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Multisystems > Micro- Cutaneous & Subcutaneous Mycoses > Flashcards

Micro- Cutaneous & Subcutaneous Mycoses Flashcards

1
Q

What are superficial mycoses?

A

non-invasive and minimally symptomatic infections of the most superficial layers of keratin of skin and hair.

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2
Q

What age group is typically affected by pityriasis [tinea] versicolor? Why?
How does it present?
What environmental factors affect it?
What is the infectious agent?

A

It classically affects young people at the beginning of puberty as the result of hormonal changes and increased sebum production.

It presents with multiple macules of variable appearance [but usually hypopigmented] surrounded by normal skin.

High temp and humidity favor tinea versicolor.

The infectious agent : malassezia furfur

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3
Q

A patient presents with black spots on the palms and soles. What fungal infection could this be?
What is the causative agent?

A

Tinea nigra- caused by Hortaea werneckii [a fungus native to soil, compost, and woods in the tropics]

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4
Q

What is Piedra?

A

nodules outside of the hair shaft [ectothrix]

Black - piedra hortae
White- trichosporon

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5
Q

How is tinea versicolor diagnosed? Confirmed?

A

Diagnosis: clinical appearance

Confirmed with:

  1. Wood’s lamp which shines UV light at 365 nm. Yellow/green fluorescence = active lesion
  2. scrapings reveal “spaghetti and meatball” appearance
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6
Q

How is tinea versicolor treated?

A

Topical agents:

  1. selenium sulfide
  2. terbinafine
  3. topical azoles

Oral treatment if topical fails:

  1. ketoconazole
  2. itraconazole
  3. terbinafine
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7
Q

What agent causes tinea versicolor?
What does a skin sample look like?
Why can the agent not be cultured?

A

It is causes by malassezia furfur.
Skin sample will have a “spaghetti and meatball appearance”
It cannot be cultured because it is lipophilic [if you add olive oil it can be cultured in 3-7 days]

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8
Q

What layer of the skin do dermatophytes invade?
How do they appear clinically?
How are they classified?

A

They invade the superficial stratum corneum of the skin, hair and nails.
They appear as serpentine or annular lesions with raised margins.
They are classified by the body region involved

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9
Q

What infectious agents cause tinea capitis?
What area of the body is affected?
What factors contribute to acquiring this infection?
Where can this disease be an epidemic?

A
  1. Microsporum canis
  2. Trichophyton tonsurans

It affects the scalp.

Factors that lead to infection:

  1. poor hygiene
  2. prolonged moist skin
  3. minor skin or scalp injuries

disease can be epidemic in inner city children

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10
Q

What infectious agent causes tinea corporis?

A

Trichophyton

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11
Q

A patient presents with athlete’s foot characterized by itching, erythema scaling, and edema. What is the cutaneous infection?
What agent most likely caused it?
What predisposes to this infection?

A

Tinea pedis caused by:

  1. Epidermophyton
  2. Trichophyton

Predisposing factors:

  1. bad hygiene
  2. tennis shoes with wet skin
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12
Q

What is tenia barbae?

A

Infection of the bearded area in men which appears as:

  1. follicular inflammation
  2. chronic cutaneous granulomatous lesion
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13
Q

What is tinea faciei?

A

dermatophyte infection of the face NOT involving the beard area

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14
Q

What is tinea unguium?

What infectious agent causes it?

A

dermatophyte infection of the nail bed caused by trichophyton

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15
Q

How does the infection pattern of zoophilic organisms differ from anthropologic organisms?

A

Zoophilic- affect exposed areas like the face, neck and arms

Anthropophilic - affect occluded areas of the skin or areas of trauma

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16
Q

Describe onychomycosis.
What are the 2 most common causes?
How does it differ from tinea unguium?

A

It refers to a non-dermatophyte nail infection or fungal nail infection caused by ANY fungus.

  • Scoplariopsis brevicaulis
  • Candida albicans

Tinea unguium can be applied ONLY if the infection is due to a dermatophyte.

