Fungal infections part III

Dermatophytosis (Ringworm Infection), Tinea capitis, Tinea faciei, Tinea barbae, Tinea corporis, Tinea manus, Tinea cruris, Tinea pedis, Tinea unguium, Onychomycosis, DERMATOPHYTID (ID) REACTION, Tinea Incognito, DDx Of Dermatophyte Infections, DIAGNOSIS OF FUNGAL INFECTION, TREATMENT OF DERMATOPHYTOSIS

1. FU NG AL IN FE CT IO NS Part III https://www.facebook.com/groups/dermatologycourseonline /

2. ﴿ الذي جعل لكم من الشجر الأخضر نارا فإذا أنتم منه توقدون أو ليس الذي خلق السموات والأرض بقادر على أن يخلق مثلهم بلى وهو الخلاق العليم ﴾

3. DERMATOPHYTOSIS

4. Dermatophytosis (Ringworm Infection) Infections that extend deeper into the epidermis , as well as hair and nail and caused by dermatophytes . Dermatophytes infect only superficial keratinized structures but not deeper tissues. They possess keratinases allowing them to utilize keratin as a nutrient & energy source  colonization  its destruction and inflammation is caused by host response to fungi & to metabolic by-products . Clinical variation of dermatophytes infection depends on: Fungal spp. Stage of infection. Body location. Immune status of the host.

5. Dermatophytosis THE MAIN 3 GENERA OF DERMATOPHYTES ARE: T richophyton (abbreviated as "T") infections on skin, hair, and nails E pidermophyton (“E") - infections on skin and nails (not the cause of TINEA CAPITIS ) M icrosporum (“M ") infections on skin and hair (not the cause of TINEA UNGUIUM )

6. Types Of Dermatophytes Based On Mode Of Transmission

7. Clinical Varieties Of Dermatophyte Infection Tinea capitis (head) Tinea faciei (face) Tinea barbae (beard) Tinea corporis   (body) Tinea manus (hand) Tinea cruris (groin) Tinea pedis (foot) Tinea unguium (nail)

8. Tinea Capitis Etymology : L. [ caput ] head. Tinea capitis is the most common pediatric dermatophyte infection worldwide . The age predilection (3 and 7 years of age) is believed to result from the presence of Malassezia furfur which is part of normal flora, and from the fungistatic properties of fatty acids of short and medium chains in postpubertal sebum so it is rare in adult population .

9. Tinea Capitis

10. Tinea Capitis

11. Mode of Infection Anthropophilic infections: such as T. tonsurans are more common in crowded living conditions. The fungus can contaminate hairbrushes , clothing , towels and the backs of seats . The spores are long lived and can infect another individual months later . Zoophilic infections: are due to direct contact with an infected animal and are not generally passed from one person to another . This produce a much greater inflammatory response and this often results in a boggy inflammatory swelling known as a kerion . Geophilic infections: usually arise when working in infected soil but are sometimes transferred from an infected animal.

12. Patterns Of Hair Invasion By Dermatophytes

13. Patterns Of Hair Invasion By Dermatophytes

14. Patterns Of Hair Invasion By Dermatophytes

15. Adamson’s fringe

16. PATTERNS OF HAIR INVASION BY DERMATOPHYTES S mall spore ectothrix La rg e spore ectothrix Ar t hrosporic endothrix Favus endothrix Species of dermatophyte M . canis , M . audouinii T. menta gr ophytes, T. ve rr ucosum T. t onsurans T. v iolaceum T. schoenleinii Fungal Growth & Hair Shaft affection Penetrates the surface  grow downwards until Adam s on’s fringe. The cuticle of the hair is destroyed Straight 1ry extrapilary hyphae Hyphae invade only the inside of the hair shaft ( intrapilary hyphae). Cuticle of the hair remains intact Inside invasion broad hyphae and significant air pockets Arthroconidia Small s pherical on outer surface of H. shaft Larger & arranged in straight manner Within hair shaft. No spores Wood’s Lamp Examination Bright green fluore s cence No fluorescence No fluorescence Pale green fluorescence Clinically H. Shaft fracture & dry s caling patch of alopecia (GPTC) ke r ion Damage of H. shaft at skin surface  Black do t s (BDTC) Scutula  Favus

17. Clinical Types of Tinea Capitis Scaly (Gray Patch) Tinea Capitis (GPTC) Black Dot Tinea Capitis (BDTC) Kerion Favus

18. Clinical Types of Tinea Capitis I. SCALY TYPE/GRAY PATCH TINEA CAPITIS (GPTC) : It begins with an erythematous , scaling, well-demarcated patch on the scalp that spreads centrifugally for a few weeks or months, ceases to spread, and persists indefinitely, sometimes for years. Single or multiple patches of scaly (grayish-white) alopecia are seen where the hairs are broken just above the level of scalp  short stumps . No subsequent scarring alopecia .

