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Dermatology Board Prep > DERM (11) Infections, Infestations, and Bites > Fungal disease > Flashcards

Fungal disease Flashcards

1
Q

What are the 3 genera of dermatophytes?

A

microsporum, trichophyton, epidermophyton

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2
Q

What are the two large subgroups between each of the 3 genera of dermatophytes?

A

Microconidia and macroconidia

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3
Q

What are conidia?

A

An asexual spore of a fungus

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4
Q

What is the importance of the conidia for the different dermatophytes?

A

For different dermatophytes, the phenotype of either the microconidia or the macroconidia can be dx.

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5
Q

What is the diagnostic appearance of Microsporum dermatophytes?

A

Macroconidia are dx, rough-walled, often spindle-shaped, thick cell wall and multi-celled

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6
Q

What is the diagnostic appearance of trichophyton?

A

Micoconidia is diagnostic: smooth-walled, one-celled. The macroconidia are not distinctive but are often cylindric to clavate

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7
Q

Which type of dermatophyte doesn’t have microconidia?

A

Epidermophyton only have macroconidia

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8
Q

What is the appearance of the macroconidia in epidermophyton?

A

smooth-walled, club-shaped, intermediate cell wall thickness, mutli-celled, occur solitary or in clusters.

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9
Q

What is the difference between anthropophilic, zoophilic, and geophilic?

A

anthropophilic: restricted to humans Zoophilic: primarily affects animals Geophilic: found in soil

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10
Q

What is the different clinical responses between anthropophilic, zoophilic, and geophilic fungi?

A

Anthropophilic: chronic, mild inflammatory response Zoophilic: causes massive inflammatory reponse in humans Geophilic: Causes severe inflammatory response and scarring in humans

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11
Q

What species of dermatophytes are anthropophilic?

A

all trichophyton spp (except T. mentagrophytes and T. verrucosum), E. floccosum, M. audouinii, and M. ferrugineum

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12
Q

What dermatophyte species are zoophilic?

A

M. Canis (cats and dogs), M. nanum (pigs), t. Verrucosum (Cattle), and T. mentagrophytes (rodents)

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13
Q

What dermatophyte species are geophilic?

A

M. gypseum

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14
Q

Histology of dermatophyte infection?

A

Septate hyphae in stratum corneum or nail plate, brisk dermal inflammation (vs minimal in tinea versicolor) +/- neutrophilic micro-abscesses in epidermis or corneum/nail plate

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15
Q

What color do dermatophytes show up as in PAS or GMS?

A

PAS = red GMS = Black

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16
Q

What is chlorazol black?

A

Chitin stain, hyphae will be green

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17
Q

Describe microsporum gypseum?

A

Geophilic, infrequent human pathogen -Ectothrix -cinammon color, granular colony on culture -Grows rapidly (5 days) -Macroconidia: thin walled, founded ends < 6 septa -+ polished rice growth

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18
Q

Describe microsporum canis?

A

zoophilic #1 cause of tinea capitis worldwide, common cause of tinea corporis -macroconidia: thick-walled; pointed ends; >6 septae -Growth on polished rice -Culture: canary yellow reverse

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19
Q

Most common organism to cause tinea capitis worldwide?

A

Microsporum canis

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20
Q

Most common cause of transmission of Microsporum canis?

A

Kittens to humans

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21
Q

What type of infection does microsporum canis cause?

A

Inflammatory infection

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22
Q

Is M. Canis an endothrix or ectothrix?

A

Ectothrix

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23
Q

Is M. audouinii an endothrix or ectothrix?

A

Ectothrix

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24
Q

What does M. audouinii cause?

A

A formerly common cause of tinea capitis

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25
Q

Characteristics of M. audouinii?

A

Anthropophilic, pectinate hyphae, culture: salmon reverse color, widely spaced radial grooves, polished rice growth

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26
Q

What color does M. Audouinii glow with woods lamp?

A

Yellow-green

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27
Q

What color does M. canis glow with woods lamp?

A

Yellow-green

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28
Q

Describe trichophyton rubrum?

A

Anthropophilic, microconidia have a teardrop or peg-shaped “birds of a wife” appearance -Culture: reverse red color, white cottony surface

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29
Q

What is the most common dermatophyte worldwide?

A

T. rubrum

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30
Q

Clinical of T. rubrum?

