English Bulldog, Boston Terrier, Great Dane, Weimaraner,
Airedale Terrier and Afghan Hound but there will be geographical variation in breeds susceptibility
((Lemarié, 1996)
The role of the immune system in the development of demodocosis remains unclear. Studies in the past
like administration of antilymphocyte serum and immunosuppressive drugs such as azathioprine and high
dose corticosteroids to dogs resulted in demodicosis indicating that immunosuppression may play an
important role in the development of demodicosis (Corbett, et al 1975, Hirsch, et al 1975) Like wise It was
hypothesized that demodicosis results from a T-cell defect that allows mites to proliferate.
Large numbers of mites with secondary pyoderma that induce humoral factors may cause generalized T-
cell suppression (Scott et al 1976 and Barriga 1992) However similar studies shown that dogs with
demodicosis had antibody titres similar to control dogs following vaccination and exhibited normal to
slightly elevated humoral immune responses (Scott et al 1976) The presence of mites may be necessary
for the immunosuppressive effects as serum samples from affected animals and not recovered /cured
dogs have been shown to exert immunosuppressive properties (Hirsh et al 1975)
More Recent studies indicated that dogs with generalized demodicosis had a significantly lower in-vitro
lymphocyte blastogenesis response, fewer cells expressing IL-2 receptors and decreased IL-2 production
than control dogs. It is also hypothesized that T cell response in demodicosis is biased towards depressed
TH1 and increased proliferation of TH2 cells - giving indirect evidence to observed decreased IL-2 level,
reduced cellular immunity and normal antibody response (Lemarie et al 1994).
Immunological studies on CD4+ cells indicated that absolute numbers of these cells were significantly
lower in affected dogs compare to healthy dogs but equalled those of the control group following
complete remission (Oliveira et al 2015)
The role of IGF-2 in pathological conditions including skin disease or would healing is well documented in
human. The IGF-2 role in pathogenesis of canine demodicosis was recently investigated. The serum IGF-
2 concentration was increased in dogs with generalized demodicosis compared to healthy dogs. In
affected dogs, slightly lower serum glucose levels negatively correlated with IGF-2 levels. (Yarim et al
2015)
Another recent study demonstrated Higher total serum protein and globulin concentrations were
detected in dogs suffering from generalized demodicosis than in healthy dogs. Serum concentrations of
albumin and A/G ratio in affected dogs were lower in demdodicosis dogs than in the healthy control dog.

A positive correlation of serum concentration of IGF-2 with serum concentrations of total protein and
globulin, as well as a negative correlation of IGF-2 serum concentration with serum concentration of
albumin and ratio of A/G in affected dogs were reported (Hagiwara et al 1974, Reddy et al 2015)
Lastly Dogs with generalized demodicosis had significantly higher concentrations of C-reactive protein and
haptoglobin and lower butyrylcholinesterase activity than dogs with localized demodicosis and healthy
dogs (Martınez-Subiela and Bernal et al 2014)
In summary, Dogs with generalised demodicosis may have a defect in Demodex mite antigen presentation
leading to a decreased IL2 response and may be directly related to a decreased Th1 cytokine response. It
is believed that there is T-cell exhaustion when dog develops generalized demodicosis which is supported
from the studies that demonstrated low production of supportive/stimulatory cytokines ( IL-2 and IL-21 )
and high levels of suppressive cytokines (IL-10 and transforming growth factor B ) and low numbers of
circulating CD4+ lymphocytes (Ferrer 2014)
This defect may manifest by itself or in conjunction with some immunosuppressive factors and would
allow the multiplication of the mites and the onset of a generalised T-cell depression predisposing to
secondary pyoderma, further depressing both the cellular and humoral immune response.
Hyperadrenocorticism, hypothyroidism, steroid administration and chemotherapy were reported as

concurrent underlying causes, while concurrent neoplastic, infectious, parasitic or metabolic disease was
uncommon in dogs with adult onset generalized demodicosis in retrospective studies ( Lemarie 1996
and Scott et al 2001)
Clinical signs
When presented with a case of canine demodicosis one should establish which clinical form is
present, since the treatment and prognosis are completely different in each case, to such an extent that
they are considered distinct clinical entities. Canine demodicosis is classified as localized (LDM) or
generalized (GDM) disease according to the extent of the disease. Additionally, GDM is subclassified as
juvenile-onset or adult-onset. “juvenile onset” presents at under 12 months in small breed dogs, 18
months in large breeds and 2 years in giant breeds. However, neither the percentage of the dog's skin
surface that is affected, nor the age of onset, which would define each clinical form, are clearly
established. This makes any comparison between the different treatments difficult. Localized demodicosis
has been defined as one where there are “6 or fewer lesions that are less than 2.5 cm in diameter” and
Generalized demodicosis can be defined as one where there are more than 12 affected areas, or a
presentation where a whole body region (e.g., head and face) is affected ( Miller et al 2013)
Pododemodicosis falls into the generalized category. In a another study , GDM was defined as demodicosis
that involved >50% of the dog's skin, or as pododemodicosis involving all four feet, and only dogs that
were >4 years old were considered to have adult-onset demodicosis.
Although some clinical lesions are similar in LDM and GDM. Table 1 the extension of the disease and the
predisposition to develop deep pyoderma produce a completely different clinical picture.

TABLE 1
Cutaneous lesions seen in the different clinical presentations of demodicosis in the dog
Localised demodicosis
Focal alopecia, desquamation, erythema, comedones, Occurs primarily in puppies, Mites found only in
lesional areas; lesions focal & limited (1–4 sites), Hyperpigmentation,& follicular plugging (comedones)
and variable pruritus
Generalised demodicosis
Multifocal/diffuse alopecia, erythema, oedema, crusting, scaling, comedones, pyoderma, furunculosis,

lichenification, lymphadenopathy. Occurs in dogs with concurrent systemic illness. Some may have
history of Localized progressing to generalized. hyperpigmentation, Papular rash, follicular plugging,
concurrent superficial or deep pyoderma (furunculosis) and Pododermatitis
Pododemodicosis
Alopecia, erythema, cellulitis, furunculosis
Otodemodicosis
Ceruminous otitis
Localised demodicosis (LDM) The localised form typically starts as one or more focal alopecic lesions in
dogs less than 1.5 years old. Usually only the head (perioral, periocular) or the forelimbs are involved,
although it can start in any area. The presence of pruritus and pyoderma is rare, as is progression to the
generalised form . However about 10% of the cases may develop into GDM.
Generalised demodicosis (GDM) This form involves, by definition, the larger part of the dog's skin and
bears a guarded prognosis. The owner must be informed that GDM can be difficult to treat and that lapses
in treatment will prolong the treatment, and may even make it less effective , especially in cases
complicated by deep pyoderma . In these cases there is usually also pruritus and peripheral
lymphadenopathy, and some dogs may show signs of septicaemia .
In juvenile-onset GDM, pure-bred dogs are more frequently affected and there is a clear breed
predisposition, to such an extent that it is not advisable to breed dogs affected by GDM. Predisposed
breeds include the Old English sheepdog, Rough collie, Afghan hound, German shepherd dog, Cocker
spaniel, Doberman pinscher, Dalmatian, Great Dane, English bulldog, Boston terrier, Dachshund,
Chihuahua, Boxer, Pug, Chinese Shar-Pei, Beagle, German shorthaired pointer, West Highland White
terrier and Scottish terrier .
Adult-onset GDM may be associated with other debilitating conditions and there is no breed
predisposition to this. The most common underlying disease is spontaneous or iatrogenic endocrinopathy,
in particular hyperadrenocorticism, which further aggravates the clinical signs of demodicosis and
interferes with the treatment. However, in many cases there is no underlying disease, or it remains
unrecognised.
Clinical signs of D. cornei infection are similar to those of D. canis infection, but D. injai infection can have
a different presentation. Demodex injai infection typically does not cause alopecia but instead is most
commonly associated with an oily coat on the dorsum of the neck and trunk. This clinical sign is consistent
with the observation of this mite histologically in the sebaceous glands of the skin. Demodex injai infection

has been observed more commonly in terrier breeds, such as West Highland white terriers, and only a low
number of mites may be found on skin scrapings
Diagnosis
Demodicosis is usually not difficult to diagnose if several deep skin scrapings are performed.
In order to increase the chance of making a definitive diagnosis, the skin should be squeezed, immediately
before skin scraping, to push the mites out of the hair follicle. The skin should then be scraped until there
is some oozing of blood, to ensure that the skin has been scraped deeply enough. A large number of adult
mites or immature forms and eggs are necessary to confirm the diagnosis, because an occasional mite
may be found on scrapings from normal dogs; however, this is rare. If an isolated mite is considered
incidental then the skin scrapings should be repeated in other areas, and especially in the face and feet,
two preferred locations for the parasite. It may also be worthwhile scraping normal skin in cases of LDM;
a large number of parasites detected may indicate a risk for subsequent generalization.
Hair plucking is considered less sensitive than skin scraping when the number of mites is low. The
diagnostic sensitivity of hair plucking was rather low (85%), and especially so in localized and
noncomplicated demodicosis. In comparison, the diagnostic sensitivity of exudate microscopy was 100%.
(Saridomichelakis et al 2007)). However, one study found that there was no significant difference between
skin scraping and hair plucking in the proportion of positive samples taken from 161 dogs suffering either
from localized or generalized demodicosis (Beco et al 2007) Acetate tape method ( tape is applied to the
test area and the skin squeezed before lifting the tape and put on a slide) reported significant increase in
mite detection compared to deep skin scraping, both in the total number of mites and in the number of
larvae and adults detected (Pereira et al 2012)
In the more chronic cases with lichenified and fibrotic lesions, especially on the feet, and in
some breeds such as the Chinese Shar-Pei, diagnosis must be made by microscopic examination of biopsy
material Retrospective histopathologic studies have indicated that mural follicullitis is the most consistent
reaction pattern in canine demodicosis, that interface folliculitis is often present, that 90% of the
lymphocytes infiltrating epithelium are CD3+ T cells, and that perifollicular melanosis is a common finding.
Treatment
When considering the prognosis and treatment of demodicosis it is important to recognise
the very different clinical behaviour of LDM and GDM . In the localised form, between 30 and 90% of the
cases will resolve spontaneously , whereas in the generalised form spontaneous resolution has never
been reported. Generalised demodicosis in the dog is, without any doubt, one of the most difficult
cutaneous conditions to manage, and, even with the new drugs currently available, cure rates of 100%
are rarely reported.
Successful outcome/Cure : As the prognosis for canine demodicosis is good, with the majority of cases
achieving long-term remission, it is recommended to scrape repeatedly the three to five most severely
affected areas and any new lesions monthly until all three to five scrapings are negative. it is
recommended to continue treatment for 1 month after the second negative monthly set of skin scrapings.
Immunosuppressive therapy must be avoided including steroids and diseases such as neoplasms,
hypothyroidism or hyperadrenocorticism must be screened when ever underlying cause suspected in dogs
with generalized demodicosis
According to a review of evidence based treatment protocols for canine demodicosis, amitraz, ivermectin,
milbemycin oxime, moxidectin, and doramectin are all recommended for treating canine demodicosis (
Muller et al 2011)

Localised demodicosis
Localised demodicosis is a spontaneously resolving disease. The individual lesion typically
heals in 6-8 weeks but can persist in some dogs for months. The dog should be in good general health,
and its management should be reviewed and corrected if indicated. Because the lesions heal
spontaneously, no treatment is necessary provided the owner understands the course of the disease. If
the decision is taken to treat the lesions, the agent selected should not include a glucocorticoid. Localized
demodectic lesions may benefit from topical antimicrobial agents such as mupirocin, benzoyl peroxide,
chlorhexidine, or ethyl lactate when secondary pyoderma is present. Juvenile-onset localized demodicosis
resolves spontaneously within one or two months in most dogs. Therefore miticidal therapy is not
required unless the disease generalizes.
Generalised demodicosis
Before therapy is instituted the owner must be made aware of the intensity of treatment
necessary for a long-term, complete, cure of the condition. They should also be made aware that regular
re-examinations of the dog will be necessary, and that adjustments to the treatment may be necessary in
the light of those examinations .
Table 2 lists some general recommendations for treating generalised demodicosis. The use of
corticosteroids deserves special consideration. Dogs with GDM are prone to secondary bacterial
pyodermas, sometimes so severe that they are life-threatening and, accordingly, the use of
corticosteroids is never justified.
TABLE 2 : General recommendations for treating generalised demodicosis

1. Rule out and treat all predisposing factors
2. Avoid both topical and systemic corticosteroids
3. Treat secondary pyoderma: systemic antibiotics and topical benzoyl peroxide
4. Monitor response by skin scrapings every 3-4 weeks
5. Scrape the same spots and all new lesions each time
6. Maintain treatment until 2 negative skin scrapings
7. Monitor at 3-monthly intervals for at least 1 year
Dogs with adult-onset demodicosis should have a complete medical evaluation performed to
identify and treat any underlying disease. If the medical evaluation fails to reveal any disease, the patient
should be monitored carefully for signs of an emerging disorder. In addition, attention should be paid to
the pyoderma that inevitably accompanies generalised demodicosis. Broad-spectrum, bactericidal
antibacterial therapy is mandatory.
Several specific antiparasitic treatment options are now available, although amitraz is the only drug
marketed worldwide for the treatment of canine demodicosis. The therapeutic efficacy of each drug varies
greatly, as is indicated in the reports of clinical studies . These discrepancies result from differences in the
populations studied, in the criteria used when differentiating LDM from GDM and in defining 'cure', and
in the follow-up periods. The variation between reports also reflects the complex nature of canine
demodicosis. Thus, treatment selection has to be based on the particularities of each case and on the
degree of co-operation afforded by the owner.

Amitraz - Topical
Amitraz is a formamidine pesticide with pharmacological activities including monoamine
oxidase inhibition, alpha-adrenergic agonism and prostaglandin synthesis inhibition . Amitraz dips will
work well in many cases and should be considered as the first choice. The licensed protocols for the use
of amitraz vary from country to country. Although it is licensed to be used as a weekly or bi-weekly
0.05% topical solution, its incomplete efficacy led to the use of unlicensed protocols with more
concentrated solutions applied weekly or even daily, in an attempt to increase its clinical efficacy. In any
case, the more aggressive protocols should be limited to the cases where bi-weekly or weekly dips prove
to be ineffective.
Table 3 lists some useful recommendations that may be employed to obtain the best results and avoid
potential hazards when using amitraz. Although the rate of cure reported for amitraz dips, especially with
the daily administration protocol, is acceptably high, there are several disadvantages in its application:
topical treatment is tedious and time-consuming, the rate of cure is variable and the probability of relapse
is high.
TABLE 3
General recommendations for amitraz dipping in generalised demodicosis
1. Use a 0.025-0.05% amitraz solution every 1-2 weeks
2. Clip the entire coat, especially in dogs with a medium to long hair coat
3. Make up fresh amitraz solution each day
4. Bathe with a benzoyl peroxide shampoo before dipping
5. Rub the solution into the skin with a sponge
6. Do not rinse
7. Allow to air-dry
8. Do not allow the dog to get wet between dips
9. Add 1-2 capfuls of bath oil rinse to the solution if the skin gets dry
10. Perform treatments in a well-ventilated room
11. Avoid clinician/owner contact with their skin and mucous membranes - wear gloves
Pododemodicosis and demodectic otitis can be treated with an extralabel mixture of amitraz and mineral
oil (1:9), although this mixture may irritate the otic epithelium in certain individuals. Amitraz collars are
not recommended for treating Demodicosis.
Pilot study using spot-on preparation with 15% amitraz and 15% metaflumizone has been used in some
countries as a monthly treatment for canine demodicosis and has shown promising results with
administration monthly and every 2 weeks ( Fourie and Kok et al 2007, Rosenkrantz 2009) but this drug
has potential to cause pemphigus foliceus in dogs
Toxicity- Mild toxicosis seen as excessive lethargy for one or two days after dipping and severe signs of
toxicosis are similar to those seen with the use of alpha2-adrenergic agonists, including sedation,
hypothermia, bradycardia, and hyperglycemia. The use of alpha2-adrenergic antagonists can reverse signs
of toxicosis and can be used before dipping in patients with a history of adverse effects. Atipamezole (50
µg/kg intramuscularly) can reverse the signs of toxicosis within 10 minutes. Avoid antidepressants and
MAOIs, such as selegiline, in dogs receiving amitraz

Macrocyclic lactones include the avermectins (ivermectin and doramectin) and milbemycins (milbemycin
oxime and moxidectin).
Milbemycin -oral
Milbemycin offers an alternative for cases where amitraz treatment has been ineffective.
Although this drug is approved only as a heartworm preventive, it was used experimentally in the
treatment of demodicosis because of its broad antiparasitic activity. The data available from these initial
reports demonstrate that milbemycin can be very effective in cases refractory to topical amitraz.
The milbemycins are natural fermentation macrolide antibiotics produced by Streptomyces
hygroscopicus. Structurally, they are closely related to the avermectins produced by S. avermitilis, and like
them, their antiparasitic activity results from disruption of invertebrate gamma-amino butyric acid (GABA)
neurotransmission .
Compared with amitraz, milbemycin oxime offers several advantages: easier administration,
lack of side-effects at the dosage used (including breeds sensitive to ivermectin such as Rough collies),
higher rate of cure and effectiveness in some of the cases unresponsive to amitraz treatment. Among the
disadvantages are the fact that milbemycin treatment is far more expensive, its optimum dosage has not
been established and although reported effective, doses vary between 0.5 and 3.8 mg/kg. Furthermore,
not all the cases will respond , the rate of relapses is high (29-75%), especially when using lower doses.(
Holm 2003, Muller et al 2011)
Milbemycin oxime is recommended for the treatment of canine generalized demodicosis at a dose of 1–
2 mg⁄ kg p.o. daily (Muller 2011) A lower efficacy is seen with adult-onset demodicosis. it is advised to
evaluate the ABCB1-D1 (MDR-1) genotype and to use lower doses or increase the dose gradually in
ivermectin sensitive breeds
Ivermectin - oral
Ivermectin is not licensed for use in canine demodicosis. Ivermectin belongs to the group of avermectins
produced by streptomyces avermitilis and has a wide spectrum of action and high anthelmintic efficacy.
Ivermectin exerts its antiparasitic activity by coupling to the binding site of GABA/glutamate and the
chloride ion channel, which results in membrane hyperpolarisation and inhibition of nerve impulse
transmission. In mammals, GABA is an inhibitory neurotransmitter found only in the central nervous
system (CNS), whereas in nematodes and arthropods it regulates peripheral muscles . In mammals in
which ivermectin does not readily cross the blood-brain barrier, the drug has a wide margin of safety.
However, ivermectin may have unfortunate consequences in the dog, especially in Rough collies, Old
English sheepdogs, Shetland sheepdogs, Bearded collies and their crosses In dogs from these breeds that
developed toxicosis, CNS concentrations of ivermectin were much higher than the concentrations in liver
or serum, which suggests greater penetration of ivermectin through the blood-brain barrier . Enhanced
sensitivity to ivermectin has also been reported in young animals, and the proposed explanation was again
the presence of greater permeability of the blood-brain barrier at this age . For these reasons, ivermectin
is marketed only as a heartworm preventive at a dosage much lower than that recommended for
demodicosis treatment.
An ABCB1-D1 (MDR-1) mutation considered responsible for the acute toxicity in collie dogs and several
other herding breeds has been identified. Ivermectin sensitivity is result of frame shift deletion mutation
of the multidrug resistance gene (ABCB1-D1 (MDR-1)), producing truncated, nonfunctional protein
product. The product of the MDR1 gene, P-glycoprotein, is a large ATP-dependent transmembrane protein
transporter found in the blood-brain barrier among other tissues. P-glycoprotein pumps substrates (e.g.

ivermectin and loperamide) within the brain back into the blood. The absent P-glycoprotein allows the
influx of ivermectin into the CNS. Dogs homozygous for this mutation (MDR1-1 delta) display an
ivermectin-sensitive phenotype, developing severe neurotoxicosis after a single dose of ivermectin.
(Mealey 2006, Mealey and Meurs 2008)
Clinical signs of toxicity include ataxia, mydriasis, altered mentation, hypersalivation, vomiting, blindness,
retinopathy, tremors, seizures, bradycardia, and/or respiratory depression (Merola et al 2009)
Dogs without an ivermectin-sensitive genotype can show signs of toxicosis if ivermectin is given with P-
glycoprotein inhibitors like Fluoxetine,Pentazocine erythromycin, Itracanazole, Tacrolimus cyclosporine
or ketaconazole. ABCB delta 1 gene ( earlier referred to as MDR1) testing is can be used to screen for
sensitivity in breeds susceptible to ivermectin toxicity
The pour-on formulation of ivermectin is not effective in treating generalized demodicosis and ivermectin
injection likely to cause toxicity /may not be well tolerated
Antidote- There are no specific antidotes for ivermectin toxicosis . Management Includes charcoal, fluids
and use of Physostigmine, an anticholinesterase agent, at 1 mg/dog IV twice a day or Picrotoxin, a GABA
antagonist - may improve neurologic status temporarily are not routinely recommended. Recently lipid
emlusion ( Intralipid 20%) at 1.5-mL/kg bolus administered over 15 minutes, then 15 mL/kg administered
over 60 minutes, reportedly reversed blindness and accelerated recovery in affected dogs. (Epstein et al
2013, Wright and Chen et al 2011)
The success of daily oral ivermectin, and the appearance of some toxic reaction at the high doses used,
prompted the trials of ivermectin at lower doses. Medleau et al. compared different doses of ivermectin
in a group of dogs with juvenile-onset and adult-onset GDM. The cure rate of 0.6 mg/kg (85%) was better
than that obtained at 0.4 mg/kg (58%), but no adverse effects were observed at this lower dosage. Other
authors have reported the use of daily oral ivermectin at 0.3 mg/kg with similar results to the 0.6 mg/kg
dosage, although they do not report any cure rate.
An evidence-based review concluded that oral Ivermectin at a dose of 0.3–0.6 mg⁄ kg daily can be
recommended as therapy for canine generalized demodicosis. To better identify ivermectin-sensitive
dogs, one report recommends initially dosing ivermectin at 50 µg/kg/day and then incrementally
increasing the dose by 50 µg/kg during the first days of treatment until the target dose is achieved.
Another way to gradually increase the dose of ivermectin is to calculate the target dose and corresponding
volume, and then give 25%, 50%, and 75% of the total volume for several days before reaching the
therapeutic volume
Moxidectin - Spot on topical and oral
A number of studies demonstrated comparable success to ivermectin and based on the published
evidence, moxidectin at 0.2– 0.5 mg⁄ kg p.o. daily can be recommended as an effecUve therapy for canine
demodicosis. ( Wagner and Wendlberger 2000, Muller et al 2011) . The spot-on containing 2.5%
moxidectin and 10% imidacloprid can be recommended as weekly treatment for dogs with juvenile-onset
and mild forms of the disease (Heine and Krieger et al 2005 Mueller et al 2011)

Doramectin- inj and oral
Doramectin is also a macrocyclic lactone that has been reported as a successful treatment for canine
demodicosis. In a recenty study, remission was achieved in 94.8% of dogs treated with weekly
subcutaneous injections of doramectin at a dose rate of 0.6 mg/kg body weight. Adverse events were rare
during average treatment period of 7.1 weeks (Hutt and Prior 2015) There is evidence that doramectin
at a dose of 0.6 mg⁄ kg p.o. or s.c. weekly may be used for the treatment of Demodicosis (Muller et al
2011)
Fluralaner - oral tablet (Bravecto from Merck ),
Fluralner is a long-acting systemic insecticide of isoxazoline class of parasiticides with selective inhibition
of arthropod γ–aminobutyric acidand L–glutamate-gated chloride channels. In a pilot study single oral
administration of Fluralaner chewable tablets once orally at a minimum dose of 25 mg fluralaner/kg was
effective with no mites detectable at 56 and 84 days following treatment. In comparison,
imidacloprid/moxidectin combination administered three times at 28-day intervals, was also highly
effective with most dogs still harbored mites at all assessment time points. (Fourie and Liebenberg et al
2015))
Sarolaner - oral tablet (Simpirica from zoetis)
Sarolaner is a member of the isoxazoline class of parasiticidesr inhibits the function of the
neurotransmitter gamma aminobutyric acid (GABA) receptor and glutamate receptor, and works at the
neuromuscular junction in insects. This results in uncontrolled neuromuscular activity leading to death in
insects or acarine. Sixteen dogs that tested positive for Demodex species mites and in which generalized
demodecosis was diagnosed were randomly assigned to treatment groups. Group 1 was treated with
sarolaner (2 mg/kg) orally on days 0, 30, and 60. Group 2 was treated with a topical product containing
imidacloprid (dose greater than or equal to 10 mg/kg) and moxidectin (dose greater than or equal to 2.5
mg/kg) solution every seven days from day 0 to day 81.In the dogs treated with sarolaner, pretreatment
mite counts were reduced by 97.1% at 14 days and 99.8% by 29 days after the first dose. No live mites
were detected after day 29. The dogs treated with imidacloprid and moxidectin showed an 84.4 %
reduction at 14 days and a 95.6% reduction at 29 days. No live mites were detected after day 59. (Six and
Becskei, et al 2016)
Axfolaner - oral tablet (Nexgard from Merial)
Afoxolaner is a member of the isoxazoline family, shown to bind at a binding site to inhibit insect and
acarine ligand-gated chloride channels, in particular those gated by the neurotransmitter gamma-
aminobutyric acid (GABA), thereby blocking pre- and post-synaptic transfer of chloride ions across cell
membranes. Prolonged afoxolaner-induced hyperexcitation results in uncontrolled activity of the central
nervous system and death of insects and acarines.
Afoxolaner was administered at the recommended dose (at least 2.5 mg/kg) on Days 0, 14, 28 and 56.
Clinical examinations and deep skin scrapings were performed every month in order to evaluate the effect

on mite numbers and the resolution of clinical signs. The percentage reductions of mite counts were
99.2%, 99.9% and 100% on Days 28, 56 and 84, respectively, in the afoxolaner-treated group, Mite
reductions were significantly higher on Days 28, 56 and 84 in the afoxolaner-treated group compared to
the imidacloprid/moxidectin-treated group. (Beugnet and Halos, et al 2016)
Others
Because chitin is found in demodex spp eggs as well as larval, nymphal and adult exoskeletons, lufenuron
was investigated for treatment efficacy and at the dose of 13.3mg/kg (once a day on the first five days of
the month) and 15.8mg/kg (3 times/week) for 2-3 months , lufenuron was ineffective as a treatment for
generalized demodicosis despite the high drug levels in the skin.
It has been reported that the oral vitamin E 200IU/dog five times daily, is effective alone and enhances
effectiveness of amitraz but serum vitamin E levels were reported to be within normal limits in dogs with
generalized demodicosis. Likewise Levamisole and injectable immune scramblers such as
Propionibacterium acnes and muramyldipeptide-parapox virus combinations were of no benefit.
Treatment failure
Some causes are not treating secondary pyoderma with appropriate antimicrobial therapy , Not selecting
right miticdal drug or not following correct dose , frequency or duration. Other causes are failure to
identify underlying cause/s and using immunosuppressive drugs including steroids. Monitoring of
treatment is a must for successful outcome
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• Yarim, Yagci, Yarim, et al (2015) Serum concentration and skin tissue expression of insulin-like
growth factor 2 in canine generalized demodicosis Vet Dermatol ; 26: 421–e99
• Wagner and Wendlberger (2000) Field efficacy of moxidectin in dogs and rabbits naturally
infested with Sarcoptes spp, Demodex spp. and Psoroptes spp. mites. Vet Parasitol
;93(2):149-158.
• Wright and Chen et al (2011) Intravenous fat emulsion as treatment for ivermectin toxicosis in
three dogs homozygous for the ABCB1–1Δ gene mutation. JVECC. ;21(6):666-672.