19. GPTC

20. Clinical Types of Tinea Capitis II. BLACK DOT TINEA CAPITIS (BDTC): It is an endothrix infection, so hair become notably fragile and break easily at the level of the scalp . The rest of the infected follicle look like "black dots" . Variable degrees of scaling . Usually begins as an asymptomatic , erythematous , scaling patch on the scalp, which slowly enlarges . Lesions may be single or multiple . Early lesions are easily overlooked and the disease is not usually noticed until areas of alopecia become evident.

21. BDTC

22. Dermoscopy of Tinea Capitis

23. Dermoscopy of Tinea Capitis

24. Dermoscopy of Tinea Capitis

25. Clinical Types of Tinea Capitis III. KERION: Usually zoonotic infection e.g. T . ve rr ucosum. Scattered painful pruritic pustular folliculitis generally associated with regional lymphadenopathy and fever. Boggy (soft & watery ) swelling studded with broken hairs and purulent sticky material "kerion" appear. Hairs  easily removed when pulled . Untreated kerion may result in permanent scarring alopecia .

26. Kerion

27. Clinical Types of Tinea Capitis IV. FAVUS (TINEA FAVOSA): Etymology : Favus=L . honeycomb Perifollicular erythema on the scalp, which progresses to the characteristic finding of concave , cup-shaped yellow crusts called scutula . The scutulum develops at the surface of a hair follicle with the shaft in the center of the raised lesion & formed of dense masses of mycelium , neutrophils , dried serum and epithelial debris . Removal of scutula reveals an oozing , moist , red base . After a period of years , atrophy of the skin occurs leaving scarring alopecia . It has unpleasant smell “ mousy odor ” .

28. Favus

29. Tinea Faciei Uncommon dermatophyte infection (most commonly T. rubrum ) of the face. It does not include infection of the beard and moustache area in men. While some dermatophyte infections of the face have classic features of tinea circinata , e.g. scale , annular configuration, pustules in the border. It is frequently aggravated by sun exposure . Others infections can be more difficult to diagnose clinically “ tinea incognito ” and require a high index of suspicion.

30. Tinea Faciei

31. Tinea Barbae It is dermatophyte infection of the beard and moustache areas of the face. Currently , it is infrequent around the world. Generally affects only adult men . The mechanism that causes tinea barbae is similar to that of tinea capitis but it is less frequently occurring . Tinea barbae was observed more frequently in the past when infection frequently was transmitted by barbers who used unsanitary razors , so it was termed BARBER'S ITCH . Tinea barbae can result in an id reaction , especially just after starting antifungal treatment.

32. Clinical Presentations of Tinea Barbae 1. INFLAMMATORY DEEP TYPE/KERION ( T. Barbae Profunda): It is the most common clinical presentation of T. barbae . Caused primarily by zoophilic dermatophytes mainly T . ve rr ucosum, T. menta gr ophytes . Most often affects farmers and is due to direct contact with an infected animal . Intense reddish inflammation and multiple follicular pustules . Abscesses , draining sinus tracts, bacterial super-infection and even kerion-like boggy plaques can develop. Most patients show solitary plaques or nodules ; however, multiple plaques are relatively common. Usually localized on the chin , cheeks , or neck , involvement of the upper lip is rare.

33. Clinical Presentations of Tinea Barbae 1. INFLAMMATORY DEEP TYPE/KERION (T. Barbae Profunda ): Surprisingly, it is not excessively itchy or painful . Hairs are loose or broken , and depilation is easy and painless. Over time, the surface of the indurated nodule is covered by exudate and crust . This variety of tinea barbae usually is associated with generalized symptoms , such as regional lymphadenopathy , malaise , and fever . Scarring alopecia may develop.

34. Tinea Barbae Profunda

35. Clinical Presentations of Tinea Barbae 2. NON-INFLAMMATORY SUPERFICIAL TYPE: Caused by anthropophilic dermatophytes. T . rubrum is usually the causative agent. This variety is less common . Typically, erythematous patches show an active border composed of papules , vesicles , and/or crusts . Hairs are broken next to the skin. Alopecia may be present in the center of the lesion, but it is reversible .

36. Tinea Corporis It is a dermatophyte infection of the skin of the trunk and extremities , excluding the hair , nails , palms , soles and groin . T. rubrum is the most common infectious agent in the world followed by T. mentagrophytes & E. floccosum . MOI: Anthropophilic : result from direct contact with infected humans including autoinoculation e.g. from t. capitis or pedis. Zoophilic : often transmitted by domestic animals, Geophilic .