A

Generally not inflammatory can cause Majocchi’s granuloma and can perforate the hair

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31
Q

Describe T. mentagrophytes?

A

Can be Zoophilic (var mentags) which is inflammatory infection w/ granular colony or anthropophilic (var interdigitale) which is non-inflammatory, cottony colony -Spiral hyphae, microconidia -In the zoophilic form microconidia abundant in round clusters -In anthropophilic form resembles T. rubrum **Positive urease test and hair penetration test** -No pigment production on rice extract-glucose agar

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32
Q

Describe T tonsurans?

A

Anthropophilic -black dot tinea capitis, non-fluorescent -large spore endothrix -microconidia are balon shaped, various sizes -Culture: yellow to cream surface, w/ feathery periphery. -Requires thiamine to grow

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33
Q

Is T. tonsurans endothrix or ectothrix?

A

endothrix

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34
Q

Is T. violaceum endothrix or ectothrix?

A

endothrix

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35
Q

What organism causes black dot tinea capitis?

A

T. violaceum

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36
Q

Describe T. violaceum?

A

Anthrophilic -Culture: dark violet color, cerebiform pattern, reverse also purple -thiamine growth requirement

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37
Q

Describe T. schoenleinii?

A

Anthropophilic -Dull, blue-green fluorescent tinea capitis -Air canals within hair -Knobby antler like hyphae, favic chandeliers -Culture: tan color; cerebriform -No growth requirements

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38
Q

Woods lamp findings from tinea capitis from T. schoenleinii?

A

Dull, blue-green fluorescence

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39
Q

What organism causes favus?

A

T. schoenleinii

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40
Q

What is favus?

A

Most commonly occurs as tinea capitis but can occur elsewhere. It starts perifollicular but then it turns to thick yellow adherent scales (scutula). Most commonly caused from T. Schoenleinii

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41
Q

Describe T verrucosum?

A

Zoophilic (cattle/horses), -rat tail macroconidia -Culture: tan to white, heaped up/folded -Inositol and thiamine growth requirement

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42
Q

Is T verrucosum ectothrix or endothrix?

A

Ectothrix

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43
Q

What dz does T verrucosum cause?

A

Inflammatory tinea barbae, kerion-like tinea barbae, corporis, and capitis

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44
Q

Describe E. floccosum

A

Anthropophilic -culture: flat feathery colonies, yellow-brown reverse -Macroconidia- club-shaped in clusters like beavertail

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45
Q

What disease is caused by E. floccosum?

A

Tinea cruris, tinea pedis, no hair invasion

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46
Q

What areas are not affected by tinea corporis?

A

Hands, feet, groin, face, scalp

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47
Q

Predisposing factors for tinea corporis?

A

DM, HIV, immunosuppression, animal/human contact, chronic scalp/foot/hand reservoir

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48
Q

What dermatophytes cause tinea corporis?

A

Microsporum, trichophyton, epidermophyton

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49
Q

What are the most common causes of tinea corporis?

A

T rubrum, T. mentagrophytes, M. canis

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50
Q

Clinical of tinea corporis?

A

Annular, erythematous, scaling plaques, often with an active border and central clearing. This annular shape has led to the lay-term “ringworm” Papules, vesicles, and crusting may develop in the active border

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51
Q

When should oral tx for tinea corporis be considered?

A

Widespread, severe, granulomatous, or verrucous lesions

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52
Q

Is the yield of KOH decreased or improved w/ tinea incognito?

A

Improved.

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53
Q

Presentation of tinea incognito?

A

Patches or papules and plaques with less erythema and more subtle scale

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54
Q

What is tinea profunda?

A

Excessive inflammatory response to the dermatophyte, like kerion in the scalp.

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55
Q

What is tinea imbricata?

A

Dermatophytosis caused by the anthropophilic dermatophyte T. concentricum. It causes chronic infections in an equatorial band encompassing the South Pacific, Asia, and Central and South America. The clinical presentation consists of concentric annular rings resembling erythema gyratum repens (but with less redness/erythema often)

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56
Q

What is nodular perifolliculitis?

A

Usually caused by T. rubrum. -follicular papulopustules or granulomatous nodules that result from a deep dermatophyte folliculitis with disruption of the follicular wall -Most common: women who have tinea pedis or onychomycosis and shave their legs, and it can also occur in the setting of immuno­suppression -The lesions may be extensive or even vegetating, and a prolonged granulomatous reaction can develop

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57
Q

What is Majocchi’s granuloma?

