Wright - Acne, Fungal, Viral Infections Flashcards
1
Q
What are the 4 key factors in acne pathogenesis?
A
- Sebaceous gland hyperplasia
- Abnormal follicular desquamation: dead skin cell buildup at opening
- Propionibacterium acnes colonization
- Inflammation
2
Q
What is this?
A
- Microcomedo:
1. Non-inflammatory comedones: blackhead (open) and whitehead (closed)
2. Inflammatory lesions: papules, pustules, nodules, cysts
3
Q
How do you assess acne patient?
A
No consensus, but combine lesion counting with global assessment of severity
4
Q
What are the topical and systemic acne treatments?
A
- Topical:
1. OTC: benzoyl peroxide, salicylic acid -> for very mild acne (sal acid less effective)
2. Prescription: antimicrobials, retinoids, combos - Systemic:
1. ABs, oral contraceptives, isotretinoin (acutane)
5
Q
Benzoyl peroxide
A
- MOA: kills P. acnes
1. Mild comedolytic
2. Mild anti-inflammatory - Limits development of P. acnes AB resistance
- Combine with retinoid to increase efficacy
- No resistance reported
- Generally recognized as safe (GRASE) by FDA: AEs include irritation, bleaching, allergic contact dermatitis (1:500; variety of formulations)
6
Q
What topical ABs are used to treat acne?
A
-
Clindamycin, erythromycin: antibac, anti-inflam
1. AEs: irritation, colitis (colon inflammation) reported with clindamycin (not a high risk) - NOT recommended as monotherapy: slow onset, resistance, and NOT comedolytic
1. Add topical benzoyl peroxide (BP), or use combo product: usually pretty easy to get, and covered by insurance - Really need to target comedone plug above all else
7
Q
Topical retinoids
A
- Adapalene, Tretinoin, Tazarotene (pregnancy X)
- MOA: normalize follicular desquamation (comedolytic), anti-inflammatory, and enhance penetration of other compounds
- Indications: FIRST-LINE tx for all types of acne
1. Preferred for maintenance therapy - Side Effects: local irritation
- Can also help with wrinkles
8
Q
What are the pros and cons of retinoid combo products?
A
- Some combo products w/AB or BP
- Pros: once a day (compliance)
- Cons: fixed retinoid (low concentration) and $$$$
9
Q
When are systemic ABs given for acne?
A
- Mod-severe inflammatory (most not FDA approved for acne -> only Minocycline)
1. On these for several months - MOA: antibacterial, anti-inflammatory -> do NOT have comedolytic effects
- Goal is maintenance w/topical
- Preferred oral ABs (pts >=8): Tetracycline, Doxycycline, Minocycline
1. Less commonly Erythromycin/Bactrim
10
Q
What are the AE’s with the systemic ABs?
A
- Generally well-tolerated: recommend taking with food (not dairy products bc can affect absorption)
- Severe AEs (uncommon):
1. Tetracycline: GI upset, teeth staining (<8 yr)
2. Doxycycline: photosensitivity, esophagitis (drink water)
3. Minocycline: dyspigmentation, lupus-like rxn, pseudomotor cerebri, SJS, DHS (drug hypersensitivity syndrome)
4. Erythromycin: GI sensitivity
11
Q
Oral contraceptives for acne
A
- Females w/mod-severe inflam/mixed acne, esp. if flare with periods
- Anti-androgen effects suppress sebum production
12
Q
What are the indications for Isotretinoin?
A
- Used to be called acutane (oral)
- Severe
- Scarring
- Refractory
- Very rarely start w/this -> most severe cases only
13
Q
What is the MOA of the oral retinoids?
A
- Target all 4 factors of acne pathogenesis:
1. DEC size/activity of sebaceous glands -> reduces sebum production by >90%
2. Normalize follicular keratinization, preventing new comedones
3. Inhibit P. acnes
4. Anti-inflammatory
14
Q
What are the common AEs of the oral retinoids? Serious AEs?
A
- Common: dry lips, skin, and eyes, nosebleeds, mild headaches, muscle aches, backaches
- Serious: TERATOGENIC -> iPledge
1. Depression, suicidal ideation (no causal relationship established)
2. Skeletal changes: more concerning for younger pts (fractures, hyperostosis, epiphyseal closure)
3. IBD: data conflicting (UC > CD)
15
Q
What is the simple treatment algorithm for acne?
A
- Mild comedonal: topical retinoid
- Mild inflammatory/mixed: topical retinoid + topical antimicrobial
- Moderate inflammatory/mixed: topical retinoid + topical antimicrobial + oral antimicrobial
- Severe inflammatory:
1. Minimal scarring: topical retinoid + topical antimicrobial + oral antimicrobial
2. Scarring or multiple treatment failures: Isotretinoin
16
Q
What is this? How would you treat it?