37. Tinea Corporis Predisposing factors include; Occupational or recreational exposure (e.g. Military housing, gymnasiums, locker rooms, outdoor occupations, wrestling). Contact with contaminated clothing and furniture. Immunosuppression. In response to the infection , the active border has an increased epidermal cell proliferation with resultant scaling . This creates a partial defense by way of shedding the infected skin and leaving new , healthy skin central to the advancing lesion.

38. Tinea Corporis caused by T. rubrum

39. Clinical Presentation of Tinea Corporis Patients can be asymptomatic or pruritic and burning . The typical incubation period is 1 to 3 weeks . Infection spreads centrifugally from the point of skin invasion , begins as an erythematous , scaly, sharply marginated plaque that may rapidly worsen and enlarge . Central resolution causes the lesion to be annular but it may be arcuate , oval or discoid . Scales , crusts , vesicles , papules and pustules often develop, especially in the advancing border .

40. Tinea Corporis

41. Tinea Corporis

42. Tinea Corporis

43. Tinea Corporis

44. Clinical Presentation of Tinea Corporis Infections due to zoophilic or geophilic dermatophytes may produce acute (sudden onset and rapid spread ) more intense inflammatory response than those caused by anthropophilic fungi chronic ( slow extension of a mild , barely inflamed lesion ).

45. Clinical Variants Of Tinea Corporis “3” MAJOCCHI GRANULOMA (Nodular Folliculitis) usually caused by T. rubrum , is characterized by perifollicular papulopustules or granulomatous nodules commonly in a distinct location, which is the lower two thirds of the leg in females who have t. pedis or onychomycosis and shave their legs, represents a deep dermatophyte folliculitis in which the follicular wall is disrupted. Also occur in immunosuppressed . TINEA IMBRICATA ( Imbricate= Overlapping) shows distinct scaly plaques arranged in concentric annular rings . TINEA PROFUNDA results from an excessive inflammatory response to a dermatophyte (analogous to a KERION on the scalp). It may have a granulomatous or verrucous .

46. Majocchi Granuloma

47. Majocchi Granuloma

48. Tinea Imbricata

49. Tinea Imbricata

50. Tinea Profunda

51. Tinea Manuum Dermatophyte infections of the palm . It shows different clinical picture due to lack of sebaceous glands on the palms . The typical causative organisms are the same as those for tinea pedis and tinea cruris: T. rubrum, T. mentagrophytes and E. floccosum. It is an uncommon dermatophytic infection .

52. Clinical Presentation of Tinea Manuum The patient may complain from mild itching . Presentation is similar to moccasin tinea pedis. Chronic erythema, dryness , scaling and hyperkeratosis of the palms and fingers affecting the skin diffusely is the commonest variety , and is unilateral in about half the cases  “ TWO FEET AND ONE HAND SYNDROME ”. The accentuation of the flexural creases is a characteristic feature because of white scale . An important clinical clue is tinea unguium of the involved hand. Tinea manuum is usually non-inflammatory .

53. Clinical Presentation of Tinea Manuum Other clinical variants include; Vesicular (on the edges of the fingers or palm) Crescentic Circumscribed Discrete Red papular Follicular scaly patches

54. Tinea Manuum

55. Tinea Cruris It is a dermatophyte infection of the inguinal region , in particular the inner aspects of the upper thighs and crural folds , with occasional extension onto the abdomen and buttocks . The three most common causative agents are T. rubrum , T. mentagrophytes and E. floccosum . Autoinoculation occurs in 50 % of cases from onychomycosis or tinea pedis . Risk factors for initial infection or reinfection include infected fomites particularly infected towels , obesity , excessive perspiration , wearing tight-fitting or wet clothing or undergarments . Tinea cruris is more common in adult men than in women .

56. Tinea Cruris

57. Clinical Presentation of Tinea Cruris Patients complain of pruritus and rash in the groin. A history of previous episodes of a similar problem usually is elicited. Large patches of erythema with central clearing are centered on the inguinal creases . Sharply demarcated lesions with a raised reddish , scaly advancing border (usually downwards) that may contain pustules , pustules or vesicles . The lesion may initially be circinate and then become serpiginous .

58. Clinical Presentation of Tinea Cruris The disease can remain unilateral but usually become bilateral . Lesions may extend to the thighs , lower abdomen , pubic area & buttocks . The penis , scrotum and vulva are typically spared .

59. Tinea Cruris

60. Clinical Presentation of Tinea Cruris ACUTE INFECTIONS , the rash may be moist and exudative with a prominent inflammation with or without pustules . Caused by zoophilic pathogens e.g. T . mentagrophytes. CHRONIC INFECTIONS typically are dry with a papular annular or arciform border and barely perceptible scale at the margin sometimes even leathery and lichenified . Caused by anthropophilic pathogens e.g. T. rubrum.

61. Clinical Presentation of Tinea Cruris Chronic infections may be modified by the application of topical corticosteroids (tinea incognito).

