Grzybica różowata
Patofizjologia i mechanizm
Grzybica różowata (Pityriasis versicolor) to powierzchowna infekcja grzybicza warstwy rogowej naskórka wywoływana przez drożdżaki z rodzaju Malassezia, które u 90-100% zdrowych osób występują jako komensale, głównie w obszarach bogatych w sebum. Patogeneza choroby opiera się na transformacji formy drożdżowej w patogenną formę mycelialną, co jest stymulowane przez czynniki środowiskowe (ciepło, wilgotność), indywidualne (łojotok, nadmierna potliwość), zaburzenia endokrynologiczne, immunosupresję oraz predyspozycje genetyczne. Charakterystyczne zmiany skórne obejmują hipopigmentację, hiperpigmentację oraz rumień, wynikające z działania kwasu azelainowego hamującego tyrozynazę melanocytów, obecności pityriacytryny absorbującej UV oraz reakcji zapalnej. W patogenezie istotną rolę odgrywają enzymy i toksyny Malassezia, takie jak fosfolipazy, lipazy, hemolizyny, malassezyna i zdolność do tworzenia biofilmu, które uszkadzają barierę skórną i modulują odpowiedź immunologiczną gospodarza.
- Patogeneza grzybicy różowatej (Pityriasis versicolor)
- Mechanizmy zaburzeń pigmentacji w grzybicy różowatej
- Czynniki wirulencji Malassezia i ich rola w patogenezie
- Rola układu immunologicznego w patogenezie
- Patogeneza wariantu atroficznego grzybicy różowatej
- Mechanizmy zaniku skóry
- Różnice histopatologiczne między zanikową grzybicą różowatą a atrofią posteroidową
- Specyfika gatunkowa Malassezia w patogenezie
- Różnice między gatunkami Malassezia w patogenezie grzybicy różowatej
- Wpływ gatunku na obraz kliniczny i syntezę melaniny
- Współczesne poglądy na patogenezę grzybicy różowatej
Patogeneza grzybicy różowatej (Pityriasis versicolor)
Grzybica różowata (Pityriasis versicolor) jest powierzchowną infekcją grzybiczą warstwy rogowej naskórka, wywoływaną przez drożdżaki z rodzaju Malassezia. Grzyb ten jest częścią prawidłowej flory skóry, występującej u 90-100% zdrowych osób, szczególnie w okolicach bogatych w sebum, takich jak skóra głowy, szyja i ramiona.12 Choroba rozwija się, gdy drożdżak przechodzi z komensalnej formy drożdżowej w patogenną formę mycelialną (strzępkową).34 Gatunkami najczęściej izolowanymi w przypadkach grzybicy różowatej są Malassezia globosa, Malassezia sympodialis i Malassezia furfur.5
Czynniki sprzyjające rozwojowi zakażenia
Transformacja Malassezia z formy drożdżowej (komensalnej) do patogennej formy mycelialnej jest związana z wieloma czynnikami:67
- Warunki środowiskowe: ciepłe i wilgotne środowisko, zwiększona temperatura i wilgotność powietrza (częściej w klimacie tropikalnym i w okresie letnim)89
- Czynniki osobnicze: nadmierna potliwość (hyperhidrosis), skóra łojotokowa, stosowanie oleistych kosmetyków1011
- Zaburzenia endokrynologiczne: ciąża, choroba Cushinga12
- Immunosupresja: stosowanie kortykosteroidów, leczenie immunosupresyjne, zaburzenia odporności komórkowej1314
- Uwarunkowania genetyczne: predyspozycja rodzinna1516
- Niedożywienie i zły stan ogólny17
Rola czynników pokarmowych i lipidów w patogenezie
Malassezia to grzyby lipofilne, które wymagają lipidów do wzrostu zarówno in vitro, jak i in vivo.18 Dystrybucja grzybicy różowatej na ciele może odzwierciedlać wymagania pokarmowe drożdżaków. Większa produkcja sebum przez gruczoły łojowe w górnej części ciała może przyczyniać się do dominacji grzybicy różowatej w tej lokalizacji.1920
Interesującym aspektem jest fakt, że pacjenci z grzybicą różowatą i osoby z grupy kontrolnej nie wykazują żadnych ilościowych lub jakościowych różnic w lipidach powierzchni skóry.21 Badania sugerują, że aminokwasy, a nie lipidy, mogą być kluczowe dla rozwoju stanu chorobowego. In vitro aminokwas asparagina stymuluje wzrost mikroorganizmu, podczas gdy glicyna indukuje tworzenie strzępek.22
Mechanizmy zaburzeń pigmentacji w grzybicy różowatej
Charakterystyczną cechą grzybicy różowatej są zaburzenia pigmentacji skóry, które mogą objawiać się jako hipopigmentacja (odbarwienie), hiperpigmentacja (przebarwienie) lub zmiany rumieniowe. Mechanizmy leżące u podstaw tych zmian są różnorodne i nie do końca poznane.23
Mechanizm hipopigmentacji
Odbarwione zmiany w grzybicy różowatej powstają na skutek enzymatycznego zahamowania aktywności tyrozynazy melanocytów przez kwas azelainowy produkowany przez Malassezia.2425 Kwas ten jest dwukarboksylowym kwasem wytwarzanym przez grzyby i wykazuje silne hamowanie reakcji dopa-tyrozynazy in vitro.26 Badania ultrastrukturalne wskazują na poważne uszkodzenia melanocytów, od zmienionych melanosomów i mitochondriów aż do degeneracji komórek.27
Pacjenci z hipopigmentowaną odmianą grzybicy różowatej często zauważają, że zaburzenie jest najbardziej widoczne latem, gdy dotknięte obszary nie opalają się po ekspozycji na słońce.28 Uszkodzenie melanocytów wyjaśnia, dlaczego repigmentacja może wymagać okresu od kilku miesięcy do lat po skutecznym leczeniu.29
Mechanizm hiperpigmentacji
Patogeneza hiperpigmentacji w grzybicy różowatej nie jest w pełni wyjaśniona. Zaproponowano dwie główne teorie:30
- Pogrubienie warstwy keratynowej skóry
- Obecność intensywnego nacieku komórek zapalnych, który działa jako bodziec dla melanocytów do produkcji większej ilości pigmentu, prowadząc do zwiększenia rozmiaru melanosomów i zmian w ich rozmieszczeniu w naskórku
Dodatkowo, specyficzny związek syntetyzowany przez Malassezia, zwany pityriacytryną, absorbuje promieniowanie UV i może przyczyniać się do hiperpigmentacji.31 Zmiany hiperpigmentowane charakteryzują się większą liczbą organizmów i bardziej wyraźnym naciekiem zapalnym w porównaniu ze zmianami hipopigmentowanymi.32
Mechanizm zmian rumieniowych
Zmiany rumieniowe (zaczerwienione) mogą być konsekwencją reakcji zapalnej na drożdżaki.3334 Odpowiedź zapalna na drożdżaki lub ich metabolity może prowadzić do łagodnego zapalenia skóry objawiającego się jako różowa odmiana grzybicy różowatej.35
Czynniki wirulencji Malassezia i ich rola w patogenezie
Malassezia wytwarza różne czynniki wirulencji i toksyny, które przyczyniają się do jej patogenności. W relacji komensalnej Malassezia pobiera składniki odżywcze od ludzkiego gospodarza bez powodowania negatywnych skutków, jednak w warunkach sprzyjających może stać się patogenna.3637
Enzymy i metabolity patogenne
Do najważniejszych czynników wirulencji Malassezia należą:3839
- Produkcja fosfolipazy
- Produkcja lipazy
- Kwaśne sfingomielinazy (odpowiedzialne za degradację lipidów sebum)
- Hemolizyna
- Zdolność do tworzenia biofilmu
- Malassezyna – indukuje apoptozę melanocytów
- Pityrialakton – związek indolowy fluoryzujący w świetle UV o długości 300 nm
- Pityriarubina – inhibitor enzymów 5-lipooksygenazy40
Sugeruje się, że wzorce enzymatyczne i tworzenie biofilmu, wraz z profilami wrażliwości na leki przeciwgrzybicze, odgrywają kluczową rolę w patogenności Malassezia i mogą wyjaśniać udział poszczególnych gatunków w inwazyjnych zakażeniach.41
Interakcje z barierą skórną i układem immunologicznym
Hyperproliferacja naskórka prawdopodobnie wynika z zaburzenia bariery skórnej spowodowanego przez wolne kwasy tłuszczowe (FFAs). Malassezia, jako grzyby zależne od lipidów, polega na wolnych kwasach tłuszczowych pochodzących z trójglicerydów sebum.4243
MGL_1304 produkowany przez M. globosa jest głównym antygenem uwalniającym histaminę, zaangażowanym w atopowe zapalenie skóry i pokrzywkę cholinergiczną.4445 Sugerowano, że bezpośrednie toksyczne uszkodzenie mieszków włosowych i/lub proapoptotyczne cytokiny indukowane przez Malassezia mogą odgrywać rolę w grzybicy różowatej, ponieważ wykazano, że Malassezia promuje zapalenie granicy skórno-naskórkowej i zwiększa ekspresję interleukin proalopekatycznych.46
Rola układu immunologicznego w patogenezie
System immunologiczny pacjenta odgrywa istotną rolę w rozwoju zakażenia. Badania sugerują obniżoną odpowiedź organizmu na specyficzne elementy grzybicze, które wywołują grzybicę różowatą.47
Zaburzenia immunologiczne a rozwój infekcji
W różnych badaniach stwierdzono następujące zaburzenia immunologiczne u pacjentów z grzybicą różowatą:48
- Defekty w produkcji limfokin i komórek T-NK (naturalnych zabójców)
- Zmniejszona stymulacja fitohemaglutyniny (PHA) i konkanawaliny A (Con A)
- Zmniejszona produkcja interleukiny-2 (IL-2), interleukiny-10 (IL-10) i interferonu gamma przez limfocyty
Limfocyty pacjentów z grzybicą różowatą wytwarzają mniej czynnika migracji leukocytów po stymulacji P. orbiculare.49 W jednym z badań u pacjenta z grzybicą różowatą i leiszmaniozą trzewną (choroba z obniżoną odpornością komórkową) zaobserwowano poprawę w zakresie grzybicy po leczeniu leiszmaniozy.50
Rola odpowiedzi Th1/Th2 w patogenezie
Odpowiedź immunologiczna typu komórkowego na antygeny Malassezia może być kluczowa w patogenezie, szczególnie w atroficznej (zanikowej) odmianie grzybicy różowatej. Zaproponowano, że reakcja nadwrażliwości typu IV napędzana przez mieszaną odpowiedź immunologiczną Th1/Th2 na Malassezia może leżeć u podstaw niektórych wariantów choroby.51
