Cutaneous fungal infections (dermatophytosis, pityriasis vesicolor) Flashcards

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1
Q

What are the clinical features of fungal foot infection?

A
  • dry
  • red
  • scaly
  • itchy
  • usually starts between the toes and speads to the soles
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2
Q

Who is most affected by athlete’s foot?

A

Men >women >children

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3
Q

How is athlete’s foot spread?

A

Indirect and direct contact

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4
Q

What causes athlete’s foot?

A

Dermatophyte (tinea pedis)

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5
Q

What conservative measures can be used in management of athlete’s foot?

A
  • wearing open shoes
  • good foot hygiene
  • wearing cotton socks (rather than synthetic or no socks at all)
  • drying feet thoroughly
  • not sharing towels
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6
Q

What is Whitfield ointment?

Why is it used for athlete’s foot?

A

Whitfield ointment = benzoic acid and salicylic acid
It is a useful keratolytic treatment but prescribed less now.

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7
Q

Which medical treatments are used for athlete’s foot?

A

Topical:
Terbinafine 1%(1st line)
+/- Aluminium acetate foot soaks BD
Imidazoles e.g. clotrimazole, ketoconazole, miconazole (2nd line)

Systemic:
Terbinafine (3rd line) - but must monitor for hepatotoxicity (LFTs)

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8
Q

Define dermatophytosis.

A

Superficial fungal infection with varying presentation depending on site. Dermatophytes are fungal organisms that require keratin for growth.

These fungi can cause superficial infections of the hair, skin, and nails. Dermatophytes are spread by direct contact from other people, animals, soil, and from fomites.

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9
Q

How common are dermatophyte infections?

A

Varies

Tinea pedis is the most common of the superficial fungal infections, occurring in up to 70% of adults

Tinea capitis is most common in children and tinea cruris in adolescents and adult men.

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10
Q

How do dermatophyte infections spread?

A
  • Directly from one person to another
  • Soil to human
  • Animal to human
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11
Q

What are the risk factors for dermatophyte infections?

A

Host factors

  • Genetic susceptibility, including atopy
  • Ethnicity
  • Immunosuppressive illnesses or medications (e.g., HIV infection, corticosteroids)
  • Presence of other skin diseases that disrupt the epidermis (e.g., atopic dermatitis)
  • Other illnesses that predispose to skin infection, including diabetes mellitus and peripheral vascular disease.

Local factors

  • Sweating
  • Occlusion
  • Occupational exposure
  • High humidity (tropical or semi-tropical climates)
  • Exposure to infected pets or farm animals, infected fomites, skin contact with the floors of public bathing facilities
  • Contact sports such as wrestling.
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12
Q

What is the pathophysiology of dermatophyte infections?

A
  • Exposure to infected desquamated cells occurs by direct contact
  • Inoculation occurs through breaks in the skin
  • Dermatophyte fungi enter, germinate and produce keratinases
  • They invade the superficial skin layers
  • The fungi require keratin for growth
  • The are restricted to hair, nails, superficial skin
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13
Q

What is the common name for dermatophyte infection?

A

Ringworm

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14
Q

What are the general clinical features of dermatophyte infection?

A
  • Rash - annular, central clearing with an active border of inflammation. Satellite lesions.
  • Scaling lesions with patchy alopecia
  • Follicular pustules
  • Fissuring, maceration and scaling in interdigital spaces of the fourth and fifth toes
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15
Q

What is the diagnosis?

A

Psoriasis - annular lesion on the elbow, with a silvery scale. No central clearing. Microscopic examination with potassium hydroxide revealed no fungal elements.

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16
Q

What are the clinical features of tinea capitis?

A
  • a cause of scarring alopecia mainly seen in children
  • if untreated a raised, pustular, spongy/boggy mass called a kerion may form
  • most common cause is Trichophyton tonsurans in the UK and the USA
  • may also be caused by Microsporum canis acquired from cats or dogs
17
Q

How do you diagnose tinea capitis?

A

Wood’s light exam - Lesions due to Microsporum canis casuse green fluorescence.

Scalp scrapings - the most useful investigation

18
Q

What is the management of tinea capitis?

A

Oral antifungals for 4-6 weeks
Terbinafine - for trichophyton tonsurans infections
Griseofulvin - for Microsporum infections

Topical ketoconazole shampoo - given for first 2 weeks to reduce risk of transmission

19
Q

What are the most common organisms causing tinea capitis?

A

Trichophyton tonsurans - most common
Microsporum canis - from cats or dogs

20
Q

What are the most common organisms causing tinea corporis?

A

Trichophyton rubrum and Trichophyton verrucosum e.g. from contact with cattle

21
Q

Which organism causes of ringworm do not fluoresce under Wood’s lamp?

A

Trichophyton species

22
Q

What is the management of tinea corporis?

A

1st line: Topical terbinafine 1% for 1-3 weeks
2nd line: Other topical antifungal e.g. miconazole 2% for 2-4 weeks and 1-2 weeks after infection subsides
3rd line: Oral antifungal e.g. terbinafine 250mg oral OD 2-4 weeks

23
Q

What is the management of tinea unguium?

A

1st line: Systemic terbinafine therapy - 12 weeks for toenails, 6 weeks for fingernails
2nd line: Systemic azole or topical e.g. fluconazole or ciclopirox topical

24
Q

What are the complications of dermatophyte infections?

A
  • Kerion
  • Bacterial infection associated with tinea pedis
25
Q

Define pityriasis versicolor.

A

Pityriasis versicolor, also called tinea versicolor, is a superficial cutaneous fungal infection caused by Malassezia furfur (formerly termed Pityrosporum ovale)

26
Q

What is the cause of pityriasis versicolor?

A

Malassezia furfur

27
Q

What are the risk factors for pityriasis versicolor?

A
  • High ambient temperature and humidity
  • Adolescent/young adult
  • Hyperhidrosis
  • Systemic corticosteroids or other immunosuppressants
  • Athletics
  • Greasy skin

NB: Malassezia are part of normal skin microbiota which usually grow on seborrhoeic areas e.g. scalp, face and chest.

28
Q

What are the clinical features of pityriasis versicolor?

A
  • No pruritus/pain
  • Dyspigmentation - hypopigmentation or hyperpigmentation
  • Macules or patches
  • Seborrhoeic distribution
  • Fine overlying scale
29
Q

What is the appearance of PV under Wood’s light?

A

Yellow or gold - but only positive in a third of cases

30
Q

How do you diagnose pityriasis versicolor?

A

Microscopy of scarpings with KOH preparation - shows short hyphae and spores on microscopy

Other:

  • Skin biopsy - hyphae and budding yeast forms within the stratum corneum
  • Culture on Dixon’s media
Microscopy of scrapings with KOH
31
Q

What are the differentials for PV?

A
  • Vitiligo
  • Tinea corporis
  • Seborrhoeic dermatitis - yeast may also be present on KOH preparation
  • Pityriasis rosea/alba
32
Q

What are the complications of PV?

A

Dyschromia - pigmentary abnormalities

32
Q

What is the management of PV?

A

1st line: Topical therapy e.g. pyrithione zinc OR selenium sulfide OR ciclopirox OR terbinafine topical
+/- UV light - for hypopogmented
2nd line: Systemic antifungal e.g. fluconazole

33
Q

What is the prognosis with PV?

A

Spontaneous resolution is uncommon
Usually persists for years if left untreated
Pigmentary abnormalities may take 6 weeks to improve after treatment
Recurrence is common