62. Tinea Pedis It is a dermatophyte infection of the soles and interdigital web spaces of the feet. Tinea pedis is thought to be the world's most common dermatophytosis . Up to 70% of the population will be infected with tinea pedis at some time . It is more common in adult men as childhood tinea pedis is rare. The lack of sebaceous glands in the soles is an important factor in its development. T. rubrum being the most common cause worldwide other dermatophytes that are typically responsible for tinea pedis are T. mentagrophytes and E . floccosum .

63. Risk Factors of Tinea Pedis A hot , humid , tropical environment. Prolonged use of occlusive footwear as it is uncommon in populations that do not wear shoes at all. Certain activities , such as swimming and communal bathing , going barefoot ( locker rooms , gyms , public facilities ) may also increase the risk of infection. Hyperhidrosis . Immunodeficiency .

64. Four Major Clinical Types of Tinea Pedis Interdigital type Moccasin type ( Chronic hyperkeratotic) Inflammatory (Vesicular) type Ulcerative type

65. Clinical Types of Tinea Pedis 1. INTERDIGITAL TYPE: The most common type , with erythema , maceration , fissuring , and scaling in the web spaces ; the two lateral web spaces are most commonly affected & may be pruritic . “DERMATOPHYTOSIS COMPLEX” ( fungal infection followed by bacterial invasion ) can develop; The clinical features of symptomatic athlete's foot are a result of the interaction of fungi and bacteria . The dorsal surface of the foot is usually clear , but some extension onto the dorsal or plantar surfaces of the foot may occur . May be caused by non-dermatophyte pathogens e.g. S. dimidiatum or Candida spp.

66. Tinea Pedis

67. Clinical Types of Tinea Pedis 2. CHRONIC HYPERKERATOTIC TYPE (MOCCASIN) Named so because it has a moccasin-like distribution pattern . Plantar erythema with slight scaling to diffuse hyperkeratosis & fissuring but not inflamed that can be asymptomatic or pruritic . Both feet are usually affected . Frequently chronic and difficult to cure because of the thickness of stratum corneum on plantar surfaces and the inability of T . rubrum to elicit sufficient immune response. Typically, the dorsal surface of the foot is clear , but, in severe cases, the condition may extend onto the sides of the foot . May be caused by non-dermatophyte pathogens e.g. S. dimidiatum .

68. Moccasin Tinea Pedis

69. Moccasin Tinea Pedis

70. Clinical Types of Tinea Pedis 3. INFLAMMATORY/VESICULAR TYPE: Painful , pruritic vesicles , pustules or bullae usually on the medial anterior plantar surface ; often associated with the id reaction. After they rupture , scaling with erythema persists . Cellulitis , lymphangitis and adenopathy can complicate this type.

71. Vesicular Tinea Pedis

72. Vesicular Tinea Pedis

73. Clinical Types of Tinea Pedis 4. ULCERATIVE TYPE: Typically an exacerbation of interdigital tinea pedis . Ulcers and erosions in the web spaces ; commonly secondarily infected with bacteria . Seen in immunocompromised and diabetic patients that may show even osteomyelitis leading to amputation .

74. Ulcerative Tinea Pedis

75. Clinical Presentation of Tinea Pedis DERMATOPHYT ID (ID) REACTION: It is an allergic eruption caused by an inflammatory fungal infection at a distant site . It is associated with vesicular tinea pedis . They develop on the palmar surface of one or both hands and/or the sides of the fingers as papules , vesicles , and, occasionally, bullae or pustules may occur, often in a symmetrical fashion . They mimic dyshidrosis ( pompholyx ) . Scattered follicular lesions mainly affect the trunk usually follows a kerion (inflammatory tinea corporis or tinea capitis ) from a zoophilic fungus .

76. Clinical Presentation of Tinea Pedis DERMATOPHYT ID (ID) REACTION: As it is an allergy or hypersensitivity response to the fungal infection it contains no fungal elements . The specific explanation of this phenomenon is still unclear . Distinguishing between a dermatophytid reaction and dyshidrosis can be difficult . Therefore, a close inspection of the feet is necessary in patients with vesicular hand dermatoses and KOH examination may help. The dermatophytid reaction resolves when the kerion or tinea pedis infection is treated , and treatment with topical steroids can hasten resolution. Occasionally systemic steroids are required for a few weeks.

77. Id Reaction

78. Id Reaction

79. Tinea Unguium and Onychomycosis TINEA UNGUIUM (Dermatophytic onychomycosis): is clinically defined as a dermatophyte infection of the nail plate . ONYCHOMYCOSIS: includes all infection of the nail caused by any fungus , including non-dermatophytes and yeasts .

80. Onychomycosis It affects men more often than women. It accounts for 20% of all nail disease . Approximately 30% of patients with dermatophyte infections on other parts of their body also have onychomycosis. Toenail infections are more common than fingernail infections. A single nail may be involved , but more commonly , multiple nails are affected.