Cytokiny Th1 przyczyniają się do atrofii i elastolizy głównie poprzez zwiększenie aktywności metaloproteinaz macierzy. Spłaszczenie listewek skórnych jest z kolei zapośredniczone przez cytokiny, takie jak czynnik martwicy nowotworu (TNF) i interleukina 1, które mogą hamować szlak czynnika jądrowego κB keratynocytów, indukując apoptozę i hamując ich proliferację.52
Odpowiedź komórek Th2, która może sprzyjać nadmiernemu wzrostowi grzybów, została wskazana, wraz z odpowiedzią Th1, w patogenezie atroficznej odmiany grzybicy różowatej.53
Patogeneza wariantu atroficznego grzybicy różowatej
Atroficzna (zanikowa) grzybica różowata jest rzadką odmianą choroby, charakteryzującą się ścieńczeniem skóry w miejscach zakażenia. Dokładna patofizjologia pozostaje nieznana, ale zaproponowano kilka hipotez.54
Mechanizmy zaniku skóry
Tatnall i Rycroft wysunęli hipotezę, że bariera skórna jest zaburzona przez grzybicę różowatą, co umożliwia lepszą absorpcję steroidów, które indukują atrofię.55 Crowson i Magro po przeprowadzeniu badań klinicznych i histologicznych u 12 pacjentów z atroficzną grzybicą różowatą, zaproponowali, że opóźnione reakcje nadwrażliwości na antygeny pochodzące z drożdżaków Malassezia kolonizujących powierzchnię naskórka i ujścia mieszków włosowych lub bezpośredni wpływ Malassezia na szlak sygnałowy czynnika jądrowego κB powodują atroficzną grzybicę różowatą.56
Levy i Magro po przeglądzie 6 przypadków atroficznej grzybicy różowatej zaproponowali, że reakcja nadwrażliwości typu IV napędzana przez mieszaną odpowiedź immunologiczną Th1/Th2 na Malassezia oraz cytokiny Th1 przyczyniają się do atrofii i elastolizy głównie poprzez zwiększenie aktywności metaloproteinaz macierzy.57
Różnice histopatologiczne między zanikową grzybicą różowatą a atrofią posteroidową
Cechy histopatologiczne ujawniają kolonizację naskórka przez strzępki i zarodniki Pityrosporum, której towarzyszy zmienna atrofia naskórka, atrofia skóry właściwej, elastoliza skóry właściwej i powierzchowny okołonaczyniowy naciek limfocytarny.58
Różnica histopatologiczna między atrofią wywołaną steroidami a atroficzną grzybicą różowatą polega na tym, że atrofia wywołana kortykosteroidami wiąże się z głęboką atrofią naskórka, teleangiektazjami i osłabieniem struktury kolagenu. W atroficznej grzybicy różowatej występuje elastoliza skóry właściwej przyczyniająca się do wystąpienia atrofii skóry.59
W atrofii wywołanej kortykosteroidami, oprócz atrofii naskórka i rozszerzenia naczyń, obserwujemy atrofię przydatków skóry oraz redukcję i fragmentację kolagenu skóry właściwej, podczas gdy w atroficznej grzybicy różowatej nie obserwujemy zmian w kolagenie, ale zmiany we włóknach elastycznych.60
| Cecha | Atrofia posteroidowa | Atroficzna grzybica różowata |
|---|---|---|
| Atrofia naskórka | Głęboka | Zmienna |
| Teleangiektazje | Obecne | Mogą być obecne |
| Kolagen skóry właściwej | Redukcja i fragmentacja | Brak zmian |
| Włókna elastyczne | Bez wyraźnych zmian | Elastoliza |
| Przydatki skóry | Atrofia | Bez wyraźnej atrofii |
| Obecność grzybów | Brak | Strzępki i zarodniki Malassezia |
| Naciek zapalny | Minimalny | Powierzchowny okołonaczyniowy naciek limfocytarny |
Specyfika gatunkowa Malassezia w patogenezie
Różne gatunki Malassezia mogą wykazywać odmienne cechy wirulencji i preferencje środowiskowe, co wpływa na obraz kliniczny i odpowiedź na leczenie.61
Różnice między gatunkami Malassezia w patogenezie grzybicy różowatej
Badania wskazują, że przypadki grzybicy różowatej reprezentowane przez dwa typy zmian skórnych u jednego pacjenta mogą być związane z różnymi gatunkami Malassezia. Każdy z wyizolowanych czynników etiologicznych może znacznie różnić się wrażliwością na leki przeciwgrzybicze, co może znacznie komplikować leczenie dermatozy, która z definicji wiąże się ze znacznym odsetkiem nawrotów.62
Podczas gdy na zdrowej skórze Malassezia rozmnaża się jako pączkujący drożdżak, w stanie wybuchu choroby komórki często rozwijają się w pseudostrzępki, prowadząc do rozwoju typowych objawów związanych z grzybicą różowatą. Taki patomechanizm zakażenia jest najbardziej typowy dla M. globosa i M. furfur, ale może również dotyczyć M. sympodialis, które mogą tworzyć pseudostrzępki w ludzkim stratum corneum i są najczęstszymi czynnikami etiologicznymi grzybicy różowatej na całym świecie.63
Wpływ gatunku na obraz kliniczny i syntezę melaniny
Najbardziej prawdopodobna wydaje się hipoteza wskazująca na rozbieżności w zdolności do syntezy melaniny przez M. furfur i M. sympodialis, po raz pierwszy sformułowana przez Gaitanisa i wsp., a później wyjaśniona przez Ianiria i wsp. w oparciu o narzędzia molekularne.64
W badaniu przeprowadzonym w 2020 roku stwierdzono statystycznie istotny związek między zakażeniem Helicobacter pylori a grzybicą różowatą, proponując zakażenie H. pylori jako czynnik etiologiczny tej infekcji grzybiczej, choć nie zostało to zweryfikowane w większych badaniach.65
Nowsze badania pokazują, że najczęściej izolowanym gatunkiem w przypadkach grzybicy różowatej jest M. furfur (35,2%), następnie M. globosa (21,6%), M. obtusa (19,6%), M. pachydermatis i M. sympodialis (po 11,8%).66
Współczesne poglądy na patogenezę grzybicy różowatej
Patogeneza grzybicy różowatej jest złożonym procesem, który obejmuje interakcje między drożdżakami Malassezia a gospodarzem, czynniki środowiskowe oraz mechanizmy odpowiedzi immunologicznej.67
Kluczowe aspekty patogenezy grzybicy różowatej obejmują:6869
- Transformację lipofilnych drożdżaków Malassezia z komensalnej formy drożdżowej do patogennej formy mycelialnej
- Wpływ czynników środowiskowych, takich jak ciepło, wilgotność oraz czynników gospodarza, takich jak predyspozycja genetyczna, zaburzenia immunologiczne i hormonalne
- Produkcję przez Malassezia różnych enzymów i metabolitów, które zaburzają funkcje skóry, w tym produkcję kwasu azelainowego hamującego tyrozynazę, co prowadzi do hipopigmentacji
- Odpowiedź immunologiczną gospodarza na antygeny Malassezia, która może prowadzić do zapalenia i zmian w pigmentacji skóry
- Zaburzenia bariery naskórkowej, które mogą prowadzić do zwiększonej penetracji leków i innych substancji
Zrozumienie złożonych mechanizmów patogenezy grzybicy różowatej ma kluczowe znaczenie dla opracowania skutecznych strategii leczenia i zapobiegania nawrotom tej częstej infekcji grzybiczej.70 Pomimo znacznego postępu w zrozumieniu i leczeniu grzybicy różowatej, niezbędne są dalsze badania. Przyszłe wysiłki powinny zmierzać do optymalizacji skuteczności leczenia, zmniejszenia częstości nawrotów i zminimalizowania działań niepożądanych.71
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Materiały źródłowe
- #1 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
Pityriasis versicolor is caused by Malassezia furfur, which may appear in two forms: oval – Pityrosporum ovale-, often in the scalp, and cylindrical – Pityrosporum orbiculare-generally on the trunk. These fungi require the addition of lipidic substances in the middle of culture, like olive oil. They grow better on average in 32-37C environments. Filaments normally seen in areas of the skin affected by infection grow when the yeasts are incubated in stratum corneum. P. orbiculare and P. ovale are similar in macromorphology, but differ in micromorphology. Observations show that the two forms are produced by the same organism, with the transformation of one into another possibly taking place; some antigenic similarities have also been reported. Three distinct forms of Malassezia furfur were recently described by Cunnigham et al., and denominated serotypes A, B and C, which differ morphologically, physiologically and serologically, with distinct cellular membrane antigens. A recent study did not describe any difference between the distribution of serotypes in affected skin when compared to the control group.
- #2 Pityriasis versicolor – Symptoms, diagnosis and treatment | BMJ Best Practice UShttps://bestpractice.bmj.com/topics/en-us/861
Pityriasis versicolor is a superficial fungal infection of the stratum corneum, due to dimorphic yeasts of the genus Malassezia, leading to hypo- or hyperpigmented macular lesions on seborrheic areas of the trunk. […] Pityriasis versicolor (PV), also known as tinea versicolor, is a common superficial fungal infection of the stratum corneum (outer layer of the epidermis) resulting from a change to the mycelial (filamentous fungus or mould) state of dimorphic yeasts of the genus Malassezia. […] The eruption is most common in the summer months in adolescents and young adults, favors oily areas of the skin, and often has a relapsing nature requiring frequent treatment.
