Pityriasis versicolor is a common superficial fungal infection of the skin caused by Malassezia furfur. It produces hypopigmented, hyperpigmented, or scaly macules on the trunk and neck. Diagnosis involves scraping skin lesions and examining under a microscope using potassium hydroxide, which reveals short hyphal fragments and clusters of yeast. Wood's lamp examination shows pale yellow-white fluorescence of lesions. M. furfur is normally present on human skin but overgrowth causes pityriasis versicolor. The fungus can be cultured using Sabouraud dextrose agar covered with oil, as M. furfur requires lipids for growth.

1. INSTITUTE OF HEALTH TECHNOLOGY, DHAKA
Department of Laboratory Medicine
BSc in Health Technology (Laboratory)- 1st Year
MYCOLOGY
Lecture No. 03 (Superficial Mycoses)
By
Sk. MIZANUR RAHMAN
Lecturer, Mycology
MS in Biotechnology & Genetic Engineering (UODA)
MS in Microbiology (SUB)

2. Superficial mycoses
pityriasis versicolor – causative fungus,
lesion produce.

3. Anatomy of Skin
Hair follicle and sebaceous
gland

4. Fungal Infections/ Mycoses
• Superficial mycoses:
– 2 types: surface and cutaneous mycoses
– Skin, hair & nails.
– Mild but chronic disease
• Deep mycoses:
– 2 types: subcutaneous & systemic mycoses
– Caused by soil saprophytes
– Infection is accidental
– Range from a symptomatic infection to fatal
disease

5. Superficial: Surface mycoses
• Live exclusively on dead surfaces of skin and
its appendages
• No contact with living tissue, hence no
inflammatory response
1. Tinea versicolor
2. Tinea nigra
3. Piedra

6. Superficial: Surface mycoses

7. Pityriasis (Tinea)Versicolor
Fungal infection of the skin
This is a very common superficial mycoses caused by a
lipophilic yeast Malassezia spp. It is seen in all countries
but is particularly common in the tropics with more than
60 % of the population infected.
The lesions are hypo or hyper pigmented. The etiologic
agent is normal flora of man so the disease re-occurs.
Multiple patchy lesions (oval shape c fine scales) either
light in color or brown
Typically occurs on the back, neck, chest, shoulders

8. Tinea Versicolor
Recent evidence suggest that seborrheic dermatitis is
also caused, or triggered by, Malassezia yeast.
There also is Malassezia folliculitis. This is seen in
patients who are usually severely ill or in patients
after sun exposure.
Tx: Topical antifungal

9. General Morphology
Tinea Versicolor
• Numerous, well-marginated, oval-to-round macules
(change in the color of the skin) with a fine white scale
when scraped.
• Pigmentary alteration uniform in each individual.
– Red
– Hypo pigmented
– Hyperpigmented
• Scattered over the trunk and neck. Seldom the face.
• M. furfur
– Normal flora of skin
• Asymptomatic.

10. Tinea Versicolor
Definition
•Asymptomatic colonization
Malassezia furfur
•Hypopigmentation
•Hyperpigmentation
•Seborrhoeic dermatitis
•Dandruff
•Fungaemia

11. Pityriasis versicolor
• Conditions:
– Health
– Sweat
– Greasy skin
– Chronic bacterial infections
– Steroids

12. Pityriasis versicolor
• Clinical manifestations:
– Maculae
– White, cream, pink, red, brown
– Scale/signs
– Painless
– Not itching

13. Superficial mycosis (Pityriasis versicolor)

14. Superficial mycosis (Pityriasis versicolor)

15. Pityriasis versicolor
Laboratory diagnosis:
• Sampling
– Scalpel (sharp bladed
instrument)
– Wood ́s lamp (producing
ultraviolet radiation)
• Direct
• Culture

16. Tinea Versicolor
Diagnosis:
•Scrape lightly – fine white scale
•KOH Positive for short hyphae and spores
(Spaghetti –hyphae and meatballs-yeasts)
•Woods Light – pale yellow white fluoresce.
•Culture rarely done.

17. Tinea Versicolor
Direct exam.
•Skin scraping
•10% KOH preparation
•Parker Ink
Culture
•Sabouraud Dextrose Agar
•Lipophilic yeast
•Flood with Olive oil

18. Tinea Versicolor

19. Tinea Vesicolor – Woods Light
Yellow White

20. •Short fragments
of hypha
•cluster of yeast

21. M.ovalae
M.paraovalae
M.furfur
Malassezia

22. Tinea Versicolor Microscope

24. Culture
 Malassezia furfur can be grown in a
laboratory but only when one covers the culture
with oil. This leads me to speculate that there is
a genetic susceptibility to this disease resulting
from qualitative or quantitative differences in
the oil content of susceptible persons.