[Lec 32] Superficial Mycoses.pdf

OUTLINE # SUPERFICIAL MYCOSES I. THE SKIN A.Layers 1. Epidermis 2. Dermis 3. Subcutaneous Tissue 4. Skin Appendages B.Skin Lesions 1. Primary Skin Lesions 2. Secondary Skin Lesions II. SUPERFICIAL MYCOSES A. Characteristics B. Types 1. Pityriasis versicolor a) Pathology b) Clinical Manifestations...

OUTLINE # SUPERFICIAL MYCOSES I. THE SKIN A.Layers 1. Epidermis 2. Dermis 3. Subcutaneous Tissue 4. Skin Appendages B.Skin Lesions 1. Primary Skin Lesions 2. Secondary Skin Lesions II. SUPERFICIAL MYCOSES A. Characteristics B. Types 1. Pityriasis versicolor a) Pathology b) Clinical Manifestations 2. Tinea nigra a) Pathology b) Epidemiology c) Diagnosis d) Treatment 3. Piedra (Trichomycosis nodularis) a) White and Black Piedra III. REVIEW QUESTIONS IV. APPENDICES 1 1 1 1 1 1 1 1 1 2 2 2 2 2 2 2 3 3 3 3 3 3 4 5 SOURCES ● Climacosa, F. (2023). Superficial Mycoses [Lecture] THE SKIN LAYERS OF THE SKIN EPIDERMIS ● Keratinized epithelium ○ Tough horny superficial layer ○ Provides protective outer surface overlying its regenerative and pigmented deep or basal layer ● Stratum corneum ○ Outermost part ● NO blood vessels or lymphatics ○ Vascular epidermis is nourished by the underlying dermis DERMIS ● Dense layer of interlacing collagen and elastic fibers ○ Accounts for: ■ Skin tone ■ Strength & toughness of skin ● Contains a lot of specialized structures ○ Deep layer of the dermis hold hair follicles with associated smooth erector muscles and sebaceous glands ○ Sweat glands provide thermoregulatory mechanisms for heat loss ● Supplied with: ○ Arteries that enter its deep surface to form a cutaneous plexus of anastomosing arteries ○ Afferent nerve endings that are sensitive to touch, irritation or pain, and temperature ■ Most nerve terminals are in the dermis ■ Few nerve endings penetrate the epidermis SUBCUTANEOUS TISSUE ● Located b/n dermis and deep fascia ● Composed of mostly loose connective tissue and stored fat ● Contains: ○ Sweat glands ■ Thermoregulation ○ Superficial blood vessel ○ Lymphatic vessels ○ Cutaneous nerves ○ Neurovascular structures SKIN APPENDAGES ● Includes: ○ Hairs ○ Glands ○ Nails SKIN LESIONS ● Skin lesions refer to any skin area that has different characteristics, i.e, color, shape, size, texture, from the surrounding skin ● Skin without any breach is a good physical barrier from any pathogenic organisms ○ When breaks occur, the environment may favor entry or even growth of pathogenic organisms ● The layer or penetration of the fungal infection determines the classification of mycoses PRIMARY SKIN LESIONS ● Originate on previously healthy skin ● Directly associated with a specific cause ● Include freckles, moles, blisters TABLE 1. Types of Primary Lesions Macules Flat, well-circumcised lesion up to 10mm Patch Similar, but larger than macule >10 mm in diameter Papules Raised bumps up to 10mm in diameter Plaque Raised, larger than 10mm Wheal Transient, smooth papule or plaque Can be erythematous, pruritus Vesicles Clear, fluid-filled blisters, up to 10mm in diameter Example: herpes simplex infection Bullae Larger than 10mm Pustules Pus-filled, elevated lesions up to 10mm Example: Pimples or acne See Appendix for visual representation. SECONDARY SKIN LESIONS ● Develop from the evolution of a primary skin lesions ○ Due to traumatic manipulation (scratching, rubbing); OR ○ Due to treatment or progression TABLE 2. Types of Secondary Lesions Scales Accumulations of thickened stratum corneum that became dry and flaky and sometimes peel off Crusts Dry exudates like sebum, pus, or blood See Appendix for more information. PH151:MICROBIO | GROUP B: MAILOM, MEDIAVILLO, PERIA, TALAGTAG, VENTANILLA 