- #3 Tinea Versicolor – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK482500/
Pityriasis versicolor, or tinea versicolor, is a common, benign, superficial fungal skin infection. The causative organism, yeast from the genus Malassezia, is part of the normal skin flora. […] Tinea versicolor is caused by Malassezia, a dimorphic lipophilic fungus previously known as Pityrosporum. Malassezia is a component of the normal skin flora. Clinical disease develops when Malassezia transforms from yeast into its mycelial form. […] The precise elements in the host’s environment that trigger tinea versicolor still need to be clarified. […] Environmental factors like heat and humidity, pregnancy, oily skin, and applying oily lotions and creams increase the risk of tinea versicolor. […] An inflammatory response to the yeast could cause hyperpigmented and erythematous lesions.
- #4 Tinea Versicolor: Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/1091575-overview
Tinea versicolor is caused by the dimorphic, lipophilic organisms in the genus Malassezia, formerly known as Pityrosporum. Fourteen species are recognized within this classification of yeasts, of which Malassezia globosa, Malassezia sympodialis, and Malassezia furfur are the predominant species isolated in tinea versicolor. […] The organism can be found on healthy skin and on skin regions demonstrating cutaneous disease. In patients with clinical disease, the organism is found in both the yeast (spore) stage and the filamentous (hyphal) form. Factors that lead to the conversion of the saprophytic yeast to the parasitic, mycelial morphologic form include a genetic predisposition; warm, humid environments; immunosuppression; malnutrition; pregnancy; and Cushing disease. […] Even though Malassezia is a component of the normal flora, it can also be an opportunistic pathogen. The organism is considered to be a factor in other cutaneous diseases, including Pityrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic dermatitis, psoriasis, and some forms of atopic dermatitis.
- #5 Tinea Versicolor: Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/1091575-overview
Tinea versicolor is caused by the dimorphic, lipophilic organisms in the genus Malassezia, formerly known as Pityrosporum. Fourteen species are recognized within this classification of yeasts, of which Malassezia globosa, Malassezia sympodialis, and Malassezia furfur are the predominant species isolated in tinea versicolor. […] The organism can be found on healthy skin and on skin regions demonstrating cutaneous disease. In patients with clinical disease, the organism is found in both the yeast (spore) stage and the filamentous (hyphal) form. Factors that lead to the conversion of the saprophytic yeast to the parasitic, mycelial morphologic form include a genetic predisposition; warm, humid environments; immunosuppression; malnutrition; pregnancy; and Cushing disease. […] Even though Malassezia is a component of the normal flora, it can also be an opportunistic pathogen. The organism is considered to be a factor in other cutaneous diseases, including Pityrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic dermatitis, psoriasis, and some forms of atopic dermatitis.
- #6 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
Malassezia is a dimorphic yeast-like fungus. It causes PV only in its pathogenic, filamentous (hyphal) form. Factors favouring the conversion from the yeast-like form include a hot and humid environment, hyperhidrosis, the application of oily emollients, using protective face masks, seborrhoea, endocrine and neuropathic disorders, pregnancy, the use of oral contraceptives and corticosteroids, malnutrition, poor general health, and genetic predisposition. […] Malassezia produces virulence factors and toxins that contribute to its pathogenicity. However, in its commensal relationship, Malassezia collects nutrients from the human host without causing negative effects. […] Understanding the role of Malassezia as a direct and indirect cause of PV (via its multifaceted interaction with the skin) is challenging. It is suspected that one of the possible causes for Malassezia virulence is the individual genetic susceptibility.
- #7 Tinea versicolor (pityriasis versicolor) – UpToDatehttps://www.uptodate.com/contents/tinea-versicolor-pityriasis-versicolor/print
Although the reasons for pigmentary variation in tinea versicolor are unconfirmed, theories have been proposed. Patients with hypopigmented tinea versicolor often notice that the disorder is most prominent during the summer, when the affected areas fail to tan after sun exposure. Inhibitory or damaging effects on melanocytes by azelaic acid (a dicarboxylic acid produced by Malassezia) may play a role in the development of hypopigmentation. Hyperpigmented and erythematous lesions may be a consequence of an inflammatory reaction to the yeast. […] External factors suspected of contributing to the transformation of Malassezia from yeast cells to a pathogenic, mycelial form include exposure to hot and humid weather, hyperhidrosis, and the use of topical skin oils. Tinea versicolor is not related to poor hygiene.
- #8 Tinea versicolor – Symptoms & causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/tinea-versicolor/symptoms-causes/syc-20378385
Tinea versicolor is a common fungal infection of the skin. The fungus interferes with the normal pigmentation of the skin, resulting in small, discolored patches. […] The overgrowth of fungus that causes tinea versicolor interferes with the normal pigment production of the skin. This creates an uneven skin pigment. […] The fungus that causes tinea versicolor can be found on healthy skin. It only starts causing problems when the fungus overgrows. A number of factors may trigger this growth, including: Hot, humid weather, Oily skin, Hormonal changes, Weakened immune system.
- #9 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
The organism is found in normal flora conditions, in percentages varying from 90 to 100% of individuals. It appears to be opportunistic, though the factors that increase susceptibility have not been completely defined yet. The simple fact of high growth does not seem to be the underlying cause, though some skin lesion cultures show much higher amounts of P. orbiculare in comparison of non-lesional skin with the skin of healthy volunteers. […] PV occurs when yeasts are converted by the micellar form due to certain predisposed factors, which may be classified as endogenic or exogenic. The exogenous factors include heat and humidity, contributing to higher disease prevalence in the tropics and during the summer in temperate climates. Other exogenous factor may be skin occlusion by clothing or cosmetics, resulting in an increase of carbon dioxide concentration and leading to microflora and pH changes. The infection has been experimentally induced by occlusive clothing. On the other hand, endogenic factors are responsible due to disease prevalence in temperate climates, including seborrheic dermatitis, Cushing’s syndrome, treatment with immunosuppressor, malnutrition and (particularly flexural) hyperhydrosis. Hereditary factors appear to perform a certain role in the disease. Positive familial history was noted in various studies, while conjugal cases are less commonly reported.
- #10 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
Malassezia is a dimorphic yeast-like fungus. It causes PV only in its pathogenic, filamentous (hyphal) form. Factors favouring the conversion from the yeast-like form include a hot and humid environment, hyperhidrosis, the application of oily emollients, using protective face masks, seborrhoea, endocrine and neuropathic disorders, pregnancy, the use of oral contraceptives and corticosteroids, malnutrition, poor general health, and genetic predisposition. […] Malassezia produces virulence factors and toxins that contribute to its pathogenicity. However, in its commensal relationship, Malassezia collects nutrients from the human host without causing negative effects. […] Understanding the role of Malassezia as a direct and indirect cause of PV (via its multifaceted interaction with the skin) is challenging. It is suspected that one of the possible causes for Malassezia virulence is the individual genetic susceptibility.
- #11 Pityriasis Versicolor (for Teens) – CareSourcehttps://kidshealth.org/CareSource/en/teens/pityriasis-versicolor.html
Pityriasis versicolor is caused by a type of yeast that normally lives on the skin. […] When the environment it lives in gets warm and moist, it can grow out of control and cause symptoms. […] Hot, humid weather and lots of sweating can create a warm, moist environment for the yeast to overgrow. […] The yeast also likes an oily environment, so oily skin can play a part (and of course, teens and young adults can have oily skin). […] Sometimes pityriasis versicolor runs in families. It’s also more likely to affect people who have a weakened immune system or who are malnourished.
- #12 Tinea Versicolor: Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/1091575-overview
Tinea versicolor is caused by the dimorphic, lipophilic organisms in the genus Malassezia, formerly known as Pityrosporum. Fourteen species are recognized within this classification of yeasts, of which Malassezia globosa, Malassezia sympodialis, and Malassezia furfur are the predominant species isolated in tinea versicolor. […] The organism can be found on healthy skin and on skin regions demonstrating cutaneous disease. In patients with clinical disease, the organism is found in both the yeast (spore) stage and the filamentous (hyphal) form. Factors that lead to the conversion of the saprophytic yeast to the parasitic, mycelial morphologic form include a genetic predisposition; warm, humid environments; immunosuppression; malnutrition; pregnancy; and Cushing disease. […] Even though Malassezia is a component of the normal flora, it can also be an opportunistic pathogen. The organism is considered to be a factor in other cutaneous diseases, including Pityrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic dermatitis, psoriasis, and some forms of atopic dermatitis.
- #13 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
Malassezia furfur has been associated to folliculitis by Pityrosporum, reticular and confluent papilloma (Gougerot-Carteaud), seborrheic dermatitis, septicemic onychomycosis. In both the pathogenic and opportunist forms, the fungus resides inside of the stratum corneum and hair follicles, where it is fed by free fatty acids, sebum triglycerides and keratinized epidermis. […] A possible factor in the development of PV is depressed cellular immunity. The lymphocytes of PV-carriers appear to produce a lower leucocyte migration factor of when stimulated with P. orbiculare stratum. In one study of a patient with PV and carrying the visceral leishmaniasis, a depressed cellular immunity disease, there was improvement in mycosis after treatment of the leishmaniasis. […] It has been suggested that the lipoperoxidation process produced by Pityrosporum could be responsible for the clinical hypopigmented appearance of lesioned skin. Culture strata containing dicarboxilic acids, like azelaic acid, has shown strong inhibition in the in vitro dopa-tirasinase reaction. Ultrastructural studies point to severe damage in the melanocytes, varying from melanossomas and altered mitochondria up to degeneration. These dicarboxilic acids may be causing the cytotoxic effects. The damage to melanocytes explains why re-pigmentation may require periods varying from months to years. Another explanation is the fact that the PV scales prevent re-pigmentation. Soon after treatment, the area affected was still hypopigmented for a variable period of time.