A
- Mild-mod comedonal acne
- Topical retinoid
17
Q
What is this? How would you treat it?
A
- Mild mixed acne
- Topical retinoid + topical AB
18
Q
What is this? How would you treat it?
A
- Moderate mixed acne
- Topical retinoid + topical AB + oral AB
19
Q
What is this? How would you treat it?
A
- Severe mixed acne
- Minimal scarring: topical retinoid + topical AB + oral AB
- More severe scarring: Isotretinoid (have to come in monthly for 6 to 9 months)
20
Q
What basic skin care should people with acne do?
A
- Gentle cleansing 1-2 times a day with mild, fragrance-free cleanser
- Oil-free moisturizer with SPF 30+ bid and prn
- Avoid OTC acne washes and topicals because too irritating/drying
21
Q
What are some common acne myths? Are they true?
A
- Acne is NOT caused by poor hygiene or dirt
- Diet controversial:
1. High glycemic index diet may lead to hyperinsulinemia and stimulate androgen synthesis (relationship to METABOLIC SYNDROME; particular subset of acne pts)
2. Milk, particularly teenage boys who drink a lot of milk
22
Q
What are some important aspects of acne pt education?
A
- Discourage picking bc can lead to permanent scarring
- Post-inflammatory hyperpigmentation
- Explain how to use medicines (pee-sized amount)
- Potential side effects
- Consistent use for 6-8 weeks minimum
23
Q
When should you refer pts with acne?
A
- Severe Acne (cysts, nodules, scars)
- No response or poor response to treatment after 12 weeks
- If systemic antibiotics needed >1 year
- Isotretinoin being considered: females will NEED OCP (oral contraceptives)
- Acne associated with a systemic disease
24
Q
What is rosacea? Causes?
A
- Relapsing and remitting facial erythema in pts over 30 years old (4 types); usually women with fair skin
- Causes:
1. Inflammation
2. Demodex folliculorum
3. Vascular abnormalities: tend to be prone to flushing
4. Genetics
5. Triggers: sunlight, exercise, hot/cold, stress, foods, alcohol
25
Q
What are the clinical manifestations of rosacea? Types?
A
- Redness, flushing, pimples
- Four types:
1. Erythematotelangiectatic
2. Papulopustular
3. Phymatous: permanent swelling in the nose
4. Ocular
26
Q
What is the tx for rosacea?
A
- Topical: usually a combo if severe
1. Metronidazole (cream or gel)
2. Azelaic acid
3. Sodium sulfacetamide with sulfur - Systemic: if more moderate to severe disease
1. Oral tetracyclines - Other: IPL (intense pulse light therapy), laser, sx
27
Q
What is this? Suspected triggers?
A
- Periorifical dermatitis: women 20-45 yrs and prepubertal children (aka, periorbital dermatitis)
- Suspected triggers:
1. Steroids, topical
2. OCP (oral contraceptives)
3. Menstruation, pregnancy
4. Fluorinated toothpaste
5. Stress
6. Candida, demodex mites
28
Q
What are the clinical manifestations of periorifical dermatitis?
A
-
Rash or “pimples” around mouth
1. Nose, eyes, labia
2. Papules, pustules, vesicles - May be kind of eczematous
- Granulomatous variant: longstanding in youth (top image)
29
Q
What is the treatment for periorifical dermatitis?
A
- Discontinue all topical steroids
- Mild: topical antibiotics
- Severe: oral antibiotics
- May need topical non-steroidal anti-inflam (like Tacrolimus)
30
Q
What causes folliculitis? How do you tell which one it is?
A
- Very common in hair-bearing areas
- Can usually determine cause via where it is occurring and PMH
-
Most common causes are bacterial:
1. Staph aureus
2. Streptococcus
3. Pseudomonas - Other Causes:
1. Fungal: pityrosporum orbiculare (yeast, fungus hybrid)
2. Mites: demodex folliculorum
3. Mechanical (i.e., on buttocks)
4. Eosinophilic folliculitis: HIV, transplant pts
31
Q
What is this? How would you treat it?
A
- Clinical manifestations of folliculitis -> follicular based papules/pustules on hair-bearing areas
- Caused often based on where it is occurring and past medical history (PMH)
- TREATMENT: AB soaps/washes
1. Topical ABs: ok to use these by themselves in this context
2. Topical antifungals
32
Q
What is hydradenitis suppurativa?
A
-
Apocrine gland bearing areas: axillary, inguinal, inframammary folds
1. Prevalence is 1-4%; mostly WOMEN - Risk factors: obesity, cigarette smoking, and family history
33
Q
What are the clinical manifestations of hidradenitis suppurativa? Txs?