A

Erythematous papules/nodules around hair follicles, particularly lower legs (may arise from tinea pedis) -Dermatophyte grows down hair follicles producing a folliculitis

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58
Q

Predisposing factors for Majocchi’s granuloma?

A
  • shaving legs (women), or topical steroid use
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59
Q

Most common pathogens to cause Majocchi’s granuloma?

A

T. Rubrum (most common) T. mentagrophytes

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60
Q

Treatment for Majocchi’s granuloma?

A

Systemic antifungals

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61
Q

Important distribution finding in tinea cruris to distinguish from candida?

A

Spares the scrotum

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62
Q

Most common pathogens causing tinea cruris?

A

Tinea rubrum> epidermophyton floccosum, Tinea interdigitale, Tinea mentagrophytes

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63
Q

What is tinea manuum?

A

Scaly, dry, hyperkeratotic lesions of palmar surfaces, often involves both feet and one hand.

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64
Q

Treatment for tinea manuum?

A

Need to use systemic usually, topicals rarely effective

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65
Q

Most common pathogens of Tinea manuum?

A

T. Rubrum, T. mentags, E. floccosum

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66
Q

Most common pathogens of Tinea Barbae?

A

T. mentagrophytes, T. verruscosum, T. rubrum, T. sonsurans

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67
Q

Clinical of tinea barbae?

A

Typically unilateral on face/neck -Papules/pustules

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68
Q

What pathogens usually cause tinea faciei?

A

Usually zoophilic species -T mentag, M. canis > T.rubrum

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69
Q

Presentation of tinea faciei?

A

Scaling present in <2/3 cases, erythematous follicular based papules, often in an annular distribution. -Itches and burns, often worse after sun exposure -most common in kids

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70
Q

Treatment of tinea faciei?

A

Systemic antifungals

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71
Q

What is the #1 cause of tinea capitis in the US?

A

Trichophyton tonsurans (less inflammatory than M. canis)

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72
Q

What is the #1 cause of tinea capitis in the world?

A

Microsporum canis (more inflammatory)

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73
Q

Clinical of tinea capitis?

A

Circular scaling patches +/- pustules +/- LAD May have black dots from broken hairs in endothrix infxn -Disease primarily of childhood, increased in black/males

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74
Q

Treatment for tinea capitis?

A

systemic antifungal

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75
Q

What antifungal is first line for kids with tinea capitis?

A

Griseofulvin

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76
Q

Which dermatophytes are ectothrix?

A

M. canis, M. audouinii, M. ferrugineum, M. distortum, M. gypseum, T. rubrum (rarely) -notice microsporum mostly ectothrix and trychophyton mostly endothrix

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77
Q

Which dermatophytes are endothrix?

A

T. tonsurans, T. violaceum, T. soudanense, T. gourvilli, T. yaoundei, T. rubrum (rarely) -notice microsporum mostly ectothrix and trychophyton mostly endothrix

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78
Q

Which dermatophytes cause yellow fluorescence with woods lamp?

A

Mostly the microsporum (ectothrix) -M. canis, M. audouinii, M. ferrugineum, M. distortum

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79
Q

What is the substance that fluoresces w/ Wood’s lamp in ectothrix species?

A

Pteridine

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80
Q

What is kerion?

A

Boggy inflamed nodule/abscess w/ pustules and possible LAD which may lead to scarring

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81
Q

Most common organisms to cause kerion?

A

M. canis, T. verrucosum, T. mentagrophytes, T. Tonsurans

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82
Q

What is pityriasis amiantacea and what can help distinguish it from tinea capitis?

A

Usually, thick yellow-white overlapping scales underlying skin normal, red or scaly. Causes can be psoriasis, LSC, seb derm, rarely tinea. -Usually partial scalp involvement, rarely whole scalp. -Some hair loss common… but regrows

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83
Q

Most common pathogens associated with tinea pedis?

A

T. rubrum >E. floccosum (moccasin), T. interdigitale (interdigital)

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84
Q

Most common pathogen associated with vesicular/bullous tinea?

A

T. mentagrophytes

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85
Q

Clinical of tinea pedis?

