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Dermatology > Infectious Dermatology Part 1 > Flashcards

Infectious Dermatology Part 1 Flashcards

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1
Q

What is the etiology of impetigo?

A
  • S. aureus: MSSA and MRSA
  • Bullous impetigo: epidermolytic toxin A producing staph aureus –> scalded skin syndrome
  • Beta-hemolytic strep group A
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2
Q

Epidemiology of impetigo

A
  • Children but can occur at any age
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3
Q

Where can impetigo be located?

A
  • Minor breaks in the skin
  • Around the nose
  • Atopic dermatitis
  • Traumatic wounds
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4
Q

What is bullous impetigo?

A
  • S. aureus exfoliative toxin A –> loss of cell adhesion in superficial epidermis
  • MC in newborn and older infants
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5
Q

What age is non-bullous impetigo seen?

A

All ages

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6
Q

Clinical manifestations of non-bullous impetigo

A
  • Often asymptomatic
  • Can be painful and tender
  • Erosions with crusts
  • 1-3 cm lesions
  • Central healing often after several weeks
  • Regional lymphadenopathy
  • Arranged in scattered, discrete lesions
  • without treatment confluent
  • satellite lesions from autoinoculation
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7
Q

Clinical manifestations of bullous impetigo

A
  • Vesicles progress to bullae
  • No erythema noted
  • Vesicles/bullae filled with serous fluid, yellow –> dark brown
  • Nikolsky sign
  • 1-2 days collapse and leave erosions with crusts
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8
Q

Clinical diagnoseis of impetigo

A
  • Clinical
  • Gram stain and culture often necessary for bullous type
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9
Q

Treatment of impetigo

A
  • Warm water soaks x 15-20 minutes twice daily followed by application of mupirocin (bactroban) x 5 days
  • For widespread infection = 7 days ABX either cephalexin or erythromycin
  • MRSA = doxycycline
  • Critically ill patients with MRSA or suspected MRSA should receive vancomycin or linezolid
  • Bullous or severe = PO ABX
  • Follow up in 1 week

Azithromycin, clindamycin, or erythromycin if penicillin allergy. Widespread pets lex erythromycin and doxycycline for MRSA

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10
Q

Patient education for impetigo

A
  • Good hygiene: clipping nails (prevent scratching), proper anti-bacterial soap, frequent washing
  • Underlying condition treatment
  • Mupirocin in other areas where skin barrier has been broken
  • Wounds covered
  • Avoid contact with others (>24 hours post ABX initiation)
  • Follow up in 1 week
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11
Q

Prevention of impetigo

A
  • BPO wash
  • Check family members for signs
  • Ethanol or isopropyl gel for hands
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12
Q

What is folliculitis

A

Infection of the hair follicle with +/- pus in the ostium of the follicle

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13
Q

Causes of folliculitis

A
  • Bacteria
  • Fungi
  • Mites
  • Virus
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14
Q

Clinical manifestations of folliculitis

A
  • Infection of hair follicle
  • +/- pus in ostium
  • Non tender/slightly tender
  • Pruritic
  • Can progress and become abscess or furuncle
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15
Q

Predisposing factors to folliculitis

A
  • Shaving hair bearing areas
  • Occlusion of hair bearing areas
  • Hot tub usage
  • Topical CS
  • Systemic ABX
  • Diabetes
  • Immunosuppression
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16
Q

Microbes that can cause folliculitis

A
  • S. aureus
  • Pseudomonas aeruginosa (hot tub) usually on trunk
  • Viral (herpetic and molloscum)
  • Fungal (candida, malassezia)
  • Syphilitic

GRAM NEGATIVE –> acne patient who worsens on systemic abx with small follicular pustules

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17
Q

An acne patient worsens on systemic antibiotics with small follicular pustules. What organism is likely responsible

A

Gram negative (gram negative folliculitis)

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18
Q

Diagnosis of folliculitis

A
  • Gram stain
  • C&S
  • KOH (fungal)
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19
Q

Treatment of mild (few) folliculitis

A
  • Warm compresses
  • Wash with BPO or antibacterial soap (dial)
  • ABX if spontaneous resolution does not occur within 2-3 weeks or if symptoms worsen
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20
Q

Treatment of moderate folliculitis

A
  • Topical ABX: clindamycin or mupirocin

Clin that mu fo follicle

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21
Q

Treatment of severe folliculitis

A
  • Oral - MSSA: cephalexin
  • Oral MRSA: doxycycline or bactrim

Follicles learning severe lessons on the bact dox

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22
Q

How do you prevent folliculitis?