A
- Clinical manifestations: recurrent, persistent painful abscesses
1. Sinus tracts: chronic drainage
2. Scars
3. Also get comedones, a key to confirming the dx - Treatment:
1. Mild: topical and/or oral antibiotics
2. Moderate to severe: intra-lesional steroids, TNF-α inhibitors, surgery
34
Q
What are the HSV types?
A
- dsDNA
-
HSV-1: peri-oral, lips, oral cavity
1. Abs in 85% of adults; can get initial outbreak when little, and not recurrences after that - HSV-2: genital -> Abs in 20-25% of adults (can also infect the mouth)
35
Q
What are the 3 infection states of HSV? What will pt hx look like for each?
A
-
Primary: direct contact (vesicles) -> 3-7 days after exposure
1. Pain, burning, tingling, fever, malaise, LAD -
Latent: via sensory nerves to ganglion
1. Tends to be milder -
Recurrent: viral shedding
1. Fever, sun exposure, stress
36
Q
What are the clinical manifestations of HSV?
A
- Clusters of monomorphous (all look the same) vesicles with an erythematous base
- “Punched out” erosions and crusted papules
- Usually start out with clear contents that become cloudy over time
37
Q
What do you see here?
A
- HSV
- Clusters of monomorphous (all look the same) vesicles with an erythematous base
- “Punched out” erosions and crusted papules
- Usually start out with clear contents that become cloudy over time
38
Q
How do you confirm HSV diagnosis?
A
-
Tzanck smear: look for multinucleated giant cells
1. Viral culture (48 hrs), PCR (faster, more $), direct fluorescent Ab -> really just depends on the institution - Most of the time this is a clinical diagnosis
- Can look like other conditions in children, however (like atopic dermatitis)
39
Q
What is this?
A
- Tzanck smear for HSV: note the multinucleated giant cells
40
Q
What should be in your differential for HSV?
A
- Impetigo: bacterial infection of skin with strep or staph (top image)
- Aphthous stomatitis (canker sore): tend to be larger and fewer in number (abscesses) -> middle image
- Syphilitic chancre: bottom image
41
Q
What is the treatment for HSV?
A
- Mild: topical antiviral -> not as effective as oral
- Moderate to severe: systemic antiviral
- Oral or IV for pts who may be immunosuppressed
42
Q
What is shingles? What are the triggers?
A
-
Reactivation of latent VZV (in dorsal root ganglia; dsDNA)
1. 20-30% lifetime risk (if you had chicken pox as a child) - Incidence/severity INC: after age 60, and in ppl who are immunosuppressed
- Triggers: trauma, stress, fever, radiation, immuno-suppression
43
Q
What are the clinical manifestations of shingles?
A
- Prodrome: pain, pruritus, burning
-
Grouped vesicles over a dermatome: can get some additional lesions outside the dermatome too-
1. Trunk most common - Trigeminal nerve (V1, ophthalmic): 10 to 15%
1. Vesicles at tip/side of nose (Hutchinson’s sign) -> nasociliary branch
1. Eye: blindness -
V2 and/or V3: facial palsy
1. Ear: tinnitus, vertigo, deafness - Rash resolves within 3-5 weeks
-
Postherpetic neuralgia (esp. common on the face, and in older patients) -> 5-20%
1. Typically over 40 yrs old - Can get permanent scarring
44
Q
What is this?
A
- Shingles: VZV
- Patients may think this is a bite at first
45
Q
How can you confirm a VZV diagnosis?
A
- Tzanck smear
- Viral culture
- PCR
- Same as with HSV (which should also be in your differential -> would not be as painful, or along the dermatome)
46
Q
Treatment and prevention of shingles?
A
- Oral antiviral w/in 72 hrs and pain med, esp. with facial type
- Vaccine (Zostavax) for people 60 yrs and older
1. Decreases risk of shingles by 51% and neuralgia by 67%
47
Q
What is molluscum contagiosum?
A
- Cutaneous infection caused by Pox virus (dsDNA)
- Transmission: skin to skin, autoinoculation, fomites
1. Risk factors: atopic dermatitis, immuno-suppression, bathing/sleeping together
2. Children should not be kept out of school; casual contact should not spread disease -
Resolve spontaneously in months to years, but may leave depressed scar (that improves over time)
1. Discoloration common
48
Q
What are the clinical manifestations of molluscum contagiosum?
A
- Small or lg pink to skin-colored 2-10 mm dome-shaped waxy papules
1. +/- central umbilication (can’t rely on this for diagnosis) - May cause “molluscum dermatitis:” pruritis
- Face, upper chest, extremities, other (common in creases: armpits, behind the knees, but really can be anywhere)
- Parents worry about eyelids -> conjunctivitis and keratitis are possible, but not common
49
Q
What is this?
A
Molluscum contagiosum
50
Q
What do you see here?