A

Erythema w/ scale, especially b/w toes (maceration) and sides of feet

86
Q

Organisms that cause onychomycosis (distal/lateral subungal)

A

This is most common… starts laterally but can invade laterally. -T. rubrum, T. interdigitale, E. floccosum -Also, non-dermatophytes: scopulariopsis brevicaulis, aspergillus

87
Q

Most common organism causing proximal sunbungal onychomycosis?

A

Least common, but common in HIV dz -Invades the proximal nail fold then nail plate -T. rubrum

88
Q

What can proximal subungal onychomycosis be associated with?

A

HIV/immunosupression

89
Q

Where does superficial white nail occur?

A

Only in the toenails, never fingernails -infection of only the surface of the nail plate

90
Q

What organism is most commonly associated with white nail?

A

T mentagrophytes (adults) vs T. rubrum in children, non-dermatophyte molds too

91
Q

Which antifungal is more effective against T. tonsurans?

A

Terbinafine

92
Q

Which antifungal is more effective against Microsporum?

A

Griseofulvin

93
Q

What are the 4 non-inflammatory superficial mycoses? (non-dermatophytes)

A

Pityriasis versicolor, white piedra, black piedra, tinea nigra

94
Q

Most common organisms to cause pityriasis versicolor (tinea versicolor)?

A

Malassezia globose, Malassezia furfur, M sympodialis (neonatal cephalic pustulosis)

95
Q

What do the different states of the Malassezia tell us about the clinical scenario?

A

Yeast form is normal skin flora, the filamentous hyphal form is seen in disease states

96
Q

What is required to grow Malassezia species in culture?

A

Olive oil

97
Q

Most common species in seb derm?

A

M. restricta

98
Q

What leads to the clinical presentation of hypopigmented plaques?

A

Azelaic acid from the yeast block melanin

99
Q

Pathogenesis of pityriasis versicolor?

A

Overgrowth of normal flora –> warmth and humidity in right host are key

100
Q

What topical or oral medications are best for pityriasis versicolor?

A

Azole-antifungals

101
Q

Clinical of pityriasis versicolor?

A

hyper- or hypopigmented finely scaling circular/oval macules/patches in sebaceous distribution (scalp, face, neck, upper chest, and upper back)

102
Q

What organism causes black and white piedra?

A

Black: piedra hortae White: trichosporon asahii, T. beigelii, t. ovoides, T. inkin and T. cutaneum

103
Q

Histology of piedra?

A

Black or white concretions along hair (encircle hair, unlike the sac-like appearance of lice) White Piedra with soft mobile nodules; black Piedra with hard nonmobile nodules

104
Q

Clinical of piedra?

A

Asymptomatic hair breakage on scalp, axillary, and pubic region

105
Q

Treatment for piedra?

A

Hair shaving/cutting and antifungal shampoos; systemic antifungals recalcitrant

106
Q

What is trichosporanosis?

A

Dissemination of trichosporon from white piedra can occur in immunocompromised hosts –> can lead to purpuric or necrotic cutaneous papules and nodules. (T. Asahii)

107
Q

Clinical distribution for white vs black piedra?

A

White piedra= facial, axillary, genital hair > scalp Black piedra= scalp>rarely beard/genitals

108
Q

The difference in texture between white and black piedra?

A

White piedra: soft and loose on the hair Black piedra: hard and firm on hair

109
Q

What organism generally causes tinea nigra?

A

Hortaea werneckii

110
Q

Microscopy of tinea nigra?

A

dark brown septate hyphae w/ budding yeast in thickened stratum corneum

111
Q

Clinical of tinea nigra?

A

dark-brown/black macule or small patch on palms/soles, limited to stratum corneum

112
Q

Treatment of tinea nigra?

A

azole creams, Whitfield’s ointment (6% benzoic acid, 3% sal acid ), oral terbinafine if recalcitrant

113
Q

What is the pathogen that causes protothecosis?

A

Prototheca wickerhamii (not a fungus but algae)

114
Q

Pathogenesis of protothecosis?

A

Introduced into skin via trauma in contaminated water

115
Q

Histology of protothecosis?

A

Distinctive morula like appearance on H&E.

116
Q

Clinical of protothecosis?

A

Nodules/ulcers/plaques and/or olecranon bursitis

117
Q

Treatment for protothecosis?

A

Excision and systemic antifungals (e.g., amphotericin B)

118
Q

Clinical of chromoblastomycosis?

