Petcare today bulletin - Cutaneous Malassezia, skin related problem

PETCARE TODAY BULLETIN ON Cutaneous Malassezia

Loving care alone cannot ensure healthy skin and smooth, shiny hair. Your pet also needs a balanced diet containing vital nutrients like Essential Fatty Acids, Vitamin E and Zinc. Deficiency of any of these can lead to various dermatoses.

This issue talks about certain salient features of skin care for the benefit of the pet owners.

Skin is a metabolically active organ that provides sensory input, protects the body from physical injuries and infections, helps in temperature control and immuno-regulation, and serves as a reservoir for some nutrients. Healthy skin and smooth, shiny hair reflect the love, affection and care you bestow on your pet. Apart from your attention, this multi-functional organ requires certain essential nutrients for its optimal functioning.

Nutritional dermatoses due to obsolute dietary deficiency are rare in dogs fed on commercial pet food. However, feeding a poorly formulated food or a home-made fiet that is not correctly balanced can lead to skin disorders. In addition, any metabolic or functional disorder that affects a pet's ability to digest, absorb or use nutrients can cause secondary nutrient imbalances that can manifest as dermatoses.

Although many components of the diet play a role in cutaneous homeostasis, the Essential Fatty Acids (EFA), vitamin A and zinc are the most important. In addition, a number of other dietary components such as biotin and vitamin E have been investigated for their ability to control skin diseases in dogs and cats.

As a component of cell membrane phospholipids and as precursors of a variety of regulatory components, the essential fatty acids maintain the health and integrity of epithelial tissue. The skin is especially susceptible to essential fatty acid deficiencies because of its high cell turnover rate. Dogs require a dietary source of linoleic acid and cats require linoleic acid and arachidonic acid.

In dogs, Essential Fatty Acid deficiency results in dry, dull coat, hair loss and eventually, skin problems develop. Consequently the skin becomes pruritic, greasy and susceptible to infection. A change in the surface lipids in the skin alters the normal bacterial flora and predispses the animal to secondary bacterial infections. Epidermal peeling, interdigital exudation and otitis externa have also been reported in essential fatty acid deficient dogs. Linoleic acid deficiency in cats results in similar changes.

The results of fatty acid supplementation may be observed after 2 weeks, but they actually take 6-8 weeks to become apparent. In many cases, fatty acid supplementation as a treatment for allergic dermatitis allows sugnificant reduction in the dose and / or frequency of other anti-inflammatory drugs uses.

Vitamin A is necessary for normal epithelium cell differentiation and maintenance and for the process of keratinisation. Vitamin A deficiency is likely to occur during growth, pregnancy or lactation, in dogs on fat restricted diets or those with poor fat absorption. Deficiency of this vitamin causes skin lesions in dogs. Signs include hair loss and poor coat condition, hyperkeratinisation of the epidermis and hair follicles, scaling of the skin, and increased susceptibility to secondary bacterial infections of the skin.

It has been suggested that Vitamin E may play a role in certain skin disorders in dogs. The occurrence of dermodicosis, a skin disease caused by the mite demodex canis, has been linked to decreased blood levels of vitamin E.

Deficiency of vitamins may occure in conditions associated with enteritis or where prolonged antibacterial therapy has reduced the synthesizing ability of enteric flora. Biotin deficiency in dogs is associated with crusted lesions on the face, neck and body with inappetence, diarrhoea and lethargy.

Zinc deficiency may occur in dogs for a number of reasons. Zinc deficiency may occur from inadequate levels of zinc in the diet, and from the presence of other nutrients or components that interfere with zinc absorption. Supplementation of the diet of growing dogs with zinc calcium also has the potential to result in dermatoses associated with zinc deficiency. the skin lesions of zinc deficiency first occur over pressure points and on the footpads, but they eventually spread over the entire body. Affected areas are characterized by hair loss, redness, inflammation, and crusting. Skin lesions show a rapid response to supplementation with complete healing within 2 weeks.

Malassezia pachydermatis (syn. Pityrosporum pachydermatis and p. canis) is a lipophilic non-mycelial yeast with a characteristic slightly elongated oval shape, a thick wall, and unipolar budding. It is commonly found on normal and abnormal canine skin and within the ear canal, anal sacs, vagina and rectum. there is an increase in incidence and organism numbers in some cases of otitis and dermatitis.