- #14 Tinea (Pityriasis) versicolor: etiology, clinical manifestations diagnosis and treatment – Online Biology Noteshttps://www.onlinebiologynotes.com/tinea-pityriasis-versicolor-etiology-clinical-manifestations-diagnosis-and-treatment/
Tinea versicolor is a common, mild, but often recurrent infection of the stratum corneum because of the lipophilic yeasts of the genus Malassezia. […] The accurate conditions which results in the development of pityriasis versicolor and other forms of superficial Malassezia infection have not been defined, but host and environmental factors both seem to be essential. […] The relationship between Malassezia species and the immune system is essential. […] It is suggested by increased incidence of Malassezia folliculitis and seborrhoeic dermatitis in persons with the acquired immune-deficiency syndrome (AIDS) and those receiving corticosteroid or other immunosuppressive treatment.
- #15 Tinea versicolor (pityriasis versicolor) – UpToDatehttps://www.uptodate.com/contents/tinea-versicolor-pityriasis-versicolor/print
Host characteristics that contribute to the development of tinea versicolor are poorly understood. A genetic predisposition may be involved. In a questionnaire-based study, 21 percent of patients reported a positive family history of the disease. Tinea versicolor also occurs more commonly in patients who are immunosuppressed, suggesting that an altered host immune response may play a role in the pathogenesis.
- #16 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
The organism is found in normal flora conditions, in percentages varying from 90 to 100% of individuals. It appears to be opportunistic, though the factors that increase susceptibility have not been completely defined yet. The simple fact of high growth does not seem to be the underlying cause, though some skin lesion cultures show much higher amounts of P. orbiculare in comparison of non-lesional skin with the skin of healthy volunteers. […] PV occurs when yeasts are converted by the micellar form due to certain predisposed factors, which may be classified as endogenic or exogenic. The exogenous factors include heat and humidity, contributing to higher disease prevalence in the tropics and during the summer in temperate climates. Other exogenous factor may be skin occlusion by clothing or cosmetics, resulting in an increase of carbon dioxide concentration and leading to microflora and pH changes. The infection has been experimentally induced by occlusive clothing. On the other hand, endogenic factors are responsible due to disease prevalence in temperate climates, including seborrheic dermatitis, Cushing’s syndrome, treatment with immunosuppressor, malnutrition and (particularly flexural) hyperhydrosis. Hereditary factors appear to perform a certain role in the disease. Positive familial history was noted in various studies, while conjugal cases are less commonly reported.
- #17 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
Malassezia is a dimorphic yeast-like fungus. It causes PV only in its pathogenic, filamentous (hyphal) form. Factors favouring the conversion from the yeast-like form include a hot and humid environment, hyperhidrosis, the application of oily emollients, using protective face masks, seborrhoea, endocrine and neuropathic disorders, pregnancy, the use of oral contraceptives and corticosteroids, malnutrition, poor general health, and genetic predisposition. […] Malassezia produces virulence factors and toxins that contribute to its pathogenicity. However, in its commensal relationship, Malassezia collects nutrients from the human host without causing negative effects. […] Understanding the role of Malassezia as a direct and indirect cause of PV (via its multifaceted interaction with the skin) is challenging. It is suspected that one of the possible causes for Malassezia virulence is the individual genetic susceptibility.
- #18 Tinea Versicolor: Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/1091575-overview
The reason why this organism causes tinea versicolor in some individuals while remains as normal flora in others is not entirely known. Several factors, such as the organism’s nutritional requirements and the host’s immune response to the organism, are significant. […] The organism is lipophilic, and lipids are essential for growth in vitro and in vivo. […] However, patients with tinea versicolor and control subjects do not demonstrate any quantitative or qualitative differences in skin surface lipids. […] Evidence has been accumulating to suggest that amino acids, rather than lipids, are critical for the appearance of the diseased state. […] Another significant causative factor is the patient’s immune system. […] Oxidative stress as shown by expression of reduced glutathione contributes to the pathogenesis of this condition.
- #19 Tinea versicolor (pityriasis versicolor) – UpToDatehttps://www.uptodate.com/contents/tinea-versicolor-pityriasis-versicolor/print
Tinea versicolor (ie, pityriasis versicolor) is a common superficial fungal infection that typically presents with hypopigmented, hyperpigmented, or erythematous macules on the trunk and proximal upper extremities. […] The causative organisms are saprophytic yeasts in the genus Malassezia (formerly known as Pityrosporum). Malassezia is a lipid-dependent, dimorphic fungus that is a component of normal skin flora. Transformation of Malassezia from yeast cells to a pathogenic, mycelial form is associated with the development of clinical disease. […] The distribution of tinea versicolor on the body may reflect the nutritional requirements of the yeast. Malassezia is lipid dependent, and the greater sebum production by cutaneous sebaceous glands on the upper body may contribute to the predominance of tinea versicolor in this location.
- #20 Can Pityriasis Versicolor Be Treated With 2% Ketoconazole Foam? – JDDonline – Journal of Drugs in Dermatologyhttps://jddonline.com/articles/can-pityriasis-versicolor-be-treated-with-2-ketoconazole-foam-S1545961614P0855X
Pityriasis (tinea) versicolor is a superficial fungal infection of the stratum corneum caused by Malassezia species. […] Most species of Malassezia are a part of normal skin flora, but as conditions become more favorable, the organism evolves from the physiologic blastospore form into its pathologic mycelial form. […] Favorable conditions include warmer temperatures, increased humidity, immunodeficiency or immunocompromise, elevated corticosteroids, pregnancy, and malnourishment. […] These conditions generally cause increased activity of sebaceous glands, which helps create the lipid-rich environment needed for Malassezia to thrive. […] This quality seems to explain why pityriasis versicolor is rarely found in very young or very elderly patients, but usually appears in postpubertal and mature ages when the sebaceous glands are most active.
- #21 Tinea Versicolor: Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/1091575-overview
The reason why this organism causes tinea versicolor in some individuals while remains as normal flora in others is not entirely known. Several factors, such as the organism’s nutritional requirements and the host’s immune response to the organism, are significant. […] The organism is lipophilic, and lipids are essential for growth in vitro and in vivo. […] However, patients with tinea versicolor and control subjects do not demonstrate any quantitative or qualitative differences in skin surface lipids. […] Evidence has been accumulating to suggest that amino acids, rather than lipids, are critical for the appearance of the diseased state. […] Another significant causative factor is the patient’s immune system. […] Oxidative stress as shown by expression of reduced glutathione contributes to the pathogenesis of this condition.
- #22 Pediatric Tinea Versicolor: Background, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/911138-overview
Tinea versicolor (or pityriasis versicolor) is a common superficial cutaneous fungal infection characterized by pityriasiform desquamation and hypopigmented or hyperpigmented macule formation, primarily located on the chest and back with a tendency to spread. The condition is frequently asymptomatic; however, some patients occasionally report pruritus. Tinea versicolor results from an overgrowth of Malassezia, which is part of normal skin flora and produces pigmentation changes when it flourishes beyond normal levels. […] The nutritional requirements of Malassezia are among the most important factors affecting the organism’s growth on the skin. Compared with normal skin, lesion sites show decreases in sebaceous gland secretions and water content, along with an increase in pH. M furfur is lipophilic, and its mycelial stage can be induced in vitro by adding cholesterol and cholesterol esters to the appropriate medium. However, the finding that significantly more amino acids are extracted from the skin of infected patients suggests that amino acids, rather than lipids, are critical for the development of the disease. In vitro, the amino acid asparagine stimulates the growth of the organism, whereas glycine induces hyphal formation.
- #23 Tinea versicolor (pityriasis versicolor) – UpToDatehttps://www.uptodate.com/contents/tinea-versicolor-pityriasis-versicolor
Although the reasons for pigmentary variation in tinea versicolor are unconfirmed, theories have been proposed. Patients with hypopigmented tinea versicolor often notice that the disorder is most prominent during the summer, when the affected areas fail to tan after sun exposure. Inhibitory or damaging effects on melanocytes by azelaic acid (a dicarboxylic acid produced by Malassezia) may play a role in the development of hypopigmentation. Hyperpigmented and erythematous lesions may be a consequence of an inflammatory reaction to the yeast.
- #24 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
With mild barrier defects, the fungus has a potential to produce hypo- or hyperpigmented patches by interacting with melanocytes. Depigmented lesions develop through enzymatic inhibition of melanocyte tyrosinase activity by azelaic acid produced by the microorganism. […] Other important virulence factors of Malassezia include the production of phospholipase, lipase, acid sphingomyelinases (responsible for sebum lipid degradation), haemolysin, and the ability to produce a biofilm. […] It has been suggested that enzymatic patterns and biofilm formation, along with antifungal susceptibility profiles, play a key role in the pathogenicity of Malassezia spp. and may explain the involvement of particular species in invasive infections. […] Epidermal hyperproliferation likely stems from the disruption of the skin barrier caused by free fatty acids (FFAs). Malassezia, being lipid-dependent fungi, rely on FFAs derived from sebaceous triglycerides.
- #25 Tinea Versicolor – Dermatologic Disorders – Merck Manual Professional Editionhttps://www.merckmanuals.com/professional/dermatologic-disorders/fungal-skin-infections/tinea-versicolor
Hypopigmentation in tinea versicolor is due to the inhibition of tyrosinase caused by M. furfur production of azelaic acid. […] Diagnosis of tinea versicolor is based on clinical appearance and by identification of hyphae and budding cells (spaghetti and meatballs) on potassium hydroxide wet mount of fine scale scrapings. […] Fluconazole 150 mg/week orally for 2 to 4 weeks is indicated for patients with extensive disease and those with frequent recurrences. […] Hypopigmentation resulting from tinea versicolor is reversible in months to years after the yeast has cleared. […] Recurrence is almost universal after treatment because the causative organism is a normal skin inhabitant.
