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• Historically it was thought that fungi were plants that did not need 
photosynthesis. 
• But now fungi are classified in their own kingdom, separate from 
plants and animals because: 
1- The cell walls of plants are made of cellulose whereas the walls of fungal cells are 
made of chitin 
2- Plants require only simple inorganic compounds such as carbon dioxide and water 
to grow. Fungi require a diet of complex organic molecules to thrive. 
• Fungi are parasites or saprophytes i.e. they live off living or dead 
organic matter.
• Growing fungi have branched filaments called 
hyphae, which make up the mycelium (like branches 
are part of a tree). Hyphae are threadlike filaments 
made up of fungal cells, whereas mycelium is the 
mass of hyphae that forms the fungal body. Some 
fungi are compartmented by cross-walls (called 
septae). 
• Arthrospores are made up of fragments of the 
hyphae, breaking off at the septae. 
• Asexual spores (conidia) form on conidiophores. The 
sexual reproductive phase of many fungi is unknown; 
these are ‘fungi imperfecta’ and include those which 
infect humans.
FORMS OF HYPHAE; 
1. Septate hyphae: In most fungi, hyphae are divided 
into cells by internal cross-walls for example 
“Aspergillus”. 
2. Coenocytic hyphae (non-septate hyphae): meaning 
their hyphae are not partitioned by septa. 
3. Pseudo hyphae: They are the result of incomplete 
budding where the cells remain attached after 
division, and Yeast can form pseudohyphae.
• Yeasts form a subtype of 
fungus characterized by 
clusters of round or oval cells. 
• These bud out similar cells 
from their surface to divide 
and propagate. In some 
circumstances they form a 
chain of cells called a 
pseudomycelium.
conidiophore
THE ORGANISMS ARE TRANSMITTED BY EITHER; 
1. Direct contact with infected host (human or 
animal). 
2. Indirect contact with infected exfoliated skin or 
hair in combs, hair brushes, clothing, furniture, 
theatre seats, caps, bed linens, towels, hotel rugs, 
and locker room floors.
• According to their appearance by microscopy and in 
culture or method of reproduction. 
BY THE METHOD OF REPRODUCTION: 
1. Sexual 
2. Asexual.
Classification of Fungal 
Infections (mycoses) 
I. SUPERFICIAL MYCOSES 
a) Non-inflammatory 
b) Inflammatory 
II. SUBCUTANEOUS MYCOSES 
III. SYSTEMIC MYCOSES
• These affect the outer layers of the skin, the nails and hair. 
• The main groups of fungi causing 
superficial fungal infections are: 
1. Yeasts 
i. Candida 
ii. Malassezia 
2. Dermatophytes (ringworm/tinea) 
3. Other Moulds e.g. 
i. Aspergillus spp. 
ii. Fusarium spp.
Infections limited to the outermost layers of the skin 
and hair: 
1. Pityriasis versicolor 
2. Candidiasis 
3. Tinea nigra 
4. Black piedra 
5. White piedra
• Infections that extend deeper into the epidermis, as well as hair and nail 
and caused by dermatophytes. 
• They colonize the keratin and inflammation is caused by host response to 
metabolic by-products: 
1. Tinea capitis (head) 
2. Tinea faciei (face) 
3. Tinea barbae (beard) 
4. Tinea corporis (body) 
5. Tinea manus (hand) 
6. Tinea cruris (groin) 
7. Tinea pedis (foot) 
8. Tinea unguium (nail)
THE MAIN 3 GENERA OF DERMATOPHYTES ARE: 
1. Trichophyton (abbreviated as "T") 
2. Epidermophyton (“E") 
3. Microsporum (“M")
1. Anthropophilic dermatophytes are restricted to human hosts and produce a mild, chronic 
inflammation e.g. 
 T. rubrum ▪ M. audouinii 
 T. interdigitale ▪ T. violaceum 
 T. tonsurans ▪ T. schoenleinii 
2. Zoophilic organisms are found primarily in animals and cause marked inflammatory reactions in 
humans who have contact with infected cats, dogs, cattle, horses, birds, or other animals e.g. 
 M. canis (originating from dogs and cats) 
 T. equinum (originating from horses) 
 T. verrucosum (originating from cattle) 
3. Geophilic species are usually recovered from the soil but occasionally infect humans and animals. 
They cause a marked inflammatory reaction, which limits the spread of the infection and may lead 
to a spontaneous cure but may also leave scars e.g. 