Dermatology : Practical Diagnostic techniques
-Notes for small Animal practitioners
Kallahalli Umesh. umeshkallahalli@gmail.com
DERM Techniques for General small Animal Practitioner
1. Coat Brushing
 Material required : Hand held metal or plastic fine tooth comb
 The simplest and most frequently employed diagnostic test
 Hairs, scale and Debris dislodged, collect for both direct and microscopic
examination
 Suspect material put onto white paper, moistened tissue or cotton wool : Flea dirt
 Further examination by Magnifying lens or microscope
2. Skin scrapings
 Materials required : Mineral oil, Glass microscope slides, Coverslips, New sterile
scalpel blade or skin scraping spatula
 Used principally for detection of ecto parasites and also for fungal hyphae an
nematode larvae
 Irrespective of depth, a size 10 scalpel blade dipped in liquid paraffin (or KOH) used
for scraping.
 Mites may stay alive in paraffin or use KOH that can kill mites, clears background.
Always use coverslip after scraped material applied on the slide. Observe under 40x.
 Deep scraping—the skin should exude a slight ooze from capillaries to indicate
entire epidermis has been removed
 Tromobiculid mites : reside on skin surface, often visible to naked eye
 Cheyletiella Sp mites : Live on surface of skin in epidermal pseudo tunnels; produce
scales. Can be difficult to find and may not be visible
 Otodectes cyanotis mites : Ear mite in vertical/horizantal ear canal, sometimes peri-
auricular and tail regions. Responsible for >50% of otitis in cats and 5-10% in dogs.
Very motile and can go undetected. Sample also can be taken using cotton swab and
rolled onto a glass slide
 Sarcoptes/Notoedres sp mites : found on surface of skin. Pregnant Females burrow
into epidermis , so deep scraping required in papulocrustous lesions. Negative
scraping for sarcoptes do not rule out scabies
 Demodex sp mites : normal follicular mite in dogs and cats. Requires deep scrapings
and skin should be gently squeezed before scraping to facilitate mites to move
distally in hair follicle. Extremely rare to find demodex mites in healthy skin of dog.
Dr. Kallahalli Umesh, Umeshkallahalli@gmail.com

3. Tape stripping
 Materials required : Clear acetate tape, Mineral oil, slides and coverslips
 For detection of surface resident parasites : lice, fleas eggs, ear mites
 The sticky side of 10 cm length of acetate tape repeatedly presed over an area
suspected
 The adherent scale, debris and hairs removed by tape are the trapped between it
and microscope slide. It is ready for immediate inspection
 Few drops of oil/paraffin on the slide before sticking to the slide improves visual
clarity when examining under microscope
 Lesional areas can sampled by simply pressing sticky side of tape onto the skin for a
few seconds. Useful for cytology study : cells, microbial organisms after staining with
wrights stain or Giemsa
Artifacts : colored threads, Pigmented plant and pollens, Blood cells mixed in mineral oil
look like round red –brown colored globular structures, Dark brown Alternaria spores
look like a macrospore of m.canis
4. Wood’s lamp examination

 Useful screening tool for Deramatophytes and often misused
 Up to 80% of Micosporum canis strains will fluoresce
 Most unusual fluorescent species are M.audoinii, M.distortum and Trichophyton
scoenleinii
 UV light 253.7 nm light filtered through cobalt/nickel oxide filter. Allow lamp to
warm up for at least 5- 10 minutes. Expose to infected hair for several minutes
before they begin fluoresce
 Positive hair will grow a bright apple green color
 Fluorescence is not seen in scales or fungal culture
 Keratin, Soap, petroleum, tetracycline’s, Bacterial infections, Sebum : can give false
positive results. Iodine can destroy Fluorescence. Lack of Fluorescence is
inconclusive
5. Trichoscopy
 Examination of Hair removed by brushing, tweezers or hemostats can be diagnostic
Bulb :
 Anagen hair(growing) : flared or rounded. Telogen : brush like.(see pictures)
 Dermatophytes can be found as arthrospores surrounding the hair. Infected hair
“fuzzy” outline. reduce aperture of iris diaphragm to visualize fungi.
 Demodex mites and eggs
Shaft :
 Lice, cheletiella, mites eggs, fungi. Louse egg larger than mite eggs and possess an
operculum.
 Large aggregates of melanin in color dilute alopecia, Mid shaft fracture in fungi,
Follicular casts, nutritional dermatosis

Tips :
 The normal hair tip tapers to a fine point. Atrumatic or trumatic ?
6. Direct examination of Hair or scale for Dermatophytes

 Materials : Culture, Tooth brush. forceps, alcohol, sterile swabs, acetate tape, slides
and cover slips and lactocotton phenol blue stain (Phenol crystals 20g, Lactic acid
20g, Glycerine 40 g, Dist water 20 ml and cotton blue dye 0.05 g)
 Dermatophytes proliferate on anagen hair , produce ectothrix spores(arthoconidia
outside hair shaft with hyphae, in mass or mosaic pattern) and fungal hyphae
 Use clearing agents to make spores/hairs more refractile and clear debris : 20 % KOH
or Chlorphenolac ( 25 ml liquid phenol + 50 g chloral hydrate + 25 ml liquid lactic
acid, store in dark glass bottle, superior to KOH). Allow 30 minutes when KOH is used
to clear or gently heat for 10-20 seconds. Chlorphenolac allows for immediate
examination.
 0.5 % calcofluor white with equal mix of KOH used as fluorescent brightener
 One part of 1-2 % dye solution of indian ink and 2 parts of KOH stain hyphae/conidia
 Hyphae may confused for artifacts such as threads, wisps of cotton, early KOH
crystallization from overheated or dry preparation
 Dermatophyte culture : Gold standar for confirming diagnosis of dermatophytosis
 Dermatophyte test medium(DTM) or Sabouraud’s dextrose agar commonly used.
Contains SDA, Antibacterial (gentamycin) and agents that kills contaminant fungi
(cyclohexamide)
 Dermatophytes initially use protein in the medium, release alkaline metabolites
which turn medium red. The red color disappears when protein has been used and
pathogen begin to use carbohydrates. Dermatophytes are aerobic
 Contaminants/non-pathogens use carbohydrate. Observed at 10-14 days of culture.
Pathogenic fungi are pale/buff in color and never heavily pigmented
 Specimen collected by sterile tooth brush ( Mackenzie method) or plucked hairs/
forceps. Swan the are with 70% isopropyl alcohol to decrease contaminants growth
 Bacteria and yeast can overgrow if plates are incunbated over 30C or 30% RH.
 Dermatophytes identified by microscopic examination of macroconidia
 Acetate tape can also be used , with lactophenol cotton blue staining
7. Cytology
 Indications : Erosive to ulcerative, Exduative, pustular, Masses/nodules and draining
lesions
 Materials required : slides, cover slips, 5-10 ml syrnge, 22-23 G needle, Fast Giemsa
and Gram’s stain. Wrights’or New methylene blue
 Impression Smear : from directly pressing slide on freshly cut surface of excised
mass or surface of lesions. Make at least 3 slide preparation after blotting excessive
moisture from surface

 Fine needle aspirates : masses or nodules. Withdraw from 2-3 sites of lesion by
redirecting the needle. can be used with /without suction
 Tooth pick : for yeast/demodex in interdigital areas or nail bed areas
 Bacteriology sample : from intact pustule, wipe with alcohol and use sterile needle.
A sterile swab used to harvest freshly expressed bead of pus and the swab is mailed
to lab in a transport medium
 Yeast samples : Malassezia or candida sp : use transport medium or contact plates
Summary of interpretation from cytology:

Vast majority of pustule samples contain a mixture of intra and extracellular
organism( usually cocci) and mixture of healthy and degenerated neutrophils,
characteristic off pyoderma. Sterile neutrophils found in autoimmune diseases like
pemphigus foliaceus and contains detached epidermal cells ( acanthocytes) that float
among neutrophils
Yeast : Considered elevated when more than Ten pea nut shaped yeast are located per
15 random microscopic slides using oil immersion (x 100) objective and tape strip
method. Or when mean yeast count from 25 high power fields is one to three or more
using impression smear
FNAC – Tips for Practice -

Remember FNAC is only a guide/screening test for diagnosis and may not replace
Biopsy
Cytological appearances: not cellular, cellular debris, cellular due to inflammation, or cellular
due to non-inflammatory cell types. If the sample is not cellular, the lesion may be a cyst or the
sample may be inadequate
Consider at least 5 characteristics for malignancy - Anisocytosis, Anisokaryosis, Binucleation,
Multinucleation, Prominent nucleoli, Multiple nucleoli, Angular or elongated nucleoli, Nuclear
molding, Abnormal nuclear shape, Aberrant mitotic figures, atypical cytoplasmic vacuolation,
Increased nuclear:cytoplasmic ratio, and Dysmaturation of nuclear and cytoplasmic morphology
Is sample cellular? – Yes- Are they leucocytes – Yes- Are they lymphocytes – yes- Is it mix of
small, medium and large Lymphocytes ?
 YES - Possibly Lymphocytic inflammation
 N0 - Consider cutaneous Lymphoma- take Biopsy
Is sample cellular? – Yes-

 Predominantly Neutrophils – Infectious- submit for culture
 Predominantly Eosinophils – immune mediated, hypersensitivity, Demodex, nematodes,
eosinophilic granuloma – Cytology samples of these lesions contain _10% eosinophils
that may be mixed with several neutrophils
 Others ( Macrophages, Giant cells etc) – Foreign body, Nocardia, Mycobacteria, Deep
Cellulitis, Fungal Keroin, Actinomycosis, Granulomas

Is sample cellular ? – Yes- Are they leucocytes – No – are the cells clustered in sheets ?
 YES - Possibly epithelial Tumors- Biopsy to identify malignancy

 NO- Are the cells spindle shaped ?
o Yes - Possibly Mesenchymal cell Tumors – Biopsy
o No- Possibly Round cell Tumors
Is sample cellular? – NO – does background look proteinaceous material ?

YES – Possibly Cyst
No- redo biopsy or FNAC
Tips for common cutaneous tumors
Round cell tumors (Transmissible venereal tumors, Cutaneous lymphomas , Plasmacytomas

Histiocytomas Mast cell tumors)
 Mast cell tumors : round cells with round, centrally located nuclei that are nearly obscured
by distinct, metachromatic cytoplasmic granules. These granules are the distinguishing
feature of this tumor. Occasionally, mast cell granules will not stain with Diff-Quik stain,
which makes identification of the mast cells difficult. If granules are not seen, but round
cells are associated with an eosinophilic infiltrate, a mast cell tumor should be suspected
 Plasmacytoma- round cells with abundant, basophilic cytoplasm and round, eccentrically
placed nuclei. A perinuclear clearing in the area of the area of the Golgi zone often can be
seen
 Histocytoma- Round cell with clear or pale-blue cytoplasm, central nuclei, and fine-to-
reticular chromatin. Cells may have basophilic cytoplasm that becomes paler toward the
edges of the cell. Nuclei are ovoid and tend to be central or eccentrically placed with or
without a prominent nucleolus. Mitotic figures can be seen.
Epithelial Tumors (Basal cell tumours, Sebacious cell adenoma, Sebacious cell carcionoma,
Squamous Cell carcinoma, Perianal tumours, Apocrine- anal sac adenocarcinoma, Apocrine
Sweat gland tumours, Mammary tumours
 SCC - cohesive, angular epithelial cells with variably basophilic cytoplasm, fine perinuclear
vacuolation, and one or multiple variably sized nuclei.
 Melonama- Spindle to rounded cells containing fine brown-to-dark-green granules
(melanin). Malignant cases may have a round, epithelial, or mesenchymal cell (spindle
shaped) appearance and may not contain melanin granules. When the cells in the lesion
contain large numbers of brown-black melanin granules,these tumors are easily diagnosed
 Sebaceous adenoma- contain clusters of round cells with abundant, highly vacuolated,
basophilic cytoplasm and small, round condensed (darkly staining) nuclei. with a dense
chromatin pattern

Mesenchymal Tumours ( Fibroma, Fibrosarcoma, Hemangiopericytoma, Hemangioma ,
Hemgiosarcoma, Myxoma , Myxosarcoma, Lipoma, Liposarcoma, Leiomyoma Leiomyosarcoma)
 Lipoma- clusters of large round cells that display small, peripheral nuclei and a single
large clear lipid vacuole. Basophilic cytoplasm and push the small oval nuclei to the edge
of the cell
 Sarcomas - Cells are typically spindle-shaped with indistinct cytoplasmic borders and
round-to-ovoid nuclei. In addition, look for Anisocytosis, anisokaryosis, and multiple
prominent nucleoli
Epidermal inclusion or follicular cyst: Abundant amorphous basophilic cellular debris is present
along with mature, anucleate squamous cells.
8. Biopsy ( from Ginel PJ and Mozos E, waltham focus, 1998, Vol 8 :1 pp 30-31)
Materials required :
 Local anesthetic(lidocaine hcl), one ml of 2% per 5kg bodyweight
 Needles and syringe, Scalpel blade,
 Suture material/skin staples,
 Small toothed forceps, Sterile surgical instruments, wooden tongue depressor,
 4 –6 mm Skin biopsy punches
 Michel’s fixative for direct immunoflorence (optional),
 10 % neutral buffered formalin ( volume should be ten times sample size and allow
to fix for 24 hours before having it processed)
Main indications for punch biopsy

1. Any pustular dermatosis that fails to respond to antibacterial therapy
2. Any ulcerated or crusting dermatosis that fails to respond to antibacterial therapy
3. Symmetrical alopecia (in the dog) that is not associated with thyroid or adrenal
endocrinopathy
4. Nodular or papule lesions that fail to respond to antibacterial therapy
5. Dermatoses associated with loss of pigmentation
6. Any dermatosis that fails to respond to apparently rational treatment
 Situations in which excision biopsy is preferred to punch biopsy

Junctional biopsies
Where the border between normal and affected tissue is important, for example,
ulcerated areas or sharply demarcated areas of chronic inflammation. In these
situations the wedge excision is traditionally taken across the border, allowing the
pathologist to orientate the sample. This orientation is not possible with a round punch
biopsy

Fragile lesions
Large, intact vesicles, bullae or very large pustules Punches are not large enough to
include the entire periphery of these lesions and the twisting action of the punch
distorts and tears the sample
Nodules or neoplastic lesions
Although a punch biopsy may provide enough tissue to allow identification of neoplastic
type, there may not be adequate tissue to permit grade of neoplasm
Suspected panniculus disease
Punch biopsy does not sample the deep tissue of the lower dermis and panniculus
adequately
• Histopathology is most reliable when utilized for diagnosing:

– Neoplastic diseases
– Auto-immune or immune-mediated diseases
– Deep infections when organisms are visible, such as blastomycosis, etc.
• Histopathology is NOT sensitive or specific for the diagnosis of:

– Allergic diseases or Endocrine diseases
9. Diagnosis of Allergic diseases

1. Intra dermal Skin testing : golden reference test for ATOPY
 Collect compatible history, signs suggestive of atopy before deciding IDST
 Used to support diagnosis, to identify potentially important allergens and to initiate
immunotherapy (hyposensitazation therapy)
 Perform on patients whose owners are prepared to be committed to at least One
year of hyposensitisation for the animal if the test is conclusive
 The allergens in the test kit are supplied by commercial companies and selection of
allergens is based on region of country
 The human allergy specialist, allergen supplier or Botany department which
conducts aeroallergens study are potential sources for information on selecting
suitable allergens in that region
 In general house dust mite (Df), House dust, Flea and mould allergens are ubiquitous
and should be part of allergens test kit. Grass, weed and tree pollens
 Mixed allergens are avoided. Allergens always stored in refrigerator

 Most use 50-70 potential allergens. Allergens are available in PNU (protein nitrogen
units or w/v ) either in glycerin o aqueous base. Use aqueous base
 Most tests in dogs are performed using 1000PNU/ml or 1:1000 w/v dilution. Irritant
allergens like dust mite (Dermatophagoides pteronyssinus) diluted to 20 PNU/ml or
1:10-50,000 w/v to avoid false positive results. Use insulin or 1 ml syringes
 Current recommendations are the 0.05 ml of minimum of 30 and max of 60
aqueous allergens is injected with positive (Histamine phosphate 1:100,000) and
negative (dilute solution supplied)
 Remember – This test is to formulate a vaccine for hyposensitization therapy
(allergen specific immunotherapy, or ASIT).
 This diagnostic tool is not used to diagnose allergic disease
Technique and Things required :

 27 G needle , I ml syringe,
 Black felt-tip marking pen,
 Electric clipper or fine razor
 Stock allergens, Sterile diluent
 The animal positioned in lateral recumbency. Some use sedation like xylazine ?? or
medotimidine 2ug/kg ??(with or without butorphanol 0.2mg/kg IV ??)
 The injections are performed on lateral thorax after clipping around 15 x 10 cm area.
 Do not use any irritant or chemicals to sterilize the area.
 Mark the injection site with indelible ink and note the time
 Inject allergens above and below marking so as to create “intradermal bleb’. Make
no Subcutaneous inj
 The results are read in batches 15-20 minutes post injection
 The positive reactions are erythematous wheal
 There are different method of reading results : scale, using formula or simply
subjective. Negative as 0 and positive as 4. Any reaction more than 2 is positive
 OR A positive wheal reaction is one with wheal equal or greater than mean
diameters of positive and negative controls
False Negative reactions:

 Anthistamines, Acepromazine, : with draw for at least 7 days before the IDST
 Glucocorticoids : Oral and topical for 6 weeks before IDST
 Grisofulvin, progesterone’s , hypotensive drugs
 Stress, Anergy (testing during peak allergy season)
 Off season, Too little quantity injected, Sc injection
 impotent allergens( expired or improper store)

False Positive reactions:
 Irritant allergens, large amount injected,
 Inflamed skin, Glycerine containing allergens,
 Needle trauma, air injection
 10-15% healthy dogs show reactions
2. Serologic testing
 There are more than 8 companies offer serum allergy testing
 All use different technologies and sources of IgE to detect allergen specific IgE in
patients serum. Eg., Heska corporation use high affinity receptor for IgE (FcR1).
 The two main technologies are RAST,ELISA and Liquid phase immunoenzymatic
assay(VARL)
 The main advantage is convenience, 2-3 ml of serum sent to lab
 Drug interference is less BUT same rule as IDST apply for steroids
 Not sensitive as IDST. Both measure different : IDST measure skin reactivity to
allergen injected intradermally where as serology measures reactivity to antibodies
present in blood
 Poor correlation between IDST and Serology tests exception being kit using on a IgE
(FcR1) ( 50-95 % ???)
Food allergy:
Withdrawal and provocative test : Diagnosis is obtained by use of a restrictive diet
consisting of ingredients not previously eaten by the animal. but Basically,one protien
and one starch source that the animal has not been fed in the past are used(example-
lamb/Fish/paneer and rice). The pet is kept on this diet with all other food excluded for
3 weeks. A homemade diet may be preferable, although owners may elect to use
commercially available hypo-allergenic diets. The length of the dietary trial is
controversial, in most cases 6-8 weeks is sufficient. Confirmation is made if pruritus and
otitis disappear during the dietary trial and resume immediately following
reintroduction of the offending foods.
 Serological tests, Endoscopy, HP etc

Contact allergy : Patch testing similar to IDST principle but applied to skin
Other test used in allergy

 CMI test, Basophil granulation tests, Basophil histamine assay, Mast granulation
test

PRURITUS : Some Key Points for Busy Practioners
Definition: It is a sensation which provokes the desire to scratch.

Pathophysiology: Inflammatory mediators (histamine, proteases peptides, prostaglandins (E2,
H2) leukotrienes (LTB4 etc) and type-I Hypersensensitivity (IgE + mastcells, basophils, histamine
releasing factors , degranulation of mastcells).
Approach
A. History:
I. Age:
 Localized demodicosis – 3 to 6 months,
 Cheyletella/fungal – more than 4 months,
 Atopy – 1 to 3 years,
 Food allergy – 4 months 4 years.
 Seniors- Autoimmune and Tumors ( histocytoma- young)
II. Breed:
 Atopy – Terriers, Delmatian, GSD, Golden Retriver, Irish Setter,Boxer, Labrador, Lhasa, Apso,
etc.
 Idiopathic seborrhea-Cockerspaniel.
 Seboorrhea Sicca – Irish Setter, GSD, Doberman, Daschund.
 Hypothyroidism – Bulldog, Boxer, Doberman, Daschung, etc.
 Superficial pyoderma – Doberman, Great Dane, Boxer, Bulldog, Dalmatian, Daschund.
 Demodcosis – Pugs,Bulldogs, Westies
 AlopeciaX- Pom
 Zinc responsive – Huskies
 Ichthyosis- Gold retrivers
 Sebacious Adenitis- Akita, Vizlas
 Dermatomyosis- Shelties and Collies
III. Sex:
Male – sertoli cell tumour, feminizing syndrome.
Female – Overian imbalance 1 and 2.
IV. Hereditary: Atopy, iodiopathic seborrhea, demodicosis, etc.

V.Contagion: Sarcoptes, otodectes, fleas, fungus and other pets at home.
VI. Environment : Kennel, bedding material, plants, trees, shrubs, etc.
VII. Skin hygiene and flea control : Soap, shampoos, insecticide, etc.
VIII. Diet, drugs and previous treatment : collect detailed History.
B. Physical examination : Localised/generalized, Symmetric/asymmetric.
Generalized pruritus: Sarcoptes, flea bite allergy, pelodera dermatitis, demodicosis, pyoderma,
food allergy, atopy – look for specific lesions and distribution.

 Facial pruritus : Sarcotes1, atopy1, food allergy, allergic contact dermatitis, fungal, bacterial
folliculitis, auto immune diseases (Pemphigus complex, SLE). Foreign bodies in ears and
eyes, zinc responsive dermatosis, idiopathic seborrhea and other rare diseases
(dermatomyositis, solar, Vogt-Koyanagi-Harada Syndrome, lethal acrodermatitis, juvenile
cellulitis, necrolytic migratory erythema).
 Pinnal pruritus: Atropy1, food allergy, sarcoptes1, fly strike.
 Pedal pruritus: Atropy, food allergy, flea bite allergy, pyoderma1, autoimmune diseases,
foreign bodies.
 Facial/pedal: Atopy, Pyoderma.
 Lumbo sacral and tail head: Flea bite allergy1, atopy, food allergy, bacterial folliculitis.
 Axillary and inguinal: Flea bite allergy1, sarcoptes1, pyoderma, atopy, food allergy, contact
dermatitis.
 Steroid responsive: Atopy**, food allergy, flea bite allergy**, allergic contact dermatitis.
 Steroid unresponsive (anti-inflammatory doses only): Parasitic – mites*, fleas, fungus*,
hook worm dermatitis*, Pelodera dermatitis, pediculosis, pyoderma*, food allergy
cutaneous neoplasia, autoimmune diseases, psychological (tail biting, acralick, flank sucking)
and some cases of flea bite allergy*.
DIFFERENTIAL DIAGNOSIS OF PRURITUS BASED ON PRIMARY SKIN LESIONS

Pruritic pustular
Infectious Impetigo, folliculities – bacterial* fungal and demoectic
Immune mediated Pemphigus, contact dermatitis, drug erruption.
Idiopathic Juvenile pyoderma, subcorneal pustular dermatosis, eosinophilic
pustulosis, sterile furunculosis.
Pruritic dermatitis with plaques
Infectious Acute moist dermatitis*, seborrheic dermatitis, dermatophytes,
bacterial hypersensitivity.
Immune mediated Eosinophilic granuloma, SLE, drug erruption.
Neoplastic Mycosis fungoides, mast cell tumour.
Papular pruritus
Infectious Folliculitis* (bacterial fungal, demodex).
Parasitic Sarcoptes*, Cheyletiella, lice, fleas.
Immune mediated Allergic – flea allergy*, food allergy, contact dermatitis, atopy,
drug erruption.
Auto immune Pemphigus, lupus erythematosis.
Idiopathic Dalmatian bronzing syndrome.
Pruritic dermatitis with erythema:

Atopy, lupus erythematosis, systemic mastocytosis, drug
erruption, staphylococcal hypersensitivity, mycosis fungoides,
contact dermatitis, Vogt-Koyonagi-Harada Syndrome.
Ulcerative pruritic: Lupus erythematosis, leukocytoclasic vasculitis, erythema
multiforme, toxic epidermal necrolysis, mycosis fungoides,
epidermolysis bullosa complex, ermatomyositis, acute contact
dermatitis, Vogt-Koyonagi-Harada Syndrome.
Lichenoid dermatitis: Systemic lupus erythematosis (SLE), discoid lupus erythematosis,
bullous pemphigoid, pembhigoid complex, Vogt-Koyonagi-Harada

Syndrome. Contact dermatitis, toxic epidermal necrolysis,
erythema multiforme, lichenold keratosis, idiopathic lichenoid
dermatitis.
__________________
 Primary rule-outs
PROPOSED DIAGNOSTIC PLAN FOR A PRURITIC DOG

1. Minimum data base – refer: Dermatology History and Examination Form.
a. Deep and superficial skin scraping.
b. KOH digest and concentration of scraping.
c. Dermatophyte and bacterial culture.
d. Response to reliable scabicide.
e. Response to antibiotics.
2. Rule out flea bite allergy – skin test, flea control.
3. Rule out atopy – history, physical examination, intradermal skin test.
4. Rule out food allergy – food allergy elimination diet.
5. Rule out contact dermatitis and drug erruption – history environmental restriction and drug
withdrawal.
6. Rule out auto immune diseases – biopsy for histopathology, direct immunofluorescence,
antinuclear antibody test, consider electromylography (EMG) and muscle biopsy.
7. Assess response to anti-inflammatory doses of corticosteroids and review history and
physical examination.
DIFFERENTIAL DIAGNOSIS OF PODODERMATITIS

Infections: Pyoderma*, dermatophytosis**, intermediate mycosis
(sporotrichosis, mycetoma), demodectic
pododermatitis**, pelodera strongyloides, hookworm,
leshmaniasis.
Allergic: Inhalant allergy* (Atopy), contact allergy.
Auto immune diseases: Pemphigus group, SLE, DLE.
Endocrine: Hypothyroidism**, cushing syndrome,
hepatocutaneous or diabetic dermatosis.
Environmental: Irritant contact dermatitis, trauma, foreign bodies.
Hyperkeratotic, nodular and pigmentary disorders:

Zinc responsive dermatitis, digital hyperkeratosis (zinc,
distempter, pemphigus and lupus), sterile
pyogranulomas (Great Dane, Boxer). Nodular
dermatofibrosis, sebaceous adenitis, vitiligo.
Neoplasia: Plasma cell pododermatitis, squamous cell carcinoma.
Psychogenic/neurological: Acral link dermatitis*, acral multilation syndrome.
___________________________________________
* Major primary rule outs
** Especially in chronic and recurrent cases

CLASSIFICATION OF PYODERMA
Conditions Examples of underlying disorders
Surface Flea allergy, otitis externa anal scacculitis,
 Acute moist dermatitis inadequate grooming.
(hotspot or pyotraumatic
dermatitis)
Anatomical defects (facial, lip, tail, vulvar,
 Intertrigo (skin fold pyoderma) obesity).
Superficial
 Impetigo Idiopathic, poor management, endo/ ecto
parasites, viral infection, poor nutrition,
dirty environment.
Hypersensitivity (atopy), ectoparasites,

 Superficial folliculitis endocrine, anatomical or immunological
factors.
Deep
 Generalized/localised Idiopathic, demidicosis, hypo-thyroidism.
 Interdigital pyoderma Demidicosis, hypothyroidism, atopy, fungal

and foreignbody.
 Muzzle or chin pyoderma Idiopathic, demidicosis.
 Anal furunculosis Idiopathic, genetic, anatomical/

immunological.
 Nasal pyoderma Idiopathic
CAUSES OF ALOPECIA
Genetic
Hairless breeds African Sand dog, Chinese crusted dog, xoloitzcuintli, Mexican
hairless, Turkish naked dog. Cat – Sphinx cat
Ectodermal dysplasia, Hypotrichosis (poodles), black hair
follicular displasia, colour mutant alopecia (Doberman, Blue
Great Dane), Pattern Baldness (Daschund – on ear flaps),
demodicosis.