A

wks-mos after inoculation, pruritic papules/nodules expand and become verrucous w/ black dots; does not invade muscle or bone; chronic lesion can turn to SCC

119
Q

Histology of chromoblastomycosis?

A

Pseudoepitheliomatous hyperplasia, granulomatous dermal inflammation w/ medlar bodies (pigmented muriform cells, “copper pennies”)

120
Q

Treatment of chromoblastomycosis?

A

Itraconazole, 5-flucytosine, among other antifungals; surgical excision for small lesions

121
Q

What are the two major types of mycetoma?

A

Eumycetoma (fungus) and actinomycetoma (bacteria)

122
Q

Most common eumycetoma species?

A

Madurella spp. Pseudallescheria boydii (MC) exophiala jeanselmei Acremonium spp.

123
Q

Most common actinomycetoma species?

A

Nocardia brasiliensis (#1) N. asteroids (both have white grains) actinomadura madurae (A. pelletieri=red grains) A.madurae=cream or pink grains) Streptomyces somaliensis (yellow-brown grains)

124
Q

Clinical of mycetoma?

A

Slow progression of tumors w/ sinus tracts draining grains, which are fungal or bacterial aggregates; MC on feet/lower legs; long standing lesions–> bone and visceral involvement Black grains only seen in eumycetoma and red grains only seen in actinomycetoma (specifically A.pelletieri); other colored grains seen in both types

125
Q

Histology of mycetoma?

A

granulomatous reaction w/ grains; serologic testing used bc of culture difficulty

126
Q

Treatment of mycetoma?

A

Euycotic mycetoma: surgical excision, several months azoles Actinomycotic mycetoma: sulfonamides and other antibiotics.

127
Q

What organisms cause sporotrichosis?

A

Sporothrix schenckii (dimorphic)

128
Q

What is the microscopy of sporotrichosis lesions?

A

Usually not well-visualized with stains; granulomatous inflammation w/ plasma cells and asteroid corpuscles (Splendore-Hoeppli phenomenon); organisms are cigar-shaped budding yeast

129
Q

Pathogenesis of sporotrichosis?

A

Traumatic inoculation from soil via plant thorns, wood splinters, and sphagnum moss>>cats/rodents/armadillo bites; inhalation of spores

130
Q

Clinical of sporotrichosis?

A

Multiple ascending ulcerated nodules or subsequent abscesses, most frequently in gardeners, agriculture/farm workers, and veterinarians -May lead to erythema nodosum

131
Q

Treatment for sporotrichosis?

A

Obtain fungal culture (difficult to find in tissue samples), itraconazole (TOC), SSKI, and amphotericin B in disseminated dz

132
Q

DDx for sporotrichoid spread?

A

NoSALT Nocardia Sporotrichosis Atypical mycobacteria Leishmaniasis Tularemia

133
Q

What is the most common cause of lymphocutaneous patterned disease?

A

Atypical mycobacterial, especially M. marinum, then sporotrichosis -nocardia, other bacteria or less common,

134
Q

What organism causes lobomycosis?

A

Lacazia (loboa loboi)

135
Q

Where is lobomycosis seen?

A

It infects freshwater dolphins in south american rivers – infects those that come in contact

136
Q

Clinical of lobomycosis?

A

keloid like verrucous fibrotic nodules that can ulcerate; men>> women; rural areas

137
Q

Treatment for lobomycosis?

A

Surgical excision

138
Q

Microscopy of lobomycosis?

A

Thick-walled yeast w/ tubular connections b/w cells- “pop bead” or “chain of coins” appearance

139
Q

What are the main 4 systemic (dimorphic) mycoses?

A

Histoplasmosis, blastomycosis, coccidiomycosis, paracoccidiomycosis

140
Q

Where is histoplasmosis seen in the US?

A

Ohio+ Mississippi river valleys

141
Q

Microscopy of histoplasmosis?

A

Tuberculoid granuloma w/ intracellular 2-4 micrometer yeast in histiocytes (looks like leishmaniasis, but see yeast have surrounding halo and are more evenly distributed throughout histiocyte cytoplasm; lacks “marquee sign” and kinetoplast)

142
Q

Pathogenesis of histoplasmosis?