81. Etiology of Onychomycosis ONYCHOMYCOSIS CAN BE DUE TO: DERMATOPHYTES (~90% of cases) most commonly T. rubrum , T. mentagrophytes or E. floccosum . YEASTS such as Candida albicans . MOULDS especially Fusarium species usually indistinguishable from tinea unguium. PREDISPOSING FACTORS: Trauma Aging Diabetes Poorly fitting shoes The presence of tinea pedis and other nail disorders represent

82. Clinical Presentation of Onychomycosis The patient often complain of discomfort and pain associated with trimming the nails, running , and other activities. Characteristically, infected nails coexist with normal-appearing nails . In addition , serious complications such as cellulitis can result from onychomycosis , especially in patients who are diabetic or immunocompromised . Onychomycosis and concurrent diabetes triple a patient’s risk of toe ulceration , infection and gangrene .

83. Clinical Presentation of Onychomycosis 4 MAJOR CLINICAL TYPES OF ONYCHOMYCOSIS : Distal/Lateral subungual onychomycosis White superficial onychomycosis Proximal subungual onychomycosis Candidal onychomycosis

84. Clinical Presentation of Onychomycosis 1. DISTAL/LATERAL SUBUNGUAL ONYCHOMYCOSIS: It is the most common type and starts by invasion of the stratum corneum of the hyponychium and distal nail bed . Infection moves proximally in the nail bed and invades the ventral surface of the nail plate . Subungual hyperkeratosis results from a hyperproliferative reaction of the nail bed in response to the infection . With further progression of infection, there is yellowing and thickening of the distal or lateral nail plate as well as distal onycholysis . Eventually , the entire nail bed and plate may become involved (TOTAL DYSTROPHIC PATTERN). 50% or more of cases of nail dystrophy are due to onychomycosis .

85. Distal/Lateral Subungual Onychomycosis

86. Distal/Lateral Subungual Onychomycosis

87. Distal/Lateral Subungual Onychomycosis

88. Distal/Lateral Subungual Onychomycosis

89. Clinical Presentation of Onychomycosis 2. WHITE SUPERFICIAL ONYCHOMYCOSIS: Direct penetration into (and usually confinement to) the dorsal surface of the nail plate often due to T. mentagrophytes. This classic form shows well-delineated discrete opaque " white islands " on the plate. Patches coalesce to involve the entire nail plate . The nail becomes rough , soft and crumbly . Transverse striate bands and deeper invasion of the nail plate can also occur . These variants are more likely be caused by T . rubrum or non-dermatophyte molds .

90. White Superficial Onychomycosis

91. Clinical Presentation of Onychomycosis 3. PROXIMAL SUBUNGUAL ONYCHOMYCOSIS: It is the least common variant of onychomycosis. It starts by fungal invasion of the stratum corneum of the proximal nail fold and subsequently the nail plate . Yellow spots appear at the lunula . Frequently in immunocompromised hosts.

92. Clinical Presentation of Onychomycosis 4. CANDIDAL ONYCHOMYCOSIS: Candida spp . are often found in association with chronic paronychia . The fingernails are usually affected, with ridging , yellow discoloration, tenderness and onycholysis . The nail fold is swollen and red . Candida spp . are a relatively common cause of onychomycosis in children less than 3 years of age, and nail involvement also represents a manifestation of chronic mucocutaneous candidiasis .

93. Candidal Onychomycosis

94. Clinical Presentation of Onychomycosis OTHER TYPES OF ONYCHOMYCOSIS Total Dystrophic Onychomycosis Endonyx Onychomycosis Fungal organisms invade only the nail plate but do not cause nail bed inflammatory changes . This type of onychomycosis is mainly confined to the lower layers of the nail plate and is characterized by a diffuse milky-white discoloration of the affected nail. The nail plate surface and nail thickness are normal and no subungual hyperkeratosis and no onycholysis .

95. Onychomycosis ONYCHOMYCOSIS IS CHALLENGING TO MANAGE DUE TO; Difficulties in diagnosis. The requirement for long treatment periods. Potential side effects of systemic medications. Frequent recurrences.

96. Tinea Incognito DEFINITION : Ringworm infections modified by systemic or topical corticosteroids prescribed for some pre-existing pathology or given mistakenly for the treatment of misdiagnosed tinea .

97. Pathogenesis of Tinea Incognito The inflammatory response of tinea may be almost totally suppressed by corticosteroids , systemic (degree of modification is often minor) or topical (degree of modification can be profound ) especially strong fluorinated steroids. At the same time, it is probable that the resistance to infection mediated by the immune response , especially the cell-mediated response, is diminished by corticosteroids.