- #26 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
Malassezia furfur has been associated to folliculitis by Pityrosporum, reticular and confluent papilloma (Gougerot-Carteaud), seborrheic dermatitis, septicemic onychomycosis. In both the pathogenic and opportunist forms, the fungus resides inside of the stratum corneum and hair follicles, where it is fed by free fatty acids, sebum triglycerides and keratinized epidermis. […] A possible factor in the development of PV is depressed cellular immunity. The lymphocytes of PV-carriers appear to produce a lower leucocyte migration factor of when stimulated with P. orbiculare stratum. In one study of a patient with PV and carrying the visceral leishmaniasis, a depressed cellular immunity disease, there was improvement in mycosis after treatment of the leishmaniasis. […] It has been suggested that the lipoperoxidation process produced by Pityrosporum could be responsible for the clinical hypopigmented appearance of lesioned skin. Culture strata containing dicarboxilic acids, like azelaic acid, has shown strong inhibition in the in vitro dopa-tirasinase reaction. Ultrastructural studies point to severe damage in the melanocytes, varying from melanossomas and altered mitochondria up to degeneration. These dicarboxilic acids may be causing the cytotoxic effects. The damage to melanocytes explains why re-pigmentation may require periods varying from months to years. Another explanation is the fact that the PV scales prevent re-pigmentation. Soon after treatment, the area affected was still hypopigmented for a variable period of time.
- #27 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
Malassezia furfur has been associated to folliculitis by Pityrosporum, reticular and confluent papilloma (Gougerot-Carteaud), seborrheic dermatitis, septicemic onychomycosis. In both the pathogenic and opportunist forms, the fungus resides inside of the stratum corneum and hair follicles, where it is fed by free fatty acids, sebum triglycerides and keratinized epidermis. […] A possible factor in the development of PV is depressed cellular immunity. The lymphocytes of PV-carriers appear to produce a lower leucocyte migration factor of when stimulated with P. orbiculare stratum. In one study of a patient with PV and carrying the visceral leishmaniasis, a depressed cellular immunity disease, there was improvement in mycosis after treatment of the leishmaniasis. […] It has been suggested that the lipoperoxidation process produced by Pityrosporum could be responsible for the clinical hypopigmented appearance of lesioned skin. Culture strata containing dicarboxilic acids, like azelaic acid, has shown strong inhibition in the in vitro dopa-tirasinase reaction. Ultrastructural studies point to severe damage in the melanocytes, varying from melanossomas and altered mitochondria up to degeneration. These dicarboxilic acids may be causing the cytotoxic effects. The damage to melanocytes explains why re-pigmentation may require periods varying from months to years. Another explanation is the fact that the PV scales prevent re-pigmentation. Soon after treatment, the area affected was still hypopigmented for a variable period of time.
- #28 Tinea versicolor (pityriasis versicolor) – UpToDatehttps://www.uptodate.com/contents/tinea-versicolor-pityriasis-versicolor/print
Although the reasons for pigmentary variation in tinea versicolor are unconfirmed, theories have been proposed. Patients with hypopigmented tinea versicolor often notice that the disorder is most prominent during the summer, when the affected areas fail to tan after sun exposure. Inhibitory or damaging effects on melanocytes by azelaic acid (a dicarboxylic acid produced by Malassezia) may play a role in the development of hypopigmentation. Hyperpigmented and erythematous lesions may be a consequence of an inflammatory reaction to the yeast. […] External factors suspected of contributing to the transformation of Malassezia from yeast cells to a pathogenic, mycelial form include exposure to hot and humid weather, hyperhidrosis, and the use of topical skin oils. Tinea versicolor is not related to poor hygiene.
- #29 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
Malassezia furfur has been associated to folliculitis by Pityrosporum, reticular and confluent papilloma (Gougerot-Carteaud), seborrheic dermatitis, septicemic onychomycosis. In both the pathogenic and opportunist forms, the fungus resides inside of the stratum corneum and hair follicles, where it is fed by free fatty acids, sebum triglycerides and keratinized epidermis. […] A possible factor in the development of PV is depressed cellular immunity. The lymphocytes of PV-carriers appear to produce a lower leucocyte migration factor of when stimulated with P. orbiculare stratum. In one study of a patient with PV and carrying the visceral leishmaniasis, a depressed cellular immunity disease, there was improvement in mycosis after treatment of the leishmaniasis. […] It has been suggested that the lipoperoxidation process produced by Pityrosporum could be responsible for the clinical hypopigmented appearance of lesioned skin. Culture strata containing dicarboxilic acids, like azelaic acid, has shown strong inhibition in the in vitro dopa-tirasinase reaction. Ultrastructural studies point to severe damage in the melanocytes, varying from melanossomas and altered mitochondria up to degeneration. These dicarboxilic acids may be causing the cytotoxic effects. The damage to melanocytes explains why re-pigmentation may require periods varying from months to years. Another explanation is the fact that the PV scales prevent re-pigmentation. Soon after treatment, the area affected was still hypopigmented for a variable period of time.
- #30 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
The pathogenesis of hyperpigmentation in PV is not entirely understood. Two theories have been presented: (I) thickening of the keratine layer; and (II) presence of intense cellular inflamed infiltrate, which acts like a stimulus for melanocytes to produce more pigment, leading to an increase in the size of melanosomes and distribution changes in the epidermis.
- #31 Pityriasis versicolor | PPThttps://www.slideshare.net/slideshow/pityriasis-versicolor/179230545
Malassezia metabolizes various fatty acids likearachidonic acids or vaccenic acid via lipase and releases Azelic acids which through inhibition of Tyrosinase in Melanin production resulting in persistent hypopigmentation of affected skin for months or sometimes years. Specific compound synthesized by Malassezia called pityriacitrin that absorbs UV light and causes hyperpigmentation. Other metabolites: Malassezin : Induces apoptosis of melanocytes. Pityrialactone : an indole alkaloids that fluroscences under 300nm uv light Pityriarubin : inhibits 5-lipoxygenase enzymes.
- #32 Dermoscopic pattern of pityriasis versicolor | CCIDhttps://www.dovepress.com/dermoscopic-pattern-of-pityriasis-versicolor-peer-reviewed-fulltext-article-CCID
Pityriasis versicolor (PV) is usually a clinical diagnosis and microscopic examination is useful when the diagnosis is uncertain. […] The present study describes the various features observed in the dermoscopy of both the hypopigmented and hyperpigmented lesions of PV. […] Dermoscopy of PV is not well described in the literature. […] In our study, nonuniform pigmentation within a lesion was the most common dermoscopic feature seen in both the hypopigmented and hyperpigmented lesions. […] Perilesional or marginal hyperpigmentation was another feature noted in the hypopigmented lesions observed in our study. […] Presence of scales was another prominent dermoscopic finding in both the hypopigmented and hyperpigmented lesions in our study. […] Hyperpigmented lesions are characterized by a higher number of organisms and more pronounced inflammatory infiltrate compared to the hypopigmented lesions.
- #33 Tinea versicolor (pityriasis versicolor) – UpToDatehttps://www.uptodate.com/contents/tinea-versicolor-pityriasis-versicolor/print
Although the reasons for pigmentary variation in tinea versicolor are unconfirmed, theories have been proposed. Patients with hypopigmented tinea versicolor often notice that the disorder is most prominent during the summer, when the affected areas fail to tan after sun exposure. Inhibitory or damaging effects on melanocytes by azelaic acid (a dicarboxylic acid produced by Malassezia) may play a role in the development of hypopigmentation. Hyperpigmented and erythematous lesions may be a consequence of an inflammatory reaction to the yeast. […] External factors suspected of contributing to the transformation of Malassezia from yeast cells to a pathogenic, mycelial form include exposure to hot and humid weather, hyperhidrosis, and the use of topical skin oils. Tinea versicolor is not related to poor hygiene.
- #34 Pityriasis versicolor. Tinea versicolorhttps://dermnetnz.org/topics/pityriasis-versicolor
Pityriasis versicolor is caused by mycelial growth of fungi of the genus Malassezia. […] Usually malassezia grow sparsely in the seborrhoeic areas (scalp, face and chest) without causing a rash. It is not known why they sometimes grow more actively on the skin surface to form pityriasis versicolor. One theory implicates a tryptophan-dependent metabolic pathway. […] The yeasts induce enlarged melanosomes (pigment granules) within basal melanocytes in the brown type of pityriasis versicolor. […] The white or hypopigmented type of pityriasis versicolor is thought to be due to a chemical produced by malassezia that diffuses into the epidermis and impairs the function of the melanocytes. […] The pink type of pityriasis versicolor is mildly inflamed, due to dermatitis induced by malassezia or its metabolites.
- #35 Tinea Versicolor – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK482500/
Pityriasis versicolor, or tinea versicolor, is a common, benign, superficial fungal skin infection. The causative organism, yeast from the genus Malassezia, is part of the normal skin flora. […] Tinea versicolor is caused by Malassezia, a dimorphic lipophilic fungus previously known as Pityrosporum. Malassezia is a component of the normal skin flora. Clinical disease develops when Malassezia transforms from yeast into its mycelial form. […] The precise elements in the host’s environment that trigger tinea versicolor still need to be clarified. […] Environmental factors like heat and humidity, pregnancy, oily skin, and applying oily lotions and creams increase the risk of tinea versicolor. […] An inflammatory response to the yeast could cause hyperpigmented and erythematous lesions.
- #36 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
Malassezia is a dimorphic yeast-like fungus. It causes PV only in its pathogenic, filamentous (hyphal) form. Factors favouring the conversion from the yeast-like form include a hot and humid environment, hyperhidrosis, the application of oily emollients, using protective face masks, seborrhoea, endocrine and neuropathic disorders, pregnancy, the use of oral contraceptives and corticosteroids, malnutrition, poor general health, and genetic predisposition. […] Malassezia produces virulence factors and toxins that contribute to its pathogenicity. However, in its commensal relationship, Malassezia collects nutrients from the human host without causing negative effects. […] Understanding the role of Malassezia as a direct and indirect cause of PV (via its multifaceted interaction with the skin) is challenging. It is suspected that one of the possible causes for Malassezia virulence is the individual genetic susceptibility.