Malassezia and Staphylococcus play a significant role in seborrheic (oily and scaly dermatitis and otitis. Malassezia dermatitis is common and should be considered a factor in any scaly, erythematous, oily, pruritic dermatitis in which other differentials have been eliminated by diagnostic tests and lack of response to treatment.

The role of Malassezia as a cause of disease has been controversial. The Pityrosorum (now Malassezia) was first described by Rivolta in 1873, and in 1874 Malassezia suggested that it was causally related to seborrheic dermatitis and dandruff in humans. Sabouraud in 1904 made the same observation. Subsequently many authors reported on the relationship, and some even fulfilled all of Koch's postulates regarding the various species of yeast in human and animal skin diseases.

It is now apparent that alterations in skin surface microclimate or host defense may allow this normally commensal organism to become a significant pathogen. Surface microclimate factors leading to Malassezia proliferation are excessive sebum production, accumulation of moisture and subsequent disruption of the epidermal barrier. The yeat produces lipases that further alter the sebum balance. Zymogen in the yeast cell wall activates the mammalian complement, further damaging the host's epidermal integrity and is believed to cause epidermal spongiosis, inflammation and pruritus.

Allergic and bacterial skin disese may also be predisposing factors. Malassezia pachydermatis is unusual in that it can proliferte in proximity to many skin bacteria and its growth has been shown to be enhanced in the presence of Staphylococcus. Malassezia from humans is lipid dependent, but Malassezia pachydermatis from animals has its growth enchanced only by sebum lipids.

A T cell-mediated hypersensitivity is responsible for recovery from acute yeast infections and the prevention of disease by normal yeast flora. In animals with Malassezia dermatitis the T cell response is (presumably) either overwhelmed or fails.

Malassezia dermatitis occurs in adults of any age and any breed. Those predisposed are the Silky, Australian, Maltese and West Highland White Terriers, Chihauhuas, Poodles, Shetland Sheepdogs, and German Shepherd Dogs. The dermatitis often starts in the summer or high-humidity months(also the allergy season) and then continues into winter. There is a second spike of cases in early spring. Clients complain of only partial relief in response to corticosteroids or a shortened relief period after increasing doses of injectable forms of the drug. Pruritis is a major sign and constant feature. Animals with generalized dermatitis have an offensive, greasy seborrheic smell that is also noticed in Malassezia otitis.

Regional (ear, muzzle, interdigital and perianal) dermatitis or generalized disease also occurs. The presenting complaint can be chronic face rubbing. This may be mild or severe, with a "frenzied fit" of scratiching the nose and lips with the front paws. Some animals that exhibit this type of nose scratching aremisdiagnosed as having a central nervous system disease and are put on anticonvulsants. Shaking the head, scratching the ears, and aural hematoma are signs of ear disease. Pododermatitis is manifested as foot licking, with discoloration of paw fur and alopecia. Perianal and ventral tail dermatitis is manifested as flank and dorsal tail self-trauma by rubbing, chewing and scooting along the ground. Skin lesions consist of diffuse erythema, with variable scale (yellow and / or slate gray), hyperpigmentation, and traumatic alopecia. The skin and hair are greasy to waxy. Focal scaly plaques, erythematous macules, and patches that may coalesce into serpiginous tracts are occasionally recorded.

Several generalised diseases present as an exfoliative erythroderma and alpeicic, hyperpigmented, lichenified areas with gray to white scale.

The clinical signs in dogs and cats are pruritic, erythematous, scaly and hyperpigmented, lichenified dermatitis and otitis; therefore, the differential diagnosis is extensive. It is even more perplexing for the clinician since Malassezia dermatitis is often associated with or triggered by most of the potential differential diagnoses. the prime differential features and associated predisposing diseases are atopy, flea allergy, food allergy, superficial pyoderma and all the etiology factors considered in an oily and scaly seborrhea complex with exfoliative erythroderma.

The most useful and readily available tool for a clinician presented with a suspected case of Malassezia dermatitis and / or otitis is cytology. A cotton swab vigorously rubbed on the surface of affected skin or in the ear canal and then pressed and rolled onto a glass slide is the preferred collection technique from oily skin. A superficial scrape with a blunt spatula or blunt scalpel blade will also provide an adequate sample. Scaly and erythematous lesions devoid of hair or after clipping will often reveal diagnostic samples with cellophane tape stripping. Clear cellophane tape is repeatedly pressed onto lesional skin and then stained and mounted without a covership. The slide is fixed with heat (skip this step if using cellophane tape) and stained with a routine cytologic stain. It is then examined under high power lens or with an oil immersion lens on a light microscope.