A
- Inflamed molluscum
- True infection is rare -> usually signals immune response and imminent resolution
51
Q
What should be on your differential for molluscum?
A
- Acne (left): comedones, no umbilication
- Folliculitis (right): papules or pustules, no umbilication
52
Q
What are the tx options for molluscum?
A
- Numerous methods, but NO CLEAR EVIDENCE to support any of them
- Active Nonintervention: self-limited
-
Physical Destruction
1. Curettage: more likely to leave scarring
2. Cryotherapy
3. Cantharidin: liquid that contains a vesicant (causes blister that dries up and falls off) - Local Irritation: topical retinoids, keratolytics
-
Immunomodulators:
1. Topical: Imiquimod -> very expensive and irritating
2. Systemic: intralesional antigens, cimetidine
53
Q
What is Cantharidin?
A
- Chemical vesicant extracted from the blister beetle that is used to treat molluscum and warts
- Research: 90% cleared after avg of 2 applications; side effects -> erythema, blistering, pain
- High rate of parental and physician satisfaction
- Superficial blisters, so NO SCARRING -> some discoloration possible, but it will go away
54
Q
What are warts? Causes?
A
- Common viral infection: HPV -> certain types have predilection to infect certain locations
- dsDNA
- >100 types
- Anywhere: hands, feet most common
- Benign, involute -> painful, embarrassing
- Some oncogenic: 16, 18, 31, 33
55
Q
How are warts transmitted?
A
-
Contact:
1. Direct: hetero or autoinoculation
2. Indirect: fomites -> warm, moist surfaces, e.g., towels - Site of entry: traumatized skin (can be subclinical abrasion or fissure)
- Incubation period: 1-6 months
- Duration variable: 2/3 resolve within 2 years
- Mechanism: cell-mediated immunity -> production of cytokines that elicit immune response against the virus
56
Q
What are 4 common types of warts?
A
- Verrucae Vulgaris: common warts
- Verrucae Plantaris: plantar warts
- Verrucae Plana: flat warts
- Condylomata Acuminata: anogenital warts
57
Q
Verrucae vulgaris
A
-
Hands most common: periungual, subungual
1. Can occur anywhere, including oral mucosa - Single or multiple skin-colored hyperkeratotic papules and/or plaques
1. Dome shaped
2. Exophytic
3. Filiform (on a stalk) - Clues to diagnosis: paring surface reveals “black dots” -> thrombosed capillaries
1. Disruption of normal skin lines
58
Q
What are these?
A
- Filiform warts: can be snipped off
59
Q
Flat warts
A
- Face, neck, arms, legs most common
- Smooth, skin-colored to slightly tan/pink flat-topped thin papules (3-5 mm) and/or plaques
- Few or many
- Shaving can facilitate spread
60
Q
What are these?
A
Flat warts
Note the Koebnerization in the bottom image (coalescing, linear lesion)
61
Q
Plantar warts
A
- Plantar foot, toes
- Tend to be most symptomatic
1. Weight bearing surfaces
2. Develop endophytic (grows inward) component, painful - Coalesce into clusters
1. Mosaic wart: big one that causes a blister (top image) - Paring surface should reveal “black dots:” if you can’t tell what it is (bottom image -> micro-thromboses)
- Note the thrombosed capillaries in the bottom image
62
Q
What are these?
A
Endophytic warts
63
Q
DDx for plantar warts?
A
- Callus: left
- Corn: top right
- Black heel (bottom right): common in athletes, and may sometimes be confused with warts
64
Q
What is the clinical presentation of anogenital warts?
A
- Skin-colored to pink/tan soft papules: 1-5 mm
1. Usually multiple
2. May form large masses (cauliflower-like) -
Usually asymptomatic
1. Irritation may cause pain, bleeding
65
Q
How are anogenital warts transmitted?
A
- Transmission:
1. Sexual contact
2. Vertical (perinatal)
3. Benign (nonsexual) heteroinoculation (like a grandparent whiping a baby’s bottom)
4. Autoinoculation: hands to genitalia or perianal area
4. Fomite (e.g., towels)
66
Q
What is the treatment for warts?
A
- No specific antiviral therapy for HPV infections -> many txs, but lack of evidence-based medicine
- Two broad categories:
1. Destructive (physical or chemical): freezing, burning (may just grow back), cutting off, laser
2. Immunomodulatory: topical, oral, injections - Best evidence for topical salicylic acid, in a review
67
Q
What are the 2 HPV vaccines?
A
- Gardasil: 16, 18, 6, 11
- Cervarix: 16 and 18
68
Q
What are the indications for tx of warts? What factors are important?
