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Orthopaedics or atopy?

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01 August 2015, at 12:00am

MICHELLE GREAVES of Virbac discusses why treating the atopic Westie shouldn’t fill you with trepidation and be the reason it disappears off your consult list onto the new graduate’s in preference to the lame puppy

SCENARIO: You’re perusing your evening consults, having had a satisfying day of rewarding surgery and straightforward boosters, when you see: “6pm Fergus – itching no better…”

The record has more pages than a Tolstoy novel and there it is, the feeling that someone is slowly hollowing out your abdomen. Pulling rank, you desperately scan your colleague’s waiting lists to see which client to swap.

Is it really that demoralising? Surely problematic skin cases aren’t all soul destroying? After all, some vets become dermatologists. In fact, skin cases can be perfect for the practice with high revenue generation and enhanced client bonding.

Here is a gentle refresher on atopy and how to keep owners satisfied and bonded to the practice.

The disease

Atopic dermatitis (AD) is a very common condition among dogs, and although true incidence is not known it is estimated at 3-15% of the canine population (Rhodes, 2011). It is also a common reason for owners to seek second opinions from other veterinary practices.

Importantly for your practice it can generate a significant amount of revenue over a pet’s lifetime and so we need to try to manage cases as best we can.

It is crucial that communication between vet and owner is improved so that a basic understanding of the condition is achieved.

This will cultivate your client’s bond to the practice and enhance compliance, with the ultimate aim of optimising the quality of life of these dogs. Poor compliance is the commonest reason for poor AD management.

Atopic dermatitis is a complex, multifactorial condition with inherited, environmental, parasitic, and sometimes dietary components. It has been described as “a genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features” and “it is most commonly associated with IgE antibodies to environmental allergens” (Miller, 2013).

AD is a chronic or relapsing skin disease and is usually initially characterised by pruritus (Bizikova, 2015). In healthy skin there is an effective barrier to prevent penetration of most bacteria, viruses and parasites (Olivry, 2001).

AD dogs have deficiencies in the intercellular lipid barrier, composition of lipid, and the arrangement of the lipid in the dermal layer (Coatesworth, 2010). Allergens are therefore able to penetrate the skin barrier before being picked up by phagocytic Langerhans cells, then processed and presented to other components of the immune system. This creates an IgE mediated immune allergic reaction to certain environmental allergens, with a TH-2 cell dominated allergic response (Marsella, 2006).

Why does this matter? It all contributes to the difficulty of treatment and the need for potent and safe treatment options (Nuttall, 2009).

Diagnosis

AD is unfortunately time-consuming and involves a cost to diagnose, as it is ultimately a diagnosis of exclusion. Explaining this to an owner will help them accept the presumed diagnosis as there is often not a convenient decisive lab test.

Inevitably, when presented with an animal with a complex disease, a thorough history is the most important first step. History charts can be useful – such as the one in the BSAVA Manual of Dermatology, chapter 2.

An extended consult is indicated for dermatology cases and a frustrated owner can be quite acceptant and appreciative of the time taken even if the consultation charge is more. In a way, the sedation and radiograph taken to work up a lameness is equivalent to the extended consultation with lesion description and mapping.

Don’t be afraid to reschedule an appointment to a more appropriate time that will give you time to work up the case properly.

From this assessment the differential diagnosis list is compiled. Next, a series of diagnostic tests are performed to rule conditions in or out. Skin scrapes, hair plucks and tape impression or direct impression cytology are all things that can be done in-house with minimal equipment and minimal expense to the practice.

Fungal and bacterial culture can be useful to diagnose concurrent infections, overgrowth of commensals such as Staphylococcus pseudintermedius and Malassezia pachydermatis.

Identification of resistant organisms can explain poor responses to previous therapies and determine antimicrobial therapy in the future. Histopathology can be very useful in certain conditions, but is not usually necessary for AD. It is important to note that allergy serology and intradermal testing are designed to target AD treatment and not as a diagnostic aid.

Remember, normal animals can be serologically positive to allergens – especially house dust mites.

Treatment

Once the process of exclusion has reached the diagnosis of AD, treatment options are discussed and owners should be reminded there is no magic cure. One treatment does not suit all, and a multimodal approach to treatment has been recommended by the International Task Force on Atopic Dermatitis (2010).