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17
Q

Are dermatophytes monomorphic or dimorphic?
Describe the microbiology.
What are the 3 main types of conidia?

A

They are monomorphic fungi with a mycelial form and NO yeast form.

Dermatophytes are/have:

  1. keratinophilic
  2. colorless conidia
    - arthroconidia [infective form]
    - micro and macroconidia [diagnostic]
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18
Q

What are the 3 main pathogenic genera of fungi?
Are they anthropophilic, zoophilic or geophilic?
Describe the conidia of each.
What tinea do they cause?

A
  1. Microsporum canis
    - zoophilic
    - spindle shaped MACROconidia
    - tinea capitis
  2. Epidermophyton floccusum
    - geophilic
    - dumbbell-shaped MACROconidia
    - tinea pedis
  3. Trichophyton
    - anthropophilic
    - microconidia only
    - ALL tineas
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19
Q

For the dermatophytes, which species will cause hair to fluoresce a greenish-yellow color when exposed to UV light [+Wood’s sign]?

A

some species of microsporum

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20
Q

What will the dermatophytes look like with KOH prep and light microscopy?
Why is this technique used?

A

They will look like branching septate hyphae

KOH lyses mammalian cells by saponifying and solubilizing the lipid membrane, but fungal carb cell walls remain intact.

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21
Q

What are the 3 modes of transmission of dermatophytes?

How long does infected material remain infectious [and able to spread to others]?

A

[Humans, animals, soil]

  1. person to person [trichophyton]
  2. animal to human [microsporum]
  3. environment [epidermophytan]

Infected material remains infectious for greater than 1 year

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22
Q

Describe the pathogenesis of dermatophytes.

  1. What cells do they infect?
  2. what allows them to infect and breakdown this tissue?
  3. What is the most favorable environment for them to est. infection?
A
  1. Dermatophytes infect keratinized tissue [hair, skin, nails] but they are unable to invade LIVING layers of the epidermis due to the fact that they are unable to grow at body temperature [they stay in stratum corneum]
  2. ability to make keratinases and proteinases enables them to breakdown and invade keratinized tissue
  3. they favor humid or moist skin
23
Q

What is an “id reaction”?

A

When immunologically mediated reactions to the fungal antigens cause small, pruritic vesicles.

24
Q

What are the three techniques that are able to make a definitive diagnosis of dermatophyte infection?

A
  1. Wood’s light [microsporum]
  2. direct mount with KOH prep
    - branching septate hyphae from skin/fingernails
  3. culture **
    - Sabouraud’s dextrose agar [SDA] adjusted to 5.2pH
25
Q 
Describe how dermatophytes are cultured [agar, special growth needs, etc] 
How will the following look on the agar?
1. epidermophyton
2. trichophyton
3. microsporum
A

Cultured using Sabouraud’s Dextrose Agar [SDA] that has:

  • pH 5.2 [skin pH]
  • chloamphenicol and cycloheximide to inhibit bacteria and saprophytic moulds
  1. greenish-brown/khaki color with suede-like surface
  2. pale, yellowish-brown, reddish-brown from reverse of plate
  3. white from the top of the plate
26
Q

What is the treatment for dermatophyte infection of skin?

What is duration of therapy?

A

Topical [OTC, no prescription]

  1. undecylenic acid
  2. terbinafine
  3. tolnaftate
  4. miconazole, clotrimazole

Systemic:

  1. griseofulvin [rarely used due to hepatotoxicity and requirement for long treatment duration]
  2. terbinafine
  3. itraconizole, ketoconazole

Duration of therapy is a couple of weeks

27
Q

What oral agent used to treat dermatophyte skin infections is rarely used due to hepatotoxicity and requirement for long treatment durations?

A

Griseofulvin

28
Q

How does treatment of onychomycosis differ from treating skin fungal infections?
What are the 3 alternative treatment courses?