98. Clinical Features of Tinea Incognito The history is characteristic. The patient is often satisfied initially with the treatment. Itching is controlled and the inflammatory signs settle. He or she stops applying the cream, the eruption relapses , with varying rapidity. Further applications bring renewed relief and the cycles are repeated . The eruption usually remains localized but , especially in E. floccosum infections, it spreads more widely than one would expect in the unmodified case .

99. Clinical Features of Tinea Incognito In the groins , the patient may develop few persistent nodules , which become unsuppressible by the steroid preparation. The usual sites are the groins , lower legs , face , hands and perianally but tinea circinata elsewhere may be steroid treated. On the face , the picture may be modified by a superimposed perioral dermatitis with papules and tiny pustules .

100. Typically , the raised margin is diminished . Scaling is lost and the inflammation is reduced to a few nodules . Often, a bruise-like brownish discoloration is seen, especially in the groins. With chronic use, atrophy , telangiectasia and, in the groins and axillae, striae are likely to be observed. In some cases, concentric rings of erythema are seen among the atrophy and telangiectasia. Presumably, these represent waves of fungal growth . Clinical Features of Tinea Incognito

101. Diagnosis of Tinea Incognito DIRECT MICROSCOPY AND CULTURE: Scrapings and culture may be difficult to obtain in a patient who is currently applying a steroid cream and may show very few fungal elements . If the patient stops steroid for a few days an upsurge of inflammation with marked scaling often occurs, making clinical diagnosis easier and facilitating the taking of scrapings . In such samples, fungal mycelium is usually abundant .

102. DDx Of Dermatophyte Infections

103. DIAGNOSIS OF FUNGAL INFECTION

104. SPECIMEN COLLECTION SKIN: Any ointments or other local applications present should first be removed with alcohol . Using a blunt scalpel, firmly scrape the lesion, particularly at the advancing border. In cases of vesicular tinea pedis, the tops of any fresh vesicles should be removed as the fungus is often plentiful in the roof of the vesicle . Skin stripped off with adhesive tape, which is then stuck on a glass slide. HAIR: Epilation of short broken hairs with tweezers especially fluorescent hairs with Wood’s lamp. Hair should be pulled out from the roots. Brushings from an area of scaly scalp. Swabs from pustular area in kerion. NAILS : Nail clippings should be taken from crumbling tissue at the end of the infected nail. The nail should be pared and scraped using a blunt scalpel until the crumbling white degenerating portion is reached. Any white keratin debris beneath the free edge of the nail should also be collected. MUCOUS MEMBRANES: Moistened swabs.

105. I. DIRECT MICROSCOPICAL EXAMINATION The material is examined by microscopy by one or more of these methods: Potassium hydroxide (KOH) preparation, stained with blue or black ink. Unstained wet-mount. Stained dried smear.

106. I. DIRECT MICROSCOPICAL EXAMINATION We add 10-20% KOH on the collected material on glass slide then it is covered with cover slip . The glass slide is gently warmed and left for 20 min . Examination under LM may shows; Dermatophytes: identified by hyaline septate branching hyphae and arthrospores . Spores inside a hair ( endothrix ) or outside a hair ( ectothrix ). Candida: Budding yeast, pseudohyphae also septate hyphae may be present. Examination under fluorescence microscopy; After applying special fluorescent stain e.g. calcoflour white (it binds to the chitin in the cell walls of the fungi ).

107. I. DIRECT MICROSCOPICAL EXAMINATION

108. I. DIRECT MICROSCOPICAL EXAMINATION Fungal elements are sometimes difficult to find , especially if the tissue is very inflamed, so a negative result does not rule out fungal infection . Repeat collections should always be considered in cases of suspected dermatophytosis with negative laboratory reports .

109. II. FUNGAL CULTURE Specimens should be inoculated onto primary isolation media, like Sabouraud's dextrose agar containing; cycloheximide (to suppress environmental contaminant fungi so it is left out if a mould requires identification) and chloramphenicol (to suppress bacterial growth) then incubated at 26-28C o for duration ranging from 2 days up to 4 weeks . The growth of any dermatophyte is significant. Fast growers: e.g. Candida, M. canis  2-3 d. Slow growers: e.g. T. schoenleinii, T. rubrum  2-3 w. Identification of fungal spp . is based on both microscopic & macroscopic appearance. Raimond Sabouraud

110. II. FUNGAL CULTURE

111. II. FUNGAL CULTURE A NEGATIVE CULTURE MAY ARISE BECAUSE: The condition is not due to fungal infection. The specimen was not collected properly. Antifungal treatment had been used prior to collection of the specimen. There was a delay before the specimen reached the laboratory . The laboratory procedures were incorrect . The organism grows very slowly .