A
- INDICATIONS: painful, extensive, enlarging, subject to trauma, cosmetically objectionable
- Choice of tx depends on multiple factors:
1. Age/personality of child
2. Number
3. Size
4. Location
5. Previous therapy
69
Q
What are the 6 types of superficial fungal infections?
A
- Tinea capitis: head
- Tinea corporis: body
- Tinea manuum: hand
- Tinea cruris: groin creases
- Tinea pedis: feet
- Tinea unguium: onychomycosis
70
Q
What is a dermatophyte? 3 primary genera? Yeast?
A
- Tinea or “ringworm”
1. Soil, on animals, on humans
2. Digest keratin and invade hair, skin, nails - 3 primary genera:
1. Trichophyton
2. Microsporum
3. Epidermophyton - Yeast:
1. Tinea versicolor
2. Candidiasis
71
Q
What is tinea capitis? Caused by?
A
- “Ringworm:” fungal infection of skin, hair of scalp
- Most common in kids: 3-7 yrs old (M>F), but freq in younger/older kids too (3-8% US prevalence)
- Caused by:
1. Trichophyton tonsurans (>90% in US; AA)
2. Microsporum canis (Caucasian) - Tends to come from cats, and AA children more than Caucasian/Hispanic
72
Q
How is tinea capitis transmitted? What are the predisposing factors?
A
- Transmission: humans (via asymptomatic carriage; most common), animals, soil
1. Fomites: brushes, combs, hats, hair clippers, etc. - Predisposing factors: large family size, crowded living conditions, and low SES
73
Q
What do these two images show?
A
- TINEA CAPITIS
- “Seb derm”-like plaques (left): look more like dandruff -> diffuse
- Localized plaques (right)
- Clinically, largely characterized by scaling and patchy alopecia, BUT variety of patterns/range of features may be seen
1. Doesn’t always look like rings, or what you see on the body
74
Q
What is this?
A
- Patchy alopecia in tinea capitis: can be subtle or quite severe
- A lot of hair breakage, particularly at the surface of the skin
75
Q
What do you see here?
A
- Patchy alopecia in tinea capitis: can be subtle or quite severe
- A lot of hair breakage, particularly at the surface of the skin
76
Q
What is going on here?
A
- Broken hair shafts in tinea capitis
- If the child has dark hair, you may see a “black dot” pattern (base of the hair is still in the follicle)
- This is generally caused by T. tonsurans, which grows on the inside of the hair shafts, weakening them and causing them to break off at the scalp
77
Q
What’s up with these dudes?
A
- Pustules in tinea capitis
- Sometimes just a few and sometimes many
- When you see pustules, even in the absence of other significant findings, you should have a high index of suspicion for a primary fungal infection and OBTAIN A FUNGAL CULTURE
- Can also be superimposed bacterial infection
78
Q
What is going on here?
A
- Kerions from tinea capitis: may cause permanent scarring alopecia -> esp likely if allowed to go on for a long time without proper treatment
- May see severe inflam rxn on the scalp -> follicles will recover and most of the hair will re-grow most of the time
1. Need to be taken seriously and treated to prevent permanent damage
79
Q
Do pts w/tinea capitis get LAD?
A
- YES!
- Studies show that presence of posterior cervical and sub-occipital LAD correlate well with a + fungal culture in the setting of scaling and alopecia
80
Q
How is a tinea capitis diagnosis confirmed?
A
-
Gold standard is FUNGAL CULTURE
1. Standard bacterial culturette
2. Moisten cotton tip of swab (tap water okay)
3. Rub vigorously over affected area - She reiterated how important this was multiple times
- M. Canis often takes even higher dose and longer course to clear, especially if more severe infection, making CULTURE IMPORTANT (even though many physicians will not do this)
- KOH of scale (attached image) & broken hairs may also be helpful
81
Q
What should be on your DDx for tinea capitis?
A
- Seborrheic dermatitis
- Psoriasis
- Alopecia areata
82
Q
What is this?
A
- Seborrheic dermatitis: usually more CHRONIC than tinea capitis
- Unusual after infancy and before puberty
1. Infants with “cradle cap:” waxy yellow scale
2. Teens and adults with “dandruff:” diffuse dry or oily white to yellow scale - Diffuse dry or oily white/yellow scale
- Thought that Malasezia is involved
83
Q
What is this?
A
- Psoriasis: frequently affects the scalp
- Erythematous plaques with silvery scale
- Favors postauricular and posterior hairline
84
Q
What do you see here?
A
- Alopecia areata: well-circumscribed, smooth bald patches
- Generally, you won’t see any scale or other skin changes
- Smooth bald patches that are very NON-INFLAM (may have pinkish-orange hue, but no scale or inflammatory pustules)
- No LAD or broken hairs
85
Q
What is the pharm treatment for tinea capitis?
