A fungi naturally found on the skin surfaces that causes most skin diseases in humans.


  1. Abstract
  2. Objectives
  3. Research
  4. Causes
  5. Method of Treatment
  6. Drugs
  7. Alternative Medicines
  8. PVGP Method
  9. References


All humans carry Malassezia fungus (as depicted above) on the skin; the commensal yeast Malassezia is a strong contributory factor to skin disease formation, but the presence of Malassezia on healthy skin indicates that Malassezia alone is not a sufficient cause. Regardless, issues occur when the fungus grows too rapidly, and the natural renewal of cells is disturbed. The outcome is the source of many skin conditions such as acne, dandruff, cradle cap, pityriasis versicolor, seborrheic dermatitis, psoriasis etc… Malassezia is hard to control and chronic prophylaxis is often required to prevent recurrences.



To successful eradicate Malassezia without harming the skin barrier. PVGP believes this can be done with cell-penetrating antimicrobial peptides that are naturally produced by the body.


The genises of Malassezia is unknown. For instance, Malassezia ribosomal DNA (rDNA) has been reported from soil nematodes, sponges, and rocks. Undeniably, much remains to be discovered about the spectrum of habitats exploited by Malassezia that would advance our knowledge on the ecological relationships between the Malassezia skin biotic community, their hosts, and the environment.[1]  The scientific consensus is that development of many skin conditions is predicated by three major factors: Malassezia colonization, sebum production and individual predisposition.


The fungus is lipophilic which means it requires fats to grow, thus most common areas occurs in places with many sebaceous glands: on the scalp, face, and upper part of the body.

Studies have shown that Malassezia flourish with fatty acids with a carbon chain length of 11 through 24.[2]



Thus applying lotions, creams, or oils which are in common in therapeutic remedies actually feed the fungus.

Naturally healthy skin has a pH around 4 making it acidic and also make it hard for Malassezia to survive in. Malassezia grows optimally in an environment when the pH is between 4 and 8. Therefore, it is critical the skin pH be around 4 or ideally slightly lower.

Keep in mind washing your face with soaps, water, and creams can easily alter your skin’s pH and make it more alkaline. There are products out there to make your skin more acidic, however, you have to be careful not over acidify because it can dry out your skin and cause your body to produce more sebum which would be counter-intuitive by creating a more food rich environment.

Due to fungus being the culprit, common treatments use antifungals. Some antifungals being used are: Climbazole, Clotrimazole, Itraconazole, Ketoconazole, Piroctone, Olamine, and Lotrimin Ultra

In theory using antifungals make absolute sense. In reality when doing so, there are two issues. First, the antifungals tend to use creams/ointments as a base which directly feeds the fungus. So although you have a substance that kills the fungus, you’re also providing a feeding ground for it. In this situation we are taking one step forward, and two steps back. The second issue, Malassezia will form a biofilm [4] which is when single-celled individuals gather together to form a sedentary but dynamic community within a complex structure, displaying spatial and functional heterogeneity. Think of this a shield around the fungus created for protective purposes, and making it hard for antifungals to penetrate and eradicate the fungus.





  • Malassezia shows significant growth in moist warm environments. Thus it’s recommended to avoid taking long hot showers, or steam baths.
  • Sweating heavily also aggravates symptoms for unknown reasons.
  • Large meals in a single sitting, especially meals high in glycemic contents, such as a fruit smoothie.
  • Washing areas even with simply just water.

The importance of skin barrier:

skin-epidermis-dermisA healthy stratum corneum (SC) forms a protective barrier to prevent water loss and maintain hydration of the scalp. It also protects against external insults such as microorganisms, including Malassezia, and toxic materials. Severe or chronic barrier damage can impair proper hydration, leading to atypical epidermal proliferation, keratinocyte differentiation and SC maturation, which may underlie some dandruff symptoms. The depleted and disorganized structural lipids of the dandruff SC are consistent with the weakened barrier indicated by elevated transepidermal water loss. Further evidence of a weakened barrier in dandruff includes subclinical inflammation and higher susceptibility to topical irritants.