A
  • BPO body wash (use on regular basis if prone to folliculitis)
  • Chlorhexidine body wash
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23
Q

What is an abscess?

A
  • Acute or chronic localized inflammation
  • Collection of pus in a tissue = inflammatory response to an infectious process of foreign body
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24
Q

Where can an abscess be located

A
  • Skin and dermis, subcutaneous fat, muscle
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25
Q

Characteristics of abscess

A
  • Tender
  • Red
  • Hot
  • Indurated nodules
  • +/- fever or constitutional symptoms
  • days/weeks = pus formation
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26
Q

Diagnosis of abscess

A
  • gram stain
  • C&S of exudate

Typically MSSA or MRSA

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27
Q

Treatment of abscess

A
  • I&D
  • ABX therapy
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28
Q

When would antibiotics be given for abscess?

A
  • Single abscess >2 cm
  • Multiple lesions
  • Extensive surrounding cellulitis
  • Immunosuppression or other comorbidities
  • S/S toxicity (fever >100.5, hypotension, or sustained tachycardia)
  • Inadequate clinical response to I&D alone
  • Indwelling medical device (prosthetic joint, vascular graft, or pacemaker)
  • High risk for transmission of s. aureus to others (athletes, group home)
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29
Q

When would IV abx be considered for abscess?

A
  • Toxic appearance: fever, hypotension, tachycardia
  • Rapid progression after 48 hr of PO ABX
  • Inability to tolerate orals
  • Close to indwelling device such as prosthetics, graft, catheter
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30
Q

When would surgery with general surgeon or plastics be considered for abscess?

A
  • Difficult areas
  • Palms
  • Soles
  • Nasolabial areas
  • Genitalia
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31
Q

Patient education for abscess

A
  • Do not squeeze
  • Prevention with antibacterial soap or BPO wash
  • Avoid heat and friction
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32
Q

Clinical manifestations of furuncle

A
  • Acute
  • Deep seated
  • Red, hot, tender nodule or abscess
  • 1-2 cm
  • Fluctuant
  • Nodule with cavitation after drainage
  • From a staphylococcal folliculitis
  • Any hair bearing region: beard, posterior neck, occipital scalp, axillae, buttocks (multiple or solitary lesions)
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33
Q

Management of furuncle

A
  • Warm compresses 10 minutes daily
  • If erythema, ABX probably necessary
  • PO ABX: bactrim x 7 days, clindamycin x 7 days, or doxycycline x 7-10 days

Doxy clin that bact fur

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34
Q

Clinical presentation of carbuncle

A
  • Deeper infection
  • Interconnecting abscesses arising in several contiguous hair follicles
  • Typically ill appearing: fever + constitutional symptoms
  • Painful/tender
  • MC location = nape of neck, back, and thighs
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35
Q

Diagnosis of carbuncle

A
  • Clinical
  • Gram stain helpful with C&S
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36
Q

Treatment of uncomplicated carbuncle

A
  • PO ABX
  • Bactrim x 7 days
  • Clindamycin x 7 days
  • Doxycycline x 7-10 days

Doxy clin the back of the car

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37
Q

Treatment of complicated carbuncle

A
  • Admission for IV abx
  • Vancomycin 1-2 IV daily
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38
Q

Criteria for carbuncle admission

A
  • Toxic appearing
  • Rapid progression
  • No improvement after 24-48 hours of PO ABX
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39
Q

Review: folliculitis definition

A

Infection of hair follicle +/- purulence at the ostium

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40
Q

Review: abscess definition

A

Localized inflammation with a collection of pus enclosed within the tissue

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41
Q

Review: furuncle definition

A

Infected nodule evolving from folliculitis

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42
Q

Review: carbuncle definition

A

Deeper infections of interconnecting furuncles

all the furuncles in a car

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43
Q

What is necrotizing fasciitis

A
  • Rapid progression of infection and destruction of subcutaneous tissue and fascia with extensive necrosis of soft tissues and overlying skin
  • AKA flesh eating disease
  • Bacteria release enzymes/gases that degrade fascia resulting in rapid proliferation, local thrombosis, ischemia, and necrosis
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44
Q

Etiology of necrotizing fasciitis

A
  • Polymicrobial
  • Beta-hemolytic GAS
  • Pseudomonas aeruginosa
  • Clostridium
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45
Q

Where can necrotizing fasciitis originate?