Biopsy of affected skin for histopathology is also useful. However, the dermatopathologist must be knowledgeable about the significance of Malassezia organisms in the skin and the type of cutaneous reaction pattern elicited. Until recently, Malassezia oranisms on skin biopsy were dismissed as an incidental finding, with no role in the development of dermatitis.

A swab of the skin surface processed routinely on bacteria or drmatophyte medium may produce Malassezia but more often will fail to isolate the yeast. Better results are obtained if the laboratory is alerted to look for yeats and to use dextrose Sabouraud agar with chloramphenicol and gentamicin added. Yeast colonies will develop in 48 to 72 hours at 37⁰C. they appear as small, white, round, glistening colonies. Oil or sebum-enriched medium is described as helpful but is not necessary.

The only way to resolve the issue of whether a commensal-turned-oathogen has played a contributory role in the dermatitis is to remove that organism. Trial therapy with an antibiotic effective against Staphylococcus intermedius is a well-established diagnostic protocol to determine the role of the bacterium in a dermatosis. When Malassezia is demonstrated and inadequate resolution of the dermatitis occurs with removal of other identified factors, then a trial therapy for 2 weeks with ketoconazole (Nizoral) or other imidazoles helps support the yeast's role in the dermatitis. Other beneficial properties of ketoconazole (e.g.: antiproliferative effects) should also be considered.

The diagnosis of Malassezia dermatitis depends on identification of the yeast via cytology, culture or histopathology, ruling out other erythematous, scaly, pruritic dermatoses and ultimately on the response to antiyeast treatment.

The treatment of Malassezia dermatitis is best accomplished with 30 days of ketoconazole at 10mg./kg. q 12h PO. Pruritis decreases noticeably in the first week and cutanesous lesions start resolving by the second week on ketoconazole. Ketoconazole is actively secreted by sebaceous glands, which explains how this imidazole is effective against surface fungi. Vomiting and vague signs of malaise are occasionally encountered and can often be overcome by giving food with the tablets. Raely, liver damage is associated with ketoconazole in humans and cats. Ketoconazole has the added disadvantage of being an expensive drug, which is compounded if monitoring of liver enzymes is recommended.

Selenium sulfide shampoo followed by rinses with enilconazole is quite effective and cheaper than ketoconazole; however, enilconazole has an offensive odor and may not be universally available. Selenium sulfide shampoo is useful with an imidazole to remove scale and sebum, on which the yeast survive, and it has a direct but weak antimicrobial effect on the organism. Twice weekly treatments are recommended during the first two weeks, and weekly threafter.

Three shampoo preparations have the potential to be effective as the sole treatment. Ketoconazole shampoo is approved in many countries for the treatment of Seborrheic dermatitis in humans. Chlorhexidine shampoos containing more than 1% active ingredient are effective in some circumstances.

Two to four percent chlohexidine preparations are more effective. A selenium sulfide, chlorhexidine, and miconazole shampoo is available in Australia and has been evaluated on Malassezia dermatitis in animals and found to be effective. Since Malassezia dermatitis can be recurrent, with frequent relapses, an effective shampoo may be valuable for maintaining control without resorting to frequent courses of ketoconazole.

Local treatment with miconazole cream (Conofite) is valuable in pododermatitis and cheilitis, as well as for the most severely affected areas in generalised dermatitis.

Mycotic (yeast) otitis should be vigorously treated at the same time, preferably with a miconazole or nystatin and antibiotic combination otic preparation. Corticosteroids in the otic preparation help settle the inflammation, speeding resolution.

Griseofulvin is not effective against this yeast. The use of concurrent systemic antistaphylococcal antibiotics is not alwasy indicated, but some cases have required combination antiyeast and antibacterial therapy. The cases requiring combination therapy often have ahistory of initially fair to good response to antistaphylococcal antibiotics and then relapse while still on a prolonged course of antibiotics or relapse soon after completing the antibiotic therapy, and failure to respond again.