A
- Requires SYSTEMIC antifungal to penetrate hair follicle (can’t use a topical anti-fungal because can’t get inside the hair shaft)
- Griseofulvin is gold standard
- M.canis infections may require higher doses and longer course for clearance
- Give with fatty food to enhance absorption; may divide bid if large volume of liquid
-
Side effects rare: headache, GI, photosensitivity, morbilliform eruption
1. Heme and hepatic toxicity very uncommon - Routine lab monitoring NOT recommended
1. CBC, LFT’s for course longer than 8 wks
86
Q
What are the non-pharm treatments for tinea capitis?
A
-
Antifungal shampoo 2-3 times per week (once per week if pt only washes hair once each week)
1. Ketoconazole 2% or Selenium sulfide 2.5%
a. Aid in removal of scale
b. Eradicate spores, which helps DEC transmission
c. Helpful adjunctive therapy
2. Consider use by all household members - Fomite education: don’t share combs, brushes, hats, etc.
87
Q
Besides Griseofulvin, what are the other tx options for tinea capitis?
A
-
Terbinafine: approval for 4 and older (6-wk course)
1. Oral; have to draw baseline LFTs and CBC (parents usually do NOT like this)
2. M. Canis doesn’t respond well to this
3. AEs: headache, GI, dizziness, drug rxns, hepatotoxicity, rare hematologic - Systemic azoles NOT routinely used -> may give Fluconazole to infants (<couple></couple>
<p>1. More $, liver toxicity, drug interactions </p>
</couple>
88
Q
How should kerions be treated in tinea capitis?
A
- Marked inflam may cause scarring and permanent hair loss (e.g., the kid might wear a hat every day for awhile, making it harder to notice the damage)
- Rapid aggressive therapy indicated
- Severe: consider systemic steroids (for 2 weeks)
1. Rapid resolution of inflammation
2. Decreased pain - If the patient has a kerion, you should think about whether you need medications in addition to the systemic anti-fungal
89
Q
What is tinea corporis?
A
- Superficial fungal infection of skin
- Transmission via contact with infected person or animal
- Young children (M. Canis > trichophyton)
- Older child/adults (T. Rubrum and o/trichophyton)
1. Young child with T. rubrum likely has parent with tinea pedis and/or onychomycosis
90
Q
What are the clinical manifestations of tinea corporis?
A
-
Classic: one or more well-defined annular scaly erythematous plaques with central clearing and a scaly, vesicular, papular, or pustular border
1. Annular: emphasized border, and central area that looks more like regular skin
91
Q
What is this?
A
Tinea corporis
92
Q
What do you see here?
A
- Tinea incognito (tinea corporis): use of topical steroids may alter appearance
- Steroid can calm inflammation, but not clear it -> ruins the appearance of the infection, leading to difficult dx (incognito)
93
Q
What is this? Tx?
A
-
Majocchi’s granuloma: granulomatous folliculitis
1. Form of tinea corporis (Trichophyton rubrum) - Erythematous plaques or patches studded with papules and/or nodules
- Deeper infection of follicles
- Usually requires systemic therapy to penetrate follicles
94
Q
How do you diagnose tinea corporis?
A
- Clinical presentation: history and PE
- KOH prep: scrape active border
- Fungal culture
- Most of the time, you’ll have to rely heavily on your presentation to make an educated guess -> often don’t have time to do a KOH in prep
95
Q
What things might be on your differential for tinea corporis?
A
- Nummular atopic dermatitis
- Psoriasis
- Granuloma annulare
96
Q
What is this?
A
- Nummular atopic dermatitis
- NOT ANNULAR (everything round is not annular)
- Very pruritic: much more itchy than typical fungal infection would be
97
Q
What do we have here?
A
- Psoriasis: “dull pink” erythema
- NOT tinea corporis because:
1. Silvery or white micaceous scale
2. Nummular lesions
3. Distribution -> tends to favor scalp, behind ears, over elbows and knees
98
Q
What is this?
A
- Granuloma annulare
- NOT tinea corporis because:
1. No scale
2. Raised, “rubbery” rim
3. Location: dorsal hands, wrists, feet, ankles
99
Q
What is the treatment for tinea corporis?
A
- Topical for superficial/localized:
1. BID for at least 2-4 weeks
2. Treat affected area and rim of “normal” skin - If no improvement, reconsider diagnosis
2. If culture +, proceed to oral therapy - Systemic therapy for: disseminated/severe, immunocompromised host, Majocchi’s, tinea faciei (on the face)
100
Q
What’s the deal with using combo products for tinea corporis?
A
- Combo antifungal/steroid often result in persistent, worsening infection
- Relatively strong topical steroids: atrophy, striae, telangiectasias
- Fairly weak anti-fungal
- Generally NOT RECOMMENDED
- Pts use the product until they get atrophy of skin, and other effects of steroid use, but still have fungal infection -> much better off doing the culture, and doing one or the other
101
Q
What is tinea manuum? Clinical manifestations?
