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The importance of recognising the role of Malassezia dermatitis in the management of allergic dogs

Unless the infection with Malassezia pachydermatis is treated, it is likely that the pruritus will continue

03 September 2020, at 7:25am

Infection with Malassezia pachydermatis is one of the most common reasons for pruritus persisting during the management of atopic dermatitis in dogs. In fact, recurrent Malassezia infection is listed as one of the criteria in making the clinical diagnosis of atopic dermatitis. The infection is a major cause of pruritus in dogs and yet it is often overlooked because of the tendency to concentrate on the atopic component. Unless the infection is recognised and treated, it is very likely that the pruritus will continue and management measures put in place for the atopic dermatitis will fail.

Microscopic view of Malassezia organisms
FIGURE (1) Malassezia organisms are oval to “footprint” in shape

Malassezia pachydermatis organisms are oval or round cells that reproduce by unicellular budding and resemble “peanuts in their shells” or a “footprint” in shape (Figure 1). They are commonly isolated from the ear canals, lip margins, chin, periocular skin, interdigital skin, anus, anal sacs and vaginas of healthy animals (Bond et al., 1995). These sites serve as reservoirs from which the organism is spread to other sites during the licking, biting and excessive grooming that are all signs of pruritus.

Pathogenesis

Malassezia organisms are known to produce virulence factors (proteases, lipases, phospholipase, lipoxygenase and many others; Coutinho et al., 2000) which break down cells and trigger the release of inflammatory mediators. They also activate the complement cascade that induces inflammation and recruits inflammatory cells. These changes influence the skin’s microclimate, which in turn favours the colonisation and proliferation of the organism. Furthermore, in a small number of individuals, these factors can induce IgE-mediated, or cell-mediated, immune responses.

The key factors that favour Malassezia overgrowth include:

  • An increase in environmental temperature and humidity
  • Inflammation, exudation and self-trauma
  • Breed predispositions
  • Underlying hypersensitivity, endocrine and paraneoplastic conditions
  • Anatomical site (eg skin folds and ear canals)

Clinical signs

Pruritus is a common presenting sign but the clinical signs vary according to the duration and intensity of the infection and the area affected. Lesions can be localised or generalised and, in the acute stages, include erythema, scaling and crusting (Figure 2), with varying degrees of hyperpigmentation. Advanced or chronic cases usually present with erythema, scaling, hyperpigmentation, lichenification and crusting. Dogs with Malassezia infections have brown exudate and/or discoloration of the skin and claws. Often, there is a concurrent bacterial infection and frequently, peripheral lymphadenopathy is present.

The distribution of the infection is usually of that seen in atopic dogs (Figure 3) and often Malassezia otitis is a common problem.

Diagnostic tests

In general practice, the cheapest, quickest and easiest way to demonstrate the presence of the organisms is by cytological examination of tape-strip preparations, direct smears or scrapes, stained with Diff-Quik. Malassezia are identified as oval to footprint-shaped organisms under oil immersion (Figure 1). The number of organisms seen under high power (x100 lens) can vary depending on the site sampled, the sampling techniques and the staining techniques. Even a small number seen can be significant, if the clinical signs and history are suggestive of Malassezia infection and there is favourable response to treatment.

Immediate hypersensitivity responses to Malassezia pachydermatis can be demonstrated by intradermal and serological tests, both of which demonstrate the presence of Malassezia-specific IgE.

Finally, if there is a high index of suspicion, but Malassezia organisms are not found, then response to treatment can be used to rule infection in or out.

Key points

  • Cytology – adhesive tape strips, direct impression smears, indirect impression smears, superficial scrapes
  • Culture
  • Response to treatment
  • Demonstrate presence of Malassezia-specific IgE by intradermal allergy test or by serum allergy testing

Treatment

Depending on the extent of the clinical signs and client and patient compliance, topical and/or systemic therapy can be considered.

Topical treatment

2% miconazole / 2% chlorhexidine shampoo or 3% chlorhexidine shampoo are the licensed treatments of choice based on evidence-based medicine (Negre et al., 2009).

Other topical antifungal preparations such as selenium sulphide shampoo, lime sulphur and enilconazole rinse may also be useful. Unlicensed shampoos, lotions and ointments containing antifungals such as ketoconazole, clotrimazole, miconazole and terbinafine may be of some use for Malassezia dermatitis in individual cases, but there is lack of evidence for their use in most cases. Wipes impregnated with chlorhexidine digluconate, climbazole 0.5%, zinc gluconate 1%, Tris-EDTA and glycerine; those with chlorhexidine 3%, climbazole 0.5% and phytosphingosine; and those with acetic acid and boric acid may be useful in reducing the yeast numbers (Bourdeau et al., 2007; Cavana et al., 2015). Other shampoos and foams containing similar combinations of ingredients are also available and can also serve the same purpose.

Systemic therapy

Ketoconazole (5 to 10mg/kg) or itraconazole (5 to 10mg/kg) once daily can be considered in cases where the infection is non-responsive to topical treatment or when topical treatment is not practical. When indicated, the author prescribes between 14 and 21 days' systemic treatment concurrently with topical medication. Depending on the individual case, the topical treatment can be continued after the course of systemic treatment is concluded as a maintenance therapy.

Side-effects include anorexia, vomiting, diarrhoea and hepatic dysfunction, which can occur with both ketoconazole and itraconazole; however, it is suggested that they are less severe and less frequent with the latter (Miller et al., 2013). In some cases, reducing the dose may help with the gastroenteric signs.

