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The enigma of color in tinea versicolor

Article in Pigment International · January 2014

DOI: 10.4103/2349-5847.135440

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Focus
The enigma of color in tinea versicolor
Divya Gupta, Devinder Mohan Thappa
Department of Dermatology and STD, Jawaharlal Institute of Postgraduate Medical Education and Research,
Puducherry, India
Tinea versicolor is a common superficial fungal infection
of the skin, especially in the hot and humid environment
of India. It is caused by the Malassezia species which is a
dimorphic, lipophilic fungus. Hence, the sebaceous areas
of the body that is, face, neck, upper back, and chest are
most frequently affected. There is a variable age distribution
of this disease, and a great majority of cases occur during
adolescence. The organism is found as part of the normal
flora of the skin in 90-100% of subjects. Tinea versicolor
results when there is an overgrowth of this commensal
fungus due to certain predisposing factors such as heat,
moisture, and occlusion of the skin by dressings, clothing,
or cosmetics.
The disease can present as hypo‑ or hyper‑pigmented
macules, initially folliculocentric, and later coalescing to form
geographic lesions with polycyclic margins. In Indians, 75-85%
of the lesions are hypopigmented [Figure 1], 5-15% are mixed
and the rest of the cases are hyperpigmented [Figure 2].[1] It is
an asymptomatic disorder and alterations of skin pigmentation
are often the presenting complaint in tinea versicolor. The
color of lesional skin in tinea versicolor varies from brown
to pink to white in different individuals. The macules and
patches, as implied by the name “versicolor”, may be hypo‑ and
hyper‑pigmented, leukodermal, erythematous, or dark brown.
Sometimes, overlapping lesions produce a striking tri‑colored
pattern of pigmentation known as “trichrome pityriasis
versicolor”.[2] Although mild pruritus can sometimes occur,
most patients are distressed by the color alteration rather
than other symptoms. However, the exact pathogenesis of
hyper‑ and hypo‑pigmentation in tinea versicolor lesions
remains an enigma to this day.
Address of correspondence: Dr. Devinder Mohan Thappa,
Department of Dermatology and STD, Jawaharlal Institute of
Postgraduate Medical Education and Research, Puducherry ‑ 605 006,
India. E‑mail: dmthappa@gmail.com
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DOI:
10.4103/2349-5847.135440
32
Amongst early theories, race and ethnicity were believed to
be important factors, and it was believed that hypopigmented
macules were more common in dark skinned patients and
hyperpigmented lesions in fair skinned individuals.[3] Aljabre
et al.[4] disproved this theory in their study, which found that
there was no correlation between the pigmentary variations of
tinea versicolor and the type of skin, sex, and age of the patients.
In fact, they observed that some patients had both hypo‑and
hyper‑pigmentation and propounded that there were other
factors involved in the production of pigmentary changes in
tinea versicolor. In their study, they also refuted the suggestions
that early lesions of tinea versicolor are light brown or
hypopigmented, which eventually evolve into hyperpigmented
macules.[5] They suggested that the pigmentary differences in
tinea versicolor were related to different strains of Malassezia;
however, this view could not be proven.
Another early theory related to the prevention of tanning
of the infected areas by fungal scales or a thinning of the
stratum corneum with subsequent loss of melanin granules
and degenerative cellular changes within the melanocytes.[6]
The damaged melanocyte theory was used to explain why
repigmentation may take months or years to occur after
resolution of infection.
However, the etiology of hypopigmentation is more complex
than can be explained by the sun‑screening effect of infected
scales in the stratum corneum. Moreover, depigmented
skin lesions of this infection have also been described over
the sun protected genital region.[7] Charles et al.[8] found
smaller melanosomes and melanosome granules in lesional
hypopigmented skin as compared to adjacent uninvolved
skin. The dendrites of melanocytes had marked “melanin
loading” with melanosomes when compared with dendrites
in the normal skin, indicating decreased melanin uptake by
the keratinocytes in the affected area. It appears then, that the
presence of the fungus in the skin initiates the production of
abnormal melanosome granules and possibly the faulty transfer
of these granules to the keratinocytes. The mechanism for this
is unknown. In addition, formation of melanosome complexes