 M. gypseum 
 M. fulvum
• These involve the deeper layers of the skin (the dermis, 
subcutaneous tissue, muscle & fascia and even bone). 
• The causative organisms normally live in the soil living on 
rotting vegetation. They can get pricked into the skin as a 
result of an injury but usually stay localized at the site of 
implantation. 
• Deeper skin infections include: 
1. Mycetoma 
2. Chromoblastomycosis 
3. Sporotrichosis
• May result from breathing in the spores of fungi, which 
normally live in the soil or rotting vegetation or as 
opportunistic disease in immune compromised 
individuals. 
A. Inhaled fungal infection (By True pathogens) 
• Although uncommon, some may infect healthy 
individuals. The result is most often a mild infection and 
long lasting resistance to further attack, but occasionally 
these infections are more serious and chronic (especially 
in the immune suppressed). The organisms causing 
systemic fungal infections include: 
1. Histoplasmosis 
2. Coccidioidomycosis (North and South America). 
B. Opportunistic infections 
• Other systemic mycoses only infect those who are already 
sick or with an immunodeficiency disorder i.e. they are 
‘opportunists’. Repeated infection may occur. Risks for 
systemic mycoses include: 
1. Serious illness and debility 
2. Cancer or leukemia 
3. Diabetes mellitus 
4. Transplant 
5. Massive doses of antibiotics 
6. Parenteral nutrition 
7. Drug addiction 
8. Infection with human immunodeficiency virus (HIV) 
• Opportunistic fungal infections include: 
1. Aspergillosis (found everywhere) 
2. Zygomycosis 
3. Cryptococcosis (where there are pigeon droppings) 
4. Trichosporon beigelii 
5. Pseudallescheria boydii
• It is a common, long-term (chronic) superficial 
fungal infection of the skin. 
• Affected skin change color and become either 
lighter or darker than surrounding skin.
• Common in adolescent and young adult males. 
Malassezia requires oil to grow, accounting for the 
increased incidence in adolescents and preference for 
sebum-rich areas of the skin. 
• Its occurrence before puberty or after age 65 years is 
uncommon. 
• A member of normal human cutaneous flora, and it is 
found in 18% of infants and 90-100% of adults and it is 
NOT CONTAGIOUS.
• Worldwide distribution but prevalence reported to 
be as high as 50% in the humid, hot environment 
and as low as 1.1% in the colder temperatures. 
• The condition is more noticeable during the 
summer months.
• The causative fungus is Malassezia furfur (previously known as 
Pityrosporon orbiculare and Pityrosporon ovale). 
• In patients with clinical disease, the organism is found in both the 
yeast stage and the filamentous (mycelial/hyphae) form. 
• Factors that lead to the conversion to the parasitic, mycelial 
morphologic form include; 
1. Genetic predisposition 
2. Oily skin (yeast is lipophilic) 
3. Excessive sweating 
4. Warm, humid environments 
5. Immuno-suppression 
6. Malnutrition 
7. Pregnancy 
8. Cushing disease
• The reason why this organism causes PVC 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. 
• Lymphocyte function on stimulation with the organism 
has been shown to be impaired in patients who are 
affected.
• Decreased pigmentation may be secondary 
to the inhibitory effects of dicarboxylic acids 
on melanocytes (these acids result from 
metabolism of surface lipids by the yeast). 
• Sun exposure may make PVC more 
apparent. Decreased tanning, due to the 
ability of the fungus to filter sunlight. 
• The yeasts induce enlarged melanosomes 
within melanocytes in the brown type of 
PVC.
• Pityriasis versicolor is usually 
asymptomatic, but in some people it 
is mildly itchy. 
• Numerous, well-marginated, finely 
scaly, oval-to-round macules. 
• Demonstration of this associated 
scale may require scratching or 
stretching the skin surface.
• Scattered over the trunk, 
shoulders and/or the chest, 
the proximal extremities 
with occasional extension 
to the lower part of the 
abdomen and the neck. 
• Less frequently, lesions are 
seen on the face (especially 
in children), scalp.
• The macules tend to coalesce, forming large irregularly shaped patches.