For those dogs where long-term management is required, pulse treatment on two consecutive days of each week can be used but monitoring of liver function and haematology are essential.

Terbinafine at 30mg/kg sid has been reported to be effective, but in an evidence-based review support for its use was lacking (Negre et al., 2009). A later study showed that terbinafine concentration in canine stratum corneum and sebum barely exceeded the reported Malassezia MIC90, when dogs were given it at 30mg/kg once daily for 21 days, suggesting that a higher dosage may be needed (Gimmler et al., 2015) for the treatment of Malassezia.

For successful long-term control of recurrent infections, it is necessary to identify and manage the underlying condition predisposing the animal to Malassezia infection. Alternatively, the underlying cause is treated but the Malassezia infection overlooked. For instance, atopy predisposes dogs to intermittent Malassezia infections, and staphylococcal infections are also associated with Malassezia infections. However, in general practice, often the atopy and/or the staphylococcal infection is treated but the Malassezia is overlooked.

Summary

Malassezia dermatitis is a common cause of pruritus and dermatitis in dogs. The clinical signs include erythema, scaling, exudations and lichenification. In-house cytological examination is the most rapid and cost-effective way of diagnosing the condition. Apart from the treatment of the Malassezia dermatitis, the underlying condition should be identified and managed, otherwise the treatment protocol for the Malassezia infection will be compromised, if not entirely ineffectual, in the long term. At the same time when an atopic dog relapses, or fails to respond to appropriate management, always look for infections as they may be preventing the resolution of the pruritus.

References
Author Year Title
Bond, R. and Lloyd, D. 1996 Factors affecting the adherence of Malassezia pachydermatis to canine corneocytes in vitro. Veterinary Dermatology, 7, 49-56
Bond, R., Elwood, C., Littler, R., Pinter, L. and Lloyd, D. 1998 Humoral and cell-mediated responses to Malassezia pachydermatis in healthy dogs and dogs with Malassezia dermatitis. Veterinary Record, 143, 381-384
Bond, R., Ferguson, E., Curtis, C., Craig, J. and Lloyd, D. 1996 Factors associated with elevated cutaneous Malassezia pachydermatis populations in dogs with Pruritic skin disease. Journal of Small Animal Practice, 37, 103-107
Bond, R., Hendricks, A., Ferguson, E., Lloyd, D. and Curtis, C. 2002 Intradermal test reactivity to Malassezia pachydermatis in atopic dogs. Veterinary Record, 150, 448-449
Bond, R., Morris, D., Guillot, J., Bensignor, E., Robson, D., Mason, K., Kano, R. and Hill, P. 2020 Biology, diagnosis and treatment of Malassezia dermatitis in dogs and cats. Clinical Consensus Guidelines of the World Association for Veterinary Dermatology. Veterinary Dermatology, 31, 27
Bond, R., Saijonmaa-Koulumies, L. and Lloyd, D. 1995 Population sizes and frequency of Malassezia pachydermatis at skin and mucosal sites on healthy dogs. Journal of Small Animal Practice, 36, 147-150
Bourdeau P., Bruet V. and Gremillet C. 2007 Evaluation of phytosphingosine-containing shampoo and microemulsion spray in the clinical control of allergic dermatoses in dogs: preliminary results of a multicentre study. Veterinary Dermatology, 18, 177-178
Cavana, P., Peano, A., Petit, J., Tizzani, P., Perrot, S., Bensignor, E. and Guillot, J. 2015 A pilot study of the efficacy of wipes containing chlorhexidine 0.3%, climbazole 0.5% and Tris-EDTA to reduce Malassezia pachydermatis populations on canine skin. Veterinary Dermatology, 26, 278-e61
Chen, T., Halliwell, R., Pemberton, A. and Hill, P. 2002 Identification of major allergens of Malassezia pachydermatis in dogs with atopic dermatitis and Malassezia overgrowth. Veterinary Dermatology, 13, 141-150
Coutinho, S. and Paula, C. 2000 Proteinase, phospholipase, hyaluronidase and chondroitin-sulphatase production by Malassezia pachydermatis. Medical Mycology, 38, 73-76
Gimmler, J., White, A., Kennis, R., Cruz-Espindola, C. and Boothe, D. 2015 Determining canine skin concentrations of terbinafine to guide the treatment of Malassezia dermatitis. Veterinary Dermatology, 26, 411-e96
Guillot, J and Bond R. 1999 Malassezia pachydermatis: a review. Medical Mycology, 37, 295-306
Miller, W., Griffin, C. and Campbell, K. ed. 2013 Fungal and algal skin diseases. In: Muller and Kirk's Small Animal Dermatology. Elsevier Health Sciences, pp. 223-283
Morris, D. O., Olivier, N. B. and Rosser, E.J. 1998 Type-1 hypersensitivity reactions to Malassezia extracts in atopic dogs. American Journal of Veterinary Research, 59, 836-841
Negre, A., Bensignor, E. and Guillot, J. 2009 Evidence-based veterinary dermatology: a systematic review of interventions for Malassezia dermatitis in dogs. Veterinary Dermatology, 20, 1-12
Nuttall, T. J. and Halliwell R. E. W. 2001 Serum antibodies to Malassezia yeasts in canine atopic dermatitis. Veterinary Dermatology, 12, 327-332

Anita Patel, BVM, DVD, FRCVS, is a diplomate and a recognised RCVS Specialist in veterinary dermatology. She has worked exclusively as a dermatologist for the last 15 years and lectures on all aspects of small animal dermatology in the UK, Europe, Africa and Asia.

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