Malassezia pachydermatis (Pytirosporum canis) is commensal, lipophilic yeast that is frequently isolated from the external ear canal and from the skin of healthy dogs. Cutaneous or immunological factors enhance its multiplication and the development of its pathogenicity. This has been recognized since the late seventies.

Aetiology and pathogenesis

The genus Malassezia includes six species of lipodependent yeasts and Malassezia pachydermatis, which is lipophilic but not lipodependent. The reproduction of Malassezia is asexual with unipolar budding. This gives a typical shape (resembling a footprint or a peanut). Their size is small (2 to 7 µm); they do not form pseudomycelia. Round, convex, yellowish cultures develop on Sabouraud’s dextrose agar.

Using various techniques, many studies have shown that Malassezia pachydermatis is a component of the normal cutaneous flora of the dog. Around 50% of healthy dogs are carriers of this yeast, which can be found in the external ear canal, the skin (particularly the anal area which could be a carriage zone, the lips and extremities) and the haircoat. The response of the host to the yeast includes non-specific defense mechanisms (phagocytosis by neutrophils) as well as cell-mediated specific defense mechanisms. In the latter, Langerhans cells present the antigen which activates T-cells. These T-cells multiply and produce lymphokines that stimulate phagocytosis by macrophages and multiplication of epidermal basal cells. This leads to the destruction of the yeasts or to their mechanical removal via scaling.

Alterations of the cutaneous microclimate or host defense mechanisms allow Malassezia pachydermatis to multiply and to become pathogenic. Cutaneous factors enhancing the multiplication of Malassezia include:

 An excessive production or a modification of sebum and/or cerumen.

 An excess of moisture.

 A rupture of the epidermal barrier.

 Cutaneous folds.

These changes may be due to underlying causes, of which the following are most common:

 Cutaneous hypersensitivity including atopic dermatitis.

 Pyoderma.

 Ectoparasitic skin disease, particularly demodicosis.

 Endocrine disorders, particularly hypothyroidism.

 Keratinization disorders: epidermal dysplasia of the West Highland White Terrier, idiopathic seborrhoea,

 Treatment with glucocorticoids or antibiotics.

Immunological dysfunction (cell-mediated immunity, IgA secretion) could also promote growth of the Malassezia population on the skin. For instance, epidermal dysplasia of the West Highland White Terrier could be associated with a genetic predisposition to a poor response of T-cells towards the yeast.

Malassezia produce many enzymes (including lipases and proteases) that can contribute to cutaneous inflammation through proteolysis, lipolysis (which alters the lipidic cutaneous film), changes of cutaneous pH, eicosanoid release and complement activation. In addition, it has been shown that Malassezia pachydermatis can play an allergenic role. In about a third of dogs with “seborrhoeic dermatitis,” skin testing with a Malassezia extract shows immediate hypersensitivity reactions. Levels of specific IgG are greater in dogs with Malassezia dermatitis than in normal dogs. There are higher levels of specific IgG in atopic dogs (with or without concurrent Malassezia dermatitis) than in non-atopic dogs with Malassezia dermatitis or normal dogs. Dogs with atopic dermatitis and Malassezia dermatitis have a high level of specific IgE whereas atopic dogs have a low level and normal dogs have no specific IgE.

Epidemiology

There is no age or sex predilection. Some breeds are predisposed to Malassezia dermatitis: West Highland White Terrier, Basset Hound, Dachshund, Cocker Spaniel, Poodle, German Shepherd, Collies, Shetland, Jack Russell Terrier, Silky Terrier, Australian Terrier, Springer Spaniel and Shar Pei. Malassezia dermatitis is often seasonal (from the end of spring to the beginning of fall which is the time at which allergic dermatites are often diagnosed). It can persist during the winter. There is no indication that Malassezia dermatitis is contagious.