1 SUPERFICIAL MYCOSES CHARACTERISTICS ● Least invasive of the pathogenic fungi ○ Invade the most superficial part ● Adapted to the keratinized outer layers of the skin ○ Fungal infections of the skin and hair ● Very common and are easily identifiable ● Treatable with antifungal agents but relapse usually occur ○ Cause little to no inflammatory response ○ ● TYPES ● Skin → Epidermis stratum corneum ○ Pityriasis versicolor ○ Tinea Nigra ● Hair → Cuticle ○ Black Piedra ○ White Piedra PITYRIASIS VERSICOLOR ● Also known as tinea versicolor ○ However, this ia a misnomer. Tinea is now used for infections caused by dermatophytes (cutaneous mycoses) ○ Versicolor → alludes to the spectrum of color changes seen on lesions ● Very common superficial fungal infection of the skin ● Characterized by discrete patcher (larger than macules) of either hypopigmentation or hyperpigmentation ○ Especially on the skin of the torso and upper arms ● Most commonly seen in adolescents and young adults ○ Age of peak sebum production ○ There is overgrowth of Malassezia furfur PATHOLOGY ● Caused by Malassezia furfur, part of the skin microbiome ○ Lipophilic dimorphic fungi ■ Grows and thrives in media supplemented with fat ■ Has two morphologies → either hyphae or yeast-like depending on the environmental conditions ○ Known to colonize our skin as early as age 3-6 months ○ Earlier colonization is associated with length of neonatal intensive care unit days ● Malassezia lacks fatty acid synthase ○ It relies on human host’s hydrolysis of sebum triglyceride ○ Leads to transition to mycelial form and invasion of stratum corneum ● Reasons on the different colors caused by Malassezia: ○ Salmon-colored ■ Free fatty acid from hydrolysis of triglyceride triggers inflammation resulting to erythematous skin ○ Hypopigmentation ■ production of azelaic acid triggers inhibition of tyrosinase and therefore inhibition of melanin synthesis ○ Hyperpigmentation ■ Malassezia induces increase in melanosomes and thickening of stratum corneum ● Risk Factors: ○ Tropical climate ■ Warm and humid environment ○ Heavy sweating ○ Immunosuppression ■ Malassezia is somehow opportunistic ○ Oral antibiotics ■ Bacterial microbiome is decreased in numbers, there is reduced competition favorable to Malassezia ○ Corticosteroids CLINICAL MANIFESTATIONS ● Causes chronic, mild, and usually asymptomatic infection of the stratum corneum ○ Can be non-itchy or mildly pruritic PH152:MICROBIO | ● Dermatology consultation is usually for the hyper- or hypopigmentation of skin Lesions: ○ Discrete (concrescent) ■ Patches coalescing into bigger patches ■ Can sometimes be plaques (have some elevation) ○ Granny (furfuraceous) ■ There are fine scales ○ Discolored (depigmented) ■ Can be hypopigmented or hyperpigmented ● For dark-skinned people, can manifest as hypopigmented ● For light-skinned people, can manifest as hyperpigmented ■ Color can be affected by: ● Normal pigmentation of patient ● Exposure to sunlight ● Severity of disease ● Chronic stage: mixed hyperand hypopigmentation Sites: ○ Neck, chest back, upper arms, scalp, abdomen, groin area Figure 1. Pityriasis versicolor lesions DIAGNOSIS ● Fairly distinctive morphology ○ Allows most trained physicians to recognize pityriasis versicolor ● Dermoscopy ○ Tool that magnifies skin to look for fine scaling that might not be seen by the naked eye ● Figure 2. Dermoscopy of hypopigmented pityriasis versicolor shows white structureless areas with background faint pigment network, and scale Wood Lamp Examination ○ Diagnostic test wherein skin or hair is observed under black light ○ Lesions fluorescence pale yellow-green GROUP