A
  • Site of nonpenetrating minor trauma
  • Bruise, muscle, or strain
  • Minor trauma
  • Laceration
  • Needle puncture
  • Surgical incision
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46
Q

Epidemiology of necrotizing fasciitis

A
  • MC middle age (mid 30s - mid 40s)
  • DM
  • ETOH abuse
  • liver disease
  • CKD
  • Malnutrition
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47
Q

Diagnosis of necrotizing fasciitis

A
  • Clinical

If skin necrosis not obvious suspect if signs of sepsis +
* Severe pain
* Indurated swelling
* Bullae
* Cyanosis
* Skin pallor
* Skin hypesthesia
* Crepitation
* Muscle weakness
* Foul smelling exudates

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48
Q

What is the progression of necrotizing fasciitis?

A
  • Local redness
  • Edema
  • Warmth
  • Pain
    Appears 36-72 hours after onset
  • Involved soft tissue becomes blue in color
  • Vesicles and bullae appear and spread along fascial plane

Progression to
* extensive cutaneous soft tissue necrosis
* Black eschar with surrounding irregular border of erythema
* Fever and other constitutional symptoms

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49
Q

Clinical red flags for necrotizing fasciitis

A
  • Severe, constant pain out of proportion to physical exam, or anesthesia
  • Erythema evolving into a dusky gray color
  • Malodorous, watery “dirty dishwater” discharge
  • Gas (crepitus or crackling sounds) in soft tissues
  • Edema extending beyond areas of erythema
  • Rapid progression despite antibiotic therapy
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50
Q

Treatment of necrotizing fasciitis

A
  • Surgical debridement
  • CBC, CMP, CK, ABG, UA, serum/deep tissue culture
  • CT, MRI, plain film, GAS?
    Start broad spectrum ABX: depending on gram stain/C&S
  • Carbapenem
  • Ampicillin/sulbactam
  • Clindamycin
  • MRSA: vancomycin

Necro CAMC (carbapenem, ampicillin/sulbactam, clindamycin, MRSA: vancomycin)

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51
Q

What is erysipelas?

A

Acute superficial infection (dermis and dermal lymphatic vessels)

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52
Q

Etiology of erysipelas

A

MC-group A B-hemolytic streptococcus

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53
Q

Epidemiology of erysipelas

A
  • MC in young children and older adults
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54
Q

Clinical presentation of erysipelas

A

Prodrome:
* fever
* chills
* anorexia
* malaise

General: +/- signs of sepsis

Lesion:
* painful/tender/hot
* bright red
* raised, edematous
* indurated plaque
* sharp borders

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55
Q

What is cellulitis

A

Acute infection of the dermis and subcutaneous tissue

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56
Q

Etiology of cellulitis

A
  • S. aureus and group a b-hemolytic streptococcus
  • Cat/dog trauma: pasteurella multocida
  • Freshwater wound: aeromonas
57
Q

Epidemiology of cellulitis

A

Middle age adults

58
Q

Clinical presentation of cellulitis

A

Prodrome
* Fever
* Chills
* Anorexia
* Malaise

General: +/- signs of sepsis

Lesion:
* Painful/tender/hot
* Bright red, edematous (+/- induration)
* Indistinct borders (not raised)

59
Q

Risk factors for cellulitis

A
  • Minor skin trauma
  • Body piercing
  • IV drug use
  • Tinea pedis infection
  • Animal bites
  • Peripheral vascular disease
  • Atopic dermatitis
  • Immune suppression (chronic systemic steroid use, neutropenia, immunosuppressive medications, alcohol use disorder)
  • Lymphatic damage (lymph node dissection, radiation therapy, vein harvest for coronary artery bypass surgery, and damage that occurs following multiple prior episodes of cellulitis)
60
Q