- #37 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://www.mdpi.com/2075-1729/13/10/2097
Malassezia is a dimorphic yeast-like fungus. It causes PV only in its pathogenic, filamentous (hyphal) form. Factors favouring the conversion from the yeast-like form include a hot and humid environment, hyperhidrosis, the application of oily emollients, using protective face masks, seborrhoea, endocrine and neuropathic disorders, pregnancy, the use of oral contraceptives and corticosteroids, malnutrition, poor general health, and genetic predisposition. […] Malassezia produces virulence factors and toxins that contribute to its pathogenicity. However, in its commensal relationship, Malassezia collects nutrients from the human host without causing negative effects. Furthermore, the concept of mutualism arises when fungal skin colonisation by Malassezia provides protection against potentially pathogenic microbes, such as S. aureus.
- #38 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
With mild barrier defects, the fungus has a potential to produce hypo- or hyperpigmented patches by interacting with melanocytes. Depigmented lesions develop through enzymatic inhibition of melanocyte tyrosinase activity by azelaic acid produced by the microorganism. […] Other important virulence factors of Malassezia include the production of phospholipase, lipase, acid sphingomyelinases (responsible for sebum lipid degradation), haemolysin, and the ability to produce a biofilm. […] It has been suggested that enzymatic patterns and biofilm formation, along with antifungal susceptibility profiles, play a key role in the pathogenicity of Malassezia spp. and may explain the involvement of particular species in invasive infections. […] Epidermal hyperproliferation likely stems from the disruption of the skin barrier caused by free fatty acids (FFAs). Malassezia, being lipid-dependent fungi, rely on FFAs derived from sebaceous triglycerides.
- #39 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://www.mdpi.com/2075-1729/13/10/2097
Understanding the role of Malassezia as a direct and indirect cause of PV (via its multifaceted interaction with the skin) is challenging. It is suspected that one of the possible causes for Malassezia virulence is the individual genetic susceptibility. […] With mild barrier defects, the fungus has a potential to produce hypo- or hyperpigmented patches by interacting with melanocytes. Depigmented lesions develop through enzymatic inhibition of melanocyte tyrosinase activity by azelaic acid produced by the microorganism. […] Other important virulence factors of Malassezia include the production of phospholipase, lipase, acid sphingomyelinases (responsible for sebum lipid degradation), haemolysin, and the ability to produce a biofilm. […] It has been suggested that enzymatic patterns and biofilm formation, along with antifungal susceptibility profiles, play a key role in the pathogenicity of Malassezia spp. and may explain the involvement of particular species in invasive infections.
- #40 Pityriasis versicolor | PPThttps://www.slideshare.net/slideshow/pityriasis-versicolor/179230545
Malassezia metabolizes various fatty acids likearachidonic acids or vaccenic acid via lipase and releases Azelic acids which through inhibition of Tyrosinase in Melanin production resulting in persistent hypopigmentation of affected skin for months or sometimes years. Specific compound synthesized by Malassezia called pityriacitrin that absorbs UV light and causes hyperpigmentation. Other metabolites: Malassezin : Induces apoptosis of melanocytes. Pityrialactone : an indole alkaloids that fluroscences under 300nm uv light Pityriarubin : inhibits 5-lipoxygenase enzymes.
- #41 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
With mild barrier defects, the fungus has a potential to produce hypo- or hyperpigmented patches by interacting with melanocytes. Depigmented lesions develop through enzymatic inhibition of melanocyte tyrosinase activity by azelaic acid produced by the microorganism. […] Other important virulence factors of Malassezia include the production of phospholipase, lipase, acid sphingomyelinases (responsible for sebum lipid degradation), haemolysin, and the ability to produce a biofilm. […] It has been suggested that enzymatic patterns and biofilm formation, along with antifungal susceptibility profiles, play a key role in the pathogenicity of Malassezia spp. and may explain the involvement of particular species in invasive infections. […] Epidermal hyperproliferation likely stems from the disruption of the skin barrier caused by free fatty acids (FFAs). Malassezia, being lipid-dependent fungi, rely on FFAs derived from sebaceous triglycerides.
- #42 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
With mild barrier defects, the fungus has a potential to produce hypo- or hyperpigmented patches by interacting with melanocytes. Depigmented lesions develop through enzymatic inhibition of melanocyte tyrosinase activity by azelaic acid produced by the microorganism. […] Other important virulence factors of Malassezia include the production of phospholipase, lipase, acid sphingomyelinases (responsible for sebum lipid degradation), haemolysin, and the ability to produce a biofilm. […] It has been suggested that enzymatic patterns and biofilm formation, along with antifungal susceptibility profiles, play a key role in the pathogenicity of Malassezia spp. and may explain the involvement of particular species in invasive infections. […] Epidermal hyperproliferation likely stems from the disruption of the skin barrier caused by free fatty acids (FFAs). Malassezia, being lipid-dependent fungi, rely on FFAs derived from sebaceous triglycerides.
- #43 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://www.mdpi.com/2075-1729/13/10/2097
Epidermal hyperproliferation likely stems from the disruption of the skin barrier caused by free fatty acids (FFAs). Malassezia, being lipid-dependent fungi, rely on FFAs derived from sebaceous triglycerides. […] Fungal MGL_1304 produced by M. globosa is a major histamine-releasing antigen, involved in atopic dermatitis and cholinergic urticaria. […] It has been suggested that direct toxic damage to the hair follicle and/or Malassezia-induced proapoptotic cytokines may play a role in PV, as Malassezia was reported to promote interface dermatitis and upregulate proalopecic interleukins.
- #44 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
Fungal MGL_1304 produced by M. globosa is a major histamine-releasing antigen, involved in atopic dermatitis and cholinergic urticaria. […] It has been suggested that direct toxic damage to the hair follicle and/or Malassezia-induced proapoptotic cytokines may play a role in PV, as Malassezia was reported to promote interface dermatitis and upregulate proalopecic interleukins.
- #45 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://www.mdpi.com/2075-1729/13/10/2097
Epidermal hyperproliferation likely stems from the disruption of the skin barrier caused by free fatty acids (FFAs). Malassezia, being lipid-dependent fungi, rely on FFAs derived from sebaceous triglycerides. […] Fungal MGL_1304 produced by M. globosa is a major histamine-releasing antigen, involved in atopic dermatitis and cholinergic urticaria. […] It has been suggested that direct toxic damage to the hair follicle and/or Malassezia-induced proapoptotic cytokines may play a role in PV, as Malassezia was reported to promote interface dermatitis and upregulate proalopecic interleukins.
- #46 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://pmc.ncbi.nlm.nih.gov/articles/PMC10608716/
Fungal MGL_1304 produced by M. globosa is a major histamine-releasing antigen, involved in atopic dermatitis and cholinergic urticaria. […] It has been suggested that direct toxic damage to the hair follicle and/or Malassezia-induced proapoptotic cytokines may play a role in PV, as Malassezia was reported to promote interface dermatitis and upregulate proalopecic interleukins.
- #47 Pediatric Tinea Versicolor: Background, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/911138-overview
Patient immune response also affects infection. Research has suggested a reduced body response to the specific fungal elements that produce tinea versicolor. In various studies, defects in lymphokine production and natural killer T cells were found; phytohemagglutinin (PHA) and concanavalin A (Con A) stimulation was decreased; and interleukin (IL)-2, IL-10, and interferon (IFN) gamma production by lymphocytes was decreased in affected patients. The exact pathophysiology of this disorder remains undefined, and additional studies are needed. […] In patients with hypopigmentation, tyrosinase inhibitors competitively inhibit an enzyme necessary for melanocyte pigment formation. In hyperpigmented macules, the organism induces enlargement of melanosomes made by melanocytes in the basal layer of the epidermis.
- #48 Pediatric Tinea Versicolor: Background, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/911138-overview
Patient immune response also affects infection. Research has suggested a reduced body response to the specific fungal elements that produce tinea versicolor. In various studies, defects in lymphokine production and natural killer T cells were found; phytohemagglutinin (PHA) and concanavalin A (Con A) stimulation was decreased; and interleukin (IL)-2, IL-10, and interferon (IFN) gamma production by lymphocytes was decreased in affected patients. The exact pathophysiology of this disorder remains undefined, and additional studies are needed. […] In patients with hypopigmentation, tyrosinase inhibitors competitively inhibit an enzyme necessary for melanocyte pigment formation. In hyperpigmented macules, the organism induces enlargement of melanosomes made by melanocytes in the basal layer of the epidermis.
- #49 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
Malassezia furfur has been associated to folliculitis by Pityrosporum, reticular and confluent papilloma (Gougerot-Carteaud), seborrheic dermatitis, septicemic onychomycosis. In both the pathogenic and opportunist forms, the fungus resides inside of the stratum corneum and hair follicles, where it is fed by free fatty acids, sebum triglycerides and keratinized epidermis. […] A possible factor in the development of PV is depressed cellular immunity. The lymphocytes of PV-carriers appear to produce a lower leucocyte migration factor of when stimulated with P. orbiculare stratum. In one study of a patient with PV and carrying the visceral leishmaniasis, a depressed cellular immunity disease, there was improvement in mycosis after treatment of the leishmaniasis. […] It has been suggested that the lipoperoxidation process produced by Pityrosporum could be responsible for the clinical hypopigmented appearance of lesioned skin. Culture strata containing dicarboxilic acids, like azelaic acid, has shown strong inhibition in the in vitro dopa-tirasinase reaction. Ultrastructural studies point to severe damage in the melanocytes, varying from melanossomas and altered mitochondria up to degeneration. These dicarboxilic acids may be causing the cytotoxic effects. The damage to melanocytes explains why re-pigmentation may require periods varying from months to years. Another explanation is the fact that the PV scales prevent re-pigmentation. Soon after treatment, the area affected was still hypopigmented for a variable period of time.
