Malassezia Furfur (Pityrosporum)
May 19, 2020
Malassezia folliculitis is a yeast overgrowth in the hair follicle. The old school name for it is pityrosporum folliculitis. It’s an “acne look-alike” with tiny red papules and superficial pustules that can itch like crazy. Factors can include oily skin, hot, humid weather, sweaty environments, occlusive clothing, oily sunscreens, pomades and emollients, seborrheic dermatitis, hormonal changes, pregnancy, diabetes, immune issues and medications like birth control pills, antibiotic overuse and systemic steroids. Typical treatment of it is with anti-fungals, sulfur, mandelic acid, and herbal remedies (Black Cumin and Tea Tree Oil amongst others). Sweating aggravates it and so it can often appear in humid climates. It is recommended that if they are doing sport that the shower immediately afterwards, wear cotton clothing and avoid synthetics.
Is it involved with Rosacea? There is no "hard proof" that it is involved directly, however those with rosacea often have concomittant diseases. Often they have malassezia as well on their skin amplifying the inflammatory reaction.
Recent research has shown a growing evidence that yeast organisms belonging to the Malassezia genus may also be involved in the pathophysiology of Atopic Dermatitis (AD).
There has now been identified seven distinct species (Malassezia furfur, Malassezia pachydermatis, Malassezia sympodialis, Malassezia globosa, Malassezia slooffiae, Malassezia restricta and Malassezia
obtusa.
Malassezia yeasts are lipophilic organisms. They are a permanent component of the microflora of normal human skin. The highest concentrations of the organism are found on the skin of the face, scalp, neck, upper chest and back; the presence of high amounts of sebaceous skin lipids is thought to favour the growth of the organism in these sites.
Generally, skin colonization with Malassezia increases after puberty, which is presumably related to the increase in skin surface lipids that results from higher sebaceous gland activity during this period. Colonization reaches a maximum in the third decade of life, and then decreases in middle-aged and elderly individuals, possibly because of decreasing skin lipid content.
15 years ago researchers investigating atopic adults with head and neck dermatitis (HND) discovered that such patients displayed greater rates of positive skin-prick tests (S PT) to Malassezia (28%) than did AD patients with dermatitis distributed in other body sites (6%).
Supporting this hypothesis at the time was an earlier report that antifungal therapy for HND patients had resulted in a definite clinical improvement in the condition. Since then, numerous groups have continued to investigate the theory that Malassezia yeasts might somehow be involved in triggering or exacerbating dermatitis in AD patients through direct stimulation of immune pathways, causing inflammation in the skin. The existing evidence suggests that both IgE-mediated and T-cell mediated immune reactions could be involved, and is outlined below.
The presence of IgE-mediated type I hypersensitivity to Malassezia in AD patients has been well documented by studies that have used radioallergosorbent testing (RAST) to detect specific IgE antibodies to the yeast. The prevalence rate of these antibodies appears to vary with age, being much higher in patients who are more than 12 years old (43–93%) compared with patients of younger age (22–39%).
Antibody levels peak at approximately 20 years of age. These same studies have also shown that Malassezia-specific IgE antibodies are almost non-existent in normal healthy individuals.
Patients with AD affecting mainly the head and neck region appear more likely to possess Malassezia-specific serum IgE antibodies compared with patients with AD located in other sites, with one study reporting rates of 100%. Furthermore, in AD patients, the prevalence of type I hyper- sensitivity towards Malassezia tends to be much greater compared with that of other fungi.
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The presence of Malassezia-induced T cell reactivity has also been demonstrated using modified epicutaneous patch testing, which has shown that direct contact with Malassezia can induce an eczematous skin reaction in sensitized AD patients.
Malassezia is able to directly stimulate keratinocytes to produce inflammatory cytokines such as tumour necrosis factor (TNF)-a, IL-6, IL-8, IL-1 and IL-18.
Various studies suggest that a difference may exist between AD patients with type I hypersensitivity to Malassezia and those without. AD patients who have Malassezia IgE anti- bodies have been reported to exhibit a more active pattern of dermatitis compared with those who lack these antibodies.
Malassezia yeasts, through their ability to stimulate IgE-mediated and cell-mediated responses, may be playing a part in triggering a variety of immunological mechanisms that lead to skin inflammation. These mechanisms could cause itch, which in turn would cause scratching leading to further skin barrier dysfunction and inflammation.
Continuous exposure to Malassezia via the normal skin flora could then be responsible for repeated triggering of the host immune system, leading to recurrent skin inflammation. Because colonization of the organism is greatest in the head and neck area, the higher antigenic stimulus in this site would provoke a greater inflammatory reaction locally, which could explain why HND patients develop a more prominent form of AD in this specific region of the body.
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