• As the name versicolor implies, the color of each lesion varies 
from almost , pink (mildly inflamed), tan to dark brown
• An INVERSE form also exists affecting the flexural regions 
antecubital fossae, sub-mammary region and groin.
• Sometimes the patches start scaly and brown, and 
then resolve through a non-scaly and white stage.
• Usually diagnosed clinically. 
• Wood’s light examination 
(revealing bright yellow-green 
fluorescence).
• SKIN SCRAPING: then it is examined under a 
microscope. 
• DIRECT MICROSCOPY: Skin scrapings taken from 
patients with PVC stain rapidly when mounted in 10% 
KOH, glycerol and Parker ink solution and show 
characteristic clusters of thick-walled round, budding 
yeast-like cells and short angular hyphal forms up to 
8um in diameter (SPAGHETTI AND MEATBALLS 
APPEARANCE). These microscopic features are 
diagnostic for Malassezia furfur and culture 
preparations are usually not necessary.
• CULTURE: is only necessary in cases of 
suspected fungaemia. M. furfur is a 
lipophilic yeast, therefore in vitro growth 
must be stimulated by natural oils or other 
fatty substances. 
• The most common method used is to 
overlay Sabouraud's dextrose agar 
containing cycloheximide (actidione) with 
olive oil or alternatively to use a more 
specialized media like Dixon's agar which 
contains glycerol mono-oleate (a suitable 
substrate for growth).
• Biopsies are usually not 
performed, as KOH examination 
of associated scale is typically 
diagnostic. 
• This section shoes; 
1. Hyperkeratosis without 
parakeratosis 
2. Few inflammatory cells in the 
epidermis 
3. Numerous yeast & plump hyphae 
(Spaghetti and meatballs)
1. Pityriasis alba 
2. Postinflammatory hypopigmentation 
3. Vitiligo 
4. Seborrheic dermatitis 
5. Pityriasis rosea 
6. Tinea corporis 
7. Secondary syphilis 
8. Progressive macular hypomelanosis
TOPICAL TREATMENT 
1. Azole creams and lotions; Clotrimazole, 
Ketoconazole, Miconazole 
2. Dandruff shampoos Ketoconazole (1% or 2%) or 
2.5% selenium sulfide twice weekly for 2 to 4 
weeks; the preparation is left on the skin for 10–15 
minutes before rinsing. Over-the-counter dandruff 
shampoo contain heavy metals e.g. Zinc, Mercury, 
Copper e.t.c.  inhibition of growth of any fungi by 
reacting in their biosynthetic pathways. Treatment 
of all the skin from the neck down to the knees, 
even if only a small area is clinically involved. 
3. Allylamine 
4. Nystatin 
5. Salicylic acid 
6. Sodium thiosulphate solution 
7. Ciclopirox cream/solution 
8. 50% propylene glycol in water
SYSTEMIC TREATMENT 
• If the rash is extensive, oral antifungal medications may be needed they are; 
1. Fluconazole (300 mg once weekly for 2 weeks) 
2. Itraconazole (200 mg daily for 5-7 days) 
3. Ketoconazole (200 mg 5 days-5 weeks), 
• Vigorous exercise an hour after taking the medication may help sweat it onto 
the skin surface, where it can effectively eradicate the fungus. Avoid bathing 
for a few hours.
• Though it is easily treated, pigment changes may last for months 
after treatment. 
• Because this rash has a high recurrence rate, medication may be 
needed periodically to prevent recurrence. The rate of recurrence 
of pityriasis versicolor is very high, especially in hot humid climates 
so avoid heat in hot weather. 
• Patients at high risk for recurrence may be helped by using 
ketoconazole shampoo once weekly as a body cleanser. Another 
preventative measure is once-monthly dosing of oral ketoconazole 
(400 mg), fluconazole (300 mg) or itraconazole (400 mg).
• It is due to infection by the fungus, 
Hortaea werneckii. 
• Occurs as a result of inoculation 
from a contamination source such 
as soil sewage, wood, or compost 
subsequent to trauma in the 
affected area. 
Note the 2 celled yeast forms
• Typically occur in tropical climates such as Central and 
South America, Africa, Asia and, occasionally, in the 
southeastern US.
• No predispositions have been identified. 
• Typically, the incubation period is 10- to 15-day. 
• A pigmentary change in the skin results from the 
accumulation of a melanin-like substance in the 
fungus.