Acquired
 Bacterial folliculitis Dermatophytosis
 Parasitic folliculitis Sarcoptes, Fleas Lice, Hook worm, Cheyletiella, Notoedres
 Allergic Atopy, Food allergy, fleabite allergy, Allergic contact
dermatitis, Bacterial allergy
 Immunologic Alopecia areta, Pemphigus complex, DLE, SLE,
 Endocrine Hypothyroidism, Hyperadernocorticism, Growth hormone
deficiency, sex hormone problems
 Nutritional Protein, fatty acids, Vitamin A, E, Biotin, riboflavin,
copper, zinc
 Stress/physical Pyrexia, infection, parturition (Telogen effluvium),
tailbiting, flank sucking, foot linking
 Toxic/chemical Arsenic, Thallium, selenium, mercuty, methotrexate,
cyclophosphamide, soaps, harsh detergents, insecticides,.
 Neoplastic Sebacious adenoma, lymphosarcoma, etc.
DERMATOLOGY HISTORY FORM FOR CLIENTS TO COMPLETE

Date: ______________
Case No.
1. Age: Month / Year
Sex: F/F
Breed:
2. What is the skin problem: Itching/Rash/Oily skin/loss of hair/
redness/Dryskin/scales/other
3. At what age did you first notice the problem?
4. Are the symptom seasonal: Yes / No – used to be –
If yes, specify the month:
5. What did problem look like Itching/redness/pimples/hair less

when it first started? rash/other
6. Where did it start? Eyes/ears/nose/neck/back/tail/

rump/legs/paws/chest/stomach/groin
7. Has it spread? Yes / No – if so, where? Explain
8. Does your pet scratch, Yes / No

rub, chew, lick or bite If yes, where? Nose/muzzle/eye/
ears/neck/back/rump/tail/front
legs/paws/chest/stomach/groin/axilla (armpit)
9. Was itching the first Yes / No
thing noticed
10. Do you have skin problems List

11. Do any have skin problems Yes / No, If yes, Explain
12. Do any people in your Yes / No, If yes, Explain

household have a skin problem
13. Percent of time your pet is

confined indoors – outdoors
14. If female and intact, has Yes / No

she had normal heat cycles?
15. If neutered, at what age
16. If male and intact, does he

have normal interest in females
17. Does your pet have fleas Yes / No / had
18. Do you use insecticides Yes / No – in your yard: Yes / No

in your home
19. What medication(s) has your Injection / topical / oral

pet been using since the
problem started
20. Did this medication help Yes / No / for a while

or cure the problem
22. Does your pet do or have Cough/sneeze/vomit/running/

any of the following runny eyes/diarrhoea/poor
appetite/worms
23. Does or did your pet have Yes / No – if yes, explain

any other illness
24. Outside environment Type of grass/shrubs/trees flower gardens,

if yes, what kind
25. Household environment
a. Type of carpets, rugs or draperies:
b. Does the pet have a favourable bed/chair
c. What fabric it is mode of

EXAMINATION REPORT
Primary lesions (Circle)

Macule Patch Papule Plaque Vesicle Bulla
Pustule Wheal Nodule Tumour
Secondary lesions (Circle)

Scale Erosion Epidermal collarette Scar Ulcer
Crust Fissure Hyperpigmentation Cyst Comedone
Abscess Erythema Hypopigmentation Callus Alopecia
Lichinification Excoriation Hyperkeratosis
Configuration of lesions (Circle)

Regiona; Linear; Annular; Grouped; Irregular;
Quality of hair coat

Epilation; Dry; Brittle; Dull;
Oily;
Foot pads; Nails; Hyperhidrosis;
Distribution of the lesions: -------------------
Laboratory test
Scraping ------ Deep and Superficial;
Workslamp; Bacterial and fungal culture;
Intradermal skin test;
Endocrine assays (T3, T4, TSH stimulation, ACTH stimulation, basal cortisol, low and high
dexamethasone, growth hormone, sex hormones, etc.).
Direct and indirect immuno-fluorescence,
Antinuclear antibody, biopsy, etc.
Differential diagnosis -------
Comments

Diagnostic outline for pruritus/alopecia in dogs
Pruritus/Alopecia
Inflammatory Non Inflammatory
Pruritic Non Pruritic pruritic Atopy

Food allergy
Psychogenic alopecia
Skin scrape Skin scrape Bilaterally symmetrical
Endocrine
Psychogenic Fleas
alopecia Sarcoptes Demodex Multifocal to diffuse Genetic Hypothyroidism
Flea bite allergy Cheylietella Cheylitella Nutritional (TSH, T4)
V/S Pelodera Bacterial culture Metabolic
Fleas infestation Demodex Stress
Response Lice (pyoderma)Bacterial folliculiits Fungal culture
to scabicides
BIOPSY Dermatophytes
Scabies Hyperaderenocortism
(ACTH, etc)
Allergic dermatitis Elimination diet
Neoplasia Immunemediated Drugs/toxins
Food allergy
Intradermal Skin test ANA, IF Hyposomatotropic
Atopy Growth hormone responsive ?
Italics: common causes Sex hormone---- Therapeutic trial

Pruritic Disorders of dogs- Differential diagnosis Summary- GUIDE LINES only
Disease Primary Level of pruritus Response to Predilection sites
lesion glucocorticoids
present
Atopy No Mild to intense Excellent Face, ears, feet, axillae, anywhere
Flea bite Hypersensitivity Yes Moderate to intense Good to excellent Lower back, thighs, ventrum
Food allergy No Moderate to intense Variable As above and/or atopy
Hormonal hypersensitivity No Intense Poor Lower back, perineum,ventrum
Internal parasite hypersensitivity ?? No Moderate to intense Poor to good Flanks, lower back, perineum
Contact dermatitis No Moderate Poor to good Feet, ventrum,perineum
Drug allergy Yes Variable Poor anywhere
Psychogenic pruritus No Mild to intense Poor Feet, flankfolds, perineum, tail
Scabies Yes Intense Poor Ears, elbows, hocks, ventrum
Cheyletiella dematitis Variable None to intense Good Dorsum
Otodectic (ear mite)) mange No Mild to moderate Good to excellent Ears, trunk
Demodicosis Yes Variable Poor to good Face, feet, anywhere
Pelodera dermatitis No Moderate to intense Good Feet, ventrum, perineum
Hookworm dermatitis Yes Moderate to intense Poor to good Feet, ventrum, perineum
Bacterial folliculitis Yes None to moderate Poor to good Anywhere
Bacterial hypersensitivity Yes Moderate to intense Poor Anywhere
Seborrhea complex Variable Mild to intense Good Face, ears, intertriginous area, anywhere
Immune-mediated disorders Yes None to intense Poor to good Head, feet, ventrum, anywhere
Subcorneal pustular dermatosis Yes Mild to intense Poor Face, trunk
Cutaneous lymphomas variable Moderate to intense Poor to good Face, anywhere

Differential diagnosis of Pruritus – Practical tips
Pruritus area Consider
Atopy Yeast Scabies AFR Flea allergy
Pinna marginal pruritus
Pinna pedal reflex
Caudal elbow pruritus
Otitis with normal pinna and

orifice, interdigital, perianal
GIT signs
Lumbosacral pruritus
Dorsal pedal without

interdigital/ventral pruritus
Face, Feet, Ears
Face, feet, Ventum, Perianal, Axilla,

ventral neck

1. Topical spot –on Products for Fleas and Ticks topical/Tabs( Min age spot ons 7-8
weeks, tabs 4 weeks in general, see details in the table)
Oral Tabs
 Nitenpyram (Capstar) oral tabs : Novartis
 Milbemycin+ lufenuron (Sentinel) oral tabs, Merial
 Spinosad : Comfortis oral chew tabs from Elanco - a sinosyn group of insecticide.
Indication : : treatment and prevention of infestations by fleas in dogs. Kills fleas in 30
minutes. Once a month. Following concomitant extra-label use of ivermectin with
Comfortis, some dogs have experienced the following clinical signs: trembling/twitching,
salivation/ drooling, seizures, incoordination, excessive dilation of pupils, blindness and
disorientation.
 Spinosad + milbemycin oxime : Trifexis® from Elanco once-monthly tablet that kills fleas,
prevents heartworm disease and treats and controls adult hookworm, roundworm and
whipworm infections.
 Afoxolaner : Isoxazoline Group Nexgard from Merial- oral chewable tabs- NEXGARD kills
adult fleas and is indicated for the treatment and prevention of flea infestations
(Ctenocephalides felis), and the treatment and control of American Dog tick
(Dermacentor variabilis) infestations in dogs and puppies 8 weeks of age and older,
weighing 4 pounds of body weight or greater, for one month: Afoxolaner is a member of
the isoxazoline family, shown to bind at a binding site to inhibit insect and acarine
ligand-gated chloride channels, in particular those gated by the neurotransmitter
gamma-aminobutyric acid (GABA), thereby blocking pre- and post-synaptic transfer of
chloride ions across cell membranes. Prolonged afoxolaner-induced hyperexcitation
results in uncontrolled activity of the central nervous system and death of insects and
acarines. The selective toxicity of afoxolaner between insects and acarines and
mammals may be inferred by the differential sensitivity of the insects and acarines’
GABA receptors versus mammalian GABA receptors
 Fluralaner : Bravecto from Merck ( sold by Intervet), Isoxazoline Group Orally once in 12
weeks, belongs to the class of isoxazoline-substituted benzamide derivatives. The mode
of action of fluralaner is the antagonism of the ligand-gated chloride channels (gamma-
aminobutyric acid (GABA)-receptor and glutamate-receptor). Bravecto kills adult fleas
and is indicated for the treatment and prevention of flea infestations (Ctenocephalides
felis) and the treatment and control of tick infestations [Ixodes scapularis (black-legged
tick), Dermacentor variabilis (American dog tick), and Rhipicephalus sanguineus (brown
dog tick)] for 12 weeks in dogs and puppies 6 months of age and older, and weighing 4.4
pounds or greater. Bravecto is also indicated for the treatment and control of
Amblyomma americanum (lone star tick) infestations for 8 weeks in dogs and puppies 6
months of age and older, and weighing 4.4 pounds or greater.
 Sarolaner (Simpirica from zoetis) Isoxazoline Group chewable tab for dogs over 6
months. Sarolaner is a member of the isoxazoline class of parasiticidesr inhibits the
function of the neurotransmitter gamma aminobutyric acid (GABA) receptor and
glutamate receptor, and works at the neuromuscular junction in insects. This results in
uncontrolled neuromuscular activity leading to death in insects or acarine. ills adult
fleas, and is indicated for the treatment and prevention of flea infestations and the
treatment and control of tick infestations

 Lotilaner (Credelio from elanco) for dogs and cats 8 weeks and above.Once a month
oral tab, Isoxazoline Group Action similar to Nexgard , control Ticks and fleas. starts
killing fleas in 4 hours and kills 99% within 8 hours for 35 days. Credelio is greater than
97% effective against labeled tick species 48 hours after administration or infestation for
30 days.
Topical spot On
 Imidacloprid + Permethrin (K9advantix) Bayer - Not for cats
 Imidocloprid + Ivermectin ( advantage duo) Bayer
 Imidacloprid + Milbemycin (Advocate) Bayer
 Selamectin 6 mg/Kg (Revolution/Stronghold) Pfizer,
 Fipronil + (S) Methoprene (Frontline plus) (Merial)
 Fipronil + Cyphenothrin (Parastar Plus) Not for cats
 Fipronil + Permenthrin ( Effitix) Virbac, Not for cats
 Pyriprole : Prac-Tic from Novartis classification: phenylpyrazole like fipronil,
indications: treatment and prevention of flea and tick infestations in dogs.
 Metaflumizone : Promeris from Fort Dodge Animal Health:, classification: unclassified, ,
indications: treatment and prevention of flea infestations in cats.
 Methaflumizone/amitraz : Promeris Duo from Fort Dodge Animal Health -,
classification: unclassified/formamidine, , indications: treatment and prevention of
infestations by fleas and ticks in dogs.
 Spinetoram 39.6% : Assurity from Elanco The primary target of action of spinetoram is
an activation of nicotinic acetylcholine receptors(nAChRs), resulting in the death of
fleas.S tarts working in 30 minutes. Kills 98-100% of fleas within 12 hours for35 days and
Lasts a full month. Kills fleas before they lay eggs.
 Dinotefuran, Permethrin, and Pyriproxyfen : Vectra3D from Summit vet
pharma.contains– Classification ; for treatment and prevention of ticks, fleas and
mosquitoes Not for cats
 4% Fipronil, 5.8% (S)-Methoprene, and 7.6% Amitraz: Certifect from Merial Topical .
Starts killing ticks in 6 hours and kills up to 100% within 18 hoursKills fleas, flea eggs, flea
larvae & chewing lice. Waterproof and keeps killing for up to one month. Not for cats
 Flumethrin4.5%,Imidocloprid10% : Seresto from Bayer waterproof collar start age 7
weeks for dogs and 10 weeks for catsfor Ticks and Fleas, prevent flea and ticks
infestation up to 7-8 months
 Indoxacard: Activyl from Merck Animal health- monthly spot-on flea control for dogs.
contains indoxacarb, -works by bioactivation – Indoxacarb is bioactivated by insect gut
enzymes into a highly potent sodium channel blocker that blocks insect nerve impulse
transmission. There is no known flea resistance to indoxacarb. Activyl® stops fleas from
feeding, kills adult fleas and flea larvae, and inhibits flea development in the
environment.
 Indoxacarb + Permthrin: Activyl® Tick Plus from Merck Animal health - for Dogs and
Puppies - combines indoxacarb for flea control with permethrin for tick protection.
Permethrin provides broad-spectrum tick protection. Activyl® Tick Plus stops fleas from
feeding, kills fleas on dogs and in the home, kills 4 major tick species (D. variabilis, R.
sanguineus, I. scapularis, and A. americanum), and repels ticks for a full month.

Control of fleas and ticks : Home and yard use
 Sentry Home Household Flea & Tick Spray contains pyriproxyfen (0.02%) and
permethrin (0.20%) for a dual action product used to kill fleas, flea eggs, flea larvae, and
ticks. The ingredient pyriproxyfen is an Insect Growth Regulator (IGR), and stops flea
eggs from hatching into biting adult fleas.
 The Virbac Knockout Fogger contains pyrethrins 0.050%,pyriproxyfen 0.1%,N-
octylbicylephenate dicarbonximide 0.4% and permethrin(0.4%), which quickly kills adult
fleas, while pyriproxyfen (Nylar) insect growth regulator sterilizes fleas and their eggs
for seven months.
 Bio Spot Inverted Carpet Spray and Bio Spot Carpet Powder (Farnam) Kills fleas and
controls reinfestation for up to 210 days and 12 months respectively. Bio Spot Inverted
Carpet Spray also kills ticks, ants, spiders, roaches and crickets. Linalool (1.000%), N-
Octyl bicycloheptene dicarboximide (1.000%), Nylar; 2-(1-methyl-2-(4-
phenoxyphenoxy)ethoxy) pyridine (0.015%), Permethrin (0.200%), Inert ingredients
(97.785%)
 Premise Treatment from Richard's Organics™ contains 100% Orthoboric acid, a salt-like
granule, which removes moisture from a flea's body causing dehydration, killing the
larvae, and therefore breaking the life cycle. Orthoboric acid is odorless and does not
repel flea larvae, so multiplying larvae will continue to stay in treated areas until they
die, which ultimately prevents adult fleas from emerging in your home. This product is
not intended to kill adult fleas; only the larval stages, therefore allow 10-14 days for it to
work. Kills flea larvae in your home, including carpets, cushions, upholstery, and your
pet's favorite places, preventing maturation and reproduction. Natural home flea
treatment, safe to use around pets and humans
 Hartz InControl Flea & Tick Home Spray: S)-Methoprene (CAS #65733-16-6) 0.01%,
Permethrin (CAS #52645-33-1) 0.28%, Other ingredients 99.71%. Use on carpeting, rugs,
upholstery and pet bedding .No lingering odor, no sticky mess, no stains. Kills flea eggs
to prevent future infestations for 7 months.
 Sergeant's Gold IGR Flea and Tick Fogger Pyrethrins (0.050%), benzeneacetate
(0.100%), Piperonyl butoxide, Technical (0.100%), N-Octylbicyloheptene Dicarboximide
(0.167%). kills fleas, flea eggs, flea larvae and ticks in your home. It controls reinfestation
of pests for up to 210 days (7 months). It also kills other insects such as, ticks,
mosquitoes, wasps and cockroaches - among many more.
 Virbac Yard Spray Concentrate (Virbac) contains Esfenvalerate(o,44%) used outdoors
on lawns and around residential premises . Kills fleas and ticks that infest your yard, so
your pet won't become infested Will not harm grass or foliage
 Sentry Home Yard and Premise Spray Concentrate Bifenthrin (0.030%), Other
ingredients (99.70%)

Common Endocrine and non endocrine diseases affecting skin
umeshkallahalli@gmail.com
Diagnosis of Hypothyroidism in dogs : Current recommendations
Key Points to remember

 ~95% of the Canine Hypothyroid cases, resulting from an immune-mediated lymphocytic
thyroiditis or idiopathic atrophy of the gland.
 Acquired secondary hypothyroidism [TSH deficiency] is rarely reported is related to pituitary
tumors or pituitary malformations. Represents less than 5%
 Tertiary hypothyroidism [TRH deficiency] has not been described in dogs.- decreased TRH -
congenital defects, tumors, or abnormal binding of TRH in the pituitary gland.
 Iatrogenic – radiation Therapy for thyroid carcinoma
 In some of the breeds there is an association with the DLA-DQA1*00101 allele (Kennedy LJ,
et al. (2006)Tissue Antigens 68:82–86.
 Congenital- Ver rare -lack or deficiency of thyroid hormone at birth, Defects in the
hypothalamic-pituitary-thyroid axis or from iodine deficiency, Deficiency or
unresponsiveness to TRH or TSH , Thyroid dysgenesis, and dyshormonogenesis. Can be
Goitrogenic or Non goitrogenic
 The prevalence of hypothyroidism is reported to be 0.2% of the referral population
(Panciera 1994).
 The two most important thyroid hormones secreted by the thyroid gland are thyroxine (T4)
and 3,5,3' triiodothyronine (T3).T4 accounts for most of the thyroid hormone secreted by
the thyroid gland, with only small quantities of T3 and minor amounts reverse T3 (rT3)
released.
 Once secreted into the circulation, more than 99% of T4 is bound to plasma proteins which
serves as a reservoir and buffer to maintain a steady concentration of free T4 (fT4) in the
plasma. The unbound, or free, T4 is biologically active, exerts negative feedback inhibition
on pituitary TSH secretion, and is capable of entering cells throughout the body.Within the
cell, fT4 is deiodinated to form either T3 or rT3, depending on the metabolic demands of the
tissues at that particular time.
 T3 is preferentially produced during normal metabolic states; rT3, is biologically inactive. T3
is believed to be the primary hormone that induces physiologic effects.
Thyroid Hormones effects - wide variety of physiologic effects,
 Increase the metabolic rate and oxygen consumption of most tissues except the adult brain,
testes, uterus, lymph nodes, spleen, and anterior pituitary.
 Role in Ca, P and Nitrogen Metabolism
 Positive inotropic and chronotropic effects on the heart. - Increase the number and affinity
of b-adrenergic receptors, enhance the response to catecholamines, and increase the
proportion of a-myosin heavy chain.
 Catabolic effects on muscle and adipose tissue- increase Fat mobilization, Oxidation,
Gluconeogenesis, Glycogenolysis and protein catabolism
 Stimulate erythropoiesis, and regulate cholesterol (increases synthesis, absorption,
conversion to bile acids) and degradation.
 Essential for the normal growth and development of the neurologic and skeletal systems.
Kallahalli Umesh
Current Diagnostic Challenges
 Vague presenting clinical signs - Clinical abnormalities do not typically develop until
approximately 75% of the thyroid glands are destroyed
 Relatively low accuracy of most biochemical tests,
 The potential influence of numerous drugs and illness on thyroid function.
 Common endocrine disorder
 It is also one of the most over diagnosed endocrinopathies in the dog ( Taeymans et al, J Vet
Intern Med 2007;21:673–684)
 Concurrent Hypoadrenocorticism and hypothyroidism and Diabetes mellitus and
Hypothyroidism reported in 22.9% and 28.6% of dogs respectively in a retrospective study
(Blios, 2011)
Use of Human Laboratory

 Significant misuse of assays designed for humans.
 Using assays that have not been specific for Canine hormones
 Most have not been validated; without consideration of methodology
 Have limited data for the computation of reference Limits
 Have failed to consider the potential influence of age, sex, breed or related and
unrelated disorders.
 Numbers have been generated but the validity of the conclusions could oftentimes be
questioned.
Thyroid hormones : Dogs Vs Man (Ferguson 1994, Roover et al 2006, Diaz-Espineira 2007)
DOG MAN
Thyroid binding proteins affinity Low High
TBG level in circulation ~ 15 % of man
TT4 - ug/dl Low – 1 to 3.5 High – 4.6 to 12

FT4 - ng/dl High - 0.8 to 3.5 Low- 0.7 to 1.9
T3/T4 Negative feedback on TRH Yes ?
Extra-thyroidal production of T3 40 to 60 % ~ 80%

Half Life T3 5 to 6 hours 24 to 36 hours
Half life T4 10 to 16 hours 7 days
 Serum T3 concentration is a poor gauge of thyroid gland function in dogs because of its
predominant location within cells and the minimal amount secreted by the thyroid gland in
comparison with the amount of T4 secreted. Thus measurement of serum T3, free T3, and
rT3 concentration is not recommended for assessing thyroid gland function in dogs and cats.
Breeds and Hypothyroidism

 English Setter, Dalmatian, Basenji, Rhodesian Ridgeback, Old English Sheepdog,, Boxer,
Maltese Dog, Chesapeake Bay Retriever, Beagle, Dobermans, Irish Setters Shar Pei, Afghans ,
Brittany Spaniel, Airedale, Cocker Spaniel, Shetland Sheepdog, Siberian Husky, Border Collie
Kallahalli Umesh
Husky, Akita and Golden Retriever Miniature Schnauzers, Poodles, Dachshunds, Irish Wolf
hounds, English Bulldogs , Great Danes, Newfoundland, Malamute
 Congenital – Boxer, French bulldog, German shepherd dog, Giant schnauzer, Miniature
schnauzer, Portuguese water dog, Rat terrier, Scottish deerhound, Terrier
Clinical signs to look for
Common Signs Reported Less common signs (Poor evidence)
Bilaterally symmetrical alopecia Peripheral neuropathies ??
(esp. at areas of friction)
Hyper pigmentation, scaling Vestibular, facial nerve paralysis, forelimb lameness ??
Recurrent pyoderma Focal myasthenia gravis
Myxedema Myopathy
Obesity- 40 % of dogs ? Hypoadrenocorticism ??
Lethargy Ocular disease: corneal lipid deposits, KCS, retinal
abnormalities
Bradycardia Myxedematous coma
Weakness Dwarfism, Infertility ??
Demodicosis
Cutaneous signs accounts for 60-80% of affected dogs. Alopecia- symmetrical -Lateral trunk-
Ventral thorax- Tail, Localized alopecia- dorsum of nose, pressure points, Perineum.
Hair coat- dry, brittle and dull. Hyperkeratosis, Hyperpigmentation, Hypothrichosis,
Scaliness/seborrhea, Comedone, Poor wound healing, Myxedema ? Predispose to Recurrent
Bacterial and yeast infections and demodicosis ??
Neuro – In a study, 29% of hypothyroid dogs had neurological abnormalities- seizures,
mentation changes and disorientation. Megaesophagus, Laryngeal paralysis, Seizures,
Peripheral neuropathy- weakness, paresis, CP deficits, Cranial nerve- Facial nerve paralysis ??,
Vestibular signs ?? Evidence to neuro signs are weak.
Eye- Corneal lipidosis, corneal ulceration, atherosclerosis, KCS reported but no strong evidence
exists to be caused by Hypothyroidism
Cardio- Sinus bradycardia and arrhythmia, Low voltages in all leads, Inversion of the T wave
Reproduction – conflicting reports on experimentally induced vs Natural cases. Some suggest
that dogs must have hypothyroid condition for more than 5 months to show reproductive
abnormalities. Increased periparturient mortality, litters with low birth weight, failure to cycle,
uterine inertia, irregular estrus cycles, testicular atrophy, low libido, and subfertility have been
linked but not proven to hypothyroidism Further investigation is necessary to determine if
fertility and other reproductive parameters is affected in natural cases.
Congenital Hypothyroidism - Usually seen at 3-8 weeks , Mental Retardation. Hypothermia,

Bradycardia, Abd distension, constipation etc ,Stunted disproportionate growth due to
epiphyseal dysgenesis; and delayed skeletal maturation, Disproportionate dwarfism, Central
nervous system (CNS) hypomyelination ? Cutaneous- Dryness and thinning of hair and Palpable
Goiter ?
Biochem and CBC :

 Can have a non-regenerative anaemia (20-32% of dogs)
 Leptocytes and An increased erythrocyte sedimentation rate is common.
Kallahalli Umesh
 Atherosclerosis and lipid abnormalities A fasting hypercholesterolemia can be
marked and occurs in approximately 70% of dogs, Hypertriglyceridemia is also
commonly present.
 Increased serum creatine kinase may be seen in 10-18% of cases.
 Mild to moderate increases in hepatic enzymes reflect altered carbohydrate and fat
metabolism. (Panciera 1994).
 In one study SDMA concentrations were significantly higher in hypothyroid dogs
compared to control dogs. and did improve with appropriate therapy for
hypothyroidism.
Summary of thyroid hormones diagnostic tests ( Daminet S 2006)

Test Advantages Disadvantages
TT4 Not expensive Decreased with SNTD
Readily available, IDDEX Decreased after administration of certain drugs
snap test available in india A decreased T4 alone does not allow a reliable diagnosis of
Normal values allow hypothyroidism (low specificity)
'exclusion' of Sensitivity Low in Human lab
hypothyroidism
TSH Easy 1/4 of hypothyroid dogs have TSH values within the
Not expensive reference range (low sensitivity), not available in India at
present
Always use in combination with T4
FT4 Is less influenced by SNTD The only reliable method includes equilibrium dialysis
or through drug (standard or modified)
administration than TT4 Not readily available in India at present
TSH Was and still is considered Bovine TSH is not easily available anymore
stimulation as the gold standard Human rhTSH : may be promising ?
test Expensive 4 to 6 hours lasting test
Anaphylactic reactions were described with bTSH
1. Influence of Age Sex and Obesity on Thyroid hormones

Age:
 TT4 is higher in puppies and may be 2-5 x the adult concentration for the first 100 days
of life. TT4 and responsiveness to TSH falls with age.
Sex:
 Female dogs in diestrus and pregnancy have a higher TT4 and TT3 than non-pregnant
females and males.
Breed:
 Sight hounds (Saluki, Deerhound, Wolfhound, Afghan) have a lower TT4 and higher TSH
compared with other breeds.
Obesity:
 TT4 and TT3 may be significantly higher.
Kallahalli Umesh
2. Summary of the effects of some drugs on canine thyroid function test results.
Drugs TT4 FT4 TSH TSH stimulation test

Glucocorticoids ↓ = or ↓ = Blunted at high dose
(immunosuppressive dosage) and duration
Phenobarbital ↓ = or ↓ = or ↓
Sulfonamides/ As ↓ ↓ ↓
Carprofen = or ↓ = (↓) = or ↓ Not studied
Opioids ↓ ↓ ↓
Aspirin ↓ = = Not studied
Clomipramine ↓ ↓ = Not studied
Ref from Daminet 2006, Bertalan et al 2013
3. Non thyroid illness on thyroid hormones

(Mooney et al (2008)Thyroid hormone abnormalities and outcome in dogs with non-thyroidal
illness, Journal of Small Animal Practice 49, 11–16) 196 dogs, TSH stimulation test
 Decrease in
Total T3 (177 nmol/l) 79.3 %
Total T4 (148 nmol/l or 11.54 ug/dl) 34.7 %
Free T4 (6.66 pmol/l ) 4.5 %
cTSH (069 ng/ml)
4. Comparison of Diagnostic tests ( %)

Test Low Total Low Total Low High Low Low
T4 T3 FT4ed TSH TT4/TSH FT4ed/TSH
Sensitivity 89/100 10 98/80 76/86.7 67/86.7 74/80
Specificity 82/75.3 92 93/93.5 93/81.8 98/92.2 98/97.8
Accuracy 85 55 95 84 82 86
( Ref from Daminet et al 2003, Kantrowitz et al 2001, Dixon et al 1999)
 Sensitivity : % of dogs Hypothyroid dogs that had abnormal tests

 Specificity : % of Euthyroid (Normal thyroid) dogs that had no abnormal tests
 Accuracy : % of cases that are neither false positive nor false negative
5. Antibody Tests for Lymphocytic Thyroiditis
 Anti-thyroglobulin antibodies (ATA) are found in 42 to 59% of hypothyroid dogs and are
believed to be the result of leakage of thyroglobulin into circulation due to lymphocytic
thyroiditis.
 A commercially available ELISA assay for ATA is a sensitive and specific indicator of
thyroiditis, with false positive results occurring in less than 5% of dogs with other endocrine
disorders.
 Tests for the presence of Tg, T3, and T4 autoantibodies in the serum of dogs can be used to
identify lymphocytic thyroiditis, to explain unusual serum T3 and T4 test results, and
possibly as a genetic screening test for hypothyroidism caused by lymphocytic thyroiditis.
Kallahalli Umesh
 Tg autoantibody is not a thyroid function test. Identification of Tg autoantibodies would
support hypothyroidism caused by lymphocytic thyroiditis if the dog has clinical signs,
physical findings, and thyroid hormone test results consistent with the disorder. A positive
Tg does not provide information on the severity or progressive nature of the inflammatory
process.
 Antibodies directed against T3 and T4 also occur in canine thyroiditis, although they are less
prevalent than ATA. Anti- T3 antibodies can be identified in approximately 30% of
hypothyroid dogs.
 Antibodies directed against T3 and T4 may interfere with hormone assays ( but not FT4)
leading to a spurious increase (most common) or decrease in the measured hormone
concentration.
 Since some euthyroid dogs also may have anti- T3 or T4 antibodies however, their presence
is not diagnostic for hypothyroidism
6. Diagnosis by Therapeutic trail, When ?