Risk factors for erysipelas and cellulitis

A
  • Compromised skin integrity: atopic dermatitis, insect bite, surgery, trauma, IV drug use
  • Compromised immune system: AIDS, DM, ESRD, CA, immunosuppressive therapy, drug/ETOH abuse
61
Q

Diagnosis of erysipelas and cellulitis

A
  • Clinical
  • Labs if systemic symptoms present
  • CBC, CMP, ESR, blood cultures
  • Imaging: US or MRI to rule out abscess, necrotizing fasciitis, pyomyositis, and gas forming anaerobic bacterial infection
62
Q

Complications of erysipelas and cellulitis

A
  • Abscess formation
  • Bacteremia
  • Endocarditis
  • Osteomyelitis
  • Metastatic infection
  • Sepsis
  • Toxic shock syndrome
63
Q

Indications for admission/parenteral therapy for erysipelas & cellulitis

A
  • Systemic presentation: Fever >100.5, hypotension, sustained tachycardia
  • Rapidly spreading lesion
  • Progression of clinical features after 48 h of oral abx
  • Unable to tolerate oral therapy
  • Comorbidities: immunosuppression, neutropenia, asplenia, cirrhosis, heart/renal failure
  • IV therapy can be switched to oral therapy once systemic s/s resolve
64
Q

What parenteral therapy would be used for erysipelas and cellulitis?

A
  • MRSA coverage: vancomycin (1st line), daptomycin (2nd line)
  • MSSA coverage: cefazolin, clindamycin, nafcillin
65
Q

What oral therapy can be used for MRSA coverage of erysipelas & cellulitis

A
  • Clindamycin (1st line)
  • AMoxicillin + one of the following:
  • Bactrim
  • Doxycycline
66
Q

What oral therapy can be used for MSSA coverage in erysipelas and cellulitis?

A
  • Cephalexin
  • Nafcillin
  • Clindamycin
67
Q

What antibiotics should be used for erysipelas and cellulitis due to a dog/cat bite?

A

Augmentin (caused by pasteurella multocida

68
Q

What antibiotics would be used for erysipelas/cellulitis due to a human bite?

A

Augmentin (caused by eikenella, group A streptococcus)

69
Q

What antibiotics would be used for erysipelas/cellulitis due to exposure to fresh water? Salt water?

A
  • Fresh water: ciprofloxacin (cover aeromonas)
  • Salt water: doxycycline (cover vibrio vulnificus)
70
Q

What is lymphagnitis?

A

Acute inflammatory process involving the subcutaneous lymphatic channels

71
Q

Etiology of lymphangitis

A

Acute:
* GAS
* S. aureus
* Herpes simplex virus

Chronic:
* Mycobacterium marinum

72
Q

What can lead to lymphangitis?

A
  • break in skin
  • Wound
  • Paronychia
  • Primary herpes simplex
73
Q

Symptoms of lymphangitis

A
  • Pain +/- erythema proximal to break in skin
  • Red linear streaks and palpable lymphatic cord
74
Q

Diagnosis of lymphangitis

A
  • Clinical
  • Resolves with correct diagnosis and treatment
  • Culture wound if open and actively weeping
  • Labs only if systemic: CBC, CMP, blood cultures
75
Q

Treatment of lymphangitis

A
  • Oral ABX dependent on sensitivity
  • Dicloxacillin or 1st generation cephalosporin
  • MRSA: clindamycin or bactrim
  • Follow up in 24-48 hours
  • Admit if toxic appearing or no improvement after 24-48 hours

The diclox named ceph has Lymphangitis so you have to clin that bacteria up

76
Q

What is cutaneous candidiasis?