followed by their subsequent destruction within lysosomes may
also contribute to the decreased pigment within the epidermis
noted in involved skin.[8]
Borgers et al. [9] found lipid laden spheres by electron
microscopy both intra and extra‑cellularly within the stratum
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Gupta and Thappa: Color in tinea versicolor
corneum, which were confirmed by lipid specific stains like
Oil Red O and Sudan Black B. Significantly, this lipid material
persisted in the skin layer even 4 weeks after treatment with
itraconazole. The authors postulated that the hypochromic
reaction was related to filtering of ultraviolet light by this
“lipid screen”. Persistence of the lipidic material for a few
weeks after treatment is consistent with the observation
that hypopigmentation persists for 3-4 weeks after the
disappearance of viable fungi from the skin.[9]
Other theories of hypopigmentation include damage to
melanocytes and inhibition of tyrosinase by dicarboxylic acid,
especially azelaic acid, produced by Malassezia furfur.[10] These
changes are most likely due to the cytotoxic effect of
dicarboxylic acids (azelaic acid, oleic acid, and vaccinic acid)
on melanocytes and melanogenesis. There may be two possible
theories that explain this effect of dicarboxylic acids. The first
is that they may interfere with mitochondrial enzymes (based
on vacuolization and degeneration in the mitrochondria). The
second is that they may be closely related to the pathway of
melanin synthesis, leading to the formation of fewer and smaller
melanosomes and partial degeneration of melanocytes.[10,11] It has
also been suggested that the lipoperoxidation process induced
by Malassezia may account for the clinical hypopigmented
appearance of the skin patches.[12]
Hyperpigmentation, on the other hand, has been explained
by abnormally large melanosomes, [13] a thick stratum
corneum,[14] and a hyperemic inflammatory response.[15,16]
Galadari et al.[14] found a definite increase in the thickness
of the keratin layer. Malassezia spores and hyphae were
more numerous in hyperpigmented lesions as compared with
hypopigmented ones. The superficial perivascular lymphocytic
inflammatory cell infiltrate was more pronounced in the
hyperpigmented areas. Hypopigmented lesions showed only
a low grade inflammatory cell infiltrate. The inflammatory
responses have been reported to act as a stimulus to the
melanocytes resulting in production of more pigment.[15,16]
In several specimens of hypopigmented and hyperpigmented
Figure 1: Hypopigmented tinea versicolor over upper back
Pigment International | Jan-Jun 2014 | Vol 1 | Issue 1 |
lesions, degenerated keratinocytes were found to be scattered
within the stratum malpighii, though their contribution to the
pigmentary disturbance was deemed unlikely.[14] The number of
melanosomes were approximately the same in hyperpigmented
lesions of tinea versicolor and the normal skin areas.[14] The
granular layer of the involved skin had more tonofilaments,
which also contributed to the dark color.[1]
In a recent study, the ratio between keratinocytes and
Malassezia was shown to be important, with the latter
inhibiting the growth rate of keratinocytes. Cytokines
like interlukin (IL)‑1α, IL‑6, tumor necrosis factor‑α and
endothelin‑1 were increased and were deemed to play a role
in hyperpigmentation.[17] The various theories of hypo‑ and
hyper‑pigmentation are summarized in Tables 1 and 2. The
histopathological differences are summarized in Table 3.
Regarding the epidemiology of tinea versicolor, there is no
difference in the prevalence of this organism in dark and light
skins. It may also be possible that hypopigmented lesions
Table 1: Theories of hypopigmentation
Theory
Race and ethnicity‑hypopigmented in dark skinned patients and
vice versa
Early hypopigmented lesions evolve into hyperpigmented lesions
Different species of Malassezia are responsible for different colors
Prevention of tanning by fungal scales
Thinning of stratum corneum and loss of melanin granules
Degenerative changes in melanocytes ‑ “Damaged melanocyte
theory”
Smaller melanosones and melanosome granules
Destruction of melanosome complexes within lysosomes
Decreased transfer of melanosomes to surrounding keratinocytes
Dicarboxylic acid induced damage to melanocytes and tyrosinase
enzyme
Lipoperoxidation induced by Malassezia
Filtering of UV light by “lipid screen” within and outside the cells in
epidermis
UV: Ultraviolet
Figure 2: Hyperpigmented tinea versicolor over the infra-axillary area
33
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Gupta and Thappa: Color in tinea versicolor