 Low TT4 and Other tests not available
 Normal TT4 and positive T4AA , others not available
 Normal TT4 and high TSH
Therapy
 Levothyroxine (Eltroxin 100ugtab) is administered orally, at the induction dose of 20 μg/kg
or 0.01-0.02 mg/kg (or 0.5 mg/m2) every 12 hours. For example, using a dose based on
body surface, a 30-kg (0.96 m2) dog would receive a dose of 500 μg instead of 660 μg; a 40-
kg (1.17 m2) dog would receive a dose of 600 μg instead of 880 μg.
 Although in North America most dogs are initially treated twice a day, it was recently proven
that once-a-day administration of an average dose of 22 μg/kg is adequate for most
hypothyroid dogs.
 Lethargy and other signs may improve by 3 weeks But classical cutaneous signs may take 6 –
8 weeks to show significant improvement. But remember that Thyroxin. Administration in
healthy/euthyroid dogs also improve Poor coat quality, seasonal flank alopecia and
Polyneuropathies
 Synthetic triiodothyronine administration is only indicated in those few situations when T4
supplementation has failed to achieve a response in a dog with confirmed hypothyroidism
 Levothyroxine has a serum half-life of 12-16 hours, and peak concentrations are present 4-
12 hours after administration.
 Monitoring : Check Immediately prior to administration and post-pill serum concentration
can be obtained, 4-6 hours (after 4-8 weeks ) or when all the clinical signs have resolved,
 The pre-pill T4 concentration should be in the normal range. The post-pill concentration
should be in the upper reference range or slightly above it. TSH levels should be in the
reference range if levothyroxine supplementation is adequate
 Toxicity ; Thyrotoxicosis (PU/PD, weight loss, panting, nervousness, and tachycardia) is rare
in the dog, due to the rapid metabolism and renal and hepatic excretion of thyroid
hormone. Be cautious in dogs suffering with kidney or hepatic diseases, diabetes mellitus,
hypoadrenocorticism,and congestive heart failure. In these instances, it has been
recommended that levothyroxine therapy be initiated at 5 μg/kg every 12 hours, and then
increased progressively over the following 3 to 4 weeks. However, if therapy is induced at 20
Kallahalli Umesh
μg/kg every 24 hours, instead of every 12 hours, potential complications are unlikely. PUPD
and Increased appetite reported in dogs
7. Options for diagnostic tests
1. Subclinical thyroiditis - Normal thyroid values but increase in Thyroglobulin auto antibodies
(TgAA)
2. Subclinical hypothyroidism- Thyroid hormone values normal but increased TSH. May be
increased TgAA if thyroiditis is cause
3. Overt Hypothyroidism- Thyroid hormone subnormal. High TSH, abnormal T4 response to
TSH stimulation test. TgAA positive in cases of thyroiditis
TSH Stimulation test :

Bovine TSH - limited availability. Gold standard test, Human β-subunit TSH (Thyrogen; Genzyme)
may work but very expensive and Not validated., Thyrotropin releasing Hormone (TRH) test
Interpretation difficult
Thyroid scintigraphy - ??
8. Guidelines for diagnosis in India ( bold)

 Appropriate clinical signs + physical findings + routine blood tests + No systemic illness
 A serum T4 concentration less than 0.5 µg/dL or 6 nmol/L
 High TSH
 FT4 less than 0.5 ng/dL(6.5 pmol/L are supportive of hypothyroidism and > 1.5 ng/dL(20
pmol/L) are consistent with euthyroidism,
 Therapeutic trail : If the dose and dosing schedule are appropriate, the serum T4
concentration should be between 2.0 and 4.5 µg/dL (25 to 60 nmol/L).
9. Reference values (check with you lab for validated range)

T3 1.15 - 3.10 nmol/L x 64.9 for nmol/L or 0.0154 for ug/dl
T4 19.0- 58.0 nmol/L or 1.0 to 3.5 µg/dL ( x 12.87 for nmol/L or 0.078 for ug/dl)
TSH 0.00- 0.35 ng/mL
T3 AA 0.0- 2.0
T4 AA 0.0- 2.0
FT3 2.00 - 4.60 pmol/L
FT4 12.0- 45.0 pmol/L or 0.8 to 3.5 ng/dL
10. Summary
 Normal FT4ed and TSH values almost always identify a euthyroid animal.
 Some laboratories have established the FT4D/TSH ratio as a valuable discriminator.
 Low TT4 or FT4D, together with high TSH, confirms hypothyroidism in most cases.
 Demonstration of positive ATA is most valuable to support abnormal TT4, FT4D, or TSH
values.
Kallahalli Umesh
Adapted from Graham P - In Practice (2009) 31, 77-82
TT4 fT4 TSH TgAA
Confidently Hypothyroidism
Low Low High Positive
Low Low High Negative
Normal or high Low High Positive
Low - High -
Hypothyroidism Likely
Low Low Normal Positive
Low Low Normal Positive
Low - Normal Positive
Low Normal High -
Low Low Normal
Confidently Euthyroidism
Normal Normal Normal Negative
Normal -- Normal Negative
Euthyroidism Likely
Low Normal Normal Negative
Normal - Normal -
Non-Thyroid illness
Low - Normal Negative
Low - Normal -
Subclinical Thyroiditis
Normal Normal Normal Positive
Subclinical Hypothyroidism
Normal Normal High
All References are available upon request
Kallahalli Umesh
Hyperadrenocorticism
In the adrenal cortex, glucocorticoids are produced in the zona fasciculata and zona reticularis,
and mineralocorticoids are produced in the zona glomerulosa. Glucocorticoid production is
stimulated by ACTH from the pituitary gland. Mineralocorticoids, on the other hand, are
released in response to either hypovolemia, which triggers the renin-angiotensin system, or
hyperkalemia, which directly stimulates adrenocortical tissue ( occasionally low Na)
 Prevalence : 0.1 % ( USA)
 Sex :,Slightly more female than males affected
 Age :Middle-aged to older dogs. 75% of dogs with PDH are older than 9 years (median
age, 11.4 years), and 90% of dogs with adrenal tumors are also older than 9 years
(median age, 11.6 years).
 Weight: SMALL BREEDS : 75% dogs with PDH are <20 kg., 50% dogs with
adrenocortical tumours >20 kg
 Breeds : Pituitary-Dependent Australian shepherd, Beagle, Dachshund , German
shepherd, Labrador retriever, poodle and terriers Adrenal Tumor ; Alaskan
malamute, Cocker spaniel, Dachshund, German shepherd, Terriers and Toy poodle
 Cushing’s syndrome(CCS) -clinical and biochemical findings that result from excessive
glucocorticoids.
 Cushing’s disease specifies pituitary-dependent hyperadrenocorticism
 Pituitary dependent (85% dogs) - usually a benign tumour secreting excessive amounts
of ACTH
 Adrenocortical tumour - 50% benign; 50% malignant
 Iatrogenic - excessive administration of exogenous steroids over a long period of time
Cutaneous signs
• Changes in coat condition and colour, slow hair regrowth after clipping
Kallahalli Umesh
• Alopecia usually bilaterally symmetrical of the flanks, sparing of the extremities. Thin skin
with poor elasticity , Hyperpigmentation, easy bruising, poor wound healing.
• Seborrhoea. Comedone formation especially on ventrum
• Calcinosis cutis is seen on dorsum especially neck and rump, axillary and inguinal areas.
Appears as whitish, gritty, firm bone-like papules and more extensive plaques
• Striae – spontaneous or at site of scar
• Secondary infection with bacteria, yeast,
• Dermatophytes or demodex – response to therapy is poor in these cases unless
hyperadrenocorticism is treated concurrently.
Non Cutaneous signs

• Neuromuscular signs – muscle atrophy, pot-bellied appearance osteomalacia, osteoporosis
(rare), pseudomyotonia.
• Urogenital signs – anoestrus (entire bitches) testicular atrophy (entire dogs), clitoral
enlargement, recurrent urinary tract infections, urolithiasis.
• Respiratory signs – panting, bronchopneumonia, coronary thrombosis, dystrophic
mineralisation and fibrosis.
• Neurological signs – blindness, head pressing, Horner’s syndrome, seizures.
• Ocular signs – exophthalmos, corneal ulcers, conjunctivitis.
• Pancreatic signs – acute pancreatitis, diabetes mellitus.
• Hypertension 40% in controlled to 86 % in untreated
Uncommon signs of hyperadrenocorticism

• Dermatological changes: coat colour changes, hyperpigmentation, calcinosis cutis
• Chronic infections / non healing wounds (e.g. cystitis, decubital ulcers)
• Pseudomyotonia (leading to a stiff hindlimb gait)
• Pulmonary thromboembolism (causing dyspnoea)
• Neurological signs (due to rapid tumour growth): ataxia, depression, apparent blindness
Screening for Diagnosis of hyperadrenocorticism (Cushing’s syndrome) in dogs :

Calculation of a cortisol:creatinine ratio by use of cortisol and creatinine concentrations
measured in a single urine sample is a simple and valuable screening test for
hyperadrenocorticism in dogs. Cortisol and its metabolites are normally excreted into the urine,
with urine cortisol excretion rising with increased adrenal secretion of the hormone. By
measuring cortisol in morning urine, an integration of cortisol secretion over a period of about 8
hours is achieved, thereby adjusting for the wide and rapid fluctuations in circulating cortisol
concentrations. Because creatinine excretion is relatively constant when kidney function is
stable, dividing the urine cortisol by the creatinine concentration negates the effect of urine
volume (and therefore the degree of urinary concentration) in interpreting the urine cortisol
concentration.
The urine cortisol:creatinine ratio is determined by dividing the urine cortisol concentration (in
µmol/L) by the urine creatinine concentration (in µmol/L).
Procedure :
Kallahalli Umesh
• The owner is instructed to collect morning urine samples at the same time of day (eg, 7
AM to 8 AM ) on two to three consecutive days.
• No special precautions are needed for the urine collection but urine samples should be
kept refrigerated until the owner is able to bring the specimens to the clinic/lab
• Determine cortisol and creatinine concentrations, and average the results of the two to
three urine cortisol:creatinine ratios.
Interpretation of results
• A high mean cortisol:creatinine ratio will be found in most dogs with
Hyperadrenocorticism, Sensitive test but lack specificity
• It is recommended that this test be used primarily for its negative-predictive value. i.e., ,
if the results of cortisol:creatine ratio remain within reference range limits, the presence
of hyperadrenocorticism is highly unlikely. On the other hand, if a high
cortisol:creatinine ratio is found, confirm Cushing’s with use of a low-dose
dexamethasone suppression or ACTH stimulation test.
• The urine cortisol:creatinine ratio cannot be used to reliably differentiate pituitary-
dependent from adrenal-dependent hyperadrenocorticism. However, the finding of very
high urinary cortisol:creatinine ratios ( > 100) make it more likely that the dog is
suffering from pituitary-dependent hyperadrenocorticism
Normal values reported : Ref : J vet Int Med ( 1993) 7, 163 –168 and (1998) 12 431-43), Clin
Tech Small Anim Pract (2007)22:2-11 )
Cortisol (nmol/L) Creatine (nmol/L)
• Normal 175.5 ± 142.3 (3-565) 13.6 ± 6.9 (1.5-30)
• Hyperadrenocorticism 562.4 ± 493 ( 85 –2252) 6.7 ± 5 (0.9- 20.3)
Ratio Cortisol: creatinine

• Normal 13.1 ± 7 ( 0.1- 31.2)
• Hyperadrenocorticism 103.1 ± 100.7 (21.3 – 432)
2nd method : The diagnosis of hypercortisolism was considered to be confirmed by finding an

increased UCCR - 8.3 x 10-6 in 2 consecutive morning urine samples collected at home.
Working example : Sample 1 Cortisol concentration is 8.34ng/dl

 First multiply the concentration by 10 to convert dl to L, 8.34 ng/dlX10 = 83.4 ng/L ,
then convert ng to µg by dividing 1000,
83.4 ng/L = 0.0834 µg/L,

1000
 To convert µg to µmol divide the µg by Molar mass of cortisol i.e. 362.46 g/mol
0.0834µg/L = 0.0002288 µmol/L

364.46
Kallahalli Umesh
Creatinine concentration is 0.49mg/dl
 First multiply the concentration by 10 to convert dl to L, 0.49mg/dl X 10 = 4.9mg/L, Then
convert mg to µg by multiplying 1000 ; 4.9mg/L X 1000 = 4900 µg/L,
 To convert µg to µmol divide the µg by Molar mass of creatinine i.e. 113.118 g/mol
4900 µg/L = 43.317 µmol/L

113.118
So cortisol to creatinine ratio
0.0002288 µmol/L = 0.00000528199 = 5.3 X 10 -6
43.317 µmol/L
B. Urine cortisol:creatinine ratios using low oral dexamethasone

 Owners collect urine from their dogs on two consecutive mornings (0800 h) for
determination of baseline cortisol:creatinine ratios
 Immediately after collection of the second urine sample, owners administer
dexamethasone at the dosage of 0.01 mg/kg, PO
 Owners walk dog at 1200 and 1400 h to ensure bladder emptying
 Owners collect a third urine sample for measurement of cortisol:creatinine ratio at 1600
h (8 h after oral administration of dexamethasone)
 Preliminary evidence suggests that a 50% suppression in the mean urinary
cortisol:creatinine ratio (and a decrease in the ratio to < 10) would be consistent with a
normal response.
 Dogs with hyperadrenocorticism would be expected to fail to show adequate
suppression of the urine cortisol:creatinine 8 hours following oral dexamethasone
administration.
Low Dose Dexamathasone suppression Test (LDDST)

 Dexamethasone given to a normal dog will cause inhibition of pituitary secretion of
ACTH and therefore decrease cortisol secretion from the adrenal glands for 24 to 48
hours. Within 2 to 3 hours after administration of dexamethasone, plasma cortisol levels
in dogs with a normal response will decrease to less than 1.4mcg/dL (reference value
dependent on the laboratory) and persist longer than 8 hours. Results should be
evaluated using the laboratory’s established reference intervals.
 Results are interpreted in light of signalment,history, physical examination findings, and
hematologic and serum biochemistry abnormalities. Phenobarbital treatment does not
appear to affect results of LDDST. A dog with no history, clinical signs, or serum
biochemistry abnormalities and a normal LDDST is considered negative for CCS.
 A dog with history, clinical signs, and minimumdatabase abnormalities consistent with
CCS andincreased cortisol levels after the 8-hourLDDST is considered to have CCS. Eight-
Kallahalli Umesh
hour plasma cortisol levels greater than1.4 mcg/dL are consistent with a diagnosis of
hyperadrenocorticism.
 Approximately 30% of dogs with pituitary-dependent hyperadrenocorticism have serum
cortisol suppression at 4 hours (1 mg/dL or 30 nmol/l), with a rise in cortisol values by 8
hours after dexamethasone administration. This escape from suppression is diagnostic
for pituitary-dependent hyperadrenocorticism,and further tests to determine the cause
of hyperadrenocorticism are not necessary. Failure to show adequate suppression of
serum or plasma cortisol at both 4 and 8 hours (ie,1 mg/dL or30 nmol/l) is diagnosticfor
hyperadrenocorticism but cannot aid in determining the cause of the
hyperadrenocorticism.
 The sensitivity of the low-dose dexamethasone suppression test is excellent,
approximately 0.90 to 0.95 in dogs with pituitary-dependent hyperadrenocorticism and
1.0 in dogswith an adrenal tumor. Thus, only 5 to 10% of dogs with the pituitary-
dependent form of the disorder show “normal”cortisol suppression with this protocol.
 The specificity of the low dose dexamethasone suppression test, however, can be low,
especially when measured in a population of sick dogs.1-5 In fact, the specificity of the
low-dose dexamethasone suppression test is considerable lower than that of the ACTH
stimulation test. Because of the low specificity of the low-dose dexamethasone
suppression test, diagnosis of hyperadrenocorticism should never be based on results of
a low-dose dexamethasone suppression test alone, especially in a dog with nonadrenal
disease. It is best to delay testing for hyperadrenocorticism until the dog has recovered
from the concurrent illness.
PDH vs AdrenalTumors
 Dexamethasone will not suppress ACTH release from the anterior pituitary in dogs with
PDH. Therefore, stimulated adrenal glands continue to release cortisol at increased
concentrations. Dogs with PDH have an 8-hour cortisol level ≥ 1.4mcg/dL.
 Dexamethasone will not suppress cortisol production in dogs with adrenal tumors
because the tumor is not under the control of ACTH. The 8-hour (and 4-hour) post
dexamethasone injection cortisol concentration will be ≥ 1.4 mcg/dL.
Sixty-five percent of dogs with PDH meet at least one of the following criteria, which separate
PDH from adrenal tumor hyperadrenocorticism:
 The 4-hour cortisol concentration is < 1.4 mcg/dL.
 The 4-hour cortisol concentration is < 50% of the basal cortisol concentration.
 The 8-hour cortisol concentration is < 50% of the basal cortisol concentration.
 Most dogs with PDH will have an 8-hour cortisol concentration > 1.4 mcg/dL.
Thirty-five percent of dogs with CCS have equivocal LDDST results that do not differentiate PDH
from adrenal tumor hyperadrenocorticism, as defined by the following criteria
 The 4-hour and 8-hour cortisol concentrations are ≥ the basal cortisol concentration.
 The 4-hour and/or 8-hour cortisol concentrations are suppressed but still > 50% of basal
concentration.
Kallahalli Umesh
 A 4-hour postinjection blood sample of cortisol concentration may be useful in
distinguishing PDH from adrenal tumor hyperadrenocorticism. If the 4-hour sample is
not suggestive of PDH,then a discriminating test (such as measurement of endogenous
ACTH concentration or a highdose dexamethasone suppression test) may be useful.
Inconclusive Results : If there is high clinical suspicion for CCS, dogs with inconclusive or normal
results should be retested or have another screening test used (urinary cortisol:creatinine ratio).
The duration of action of dexamethasone is over 48 hours, with half-life of 119 to 136 minutes
in the dog; therefore, retesting can be done in 1 to 2 weeks.
Test Limitations
 LDDST cannot distinguish iatrogenic hyperadrenocorticismfrom naturally occurring CCS.
 The 8-hour LDDST cannot differentiate PDH from adrenal tumor hyperadrenocorticism.
 Stress from confinement and handling, spontaneous fluctuations in cortisol, and
nonadrenal
 diseases may interfere with results (false positives). Cortisol levels in these dogs may fail
to suppress normally and therefore results of the LDDST may be misleading.
 In addition, the testing period is long (8 hours) and multiple blood samples are needed.
High dose Dexamethasone test; Not routinely done

Normal dogs suppress at 4 and 8 hours with dexamethasone. Higher doses of dexamethasone
should suppress a pituitary tumor but not an autonomously secreting adrenal tumor.
Dexamethasone is given at 0.1 mg/kg IV and a pre, 4 hour and 8 hour cortisol level is measured.
Suppression occurs if the 8 hour is less than or equal to a 50% decrease from baseline or the 8
hour cortisol is within or below the reference range. The utility of the 4 hour cortisol is
questionable since it is the 8 hour cortisol level that is used for interpretation. Dogs with PDH
should adapt at least one of the criteria stated above. Unfortunately 25% of dogs with PDH fail
to suppress as stated above. Almost all dogs with AT fail to suppress. Even though the ability of
glucorticoids, such as dexamethasone,to suppress pituitary ACTH secretion in dogs with
pituitary-dependent hyperadrenocorticism is abnormal and is resistant to suppression with low
doses of dexamethasone, much higher doses of dexamethasone will usually overcome this
resistance to negative-feedback inhibition. Therefore, most dogs with pituitary-dependent
hyperadrenocorticism demonstrate suppression of serum cortisol levels following
administration of a high dose of dexamethasone. In contrast, because pituitary ACTH secretion
has already been chronically suppressed in dogs with cortisol-secreting adrenal tumors,
administration of dexamethasone, no matter how high the dose, will fail to suppress serum
cortisol concentrations.
Additional tests
 ACTH : EDTA samples -not always accurate
 Measurement of 17 hydroxyprogesterone, before and after ACTH stimulation, has been
suggested to be useful in helping to confirm the diagnosis of HAC in cases with equivocal
results.
 MRI and CT scan : PDH
 Radiograph and US : PT : Normal adrenal glands are less than 6.0 mm.
Treatment of PDH
Kallahalli Umesh
 Reduce ACTH secretion ; Hypophysectomy?, Selegiline , Bromocriptine ,Cyproheptadine
 Reduce adrenal cortisol production : o,p’DDD (Mitotane, Lyosdren), Ketoconazole,
Trilostane, Metyrapone , Adrenalectomy
Mitotane /lysodern :
Controlled destruction of the zona reticularis and fasciculata , spare the zona glomerulosa
(mineralocorticoid secretion).
 Loading dose : 50mg/kg/day (divided), Must be given with food
 ≤5 days treatment then stop, wait 2 days then test responsiveness to ACTH
 Repeat this process until mild early signs of hypoA OR until adequate suppression of adrenal
function on ACTH stimulation test
 Maintain contact with the client, and dispense cortisone acetate for emergency use
Maintenance dose
 ~ 50mg/kg/week (divided), Must be given with food
 Test after 1 month then every 3 months, May require ↑ or ↓of 25% maintenance dose
 Sometimes a repeat “pulse therapy” is required, Sometimes have to re-induce
 Sometimes have to withhold drug if over controlled, Occasionally induce
hypoadrenocorticism
Adverse effects
 Direct adverse drug reactions occur in about 25% dogs treated with mitotane.
 Gastrointestinal signs (vomiting, diarrhoea and/or Inappetence), lethargy, and/or
neurological signs such as ataxia or depression. Hepatotoxicity is very rare.
 With the exception of hepatotoxicity, most dogs will not have recurrence of these signs if
the dose is divided into smaller doses, +/- spread out over a longer time.
 Some individuals will not tolerate the drug at all and alternative treatments should be used.
Trilostane
 Initially, <5 kg receive 30 mg, 5 –19.9 = 60mg and ≥20kg =120 mg. Dose 2.2 to 6.7 mg/Kg Q
24 hrs, The drug is given in the morning if given once daily to facilitate testing at time of
peak effect (4 – 6 h post-dose).
 Drug absorption is not affected by food. Recheck at days 10, 40,and 120 of trilostane
treatment
 Adverse effects are not common, are generally mild, and easily managed. should not be
used in renal failure, primary liver disease, lactating animals or those intended for breeding.
 Signs resolve in 4-7 weeks and Derm signs in 6-12 months
Which is better ?
 Median survival on trilostane given SID was 662 days (8-1971) while survival on mitotane
was 708 days (33-1399) (Barker et al 2005).
Kallahalli Umesh
 3 year study -Median survival of dogs was 24 months for dogs given mitotane and 30
months for dogs given trilostane BID (Arenas et al 2006Proc).
Ketacanazole ( Fungicide 200mg tabs) interferes with gonadal and adrenal steroid synthesis in
mammals by inhibiting cytochrome p - 450 dependent enzymes.
 A dose of 5-25 mg/kg q 12 hours, results in a rapid reduction of serum cortisol
concentrations in most animals.
 Toxicity can be minimized by gradual increase of the dose.
 In a study of 48 dogs with PDH treated with ketoconazole, median survival was 25
months.
Selegiline ( L-Deprenyl) Jumax, Jumex, Selerin 5mgtab

 selective monoamine oxidase type B inhibitor which increases CNS dopamine- Supress
ACTH from pars intermedia in Pituitary gland
 The dose is 1 mg/kg orally every 24 hours for 60 days, increasing to 2 mg/ kg after this
time if there is no response.
 If there is no response after a further month, alternative therapy should be considered.
 Recently been reported to be effective in less than 20% of dogs with PDH.
 The current evidence indicates that there is minimal endocrinologic but some clinical
improvement with selegiline therapy (Reusch, Steffen,and Hoerauf, 1999).
 Do not use in dogs with diabetes mellitus, pancreatitis, heart failure, renal disease, or
other severe illness
Others
 Retinoic acid and cabergoline have also been reported to have efficacy in treatment of
canine PDH.
 Treatment with melatonin, lignins and flaxseed oil has been recommended for
treatment of atypical hyperadrenocorticism
 Bilateral adrenalectomy is an option in dogs with PDH that do not tolerate or respond to
medical therapy.
Alopecia X
Pseudo-Cushing ,Adult-onset growth hormone deficiency ,Growth hormone-responsive alopecia
,Hyposomatotropism of the adult dog ,Sex-hormone alopecia ,Castration-responsive dermatosis
,Gonadal sex hormone dermatoses ,Sex hormone/growth hormone dermatosis, Follicular
dysplasia of Nordic breeds ,Siberian Husky follicular dysplasia ,Follicular growth dysfuntion of
the plush coated breeds ,Adrenal sex hormone imbalance ,Biopsy-responsive alopecia,
Congentital adrenal hyperplasia-like syndrome, Lysodren-responsive dermatosis
 Adult onset (typically 9 months to 3 yrs) symmetrical alopecia which progresses to
involve the neck, back, hindlegs, chest, rump and tail
 May or may not have hyperpigmentation in affected areas
Kallahalli Umesh
 Hair on head, tail and feet are usually not affected
 Affects dogs more than bitches
 May occur before or after neutering
 Coat is dry and dull
 loss of guard coat
 Hair may regrow at site of biospy
 The breeds most affected by alopecia X are Pomeranians, Chow Chows, Miniature
Poodles, Siberian Huskies, Keeshunds and Samoyeds.
Management
Melatonin ( Meloset, Zytomin 3mg, 6 mg tab)
• Involved in neuroendocrine control of photoperiod dependent moulting and colour.
• Inverse relation to prolactin and photo-period.
• Canine recurrent flank alopecia -boxers
• Canine pattern alopecia : post-auricular region, ventral neck, thorax and abdomen,
caudo-medial thighs
• Alopecia X
• Recommended dose : 3-6 mg q 8-12 hours for 1-2 months
• Success rate - range of 25-35% in alopecia X
• Rare side effects like lethargy and flatulence
• Deslorelin - Gnrh analogue - < 30 kg - 4.7 mg and >30 kg - 9.4 mg
• Trilostane ( Vetoryl, Modrenal) -2 mg/kg Q 24 H or 1 mg/kg Q 12 H
• Osaterone acetate (Yposane)- anti-androgen also has been tried . Finasterid ?
• Gonadectomy works in only about 50% of male dogs.
Kallahalli Umesh
Otitis externa: Refreshing Best practice: Notes for busy Practice
Kallahalli Umesh, kallhalli.umesh@effem.com
1. How common is Otitis externa ?