A
  • superficial fungal infection of the skin
  • MC: candida albicans
  • MC neonates and adults >65 years old
77
Q

Common areas involved in cutaneous candidiasis

A
  • Genitocrural
  • Gluteal
  • Interdigital
  • Inframammary
  • Axilla
  • Under pannus
78
Q

Risk factors for cutaneous candidiasis

A
  • Obesity
  • DM
  • Local occlusion/moisture
  • Steroid/abx use
  • Hyperhidrosis
  • Incontinence
79
Q

Presentation of cutaneous candidiasis

A
  • Pruritic
  • Tender/painful
  • Macerated
  • Erythematous
  • Satellite lesions typically present
80
Q

Diagnosis of cutaneous candidiasis

A
  • Clinical
  • KOH prep
81
Q

Treatment of mild to moderate cutaneous candidiasis

A
  • Topical antifungals 2-3 weeks, continue x 2 weeks after clearance
  • Ketoconazole
  • Econazole
  • Clotrimazole
  • Miconazole
82
Q

Treatment of severe cutaneous candidiasis

A
  • Oral antifungals: fluconazole
83
Q

Patient education for cutaneous candidiasis

A

Prevention is key
* Keep areas dry
* Powders
* Hair dryer
* Avoid occlusive clothing

84
Q

What is balanitis

A
  • Inflammation of the glans penis, can be triggered by numerous factors
  • Affects uncircumcised men with poor hygiene
85
Q

Common infectious triggers of balanitis

A
  • Candida
  • Trichomonas vaginalis
  • Gonorrhoeae
  • Streptococcus
86
Q

Diagnosis of balanitis

A
  • Culture
  • KOH
  • Tzank smear
  • RPR-syphilis
  • Patch test
  • depending on history
87
Q

Treatment of balanitis

A
  • Improved personal hygiene
  • Use of low to medium potency topical steroid until improved
88
Q

What is dermatophyte infection

A
  • Fungal infection that infects nonviable keratinized cutaneous structures
  • Includes: stratum corneum, nails, hair (can surviva in human scales for 12 months)
89
Q

What are the 3 genera of dermatophytes?

A
  • Trichophyton (MC): hair and nail
  • Microsporum
  • Epidermophyton
90
Q

What is the most common area of dermatophyte infection by age?

A
  • Scalp MC in children
  • Intertriginous areas in young and older adults
91
Q

How are dermatophytes transmitted?

A
  • Person to person (MC)
  • Animals
  • Soil (least common)
92
Q

Pathophysiology of dermatophytes

A
  • Dermatophytes produce enzymes that break down keratin allowing fungi to invade epidermis, nail, and hair shaft
93
Q

Areas affected by dermatophytes

A
  • Feet (tinea pedis)
  • Groin (tinea cruris)
  • Trunk/extremities (tinea corporis)
  • Hands (tinea manuum)
  • Face (tinea facialis)
  • Hair (tinea capitis)
  • Facial hair (tinea barbae)
  • Nails (onychomycosis)
94
Q

Classifications of dermatophytes

A
  • Person to person = anthropophilic
  • Animal to human = zoophilic
  • Environmental = geophilic
95
Q

Predisposing factors to dermatophytes

A
  • Atopy, ichthyosis
  • Collagen vascular disease: RA, SLE, temporal arteritis, scleroderma
  • Steroid use (oral/topical)
  • Sweating, local occlusion
  • Occupational exposure
96
Q

Diagnosis of dermatophytes

A
  • Skin and nail for KOH and direct microscopy
  • Woods lamp with microsporum blue green fluorescence
  • Fungal culture
  • Dermatopathology via skin biopsy
97
Q

How is a KOH prep done?

A
  • Skin: use blade to scrap skin cells from area
  • Nail: use dull scalpel to remove excess keratin from nail
  • Hair: remove hair at root
  • 2 drops of 10% KOH on glass slide and let sit for 15 minutes
  • Inspect under low and high power: hyphae and spores will be present
98
Q

How is fungal culture performed?