112. III. WOOD’S LAMP EXAMINATION This is a source of ultraviolet light from which most visible light have been excluded by a Wood’s (9% nickel oxide) glass filter and allows passage of UV-A of wavelength ~ 365 nm .

113. III. WOOD’S LAMP EXAMINATION USES IN FUNGAL INFECTIONS: Tinea capitis: Large spore ectothrix & Arthrosporic endothrix : do not fluoresce, so a negative test does not exclude the diagnosis but may help in screening to control epidemics. M . canis, M . audouinii → bright green fluorescence. T . schoenleinii → pale green fluorescence. Pityriasis (Tinea) Versicolor: Golden yellow fluorescence.

114. III. WOOD’S LAMP EXAMINATION

115. III. WOOD’S LAMP EXAMINATION OTHER USES OF WOOD’S LAMP: Bacterial infections e.g . Erythrasma, Pseudomonas Infestations  Scabies. Porphyrias Pigmentary disorders Detection of Drugs and chemicals Detection of certain Tumours e.g . SCC Miscellaneous; e.g. PDT, Bromhidrosis

116. IV . HISTOPATHOLOGICAL EXAMINATION IN TINEA CAPITIS: Endothrix infections  There is minimal epidermal response aside from mild hyperkeratosis. The hyphae extend within the hair shaft and produce spores. This form is caused by T. t onsurans , T. v iolaceum . Ectothrix infections  There is also often minimal inflammatory reaction. The fungal forms coat the outside of the hair shaft without significant invasion of the shaft itself. This is typically caused by M. Canis, M. audouinii .

117. IV. HISTOPATHOLOGICAL EXAMINATION TINEA CERCINATA: Typically show foci of parakeratosis with epidermal acanthosis , spongiosis , and collections of neutrophils in the upper layers of the epidermis. The dermis may display edema and predominantly chronic inflammatory changes. Prolonged topical treatments with corticosteroids may result in attenuation of these inflammatory changes and extensive proliferation of the organisms which become easy to identify , even with routine H & E stain . Special stains : PAS or GMS stains.

118. Dermatophytes in PAS-stained skin

119. PAS-stained nail plate

120. TREATMENT OF DERMATOPHYTOSIS

121. TREATMENT OF DERMATOPHYTOSIS GENERAL MEASURES TOPICAL TREATMENT SYSTEMIC TREATMENT

122. I . GENERAL MEASURES Good hygiene of the skin , hair and nail . In tinea capitis asymptomatic carriers should be detected and treated (Antifungal shampoo twice weekly). Surveillance in schools would be helpful. Personal objects , such as combs and hairbrushes  disinfected or discarded . Avoiding prolonged wetting or humidity of skin and feet . In tinea pedis footwear should be disinfected , and patients should avoid walking barefoot in public areas such as locker rooms. Other measures to reduce recurrence include controlling hyperhidrosis with powders and wearing absorbent socks and nonocclusive footwear . Treatment of any associated fungal infection e.g. treatment of tinea pedis helps prevent onychomycosis . In tinea cruris include wearing clean loose clothing , drying thoroughly after bathing, using topical powders , weight reduction (if obese), laundering contaminated clothing and linens , and treating concomitant tinea pedis .

123. II. TOPICAL TREATMENT Topical antifungal Whitfield's ointment (benzoic acid) Undecylenic alkanolamide Topical azoles Clotrimazole ( Canesten ®) Ketoconazole ( Nizoral ®) Miconazole ( Daktarin ®) Tioconazole ( Trosyd ®) Sertaconazole ( Dermofix ®) Econazole ( Ecreme ®) Allylamine (higher cure rates and more rapid responses than older topical antifungals) Terbinafine (Lamisil ®) Ciclopirox olamine ( Batrafen ®) Thiocarbamates e.g. Tolnaftate Dandruff shampoos : Ketoconazole 2 %, selenium sulfide 2.5% , zinc pyrithione 1 % to 2% for t. capitis. Mild steroid to  inflammation for short period also in tinea incognito  few applications of topical steroid to continue until the oral antifungal has begun to take effect. It is wise to use a weaker steroid than that originally prescribed.

124. III. SYSTEMIC TREATMENT Oral antifungals Oral antihistamines Oral antibiotics Oral corticosteroids

125. III. SYSTEMIC TREATMENT Oral antifungals Oral antihistamines for symptomatic relief of itching. Oral antibiotics Oral corticosteroids

126. III. SYSTEMIC TREATMENT Oral antifungals Oral antihistamines Oral antibiotics for 2ry infection e.g. kerion , ulcerative t. pedis. Oral corticosteroids

127. III. SYSTEMIC TREATMENT Oral antifungals Oral antihistamines Oral antibiotics Oral corticosteroids for short period in id reaction & marked inflammatory tinea capitis.