A
- Skin of hands; most comm in MEN (Trichophyton)
- Rare in children
- Clinical manifestations:
1. Chronic dryness of palms
2. Redness/scaling
3. Two patterns:
a. Palmar: fine scale, may be unilateral
b. Dorsal: annular, red, scaly
102
Q
What is this? Dx?
A
- Tinea manuum
- Diagnosis via KOH (branched septated hyphae) and fungal culture
103
Q
What is the differential for tinea manuus?
A
- Other dermatitis: irritant, contact
- Psoriasis
- Really important to GET CULTURE and see what this is
104
Q
How do you treat tinea manuus?
A
- Topical antifungal for dorsum, limited
- Palms require oral antifungal
105
Q
What is tinea cruris?
A
- Skin of groin, aka, “jock itch” -> rare in children
- MEN > women
- Risk factors: obesity, heat, humidity
- Trichophyton
106
Q
What are the clinical manifestations of tinea cruris?
A
- Pruritic
- Red, annular, scaly plaques over groin and medial thighs
- Penis, scrotum not affected
107
Q
What is this? How would you dx it?
A
- Tinea cruris (jock itch)
- KOH and fungal culture
108
Q
What should be in your DDx for tinea cruris?
A
- Candidiasis: NOT tinea bc much more irregular border satellite pustules
- Erythrasma: NOT tinea bc no scale and coral red fluorescence (see attached image)
- Other: psoriasis, seb derm
109
Q
What is the treatment for tinea cruris?
A
- Topical anti-fungal if it is pretty limited
1. Powders helpful (dry up the area) - Oral AF if refractory, severe (or have deeper follicular involvement)
- Treat tinea pedis also -> LOOK AT WHOLE BODY
- Recurrences are common
110
Q
What is tinea pedis? Risk factors?
A
- “Athlete’s foot” -> 10% world population
- Males
- Risk factors: occlusive shoes, communal pools, showers
111
Q
What are the clinical manifestations of tinea pedis?
A
- Itching, scaling on soles, between toes
1. Blistering - Moccasin: fine dry scale over soles (T. rubrum)
- Vesiculobullous: vesicles/bullae on soles, esp. insteps (T. mentagrophytes)
112
Q
What is this?
A
Tinea pedis: usually more concentrated on medial edge of the foot
113
Q
How do you diagnose tinea pedis?
A
KOH and fungal culture
114
Q
What should be on your differential for tinea pedis?
A
- Contact dermatitis: dorsal feet affected
-
Dyshidrotic eczema: “tapioca vesicles”
1. Can be hard to differentiate between this and vesiculobullous type, but CULTURE is what helps here
115
Q
What is this?
A
Contact dermatitis: e.g., leather, etc.
NOT tinea pedis
116
Q
What is this?
A
- Dyshidrotic eczema
- Usually a lot itchier than tinea pedis, but this is a very subjective thing
- CULTURE is the key
117
Q
What is tinea unguium? Risk factors?
A
- Nail infection -> 60% over age 70
- Males
- Tricophyton
- Non-dermatophyte molds, yeasts
- Risk factors: immunosuppressed, diabetes, HIV, poor circulation, trauma, dystrophy (already abnormal and more susceptible)
118
Q
What are the clinical manifestations of tinea unguium? Patterns?
A
- Discoloration, thickening, onycholysis
- 4 patterns:
1. Distal subungual: most common
2. Proximal subungual
3. White superficial
4. Candida - Nails may separate from the nail bed
119
Q
What is this?
A
- Distal subungual = most common of the 4 types of tinea unguium
- Invasion of distal nail plate, onycholysis with thickening and discoloration
120
Q
What is this?
A
- Proximal subungual variation of tinea unguium
- Uncommon
- HIV positive patient: considered pathognomonic for HIV
121
Q
What is this?
A
- Proximal subungual variation of tinea unguium
- Uncommon
- HIV positive patient: considered pathognomonic for HIV
122
Q
What is this?
A
- White superficial variation of tinea
- White plaques on dorsal nail plate: from top downward
123
Q
What is this?
A
- Candida
- Distal fingertips red and swollen, and nails destroyed
- Won’t see this in typical dermatophyte infections
124
Q
What is chronic paronychia?
A
- Nail dystrophy
-
Candida albicans
1. Confirm with stain and culture
2. Treatment
a. Topical ketoconazole if mild
b. Oral fluconazole if severe (3 mos for fingernails) -> baseline CBC, LFT’s - Most of the time this has been going on for quite awhile, and you will give Fluconazole
125
Q
What do you see here?
