2. INTRODUCTION
Pityriasis versicolor is a mild chronic superficial fungal
infection of stratum corneum caused mainly by Malassezia
species.
Infection usually results from change from its lipophilic
yeast form to mycelial form of Malassezia.
Also called as ‘Tinea versicolor’ the term best discarded as
not caused by Dermatophytes.
Malassezia species are normal flora of the skin and can be
cultured from both normal and affected skin.
Also thought to be responsible for other dermatological
condition like Seborrheic dermatitis and is not contagious.
3. ETIOLOGY
Pityriasis versicolor is caused by dimorphic lipophilic
organisms in the genus Malassezia formerly known as
pityrosporum.
Fourteen species are recognized in this classification
of Yeast of which Malassezia globosa , Malassezia
sympodalis and Malassezia furfur are predominant
species isolated in P. versicolor.
Malassezia is naturally found on skin surfaces of many
animals including humans. It can be isolated in 18% of
infants and 90-100% of adults.
4. PATHOGENESIS
Malassezia spp. are commonly found in the stratum corneum
of normal skin mostly around lipophilic zones like upper
trunk neck and upper arms in its yeast form
Under appropriate conditions
Warm, Humid environment
Hyperhidrosis(Sweating)
Oral Contraceptives, Steroids
Cushings Disease
Immunocompromised,
Malnourished state
Saprophytic Yeast cell
of Malassezia
converted into
parasitic mycelial form
which causes clinical
disease
5. 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
6. CLINICAL PRESENTATION
FORM 1: Most Common Form
Patient with pityriasis versicolor present with a rash
consisting of well demarcated, finely scaling
hypopigmented (less commonly hyperpigmented or
erythematous) macules mainly starts around
perifollicular region.
Scale is fine , powdery and branny.
M/C site of lesions are on oily regions which are also
very sweaty like upper trunk often spreading to the
neck and upper arms.
7. Lesion appears to be sitting on the skin.
Lesion frequently coalesces to form patches but
the distinct perifollicular character of the lesions
invariably retained at periphery.
Scratch sign: Lesion surmounted by branny scales
which can be accenuated by scratching lesion
gently with the help of glass slides also known as
‘coup d’ongle sign’ or ‘Besnier’s sign’ or
‘Stroke of the nail sign’
Itching is minimal but mild pruritus may be
present.
11. OTHER FORMS
FORM 2 : Inverse Form
Distributed typically in flexular region
More commonly seen in immunocompromised
FORM 3 : Folliculitis form
Perifollicular erythematous papule or pustule
FORM 4 : Multiple , Firm , Red-Brown inflammatory papules
May or may not demonstrate scales
Usually found on torso and usually asymptomatic.
12. DIFFERENTIAL DIAGNOSIS
Hypopigmented Lesions
Vitiligo
Pityriasis alba
Leprosy
Hyperpigmnted Lesions
Tinea Corporis
Pityriasis rosea
Guttate psoriasis
Nummular Eczema
Confluent and Reticulate papillomatosis
Post inflammatory hyperpigmentation
13. INVESTIGATIONS
The Diagnosis of P. Versicolor is usually made clinically on
the basis of typical lesion surmounted with scales.
Culture of organism is of little value .
1. However the KOH wet mount test can be done
Shows “Spaghetti and Meat ball” appearance
• Spaghetti represents the fungal hyphae of Malassezia
• Meat ball represents spore form
15. 2. WOOD LAMP EXAMINATION
On wood lamp examination of the lesion pityriasis
versicolor gives the yellow fluroscence.
16. Fig Wood Lamp Examination of lesion of Pityrasis versicolor
17. 3. Histology
Not done usually but on histopathological examination
shows the superficial budding yeast (Blastoconidia) and
short septate hyphae (Pseudomycelium) in stratum
corneum layer of skin.
18. TREATMENT
TOPICAL PREPARATION
Selenium sulphide
Zinc pyrithione
Sodium sulfacetamide
Azoles like Ketoconazole(2%),
Allylamines like Terbinafine (1%)
SYSTEMIC THERAPY
Ketoconazole (200mg OD for 7-10 days or SOD of 400 mg)
Fluconazole (Single oral dose of 400 mg)
Itraconazole (200-400 mg OD for 3-7 days)
19. PREVENTION
TOPICAL OR ORAL TREATMENTS ARE USED FOR
PROPHYLAXIS IN CASE OF EXTENSIVE DISEASE.