A
  • Skin: specimen obtained with brush
  • Hair: specimen remove 5-10 hairs with forcep/hemostat at one time, use brush to obtain scales and inoculate fungal medium
  • Nail: use fingernail clipper or sharp curette to obtain keratinous debris from under nail
  • Place specimen inside fungi culture medium

Limitations: requires days - wks to return definitive diagnosis; benefits: differentiates between fungal spp

99
Q

Treatment of dermatophyte infection

A

Topical antifungals
* Imidazoles: clotrimazole, miconazole, ketoconazole

Allylamines: Naftfine, terbinafine

Systemic antifungals
* CBC, Cr, LFTs
* Imidazoles: itraconazole, ketoconazole, fluconazole
* Allylamine: terbinafine

100
Q

Benefits and limitations of dermatopathology via skin biopsy for dermatophytes

A
  • Benefits: most sensitive form of diagnosis
  • Limitations: skin biopsy sample required, more invasive testing
101
Q

Epidemiology of tinea capitis

A
  • MC in children
  • MC in african americans
102
Q

What are the parts of tinea capitis

A
  • Ectothrix outside of hair shaft: grey patch that is scaly, circular with hairs broken off, very brittle
  • Endothrix within hair shaft: black dot, kerion, favus
103
Q

Presentation of non-inflammatory tinea capitis

A
  • Scaling
  • Pruritis
  • Alopecia
  • Adenopathy
104
Q

Presentation of inflammatory tinea capitis

A
  • Pain
  • Tenderness
  • Alopecia
105
Q

Why does tinea capitis have a black dot at the endothrix?

A
  • Broken off hairs near the scalp –> swollen hair shafts
  • Diffuse and poorly circumscribed
  • Caused by T. tonsurans. or T. violaceum
106
Q

What is a kerion?

A
  • In tinea capitis
  • Inflammatory mass where remaining hairs are loose
  • Boggy, purulent, inflamed nodules, and plques
  • Painful –> drains pus from multiple openings
  • Hairs do not break off but fall out or pulled without pain
  • Crusting and matting of surrounding hairs
  • Caused by T. verrucosum, t. mentagrophytes, heals with scaring alopecia
107
Q

What is a favus?

A
  • Tinea capitis
  • Perifollicular erythema and matting of hair
  • Thick/yellow crusts
  • Odor
  • Doesn’t clear spontaneously
  • Results in scarring alopecia
108
Q

Diagnosis of tinea capitis

A
  • Woods lamp: T. tonsurans doesn’t fluoresce
  • Direct microscopy
  • Fungal culture: usually growth seen in 10-14 days
  • Bacterial culture: to rule out bacterial with staph (can have superimposed infections)
109
Q

Treatment of tinea capitis

A
  • If left untreated permanent hair loss!
  • PO antifungals: terbinafine, griseofulvin
  • Antifungal shampoos: ketoconazole 2% shampoo
110
Q

Prevention of tinea capitis

A
  • Wash clothing, bedding, and towels
  • Wash furniture if in contact
  • Avoid used pillow cases
  • Avoid head to head contact
  • Disinfect combs and other hair products

`

111
Q

What is tinea cruris?

A
  • “Jock itch”
  • Tinea of inguinal folds and thighs
  • MC in males, coexists with tinea pedis typically
  • Subacute or chronic dermatophytosis of upper thigh and adjacent inguinal and pubic regions
112
Q

Clinical presentation of tinea cruris

A
  • Large scaling, well demarcated dull red/tan/brown plaques
  • Central clearing
  • Papules and pustules @ margins
  • Treated = lack scale
  • Post-inflammatory hyperpigmentation in darker skinned persons
  • Scrotum and penis rarely involved
113
Q

Diagnosis of tinea cruris

A

Clinical diagnosis

114
Q

Treatment of tinea cruris

A

Topical antifungal x +/- 3 weeks:
* Ketoconazole
*Econazole: zeasorb AF powder

PO antifungals if failure of topicals:
* Griseofulvin

115
Q

Management/prevention of tinea cruris

A
  • Wear shower shoes while bathing
  • Put on socks before pants
  • Antifungal/drying powders
  • Benzoyl peroxide wash
  • Alcohol based sanitizer gels
  • Avoid tight fitted clothing/use cotton underwear
116
Q

What is tinea corporis?

A
  • Ring worm
  • Fungal/dermatophyte infection involving anywhere on the body
  • Wrestlers infection
117
Q

diagnosis of tinea corporis

A
  • Clinical
  • Biospy if unsure
118
Q

Findings of tinea corporis

A
  • Asymptomatic
  • Pruritis depending on area
  • Sharply marginated plaques
  • Vesicles and papules
  • Central clearing
119
Q

Treatment of tinea corporis

A
  • Topical antifungals
  • Oral antifungals: terbinafine; need CBC, Cr, LFT’s
120
Q

What is tinea pedis?