B: MAILOM, MEDIAVILLO, PERIA, TALAGTAG, VENTANILLA 2 ○ Oral ketoconazole is not given anymore ■ Associated with high risk of liver damage and adrenal dysfunction ■ Structure ko ketoconazole is similar to cortisol ○ It may take months for lesions to disappear ■ Counseling to manage expectations are needed ■ Prophylactic long term treatment may be warranted due to high propensity of pityriasis versicolor for recurrence ● Periodic use of shampoo w/ selenium sulfide or ketoconazole, and even oral itraconazole for 6 months TINEA NIGRA ● Characterized by brown to black macular lesions, usually on the palms or soles ● Usually misdiagnosed as melanoma due to coloration and location ○ Unlike tinea nigra, there is extensive involvement and possible disfiguration in melanomas Figure 3. Wood Lamp Examination ● ● Direct Examination: 10-15% KOH ○ There is presence of hyphal and yeast forms ○ Resemble a “spaghetti-and-meatballs” appearance Culture ○ Not generally used to confirm Malassezia ○ Grows at 37 degrees celsius ○ Media: Malt agar / Sabouraud’s agar ■ With streptomycin, penicillin, and actidione ■ Covered with a layer of supplemental olive oil Figure 5. Macular lesion caused by tinea nigra PATHOLOGY ● Caused by Hortaea werneckii ○ Melanized, black-pigmented fungi ○ Dematiaceous fungi ○ Found in soil, sewage, and decaying vegetation ● Infection occurs after trauma to the skin ○ Incubation period: 2-7 weeks ● Infection is confined in the stratum corneum with no disfiguration ○ Asymptomatic and non-pruritic EPIDEMIOLOGY ● Occurs in tropical or subtropical areas (Central and South America, Africa, and Asia) ● Low incidence in the USA and Europe (cases associated with tropical travel) ● Person-to-person transmission is rare ● Female-to-male predilection: 3:1 Figure 4. Diagnosis of Pityriasis Versicolor. (A) Direct mycological examination of a sample collected through skin lesion scraping, clarified with KOH 10%, illustrating yeasts grouped in a “grape bunch” format, and of short and thick pseudo-hyphae, (B) Sabouraud agar culture, enriched with olive oil, with beige yeast-like colony. DIAGNOSIS ● Microscopic examination of skin scrapings with 10% KOH ○ Brown or black septate hyphae ○ Oval- to spindle-shaped yeast cells when stained ● Culture on Sabouraud dextrose agar (SDA) with cycloheximide and chloramphenicol additive ○ Definitive diagnosis ○ Growth visible within one week ○ Initially yeast-like colony → fuzzy, grayish-black colony after mycelial growth TREATMENT TREATMENT ● First line (topical ○ Shampoos (pyrithione zinc or selenium sulfide) ● Topical therapy: ○ Propylene glycol in aqueous solution ○ Keratolytic (Whitfield ointment, 2% salicylic acid) ○ Topical imidazoles (ketoconazole) ○ Tincture of iodine ● Second line (oral) ○ Topical antifungal ○ Usually if there is extensive skin involvement and ● Continued for 2-4 weeks after clinical resolution to prevent refractory to topicals (recurrent) relapse ○ Oral fluconazole ● Systemic antifungals are effective but rarely indicated: ○ Oral itraconazole PH152:MICROBIO | GROUP B: MAILOM, MEDIAVILLO, PERIA, TALAGTAG, VENTANILLA 3 ○ Oral ketoconazole, itraconazole, terbinafine PIEDRA (TRICHOMYCOSIS NODULARIS) ● Asymptomatic superficial fungal infection of the hair shaft ○ Has characteristic white or black nodules attached to the hair shaft dematiaceous etiologic agents Epidemiology ● Temperate and ● semitropical climates of South America, Asia, Middle East, India, Africa, and Japan ● Transmission ● Person-to-person transmission is rare Not associated to travel in endemic areas WHITE AND BLACK PIEDRA ● Figure 6. White Piedra (Left) & Black Piedra (Right) Management/ Treatment ● TABLE 3. Comparison Between White and Black Piedra Characteristic White Piedra General Features ● ● ● Black Piedra Softer ● Less adherent to ● hair shaft ● Hair breakage may still occur but less common ● ● ● Causative Agent ● ● ● ● ● ● Hard/gritty Firmly attached Brown/black compressions on hair shaft (varying size) Frontal area of scalp Infection leads to weakening of hair shaft Hair breakage common Trichosporon ● asahii (other body surfaces) T. ovoides (scalp) T. inkin (pubic hair) T. mucoides T. asteroids T. cutaneum Piedraia hortae ○ In soil, stagnant water, and crabs ○ Mostly affects scalp hair Growth ● Infects the shaft ● in a hyphal form that can fragment into component buds Grows as branched hyphae in the hair shaft Nodules ● Mature nodules ● attached to hair shaft Appears easily ● detachable Higher magnification shows closely aligned fungal arthrospores Attached and more adherent to hair shaft Higher magnification shows ascus (round structures) ● ● Culture ● ● Sabouraud Dextrose Agar Trichosporon yield characteristic white colonies ○ Convoluted ○ Cerebriform (cerebrum/ brain-like) PH152:MICROBIO | ● Sabouraud Dextrose Agar ○ Does not require cycloheximide for growth ○ Takes long to culture ● Resembles colonies of Tinea nigra since both are caused by ● Shaving infected ● hair (curative) + topical azole Systemic antifungal agent (i.e. oral itraconazole) due to high relapse rates Humans and primates in tropical areas of South America, Pacific Islands, and the far east Less common in Africa and Asia — Shaving infected hair (curative) + topical azole REVIEW QUESTIONS 1. The layer of the skin that contains the sweat glands is: a. Epidermis b. Dermis c. Subcutaneous tissue d. Skin appendages 2. The type of primary skin lesions that can be erythematous, pruritus is: a. Macules b. Wheal c. Vesicles d. Pustules 3. TRUE OR FALSE: Scales are accumulations of thickened stratum corneum 4. TRUE OR FALSE: In Tinea nigra, infection can spread to other parts of the body. 5. TRUE OR FALSE: The male-to-female predilection in Tinea nigra is 3:1 6. Microscopic examination of skin scrapings in Tinea nigra is with __% KOH 7. TRUE OR FALSE: White piedra occurs in the frontal area of scalp 8. The definitive diagnosis of Tinea nigra is: a. Culture on SDA with cycloheximide and chloramphenicol additive b. Culture on SDA with chloramphenicol additive only c. Microscopic examination of skin scrapings with KOH 9. Malassezia lacks: a. Tyrosinase b. Azelaic acid c. Triglyceride d. Fatty acid synthase 10. TRUE OR FALSE: Pityriasis veriscolor is caused by an undergrowth of Malassezia furfur. Answer Key 1. C 2. B. 3. True 4. False 5. False (female-to-male) 6. 10% 7. False (Black Piedra) 8. A 9. D 10. False GROUP B: MAILOM, MEDIAVILLO, PERIA, TALAGTAG, VENTANILLA 4 APPENDIX LAYERS OF THE SKIN Epidermis Keratinized epithelium ● A tough, horny superficial layer that provides protective outer surface overlying its regenerative and pigmented deep or basal layer Stratum corneum ● Outermost layer consisting of dead skin cells Has no blood vessels or lymphatics ● Vascular epidermis is nourished by the underlying dermis. Dermis Dense layer of interlacing collagen and elastic fibers accounting for skin tone, strength, and toughness Contains a lot of specialized structures: Hair follicles ● With associated smooth erector muscles and sebaceous glands Sweat glands ● Function in thermoregulation Arteries ● Supplied in the dermis form a cutaneous plexus of anastomosing arteries Afferent nerve endings ● Sensitive to touch, irritation or pain, and temperature. ● Most nerve terminals are in the dermis; only a few penetrate the epidermis. Subcutaneous