A
  1. topical therapy is INEFFECTIVE
  2. systemic therapy must last MONTHS not weeks

Treatment courses:

  1. griseofulvin or intraconazole daily for 90 days [fingers/toes]
  2. griseofulvin or itraconazole first week of the month for 4 months [fingers]
  3. terbinafine - incorporates into the growing nail so the discoulored nail doesn’t become normal, but normal nail replaces it so it takes 12 weeks for toes, 6 for fingers
29
Q

What is the mechanism of action of terbinafine in onychomycosis?

A

Terbinafine incorporates into the growing nail so with growth, the normal nail replaces the abnormal nail.

Duration is 12 weeks for toes, 6 for fingers

30
Q

What are the 3 main drugs to treat onychomycosis?
What is the side effect of all?
Which 2 are first line?

A
  1. griseofulvin
  2. itraconazole**
  3. terbinafine **

All three are hepatotoxic.
Itraconazole also interacts with p450s

31
Q

A patient was gardening and pricked herself with a rose thorn. Now she presents with a chronic, firm, non-healing nodule. Sometimes it ulcerates and oozes serous fluid. It spread slowly proximally along lymphatic vessels becoming firm and cord-like and appearing as a string of nodules in a linear arrangement. The lymph nodes do not seem to be involved.

What is the likely cause?

A

Sporotrichosis -

  1. minor trauma
  2. inoculation of fungi through skin
  3. growth in subcutaneous area –> nodules
  4. fungus spreads slowly along lymphatic vessels resulting in nodules in a linear arrangement
32
Q

What is the most common form of extracutaneous sporotrichosis in immunoCOMPETENT people?

What does it cause in immunoCOMPROMISED people?

A

COMPETENT
Osteoarthritis due to:
1. direct spread
2. hematogenous spread

COMPROMISED [HIV. sarcoidosis, malignancies, transplant] :

  1. disseminated disease –>
  2. osteoarticular
  3. pulmonary sporotrichosis
33
Q

What occurs when sporothrix schenckii conidia are inhaled?

A
  1. Subacute pneumonia

2. chronic cavitary pneumonia [looks like TB, histo]

34
Q

What is the infectious agent that causes sporotrichosis?
What kind of fungi is it [yeast, mold, dimorphic]?
What region is it more likely to occur?
How is it acquired?

A

Sporothrix schenckii is a dimorphic fungi.

It is worldwide but more likely in the tropics/subtropics

It is acquired by:

  1. direct inoculation into the skin
  2. rarely inhalation of conidia
35
Q

Sporothrix schenckii is a dimorphic fungus. Describe where each form grows?

Why is demonstration of the organism on tissue or skin biopsy difficult?

A
  1. Mould - compost soil, lab media at room temperature
  2. Yeast- infected subcutaneous tissue [ovoid/cigar-shaped; 3-5 microns], nutrient rich media at 37 degrees

Demonstration on biopsy is difficult because the organisms are NOT numerous. Most of the lesion size is a result of the host immune response.

36
Q

You are examining a specimen that when cultured on SDA at 22 degrees was a darkly pigmented mould. You stain it with lactophenol blue and see:

  1. slender hyphae
  2. microconidia in flora/daisy arrangement

What are you suspicious of?

A

Sporothrix schenckii

37
Q

Where is sporothrix schenckii found?

A

All parts of the world specifically in:

  1. sphagnum moss
  2. hay
  3. soil
38
Q

What organism is responsible for “rose handler’s disease”?

A

sporothrix schenckii

39
Q

Describe pathogenesis of sporotrichosis.

A
  1. skin is punctured by sphagnum moss, hay, rose thorn, etc
  2. localized infection with initial erythematous papulonodular lesion that are painless and less that 3cm
  3. spreads via lymphatic channels [though nodes are not involved] forming a chain of nodular lesions
40
Q

What is the histology of a nodular lesion of sporothrix schenckii?

A

suppurating granulomas:

histiocytes and giant cells surrounded by neutrophils, lymphocytes, and plasma cells

41
Q

Why can you not make a clinical diagnosis of sporotrichosis?