• Asymptomatic brown-to-black sharply 
marginated macule or patch, resembling 
silver nitrate or India ink stains. 
• The surface may appear mottled, velvety or 
have mild scale. 
• The lesions are typically solitary, although 
may be multiple. 
• Although most frequently seen on the 
palms, tinea nigra can also appear on the 
soles, neck and trunk.
• The shape of the lesion varies, and they may appear 
ovoid, round, or irregular. 
• The lesion slowly grows over weeks to months. 
• The size may range from a few millimeters to 
several centimeters in diameter, depending on the 
duration. 
• It may have darker pigmentation of the advancing 
border as compared to the center. 
• While the disease tends to be chronic, recurrence 
after effective treatment is infrequent except in the 
case of re-exposure.
• KOH EXAMINATION reveals highly 
branched and septate pigmented 
hyphae. 
• BIOPSY specimens have similar findings 
observed within the stratum corneum. 
• CULTURES of H. werneckiifirst appear 
as pasty, green-black colonies with a 
yeast-like appearance, and then change 
after approximately 2 weeks to a fuzzy, 
dematiaceous (dark in color) mold.
1. Acral melanocytic nevi. 
2. Fixed drug eruption. 
3. Postinflammatory hyperpigmentation. 
4. Staining from chemicals, pigments and dyes. 
5. Melanoma.
1. Topical keratolytic agents such as Whitfield’s ointment 
(typically 6% benzoic acid plus 3% salicylic acid) 
2. Topical azole 
3. Topical Allylamine 
• Several weeks of therapy may be required to prevent 
recurrence of disease. 
• Systemic therapy is generally not indicated.
• It is a superficial non-inflammatory nodular fungal 
infection confined to hair shafts. 
• “Piedra” means “stone”, reflecting the fungal 
elements’ adherence to one another to form 
nodules along the hair shaft, the surrounding skin is 
healthy. 
• Favored climate; tropical areas. 
• There are 2 types Black Piedra & White Piedra.
BLACK PIEDRA WHITE PIEDRA 
CAUSATIVE FUNGI Piedraia hortae 
Trichosporon beigelii (6 
pathogens) 
PATHOGENESIS 
• Infection usually begins 
under the cuticle of the 
hair shaft and extends 
outward. 
• Hair breakage may occur 
as a result of shaft rupture 
at the site of the nodules. 
• As the nodules enlarge, 
they can even envelope 
the hair shaft. 
• Infection also begins 
beneath the cuticle and 
grows through the hair 
shaft, causing weakening 
and breakage of the hair.
CLINICALLY BLACK PIEDRA WHITE PIEDRA 
NODULE COLOR 
Brown to black 
along the hair shaft. 
Generally white but may also be red, green or 
light brown in color. 
NODULE FIRMNESS Hard Soft 
NODULE ADHERENCE TO 
THE HAIR SHAFT Firm Loose 
TYPICAL ANATOMIC 
LOCATION 
Face, axillae and 
pubic region 
(occasionally scalp) 
Scalp and face (occasionally pubic region its 
incidence has increased since the start of the 
HIV pandemic) 
SYSTEMIC INFECTION Non 
In immunosuppressed patients, T. beigelii can 
cause TRICHOSPORONOSIS, a serious with 
fungemia, fever, pulmonary infiltrates, skin 
lesions (papulovesicular and purpuric, often 
with central necrosis) and renal disease.
INVESTIGATIONS BLACK PIEDRA WHITE PIEDRA 
KOH EXAMINATION 
“crush preparation” 
• Dematiaceous hyphae 
• Organized cluster of asci, each of 
which contains eight ascospores 
(sexual phase of P. hortae-the only 
sexual phase detected that is 
pathological to human) 
• Non-dematiaceous 
hyphae 
• Blastoconidia and 
arthroconidia 
(representing the 
asexual state) 
CULTURE ON 
SABOURAUD’S AGAR 
• Very slow-growing 
• Dark green to dark brown–black 
colonies with a velvety texture 
(asexual phase) 
• Grows rapidly 
• Moist, cream-colored, 
yeast-like colonies 
• Cycloheximide inhibits 
growth.
1. Pediculosis (nits) 
2. Hair casts 
3. Trichorrhexis nodosa 
4. Trichomycosis axillaris 
5. Scaly scalp conditions
1. Clip affected hairs. 
2. Wash affected hairs with antifungal shampoo 2% 
ketoconazole shampoo or selenium sulfide. 