• 3rd most common dermatological problem for dogs, and 2nd commonest for cats
• 22% canines (up tp 40 % in tropical countries) and 19% of felines of Dermatological cases
Banfield database :
• 13.7% of canines and 5.2% of felines
• Secondary bacterial infections -15.2% in dogs and 19.8% in cats.
• Yeast infections -26.2% in dogs, while no cases were documented in cats during the past five
years
2. Predisposing factors
• Climate temperature and humidity • Excessive ear cleaning Cotton swabs &
• Excessive cerumen production. vigorous hair plucking
Sebaceous gland and hair follicle • Immune suppression
density (Cocker Spaniels, Springer • Inappropriate treatment
Spaniels, Labradors) • Irritant
• Increased moisture--(excessive
swimming or bathing)-breakdown of Breeds ( Benfield database)
lipid barrier- microbes invade • Spaniels
• Water or peroxide • Pugs,
• Obstructive ear disease (can be primary • Hounds,
factor too)-- Neoplasia, polyp • Beagles,
• Systemic diseases--FeLV, FIV, Parvo, • Lhasa Apso,
distemper • Retrievers,
• Conformation • Shih Tzu,
• Stenosis of the ear canal (Chinese Shar • Poodles,
pei, chow-chow) • Rottweiler
• Pendulous pinna • German Shepherd
• Excessive hair on pinna (cockers) or in
canal (poodles)

3. Primary causes
• Allergies/Hypersensitivity • ceruminous gland adenocarcinoma- -
• Atopy : 50-80% and 5% as sole irregular,friable, ulcerative mass,
• Food reaction : 80% and 20% as attached to the wall
sole • Juvenile cellulitis
• Contact • Eosinophilic granuloma
• 56% of both cats and dogs had • Sterile eosinophilic folliculitis
nonspecific hypersensitivity • Vasculitis.
(Banfield) • Trauma
• Foreign objects
• Parasites
• Otodectes cynotis 50% cats, 5- • Keratinization disorders
10% dogs o Seborrhea
• Demodex sp o Zinc-responsive
• Psoroptes o Vitamin A-responsive
• Otobius megnini (spinous ear
tick), • Endocrine
• Sarcoptes scabiei, o Hypothyroidism
• Notoedres cati, o Hyperadrenocorticism
• Eutrombicula alfreddugesi o Adrenal sex hormone
(chiggers) imbalance
• Glandular disorders • Bacteria

o Ceruminal gland hyper or o Gram positive
hypoplasia. o Gram negative
o Sebaceous gland hyper or
• Malassezia
hypoplasia.
o Altered type or rate of
• Otitis media
secretion.
o 50- 89% of dogs with chronic
• Auto-immune diseases
otitis externa
o SLE, DLE
o Cholesteatoma
o Pemphigus complex
• Progressive pathologic changes
• Viral disease
o Failure of epithelial migration
o Distemper virus
o Edema
o Stenosis
• Neoplasia and other masses o Glandular hypertrophy
o Nasopharyngeal polyps-young o Folding
cats o Fibrosis
o SCC o Ossification

4. Perpetuating factors
• Bacteria :
o Staphylococcus pseudointermedius (30-50%).
o Proteus mirabilis, Coagulase-negative Staphylococcus sp
Beta hemolytic Streptococci, Pseudomonas aeruginosa
Corynebacterium sp, Escherichia coli
• Yeast : Malassezia pachydermatis : 49% of normal dogs and 23% of normal cats
• Topical drugs : reaction to PG, Neomycin etc
• Otitis Media
• Progressive Pathological changes in ear : Stenosis, Raptured TM, Mineralization,
Hyperkeratosis, Hyperplasia
5. Recurrent or chronic ear disease

• The infection is caused by an unusual or very resistant organism, - some strains of
Pseudomonas aeruginosa.
• The infection is very deep (e.g., otitis media, osteomyelitis of the bulla) and not treated
aggressively enough.
• The patient has an anatomic ear problem—stenosis, tumor, excessive hair, and poor
conformation
• The patient has an underlying disease (often inflammatory, such as atopic dermatitis or
seborrheic disease)
• Underlying inflammatory disease that creates chronic inflammation in the ear canal can initiate,
promote, or maintain otitis externa
• Diseases of defective cornification (seborrhea), - primary or secondary- re accompanied by
ceruminous OE
• Chronic inflammation induces changes in the ear canal tissue
• Certain breeds have unique issues that may complicate the clinical picture.
6. Biofilms
• Biofilms can be identified on otoscopy or cytology.
• Clinically, the form an adherent, thick and slimy discharge that is often dark brown or black.
• On cytology they appear as variably thick veil-like material that may obscure bacteria and cells.
• Biofilms are clinically important as they inhibit cleaning, prevent penetration of antimicrobials
and provide a protected reservoir of bacteria.
• Also, Bactericidal antibiotics less effective, as biofilm-forming bacteria are usually in a quiescent
state.
• Biofims may enhance resistance, especially in Gram-negative bacteria - mutations to
concentration-dependent antibiotics.
• Topical trizEDTA and, n-acetylcysteine can disrupt biofims facilitating their removed and
enhancing penetration of antimicrobials

7. Chronic Otitis Externa
• Erosion/ulceraton leading to crust formation.
• Otic exudate, nature dependent on cause:
• Moist brown - cocci and yeast.
• Purulent creamy - gram-negative.
• Ceruminous waxy yellow - keratinizing.
• Glandular, chronic allergic.
• Dry coffee grounds - Otodectes- not sensitive sign.
• Pruritus or pain.
• Pinnal lesions (erythema, swelling, scaling, crusting, alopecia).
8. Otitis Media
• Thickened and/or ruptured eardrum, with opacity or color changes
• Ruptured eardrum with debris in middle ear
• Deformed and/or radio-opaque bulla on radiography
• Head tilt due to vestibular involvement.
• Facial nerve paralysis
• Sympathetic system involvement (Horner’s syndrome: miosis, enophthalmos and
protrusion of the nictitating membrane)
• Parasympathetic system involvement (KCS)
• Pain when opening mouth and/or palpating bulla
• Head shaking, hearing defects, pain, odor and lethargy
9. Otitis Interna
• Asymmetrical ataxia with wide-based stance
• Head tilt
• Walking in circles/falling
• Horizontal or rotational Nystagmus
• Vomiting (in the acute stage)
10. Before you initiate the treatment

• Age of onset-
a. Young: Allergy,Parasites
b. Old: Tumour/endocrine
• Breeds
• Type and duration of treatment
• Past occurrences
• Concurrent or historic dermatologic complaints
• Seasonality
• Gastrointestinal complaints
• General health ( systemic signs)
• Mixed infections

Diagnostic choices
Dermatologic Exam
Skin and hair changes
Evidence of pruritus
• Culture of ear swabs, needle aspirate >> Aerobic bacteria isolated and identified from ear
• Otoscopy/Videotoscopy >> Ear canal – Wax, Hyperplasia, Inflammation, growths
o Tympanum assessment if possible
o Ulceration
o Obstructive disease rule-out
• Culture of Tissues/Swabs >> Anaerobic bacteria isolated and identified
Rods and/or cocci seen. The most suitable antibiotic treatments can only be chosen
if the organisms are known.
Marked purulent discharge without organisms being noted. Possibility of finding a
pathogen that is relevant, but also may grow organisms that are irrelevant clinically.
Pyogranulomatous inflammation. Organisms are often difficult to see with cytology
in this uncommon ear inflammation, so culture is obligatory.
In the event of treatment failure regardless of the organisms found, culture should
help direct secondary and further treatments.
If there is a suspicion of methicillin-resistant Staphylococcus species (MRS).
The dog or cat has previously suffered MRS or has been in-contact with MRS
‘carriers’ or MRS is common in the hospital environment.
If considering video otoscopy or ear flush for diagnosis or treatment in a bacterial
otitis.
• Biopsy >> Inflammatory cell infiltration of neoplasia
• Endocrine Panel >> Thyroid, Adrenal
• Scraping>> Ear mites
• Cytology
o Quick and easy to perform.
o If the mean number of bacterial or yeast is > 4, - considered pathogens.
o Mean counts of yeast > 5and bacterial > 25 per HPF - abnormally increased.
o Mean counts of yeast > 12 and bacteria > 15 per HPF in cat - abnormally increased.
o Artifacts –Melanin granules and stain precipitates
o Type of Inflammatory cells : neutrophils, eosinophils, lymphocyte, Blast cells,
Mitiotic cells
o Cerumen is clear - does not stain due to its high lipid content.
o Inflammation in Ears - lower lipid content than normal - bluer than a smear from a
normal ear.
o Keratinized squamous epithelial cells are usually anucleate and stain blue/purple.
o Melanin granules may be present in the keratinized squamous epithelial cells and
should not be confused with rod bacteria.
o The melanin granules will stain brown, while rod bacteria will stain blue/black.
o Precipitates on the slide stain blue/black and may be mistaken for coccoid bacteria.
o They differ from bacteria, since they form large, indistinguishable clumps while
coccoid bacteria are very round and uniform in size.
o This artifact is due to inadequate stain filtration. This can be avoided by periodically
filtering the stain and replenishing the buffer solution

Color/ Appearance Possible cause
Dry Coffee Grains Ear Mites
Humid/Moist Pale brown to yellow Cocci
Purulent creamy yellow, foul odor Gram Negative
Yellow Brown waxy greasy, stale odor Ceruminous- seborrheic /Ketatinizing
Adherent
Gray caseous, stale odor Mycotic ?
Dark to Green Black, Thick and slimy Biofilm
Pale brown to Gray, waxy to seborrhic Malassezia
11. Canine Ear margin Dermatosis

o Scaly condition of the margin of the pinnae.
o Mainly in dachshunds but other breeds with pendulous ears.
o Follicular casts and partial alopecia are common.
o In severe cases secondary infections, necrosis or fissures can develop.
o Moisturizing agents, topical sulfur salicylic acid shampoos and topical glucocorticoid
creams.
o Pentoxifylline may be beneficial in some cases.
o Underlying hypothyroidism ?
o Pemphigus foliaceous
12. Pinnal Dermatoses

o Alopecia on Pinnae
o Pattern baldness 14. Ulceration -Tip of Pinnae
o Demodex o Vasculitis
o Dermatophytosis o SLE
13. Papular Eruption on Pinnae o Dermatomyositis
o Scabies o Frost bite
o Contact allergy o Fly strike
o Food allergy o Cold Hemagglutinin disease
o Dermatophytosis o Fissures
o Drug eruption o Thrombovascular necrosis
o Pemphigus erythematosus

15. Scaling/Erosions/Alopecia Eyelids, pinna, Periocular,
o Necrolytic Migratory and muzzle
Erythema o Papules and pustules
o Zinc responsive develop which then
o Sebaceous adenitis fistulate, drain and crust.
16. Ceruminous Otitis o Systemic signs of fever,
o Primary seborrhea depression, and anorexia
o Demodex Submandibular
o Yeast lymphadenopathy
o Hypothyroidism o oral glucocorticoids +/-
17. Plaques antibiotic
• Lichenoid psoriasiform 22. Pattern baldness

dermatosis of Springer spaniels o Non-inflammatory hair loss
in dogs
18. Nodules
o Genetic basis -dachshunds,
o Leprosy in the dog
Chihuahuas, whippets and
o Crypto in cats
Boston terriers.
o Folded pinnae with steroid
o 6mom to 1 year.
use in cats
o Other body locations -
19. Erythema and Alopecia Secondary to
ventrum, caudal thighs and
Trauma
o Treatment with oral
o Atopic dermatitis
melatonin
o Otitis
20. Ear Tip Vasculitis
23. Proliferative thrmobovascular necrosis
o Idiopathic or secondary to
o Uncommon disease
vaccines, drug reactions
recognized in dogs.
and infections, lupus
o Begin at the apical margin
Erythematosus and other
of the ears and spread
immune mediated diseases.
along the concave surface.
o Breed -Jack Russell Terriers
o An ulcer may be located in
o Early lesions -scale, alopecia
the center of the lesions.
-symmetrical.
o A scaly, thickened,
o Erythema or cyanosis >
hyperpigmented zone
Necrosis
surrounds the ulcer.
o Distal extremities (tip of
o Prominent vessels can be
tail), foot pads, and nose –
seen coursing the margins
look for signs of vasculitis.
of the lesions.
o Pentoxifylline. Dapsone.
o Diagnosis: HP
Glucocorticoids
o Slowly progressive and
Prednisolone (2 to 4 mg/kg
unresponsive Pentoxifylline
orally q24h)
+ partial pinnectomy
21. Juvenile cellulitis ( Puppy Strangles)
o Puppies- 6 to 14 weeks of
age.
o Golden Retrievers,
Dachshunds, and Pointers.

Ideal ear cleaning protocol : Ceruminolytics > Drying agents > Antiseptics- specific treatments
• 0.5-1ml enough to cover the entire epithelium. 1 drop is ~0.025ml,

• Flushing -2 -3ml of the ear cleaner , Contact Time : 2-5 minutes
• Aware about ototoxic drugs – Aminoglycosides, PG, Chlorhexidne > 0.2 % ? some reported
gentamycin to be safe.
• Otitis more than 4 weeks old – 50% chance of raptured TM
o Surfactants : Reduce surface tension, Act as detergent or Humectant : Docusate sodium

o Detergents : Emulsify fats and waxes : Sodium Lauryl Sulfate
o Humectants : Humidify and stabilize water content ,draw moisture from dermis : urea,
propylene glycol, glycerin, lactic acid, Allantoin, Sodium lactate, Glycolic acid, Colloidal oatmeal,
fatty acids, polyvinyl pyrrlidone. Squalene, Saline
o Emollients /Occlusive : Seal moisture at the skin surface and reduces TEW loss : Oils - Olive,
Cottonseed, Corn, Almond, Peanut, Persia, cocounut, Sesame and Safflower, Animal Fats :
Lanolin, Hydrocarbons : Paraffin, Petrolatum, Mineral Oils
o Acids/Alcohol: Act as desiccants: Isopropyl alcohol, Boric acid, benzoic acid, aceticacid, sal.acid,
lactic acid
o Proteolytic agents : Protein degradation : Proteases. Lysozyme, Lactoperoxidase, Lactoferrin
o Alkalizing : Bactericidal, enhance AB action : TrisEDTA
o Regenerating agents : Skin barrier, anti-inflammatory and anti-microbial : Phytosphingosine
o Antiseptics : 0.05% chlorhexdine, 2% boric acid, 2% acetic acid. Avoid chlorhexidine in cats
24. Ear Cleaning agents

Ceruminolytics • Surfactants
• Propylene glycol o detergents
• Mineral oils DSS/docusate
• Glycerine Calcium sulphosuccinate
• Xylene o Emulsify debris
• Essential oils o Can be irritating
• lanolin, o Care if TM ruptured
• squalene, o Astringents
• butylated o Drying agents
hydroxytoluene, o Help to prevent maceration
• cocamidopropyl o Increase humidity- favor bacteria ?
betaine • Isoproponol/isopropyl alcohol
• Useful in purulent otitis • Boric acid
? • Benzoic acid
• Salicylic acid
• Sulphur
• Aluminium acetate
• Silicon dioxide

25. Popular Cleaning and drying agents combination of agents
o Acetic acid, lactic acid, salicylic acid in a surface-active vehicle containing docusate and
propylene glycol
o Isopropyl alcohol, salicylic acid, eucalyptol, acetamide MEA, propylene glycol, acetic acid,
aluminum acetate, hydrolyzed oat protein, wheat amino acids
o Deionized water, glycerol disterate, alkyl benzoate, glycerin, sodium olefin sulfonate,
cholesterol, allantoin, methylparaben, citric acid, sodium citrate, propylparaben
o Acetic acid, boric acid, surfactants
o Lactic acid and salicylic acid are present in encapsulated and free forms, chitosanide is present in
encapsulated form, in docusate sodium and propylene glycol base
o Propylene glycol, malic acid, benzoic acid, eucalyptus oil
o Lactic acid, salicylic acid in propylene glycol
o Benzoic acid, malic acid, salicylic acid, oil of eucalyptus
o Deionized water, isopropyl alcohol, propylene glycol, glycerine, fragrance, salicylic acid, PEG 75
lanolin oil, lidocaine hydrochloride, boric acid, acetic acid
o Propylene glycol, malic acid, benzoic acid, salicylic acid
o Water, propylene glycol, SD alcohol 40, DSS, glycerine, nonoxynol-12, salicylic acid, benzoic acid,
benzyl alcohol, fragrance, aloe vera
o 2% boric acid, 2% acetic acid, surfactants
o De-ionized water, isopropyl alcohol, propylene glycol, glycerine, fragrance, salicylic acid, PEG 75
lanolin oil, lidocaine hydrochloride, boric acid, acetic acid
26.Tris EDTA
o Apply 15-20 minutes before antibiotic or with antibiotic.
o Can over come partial resistance
o EDTA chelates metal ions, such as calcium and magnesium, which are necessary to maintain the
integrity of the cell membrane. Tris buffer enhances this effect
o Acts as a buffer to keep the ear canal at pH of 8.0, which is optimum for function of the
aminoglycosides and fluoroquinolones.
o 1.2 g EDTA, 6.05 g Tris buffer, 1 L distilled water, ph 8; autoclave 15 minutes.
27. Antibiotics
o Systemic : when?
• Stenosis, Severe ulceration
• Unusually severe or longstanding otitis
• Otitis that has been resistant or recurrent with prior topical treatment
• An obviously ruptured tympanic membrane
• If > 4 weeks, 50% chance of tympanic membrane rupture.
• In any situation where there is evidence of otitis media or otitis interna (pain, vestibular
signs, hearing loss etc)
•
Licensed : Enrofloxacin- Good MIC, Gentamycin, polymyxin- inactivated by purulent material

Non-Licensed :
• Silver sulphadiazene*-Promote healing, well tolerated 1:1 in water : Silver sulphadiaze

(Ceptidar, silveleb 1 % cream)
• Sulphdiazene 1% + chlorhexidine 0.2% (Silverex, Burnkul, Argisept),
Amikacin/Tobramycin, Pencillins/Cephalosporins
• Antibiotic sensitivity data is less useful with topical therapy as the concentrations achieved in
the ear canal will be ~1-4,000x that predicted by in vitro sensitivity tests.
• This can overcome resistance, and the response to treatment is best assessed by clinical signs
and cytology.
Staphylococcus Pseudontermedius -Percent of susceptible isolates (Kwochka KW ,2010, CVC )
Antibiotic Horizontal Canal Middle Ear
Cephalothin 77.8% 92.9%
Amoxicillin/Clavulanic Acid 100% 100%
Enrofloxacin* 96.3% 85.7%
Or Marbofloxacin , Difloxacin and orbifloxacin.
Gentamicin 96.3% 100%
Neomycin 88.5% 75%
Polymyxin B 100% 100%
Tobramycin 100% 100%
Trimethoprim/Sulfa 51.9% 35.7%

28. Recommended Topicals
• Nystatin,
• Thiabendazole,
• Clotrimazole,
• Miconazole, and
• Ketoconazole
• Neomycin, Gentamicin, Amikacin, Tobramycin
• Polymyxin (Neomycin, polymyxin B, and hydrocortisone
• 1 part injectable enrofloxacin (22.7 mg/ml) + 4 parts of 1% hydrocortisone or saline,
• Silver sulfadiazine 1% 1 part cream + 9 parts water - 0.5 ml, q12h.
• Enrofloxacin/Silver sulfadiazine
29. Glucocorticoids
• are antipruritic, anti-inflammatory, and antiproliferative.
• Proactive therapy gives a much better prognosis.
• Reactive treatment of each bout of infection gives short-term relief, but misses the ongoing
inflammation in the absence of infection - result in more frequent and severe infections
• Dexa /Vetalog twice daily topically for 3 wks- caused HPA suppression persisted even after 2 wks
stopping medications
• No evidence that NSAIDS benefit in reducing inflammation in Otitis externa
• Prednisolone -1 to 2 mg/kg every 12 to 24 hours- for 1 to 3 wks - control inflammation and
stenosis
• Betamethasone or dexamethasone - severe fibrosis and stenosis,
• Ciclosporin has also been shown to be effective in some cases of chronic otitis.
• Long-term treatment- prednisolone, or ciclosporin - lowest frequency and dose
• Dexamethasone can be used with care twice weekly.
Topical steroids –
• Appropriate for managing mild to moderate inflammation in acute otitis externa.
• Soluble preparations- 0.1 per cent dexamethasone + trizEDTA solutions to create rinses with an
appropriate glucocorticoid concentration
30. Ear Parasities

• Pyrethrin, Rotenone, Thiabendazole, Fipronil , Amitraz ,Ivermectin ,Moxidectin
• Spot-on 10% imidacloprid +1% moxidectin or selamectin, once or twice 30 days apart was best
31. Medical Grade Honey

• 70% of dogs achieving clinical cure between days 7 and 14
• 90% having resolved by Day 21.
• There was a decrease in clinical score throughout the duration of the trial

32. Delivering technology
• Microvesicle technology
• very small unilamellar, spherical structures made up of bipolar lipid molecules; Chitosanide .
o Delivers the active ingredient to the skin it attracts
o Traps dirt and debris - rinsed away at the end of the shampoo.
o Novasome® : non-phospholipid microvesicles ; deliver long lasting moisture to the skin
o Spherulites (Virbac)® : Plant-derived surfactants - Allow active ingredients for lasting
activity in skin
o Ceramides, essential fatty acids, and cholesterol are added -Hydration and epidermal
integrity
• Glycotechnology :
• Anti-adhesive technology - mimic the sugar moiety in cutaneous glycoproteins
o Bind both the cutaneous sugars and microbial lectins, and thus keep microbes from
binding to the skin
o D-mannose, Dgalactose, L-rhamnose and alkylpolyglucoside
33. Ear wicks

o Polyvinyl acetate wicks
o Inserted under GA
o Soaked in antibiotic or cleaning agent
o Expand to fill canal
o Replace after 3-5 days
34. When to consider surgery
o Neoplasia
o Stenosis of ear canal
o Proliferative/nodular hyperplasia
o Calcification of ear cartilages
o Bony changes to bulla
o Granulation tissue in middle ear
o Neurological deficits, deafness
o Failure to respond to medical therapy
35. Pseudomonas Otitis

o Painful, not pruritic
o Usually unilateral
o Yellow/green malodorous suppurative mucoid discharge
o Severe inflammation and ulceration of the canal
o Otitis media (~83% of cases of chronic disease)
o Head shaking
o Pain on palpation of the ear pinna
o Discomfort on opening the jaw
o Occasional neurologic signs, including:
o Horner’s syndrome
o Facial nerve paralysis
o Keratoconjunctivitis sicca

Treatment for least for 3 weeks- Systemic + Topical
o Flush with saline followed by an antiseptic flush.

o Lower the pH -kill Pseudomonas
o 2% Acetic acid - lethal within 1 minute of contact
o Can be used daily to flush the ear canal before applying a topical antibiotic solution.
o Safe even if the eardrum is ruptured.
If resistance is shown
o Tris EDTA), may be used as a final rinse that is not flushed away.
o Used as a prepared solution (12 mL + 4 ml Enro/Marbo or 1ml Genta) instill 0.5 mL into
ear Q 12 H
o Or + chlorhexidine or ketoconazole
o Silver sulfadiazine : dilute 0.1 to 0.5% in saline, combine with enrofloxacin
o Erofloxacin 20mg?kg Q 24hrs, Injectable dilute 1:4 with saline, ).15 to 0.3ml/Ear Q 24
hrs
o A Tris EDTA flush should be used twice daily prior to antibiotic administration.
o Enrofloxacin, Morbofloxcacin +/- Silversuphadiazne cream even in raptured TM
o Amikacin, Tobramycin, and Ticarcillin. +/- Tris EDTA
o Can replace 4 ml TrisEDTA with Dexamethasone
References available upon request

Topical Shampoo therapy in practice; Guidelines
Umeshkallahalli@gmail.com
 Shampoo therapy is rarely the sole form of treatment but can be invaluable in reducing the time to
clinical resolution while providing a window of increased comfort for the pet until a definitive
diagnosis and more specific treatment options can be identified.
 Useful in conditions where the barrier is abnormal (primarily in atopic dermatitis, and secondary to
infections, keratinization disorders,hypothyroidism, exfoliative dermatitis)
 Duration, type and interval of treatment can be adjusted based on the individual’s response. The
process mechanically removes dirt, keratinaceous debris , bacteria ? and allergens from the skin.
 Most of shampoos available in India are not validated and there is no control on the formulations
and manufacturing process
 Hair follicle density, PH and thickness of dog skin make them more sensitive to shampoos than man
 The potency, stability, efficacy and safety of many shampoos sold in india are uncertain- Most vets
choose the products based on their experience
 Normal skin should be relatively smooth and range in color from pink to black. Some dogs develop
blackening (hyperpigmentation) of the skin and could be a normal finding over time. The skin
secretes oil and sweat but should not be greasy or oily. A few exfoliated cells can be found
(sometimes confused as pathology called seborrhea) but should be difficult to find and not adhered
to the skin or hair shafts. Normal skin should not be thickened (lichenification) unless it is in an area
of trauma or pressure. Normal pressure point calluses occur in areas of trauma over boney
prominences such as the elbows, lateral tarsi, and points of the hips. Some breeds such as bull
terriers can develop large pressure points over odd places such as the dorsal bridge of the nose.
 Some areas can have increase moisture or exudation (oil) under normal conditions and can include
skin fold areas, lip folds, vulvar folds and ear canals. These areas trap moisture, and unless pruritus,
alopecia, erythema, or odor and discharge are evident may be a normal finding
 The active ingredients penetrate the skin through intercellular spaces (lipophilic molecules), through
keratinocytes (negatively charged), and through the hair follicles. Newer technologies (liposomes,
novasomes, spherulites, micelles, etc) allow these active ingredients to stay in contact with the skin
longer resulting in prolonged effect
Basics
 Shampoos may have either a soap base or a detergenet base and some are mix. Base- Sodium or
potassium salts of high MW aliphatic acids and to get desired qualities and specific therapeutiuc
effects – emollient oils, emulsifiers, surfactants, Stabilizers, Foam boosters, pH adjusters,
Preservatives, Antioxidants, Coloring agents, Fragrances, thickening agents and solvents are
added
 Surfactants are amphiphilic compounds ( affinity to both water and oil) and they form Micelle
structure in water- ability to emulsify, render soluble and detach oils, dirt and debris, facilitating
their elimination with water
 Surfactants classified into Anionin and cationic, nonionic and amphoteric.
Kallahalli Umesh,. This notes is for education and internal use only. Reproduction in any form is not
allowed.
o Anioninc : negatively charged- has - fats and oils salts eg., soaps- cleaning and foaming
properties
o Cationic: positively charged- qauternery ammonium compounds, aminooxides-
alkylamine salts and alkyl pyridinium salts- absorb on negative things like hair- used as
conditioners to improve texture and volume
o Nonionic: resistant to PH variation, glycol and fatty acid esters, alkanolamides,
polyethoxylated and polyhydroxy derivatives – generally used with anionin and cationic
surfactants
o Amphoteric : isoelectric point and behave as anionic or cationic depending on pH of
aqueous phase. Betaines, imidazolines and aminiacid derivatives commonly used.
 A cleansing shampoo with sufficient surfactants to break up and remove accumulated debris is
done first to prepare the skin to receive the maximum benefit from the selected medicated
shampoo.
 A medicated shampoo is chosen based on the condition needing attention. It must be massaged
into the skin for 10-15 minutes to allow the active ingredient(s) to penetrate and have its effect,
and then rinsed thoroughly. Shampoos should be used 2–3 x/week as long as active disease is
present . At least 2 weeks is indicated for treatment initially in severe cases and then frequency
decreased.
 Clipping the fur short may be needed to facilitate this process.
 Shampoo, when lathered with water, cleans the fur and skin but will also remove the natural oils
(sebum) resulting in a dry skin condition.
 Water (hydrotherapy) rehydrates the stratum corneum but the benefit is only temporary unless
a moisturizer is used to trap the water in the SC. So the best use of a moisturizer is after a
cleansing shampoo to trap water in the SC and prolong rehydration
 Hydrotherapy (just water) has the benefit of mechanically removing dirt, crusts, dead skin cells,
allergens, as well as being cooling and rehydrating.
-------------------------------------------------------------------------------------------------------------------------
 The term moisturizer implies that the substance applied adds or retains water in the skin
Moisturizing factors are often either added to the shampoo or placed in an after-shampoo
spray or rinse to help reverse the dryness that can occur as a result of stripping the normal
moisturizers from the skin with the medicated shampoo, or to help re-establish the normal skin
environment.. This may be done by providing natural exogenous humectants (urea, propylene
glycol, glycerin, lactic acid) or an exogenous barrier to water loss (petrolatum or natural or
synthetic oils). Other moisturizing factors include emollients, humectants, occlusives (heavier
seal than emollients), fatty acids (incorporated into intercellular space to help maintain the
epidermal barrier), and emulsifiers (help distribute oil or humectants evenly over the skin).
allowed.
 Emollients (seal moisture at the skin surface) and humectants (draw moisture from the dermis
into the skin) prolong the rehydrating benefits of hydrotherapy by trapping the water close to
and in the skin, and are often applied after the medicated shampoo to help prevent dryness.
They also prevent excessive water loss. Oils mixed with surface acting agents and aid to
soften/soothe the skin. Smoothen the roughened surface of Stratum corneum (SC) by filling the
space between dry skin flakes with oil droplets. The term ‘emollient’ covers a diverse range of
products, including soap substitutes, bath additives, creams, ointments and even aerosol spray
products. They are important in the management of itchy, dry skin conditions, giving
symptomatic relief, and may reduce requirements for topical corticosteroids.
 Consists of
o Oils - Olive, Cottonseed, Corn, Almond, Peanut, Persia, cocounut, Sesame and Safflower
o Animal Fats : Lanolin
o Hydrocarbons : Paraffin, Petrolatum, Mineral Oils
 Occlusive agents : Block surface of SC and reduces transepidermal (TEW) water loss, allow more
effective penetration of medications. (petroleum, mineral oil, lanolin, corn/peanut/cotton seed
oils)
 Emulsifiers : Highly dispersible agents- oil in water- PEG-4 dilurate,Stearic acid,Stearyl alcohol,
Cetyl alcohol, lecithin, Laureath-4 etc
 Humectants absorb moisture from the air into stratum corneum, Soften keratin on the surface
by bonding to stratum corneum. They prevent water loss without oils.
o Glycerin, propylene glycol(PG), allantoin, Sodium lactate lactic acid, Glycolic acid, urea,
Colloidal oatmeal, fatty acids, polyvinyl pyrrlidone
o Lactic acid used in free form or in liposomes as sprays or lotion. Glycerine, PG and urea
coat skin surface and alleviate pruirtus
o PG- hygroscopic, antibacterial and anifungal at 40-50%, excellent vehicle for most drugs
and enhance penetration of drugs. Keratolytic at 50% and above by denaturing proteins
o Urea: Hygroscopic, < 20% - Humecatant and > 20% - Keratolytic by proteolytic action,
promotes hydration
 Calcineurin inhibitors are a new class of topical immunomodulators that act by reducing
inflammation via T-cell suppression : Tacrolimus and pimecrolimus
 Keratomodulating products work to restore normal keratinocyte growth and differentiation by

working on the basal cell layer and reducing the rate of division. Products that work in this way
are called keratoplastic. Keratolytic products may remove excess scaling by increasing
desquamation and/or reducing intercellular cohesion. Many products are both keratolytic and
keratoplastic and include salicylic acid, sulfur, selenium sulfide, benzoyl peroxide and tar. Tar
and selenium sulfide should never be used on cats.
o Keratolysis means softening, separating, and desquamation of the cornified epithelium
(SC). This is caused by cellular damage to the corneocytes resulting in ballooning of the
cells and reduction of intercellular cohesion.
o Keratolytic agents basically loosen the outer layer of the skin (SC)
o Keratoplastic is when there is a "normalization" of epidermal cell kinetics and
keratinization, usually by cytostatic effects on the basal cell layer. Keratoplastic agents
normalize epidermal turnover time.
allowed.
 Menthol, camphor, and thymol act by substituting other sensations for itching. A cooling
sensation helps decrease itching and may also help increase the itching threshold.
 Phytosphingosine is a lipid that occurs naturally in the stratum corneum, both in its free form
and as part of ceramides. It has both anti-inflammatory and anti microbial activities. It has also
been synthesized and incorporated into shampoo as a means of barrier repair.
 Lysozyme, Lactoperoxidase, and Lactoferrin are 3 enzymes derived from milk products. Each
enzyme has its own unique antimicrobial properties. Lactoperoxidase, which when combined
together with hydrogen peroxide, thiocyanate and/or iodide, produce a potent antibacterial
system known as the Lactoperoxidase System. Two hypohalous ions, hypothiocyanate or
hypoiodite, are both bactericidal and fungicidal. Lysozyme kills bacteria by disrupting the
formation of a glycosidic bond between the two components of peptidoglycan in bacterial cell
walls. Lactoferrin is an iron binding protein. It is bacteristatic against a wide range of
microorganisms including gram-negative and gram-positive bacteria and may inhibit the growth
of bacteria by depriving them of iron.
Formulations
 Oils, creams and gels : All tend to soften and protect and many absorb water and can hold large
quantities of medication, Only useful for localized applications
 Vehicles hydrate the skin, can have an antiinflammatory effect, and help the active drug
penetrate the skin.
 Creams are water-based products with a cooling and emollient effect. They contain
preservatives to prevent bacterial and fungal growth, but the preservatives may lead to
sensitization and allergic contact dermatitis. Creams are less greasy than ointments and are
cosmetically better tolerated.
 Ointments contain no water; they are oil-based products providing an occlusive layer over the
skin surface that helps to retain water. This hydrates dry and scaly skin and enhances
absorption, and ointments are therefore useful in chronic dry conditions. They contain no
preservatives.
 Lotions are watery suspensions that can be used over hairy and large body surface areas. They
have a drying, cooling effect.
 Gels are watery suspensions of insoluble drugs such as corticosteroids, salicylic acid, and
retinoids. Gelling agents are added to aid their absorption. clear, greaseless, water miscible,
minimally occlusive
 Topical Steriods: Useful in non-exudative, non-ulcerated acutely inflamed lesions and on
chronically inflamed uninfected lesions
 Soaks/Rinses/Dips/Sprays - all water based : can be used on whole animal, even with thick
coat; non-messy and can be cleansing, soothing, antipruritic, antimicrobial, anti-inflammatory,
keratolytic. Disadvantages : requires frequent and prolonged administration and Poor
penetration of intact stratum corneum (although hydration during therapy increases
penetration) Uses: Treatments of Choice for acute exudative processes - removal of crust,
exudate
- Soaks : Plain water, Colloidal oat meal, Aluminium acetate 1:10/20 in water, Epsom salt (
Mgso4) 1: 65 in water, Chlorhexidine, Betadine solutions in water or normal saline; removes
exudate, antimicrobial, good in whirlpool baths.
allowed.
Clinical Uses
 Antiseborrheic products theoretically reduce sebum production and help remove stagnant oil
and debris from the sebaceous gland ducts. Certainly, products in this category are degreasing
and can be drying if an effort is not made to re-establish a moist, healthy environment after
stripping away the debris. Antiseborrheic products include benzoyl peroxide, sulfur, tar and
selenium sulfide.
 Antimicrobial shampoos are used to treat both superficial and deep infections, remove
exudates, and help prevent infections in animals that are prone to reoccurrence. These
shampoo ingredients reduce the surface colonization of the skin and fur. Antibacterial products
include acetic acid and ethyl lactate. Chlorhexidene (0.5-4%), povidone iodine, triclosan, ethyl
lactate (enzymatically changed to ethanol (lipid solubilizer) and lactic acid (lowers pH by
bacterial lipases in hair follicles and sebaceous glands), and benzoyl peroxide (BP-2-3%) all have
antibacterial effects. Benzoyl peroxide has the highest antibacterial activity as it oxidizes to BP
free radicals which then disrupt bacterial cell walls. Phytosphingosine is both antibacterial and
antiseborrheic.
 Antifungal products include the keratomodulating products in addition to products with direct
antifungal properties. Chlorhexidene, ketoconazole (2%), miconazole (2%), benzoyl peroxide and
acetic acid are all effective in killing fungus
 Anti-pruritic therapy is multifactoral. Anything that reverses dryness, removes allergens and
surface debris, and prolongs rehydration of the Stratum corneum has the potential to be
antipruritic. Products that restore barrier function, kill bacteria and malassezia, and reduce
inflammation are also antipruritic. Ingredients with specific antipruritic activity have also been
added to shampoos, sprays and rinses and include colloidal oatmeal, pramoxine (a topical
anesthetic), diphenhydramine, hydrocortisone and triamcinolone.
New delivery system

