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MSII Micro Unit 2 > Superficial, Cutaneous, and Subcutaneous Mycoses > Flashcards

Superficial, Cutaneous, and Subcutaneous Mycoses Flashcards

1
Q

What are the superficial/ cutaneous mycoses?

A
  • Dermatophytosis
  • Tinea Versicolor
  • Tinea Nigra
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2
Q

What are the subcutaneous mycoses?

A
  • sporotrichosis
  • chromomycosis
  • mycetoma
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3
Q

What is the opportunisitc mycosis?

A

-candidiasis

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4
Q

What are molds?

A
  • they are asexual or sexual reproduction with spores

- multicellular: not very mobile in the body

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5
Q

What are the yeasts?

A
  • asexual by budding
  • single-celled: can circulate
  • resistant to phagocytosis
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6
Q

What are the organisms involved with dermatophytosis?

A
  • dermatophytes
  • infect only superficial keratinized structures- skin, hair, nails
  • three major genera- Epidermophyton (direct contact), Trichophyton (direct contact), Microsporum (direct contact, also zoonosis from pets)
  • all three produce keratinases that allow invasion of the cornified cell layer
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7
Q

What is the pathogenesis of dermatophytosis?

A
  • from chronic infections in warm, humid areas on body surface- mold form
  • inflamed circular border of papules and/or vesicles, broken hairs, thickened broken nails
  • skin within border may be normal
  • named for affected body part: Tinea capitis (head), Tinea corporis (ringworm), Tinea cruris (Jock itch), Tinea pedis (Athlete’s foot)
  • transmitted by fomites or by autoinoculation from other sites on body
  • no morbidity results from the primary infection, but prolonged itching can lead to bacterial superinfection
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8
Q

What is a dermatophytid reaction?

A
  • hypersensitive dermatophytid reactions: vesicles on fingers
  • caused by hypersensitivity to circulating fungal antigen
  • vesicles do not contain live fungus or spores
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9
Q

How is dermatophytosis diagnosed?

A
  • exam: itching, redness, history of tight or wet clothing
  • microscopic exam: scraping from affected skin or nail, treat with 10% KOH, examine remains for hyphae and spores
  • culture on Sabourand’s agar at room temp
  • PPD with trichophytin
  • microsporum show fluorescence when examined under Wood’s lamp
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10
Q

How do you treat dermatophytosis?

A
  • topical antifungal cream- Terbinafine, Undecylenic acid, Micronazole, Tolnaftate
  • treat all affected body sites simultaneously
  • alternate: oral griseofulvin
  • keep skin dry and cool
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11
Q

What is the pathogenesis in tinea versicolor?

A
  • common overgrowth of dimorphic normal flora Malassezia furfur or globosa
  • superficial skin infection only cosmetic importance
  • hypopigmented or hyperpigmented areas with slight scaling/itching
  • usually on trunk, back or abdomen
  • most frequent in hot, humid weather
  • other presentations (face, extremities, folliculitis) may occur, particularly with immunocompromise
  • family often has a history o infection- uncharacterized genetic predisposition
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12
Q

How do you diagnose Tinea Versicolor?

A
  • take skin scrapings: light scraping of the area with a scalpel blade releases lots of keratin
  • treat scrapings with 10% KOH and stain
  • examine microscopically for mix of budding yeasts and short cigar butt hyphae
  • examination with wood lamp may show coppery-orange fluorescence
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13
Q

How do you treat tinea versicolor?

A
  • Topical selenium sulfide or azole used daily for 2 weeks
  • tends to recur, repeat as needed
  • alt: oral azoles
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14
Q

What is the pathogenesis of Tinea Nigra?

A
  • Organism- look for weneckii
  • spores in soil enter injury
  • germinate in the keratinized skin layers
  • generate a brown pigment which appears as a brown spot
  • seen in southern coastal US, mostly peds, not comon
  • may alarm with resemblance to melanoma, but benign and curable
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15
Q

How is Tinea Nigra diagnosed?

A
  • patient reports new brown spot on an extremity, may itch slightly, possible travel to Caribbean, Asia, Africa
  • take skin scrapings, treat with 10% KOH and examine microscopically for thick, septate, branching hyphae with dark pigment in their walls
  • culture on Sabourand’s agar at room temp. Yeastlike shiny black colonies grow in about 1 week, form mix of yeast and septate hyphae
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16
Q

What is the treatment of Tinea Nigra?

A

-treat with topical keratolytic agent (Salicyclic acid) to break down infected skin and a topical azole

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17
Q

What is the organism that causes Sporotrichosis?