3. Topical imidazole cream. 
4. Oral terbinafine may also be used for black piedra. 
5. Oral itraconazole may also be used for white 
piedra.
Fungal infections part I
Fungal infections part I

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Fungal infections part I

  • 2.
  • 3.
  • 4. • Historically it was thought that fungi were plants that did not need photosynthesis. • But now fungi are classified in their own kingdom, separate from plants and animals because: 1- The cell walls of plants are made of cellulose whereas the walls of fungal cells are made of chitin 2- Plants require only simple inorganic compounds such as carbon dioxide and water to grow. Fungi require a diet of complex organic molecules to thrive. • Fungi are parasites or saprophytes i.e. they live off living or dead organic matter.
  • 5. • Growing fungi have branched filaments called hyphae, which make up the mycelium (like branches are part of a tree). Hyphae are threadlike filaments made up of fungal cells, whereas mycelium is the mass of hyphae that forms the fungal body. Some fungi are compartmented by cross-walls (called septae). • Arthrospores are made up of fragments of the hyphae, breaking off at the septae. • Asexual spores (conidia) form on conidiophores. The sexual reproductive phase of many fungi is unknown; these are ‘fungi imperfecta’ and include those which infect humans.
  • 6. FORMS OF HYPHAE; 1. Septate hyphae: In most fungi, hyphae are divided into cells by internal cross-walls for example “Aspergillus”. 2. Coenocytic hyphae (non-septate hyphae): meaning their hyphae are not partitioned by septa. 3. Pseudo hyphae: They are the result of incomplete budding where the cells remain attached after division, and Yeast can form pseudohyphae.
  • 7.
  • 8. • Yeasts form a subtype of fungus characterized by clusters of round or oval cells. • These bud out similar cells from their surface to divide and propagate. In some circumstances they form a chain of cells called a pseudomycelium.
  • 9.
  • 11.
  • 12. THE ORGANISMS ARE TRANSMITTED BY EITHER; 1. Direct contact with infected host (human or animal). 2. Indirect contact with infected exfoliated skin or hair in combs, hair brushes, clothing, furniture, theatre seats, caps, bed linens, towels, hotel rugs, and locker room floors.
  • 13. • According to their appearance by microscopy and in culture or method of reproduction. BY THE METHOD OF REPRODUCTION: 1. Sexual 2. Asexual.
  • 14. Classification of Fungal Infections (mycoses) I. SUPERFICIAL MYCOSES a) Non-inflammatory b) Inflammatory II. SUBCUTANEOUS MYCOSES III. SYSTEMIC MYCOSES
  • 15.
  • 16. • These affect the outer layers of the skin, the nails and hair. • The main groups of fungi causing superficial fungal infections are: 1. Yeasts i. Candida ii. Malassezia 2. Dermatophytes (ringworm/tinea) 3. Other Moulds e.g. i. Aspergillus spp. ii. Fusarium spp.
  • 17. Infections limited to the outermost layers of the skin and hair: 1. Pityriasis versicolor 2. Candidiasis 3. Tinea nigra 4. Black piedra 5. White piedra
  • 18. • Infections that extend deeper into the epidermis, as well as hair and nail and caused by dermatophytes. • They colonize the keratin and inflammation is caused by host response to metabolic by-products: 1. Tinea capitis (head) 2. Tinea faciei (face) 3. Tinea barbae (beard) 4. Tinea corporis (body) 5. Tinea manus (hand) 6. Tinea cruris (groin) 7. Tinea pedis (foot) 8. Tinea unguium (nail)
  • 19. THE MAIN 3 GENERA OF DERMATOPHYTES ARE: 1. Trichophyton (abbreviated as "T") 2. Epidermophyton (“E") 3. Microsporum (“M")
  • 20. 1. Anthropophilic dermatophytes are restricted to human hosts and produce a mild, chronic inflammation e.g.  T. rubrum ▪ M. audouinii  T. interdigitale ▪ T. violaceum  T. tonsurans ▪ T. schoenleinii 2. Zoophilic organisms are found primarily in animals and cause marked inflammatory reactions in humans who have contact with infected cats, dogs, cattle, horses, birds, or other animals e.g.  M. canis (originating from dogs and cats)  T. equinum (originating from horses)  T. verrucosum (originating from cattle) 3. Geophilic species are usually recovered from the soil but occasionally infect humans and animals. They cause a marked inflammatory reaction, which limits the spread of the infection and may lead to a spontaneous cure but may also leave scars e.g.  M. gypseum  M. fulvum
  • 21.