 Microvesicle technology - Micelles (Spherulites® and Novasomes®) are very small unilamellar,
spherical structures made up of bipolar lipid molecules that have hydrophilic (head) and a
hydrophobic (lipophilic) ends. These microvesicles can be charged or neutral. The positively
charged (cationic) microvesicles bind to negatively charged skin allowing prolonged contact of
the active ingredient with the surface of the skin and hair. On contact with the skin the chemical
bonds in the micelle break down delivering the content of the micelle to the skin. At the same
time it delivers the active ingredient to the skin it attracts and traps dirt and debris. This trapped
debris is rinsed away at the end of the shampoo. Neutral micelles pass through the surface
barrier and are deposited in the deeper layers of the skin where they have the desired effect.
Cutaneous bio-mimetic ingredients such as ceramides, essential fatty acids, and cholesterol are
added to the microvesicle to help re-establish hydration and epidermal integrity. There are
commercially available sources of procerumides (phytosphingosine) in a shampoo, spray, wipe
and ampule treatments, some of which contain chlorhexidine.
The protonated amino groups contained in Chitosan is produced commercially by deacetylation
of chitin, the structural element in the exoskeleton of crustaceans (such as crabs and shrimp)
and cell walls of fungi. it has a high affinity for normal negatively charged skin, hair, and nails.
Chitosan readily adsorbs to skin and hair surfaces, providing a protective elastic film as its high
molecular weight will not allow it to penetrate the skin. Additionally, it enhances the transport
of polar drugs across epithelial surfaces and can trap non-polarized drugs on the skin surface.
Chitosanide coats skin and fur and traps the spherulite next to skin to extend the activity of the
active product increasing moisturizing effect. Novasome® are non-phospholipid microvesicles
allowed.
that incorporate water or lipids. They are designed to deliver long lasting moisture to the skin
Spherulites (Virbac)® multiple layers of plant-derived surfactants and In contrast to Novasomes,
it incorporates active ingredients into these layers allowing long lasting activity
 Glycotechnology : This is an anti-adhesive technology where sugars like D-mannose,
Dgalactose, L-rhamnose and alkylpolyglucoside, mimic the sugar moiety in cutaneous
glycoproteins and bind both the cutaneous sugars and microbial lectins, and thus keep
microbes from binding to the skin. Studies have shown that these sugars bind lectins on the
surface of Staphylococcus intermedius, Pseudomonas auregenosa, and Malassezia thus
preventing them from adhering to the skin surface. In addition, Glycotechnology reduces
keratinocyte activation and cytokine signaling thereby reducing inflammation.
Keratinization disorders
Keratnization (means normal production and development of skin cells) disorders are caused by
alterations in proliferation, differentiation or desquamation or combination of these abnormalities. It
takes 20-22 days from birth of keratinocytes by cell division in the basal cell layer to desquamation as
dead dehydrated cells from stratum corneum. Dryness of skin is caused by decreases water content
which must be > 10% for skin to appear and feel normal. It can be retention ( eg, sebaceous adenitis) or
proliferative ( eg., allergic, parasitic infections) keratnization disorders.
Scale is accumulation of loose skin cells from stratum corneum caused either by increased production of
keratinocytes or insufficient shedding of squames. By contrast, crust consists of dried serum, pus,
exudates, blood or medication mixed with keratinocytes.
The term seborrhea is commonly used to describe the clinical aspect of the skin and/or hair coat,
including conditions associated with excessive scaling, flaking, malodor, and/or greasiness.
Keratoseboorhic disorders, keratnization or cornification disorders are other terms used frequently by
dermatologists. It is important, however, to differentiate between primary seborrhea (heritable
disorders) and secondary seborrhea (secondary to another underlying disease) for diagnostic purposes,
because treatment and recommendations for owner and breeder will differ.
• Primary seborrhea describes specific, heritable disorders of keratinization or cornification. The

pathophysiology involves a defect in the keratinizing epithelium or cutaneous glandular function, and is
manifested clinically by excess scale formation. There are marked breed predilections and animals
affected with the condition should not be bred. Primary seborrhea is rare; most animals have underlying
diseases that lead to seborrhea. The dermatologists suggests that the term seborrhea as a diagnosis be
limited to the breed-specific disease
• Secondary seborrhea. - Most cases of seborrhea are secondary to a primary skin disease, such as
allergy, superficial pyoderma, Malassezia dermatitis, ectoparasitosis, or hypothyroidism. Once the
underlying disease is cured, the seborrhea clears up. Secondary seborrhea includes
 seborrhea sicca to describe dry scaly conditions . After washing your hands it feels like you have
candle wax on tips of your fingers
 seborrhea oleosa to describe greasy, oily,malodorous conditions; hairs may become matted in
greasy tufts
 seborrheic dermatitis to describe more inflammatory conditions usually involving secondary
pyoderma and Malassezia. Can be focal or generalized. Blackish, scaly, partially alopecic and
allowed.
lichnified macule surrounded byscaly annular zone of erythema and /or bordered by epidermal
collerate
Primary Cornification disorders /keratoseborrheic disorders / keratinization disorders are usually

inherited (ie, genetically determined).
Localized
 Nasal hyperkeratosis (Labrador retriever – autosomal recessive)
 Footpad hyperkeratosis (Irish Terrier and Dogue de Bordeaux)
 Schnauzer comedone syndrome (miniature Schnauzer)
 Ear margin dermatosis ( eg., Daschunds)
 Acne
 Stud tail
Generalized
 Idiopathic primary seborrhea in dogs (cocker and Springer spaniels, dachshund, etc.)
 Follicular dystrophy (color dilution alopecia of Doberman)
 Hereditary seborrhea oleosa in cats (Persian, Himalayan and exotic shorthair cats; autosomal
recessive)
 Ichthyosis
Secondary Cornification disorders

 Infectious : Pyoderma, Malassezia dermatitis, Dermatophytosis, Leishmaniasis
 Parasitic : Cheyletiellosis, Pediculosis, Demodicosis, Sarcoptic acariosis
 Hypersensitivity : Atopic dermatitis, Fleabite hypersensitivities*, Food hypersensitivities
 Metabolic : Malabsorption/maldigestion, Metabolic epidermal necrosis
 Endocrine : Hypothyroidism, Hyperadrenocorticism, Sex hormone imbalance
 Autoimmune or immune-mediated : Pemphigus foliaceus or erythematosus, Systemic lupus
erythematosus, Cutaneous drug reaction, Sebaceous adenitis
 Nutritional : Zinc responsive dermatosis, Essential fatty acid deficiency
 Environmental : Frequent baths, Warm and dry environment
 Neoplastic : Epitheliotropic lymphoma (Mycosis fungoides), Exfoliative dermatitis associated with
thymoma in cats
Pruritic diseases causes keratoseborrhoea : Flea bite allergy, Scabies, Cheyletiella, Pyoderma,
Malassezia (yeast), Adverse food reaction, Atopy, epitheliotrophic lymphoma
1. Topical Antiseborrheic Agents
Sulfur
 is mildly keratolytic (increases desquamation), keratoplastic (by a reaction with cysteine in the
skin to form cystine and hydrogen sulfide, which are the building blocks for normal
keratinization; or by dysregulation of normal maturation of keratinocytes by suppressing
epidermal growth).
 Smaller the particle size greater the surface area of interaction with skin- Colloidal sulfur.
 It is also Antibacterial and antifungal due to hydrogen sulfide and pentathionic acid that forms.
allowed.
 It is also anti-parasitic and anti-pruritic. - Its side effects include its odor and staining potential
as well as its drying effects. Sulfur can cause re -bound increasein seborrhea.
 Indications- scaling, pruritic, some infectious (bacterial or fungal) or some parasitic dermatoses
 Known drug interaction -sulfur is synergistic with salicylic acid and shampoos typically contain
2% sulfur and 2% salicylic acid
Salicylic acid
 is keratolytic (by disrupting intercellular cement), keratoplastic, anti-pruritic, and decreases the
pH of skin resulting in increased hydration of the stratum corneum- swelling of SC
 In the desquamation process, has a direct effect on intercellular cement and the intercellular
junction system (desmosomes).These actions help soften the corneal layer
 Indications - scaling dermatoses typically in combination with sulfur.
Tar
 is another antiseborrheic ingredient and comes in a variety of forms (coal tar, solubilized tar,
coal tar solution).
 It is often included with sulfur and salicylic acid. It is keratoplastic (antimitotic on the basal cell
layer), antipruritic, vasoconstrictive, and degreasing. Shampoos contain 0.5% tar ( 2.5 %
solution) is les irritating and acceptable.
 indications -recommended for treatment of greasy dermatoses in dogs . 3-4 % is ideal and has
better clinical efficacy. Reserve for severe greasy, primary idiopathic seborrhea and thise cases
not responding to sulfur, salicylic acid or benzyl peroxide
 Side effects include photosensitivity and pruritus and irritation
 Contraindicated in patients with dry skin and in CATS
Ammonium Lactate:
 Keratoplastic and ketarolytic stimulate living epidermis, correct defects in keratinocytes
multiplication and maturation, , has moisturizing properties
Selenium Sulfide
 Keratolytic- depress epidermal cell turnover rate and interfere with hydrogen bond formation in
keratin(impair disulphide bridge formation) , keratoplastic and degreasing. May stain, dry and
irritating. Rarely used. Use at 1%. can cause re -bound increase in seborrhea. Contraindicated in
cats
Benzoyl peroxide
 is quite versatile in that it is not only antiseborrheic and keratolytic, but it is antimicrobial and is
reported to have follicular flushing effects as well but with poor evidence. Residual antibacterial
activity up to 48 hours on skin? 5 hours in experimental
 When applied to the skin, it is broken down to benzoyl peroxy radicals, benzoic acid, benzoate
salts and nascent oxygen, which exert the antimicrobial effect. Lowers PH- disrupts cell
membrane-oxidizing agent- release nascent oxygen- rupture of bacterial membrane
 Side effects include dryness and increased pruritus. >5% causes irritation, bleaching action on
fabrics
 The antibacterial effect at 2.5-5% concentrations has been shown to persist for 48 h,
 indications- bacterial pyoderma, acne, adjunctive therapy for demodicosis (follicular flushing).
allowed.
Phytosphingosine (PS)
 Recently released (Sogeval®,DOUXO®) combination antiseborrheic, antiinflammatory, and
antimicrobial product. Used for primary and secondary seborrheic conditions. Combined
properties are valuable for cases of seborrhea that have concurrent inflammation and infection.
Because PS is a key molecule in the natural defense mechanism of the skin and a major
component of ceramides in the skin, PS can be invaluable in maintaining the cohesion of the
stratum corneum, controlling local flora, and preserving the correct moisture
balance.Preliminary clinical evaluations have shown great promise for all forms of seborrheic
skin conditions.
Zinc gluconate
 is a type I 5-reductase inhibitor and downregulates sebum production.Down regulates sebum
production. Zinc gluconate and vitamin B6 are combined with essential fatty acids in a newer
shampoo that has both antiseborrheic and antibacterial properties.
Localize scaling :
 Treinoin at 0.05% as gel increase epidermal turn over rate and reduces cohesion of
keratinocytes. Useful in acne and Nasal hyperpigmentation.
 Lactic acid useful in Callus and ear margin dermatoses and nasal hyperpigmentation.
 Sulfur-6%, Urea 5%, and sodium lactate 5 % useful in callus, ear margin dermatosis and acne
2. Topical Anti-bacterial in shampoo
Chlorhexidene
 Biguanide antiseptic, act on bacterial cytoplasm membrane causing leakage.higher con causes
coagulation of proteins
 Rapid acting and less irritation. Work in organic matter, residual action up to 29 hours ? ( 4-8
hours in experimental)
 0.5% chlorhexidine solution provided better antimicrobial activity, it also slowed granulation tissue
formation. In view of this fact, it is recommended that 0.5% chlorhexidine should not be used as a wound
antiseptic for prolonged contact with the tissues
 Side effects – Few – chlorhexidine is safe in cats, although corneal ulceration and irritation have
been reported. Incompatible with anionic surfactants
 Phytosphingosine + chlorhexidine is excellent combination
 indications - for bacterial and some fungal skin infections in dogs and cats. (At least a 3-4%
concentration is needed for a good effect against Malassezia or dermatophytes if used as a sole
ingredient.)
Ethyl Lactate (EL)

 Lipid soluble, Hydrolyze to ethanol and lactic acid by bacterial lipase, penetrate hair follicles and
sebaceous glands, reduces pH and reduces sebum
 indications - EL is used for mild surface and superficial bacterial infections. Found in shampoo
formulations in a concentration of 10%
 Side effects – Irritation, erythema, pruritus seem less frequent than with benzoyl peroxide.
allowed.
Triclosan
 Appears to be less effective in dogs than benzoyl peroxide as a prophylactic agent against S.
intermedius. It is not effective against Pseudomonas
 Side effects – Allergic contact reactions to the product may occur.
 indications – for bacterial skin infections in dogs and cats
Povidine-Iodine-
 Bactercidal, funficidal , sporicidal and virucidal. Residual action up to 6 hours. Dry and irritate
use at 2%. persists for 4-8 hours on skin in experimental
Topical antibacterial Creams, ointment, solution , gels and wipes

 contact time of more than 10 minutes is required for to exert its antibacterial benefit
 Mupirocin : produced from Pseudomonas fluorescens bacteria. It is bacteriostatic at low
concentrations and bacteriocidal at higher concentrations. Kills bacteria by selective inhibition
of bacterial protein synthesis (isoleucin transfer RNA- Bacaterial synthetase). Staph resistance to
is rare in dogs and cats but possible when used over a prolonged period of time . Useful in
treating interdigital abscesses, callous pyoderma and acne in both dogs and cats. Mupirocin ointment
can be dissolved in (30g in warm water ) 60 mL of warm water to make a 1% solution. The
mupirocin stays in solution without precipitating and maintains its potency for at least 1 month.
 Fusidic acid, produced from Fusidium fungus, Fusidic acid works by inhibiting bacterial protein
synthesis and is bacteriocidal at all concentrations. It readily penetrates skin and there is almost
no known staphylococcal bacterial resistance. Studies have shown fusidic acid to be as effective
as mupirocin for killing Staphylococcus infections.
 Sulfadiazine, clindamycin, Triclosan -0.5%, Acetic acid : 1;! In water 1-2 times a week, Lime
sulfur 2% 1:16. Retapamulin is a derivative of the antibacterial pleuromutilin, a product of
Pleurotus mutilus, an edible mushroom. This 1% ointment is a new antibacterial licensed for
treatment of impetigo, infected lacerations, and sutured wounds in human medicine
 Both sodium hypochlorite, common household bleach, and its active ingredient hypochlorous
acid are effective antibacterial agents. - If one half cup of common household bleach is added to
a bathtub filled one quarter of the way, the resultant 2.5-uL/mL concentration of bleach kills
99.94% to 100% of methicillin resistant Staphylococcus aureus organisms in vitro after 10
minutes of contact time. The pet should be thoroughly bathed with shampoo after the 10-
minute to avoid potentially bleaching the coat or its surrounding environment.
 Lantibiotics (lanthionine-containing antibiotics) available as Wipes are a group of antimicrobial
peptides that are produced by and primarily act on Gram-positive bacteria, of which nisin is a
member. Nisin is bacteriocidal and is derived from Lactococcus bacteria- target the Staph
cytoplasmic membrane, which it disrupts, causing rapid efflux of cytoplasmic contents. Because
nisin is an edible protein, there is no chance for toxicity if the dog licks or chews the site of its
application. Further studies required for routine clinical uses.
allowed.
3. Topical antifungal agents
 Chlorhexidine 2% + Micanazole 2% better than single agent alone

 Povidieniodine
 Lime sulfur 1:16, 2 %
 Enilconazole, ketacanozole 1% and Micanazole 2%
 Piroctone Olamine: used in human shampoos to treat malassezia furfur, useful in pets and
also as keratomoduilating agent and M.pachydematis
4. Topical Antipruritic Agents
"When it is dry, wet it" and "When it is wet, dry it"
Shampoo therapy for dog with atopy is helpful by removing antigens from the skin and haircoat and
also by rehydrating the skin Antipruritic shampoos in general, are used as adjunctive treatments for
short-term relief – they may allow lower dosages of systemic antipruritic agents to be used
 Glucocorticoids –
o 0.01% fluocinolone shampoo applied to allergic dogs twice weekly for 6 months had no
adverse effects.
o Hydrocortisone (1%) shampoo is not significantly absorbed and may help treat allergic
reactions
o 0.0584% hydrocortisone aceponate (HCA) spray (Cortavance® from Virbac )
o Tacrolimus can be used along steroids to reduce side effects of skin atrophy etc
 Colloidal Oatmeal : Antipruritic and soothing
 Phytosphingosine is antiprutiuc as well antiseboorrehic
 Lime sulfur is excellent antipruritic but odour, bleaching are issues
 Pramoxine Hydrochloride– Found in combination with colloidal oatmeal, hydrocortisone,
menthol and petrolatum. Pramoxine was shown to be useful in the management of pruritus in
dogs with atopic dermatitis Side effects – Sensitizing potential.
 Tar - anesthetizes peripheral nerves
 Diphenhydramine
 Linoleic acid + Gamma Linolenic acid
 Mono and oligosacccharides – restore barrier function, imunomodulatory and inhibit
inflammatory cytokines like TNFalpha
 Vitamin E- a study shown to have Antioxidant, stabilize lysosomes, redice PGE2 synthesis,and
increase interleukin -2
 Acute cases - Red, wet and itchy or painful. Avoid occlusive therapy; Use water-based or
hydrophilic vehicles
 Chronic disease - usually cool, dry, thickened and hyperpigmented. Scale and itching are
variable - Occlusive vehicles may be required for effective penetration and to allow rehydration.
(Eg Oil base)
 Mild dry scaling : use mositerizers and hypoallergenic shampoo, If no response use sulfur and
sal. Acid along with bath oil rinses or humectants to avoid drying. If scaling is severe and not
responding to above use tar and moisturizing agents must follow.
 For oily/Greasy skin- use benzyl peroxide or/and sufur/tar alone or in combinations
 Dry scaling with pyoderma : Chlorhexidine is choice
allowed.
Topical therapy Ingredients - Indications
O Dry Oily
Nor Itc Dr il flack flack Follicu Pyode Malass Dermatop Kerato Kerat Follicul Rehyr
Ingredient mal hy y y ing ing litis rma ezia hytes plastic olytic flushin dating
Benzyl
peroxide Y Y Y Y Y Y Y ?
Sulfur Y Y Y Y Y Y Y Y Y
Salicylic acid Y Y Y Y Y Y Y Y Y
Tar Y Y Y Y Y Y
Selenium
sulfide Y Y Y Y Y Y Y
Chlorhexiden Y Y Y Y Y Y Y Y?
Ketacanazole Y Y
Micanazole Y Y
Triclosan Y
Pramoxine Y Y Y Y Y Y
Colloidal oat
meal Y Y Y Y Y
Aloevera Y Y Y?
Acetic acid Y Y Y Y Y Y Y Y
Hydrocortison Y
Zinc
gluconate Y Y Y Y Y
Ethyl lactate Y Y Y Y Y
Boric acid Y Y Y Y Y
Menthol Y Y Y Y Y Y Y Y Y Y Y Y Y
Moisteruiring
agents y y y y y y y y y y y y Y
Phytosphingo
sine y y y y y y Y
Novasome
microvesicles y y y y y y y y y y y y Y
Glyoctechnol
ogy y y y y y y
Spherulites y y y y y y y y y y y y
Mono/oliosac
charides y y y y y y y y
Milk enzymes y y y y y y y y y
allowed.
Frequent cause for scaling in dogs ( other than Primary Keratinization disorders)
Infectious Pyoderma, Malassezia dermatitis, Dermatophytosis, Leishmaniasis
Immunologic Atopic dermatitis, Fleabite hypersensitivities*, Food hypersensitivities
Endocrine Hypothyroidism, Hyperadrenocorticism, Sex hormone imbalance
Autoimmune Pemphigus foliaceus or erythematosus, Systemic lupus erythematosus,

Cutaneous drug reaction, Sebaceous adenitis
Nutritional Zinc responsive dermatosis, Essential fatty acid deficiency
Environmental Frequent baths, Warm and dry environment
Parasitic Cheyletiellosis, Pediculosis, Demodicosis, Sarcoptic acariosis
Neoplastic Epitheliotropic lymphoma (Mycosis fungoides), Exfoliative dermatitis

associated with thymoma in cats
Primary scaling causes

Localized
 Nasal hyperkeratosis (Labrador retriever – autosomal recessive)
 Footpad hyperkeratosis (Irish Terrier and Dogue de Bordeaux)
 Schnauzer comedone syndrome (miniature Schnauzer)
 Ear margin dermatosis ( eg., Daschunds)
 Acne and Stud tail
Generalized
 Idiopathic primary seborrhea in dogs (cocker and Springer spaniels, dachshund, etc.)
 Follicular dystrophy (color dilution alopecia of Doberman)
 Hereditary seborrhea oleosa in cats (Persian, Himalayan and exotic shorthair cats; autosomal
recessive)
 Ichthyosis
allowed.
Practical approach to Uncommon skin diseases in General Practice
Kallahalli Umesh, MVSc, MSc, Mars India International
Uncommon diseases causing Cutaneous Ulceration and erosions in dogs
Ulceration - Epidermis has been lost and the basement membrane disrupted. It is therefore a
deep lesion that bleeds easily
Erosion is less severe, the damage to the epidermis leaves the basement membrane intact. It
does not bleed.
• May be difficult clinically to differentiate between ulcerations and erosions clinically.

• Erythema and tissue haemorrhage may be differentiated by diascopy-pressing a glass
slide onto the lesion. Blanching indicates vasodilatation, and a failure to pale indicates
haemorrhage into the tissues.
• Crust is formed from the accumulation of dried serum, pus or haemorrhage, and may
include hair, cells and, sometimes, medication on the skin surface. Crust is representative
of a breach of epithelial integrity and there are many diseases that can result in its
formation, including vesicular, pustular, erosive or ulcerative disorders
• Ulcers and erosins formed by External factors (Thermal, chemical, mechanical trauma
from pruritus or Internal factors: Damage to the blood supply; vasculitis, neoplasia,
Neoplastic invasion of epidermis, Immune-mediated insult of the epidermis or basement
membrane: i.e. cutaneous lupus erythematosus, pemphigus, bullous pemphigoid and
variants, erythema multiforme, Hotspot ( pyotrumatic dermatitis), skin fold pyoderma,
Thermal or chemical burns
Autoimmune Skin diseases

These diseases are usually rare to uncommon and vary in severity from mild to life threatening
Signs to look for suspected autoimmune diseases
• Ulceration and erosions- foot pads, Nasal planum ear pinnae etc
• Mucocutaneous involvement – Oral, Ocular or genital
• Depigmentation at site of old lesions
• Symmetrical distribution – most cases
• Positive Nikolsky sign - new or extended erosive lesions can be induced with pressure on
adjacent skin
• Poor or No response to conventional therapy including anti-bacterials
Autoimmune diseases are the result of an aberrant immune response against structures of self,
or self-antigen. The cause of autoimmune diseases is complex and multifactorial, with a
polygenic genetic background interacting with triggering environmental and/or individual
factors. Some proposed causes are overexpression of self-antigen, Exposure of cryptic or
sequestered self-antigen, Aberrant expression of MHC molecules, Epitope spreading, Molecular
mimicry, Failure of central tolerance – all could be triggered by drugs, infection, trauma,

inflammation or UV rays etc (Bizikova P (2013) 11-16, 26th ESVD-ECVD conference) Diagnosis of
autoimmune skin disease generally relies on ruling out more common cutaneous diseases
(pyoderma, demodex etc) and performing skin biopsies. Obtaining the right skin biopsy is critical
to confirming a diagnosis. Serological evaluation for the presence of autoantibodies can be
performed in some cases at specialized institutions. It is recommended to contact
immunopathology lab before sending sample for diagnosis. DO NOT treat without a diagnosis.
False negative results for histopathology are often seen due to: Absence of recent lesions,
improper selection and handling of biopsies, prior steroid therapy. Biopsy sample before starting
immunosuppressive treatment.
Guidelines for biopsy

Carefully clip the hair coat without disturbing crusts or any surface lesions. Do not scrub, shave
and disinfect the skin surface, unless the biopsy is used for culture. Inject the local anesthetic
strictly subcutaneously. Never biopsy an entirely ulcerated area and select a new lesion proximal
to an ulcerated area. In most instances punch biopsies are the technique of choice. Wedge
biopsies are most suitable to sample large solitary lesions, intact vesicles and pustules, deep
pannicular lesions and ulcerated lesions. Avoid pinching of the samples while removing them.
Generally non infected “early lesion” for direct antibody testing in preferred but diseases like
DLE may require older lesion. It must be noted that tissue in nasal planum or food pads may
contain immunoglobulins in healthy dogs. 10% buffered saline (1:10) can also be used for most
special stains, Immunohistology with antibodies suitable for formalin-fixed tissues, Clonality
testing (T cell receptor gamma: TCRG; immunoglobuline heavy chain: IgH; kappa deleting
element: KDE) and Polymerase chain reactions for infectious pathogens. Fresh samples are
wrapped in saline dampened gauze and placed in a plastic container or ziplock bag. The samples
need to be kept cool (+4oC). Michel fixative may be used for direct immunofluorescence . Tissues
can be quickly frozen and kept for 2 weeks in Michel fixative.
Examples of Autoimmune diseases of the epidermis and epidermal basement membrane :

Pemhigus Complex
Pemphigus Foliaceus ( PF) -
• PF is the most common form of pemphigus and is probably the most frequently diagnosed
autoimmune skin disease affecting cats and dogs
• PF is a Pustular disease- leading to erosions and crusting
• Pemphigus foliaceus is a specific type of superficial pemphigus and is clinically distinct
from deep pemphigus diseases. Pemphigus erythematosus is also superficial where as
Paraneoplastic pemphigus, pemphigus vulgaris, and bullous pemphigoid are deep
pemphigus diseases
• Desmosomes are responsible for cell-to-cell adhesion and present in all kerationcytes (
three types- Plakins, armadillo proteins and cadherins. The main cadherins, Desmogleins
and desmocollins are important for the discussions here.