How is the lab diagnosis of sporothrix schenckii made?

A

You cannot rely on presentation along because bacterial infections mimic the presentation [actinomycotic, MAC]

  1. special histochemical stain for fungi [GMS silver]
  2. culture of a biopsy, pus or exudate on SDA showing microconidia with floral arrangement
42
Q

What is treatment for sporotrichosis?

A
  1. saturated solution of potassium iodide

2. itraconazole and terbinafine orally

43
Q

An immigrant presents with chronic raised, warty, scaly lesions on the legs. They are hyperkeratotic and hyperpigmented. They appear “cauliflower-like”.

What is the concern that this is?
How did this lesion occur and progress?
How long are lesions present before patients present for care?
What is a common sequelae?

A

Chromoblastomycosis is a chronic localized fungal infection of the skin and subcutaneous tissue.

  1. minor traumatic inoculation to the skin.
  2. small papule
  3. papule enlarges to form nodule with friable irregular surface
  4. spreads laterally with satellite lesions
  5. enlarge to encircle the leg and if extensive cause lymphatic obstruction

Patients usually present 1-3 years after infection.
Sequelae is bacterial superinfection

44
Q

What do the organisms that cause chromoblastomycosis have in common?
Where is their habitat?
What is the most common cause?

A

A large number of organisms can cause these infections but are all:
dematiaceous fungi [dark-walled, pigmented fungi] that grow in soil, wood, vegetation and produce melanin

The most common cause: Fonsecaea pedrosoi

45
Q

How is diagnosis made for chromoblastomycosis?

A
  1. skin scrapings and punch biopsies
    Stains:
    H&E = large clusters of fungal cells that are naturally brown due to melanin production
    GMS = hyphae
  2. culture on SDA
    - 4 weeks to grown
    - characteristic brown pigment
46
Q

What is treatment for chromoblastomycosis?

How long is it given?

A
  1. itraconazole
  2. terbinafine

6 months to a year

47
Q

What region is most likely to have mycetoma [madura foot, maduromycosis]?
What people are most frequently affected?

A

It is in tropical and subtropical areas in South Asia, Africa and South and Central America.

Most cases occur in males 20-40 with outdoor occupations that expose them to environmental trauma and implantation of soil into the skin

48
Q

A patient presents with a swollen foot with draining sinus tracts, and the production of granules in the tracts.

What is this and what would it look like on histology?
What layers of tissue can be involved?

A

Madura foot, maduromycosis, mycetoma

It is a chronic, progressive granulomatous infection of:

  • skin
  • subcutaneous tissue
  • underlying bone
49
Q

Describe the pathogenesis of mycetoma.

A
  1. minor trauma
  2. acute inflammation, but PMNs cannot engulf and destroy organisms
  3. granulomatous inflammation with macrophage derived cells and lymphocytes
50
Q

What is the incubation period for mycetoma?
How does it spread?
What skin changes do you notice?

A

Incubation is 5-10 years.
It spreads to involve deep soft tissue and contiguous bone.
The overlying skin changes color [hypo or hyper] but is NOT erythematous or warm [showing it is chronic and not acute]. Sinus trancts are present.

51
Q

What are the 2 main agents that can cause mycetoma?

How do they differ?

A
  1. Actinomycotic
    - filamentous bacteria like nocardia, actinomadura, streptomyces
  2. eumycotic
    - fungi
    - white grain = pseudoallascheria boydii
    - dark grain = pigmented dematiaceous fungi
52
Q

How is diagnosis of mycetoma made?

A
  1. epidemiology, long duration of symptom
  2. painless soft tissue swelling
  3. sinus tracts with grains in the drainage
  4. culture of the drainage
53
Q

What is treatment for mycetoma?

A
  1. Eumycotic = terbinafine, itraconazole, voriconazole for several months to a year
  2. amputation if necessary

Multisystems (29 decks)

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