  • 22. • These involve the deeper layers of the skin (the dermis, subcutaneous tissue, muscle & fascia and even bone). • The causative organisms normally live in the soil living on rotting vegetation. They can get pricked into the skin as a result of an injury but usually stay localized at the site of implantation. • Deeper skin infections include: 1. Mycetoma 2. Chromoblastomycosis 3. Sporotrichosis
  • 23.
  • 24. • May result from breathing in the spores of fungi, which normally live in the soil or rotting vegetation or as opportunistic disease in immune compromised individuals. A. Inhaled fungal infection (By True pathogens) • Although uncommon, some may infect healthy individuals. The result is most often a mild infection and long lasting resistance to further attack, but occasionally these infections are more serious and chronic (especially in the immune suppressed). The organisms causing systemic fungal infections include: 1. Histoplasmosis 2. Coccidioidomycosis (North and South America). B. Opportunistic infections • Other systemic mycoses only infect those who are already sick or with an immunodeficiency disorder i.e. they are ‘opportunists’. Repeated infection may occur. Risks for systemic mycoses include: 1. Serious illness and debility 2. Cancer or leukemia 3. Diabetes mellitus 4. Transplant 5. Massive doses of antibiotics 6. Parenteral nutrition 7. Drug addiction 8. Infection with human immunodeficiency virus (HIV) • Opportunistic fungal infections include: 1. Aspergillosis (found everywhere) 2. Zygomycosis 3. Cryptococcosis (where there are pigeon droppings) 4. Trichosporon beigelii 5. Pseudallescheria boydii
  • 25.
  • 26.
  • 27. • It is a common, long-term (chronic) superficial fungal infection of the skin. • Affected skin change color and become either lighter or darker than surrounding skin.
  • 28. • Common in adolescent and young adult males. Malassezia requires oil to grow, accounting for the increased incidence in adolescents and preference for sebum-rich areas of the skin. • Its occurrence before puberty or after age 65 years is uncommon. • A member of normal human cutaneous flora, and it is found in 18% of infants and 90-100% of adults and it is NOT CONTAGIOUS.
  • 29. • Worldwide distribution but prevalence reported to be as high as 50% in the humid, hot environment and as low as 1.1% in the colder temperatures. • The condition is more noticeable during the summer months.
  • 30. • The causative fungus is Malassezia furfur (previously known as Pityrosporon orbiculare and Pityrosporon ovale). • In patients with clinical disease, the organism is found in both the yeast stage and the filamentous (mycelial/hyphae) form. • Factors that lead to the conversion to the parasitic, mycelial morphologic form include; 1. Genetic predisposition 2. Oily skin (yeast is lipophilic) 3. Excessive sweating 4. Warm, humid environments 5. Immuno-suppression 6. Malnutrition 7. Pregnancy 8. Cushing disease
  • 31. • The reason why this organism causes PVC 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. • Lymphocyte function on stimulation with the organism has been shown to be impaired in patients who are affected.
  • 32. • Decreased pigmentation may be secondary to the inhibitory effects of dicarboxylic acids on melanocytes (these acids result from metabolism of surface lipids by the yeast). • Sun exposure may make PVC more apparent. Decreased tanning, due to the ability of the fungus to filter sunlight. • The yeasts induce enlarged melanosomes within melanocytes in the brown type of PVC.
  • 33. • Pityriasis versicolor is usually asymptomatic, but in some people it is mildly itchy. • Numerous, well-marginated, finely scaly, oval-to-round macules. • Demonstration of this associated scale may require scratching or stretching the skin surface.
  • 34. • Scattered over the trunk, shoulders and/or the chest, the proximal extremities with occasional extension to the lower part of the abdomen and the neck. • Less frequently, lesions are seen on the face (especially in children), scalp.
  • 35.
  • 36.
  • 37.
  • 38. • The macules tend to coalesce, forming large irregularly shaped patches.
  • 39. • As the name versicolor implies, the color of each lesion varies from almost , pink (mildly inflamed), tan to dark brown
  • 40.