One of the aims of treatment is to repair and restore the defective epidermal barrier, which will reduce percutaneous allergen penetration, therefore reducing clinical signs. Barrier restoration can be achieved in a number of ways. Oral essential fatty acid supplements, dermatological diets and fatty acid spot-on treatments can help to enhance the lipid bilayer in the skin.

Many shampoos, lotions, gels, rinses and creams are available on the market for dermatology disorders, and it can be confusing for owners and vets alike to know which one is suitable.

Not all shampoos with the same ingredients have the same effects, as the success is often in the shampoo formulation, with some shampoos having residual activity on the hair shaft and skin surface (Mueller, 2014).

When choosing a topical treatment consider which action you are looking for – be it drying, rehydrating, keratoplastic, keratolytic, antibacterial, antifungal, antiparasitic or antipruritic – and choose one with this action. It is outwith the scope of this article to discuss all the individual ingredients.

Topical steroid treatments can be very useful for localised lesions and may limit systemic side-effects, especially hydrocortisone aceponate (Cortavance, Virbac) which is metabolised in the skin layers to cortisol, and therefore has negligible systemic absorption (Nuttall, 2009).

Oral immunomodulatory medications have evolved beyond the stalwart prednisolone to include molecules like ciclosporin. Ciclosporin A is an immunosuppressant and immunomodulatory molecule which can alleviate inflammation, reduce pruritus and help improve barrier function.

With the recent introduction of liquid formulations (Cyclavance, Virbac; Sporimune, Dechra; Modulis, Ceva) onto the market, increased flexibility and tailored dosing can be achieved. Ciclosporin has had market authorisation for over 10 years and has proven safety and efficacy (Forsythe, 2014).

Oclacitanib (Apoquel, Zoetis) is a newer introduction to the market, as a JAK kinase inhibitor with anti-pruritic activity. With any immunomodulant, there are potential side-effects and datasheets should be consulted and discussed with the owner, so that their expectations are not unrealistic, and additional requirements like monitoring blood biochemistry, haematology and urine testing are explained and factored into the cost.

With all the products available and a good understanding of AD, it should be possible to obtain satisfactory, safe, lifelong control of clinical signs. By increasing client awareness and understanding of the treatments, compliance can be greatly increased.

Client communication is the key to success and as long as the client knows what to expect from the treatment, and why certain treatments are being used, dermatology cases can be very rewarding and something to look forward to!

References

Bizikova, P., Santoro, D. et al (2015) Review: Clinical and histological manifestations of canine atopic dermatitis. Veterinary Dermatology 26: 79-83.

Coatesworth, J. (2010) Canine Atopic Dermatitis. UK Vet Companion Animal 15 (1): 33-37.

Coatesworth, J. (2010) Management of Canine Atopic Dermatitis. UK Vet Companion Animal 15 (2): 47-51.

Forsythe, P. and Paterson, S. (2014) Ciclosporin 10 years on – indications and efficacy. Review. Vet Record 174 (Supplement 2): 13-21.

Marsella, R. (2006) Atopy: New Targets and New Therapies. Veterinary Clinics Small Animal Practice 36: 161-164.

Meuller, R. (2014) Topical Therapy and Hygiene. British Veterinary Dermatology Study Group Spring Proceedings: Bacterial Skin Diseases, pp25-30.

Miller, W., Griffin C. and Campbell, K. (2013) Hypersensitivity Disorders. In: Muller and Kirk’s Small Animal Dermatology. 7th Edition. pp365-388.

Nuttall, T., Mueller, R., Bensignor, E. et al (2009) Efficacy of a 0.0584% Hydrocortisone Aceponate Spray in the Management of Canine Atopic Dermatitis: A Randomised, Double Blind, PlaceboControlled Trial. Veterinary Dermatology 20 (3): 191-198.

Olivry, T., Marsella, R. and Hillier, A. (2001) The ACVD Task Force on Canine Atopic Dermatitis (XXII): Are Essential Fatty Acids Effective? Veterinary Immunology and Immunopathology 81: 347-362.

Olivry, T. and Sousa, C. A. (2001) The ACVD Task Force on Canine Atopic Dermatitis (XX) Glucocorticoid Pharmacotherapy. Veterinary Immunology and Immunopathology 81: 317-322.

Rhodes, K. and Werner, A. (2011) Atopic Dermatitis. In: Blackwell’s 5 Minute Consult. Clinical Companion. Small Animal Dermatology. 2nd Edition. pp94-103.