Table 2: Theories of hyperpigmentation Table 4: Treatment options for TV

Theory Topical treatment Systemic treatment
Thickened stratum corneum 2% ketoconazole shampoo Fluconazole single
Granular layer contains increased tonofilaments oral dose 400 mg
Abnormally large melanosomes Ciclopirox shampoo left on for 10 min Itraconazole 200 mg
Increased number of hyphae and spores before rinsing ×2 weeks OD ×7 days
Cytokine production‑IL‑1α, IL‑6, TNF‑α and ET‑1 Topical imidazoles and allylamines Ketoconazole 200 mg
b.i.d. ×2 weeks OD ×10 days
Perivascualr lymphocytic inflammatory infiltrate in dermis
stimulates melanogenesis Zinc pyrithione shampoo for 5 min
IL: Interlekuin, TNF‑α: Tumor necrosis factor alpha, ET: Endothelin
daily ×2 weeks
Selenium sulfide suspension for
5-10 min ×2 weeks
Table 3: Histopathological differences between hypo- and Keratolytic creams, ointments or
hyper‑pigmented TV lotions containing 3-6% salicylic acid
Hyperpigmented TV Hypopigmented TV 25% sodium hyposulfite
Thickening of stratum corneum Thinning of the stratum corneum b.i.d ×several weeks
Thickened granular layer Normal granular layer Retinoic acid cream b.i.d. ×2 weeks
to lighten
Increased number of hyphae and Not seen
spores seen Post inflammatory hyperpigmentation
TV: Tinea versicolor, OD: Once daily, b.i.d.: Two times in a day
Hyperemic inflammatory response Not seen
with increased lymphocytic
infiltrate in dermis seen through hitherto unknown mechanisms. It may, on the strength
TV: Tinea versicolor of current evidence, be tempting to think that the variation
in appearance of these lesions may be due to differences in
in light skinned individuals are less noticeable as compared ultrastructural composition already present in healthy dark or
to hyperpigmented lesions (and vice versa) and thus escape light skin.
attention.[1] In a study by Park et al., higher humidity, increased
sebum excretion rate and increased transepidermal water References
loss were seen in both hyper‑ and hypo‑pigmented pityriasis
versicolor skin lesions by multiprobe adapter 5‑a noninvasive 1. Kallini JR, Riaz F, Khachemoune A. Tinea versicolor in
physiological parameter of the skin. However, there was no dark‑skinned individuals. Int J Dermatol 2014;53:137‑41.
significant difference in the type of Malassezia species between 2. Ritter SE, Bryan MG, Elston DM. Photo quiz. Trichrome tinea
versicolor. Cutis 2002;70:92, 121‑2.
hyper‑ and hypo‑pigmented skin lesions.[18]
3. Lewis GH, Hopper ME. Pseudo‑achromia of tinea versicolor.
Arch Dermatol Syphilol 1936;34:850‑61.
The differential diagnosis of tinea versicolor includes pityriasis
4. Aljabre SH, Alzayir AA, Abdulghani M, Osman OO.
rosea, pityriasis alba, seborrheic dermatitis, and vitiligo.
Pigmentary changes of tinea versicolor in dark‑skinned
There are a number of therapeutic options for treating tinea patients. Int J Dermatol 2001;40:273‑5.
versicolor. The antifungals used can be divided into topical and 5. Borelli D, Jacobs PH, Nall L. Tinea versicolor: Epidemiologic,
oral medications. Topical medications must be applied over clinical, and therapeutic aspects. J Am Acad Dermatol
entire trunk (from neck to waist) as lesions may be widespread 1991;25:300‑5.
and sometimes clinically unapparent. Systemic medication is 6. Lewis GM, Hopper ME. An Introduction to Medical
preferred in patients with severe disease, frequent relapses, or Mycology. Chicago: Year Book Publishers; 1958.
in whom topical agents have failed. The yeast is part of the 7. Smith EL. Pityriasis versicolor of the penis. Br J Vener Dis
normal flora, and sometimes resides deep in the hair follicles. 1978;54:441.
This may contribute to the high recurrence rate. Other reasons 8. Charles CR, Sire DJ, Johnson BL, Beidler JG. Hypopigmentation
for recurrence include endogenous or exogenous predisposing in tinea versicolor: A histochemical and electronmicroscopic
factors that are still present after treatment. Therefore, it study. Int J Dermatol 1973;12:48‑5.
may be considered a chronic disease with prophylaxis being 9. Borgers M, Cauwenbergh G, Van de Ven MA, del Palacio
an integral part of the overall treatment.[1] In dark skinned Hernanz A, Degreef H. Pityriasis versicolor and Pityrosporum
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10. Nazzaro‑Porro M, Passi S. Identification of tyrosinase
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Gupta and Thappa: Color in tinea versicolor

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How to cite this article: Gupta D, Thappa DM. The enigma of color in
tinea versicolor. Pigment Int 2014;1:32-5.
Source of Support: Nil. Conflict of Interest: None declared.

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