Located between dermis and deep fascia Tissue Composed of mostly loose connective tissue and stored fat Contains: ● Sweat glands, ● Superficial blood vessel, ● lymphatic vessel, ● cutaneous nerves, ● neurovascular structures Appendages ● ● ● PH152:MICROBIO | Hairs Glands Nails GROUP B: MAILOM, MEDIAVILLO, PERIA, TALAGTAG, VENTANILLA 5 SUPERFICIAL MYCOSES Characteristics Pityriasis versicolor ● ● ● General Features ● ● ● ● Pathogenesis PH152:MICROBIO | Tinea nigra Piedra/Trichomycosis Nodularis White Piedra Black Piedra Also known as tinea versicolor ● Characterized by brown to black macular lesions ○ Versicolor → alludes to the ● Often misdiagnosed as melanoma spectrum of color changes seen on lesions Very common superficial fungal infection of the skin Characterized by discrete patcher (larger than macules) of either hypopigmentation or hyperpigmentation ○ Especially on the skin of the torso and upper arms Most commonly seen in adolescents and young adults ○ Age of peak sebum production ● Softer ● Hard/gritty ● Less adherent to hair shaft ● Firmly attached ● Hair breakage may still occur but less ● Brown/black compressions on hair common shaft (varying size) ● Frontal area of scalp ● Infection leads to weakening of hair shaft ● Hair breakage common Caused by Malassezia furfur, part of ● Etiologic agent: Hortaea werneckii the skin microbiome ○ Melanized, black-pigmented fungi (dematiaceous) ○ Lipophilic dimorphic fungi ○ Found in soil, sewage, and decaying vegetation ○ Known to colonize our skin as ● Infection occurs after trauma to the skin (IP: 2-7 weeks) early as age 3-6 months ○ Earlier colonization is associated with length of neonatal intensive care unit days Malassezia lacks fatty acid synthase ○ It relies on human host’s hydrolysis of sebum triglyceride ○ Leads to transition to mycelial form and invasion of stratum corneum Reasons on the different colors caused by Malassezia: ○ Salmon-colored ■ Free fatty acid from hydrolysis of triglyceride triggers inflammation resulting to erythematous skin ○ Hypopigmentation ■ production of azelaic acid triggers inhibition of tyrosinase and therefore inhibition of melanin synthesis ○ Hyperpigmentation ■ Malassezia induces increase in ● Causative agents: ● Causative agent: ○ Trichosporon asahii (other body ○ Piedraia hortae surfaces) ■ In soil, stagnant water, and crabs ○ T. ovoides (scalp) ■ Mostly affects scalp hair ○ T. inkin (pubic hair) ○ T. mucoides ○ T. asteroids ○ T. cutaneum ● Person-to-person transmission is rare ● Not associated to travel in endemic areas GROUP B: MAILOM, MEDIAVILLO, PERIA, TALAGTAG, VENTANILLA 6 melanosomes and thickening of stratum corneum ● Risk Factors: ○ Tropical climate ■ Warm and humid environment ○ Heavy sweating ○ Immunosuppression ■ Malassezia is somehow opportunistic ○ Oral antibiotics ■ Bacterial microbiome is decreased in numbers, there is reduced competition favorable to Malassezia ○ Corticosteroids ● Occurs in tropical or subtropical areas (Central and ● Temperate and semitropical climates of ● Humans and primates in tropical South America, Africa, and Asia) South America, Asia, Middle East, India, areas of South America, Pacific ● Low incidence: USA and Europe (associated with tropical Africa, and Japan Islands, and the far east travel) ● Less common in Africa and Asia ● Person-to-person transmission is rare ● Female-to-male predilection: 3:1 Epidemiology ● ● Clinical Manifestations PH152:MICROBIO | Causes chronic, mild, and usually ● Brown to black macular lesions usually on the palms or asymptomatic infection of the stratum soles corneum ● Infection is confined in the stratum corneum with no ○ Can be non-itchy