A

Inhalation (esp. bird and bat feces) w/ hematogenous spread (can go to liver, spleen, bone marrow, brain; skin involvement more common in HIV, often p/w umbilicated or “molluscoid” papules)

143
Q

Clinical of histoplasmosis?

A

primary cutaneous chancre w/ lymphangitis and lymphadenitis (rare); More commonly, secondary cutaneous molluscoid nodules, cellulitis, ulcers, panniculitis, and oral lesions -Pulmonary manifestations=MC presentation

144
Q

Diagnosis of Histoplasmosis?

A

Culture is gold standard (also urinary ELISA or PCR)

145
Q

Treatment for histoplasmosis?

A

Itraconazole (mild-mod dz) or amphotericin B (severe dz)

146
Q

Geographic areas affected by blastomycosis?

A

Southeastern U.S, Great Lakes, KY, Miss, Chicago

147
Q

Histology of blastomycosis?

A

Pseudoepitheliomatous hyperplasia, granulomatous dermal inflammation w/ unipolar budding yeast (8-18micrometers) (Broad-based buds)

148
Q

Pathogenesis of blastomycosis infection?

A

Inhalation w/ subsequent hematogenous spread to skin (>75% of cases), bones, and GU tract (e.g. prostate, spleen, liver, brain)

149
Q

Clinical of blastomycosis?

A

-Primary cutaneous form (rare) presents w/ lymphangitis and lymphadenitis at injury site -Secondary cutaneous form (more common); due to hematogenous dissemination from lungs to skin), presents w/ verrucous nodules, abscesses and ulcers (can occur orally as well) -Pulmonary manifestations: most common presentation

150
Q

Diagnosis of blastomycosis?

A

KOH of purulent exudate, DNA probe assay, (culture is difficult), serology

151
Q

Treatment of blastomycosis?

A

Polyene and azole antifungals (Itraconazole 200-400 mg/day for 6 mos) and amphotericin B (Severe disease)

152
Q

Geography of coccidiomycosis?

A

Desert SW United States (esp. Central Valley/San Joaquin Valley, California), Mexico, and Central/South America

153
Q

Histology of coccidiomycosis?

A

Large (up to 100 micrometer) spherules containing endospores; also has PEH and granulomatous inflammation

154
Q

Pathogenesis of coccidiomycosis?

A

Inhalation w/ hematogenous spread to skin (as well as CNS and bone); very rarely primary cutaneous infection

155
Q

Clinical of coccidiomycosis?

A

Verrucous nodules/ papules, pustules, abscesses, or ulcerative lesions Pulmonary manifestations= MC presentation

156
Q

Treatment for coccidiomycosis?

A

limited and cutaneous: itraconazole Severe: amphotericin B Meningeal: amphotericin B and fluconazole

157
Q

Geography of paracoccidioidomycosis?

A

Southern US, Mexico, and Central/South America

158
Q

Microscopy of paracoccidioidomycosis?

A

Pseudoepitheliomatous hyperplasia, granulomatous dermal inflammation w/ multipolar budding yeast (mariner’s wheel)

159
Q

Pathogenesis of paracoccidioidomycosis?

A

Inhalation of infected soil (can disseminated to skin, liver, adrenal glands, LN, GI tract, and spleen); rarely may arise from direct inoculation in skin

160
Q

Clinical of paracoccidioidomycosis?

A

-Granulomatous ulcerative oropharyngeal and perioral involvement in 70% of adults; cutaneous lesions can be contiguous, hematogenous, or via inoculation -Clinical appearance of ulcers w/ infiltrated borders and hemorrhagic dots, and associated LAD (can be massive) -Men>>>women -Pulm disease (granulomatous and chronic) most common presentation

161
Q

Most common candida species in localized and generalized infections?

A

Albicans

162
Q

Candida species commonly seen in chronic paronychia?

A

C. parapsiosis

163
Q

What canidida species can be seen in HIV patients w/ oropharyngeal candidiasis?

A

C. Dubliniensis

164
Q

Diagnosis of superficial candidiasis?

A

KOH w/ budding yeasts w/ pseudohyphae -If concern for systemic w/ skin lesions –> bx showing organisms in dermis and blood vessels; stain with PAS or methenamine silver -Culture of skin lesions -Blood cx often negative

165
Q

Clinical of median rhomboid glossitis?