A
-
Trachyonychia: 20 nail dystrophy (may not affect all nails)
1. Ridging, grooves, pitting, discoloration, fragility
2. Pretty rapidly progresses to involve all nails -
Causes: idiopathic, lichen planus, psoriasis, other
1. Don’t really know what causes this (idiopathic), but can see in setting of psoriasis
126
Q
What do you see here?
A
- Beau’s lines: transverse grooves or furrows
-
Stress causes temporary arrest of nail matrix
1. Usually after some type of viral or febrile illness in kids
2. Plate stops growing, and re-starts, leaving a gap (totally common, and nails grow back normally) -> NOT fungus - Nail may shed completely (onychomadesis)
127
Q
What is going on here? Why?
A
- Usually symmetrical: often both great toes, 2nd toes, or 5th toes, e.g., pressure from ill-fitting shoes
- Jamming will show breakage, splitting, hemorrhage
1. Smaller toes often times a little thicker (due to friction) - NOT fungus -> if symmetrical, less likely to be fungus
128
Q
What happened here?
A
- Habit tic deformity
- Habitual picking at the cuticle
129
Q
How would you diagnose a nail fungal infection?
A
- KOH prep: preferably from subungual debris
- Fungal culture of nail clipping (couple pieces of nail)
- Fungal stain of nail clipping: PAS = periodic acid-Schiff (see attached image; kind of old-fashioned)
130
Q
What is the treatment for tinea unguium?
A
-
Topicals generally not very effective bc they:
1. Do not penetrate nail plate well
2. Do not reach nail matrix
3. Penlac (Ciclopirox) for superficial infection not involving lunula (visible, crescent-shaped part of the root of the nail) -> w/softening agent (urea cream) -
Systemic therapy: Griseofulvin in the past (but low cure rate and high recurrences)
1. Terbinafine: 6 wks for fingernails, and 12 wks for toenails -> baseline CBC and LFTs (repeat in 2-4 weeks)
2. Other: itraconazole, fluconazole -> tend to be more expensive and have more potential side effects
131
Q
How long does it take fingernails and toenails to grow out?
A
- Fingernails: 4 to 6 months
- Toenails: 12 to 18 months
132
Q
What is tinea versicolor?
A
- Aka, pityriasis versicolor (not a true infection)
- Common superficial fungal disorder of skin
- Yeast forms of dimorphic fungus Malassezia furfur (same as seb derm); also pityrosporum orbiculare and pityrosporum ovale
1. Normal skin flora - Usually presents in adolescence (when oil and sebaceous glands are more active), but may be seen in younger children too
133
Q
What are the clinical manifestations of tinea versicolor?
A
- Multiple scaling, oval macules, patches and thin plaques over upper trunk, prox arms, & sometimes face and neck
-
Hyper- or hypopigmented: azelaic acid production (diffuses down and impairs melanocyte function)
1. Depending on baseline complexion, level of sun exposure (may look lighter on dark skin and darker on light skin) - More prominent in summer when sun exposure intensifies pigmentation differences
134
Q
What is this?
A
- Multiple scaling, oval macules, patches and thin plaques over upper trunk, prox arms, & sometimes face and neck
-
Hyper- or hypopigmented: azelaic acid production (diffuses down and impairs melanocyte function)
1. Depending on baseline complexion, level of sun exposure (may look lighter on dark skin and darker on light skin) - More prominent in summer when sun exposure intensifies pigmentation differences
135
Q
What do you see here? Dx?
A
- Pityriasis alba
- Most common on face (mostly children, and more M than F)
- Usually atopic background
- Less extensive than pityriasis versicolor
-
Diagnosis: KOH prep w/spaghetti and meatball appearance (hyphae and spores)
1. Usually don’t culture, but DIAGNOSE CLINICALLY
136
Q
How do you treat pityriasis?
A
- Education: course tends to be chronic, and recurrences common, esp. when weather gets hot
-
Topical therapy: selenium sulfide lotion/shampoo 2.5% OR ketoconazole shampoo 2%
1. Applied for 10 min. daily for 1-2 weeks, then 2-3 times per week for maintenance
2. May need maintenance tx, esp. in warmer months -
Severe, recurrent, fails topical therapy -> systemic therapy (adult dosing)
1. Ketoconazole 400 mg po x 1: work up sweat, wait 10-12 hr to shower and repeat in 1 week
2. Fluconazole 200-400 mg po x 1: may repeat in 1 week if severe
3. Should still use topical for maintenance
137
Q
Candidiasis? Clinical manifestations? Tx?
A
- Intertriginous
- Paronychia
-
Angular Cheilitis: oral commissures (increased moisture) -> elderly, lip lickers, denture (see attached image)
1. Clinical manifestations: painful, erythematous fissures and small pustules
2. Treatment: topical anti-yeast cream -> DEC moisture