• Hemidesmosomes are responsible for cell-to-matrix adhesion and located in basal cells
and basal membrane. In the skin, hemidesmosomes bind the deep or basilar epidermal
keratinocytes to the basement membrane (Epidermal-dermal adhesions)
• The autoantibodies involved in autoimmune diseases are still unclear in dogs
Autoantibodies (usually IgG) are directed against components of the epidermal cell
membrane responsible for cellular adhesion (majority being Desmocollin-1 and possibly
Desmoglein-1, Dsg1).
• The binding of anti-desmoglein antibodies causes desmosome disruption (release of the
cellular attachments) results in separation of the keratinocytes, which is referred to as
acantholysis.
• Keratinocytes that have lost their cell-to-cell adhesion are called acantholytic
keratinocytes, not acanthocytes (i.e. crenated red blood cells).
• Vesicles and pustules appear when the tight bonds between superficial keratinocytes are
affected. Likewise Bullae (Large blisters)and ulcers appear when the tight bonds between
basilar keratinocytes and the skin's basement membrane are affected.
• Acantholytic cells are the hallmark of pemphigus diseases.
• Sex and age appear to be unrelated to the development of pemphigus foliaceus in dogs
and cats. Most cases are in middle age to old dogs. In a study, Sixty five percent of the
dogs have the disease before 5 years of age
• Incidence unknown but may represent 2 % of cases in dermatology practice
• Overrepresented in certain breeds such as: Akitas, Chows, Dachshunds, Collies,
Doberman Pinschers, Newfoundlands.Labrador retrivers Cocker spaniels etc
• Can be Spontaneous - Most common or Drug/ tumor/ infection induced/triggered form
Currently there is no way/test to identify which drug induced or drug triggered. There are
reports of PF in dogs from topical spot-on product containing metaflumizone &amitraz
(promeris) and fipronil, amitraz and S-methoprene (Certifect)
• Ultraviolet exposure from the sun is a potential environmental trigger for pemphigus
foliaceus. The skin lesions in dogs with pemphigus foliaceus can worsen in the summer
and improve in the winter.
• Generally history of lesions that wax and wane, - slow progressive if localized like in face
or can be acute eruptions with generalized disease
• Lesions: Lesions are usually bilateral and symmetrical. The lesions progress from an
erythematous macule pustule collarettes erosions yellow brown crusts. Pustules and
crusts that can wax and wane despite therapy
• The primary lesions of PF are large “nonfollicular” pustules in the affected
regions. Where as in bacterial pyoderma -are follicularly oriented, usually involve the
ventral abdomen and/or trunk and are much smaller.
• As pustules are fragile and easily ruptured, only crusts or the dried exudate from ruptured
pustules may be noted Therfore, crusts rather than pustules are the most commonly seen
lesion in cases of pemphigus foliaceus.
• Ulcers are rare unless accompanied by deep pyoderma

• Distribution: Head, face and ears affected in more than 80% of cases, usually symmetrical.
Facial is most common form which involves the bridge of the nose, nasal planum,
periorbital and only Ear pinnae only (not an otitis externa), Pinnal lesions well-
demarcated rather than diffuse. Feet, footpads and groin also often involved. Footpads -
ameness and hyperkeratosis but affection of only footpads pads rare. Can mimic
pyoderma (pustules, crusts) pain/ pruritus - variable (not usually as pruritic as allergic
patients).
• Pruritus with any form varies from non-existent to moderately intense. The pruritus is
usually noted AFTER the development of crusted lesions, whereas an allergic patient is
typically pruritic BEFORE the development of crusted lesions. Systemic signs uncommon
.Secondary pyoderma may be present, but the patient usually feels good
• Differential diagnosis would include any pustular, crusting and scaling disease such as:
pemphigus erythematosus; zinc responsive dermatosis (especially with foot pad
involvement); metabolic epidermal necrosis (especially with foot pad involvement);
bacterial and fungal (dermatophytosis) infections; demodicosis, DLE (facial/nasal form);
erythema multiformae; mycosis fungoides; Leishmaniasis; and sebaceous adenitis.
Diagnosis:
• Clinical signs. CBC, Serum chemistries, UA – usually normal but rarely some inflammatory
changes will be present - hyperglobulinemia ± hypoalbuminemia, Leukocytosis due to
neutrophilia. Antinuclear antibody test (ANA) - negative
• Cytology – from pustule or crust - acantholytic keratinocytes, either individually or in
clusters, surrounded by non-degenerative neutrophils and/or eosinophils- bacteria
should not be seen (unless secondary Pyoderma).
• Histopathology is the only definitive means to diagnose pemphigus- subcorneal vesicles
or pustules containing acantholytic cells, neutrophils ± eosinophils. An intact pustule (or
if none are present, a crusted lesion) should be biopsied. do not scrub the biopsy site.
Instead, gently clip the biopsy site while avoiding the removal of surface crusts. The biopsy
site can then be gently blotted with alcohol. Discontinue steroids for at least one week
before biopsy
• Some occasions acantholytic cells may be present in a pyoderma (but will have bacetria
and degenerative neutrophils) or Trichophyton mentagrophytes (use Periodic acid-Schiff
(PAS) stain to differentiate)
• Immunofluorescence testing - primarily for research purposes, Indirect IF test is not
sensitive and reliable
• Therapy - There is no “best” treatment that works for all PF patients so treatment must
be individualized for each patient. Most cases can be successfully treated or managed,
while some may fail to respond The total duration of immunosuppressive therapy varied
between few months and few years. Prognosis is variable and many dogs may stay in
remission for months to years. Prednisolone alone or with azathioprine are frequently
used combinations. Topically steroid and /or Tacrolimus may be tried

Pemphigus Vulgaris
• Antibody targets desmoglein3, Dsg3 and possibly Dsg 1 -strongly expressed in the supra
basilar keratinocytes and mucous membranes and autoantibody deposition just above the
basement membrane zone results in ulcer formation
• Rare disease with a very poor prognosis and Most severe form - lesions are deeper than those
associated with Pemphigus foliaceus
• Vesicles, bullae rare ,Ulcerative lesions, erosions, epidermal collarettes, blisters, and crusts
Deep lesions are painful and the secondary systemic signs -pyrexia, anorexia, depression.
• Distribution may involve: High percentage of patients will present with oral ulceration and
may precede skin lesions, often the chief complaint. nasal planum, ear pinnae, foot pads and
the oral cavity (80% of cases, mucocutaneous junctions, claw folds, axillary and inguinal
region—areas of friction especially.
• DD- Bullous pemphigoid, Epidermolysis bullosa , Drug eruption, Stevens–Johnson syndrome
and toxic epidermal necrolysis, Systemic lupus erythematosus , Cutaneous neoplasia and
Mucocutaneous candidiasis
• Diagnosis Immunofluorescence and immunohistochemistry, Cytology - Acantholytic cells,
neutrophils, few bacteria ANA negative
Pemphigus Erythematosus
• Autoantibody targets Desmoglein-1 and antigens expressed on epidermal cells

• Benign/Mild form of Pemphigus foliaceus with some similarities to discoid Lupus
Erythematosus
• Lesions - similar to PF but restricted to Face and ears in majority of cases. ANA may be
positive
• Depigmentation of the nasal planum, dorsal muzzle, lip margins, and eyelid margins
common, and may precede crusting No oral or mucosal lesions.
Lupus Erythematosus
These autoimmune diseases will have distinctly different clinical presentations but may have
similar pathogenesis and histopathologic findings. Typically these diseases are divided into those
with systemic symptoms and a poorer prognosis, in contrast to those with only cutaneous
involvement, which are considered more cosmetic diseases.
Systemic Lupus Erythematosus
SLE is considered to be an uncommon multi-system disease affecting dogs and cats SLE is a
generalized connective tissue disorder with presence of antinuclear antibodies. The dog
spontaneously develops autoantibodies to nuclear proteins resulting in a Type III (immune
complex) hypersensitivity reaction. The immune complexes that form lodge in small vessels and
cause small vessel. Vasculitis with anoxia of the tissues beyond the vascular damage. Therefore
all organ systems are affected (joints, skin, bone marrow, kidney, etc.). Approximately 40-50 %

of dogs with systemic lupus erythematosus (SLE) present with skin lesions, these can include
erosions, ulcerations, depigmentation, vasculitis, panniculitis and disordered epidermal
maturation manifesting as scaling/ hyperkeratosis. Some animals do not have skin lesions at all.
And Patient is usually sick Systemic manifestations include glomerulonephritis, Polyarthritis,
Hemolytic anemia, Fever, renaldiseases, Pericarditis ,myocarditis, Pneumonitis, pleuritis,
Polymyositis, Neurologic disorders, Lymphedema RBC, WBC, platelet abnormalities, Bone
marrow abnormalities with the potential for a spectrum of other system involvement.
Cutaneous manifestations of lupus (with or without systemic signs)
The insult to the skin in these diseases is the basal epidermal layer. Depending on the severity of
the disease separation and ulceration may be present or local inflammation can result in
depigmentation and disruption of the normal epidermal contours. Sunlight may be involved in
the pathogenesis. The classic histopathological finding on examination of the skin is an “interface
dermatitis”, that is damage to the cells of the basal layers of the epidermis evident on
histopathology. Special techniques can be used to demonstrate immunoglobulin deposition at
the dermo-epidermal junction.
The initial lesions are small, hairless, erythematous, and scaly. With time, the lesions enlarge in
size and depth and become crusted and ulcerated. These lesions always heal with scarring. The
active and scarred lesions are temperature- and photo- aggravated. Animals can develop any kind
of skin lesion from chronic, mild skin lesions to severe, deep and potentially life threatening
disease. Vesicular/bullous , Variable pruritus, Vasculitis, Oral lesions similar to PV and BP,
Seborrheic disease, Alopecia, Diffuse or regional erythema , Footpad ulcers and hyperkeratosis,–
onychodystrophy, Panniculitis, Refractory secondary pyoderma etc
Diagnosis : is made by skin biopsy, standard hematologic and biochemical tests, serology (ANA
titer), and the exclusion of all other possibilities. Serology for all of the infectious disorders
present in the region is mandatory as is a complete drug history with withdrawal of suspect
agents, especially potentiated sulfa antibiotics. Finding LE cells ( neutrophil containing an
engulfed mononuclear cell) are not diagnostic
American Rheumatism Association Guidelines: Modified criteria for diagnosis: Erythema, discoid
rash, photosensitivity, oral ulcers, arthritis, serositis, renal disorders, neurologic disorders,
hematologic disorders, immunologic disorders, antinuclear antibodies. SLE likely using four
modified criteria experienced during any observation period and probable SLE using 3 modified
criteria with positive ANA. However, these are not reliable always (Non-erosive polyarthritis, Skin
lesions, Coombs positive anemia Thrombocytopenia, Glomerulonephritis (proteinuria),
Polymyositis, Marked neutropenia ANA positive)
DD : Pemphigus foliaceus, pemphigus erythematosus,Drug reactions, erythema multiforme, and
toxic epidermal necrolysis,: infectious conditions; Insect hypersensitivity: Metabolic epidermal
necrosis, and Infectious diseases
Treatment is lifelong. Photoprotection is mandatory. Treatment with steroids , Tetracycylines &
niacinamide will help improve the skin lesions but will have no effect on the kidney, joint, or
other systemic problems. Pentoxifylline will help the lesions everywhere but probably won't

entirely resolve the visceral lesion. Typically azathioprine or cyclosporine is added to maintain
maximum control of the disease and also Gene therapy using recombinant canine CTLA-4 and IgA
domains tried
There appears to be a subset of this group of diseases, which can have focal or more generalized
areas of skin, affected (cutaneous lupus erythematosus). The disease may be limited to the
mucocutaneous junctions or nasal planum or be more generalized such as is seen in the rare
ulcerative dermatosis disease of Shetland Sheepdogs and Collies (vesicular cutaneous lupus
erythematosus – VCLE). These dogs have no demonstrable systemic involvement and
characteristic histopathological findings as described. Exfoliative CLE in German short haired
pointers- scaling and alopecia on muzzle, pinnae and dorsal trunk- may involve limbs and ventra
trunk with lymhodenopathy
Discoid (cutaneous) lupus erythematosus

Second most common autoimmune disease after PF and Similar to Systemic Lupus
Erythematosus but so systemic signs and confined only to skin. classically describes a
depigmenting ulcerating disease of the nasal planum, occasionally involving the periorbital skin
and bridge of the nose. May look similar to PE. The normal cobblestone appearance of the nose
is lost. No systemic involvement occurs. Middle aged German Shepherd dogs and Collies are
predisposed. The condition is photo aggravated and unprotected exposure to sun light will
accelerate the progression of the condition and decrease the response to therapy. Clinical lesions
range from mild to severe.
Diagnsosis – Unique location and lesion make easy for diagnosis but must be differentiated from
mucocutaneous pyoderma. Collie nose or Nasal solar dermatitis could be DLE. Therefore treat
with appropriate antibiotics for at least 3 weeks before skin biopsies are undertaken. Other
diffrentials includes Actinic dermatitis, Dermatophytosis, Nasal pyoderma Demodicosis,
Pemphigus complex, Drug eruption, Systemic lupus erythematosus, Uveodermatologic
syndrome, Proliferative nasal arteritis/vasculitis, Parasympathetic nasal dermatitis, Idiopathic
nasal depigmentation and Proliferative arteritis of the nasal philtrum
Topical therapy includes steroids, tacrolimus and sunscreen. Systemic glucocorticoids with
tetracycline / niacinamide, Vitamin E, fatty acids also has been proposed for mild cases. Biopsies
may be non-diagnostic in chronic cases.
Uveodermatological syndrome
This is a very rare dermatosis similar to a disease in people called Vogt- Koyanagi- Harada (VKH)
syndrome.common in young to middle age dogs of Akitas, Samoyeds and Siberian Huskies are
predisposed. Reported in Chow Chow, GSD Dachshund and other breeds The disease is caused
by an immune mediated attack on melanocytes. Histological examination of an affected area will
demonstrate the loss of melanocytes from the basal epidermis accompanied by an histiocytic
interface dermatitis.
This is characterized by depigmentation of the skin and mucous membranes in some cases
progressing to ulceration. The cutaneous lesions are accompanied by ocular changes; corneal
edema, sudden onset uveitis, blepharospasm, conjunctivitis and lacrimation cataract to
blindness. Patchy leukotrichia may be present around depigmented areas and subsequently
leukoderma of the nose, lips, and eyelids. If overlooked the ocular disease can progress to

complete blindness - early diagnosis and therapeutic intervention is indicated. Must be
differentiated from pemphigus complex, SLE, DLE, bullous pemphigoid, vitiligo and vasculitis
Treatment of ocular lesions should be instituted as soon as possible as the course of the disease
is acute and irreversible damage may result. Oral Steroids and or Cyclosporine as well topical
steroids and cycloplegics for uveitis
Toxic epidermal Necrolysis (TEN)/ Stevens-Johnson syndrome(SJS) / Erythema multiforme (EM)

This group of diseases represents a spectrum of severity of diseases that share similar pathogenic
mechanisms. The chief underlying pathomechanism is a cytotoxic response by CD8+ T
lymphocytes and natural killer cells directed against keratinocytes, whose antigenicity is altered
by infectious agents or drugs. Apoptosis results largely from direct cellular cytotoxicity (EM) or
by actions of soluble mediators of cell death (SJS/TEN). The soluble mediators include Fas ligand,
granzymes, perforin and, most importantly, granulysin. The relationship of EM, SJS and TEN in
veterinary dermatology has also been controversial and no clear census exits at present and
further Histopathological lesions do not reliably differentiate EM, SJS and TEN.
Lesions- Typical target lesions- round and well defined borders and three zones of color-
erythematous or purpuric centre followed by lighter raised erythema and another eryhtemtous
ring. Other lesions are raised and edematous atypical target with only two zones or flat atypical
target lesions without raised erythema or Macular lesions.
Toxic epidermal necrolysis is a severe, extremely rare life threatening drug reaction in which full
thickness epidermal necrosis occurs with minimal inflammation. Patients need intensive care
treatment.
In erythema multiforme an interface dermatitis is accompanied by single cell necrosis/apoptosis

of cells(epidermal /follicularcells) in the epidermis. Clinically this presents with erythematous
macules that spread peripherally (EM minor). Urticaria, vesicles, bullae and ulceration can also
occur. Lesions can be local or generalized. More severe forms involve the mucous membranes
(EM major, Stevens-Johnson syndrome). EM minor and EM major are most commonly idiopathic
or associated with infections and neoplasia, whereas Generalized EM and SJS/TEN is clinically
similar in people and animals and is mostly triggered by drugs; occasionally by infectious agents.
SJS- Lesions includes Erythematous or purpuric, macular or patchy eruption Epidermal

detachment <10%. Distribution of lesions - Trunk, often axillary and inguinal, mucocutaneous
junctions, generalized trunk and Face. Severe mucosal involvement with systemic signs reported.
TEN- Erythematous or purpuric, macular or patchy eruption Epidermal detachment >30%. Trunk,
often axillary and inguinal, mucocutaneous junctions, generalized
Management of TEN/SJS- Drug withdrawal, Immunosuppressive therapy- glucocorticoids,
azathioprine, Cyclosporine, Intravenous immunoglobulin

Erythema multiforme
A significant number of EM cases in animals are idiopathic. Drug reactions account for between
19 and 59% of canine in 2 reports
EM Minor – believed to caused by Drugs, dietary, vaccine or idiopathic. Wide range of lesions -
Erythematous macules or papules, often crusted; raised or flat targetoid lesions, typical targets
rare, polycyclic, arciform, erythematous or purpuric lesions (<50%), vesicles, bullae, ulcers,
urticarial, scaly erythematous macules, papules, plaques(hyperkeratotic ‘EM’), alopecia
(follicular ‘EM’), generalized scaling. Mucosal involvement restricted to not more than one.
Lesions typically seen in Trunk , often axillary and inguinal, mucocutaneous, head, generalized.
NO systemic signs
EM Major- drugs or infection may be cause. Flat or raised, focal or multifocal polycyclic, targetoid
(rarely typical) lesions; erythematous or purpuric macular or patchy eruptions; <10%
detachment. Mucosal involvement more than one. Distribution of lesions are similar to EM
minor but with Systemic signs
Management of EM - Drug withdrawal in appropriate cases, Immunosuppressive therapy in
refractory cases. Azathioprine, glucocorticoids, Pentoxyphylline, cyclosporin
Vasculitis
Vasculitis is characterized by an aberrant immune response directed toward blood vessels. It is a
cutaneous reaction to multiple causes and therefore always look for an underlying disease or
factor that may have incited the immunological attack. It has been hypothesized that cytokine-
mediated changes in the expression and function of adhesion molecules together with
inappropriate activation of leukocytes and endothelial cells are key factors influencing vessel
inflammation and damage.(Type II or III hypersensitivity ?)
Some causes are bacterial, viral, fungal or Rickettsial infections – Ehrlichiosis or bacterial sepsis
(either induced by direct invasion of the vessel walls by the pathogen or as a result of immune
complex formation (type III hypersensitivity), autoimmune disease such as systemic lupus, cold
agglutinin disease and neo-antigens incited by vaccination, drugs or neoplasia.
Cutaneous small vessel vasculitis affects small dermal vessels especially the post capillary
venules. This is the most common form of canine cutaneous vasculitis. It could be neutrophilic
leukocytoclastic, neutrophilic non-leukocytoclastic, lymphocytic, eosinophilic or granulomatous.
Clinically, vasculitis can involve just the skin or there can be systemic involvement (eg uveitis,
glomerulonephritis, hepatopathies, synovitis-arthritis, gastroenteritis, pleuritis/pericarditis)
and/or due to the underlying disease (eg anemia and/or thrombocytopenia with SLE).
If superficial vessels affected – may be present as Focal alopecia, scaling, alopecia, purpura
(bleeding into the skin manifested as petechiation and/or ecchymoses), ulcers, wheals, nodules,
dependent edema, acrocyanosis, and panniculitis. Usually seen in extremities –paws, tail, ear
tips, nose. In some cases, the claws may be affected and exhibit signs of onychodystrophy,
onychomadesis, petechiae, and exudate within the claw. Erosive, ulcerative or hyperkeratotic
lesions may affect the pads. Pitting edema may also be present
The “classic” lesion of vasculitis is a circular punched out defect representing the segment of skin

supplied by the affected vessel (deep vessel arteritis). Scarring or foacl alopecia or
depigmentation is common with healing
Vasculitis may be demonstrated on skin biopsies from recently affected areas. It is important to
take multiple biopsies, avoid ulcerated skin and alert the pathologist to the possibility of vascular
disease. It is a diagnosis that can have very subtle changes on histopathology.
There are a number of subtypes of vasculitis/vasculopathy including
• Urticarial vasculitis that represents a peculiar subset of small vessel vasculitis. - lesions
are slow to resolve, - frequently associated with cutaneous adverse food reaction.
• Proliferative thrombovascular necrosis of the pinna - begin on the pinnal tip and spread
proximally on the concave surface. - ulcers, crusting and scaling present.
• Cutaneous vasculopathy in German Shepherd - Rare ?
• Proliferative arteritis of the nasal planum – reported only in Saint Bernards and Giant
Schnauzer. - linear ulcers on the nasal planum , non-pruritic.
• Idiopathic cutaneous and renal glomerular vasculopathy in racing
• Vasculitis of Scottish terrier
• Vasculitis of Jack Russell Terriers
• Dermatomyositis - in collies and shelties or spontaneously in adults of other breeds. -
usually before 6 months of age. - alopecia, scaling, crusts, erosions, ulcers,
depigmentation, hyperpigmentation and scarring. These lesions occur on the face,
mucocutaneous junctions, carpal and tarsal regions and the tip of the tail and ears. Some
may megaesophagus or muscle atrophy involving the muscles of mastication and
ambulation.
• Post rabies vaccination alopecia – lesions develop 2-12 months after administering a
rabies vaccine. scaling, alopecia, plaques, hyperpigmentation, nodules, erosions, crusts
and cutaneous atrophy (scarring).
Diagnosis - history , identification of primary lesions, distribution of lesions, laboratory testing

(Tick titers, blood, tissue or urine cultures, Coomb's test, ANA) and therapeutic trials. thoracic or
abdominal radiographs or ultrasound. HP is most useful in early stages
Therapy - The first step is to identify and treat the underlying cause if known and/or avoid it (eg
drug induced). Depending on the severity of the symptoms therapy may include: pentoxifylline,
glucocorticoids,Vitamin E, Omega fatty acids, Tetracycline/Niacinamide Azathioprine,
Chlorambucil when azathioprine fails. Cyclosporine can be addition and Dapsone and food trial
Examples of Subepidermal Blistering disease
A. Bullous Pemphigoid : Blisters are not common in dogs and usually results in ulcers or erosions.
Autoantibodies (usually IgG) are directed against a component of the basal hemidesmosome
(Bullous pemphigoid antigen, BPAG- collagen XVII). Activation of complement with subsequent
cellular infiltration are essential for the pathogenesis of the lesions (unlike Pemphigus) - loss of

dermo-epidermal cohesion followed by epidermal separation and vesicle formation.
Idiosyncratic drug reactions may also play a role in the pathogenesis of bullous pemphigoid.
Lesions: similar to Pemphigus vulgaris. Head, ears, axillae, ventral abdomen, Inguinum. Majority
of lesions in Oral cavity (~80% of cases)- to ulcerations of the oral cavity and lip margins. Patient
is usually sick. Cytology- Purulent inflammation and NO acantholysis. Differentials includes
Pemphigus vulgaris, Epidermolysis bullosa acquista, Systemic lupus erythematosus, Vesicular
cutaneous lupus erythematosus, Drug eruption (Stevens–Johnson syndrome and toxic epidermal
necrolysis) and Cutaneous neoplasia
B. Mucous Membrane Pemphigoid - Most common blistering disease targeting variable antigens
of the basement membrane zone like collagen XVII. Common n German shepherds and husky
breeds. Most cases are in Adults and slow progression and symmetrical affecting mucosa. In a
recent review, dogs exhibited erosions and ulcers in the oral cavity ( 69%), nasal (56%), periocular
(50%) and genital 38%) regions. Haired skin lesions were less frequent (38%) and involved mostly
concave pinnae. Treatment regimens varied widely but six of 60% dogs received a combination
of tetracycline and Nacinamide (Tham et al (2016) Vet derm Vol 27, 5 376–94)
Both above diseases requires Histopathology, cytology, and direct and/or indirect
immunofluorescence tests to support diagnosis
Principles of therapy of cutaneous immune-mediated and autoimmune diseases ( Please refer

the table for drugs and doses)
There are many recommendations and treatment schedules for management of these diseases.
In practice the dose and regimen often has to be tailored for the particular individual. Primary
objective is to stop the inflammation and immunological destruction without causing side effects
that the patient and client will not tolerate
• Never institute treatment without having a definitive diagnosis
• Use the least potent drug or combination of drugs that will control the disease-
Combination drug therapy is generally more effective and has fewer side effects than
monotherapy. Monotherapy is generally with low immunosuppressive dose of
glucocorticoids.
• Mild or localized cases may initially be treated less aggressively - relying on more topical
therapy.
• Clients should be advised that some dogs may be cured or reach long-term remission,
depending on the cause and even when no cause if found there may be some chance for
cure, though controlled studies providing prognostic statistics are lacking for most
immune mediated diseases.
• Monitor the animal regularly for side effects/ toxicity of drug therapy -The side effects of
therapy should be acceptable to the client and not adversely affect the patient
• Regular monitoring of a CBC and chemistry panel will be necessary.
• Don’t assume that when lesions recur that it is the same disease - Secondary pyodermas,
yeast infections and demodicosis are potential complications in these immuno-
suppressed animals.
• Clinical signs should improve by 50-75% within 1 month of starting treatment

• No new lesions should be noted after 3-4 weeks of therapy.
• Azathioprine and cyclosporine are two systemic drugs often combined with the steroid
for PF in dogs
Planning the therapy
• Induction phase - is selected to stop the inflammation and suppress the immunologic
response against the epidermis. The response is generally good with drying of lesions
with no new pustules or erosions and patient will show improvement in overall attitude.
This phase generally required higher dosed of immunosuppressive drugs. If the response
is poor in first 2 weeks time, then a different induction treatment should be selected.
• Transition phase - involves tapering the drugs to reduce risks of toxicity or adverse
reactions as well as the cost. All medications are slowly tapered until there is a recurrence
of clinical signs. Taper the drug which is more likely to cause side affects when using
combination therapy
• Maintenance phase – Maintenance doses are the lowest doses that result in a stable
degree of disease that is acceptable to the client and clinician. Medication doses are
raised again sufficiently to reinduce remission when ever recurrence occurs and then
doses are maintained at the level reached prior to the recurrence.
Summary of approach to Ulcers and erosions based on location
• NO Pruritus - Rule out Trauma, Caustic agents, Thermal injury , Drug reactions.
Impression smear or cytology to rule out Demodex, Infection or Neoplasms
• Focal – Lipfold pyoderma, Calcinosi cutis, Neoplsam, Pyotrumatic dermatitis ( Hot spot),
Fungal Keroin
• Nasal and Facial- DLE, Squamous cell carcinoma, UV syndrome, PF/PE, Dermatomyositis
• Axillary/Inguinal- Bullous Pemphgoid, SLE, Skin fold pyoderma, TEN/EM, Drug reaction,
Urine scald
• Mucocutaneous- Bullous Pemphgoid, SLE, TEN/EM, Drug reaction, Uremia
• Large or regional - Demodicosis, fungal, drug reactions, SLE, TEN/EM, Deep Pyoderma,
GSD pyoderma
Uncommon diseases causing Nodules and draining tracts
A nodule is a circumscribed elevation of the skin greater than 1cm diameter. Nodules are formed
by a localized cellular or fluid infiltrate of the dermis and / or subcutis which may be inflammatory
or neoplastic. May manifests as multifocal areas of punctate ulceration through with draining
sinus tracts.
Nodular diseases can be broadly separated into:Infectious, Non Infectious and neoplastic
Diagnostic approach – Cytology, Histopathology ad culture

Infectiuous causes - Fungal, Mycobacteria, Deep pyoderma (pressure point), Leishmania,
Pythium, Acral lick dermatitis, Botryomycosis, Nocardia, Actinomyces, Actinobacillus
Noninfectious/sterile- Foreign body, Nodular panniculitis, Eosinophilic granuloma, Sterile
pyogranulomas, Cysts, Acral lick dermatitis, Histiocytoses
Neoplastic - Mast cell tumor, Basal cell tumor, Cutaneous lymphoma, Glandular tumors,
Histiocytoma, Other tumors and Sarcoid
Infectious nodular diseases