The loss of barrier function initiates a signaling cascade within the underlying epidermis that stimulates a repair response designed to normalize stratum corneum function. The primary response is a temporary increase in the biosynthesis of major lipid species (i.e. ceramides, cholesterol and fatty acids) . The so-called lamellar bodies responsible for the delivery of these lipids into the extracellular domains of the stratum corneum have also been shown to contain antimicrobial peptides vital to reducing pathogenic infections. Hence, there is a coordinated restoration of both the epidermal permeability and the antimicrobial barriers following damage to the stratum corneum.

Consistent with the hypothesis of SC disruption, several observations about dandruff susceptibility are consistent with poor EPB function. First, only individuals prone to dandruff respond to the topical application of oleic acid (a known skin penetration enhancer and irritant) , and secondly, dandruff sufferers are more responsive (i.e. report a higher perception of itch) to histamine topically applied to the scalp. Individuals with healthy scalps only respond to topically applied histamine following ‘active’ delivery of the pruritogen into the scalp with iontophoresis, whereas dandruff sufferers report itch before the iontophoretic current is applied.

Although antifungal activity is a key driver of efficacy, it has long been recognized that many of the known antidandruff agents may also have non-antifungal effects that may contribute to the overall clinical benefit. Examples of this are the cytostatic effects ascribed to selenium sulphide and the intrinsic anti-inflammatory properties of ketoconazole Zinc pyrithione is unquestionably the most widely used of the available active agents, offering an effective combination of antimicrobial potency, high efficiency deposition from modern shampoo systems and a demonstrated ability to deliver active material into the hair follicle, enhancing the ability of the active agent to target both scalp surface and infundibular Malassezia.

Although there is no doubt that treatments such as zinc pyrithione and climbazole are effective antifungals, they do not directly address the deleterious changes in SC biology as measured by increased TEWL and lipid levels observed in individuals with dandruff. Although a normalization of scalp barrier lipids is reported to accompany zinc pyrithione treatment, this effect is believed to be an indirect change arising from the removal or reduction of the microbial irritant. Thus, the reduction in microbial challenge subsequently and indirectly leads to the recovery and normalization of cellular processes, including keratinocyte proliferation and lipid biosynthesis, which in turn allow the underlying epidermal layers to recover and gradually repair the SC barrier over a period of days or weeks. Given the indirect nature of antifungal-derived EPB repair, the opportunity exists to drive a more immediate and selective barrier replenishment strategy through the topical application of lipids to directly replenish the SC and deliver a more rapid restoration of barrier quality.

In addition, shampooing with harsh surfactants will undermine the efficacy of conventional cosmetic antidandruff treatments by repeatedly damaging the SC permeability barrier already compromised by the reduction in lipid content apparent on the dandruff scalp. Such damage will manifest itself after-wash tightness, dryness, barrier damage , irritation and itch .

Harsh surfactants, with their ability to damage lipids and proteins, are closely associated with loss of SC barrier lipids, water-soluble NMF and a reduction in the enzyme activity fundamental to the normal functioning of the SC. Collectively, these changes in SC composition impact the overall barrier quality, impair desquamation and promote flaking. [5]

Current Treatments

  • Antifungals
  • Steriods
  • Phototherapy (UV radiation)
  • Other Medications
    • Pimecrolimus
    • Isotretinoin

PVGP Treatment Method

To successful eradicate Malassezia without harming the skin barrier. PVGP believes this can be done with cell-penetrating antimicrobial peptides that are naturally produced by the body.

Case Study:


1. Aristea Velegraki, Claudia Cafarchia, Georgios Gaitanis, Roberta Iatta, and Teun Boekhout. (2015) Malassezia Infections in Humans and Animals: Pathophysiology, Detection, and Treatment.  [PMC free article] 
2. Peter F. Wilde, Patrick S Stewart. (1968) A Study of the Fatty Acid Metabolism of the Yeast Pityrosporum ovale. 3. [PMC PDF] 
3. Lambers H, Piessens S, Bloem A, Pronk H, Finkel P. (2006) Natural skin surface pH is on average below 5, which is beneficial for its resident flora. [Pub Med] 
4. Aron G. Nusbaum, Robert S. Kirsner, Carlos A. Charles. (2015) Biofilms in Dermatology. [Skin Therapy Letter] 
5. G A Turner, M Hoptroff, and C R Harding. (2012) Stratum corneum dysfunction in dandruff. [PMC]