  • 41.
  • 42.
  • 43. • An INVERSE form also exists affecting the flexural regions antecubital fossae, sub-mammary region and groin.
  • 44.
  • 45. • Sometimes the patches start scaly and brown, and then resolve through a non-scaly and white stage.
  • 46. • Usually diagnosed clinically. • Wood’s light examination (revealing bright yellow-green fluorescence).
  • 47. • SKIN SCRAPING: then it is examined under a microscope. • DIRECT MICROSCOPY: Skin scrapings taken from patients with PVC stain rapidly when mounted in 10% KOH, glycerol and Parker ink solution and show characteristic clusters of thick-walled round, budding yeast-like cells and short angular hyphal forms up to 8um in diameter (SPAGHETTI AND MEATBALLS APPEARANCE). These microscopic features are diagnostic for Malassezia furfur and culture preparations are usually not necessary.
  • 48.
  • 49. • CULTURE: is only necessary in cases of suspected fungaemia. M. furfur is a lipophilic yeast, therefore in vitro growth must be stimulated by natural oils or other fatty substances. • The most common method used is to overlay Sabouraud's dextrose agar containing cycloheximide (actidione) with olive oil or alternatively to use a more specialized media like Dixon's agar which contains glycerol mono-oleate (a suitable substrate for growth).
  • 50. • Biopsies are usually not performed, as KOH examination of associated scale is typically diagnostic. • This section shoes; 1. Hyperkeratosis without parakeratosis 2. Few inflammatory cells in the epidermis 3. Numerous yeast & plump hyphae (Spaghetti and meatballs)
  • 51.
  • 52.
  • 53. 1. Pityriasis alba 2. Postinflammatory hypopigmentation 3. Vitiligo 4. Seborrheic dermatitis 5. Pityriasis rosea 6. Tinea corporis 7. Secondary syphilis 8. Progressive macular hypomelanosis
  • 54. TOPICAL TREATMENT 1. Azole creams and lotions; Clotrimazole, Ketoconazole, Miconazole 2. Dandruff shampoos Ketoconazole (1% or 2%) or 2.5% selenium sulfide twice weekly for 2 to 4 weeks; the preparation is left on the skin for 10–15 minutes before rinsing. Over-the-counter dandruff shampoo contain heavy metals e.g. Zinc, Mercury, Copper e.t.c.  inhibition of growth of any fungi by reacting in their biosynthetic pathways. Treatment of all the skin from the neck down to the knees, even if only a small area is clinically involved. 3. Allylamine 4. Nystatin 5. Salicylic acid 6. Sodium thiosulphate solution 7. Ciclopirox cream/solution 8. 50% propylene glycol in water
  • 55. SYSTEMIC TREATMENT • If the rash is extensive, oral antifungal medications may be needed they are; 1. Fluconazole (300 mg once weekly for 2 weeks) 2. Itraconazole (200 mg daily for 5-7 days) 3. Ketoconazole (200 mg 5 days-5 weeks), • Vigorous exercise an hour after taking the medication may help sweat it onto the skin surface, where it can effectively eradicate the fungus. Avoid bathing for a few hours.
  • 56. • Though it is easily treated, pigment changes may last for months after treatment. • Because this rash has a high recurrence rate, medication may be needed periodically to prevent recurrence. The rate of recurrence of pityriasis versicolor is very high, especially in hot humid climates so avoid heat in hot weather. • Patients at high risk for recurrence may be helped by using ketoconazole shampoo once weekly as a body cleanser. Another preventative measure is once-monthly dosing of oral ketoconazole (400 mg), fluconazole (300 mg) or itraconazole (400 mg).
  • 57.
  • 58.
  • 59. • It is due to infection by the fungus, Hortaea werneckii. • Occurs as a result of inoculation from a contamination source such as soil sewage, wood, or compost subsequent to trauma in the affected area. Note the 2 celled yeast forms
  • 60. • Typically occur in tropical climates such as Central and South America, Africa, Asia and, occasionally, in the southeastern US.
  • 61. • No predispositions have been identified. • Typically, the incubation period is 10- to 15-day. • A pigmentary change in the skin results from the accumulation of a melanin-like substance in the fungus.