Primary or secondary - Present as chronic - unresponsive to routine antibacterial treatment..
Deep pyoderma (bacterial furunculosis) : draining sinus tracts arise from the development of a
folliculitis into a furunculosis. Staphylococcus pseudointermedius is the usual pathogen although
other opportunistic bacteria may become involved. Deep pyoderma may be generalized or
localized. Remember that RECURRENT pyodermas are usually considered secondary to an
underlying disease until an exhaustive search has suggested otherwise. Examples -
Folliculitis/furnculosis associated with demodicosis, Acne, Callus pyoderma, Breed associates –
German shepherd and English bull terrier, Acral lick
Deep pyoderma is less common than superficial pyoderma however, it is a more serious disease
and warrants aggressive investigation and management. Affected dogs may be febrile, anorectic,
and painful and have a marked reactive local lymphadenopathy. Rupture of the hair follicle
results in liberation of follicular cells and hair shaft fragments into the dermis where they are
perceived as foreign and a pyogranulomatous reaction results.
Failure to response to routine antibacterial therapy should alert you to the possibility of an
unusual infection. Examples are Dermatophyte Keroin (nodular dermatophytosis), subcutaneous
or systemic fungal diseases, actinomyces or Nocardia, Mycobacterial or anaerobic infections
Non-infectious (sterile) nodular diseases

Cellular debris and hair shafts or calcium deposition in dermis or subcutis may act as foreign
body durig folliculitis or furnculosis A sterile reaction may also be initiated by bacterial or viral
antigens,
Sterile panniculitis/Sterile Nodular pannicultis

Idiopathic sterile inflammation of the hypodermis (panniculitis) has been recognized in dogs.
Some of these cases have been associated with lipase releasing pancreatitis or pancreatic tumors.
Panniculitis is an inflammatory condition of subcutaneous fat with a wide variety of causes and
clinical presentations. These causes include infection, trauma, foreign body, postinjection site
inflammation, vasculitis, nutritional (vitamin E deficiency), drug eruption, insect bite, neoplasia,
and sterile nodular panniculitis. Lesions often present as deep nodules with or without clinically
observed draining tracts, fistulae and ulcers. These lesions can be confused with deep
pyoderma, cutaneous neoplasia or a cutaneous cyst. Clinical signs consist of firm to fluctuant
nodules that rapidly evolve into tracts draining a lipid-rich material. Single or multiple deep, soft
to firm nodules. The most common gross lesions reported are cutaneous and subcutaneous
nodules. Most cases (84.6%) will have multiple lesions, the majority of which are found on the
trunk and neck. In previous studies, the majority of dogs with SNP had multiple lesions. In another

study study, 83% of dogs with SNP had lesions on the trunk and 33.3% had lesions on the neck
and ventral cervical area (Yamagishi et al. J Vet Med Sci 2007; 69: 915–924 and O’Kell et al. J Vet
Intern Med 2010; 24: 278–284) The lesions may ulcerate and develop draining tracts. They
discharge an oily, yellowish-brown to bloody fluid .There were no correlation between
inflammatory patterns of panniculitis and other histological and clinical factors (Contreary et al
Vet Dermatol 2015; 26: 451–e105)
Most dogs will have systemic signs, such as fever, inappetence, lethargy, and multiple lesions.
Common clinicopathologic findings included neutrophilia with or without left shift, increased
alkaline phosphatase activity, mild hypoglycemia, hypoalbuminemia, and proteinuria.
Concurrent diseases includes pancreatic disease, SLE, rheumatoid arthritis, polyarthritis,
lymphoplasmacytic colitis, and hepatic disease.
Common differentials are abscess, Cutaneous bacterial or fungal granuloma, Deep bacterial
folliculitis and furunculosis, Cutaneous mycobacterial infection, Deep mycotic infections,
Cutaneous cysts Infestation, Cutaneous neoplasia, Foreign body reactions
Once infections and pancreatic pathology have been ruled-out, then corticosteroid therapy
(immune-suppressive doses) may be beneficial. Corticosteroids with combination of a
tetracycline antibiotic, usually doxycycline and niacinamide, Cyclosporin, Azathioprine, and
chlorambucil and Vitamin E can be tried.
Juvenile cellulitis (Puppy strangles)

Juvenile cellulitis is a common disease of puppies. The mechanisms of lesion formation have not
been characterized precisely. Attempts to isolate or characterize infectious agents have
remained unsuccessful. Large coalescing pustules and suppurative (abscessing) lymphadenitis
develop rapidly on the anterior aspect of the body. There is usually marked swelling of the face.
Multiple puppies in a litter may be affected. This diseases may be confused for Angioedema
Demodicosis, Pyoderma, Pemphigus foliaceus and Adverse drug reaction. Definitive diagnosis
involves histopathology. Once an infection has been ruled-out, the treatment of choice involves
prednisone (1-2 mg/kg per os daily) until lesions resolve (14-21 days). If there is concern about
sepsis, then antibiotics should be given.
Sterile pyogranulomas and granulomas
Occasional sterile pyogranulomas/granulomas develop on the skin of dogs and cats. These may
represent an abnormal immune reaction to an infectious agent or other antigen. Reported in
Great Dane, Boxer, Golden Retriever, Collie, and Weimaraner. The lesions may appear as non-
painful, papules, nodules that occur commonly on the head ( bridge of the nose and the muzzle)
and also pinna, neck, trunk, and extremities. Once an infection has been ruled out by
conventional methods, treatment involves corticosteroid therapy as needed to control the
symptoms. Tetracyclines with Niacinamide, Azathioprine and cyclosporine has also been used by
some dermatologists.
Eosinophilic collagenolytic granulomas
Sterile eosinophilic plaques and nodules have been recognized in dogs, cats and horses. In cats,
they have been reported in association with allergic dermatoses. In dogs, the disease is more
prevalent in the Husky breed. Treatment involves corticosteroids.

Metatarsal fistula
Believed to immune mediated - circulating antibodies to types I and II collagen ? reported
commonly in German Shepherd Dogs, but can occur in crossbreeds or other breeds. Presented
initially as soft swelling in the skin that may lead to single or multiple tracts containing a
serosanguineous discharge. Most cases appear on the plantar metatarsal skin surface just
proximal to the metatarsal pad of both hindlimbs. The condition can be part of the German
Shepherd Dog pyoderma syndrome. Therapy includes steroids, cyclosporine, Oxytertacycline and
Niacinamide and topical tacrolimus. Antibiotics for secondary infections.
Recurrent Inter-digital cysts / Recurrent inter-digital pyogranuloma
Common in American Staffordshire terriers and bull terriers, Labrador retrievers ,Great danes
etc. There is a failure to respond to antibiotic; new draining lesions develop while on antibiotics
Cause not known but believed to be inflammatory response to keratin and triglycerides liberated
from ruptured hair follicles, sebaceous glands, and the panniculus. Interdigital dermatitis
(pododermatitis, pedal folliculitis and furunculosis, interdigital furunculosis) in dogs is a
multifaceted disease that is often recurrent and difficult to diagnose and treat. Causes are varied
and include exogenous foreign bodies, contact irritants, hypersensitivity reactions, parasitism
(demodicosis, hookworm dermatitis, Pelodera sp. dermatitis), infections with yeast, fungi, and
bacteria, and disorders associated with immunosuppression. Lesions consisting of multiple
comedones and follicular cysts in palmar or plantar (ventral) interdigital skin that result in sinus
tracts that open and drain on the dorsal interdigital skin surface giving the false impression that
lesions develop dorsally (Doclas et al (2008), Vet Derm Vol 19,3, P 134-141)
Most dogs have history of that this problem started at a young age (1–3years). The clinical lesions
consist of recurrent nodules that are erythematous, and ulcerate and drain a purulent to
serosanguineous exudate and this condition have no other clinical disease and only the recurrent
interdigital draining tracts. The front feet are most commonly affected with interdigital space
most often affected in the lateral space between digits IV and V.
Suggested Therapy for Recurrent Inter-digital cysts (following complete investigations and
ruling out of common causes)
• Antibiotics : control with Cytology : Intracellular bacteria : Fluroquinolones
• Cyclosporine, Vit E,
• Tetracycline + Niacinamide
• Retinoids (Isotretinoin - Isotane, Isac, Isotrion 10,20mg caps)- Sebaceous adenitis,
ichthyosi s 1-3 mg/Kg Q24 h, Etretinate-Idiopathic seborrhoea, S. adenitis.0.75-1mg/Kg
Q24 h
• Pentoxyfylline 10mg/Kg ( Rx Flextal, Flopent, trental 400mg tabs)
• Topical : DMSO, Sodium fusidate( (fucidin,siofin cream) Mupirocin ( T-bact cream), Benyl
peroxide, 0.3% tacrolimus and interferon 2 alpha (Virbagen omega from Virbac :1.5 - 2.5
x106 units/Kg IV for 3 days, Once a week SC or buccal mucosa spray. Human prep in India
- Veraferon, Zavinex 3/5 million units).
• Fusing Podoplasty
• CO2 laser ablation of the ventral cysts

Neoplastic nodular skin diseases
Neoplasia is a very important differential for nodular skin diseases and often cannot be
differentiated from inflammatory skin diseases on clinical grounds. The most common skin
tumors are sebaceous adenomas, mast cell tumors, squamous cell carcinomas and cutaneous
lymphosarcomas. Be familiar however, with the cytological findings that might support a
diagnosis of neoplasia.
Cutaneous epitheliotropic T-cell lymphoma (CETL) including mycosis fungoides, Se´zary

syndrome,and pagetoid reticulosis, is defined as a spontaneous neoplasm of skin and mucous
membranes in which neoplastic T lymphocytes infiltrate the epidermis and adnexal structures. All
lymphomas (epitheliotropic and non-epitheliotropic) combined represent only 1% of canine skin
tumours and cutaneous lymphomas represent only 3 – 8% of all canine lymphomas. The average
age at onset is 9-11 years which should be the first clue when trying to distinguish from allergic
disease. Several clinical forms or manifestations will occur in the dog and include an exfoliative
erythroderma, plaques and nodules, ulcers or erythema of the oral mucosa and mucocutaneous
lesions. An exfoliative erythroderma is defined as erythematous scaly skin along with alopecia
and potential hypopigmentation. The pruritus can be variable but up to 50% of the patients with
a CETL are pruritic which is why it is misdiagnosed as allergic disease. The case may be preseted
in any form as A - Pruritus and erythema with scaling, depigmentation and alopecia, B -
mucocutaneous inflammation with erythema, depigmentation, and ulceration, C- solitary or
multiple plaques or nodules that may be covered with scale or crust and D- oral with ulceration
of the gingiva, palate, or tongue.
Percentage of lesion reported in a study includes Erythema (80.8),Plaques (61.5) Scaling (61.5)
Nodules (57.7) Erosion/ulceration (42.3) Crusting (38.5)Mucosal lesions (38.5) Pruritus (38.5)
Papules ( 15.4) (Beale et al Advances in Veterinary Dermatology , Vol. 2, 1993 : 273 – 284 ).
Diagnosis is based on histopathology although cytology of lesions will sometimes reveal
numerous lymphocytes which raise the index of suspicion for CETL and further mandate biopsies.
Biopsies of scale, plaques, hypopigmentation or significantly erythematous lesions are the best
for sampling. The differentials are Atopic dermatitis, Yeast infection, Cutaneous adverse food
reaction, Mucocutaneous pyoderma, Pemphigus vulgaris, Bullous pemphigoid, Lupus
erythematosus and stomatitis. The long-term prognosis of CETL is poor with an average survival
time of six months after the diagnosis is made. Treatment is not known to extend the survival
rate, but is known to improve the quality of life. Retinoids, cyclosporine, Fatty acids, L-
asparaginase etc have been tried but steroids and lomustine are two of the drugs of choice when
treating CETL.
Other uncommon diseases

Vitiligo
Vitiligo is a disease in which immune cells target melanocytes in the skin leading to
depigmentation. Common in “young dogs” and breeds like Rottweiler, Doberman, GSD and collie.
As this is a merely cosmetic condition, treatment is not needed. However, breeding is not
recommended, as a hereditary basis is suspected. Symmetrical Macular leuoderma with or

without leutrichia typically seen on face but nasal planum, lips, Muzzle, buccal mucosa, and
footpads. Uveodermatologic syndrome, Cutaneous lupus erythematosus, Dermatomyositis and
Systemic lupus erythematosus can also cause depigmentation in these areas. Treatment tried
with some success - Folic acid 1 mg PO BID , B12 injection at 50 microgram IM q 14 days and
Vitamin C 500 mg BID , l-phenylalanine orally at 50 mg kg SID.
Sebaceous adenitis
more common skin disease in breeds like Poodles, Akitas, Samoyeds, Chow Chows, English
Springer Spaniels and Vizslas etc. The reduced number or even complete absence of sebaceous
glands reduces sebum production, resulting in clinical signs. These include a dry, brittle hair coat,
scale, follicular casts and alopecia. Frequently seen in young to middle age presented as nodular
to plaque with scales and alopecia. The clinical disease differs in short-coated versus long coated
breeds of dogs. In the short coat dogs – nodular with multifocal annular and serpiginous areas
of alopecia and fine white scaling. The head and pinnae are usually the first areas involved, and
the condition often progresses to involve the trunk. The condition tends to give the dogs a ‘‘moth-
eaten’’ appearance. In long hair coat - clumps of adherent scales, many adhering to the hair
shafts, and minimal alopecia, generally symmetrical and Dull brittle hair. Lesions common along
dorsal midline and dorsum of the head. Follicular cast (waxy and keratinous material attached to
the hair shafts) are common. The diagnosis of is made on the basis of the clinical appearance but
should always be backed by histopathology.
DD includes Vitamin A responsive dermatitis, Primary keratinization defects, Leishmaniasis,

Dermatophytosis, Demodicosis, Superficial pyoderma, Zinc responsive dermatosis,
Endocrinopathies, Color-dilution alopecia, Follicular dysplasia, Pemphigus foliaceus and
Epitheliotropic lymphoma, Successful management is achieved by a combination of topical
treatments with Propylene glycol ( 50 –75% in water) or Baby oil, Oral fatty acids, nutraceuticals,
Reteniods and Cyclosporine
Follicular Dysplasia and Non-inflammatory/Non endocrine alopecia

Frequent problem in dogs. the pathogenesis of this group of disorders is still unclear, and
diagnosis is based on the history, clinical findings, histopathology of skin biopsies and laboratory
findings. Histopathology findings in skin biopsies, however, are often unspecific and do not
discriminate between different hair cycle disorders.
The term follicular dysplasia is used to describe a variety of hair loss conditions which are due to
structural defects in follicular anatomy, abnormal follicular production, or abnormal follicle
cycling. The group includes Congenital Hypotrichosis or Alopecia, Black Hair Follicle Dysplasia,
Follicular Dysplasia ( Doberman Pincher, Siberian Husky Boxer, Yorkshire terriers and Silky
Terriers etc ) color dilution alopecia, Pattern baldness, Seasonal Flank Alopecia etc
Treatment - Gentle bathing with mild shampoos antimicrobial, keratolytic, and moisturizing
products tailored to the each case, Systemic antibiotics when secondary infections High-quality
diets and essential fatty acids and Melatonin

Pattern Baldness: common in dachshunds, Boston terriers, and greyhounds but reported in
short-coated breeds. Pathogenisis may be similar to as seasonal flank alopecia. Most cases will
have post-auricular region, the ventrurn, and posterior thighs. Normal puppy coat replaced with
thinner then normal adult in the affected regions and those hairs are slowly lost with increasing
age. Common rule outs are Endocrinopathies, Demodicosis Dermatophytosis, Follicular
dysplasia,Telogen effluvium and telogen defluxion. Some claims that melatonin 3mg small and 6
mg large dogs for 6 weeks improves these dogs
Recurrent Flank alopecia : recurrent episodes of bilateral trunk hair loss- abrupt onset of alopecia
with well demarcated borders usually symmetric in the flanks. Photo period may have role.
Mild alopecia of the dorsum of the nose, base of the ears, base of tail and/or perineum seen in
some cases. Infectious diseases like Demodicosis and Dermatophytosis as ell as Endocrinopathies
and Follicular dysplasia must be considered in differential diagnosis. Spontaneous regrowth of
hair may take 3 to 8 months and most may develop recurrent episodes. Frequently reported in
Boxers, English bulldog, Airedale Terrier and Schnauzer. Melatonin can be tried
Alopecia-X : Or hair cycle arrest is a relatively frequent hair growth disorder in Pomeranians and
several other breeds, ( Group of non-endorine or non inflammatory disorders includes
hyposomatotropism of the adult dog, growth hormone responsive alopecia, castration-
responsive dermatosis, gonadal sex hormone dermatoses, sex hormone/growth hormone
dermatosis, adrenal sex hormone imbalance, congenital adrenal hyperplasia-like syndrome,
follicular dysplasia of Nordic breeds, Siberian Husky and plush-coated dogs follicular dysplasia) .
characterized by symmetrical, noninflammatory alopecia without systemic signs Initially Loss of
primary hairs around the neck, tail, caudal-dorsum and caudal thighs and Gradually, all hair is lost
in trunk regions. The head and distal legs are usually spared. Breeds more at risk are the
plushcoated Nordic breeds and Poodles, Miniature poms. Currently recommended treatments
include neutering, melatonin, trilostane, deslorelin, growth hormone, mitotane and
medroxyprogesterone acetate and recently Microneedling with variable or partial clinical
success.
Color dilution Alopecia: or color mutant alopecia, uncommon skin problem in some dogs with
diluted (blue or fawn) hair coats. Most common in in blue Doberman Pinschers, but reported in
Dachshund, Great Dane, Whippet, Chow Chow, Yorkshire Terrier and Chihuahua. Presented as a
hypotrichosis involving exclusively hair follicles in the dilute areas. Initial clinical signs usually start
between 6 months or 2 to 3 years of age and most light colored dogs are almost completely
alopecic by 2 to 3 years of age. These dogs may develop follicular plugging and secondary
recurrent bacterial folliculitis. Rule out common endocrine, Follicular dysplasia, Cyclical flank
alopecia, Demodicosis and Dermatophytosis. Oral retinoids and fatty acids ,Oral antibiotic of
melatonin can be attempted
References are available upon request

Summary of the commonly used drugs used for Autoimmune or Immune mediated diseases
(Modified from the table with permission , Shumaker (2015) Canine cutaneous autoimmune
disease Veterinary Focus / Vol 25, 2, PP4 )
Drug Dosage and notes Mechanism of action Side effects

Examples of Immuno-suppressants
Glucocorticoids Prednisone/predn Decreases circulating levels Symptoms of
isolone 2.2-4.4 of T lymphocyctes; hyperadrenocorticism,
mg/kg q24H inhibits lymphokines; panting, vomiting, diarrhea,
Dexamethasone inhibits neutrophil, hepatic enzyme elevations,
0.2-0.4 mg/kg macrophage and monocyte pancreatitis, GI ulceration,
q24H. migration; inhibits lipidemias, urinary tract
Triamcinolone 0.2- phagocytosis and infections,
0.6 mg/kg q24H. chemotaxis; reduces diabetes mellitus, muscle
The above are production of interferon atrophy, behavioral changes
induction dosages
that are then
tapered to the
lowest dose q48H
(prednisone) –
72H
(dexamethasone,
triamcinolone) to
maintain
remission
Cyclosporine Induction: 5-10 Immunosuppressant: Vomiting, diarrhea,
mg/kg q24H blocks IL-2 transcription anorexia, gingival
Maintenance: 5- and T-cell responsiveness to hyperplasia, papillomatosis,
10 mg/kg q48H or IL-2; inhibits IFN-a hirsutism, bacteriuria, bone
less transcription, marrow suppression,
inhibits mononuclear cell nephropathy
function
Azathioprine Induction: 1.5-2.5 Affects rapidly proliferating Anemia, leukopenia,
mg/kg q24H cells Greatest effects on thrombocytopenia,
(Imuran, Zymurine Maintenance: 1.5- cell-mediated immunity vomiting, hypersensitivity
50mg tab) 2.5 mg/kg q48H and T-cell-dependent reactions, pancreatitis,
but can be tapered antibody synthesis. Can also elevated ALP and ALT,
to as low as 1 be used in sterile rashes, alopecia, diarrhea,
mg/kg q72H pyogranulomatous hepatotoxicity, increased
disorders, histocytic risk of infections. should not
diseases and vasculitis be used in cats

Mycophenolate Inhibits de novo purine Nausea, vomiting, diarrhea,
mofetil 10-20 mg/kg q12H synthesis and suppresses T bone marrow suppression,
and B lymphocytes and increased incidence of
(Fenograf,Mycoral production of antibodies infections
250,180,360, 500 mg
tab)
Chlorambucil Induction: 0.1-0.2 Cytotoxic effects via cross- Anorexia, vomiting,
mg/kg q24-48H linking of DNA diarrhea, myelosuppressio
(Leukeran 2 and 5 mg Maintenance: 0.1-
tab) 0.2 mg/kg q48H or
less
Cyclophosphamide 1.5 mg/kg q48H Inhibits mitosis; Sterile hemorrhagic cystitis,
Due to side immunosuppressive to bladder fibrosis,
(Endoxan-ASTA 50mg effects, often humoral and cell-mediated teratogenesis, infertility,
tab) recommended for systems, suppresses alopecia, nausea, GI
use in induction antibody production inflammation, increased
phase only; rarely infections, bone marrow
used currently for suppression
cutaneous
autoimmune
diseases
Human IV 0.25 g/kg to 2.2 Fc receptor blockade, Limited data. Acute
immunoglobulins g/kg, with infusion autoantibody elimination, hypersensitivity reaction
durations cytokine modulation,
( IV Gobulin, Gamma IV, ranging from 4 complement inhibition, and
Norglobulin, 2, 2.5,5 hours to 12 hours. Fas–Fas ligand blockade.
and 10 G ) 5–6% solution is
prepared with
0.9% NaCl.
Leflunomide 2–4 mg/kg PO q 24 isoxazole derivative that is lethargy, gastrointestinal
h metabolized to upset, and mild
( Arava, Cleft, Lefra, 10 Teriflunomide -selective bone marrow suppression
and 20mg tab) pyrimidine synthesis
inhibitor and
inhibition of tyrosine kinase
activity,
Lomustine (CCNU) 60–90 mg/m2 p.o. Interferes with the Myelosuppression is the
q21d. synthesis and function of dose-limiting toxicity -
(Lomustine 40mg cap) DNA, RNA and proteins. neutropenia
Antitumour activity Thrombocytopenia can also
Mast cell tumours and correlates best with be seen,. GI and potentially
epitheliotrophic formation of interstrand irreversible hepatic toxicity
lymphoma. crosslinking of DNA.
Others - injectable gold salts,

Examples of Immunomodulators
Tetracyclines 5 mg/kg q12H Anti-inflammatory Vomiting, anorexia, lethargy,
Doxycycline: Minocycline: 5-10 properties that affects diarrhea, increased liver
mg/kg q12H chemotaxis, antibody enzyme activity.
Response is Tetracycline: 500 mg production, complement Used with Niacinamide in
excellent in for dogs >10 kg q8H activation; down-regulates DLE, vesicular CLE, lupoid
combination with 250 mg for dogs <10 cytokines; inhibits onychodystrophy, PE, GSD
Niacinamide in 25 to kg q8H prostaglandin synthesis, metatarsal fistulae, sterile
65 % of PF and DLE lipases and collagenases panniculitis, sterile
granuloma-pyogranuloma
syndrome, vasculitis,
dermatomyositis and
cutaneous histiocytosis,
Uveodermatologic
syndrome
Niacinamide. 500 mg for dogs > 10 Blocks antigen IgE induced Anorexia, vomiting, lethargy,
Or Nicotinamide kg q12H histamine release and occasional hepatic enzyme
Niacinamide is the 250 mg for dogs < 10 degranulation of mast cells; Elevation. Avoid in dogs with
amide of niacin. kg q12H photoprotectant and seizures ?
Niacinamide is not Given q8H if cytoprotectant that blocks
niacin. administered with inflammatory cell activation
tetracycline and apoptosis; inhibits
phosphodiesterases;
decreases protease release
Pentoxifylline 10-30 mg/kg q8-12H inhibit phosphodiesterase Vomiting, anorexia, CNS

(PDE) enzymes, decreases excitement or nervousness
(Trental 400mg tab) fibronectin, reduces the
production of cytokines
(TNF-alpha, IL-1, 6 and 8),
decreases leukocyte
response to interleukins,
impairs T-lymphocyte
binding to keratinocytes,
decreases fibroblastic
activity
Dapsone 1 mg/kg q8h for 2 –3 Inhibition of the Anaemia, neutropenia,
(Vasculitis, weeks, then taper to neutrophilic-cytotoxic thrombocytopenia and
pemphigus) 1 mg/kg q12h system and interference in hepatotoxicities
for 2 weeks, and then alternate complement
(Dapsone 25, 50 and taper further to 1 pathway. decreases
100mg tab) mg/kg q24h for antibody and lysozymal
2weeks, and then 1 enzyme synthesis.
mg/kg Antibacterial- inhibits
every 48 hrs dihydropteroate synthase
in susceptible organisms.

Examples of Topical medications
Tacrolimus , 0.1% Applied 1-2 Inhibits T-cell activation and Localized erythema,
(Tacroz,Mustopic times per day then proliferation via irritation,
0.1% ) Sirolimus: taper down to less cytokinesuppression Pruritus. Owners should
frequent use Sirolimus blocks the action wear gloves
of cytokines and diverse
cellular growth factors by
affecting their signal
transduction pathways. It
also inhibits B-cell
immunoglobulin synthesis
triggered by interleukins
Betamethasone 0.1% Applied 1-2 Similar effects as with Dermal atrophy; increased
Others - times per day then systemic glucocorticoids; risk of induction of
Fluocinolone taper down to ess inhibit migration of hypothalamicpituitary-
acetonide, frequent use (ideally lymphocytes and adrenal axis suppression;
Mometasone, twice weekly for macrophages locally systemic glucocorticoid
Budesonide chronic use) effects; development of
milia and comedones; local
skin reactions
• Imiquimod topical ( Aldara® 5% cream) Indications : Topically 2-3 applications for canine Oral
papilomatosis, Feline herpes virus infections, Equine sarciods, Epithelial diseases in cats, Keloids etc
• Retinoids (Isotretinoin - Isotane, Isac, Isotrion 10,20mg caps)- color dilution alopecia, Sebaceous
adenitis, ichthyosis 1-3 mg/Kg Q24 h, Etretinate- Idiopathic seborrhoea, S. adenitis.0.75-1mg/Kg Q24 h
• Melatonin : ( Meloset 3mg tabs) Involved in neuroendocrine control of photo period dependent
moulting and colour. And Inverse relation to prolactin and photo-period. Indicated in Canine recurrent
flank alopecia and Canine pattern alopecia, Alopecia X, Telogen effluvium ?? Recommended dose : 3mg
for small and 6 mg for large dogs q 8-12 hours for 1-2 months

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Allergic Skin Diseases-Practical Approach in India ( Atopy and Adverse food reaction)

Approach to pruritus - some key examples

IV. Hereditary: Atopy, iodiopathic seborrhea, demodicosis, etc.

B. Physical examination : Localised/generalized, Symmetric/asymmetric.

 Pinnal pruritus: Atropy1, food allergy, sarcoptes1, fly strike.

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Differential diagnosis of pruritus based on primary skin lesions

PROPOSED DIAGNOSTIC PLAN FOR A PRURITIC DOG

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Atopic dermatitis (Inhalant dermatitis)

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Diagnosis of canine atopic dermatitis

1. Onset of signs under 3 years of age

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2. Control secondary infections

Management of Acute flare

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Side effects reported:

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When to use oclacitinib

3. LOKIVETmab (Cytopoint –Zoetis)- Monoclonal ab against IL-31

When to use LokiVETmab

How to reduce Itching quickly

5. Recombinant canine interferon-gamma (Interdog, Toray Industries),

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Hydrocortisone aceponate 0.058% (Nuttall et al 2009; Nuttall et al 2011; Lourenco-Martins et al 2012)

9. Topical Calcineurin inhibitors

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11. Immunotherapy ( refer publications or books)

Client education on atopy

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Topical Steroid cyclosporine Oclacitinib Lokivetmab

Spectrum Broad Broad broad semi Narrow

Cost ++ + +++ ++++ +++++

Onset of action Rapid Very Rapid 2-3 weeks Rapid Rapid

Acute effective effective Less effective effective effective

Chronic effective effective effective Less effective Less effective

Otitis effective effective effective Less effective Less effective

Adverse effects Rare common Common Com to Uncommon

Long term safety Moderate Poor Good Unknown Unknown

Monitoring clinical Clinical, Clinical and Clinical, Clinical

Adverse Food Reactions : Basics

1. Immunologic food reactions can be

 IgE mediated ( Immediate or anaphylaxis) or Intermediate Type 1hypersensitivity : occurs with in

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1. Food intolerance – classified as

2. Dietary Indiscretions – classified as

Proposed pathophysiological mechanisms of Food Hypersensitivity

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2. Gastrointestinal manifestations - scant data

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III. Other tests studied but not validated:

References are available upon request

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A good level of evidence - High efficacy

A fair level of evidence -Moderate to High efficacy