Clinical signs

Pruritus is always present and severe. Animals are presented with a strong odour of rancid fat. At the beginning of the disease, there are localized or diffused erythema, erythematous papules and macules, and a keratoseborrhoeic disorder with scaling, crusting and alopecia and a greasy aspect of the skin and hair. Secondary lesions such as lichenification and hyperpigmentation follow this rapidly. Malassezia dermatitis can be localized, e.g., on the ventral side of the body (neck, axillae, ventrum and inguinal area), face (ear pinnae, lips, muzzle), peri-anal area and legs (forearms, caudal thighs and feet). It can also be generalized. It is not uncommon to observe concurrent otitis externa. Lymph node enlargement is sometimes seen, but most often, there are no general signs.

Diagnosis

Diagnosis of Malassezia dermatitis is based upon history, physical examination, appropriate complementary diagnostic aids to show the presence of Malassezia on the skin, response to specific therapy and exclusion of other dermatoses.

Cytological examination can show yeasts and allow for semi-quantification. The result is immediate using the immersion power objective after staining with lactic blue or, preferably, a rapid staining method. Several cytological techniques can be used: 1) impression smear; 2)“Scotch tape test” using pieces of tape (clear cellophane) strip or even “sticky slides;” 3) scrape smear; and 4) swab smear. In many hands, impression and above all tape strip smears appeared to be the most reliable methods. Swab smears should be reserved for cytological examination of the external ear canal. Cytological examination will show oval or elongated cells of 3 to 5 µm in diameter, with a typical single polar budding (“footprints, peanuts, Perrier bottles”). Yeasts can adhere to scales. A suppurative reaction is not uncommon.

The minimum number of yeasts that indicates the possibility of a true Malassezia dermatitis is not really known. Some authors feel that even a few yeasts are significant whereas others would consider the disease only if there is a higher number of yeasts per high power field. Perhaps the number of yeasts is an indication. In addition, there are variations between breeds and body sites. Lastly, there are cases in which a small number of yeasts trigger a hypersensitivity reaction and so the ultimate criterion will be the response to antifungal therapy.

Fungal cultures can show the presence of Malassezia on the skin and hair of dogs. Sampling can be done using hairs, swabs, contact plates or the “pieces of rug,” or detergent scrub techniques. Appropriate media for Malassezia pachydermatis are Sabouraud’s dextrose agar with chloramphenicol and cycloheximidine (which improves the growth of the yeast) and modified Dixon’s agar, which grow all species of Malassezia. As the yeast is a normal component of the cutaneous flora of the dog, by itself a positive culturing has no or little value. However, as for all opportunistic agents, the number of colonies is perhaps an indication (this is comparable to the number of yeasts demonstrated by cytological examination).

Cutaneous histopathology can sometimes show the yeasts on the surface of the epidermis and in the infundibula, particularly in PAS stained sections (although they are occasionally visible on HE stained sections). However, if they are not seen on biopsy, this does not exclude their presence. False negative results could be caused by the sampling of a non-infected area, removal of the stratum corneum during processing, etc. Cutaneous histopathology is a less sensitive technique than cytology. As for cytology, the presence of the yeast on the skin may have a variable meaning since it can be discovered in normal dogs and dogs with various dermatoses. In contrast, the finding of Malassezia inside hair follicles could indicate a real pathogenicity.

There are common findings in biopsies from dogs with Malassezia dermatitis, leading to a pattern including:

 Orthokeratotic hyperkeratosis with prominent foyers of parakeratosis.

 Acanthosis and spongiosis with irregular rete ridges.

 Lymphocytic exocytosis of the epidermis.

 Intraepidermal neutrophilic or eosinophilic pustules.

 Moderate dermal inflammatory reaction, perivascular to diffuse, with lymphocytes, plasma cells, histiocytes and often neutrophils, eosinophils and mast cells.

 Supepidermal linear alignment of mast cells (SLAM).

Signs of concurrent bacterial folliculitis are not uncommon. Rarely, folliculitis and furunculosis can be observed in association with the presence of yeasts inside the hair follicles.

Therapeutic challenge is, in fact, the ultimate tool to confirm that in a particular case the commensal Malassezia has become a pathogen, thereby playing a role in the development of the dermatitis.