  • 62. • Asymptomatic brown-to-black sharply marginated macule or patch, resembling silver nitrate or India ink stains. • The surface may appear mottled, velvety or have mild scale. • The lesions are typically solitary, although may be multiple. • Although most frequently seen on the palms, tinea nigra can also appear on the soles, neck and trunk.
  • 63.
  • 64.
  • 65. • The shape of the lesion varies, and they may appear ovoid, round, or irregular. • The lesion slowly grows over weeks to months. • The size may range from a few millimeters to several centimeters in diameter, depending on the duration. • It may have darker pigmentation of the advancing border as compared to the center. • While the disease tends to be chronic, recurrence after effective treatment is infrequent except in the case of re-exposure.
  • 66.
  • 67. • KOH EXAMINATION reveals highly branched and septate pigmented hyphae. • BIOPSY specimens have similar findings observed within the stratum corneum. • CULTURES of H. werneckiifirst appear as pasty, green-black colonies with a yeast-like appearance, and then change after approximately 2 weeks to a fuzzy, dematiaceous (dark in color) mold.
  • 68.
  • 69. 1. Acral melanocytic nevi. 2. Fixed drug eruption. 3. Postinflammatory hyperpigmentation. 4. Staining from chemicals, pigments and dyes. 5. Melanoma.
  • 70. 1. Topical keratolytic agents such as Whitfield’s ointment (typically 6% benzoic acid plus 3% salicylic acid) 2. Topical azole 3. Topical Allylamine • Several weeks of therapy may be required to prevent recurrence of disease. • Systemic therapy is generally not indicated.
  • 71.
  • 72.
  • 73. • It is a superficial non-inflammatory nodular fungal infection confined to hair shafts. • “Piedra” means “stone”, reflecting the fungal elements’ adherence to one another to form nodules along the hair shaft, the surrounding skin is healthy. • Favored climate; tropical areas. • There are 2 types Black Piedra & White Piedra.
  • 74.
  • 75.
  • 76.
  • 77.
  • 78.
  • 79.
  • 80.
  • 81. BLACK PIEDRA WHITE PIEDRA CAUSATIVE FUNGI Piedraia hortae Trichosporon beigelii (6 pathogens) PATHOGENESIS • Infection usually begins under the cuticle of the hair shaft and extends outward. • Hair breakage may occur as a result of shaft rupture at the site of the nodules. • As the nodules enlarge, they can even envelope the hair shaft. • Infection also begins beneath the cuticle and grows through the hair shaft, causing weakening and breakage of the hair.
  • 82. CLINICALLY BLACK PIEDRA WHITE PIEDRA NODULE COLOR Brown to black along the hair shaft. Generally white but may also be red, green or light brown in color. NODULE FIRMNESS Hard Soft NODULE ADHERENCE TO THE HAIR SHAFT Firm Loose TYPICAL ANATOMIC LOCATION Face, axillae and pubic region (occasionally scalp) Scalp and face (occasionally pubic region its incidence has increased since the start of the HIV pandemic) SYSTEMIC INFECTION Non In immunosuppressed patients, T. beigelii can cause TRICHOSPORONOSIS, a serious with fungemia, fever, pulmonary infiltrates, skin lesions (papulovesicular and purpuric, often with central necrosis) and renal disease.
  • 83. INVESTIGATIONS BLACK PIEDRA WHITE PIEDRA KOH EXAMINATION “crush preparation” • Dematiaceous hyphae • Organized cluster of asci, each of which contains eight ascospores (sexual phase of P. hortae-the only sexual phase detected that is pathological to human) • Non-dematiaceous hyphae • Blastoconidia and arthroconidia (representing the asexual state) CULTURE ON SABOURAUD’S AGAR • Very slow-growing • Dark green to dark brown–black colonies with a velvety texture (asexual phase) • Grows rapidly • Moist, cream-colored, yeast-like colonies • Cycloheximide inhibits growth.
  • 84.
  • 85. 1. Pediculosis (nits) 2. Hair casts 3. Trichorrhexis nodosa 4. Trichomycosis axillaris 5. Scaly scalp conditions
  • 86. 1. Clip affected hairs. 2. Wash affected hairs with antifungal shampoo 2% ketoconazole shampoo or selenium sulfide. 3. Topical imidazole cream. 4. Oral terbinafine may also be used for black piedra. 5. Oral itraconazole may also be used for white piedra.