A
  • MC dermatophyte infection: athlete’s foot
121
Q

Presentation of tinea pedis

A
  • Erythema
  • Scaling
  • Maceration
  • +/- bullae formation (if tinea cruris diagnosed check feet)
  • MC age 20-50 y/o
122
Q

Risk factors for tinea pedis

A
  • Hot
  • Humid climate
  • Occlusive footwear
  • Hyperhidrosis
123
Q

Subtypes of tinea pedis

A
  • Interdigital
  • Moccasin
  • Inflammatory
  • Ulcerative
124
Q

Presentation of interdigital type of tinea pedis

A
  • Dry scaling
  • Maceration
  • Fissuing: hyperhidrosis common; MC site between 4th and 5th toe
125
Q

Presentation of moccasin type of tinea pedis

A
  • Well demarcated
  • Scaling with erythema
  • Papules at margin
  • Fine white scale
  • Hyperkeratosis: MC on soles or lateral border of feet; MC bilateral
126
Q

Presentation of inflammatory type of tinea pedis

A
  • Vesicles or bullae with clear fluid
  • Pus usually indicates secondary bacterial infection
  • After rupture erosions like ragged ringlike border
  • ID reaction can occur
  • MC on sole, instep, and web spaces
127
Q

Presentation of ulcerative type of tinea pedis

A
  • Extension of interdigital tinea pedis onto the plantar and lateral foot
  • May have secondary bacterial infection –> S. aureus
128
Q

Treatment of tinea pedis

A

Topical antifungal
* BID x 2-4 weeks
* Ketoconazole & Econazole BID

Oral antifungal: best for hyperkeratotic
* Terbinafine; Blood work prior (Cr, LFT’s CBC) and monitor

129
Q

Prevention of tinea pedis

A
  • Wash with BPO daily
  • Use antifungal powder
  • Shower shoes in communal showers
  • Alcohol based sanitizers
130
Q

What is tinea versicolor?

A
  • Pityriasis versicolor
  • Not part of group caused by dermatophyte
  • MC adolescents
  • Overgrowth of malassezia furfur
  • Seen often in patients with oily skin
  • Not contagious
131
Q

Risk factors for tinea versicolor

A
  • Climate
  • Sweating
  • Immunodeficiency
  • Products
  • Steroid use
  • Oily skin
132
Q

Presentation of tinea versicolor

A
  • Some itching, possibly psychological
  • Macules +/- scale
  • Patches +/- scale
  • Plaques +/- scale\
  • Hypo/hyperpigmentation
  • Erythema
133
Q

Diagnosis of tinea versicolor

A
  • KOH shows hyphae and budding yeast (spaghetti and meatballs)
  • Woods light
134
Q

Treatment of tinea versicolor

A
  • Selenium sulfide or zinc pyrithione
  • Topical antifungals –> ketoconazole
  • PO therapy not recommended unless failure of topicals
135
Q

A 8 year old boy is brought in for evaluation of a chronic rash on his trunk. Examination reveals multiple erythematous, scaling plques and papules with raised borders and some central clearing. What is the best next step in management?

A

Examine scrapings in a 20% KOH solution by direct microscopy

136
Q

A 26 year old female presents with a rash consisting of hypopigmented macules and papules with fine scales located on the lower back and abdomen. Which of the following laboratory findings is consistent with the most likely diagnosis?

A

Large blunt hyphae with budding spores

tinea versicolor

137
Q
A
138
Q

A 19 year old male college student presents with an asymptomatic rash extending over his upper trunk, shoulders, and neck. The hypopigmented annular lesions vary in size from 4 to 5 cm in diameter to larger, confluent areas. There is no visible scale associated with the lesions What organism is the most likely cause of his symptoms?

A

Malassezia furfur

tinea versicolor

139
Q

What is the best description of erysipelas?

A

Localized painful, distinctly demarcated, raised erythema and edema often with streaking and prominent lymphatic involvement

Dermatology (12 decks)

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