- #50 SciELO Brazil – PitirÃase Versicolor PitirÃase Versicolorhttps://www.scielo.br/j/abd/a/dtycs4DqQTZ3mxB6mMKGSbr/?lang=en
Malassezia furfur has been associated to folliculitis by Pityrosporum, reticular and confluent papilloma (Gougerot-Carteaud), seborrheic dermatitis, septicemic onychomycosis. In both the pathogenic and opportunist forms, the fungus resides inside of the stratum corneum and hair follicles, where it is fed by free fatty acids, sebum triglycerides and keratinized epidermis. […] A possible factor in the development of PV is depressed cellular immunity. The lymphocytes of PV-carriers appear to produce a lower leucocyte migration factor of when stimulated with P. orbiculare stratum. In one study of a patient with PV and carrying the visceral leishmaniasis, a depressed cellular immunity disease, there was improvement in mycosis after treatment of the leishmaniasis. […] It has been suggested that the lipoperoxidation process produced by Pityrosporum could be responsible for the clinical hypopigmented appearance of lesioned skin. Culture strata containing dicarboxilic acids, like azelaic acid, has shown strong inhibition in the in vitro dopa-tirasinase reaction. Ultrastructural studies point to severe damage in the melanocytes, varying from melanossomas and altered mitochondria up to degeneration. These dicarboxilic acids may be causing the cytotoxic effects. The damage to melanocytes explains why re-pigmentation may require periods varying from months to years. Another explanation is the fact that the PV scales prevent re-pigmentation. Soon after treatment, the area affected was still hypopigmented for a variable period of time.
- #51https://journals.lww.com/ders/fulltext/2021/39020/atrophying_pityriasis_versicolor__a_rare_variant.6.aspx
Levy and Magro reviewed 6 cases of atrophying pityriasis versicolor proposed that type IV hypersensitivity reaction driven by mixed TH1/TH2 immune response to Malassezia, and TH1 cytokines contribute to atrophy and elastolysis mainly by upregulation of matrix metalloproteinase activity. […] Histopathologic features reveal epidermal colonization with pityrosporum hyphae and spores accompanied by variable epidermal atrophy, dermal atrophy, dermal elastolysis, and superficial perivascular lymphocytic infiltrate. […] The histopathological difference between steroid atrophy and atrophying pityriasis versicolor is that corticosteroid-induced atrophy is associated with profound epidermal atrophy, telangiectasias, and attenuation in the collagen framework. In atrophying pityriasis versicolor, there is dermal elastolysis contributing to the occurrence of skin atrophy.
- #52 Atrophying Pityriasis Versicolor | Actas Dermo-Sifiliográficashttp://www.actasdermo.org/en-atrophying-pityriasis-versicolor-articulo-S1578219018301306
Flattening of the rete ridges, on the other hand, is mediated by cytokines, such as tumor necrosis factor and interleukin 1, which can inhibit the nuclear factor B pathway of keratinocytes to induce apoptosis and hinder proliferation thereof. […] Furthermore, a type 2 helper T cell response, which could favor fungal overgrowth, has been implicated, together with the type 1 response, in the pathogenesis of atrophic PV.
- #53 Atrophying Pityriasis Versicolor | Actas Dermo-Sifiliográficashttps://www.actasdermo.org/es-atrophying-pityriasis-versicolor-articulo-S1578219018301306
Crowson and Magro proposed that this form of PV appeared through a type 1 helper T-cell immune response to Malassezia antigens, in which histocytes recruited and activated by interferon- would generate the elastases responsible for the dermal elastolysis observed. Flattening of the rete ridges, on the other hand, is mediated by cytokines, such as tumor necrosis factor and interleukin 1, which can inhibit the nuclear factor B pathway of keratinocytes to induce apoptosis and hinder proliferation thereof. In parallel, the reduced thickness and loss of hair in areas of PV has also been related to this mechanism. Furthermore, a type 2 helper T cell response, which could favor fungal overgrowth, has been implicated, together with the type 1 response, in the pathogenesis of atrophic PV.
- #54https://journals.lww.com/ders/fulltext/2021/39020/atrophying_pityriasis_versicolor__a_rare_variant.6.aspx
Pityriasis versicolor is a superficial fungal infection caused by Malassezia species and characterized by roundish to oval maculopatches varying in color from hypopigmentation to red to hyperpigmentation. […] The exact pathophysiology remains unknown. Tatnall and Rycroft hypothesized that the skin barrier is disrupted by pityriasis versicolor, allowing better absorption of the steroid, which induces atrophy. […] Crowson and Magro conducted clinical and histological studies in 12 patients with atrophying pityriasis versicolor, however, only one used topical steroids chronically, proposed that delayed hypersensitivity reactions to antigens derived from components of the Malassezia yeast colonizing the epidermal surface and hair follicle orifices or the direct effect of Malassezia on nuclear factor kappa B signaling causing atrophying pityriasis versicolor.
- #55https://journals.lww.com/ders/fulltext/2021/39020/atrophying_pityriasis_versicolor__a_rare_variant.6.aspx
Pityriasis versicolor is a superficial fungal infection caused by Malassezia species and characterized by roundish to oval maculopatches varying in color from hypopigmentation to red to hyperpigmentation. […] The exact pathophysiology remains unknown. Tatnall and Rycroft hypothesized that the skin barrier is disrupted by pityriasis versicolor, allowing better absorption of the steroid, which induces atrophy. […] Crowson and Magro conducted clinical and histological studies in 12 patients with atrophying pityriasis versicolor, however, only one used topical steroids chronically, proposed that delayed hypersensitivity reactions to antigens derived from components of the Malassezia yeast colonizing the epidermal surface and hair follicle orifices or the direct effect of Malassezia on nuclear factor kappa B signaling causing atrophying pityriasis versicolor.
- #56https://journals.lww.com/ders/fulltext/2021/39020/atrophying_pityriasis_versicolor__a_rare_variant.6.aspx
Pityriasis versicolor is a superficial fungal infection caused by Malassezia species and characterized by roundish to oval maculopatches varying in color from hypopigmentation to red to hyperpigmentation. […] The exact pathophysiology remains unknown. Tatnall and Rycroft hypothesized that the skin barrier is disrupted by pityriasis versicolor, allowing better absorption of the steroid, which induces atrophy. […] Crowson and Magro conducted clinical and histological studies in 12 patients with atrophying pityriasis versicolor, however, only one used topical steroids chronically, proposed that delayed hypersensitivity reactions to antigens derived from components of the Malassezia yeast colonizing the epidermal surface and hair follicle orifices or the direct effect of Malassezia on nuclear factor kappa B signaling causing atrophying pityriasis versicolor.
- #57https://journals.lww.com/ders/fulltext/2021/39020/atrophying_pityriasis_versicolor__a_rare_variant.6.aspx
Levy and Magro reviewed 6 cases of atrophying pityriasis versicolor proposed that type IV hypersensitivity reaction driven by mixed TH1/TH2 immune response to Malassezia, and TH1 cytokines contribute to atrophy and elastolysis mainly by upregulation of matrix metalloproteinase activity. […] Histopathologic features reveal epidermal colonization with pityrosporum hyphae and spores accompanied by variable epidermal atrophy, dermal atrophy, dermal elastolysis, and superficial perivascular lymphocytic infiltrate. […] The histopathological difference between steroid atrophy and atrophying pityriasis versicolor is that corticosteroid-induced atrophy is associated with profound epidermal atrophy, telangiectasias, and attenuation in the collagen framework. In atrophying pityriasis versicolor, there is dermal elastolysis contributing to the occurrence of skin atrophy.
- #58https://journals.lww.com/ders/fulltext/2021/39020/atrophying_pityriasis_versicolor__a_rare_variant.6.aspx
Levy and Magro reviewed 6 cases of atrophying pityriasis versicolor proposed that type IV hypersensitivity reaction driven by mixed TH1/TH2 immune response to Malassezia, and TH1 cytokines contribute to atrophy and elastolysis mainly by upregulation of matrix metalloproteinase activity. […] Histopathologic features reveal epidermal colonization with pityrosporum hyphae and spores accompanied by variable epidermal atrophy, dermal atrophy, dermal elastolysis, and superficial perivascular lymphocytic infiltrate. […] The histopathological difference between steroid atrophy and atrophying pityriasis versicolor is that corticosteroid-induced atrophy is associated with profound epidermal atrophy, telangiectasias, and attenuation in the collagen framework. In atrophying pityriasis versicolor, there is dermal elastolysis contributing to the occurrence of skin atrophy.
- #59https://journals.lww.com/ders/fulltext/2021/39020/atrophying_pityriasis_versicolor__a_rare_variant.6.aspx
Levy and Magro reviewed 6 cases of atrophying pityriasis versicolor proposed that type IV hypersensitivity reaction driven by mixed TH1/TH2 immune response to Malassezia, and TH1 cytokines contribute to atrophy and elastolysis mainly by upregulation of matrix metalloproteinase activity. […] Histopathologic features reveal epidermal colonization with pityrosporum hyphae and spores accompanied by variable epidermal atrophy, dermal atrophy, dermal elastolysis, and superficial perivascular lymphocytic infiltrate. […] The histopathological difference between steroid atrophy and atrophying pityriasis versicolor is that corticosteroid-induced atrophy is associated with profound epidermal atrophy, telangiectasias, and attenuation in the collagen framework. In atrophying pityriasis versicolor, there is dermal elastolysis contributing to the occurrence of skin atrophy.
- #60 Atrophying Pityriasis Versicolor | Actas Dermo-Sifiliográficashttps://www.actasdermo.org/es-atrophying-pityriasis-versicolor-articulo-S1578219018301306
Pityriasis versicolor (PV) is a common superficial fungal infection caused by yeasts of the genus Malassezia. […] The mechanism by which species of Malasezzia can induce atrophy in the skin remains unclear. Since many of the patients reported were being treated with topical corticosteroids or systemic corticosteroids, atrophy was associated with the atrophogenic effect of the drugs. The fungal infection is thought to alter the epidermal barrier, thus increasing absorption of corticosteroids in the PV lesions and inducing local cutaneous atrophy. However, in corticosteroid-induced atrophy, in addition to epidermal atrophy and vasodilation, we can see atrophy of skin adnexa and reduction and fragmentation of dermal collagen, whereas in atrophic PV, we do not see alteration of collagen but alteration of the elastic fibers.