or mildly pruritic disfiguration ○ Dermatology consultation is usually for ○ Asymptomatic and non-pruritic the hyper- or hypopigmentation of skin Lesions: ○ Discrete (concrescent) ■ Patches coalescing into bigger patches ■ Can sometimes be plaques (have some elevation) ○ Granny (furfuraceous) ■ There are fine scales ○ Discolored (depigmented) ■ Can be hypopigmented or hyperpigmented ● For dark-skinned people, can manifest as hypopigmented ● For light-skinned people, can manifest as hyperpigmented ■ Color can be affected by: ● Normal pigmentation of patient ● Exposure to sunlight ● Severity of disease GROUP B: MAILOM, MEDIAVILLO, PERIA, TALAGTAG, VENTANILLA ● Infects the shaft in a hyphal form that can ● Grows as branched hyphae in the hair fragment into component buds shaft ● Mature nodules attached to hair shaft ● Attached and more adherent to hair ● Appears easily detachable shaft ● Higher magnification shows closely ● Higher magnification shows ascus aligned fungal arthrospores (round structures) 7 ● ● Sites: ○ Neck, chest back, upper arms, scalp, abdomen, groin area ● Fairly distinctive morphology ● Microscopic examination of skin scrapings with 10% KOH ● Culture on SDA ● Culture on SDA ○ Allows most trained physicians to ○ Brown or black septate hyphae ● Trichosporon yield characteristic white ○ Does not require cycloheximide for recognize pityriasis versicolor ○ Oval- to spindle-shaped yeast cells when stained colonies -growth Dermoscopy ● Culture on SDA with cycloheximide and chloramphenicol ○ Convoluted ○ Takes long to culture ○ Tool that magnifies skin to look for fine additive ○ Cerebriform (cerebrum/ brain-like) ● Resembles colonies of Tinea nigra scaling that might not be seen by the ○ Definitive diagnosis since both are caused by naked eye ○ Growth visible within one week dematiaceous etiologic agents Wood Lamp Examination ○ Initially yeast-like colony → fuzzy, grayish-black colony ○ Diagnostic test wherein skin or hair is after mycelial growth observed under black light ○ Lesions fluorescence pale yellow-green Direct Examination: 10-15% KOH ○ There is presence of hyphal and yeast forms ○ Resemble a “spaghetti-and-meatballs” appearance Culture ○ Not generally used to confirm Malassezia ○ Grows at 37 degrees celsius ○ Media: Malt agar / Sabouraud’s agar ■ With streptomycin, penicillin, and actidione ■ Covered with a layer of supplemental olive oil ● ● Diagnosis Chronic stage: mixed hyperand hypopigmentation ● ● ● ● Treatment PH152:MICROBIO | First line (topical ● Topical therapy: ● Shaving infected hair (curative) + topical ● Shaving infected hair (curative) + topical ○ Shampoos (pyrithione zinc or selenium ○ Keratolytic (Whitfield ointment, 2% salicylic acid) azole azole sulfide) ○ Tincture of iodine ● Systemic antifungal agent (i.e. oral ○ Propylene glycol in aqueous solution ○ Topical antifungal itraconazole) due to high relapse rates ○ Topical imidazoles (ketoconazole) ○ (continued for 2-4 weeks after clinical resolution to prevent Second line (oral) relapse) ○ Usually if there is extensive skin ● Systemic antifungals are effective but rarely indicated: involvement and refractory to topicals ○ Oral ketoconazole, itraconazole, terbinafine (recurrent) ○ Oral fluconazole ○ Oral itraconazole ○ Oral ketoconazole is not given anymore ○ It may take months for lesions to disappear ■ Counseling to manage expectations are needed ■ Prophylactic long term treatment may be warranted due to high propensity of pityriasis versicolor for recurrence ● Periodic use of shampoo w/ selenium sulfide or ketoconazole, and even oral itraconazole for 6 months GROUP B: MAILOM, MEDIAVILLO, PERIA, TALAGTAG, VENTANILLA 8