Differential diagnosis includes many pruritic dermatoses with erythema, hyperpigmentation and seborrheoa including allergic skin diseases, bacterial folliculitis, demodicosis, scabies, drug reaction, idiopathic acanthosis nigricans, epitheliotropic lymphoma, and all causes of seborrhoea with cutaneous inflammation. In fact, clinical signs of Malassezia dermatitis are so variable that it may mimic many dermatoses. Furthermore, Malassezia dermatitis is often associated with or even promoted by most of the dermatoses that are included in its differential diagnoses.

Treatment

Systemic therapy is necessary in many cases, particularly when clinical signs are severe and when the lesions are extensive. Ketoconazole is the most commonly used drug. As with all azole derivatives, ketoconazole acts in binding to cytochrome P450, which inhibits synthesis of ergosterol, an important component of the fungal cell membrane. This results in alterations of cellular permeability and activity of various membrane enzymes. Ketoconazole also has anti-inflammatory properties through an action on leucotriene synthesis and it has an action on the keratinization process through an action on alltrans retinoic acid. The dose is 10 mg/kg q24h (the author would not, however, give more than 200 mg/day, the human daily dose, to a dog). It is recommended to give the drug with some food. Tolerance is usually good but periodic biochemistry panels are necessary during a long course of treatments. In effect, an increase in serial transaminases may be followed by signs of intolerance (anorexia, vomiting) due to hepatic toxicity. Itraconazole could also be used (5 to 20 mg/kg every day or other day). To our knowledge, Malassezia pachydermatis has not shown any resistance to antifungal agents commonly used against yeasts (azole derivatives, nystatin, amphotericin B, 5- fluorocytosin). Griseofulvin and allylamine derivatives are not effective in treating Malassezia.

Topical therapy is an alternative to systemic treatment, particularly for localized lesions (creams, gels, lotions, or sprays). For extensive lesions, antifungal shampoos or lotions are preferable. They can be used with systemic therapy, although there is no formal evidence that the combination is of greater value than systemic treatment alone. Topical therapy alone should not be used as a diagnostic challenge, but it can maintain a remission, thus confirming the diagnosis. Shampoos containing miconazole (2%), chlorhexidine (at least 3%), a combination of both (2% each) and ketoconazole (2%) are the best whereas the most appropriate leave-on rinses (lotions) are lime sulfur and above all enilconazole (10 % diluted 50 times, i.e., 0.2 %). Topical treatments should be administered two to three times a week for two weeks then once a week.

Therapeutic follow-up is very important. First, an improvement confirms the diagnosis. Pruritus usually decreases within one week, whereas lesions will clearly diminish after two weeks of treatment. The duration of treatment should be at least one month and may be as long as two months to get a complete recovery. Usually therapy is continued for seven to 10 days beyond clinical cure. Otitis externa should be treated vigorously to limit the fungal reservoir (nystatin, thiabendazole, clotrimazole, miconazole, antiseptic cleansing agents, etc). In cases of concurrent superficial pyoderma or bacterial overgrowth, antibiotic therapy should be used simultaneously because Malassezia dermatitis is often a secondary problem. It is important to diagnose and treat the underlying problem. In case of “idiopathic “ Malassezia dermatitis, or if such control is impossible, relapses can be prevented either by weekly topical treatments or by oral administration of ketoconazole one or two days a week.

Conclusion

Malassezia dermatitis is a relatively common skin disease in dogs and can mimic and be secondary to a number of other dermatoses. It should be looked for as soon as history and clinical signs are compatible. Cytological examination should then always be done and an appropriate antifungal treatment should be used to confirm the diagnosis. In all cases, an underlying cause should be considered such as allergic skin disease, ectoparasitoses, endocrine disorders and/or keratinization disorders. However, there is no doubt idiopathic (“primary “) Malassezia dermatitis exists, particularly in the above-mentioned predisposed breeds. Long-term control of the disease is often obtained by treating an underlying cause. A rigorous dermatological approach is mandatory to achieve this purpose.

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