128. Oral Antifungals For Dermatophytosis Oral antifungal medications may be required for a fungal infection if: It is extensive or severe . It resists topical antifungal therapy. It affects hair-bearing areas (tinea capitis and tinea barbae ).

129. Oral Antifungals For Dermatophytosis Griseofulvin* Terbinafine* Itraconazole Fluconazole Ketoconazole  

130. Oral Antifungals For Dermatophytosis 1. DOSE REGIME FOR GRISEOFULVIN: Adults : 500 mg to 1 g /day. Children : 10-25 mg/kg/day . Tinea pedis, Tinea cruris, tinea manuum, tinea corporis etc. for 2-6 weeks. Tinea unguium for 12-18 months until all signs of nail infection have gone.

131. Oral Antifungals For Dermatophytosis 2. DOSE REGIME FOR TERBINAFINE: The oral dose of terbinafine for adults is 250 mg daily. For children, the tablets can be hidden in food – the tablets taste unpleasant: Weight 10-20 kg, 62.5 mg per day Weight 20-40 kg, 125 mg per day Weight >40 kg, 250 mg per day Sometimes , if the fungal infection does not clear, the dose in children may need to be increased. Tinea corporis, tinea cruris, tinea pedis, tinea manuum: 1 to 4 weeks. Tinea unguium: for 6-8 weeks (fingernails) or 3-4 months (toenails ). Treatment can be repeated if necessary.

132. Oral Antifungals For Dermatophytosis 3. DOSE REGIME FOR ITRACONAZOLE: Tinea corporis , tinea cruris : 200 mg daily for one week OR 100 mg daily for 2 weeks. Tinea pedis, tinea manuum: 200 mg twice daily for one week OR 100 mg daily for 2-4 weeks. Tinea unguium: 200 mg/day for 6-8 weeks (fingernails) or 3-4 months (toenails), OR 200 mg twice daily for 7 days, repeated monthly for 2 months (fingernails) or 3-4 months (toenails ).

133. Oral Antifungals For Dermatophytosis 4. DOSE REGIME FOR FLUCONAZOLE: Either 50 mg daily or 150 mg once weekly is taken for two to six weeks. Fluconazole is not normally used in children but doses of 5 mg/kg/day have been safely prescribed for serious infection.

134. Oral Antifungals For Dermatophytosis 5. DOSE REGIME FOR KETOCONAZOLE: In adults is 200 to 400 mg daily, taken for two to eight weeks. Nail infections are treated for up to twelve months. The dose in children is usually 50 mg per day for those weighing less than 20 kg and 100 mg daily for those 20-40 kg.

135. Oral Antifungals For Dermatophytosis In August 2013 , the FDA announced that clinicians should no longer prescribe ketoconazole ( Nizoral ) tablets as a first-line therapy for any fungal infection , including Candida and dermatophyte infections, because of the risk for severe liver injury , adrenal insufficiency , and adverse drug interactions . Ketoconazole tablets were also withdrawn from the market in the European Union in July 2013 .

136. Oral Antifungals For Dermatophytosis TREATMENT OF TINEA CAPITIS Oral antifungal medicines, including Grizofulvin he most effective agent for infection with Microsporum canis, terbinafine and itraconazole or fluconazole for 4 to 6 weeks . Trichophyton infections.

137. TREATMENT TINEA PEDIS Interdigital : Topical antifungal; may require topical or oral antibiotic if superimposed bacterial infection. Moccasin : Topical antifungal plus product with urea or lactic acid; may require oral antifungal therapy. Vesicular : Topical antifungal usually sufficient. Ulcerative : Topical antifungal; may require topical or oral antibiotics if secondary bacterial infection ( common ).

138. DEVICES USED TO TREAT ONYCHOMYCOSIS Recently , non-drug treatment has been developed to treat onychomycosis thus avoiding the side effects and risks of oral antifungal drugs. Lasers emitting infrared radiation are thought to kill fungi by the production of heat within the infected tissue. Laser treatment is reported to safely eradicate nail fungi with one to three, almost painless, sessions. Several lasers have been approved for this purpose by the FDA and other regulatory authorities. Nd:YAG continuous, long or short-pulsed lasers Ti:Sapphire modelocked laser Diode laser Photodynamic therapy using application of 5-aminolevulinic acid or methyl aminolevulinate followed by exposure to red light has also been reported to be successful in small numbers of patients, whose nails were presoftened using urea ointment for a week or so. Iontophoresis and ultrasound are under investiation as devices used to enhance the delivery of antifungal drugs to the nail plate.

139. Ihab Younis , M.D. Fungal skin infections (Presentation) http:// dermnetnz.org Google images Bolognia 3 rd ed. http:// www.mayomedicallaboratories.com Oral Candidiasis by Hemam Shankar Singh ) Presentation ( Assoc. Prof. Ivan Lambev (Presentation ) medscape.dermatology.com References

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