A

Central smooth erythema of tongue, 2/2 candida. Can get loss of lingual papillae giving it the look of atrophy

166
Q

Clinical of candida intertrigo?

A

Beefy red color + satellite pustules +/- erosions. Compare with irritant intertrigo w/o pustules and erosions, not as beefy red

167
Q

What is the #1 cause of infectious balanitis?

A

Candida

168
Q

Clinical of candidal balanitis?

A

Papules, pustules on glans, may extend to the prepuce

169
Q

Cause of black hairy tongue?

A

Altered normal flora –> overgrowth of bacteria and fungi Papillary hypertrophy and abnormal desquamation involved.

170
Q

Treatment for black hairy tongue?

A

Physical debridement and good hygiene

171
Q

Differentiation of tinea cruris and candidal involvement?

A

Scrotum often involved in candidal form. You can also see satellite pustules and subcorneal pustules. **Look for fold involvement. Irritant will often spare the fold whereas candida involves the folds.

172
Q

What do you can candidiasis between the web toe spaces?

A

Erosion interdigitalis blastomycetica (often third or 4th web space of toes or fingers)

173
Q

Clinical of congenital candidiasis?

A

Pink maculopapular eruption progressing to vesicles/pustules with desquamation

174
Q

Treatment for congenital candidiasis?

A

topicals +/- systemic

175
Q

Diagnosis of congenital candidiasis?

A

KOH or gram stain of pustular or vesicular contents

176
Q

What is the source of most systemic candidiasis?

A

Usually starts in GI tract; 10% of bloodstream infections

177
Q

Clinical of deep-seated or systemic candidiasis?

A

See scattered papules/nodules, occ. Hemorrhagic and ecthyma gangrenosum-like

178
Q

Which Candida species have lower sensitivities to azoles?

A

Glabrata and Krusei

179
Q

Geography of cryptococcosis?

A

In bird droppings, especially pigeons and bark/fruit of tropical trees. Cryptococcus neoformans is ubiquitous, Cryptococcus gattii is tropical/sub-tropical

180
Q

Histology of cryptococcus?

A

Single-cells sphere w/ double cell wall and thick capsules (“halo” appearance), may have one or more buds (blastoconidia); a collection of organism look like soap bubbles Stains: India ink, PAS, mucicarmine, GMS, Fontana-Masson

181
Q

Pathogenesis of cryptococcosis?

A

Inhalation–> lungs (Primary pulm infection, usually mild) hematogenous spread (CNS, bones, skin); can also arise from primary inoculation of skin (rare) -More common in immunosuppressed (esp HIV/AIDS, but also a/w sarcoidosis and pregnancy)

182
Q

What is the virulence factor for cryptococcus?

A

Glucuronoxylomannan polysaccharide capsule

183
Q

Clinical of cryptococcosis in the skin?

A

Papules/ nodules (often molluscum-like) that can be umbilicated and/or ulcerated, and prefer head/neck, mouth, nose -Patients w/ secondary cutaneous lesions have a high mortality rate -Nodular lymphangitic syndrome- a nodule at the inoculation site, nodular lymphangitis, and adenopathy -Meningoencephalitis is a serious and common manifestation

184
Q

Treatment for cryptococcosis?

A

-oral fluconazole, -CNS: amphotericin B and Flucytosine

185
Q

Most common organisms to cause aspergillosis?

A

Aspergillus fumigatus (most common), Aspergillus Flavus (2nd most common), Aspergillus niger (can lead to otomycosis)

186
Q

Histology of aspergillus sp?

A

Septate hyphae w/45-degree angle branching?

187
Q

Pathogenesis of aspergillosis?

A

Can be primary cutaneous disease (MC A. Flavus) via direct inoculation (e.g., IV catheter, trauma sites, burn sites, and disturbed skin under dressings) vs secondary cutaneous disease (MC A. fumigatus; more common, typically in immunosuppressed, esp. neutropenia) via inhalation–>pulm aspergillosis –>disseminated disease Both can–> hematogenous spread w/ tendency for vascular invasion causing thrombus and necrosis

188
Q

Clinical of aspergillosis in the skin?

A

Six clinical forms including erythematous edematous plaques, nodules w/ necrotic centers, hemorrhagic bullae, and necrotic ulcers can involve CNS, heart, kidneys, bone, GI tract

189
Q

What species of aspergillus most commonly causes primary cutaneous disease?