- #61 A case of anti- pityriasis versicolor therapy that preserves healthy mycobiome | BMC Dermatology | Full Texthttps://bmcdermatol.biomedcentral.com/articles/10.1186/s12895-020-00106-x
The impact of Malassezia yeasts on skin mycobiome and health has received considerable attention recently. Pityriasis versicolor (PV), a common dermatosis caused by Malassezia genus worldwide, is a manifestation of dysbiosis. PV can be associated with hyper- and/or hypopigmented skin lesions. This disease entity is characterized by high percentage of relapses, which demands a proper antifungal therapy that is based on unambiguous species identification and drug susceptibility testing. […] Comprehensive analysis of PV case in man presenting simultaneously hyper- and hypopigmented skin lesions was performed. Conventional and molecular diagnostic procedures revealed Malassezia furfur and Malassezia sympodialis, respectively as etiological agents of skin lesions observed. Susceptibility tests showed significantly lowered sensitivity of M. furfur cells to fluconazole. Based on susceptibility profiles local antifungal therapy with drugs characterized by entirely different mechanism of action was included.
- #62 A case of anti- pityriasis versicolor therapy that preserves healthy mycobiome | BMC Dermatology | Full Texthttps://bmcdermatol.biomedcentral.com/articles/10.1186/s12895-020-00106-x
Our study indicates that cases of PV represented by two types of skin lesions in one patient may be associated with distinct Malassezia species. Moreover, as observed in this case, each of the isolated etiological agents of PV may differ significantly in susceptibility to antifungals. This can significantly complicate the treatment of dermatosis, which by definition is associated with a significant percentage of relapses. […] Pityriasis versicolor (PV) also known as tinea versicolor is caused by basidiomycetous yeasts of the genus Malassezia, characterized by lipid-dependent growth and narrow specialization in the context of occupied ecological niches. […] Under certain conditions, however these Malassezia species, similar to other opportunistic pathogens, break out of the internal control of the host and overgrow leading to skin infections.
- #63 A case of anti- pityriasis versicolor therapy that preserves healthy mycobiome | BMC Dermatology | Full Texthttps://bmcdermatol.biomedcentral.com/articles/10.1186/s12895-020-00106-x
While on healthy skin Malassezia proliferates as budding yeast, during an outbreak state cells often develop into pseudohyphae leading to the development of typical symptoms associated with PV. […] Such pathomechanism of infection is most typical for M. globosa and M. furfur, but can also involve M. sympodialis which are able to form pseudohyphae in human stratum corneum and are the most common etiological factors of PV worldwide. […] The most probable seems the hypothesis pointing to dissimilarities in the ability to synthesize melanin by M. furfur and M. sympodialis, first time formulated by Gaitanis et al. and later explained by Ianiri et al. based on molecular tools. […] One of the causes of depigmenting effect, observed also in case of our patient on tanned skin of forearms and lower parts of arms, could be azelaic acid, which inhibits the melanogenesis process.
- #64 A case of anti- pityriasis versicolor therapy that preserves healthy mycobiome | BMC Dermatology | Full Texthttps://bmcdermatol.biomedcentral.com/articles/10.1186/s12895-020-00106-x
While on healthy skin Malassezia proliferates as budding yeast, during an outbreak state cells often develop into pseudohyphae leading to the development of typical symptoms associated with PV. […] Such pathomechanism of infection is most typical for M. globosa and M. furfur, but can also involve M. sympodialis which are able to form pseudohyphae in human stratum corneum and are the most common etiological factors of PV worldwide. […] The most probable seems the hypothesis pointing to dissimilarities in the ability to synthesize melanin by M. furfur and M. sympodialis, first time formulated by Gaitanis et al. and later explained by Ianiri et al. based on molecular tools. […] One of the causes of depigmenting effect, observed also in case of our patient on tanned skin of forearms and lower parts of arms, could be azelaic acid, which inhibits the melanogenesis process.
- #65 Tinea Versicolor: Practice Essentials, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/1091575-overview
In steroid-associated atrophying tinea versicolor, the Malassezia infecting the epidermis may impair the barrier function of skin, thus allowing improved penetration of topical corticosteroids. […] This theory suggests that Th1 cytokines recruit histiocytes to the site of epidermal infection. These histiocytes serve as a source of elastases and they up-regulate the metalloproteinase activity, ultimately leading to atrophy of the affected epidermis. […] A study from 2020 found a statistically significant relationship between Helicobacter pylori infection and tinea versicolor, proposing H pylori infection as an etiologic factor for this fungal infection, although this has not been verified in larger studies and the controls population with telogen effluvium was not clearly demographically matched.
- #66https://journals.lww.com/10.4103/ijd.ijd_391_24
Pityriasis versicolor (PV) is an asymptomatic, superficial fungal infection caused by the Malassezia species and causes discolouration of the skin leading to altered pigmentation. […] The genus Malassezia includes a group of dimorphic fungi that occurs as normal flora on the human skin. It is usually associated with mild superficial infection, but in immunocompromised patients, it is now emerging as an opportunistic fungal pathogen. […] Dermoscopy is a new, popular non-invasive diagnostic modality, which shows specific features like fine scaling, pigment alteration, ridges and furrows with perifollicular involvement, and can be used to diagnose doubtful cases of PV as an adjunct or substitute to a KOH mount. […] Various predisposing factors have been described in the development of PV. In our study, 42.6% of the patients noticed increased sweating, with summer aggravation observed in 24.3% of the patients. […] Growth in fungal culture was seen in 44.3% of the patients. Out of 51 isolates, M. furfur was the most common species isolated in 35.2% of culture-positive PV cases, followed by M. globosa in 21.6%, M. obtusa in 19.6%, M. pachydermatis and M. sympodialis in 11.8%.
- #67 Tinea Versicolor | Treatment & Management | Point of Carehttps://www.statpearls.com/point-of-care/30211
Tinea versicolor is caused by Malassezia, a dimorphic lipophilic fungus previously known as Pityrosporum. Malassezia is a component of the normal skin flora. Clinical disease develops when Malassezia transforms from yeast into its mycelial form. […] The precise elements in the host’s environment that trigger tinea versicolor still need to be clarified. Although experimental inoculations using topical oils and occlusion have proven successful, tinea versicolor is not contagious. […] Environmental factors like heat and humidity, pregnancy, oily skin, and applying oily lotions and creams increase the risk of tinea versicolor. […] Genetic predisposition and a hereditary component may play a role. […] An inflammatory response to the yeast could cause hyperpigmented and erythematous lesions.
- #68 Pityriasis VersicolorâA Narrative Review on the Diagnosis and Managementhttps://www.mdpi.com/2075-1729/13/10/2097
Understanding the role of Malassezia as a direct and indirect cause of PV (via its multifaceted interaction with the skin) is challenging. It is suspected that one of the possible causes for Malassezia virulence is the individual genetic susceptibility. […] With mild barrier defects, the fungus has a potential to produce hypo- or hyperpigmented patches by interacting with melanocytes. Depigmented lesions develop through enzymatic inhibition of melanocyte tyrosinase activity by azelaic acid produced by the microorganism. […] Other important virulence factors of Malassezia include the production of phospholipase, lipase, acid sphingomyelinases (responsible for sebum lipid degradation), haemolysin, and the ability to produce a biofilm. […] It has been suggested that enzymatic patterns and biofilm formation, along with antifungal susceptibility profiles, play a key role in the pathogenicity of Malassezia spp. and may explain the involvement of particular species in invasive infections.
- #69 Antifungal Treatment for Pityriasis Versicolorhttps://www.mdpi.com/2309-608X/1/1/13
Pityriasis versicolor (PV) is a chronic cutaneous fungal infection caused by proliferation of lipophilic yeast (Malassezia species) in the stratum corneum. The most common Malassezia species associated with PV is M. globosa, with M. sympodialis and M. furfur also frequently seen. In most cases of PV, Malassezia, as a part of normal skin flora, are not pathogenic unless they assume a mycelial form. This may be triggered by various factors, including humidity and high temperature, hyperhidrosis, familial susceptibility, and immunosuppression. Consequently, PV occurs more frequently in tropical climates (as much as 40%) as compared to temperate climates. PV is difficult to cure, as relapse following treatment can be as high as 80% within 2 years. […] Diagnosis of PV is confirmed by microscopy using skin scrapings from the borders of lesions, or, if this is not possible, obtaining samples using the transparent tape method. Woodâs light examination may also aid in diagnosis, with lesions appearing yellow or gold. Topical antifungals are currently the first line of treatment for PV and systemic antifungals are recommended for severe or recalcitrant cases. There are, however, many non-specific topical treatments that may be effective in treating PV. In some cases, misdiagnosis may lead to inappropriate and ineffective treatment (e.g., antibiotics, corticosteroids). The focus of the present review is to highlight the clinical evidence supporting the use of topical and systemic antifungal medications in treating PV.
- #70https://apcz.umk.pl/JEHS/article/view/57171
Pityriasis versicolor is a prevalent superficial mycosis caused by saprophytic yeasts of the Malassezia genus. […] Pityriasis versicolor is well-characterized in terms of its etiology and clinical manifestations. […] Despite significant progress in understanding and managing pityriasis versicolor, further research is essential. Future efforts should aim to optimize treatment efficacy, reduce relapse rates, and minimize adverse effects.
- #71https://apcz.umk.pl/JEHS/article/view/57171
Pityriasis versicolor is a prevalent superficial mycosis caused by saprophytic yeasts of the Malassezia genus. […] Pityriasis versicolor is well-characterized in terms of its etiology and clinical manifestations. […] Despite significant progress in understanding and managing pityriasis versicolor, further research is essential. Future efforts should aim to optimize treatment efficacy, reduce relapse rates, and minimize adverse effects.