Topical Ketoconazole, Zinc pyrithione or Selenium
sulphide shampoo applied 5-10 minutes , 1-4 times
monthly
Oral itraconazole 200 mg BD per month or
Fluconazole or Ketoconazole
21. INTRODUCTION
Pityriasis Rosea is a papulosquamous rash usually affects teen and
young adults which is usually self limiting type of disease.
Exact aetiology of this disorder remains to be unknown however a
virus HHV-7 more frequently and HHV-6 less frequently been
implicated in the pathogenesis of this disease though the disease is
non contagious.
Probably related to respiratory infections and slightly more common
in females.
Like other viral rashes most person will have this condition only once.
22. CLINICAL FEATURE
Disease is characterized by initial appearance of
Herald’s patch followed by secondary lesions.
HERALD’S PATCH
First lesion of Pityriasis Rosea and is seen in 80% of
patients.
Annular lesion with wrinkled salmon pink centre and
collarette of scales at the periphery.
Scales are just attached within leading edgeand free
towards the centre.
Primarily on trunks and upper arms.
24. SECONDARY ERUPTIONS
Begins as a scaly papules which enlarges to form
oval , annular plaques similar to Herald patch.
These are smaller , less scaly and less
erythematous than Herald patch.
Are arranged characteristically with the long axis
of patches runs downward and outward from spine
along the line of Ribs with Fir tree or Christmas
tree appearances.
26. HERALD’s PATCH
Phase of evolution(1-2wks)
SIMILAR LESIONS, WHICH ENLARGES SLOWLY
Phase of resolution (2-10 wks)
MILD PIGMENTARY CHANGES
FADES SLOWLY
Fig. Pityriasis Rosea, Course A Self limiting Disease
27. HANGING CURTAIN SIGN
When invidual lesions are scratched along long axis
the scales tends to fold across the line of stretch.
28. Atypical Variants
Inverse Form : Secondary eruptions are usually
seen in Predominantly over axilla, groins
and neck.
Papular Form : When secondary eruptions is
predominantly popular.
Bullous Form : When secondary eruptions is
predominantly vesicular.
29. Differential diagnosis
1. Tinea Corporis
2. Secondary Syphilis
3. Guttate Psoriasis
4. Pityriasis Licheoides Chronica(PLC)
5. Drug Eruptions
Like Gold, Captopril, Barbiturates, and
Penicillamines
30. INVESTIGATIONS
Usually no investigation is required, Pityriasis
Rosea is clinical diagnosis.
Serology to rule out Syphilis as it can closely
mimic secondary syphilis.
KOH wet mount to differentiate from fungal
infections.
31. TREATMENT
Counsel patient regarding self limiting course of Disease.
Symptomatic Treatment :
Pruritus :Topical Calamine lotion and Antihistaminics
Very Scaly/Erythematous Lesions: Coal Tar in Petroleum and
Low- Medium Potency Steroids
Recalcitrant Lesions : Sunlight, PUVA/PUVA SOL
33. INTRODUCTION
Often occurs on face, with chest being particularly common
site.
Etiology unknown maybe secondary to atopy and
postinflammatory changes.
34. EPIDEMIOLOGY
Exact incidence not known upto 5% of children may have Pityriasis
alba.
Prevalence : 5.2% in Nepal.
Both gender equally affective.
Age : 3-16 years of age.
35. CLINICAL FEATURES
Rounded , Oval or Irregular plaques
Red, Pink or Skin coloured
Presence of Fine lamellar or Branny scaling
Indistinct margins
Usually 1-4 cm in diameter
Generally asymptomatic but maybe mildly pruritic
Site : often occurs on face , with cheek being
particularly common site.
Most common age group 3-16 years of age
38. Recurrent crops of new lesions may develop at
intervals with the duration of Pityriasis alba
varying from 1 month to 10 years . Most cases
however resolve over a period of several
months to years.
41. INVESTIGATION
Investigation to rule out other causes
KOH wet mounts
Wood’s Lamp : Vitiligo rash will glow more brightly and have edges
with sharper demarcation.
SKIN BIOPSY
Hyperkeratosis
Parakeratosis
Acanthosis
Spongiosis
Perivascular infiltrates
42. TREATMENT
Reassurance
Sun Protection
Topical Steroids : For erythema and Pruritus.
Bland Emolient creams to reduce scaling of the
lesions.
PUVA in extensive cases.
43. References
DERMATOLOGY AND SEXUALLY TRANSMITTED DISEASE – DR. NEENA KHANNA
DERMATOLOGY IN GENERAL MEDICINE – FITZPATRICK’s
MEDSCAPE