A

Aspergillus flavus (hemorragic bullae or mulluscum lesions)

190
Q

Treatment for aspergillosis?

A

Amphotericin B (esp. w/ invasive) or voriconazole (in combo with caspofungin)

191
Q

What species of aspergillus is the most common to cause disseminated dz w/ cutaneous findings?

A

Aspergillus fumigatus

192
Q

What organisms cause hyalohyphomycosis?

A

Penicillium, Paecilomyces, and Fusarium

193
Q

Histology of Fusarium infections?

A

45 degree angle branching, similar to Aspergillus

194
Q

Pathogenesis of Fusarium infections?

A

More common in immunosuppressed; severe burns **Most common fungus cultured in burn patients** -Cutaneous disease via direct inoculation and hematogenous spread w/ tendency for vascular invasion causing thrombus/necrosis

195
Q

What is the most common fungus cultured from burn patients?

A

Fusarium

196
Q

Clinical of Fusarium infections?

A

erythematous; edematous plaques more common than subq nodules (purpuric or ecthyma gangrenosum-like); panniculitis

197
Q

What organism causes penicilliosis?

A

Penicillium marneffei is the only pathogenic species

198
Q

Where does penicilliosis occur?

A

SE Asia

199
Q

Histology of penicilliosis?

A

Intracellular parasitic phase in macrophage

200
Q

Pathogenesis of penicilliosis?

A

Acquired by inhalation or possibly abrasions; bamboo rat exposure may be RF

201
Q

Clinical of penicilliosis?

A

Similar to histoplasmosis: fever, wt loss, LAD, cough, and hepatosplenomegaly -Cutaneous manifestations: papules w/ central necrosis and molluscum like lesions; face, arms, and trunk are most common sites

202
Q

Treatment of penicilliosis?

A

Polyenes (amphotericin B and terbinafine) and azole antifungals

203
Q

Why are the 2 orders of organisms that can cause zygomycosis (mucormycosis) and what organisms are in each?

A

Order Mucorales: Rhizopus, Mucor, Absidia, and others = systemic and cutaneous dz Order Entomophthorales: conidiobolus coronatus = rare, chronic, cutaneous and subcutaneous infection in the tropics

204
Q

Microscopy of mucormycosis?

A

Broad ribbon-like nonseptate hyphae w/ 90 degree angle branching, angioinvasive w/ thrombosis

205
Q

Pathogenesis of mucormycosis?

A

Most commonly enter via respiratory tract (though there are other portals of entry like skin), and can invade blood vessels–>thrombosis/infarction/necrosis. More common in immunosuppressed, but also nonimmunodeficient (e.g., severe diabetes and severe burns)

206
Q

Clinical of zygomycosis (mucormycosis)?

A

subtypes include: rhinocerebral (MC subtype; usually in diabetes pt w/ DKA), pulmonary, GI, primary cutaneous (from surgery, catheterization, or burns), and disseminated -All forms are rapidly progressing and commonly fatal -Cutaneous lesions (can be primary or secondary) typically indurated, necrotic black plaque/eschars most commonly seen on the face (nasal and oral in rhinocerebral type) -Rhinocerebral type may have epistaxis, facial pain, periorbital cellulitis, proptosis, and loss of EOM movement (secondary to cranial nerve palsies)

207
Q

Treatment for zygomycosis (mucormycosis)?

A

Aggressive surgical resection of all necrotic areas (crucial to survival of patient) and amphotericin B (lipid formulation); posaconazole may be alternative

208
Q

What organisms cause phaeohyphomycosis?

A

Dematiaceous (pigented) fungi: Exophiala jeanselmei (most common cause), Wangiella dermatitidis, Alternaria bipolaris, Phialophora, Curvularia

209
Q

What areas does phaeohyphomycosis occur?

A

Tropics and temperate zones

210
Q

Clinical of phaeohyphomycosis?

A

Subcutaneous, potentially draining, inflammatory abscess or cyst. It can mimic baker cysts or other cysts.

211
Q

Microscopy of phaeohyphomycosis?

A

Cyst composed of macrophages and short hyphae, with a fibrous capsule -Hyphae are pigmented/brown, and stain + w/ Fontana-Masson

212
Q

Treatment of phaeohyphomycosis?

A

Excision and intraconazole

DERM (11) Infections, Infestations, and Bites (13 decks)

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