A
  • Sporothrix schenckii and other species
  • Thermally dimorphic
  • found on vegetation
  • often seen in gardeners, particularly of roses (thorns) “rose-picker’s disease”
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18
Q

What is the pathogeneis of Sporotrichosis?

A
  • introduced into skin by thorn puncture
  • yeasts grow at site and form painless pustule or ulcer
  • draining lymphatics form suppurating subcutaneous nodules
  • symptoms wax and wane over years
  • may progress to disseminated disease and meningitis if immunosuppressed
  • patients with COPD and long term corticosteroid use may develop pulmonary symptoms from inhaling the spores; difficult to distinguish from TB or histoplasmosis
19
Q

How does Sporotrichosis look on exam?

A
  • painless pustule or ulcer on hand or arm: reddish, necrotic, nodular papules may extend along lymphatic from initial injury site
  • history of gardening, farming, landscaping, berry-picking
  • history of ineffective antibiotic treatment
  • in AIDS, may see nodules disseminated over whole body
  • in COPD + alcholism, respiratory distress
20
Q

What are the labs for Sporotrichosis?

A
  • tissue biopsy: round or cigar-shaped budding yeasts- hard to see
  • culture at room temp from pus, biopsy: hyphae with oval conidia in clusters at tip of slender conidiophores (resembles a daisy)
21
Q

What is the treatment and prevention for Sporotrichosis?

A
  • treatment: 3-6 months itraconzaole or other azoles for normal form of disease
  • for more serious types, admit for Amphotericin B
  • prevention: gardening gloves
22
Q

What is the organism for Chromomycosis?

A
  • also called chromoblastomycosis or dermititis verrucosa
  • caused by a variety of dermatiaceous fungi: Fonsecaea, Phialophora, Cladosporium
  • found in soil in the tropics
  • condidia or hyphae are gray or black
23
Q

What is the pathogenesis for Chromomycosis?

A
  • introduced into legs or feet with injury by wood splinters or thorns
  • gradually progressive subcutaneous disease
  • granulomas form as immune system attempts to contain
  • wartlike lesions gradually spread from initial site over years
24
Q

How does Chromocysosis look on exam?

A
  • history of farming, travel to tropical locations
  • warlike dark colored lesions
  • crusting abscesses extending along lymphatics
  • black dots scattered among lesions
  • secondary infection with bacteria produces an ill odor and elephantiasis
25
Q

What labs are used for Chromomycosis Diagnosis?

A
  • KOH mount from skin scraping: dark colored septate hypache or conidia
  • Biopsy: H and E stain for dark brown, round fungal cells inside leukocytes or giant cells
  • ELISA is available for some species
26
Q

How is Chromomycosis treated or prevented?

A
  • hard to treat sucessfully
  • oral flucytosine and/or itraconazole
  • combine with local surgery: cryosurgery can be effective
  • topical application of heat from pocket warmers also helps reduce and reverse fungal growth over months
  • prevention: shoes
27
Q

What is the organism to cause Mycetoma?

A
  • organism: Petriellidium or Madurella
  • found in soil
  • enters through wounds
  • rare in US
28
Q

What is the pathogenesis of Mycetoma?

A
  • replicating fungi form abscesses
  • pus containing compact colored granules forms and drains through the local sinuses
  • looks very similar to actinomycosis, forms in foot, lower leg, or hand rather than face
  • granulomatous inflammatory response in the deep dermis and subcutaenous tissue may extend to bone
  • after years of infection, initial painless nodule swells and bursts, becomes painful
29
Q

How is Mycetoma Diagnosed?

A
  • need biopsy for culture
  • H and E staining of biopsy reveals grains in pus
  • Xray to determine whether bone is involved
  • differentiate from actinomycosis by staining
  • tissue gram stain to detect fine, gram-positive, branching filaments within the actinomycetoma grain
  • Gomori methanamine silver or periodic acid-Schiff stain to demonstrate the larger hyphae of eumycetoma
30
Q

How is Mycetoma Treatment?

A
  • first attempt antifungal therapy: admit for initial IV Amphotericin B
  • add antibiotics for secondary infections, send home with oral azole
  • surgical excision of abscesses usually necessary
31
Q

What is the organism that causes Candidiasis?

A
  • primarily Candida albicans
  • largely yeastlike, oval with single bud
  • may also appear as pseudohyphae or hyphae when invading tissues
32
Q

What is the pathogenesis of Candidiasis?

A
  • Virulence factors: adhesins for surface attachment, acid proteases and phospholipases for tissue invasion, phenotypic switching/morphogenesis: changes antigen expression and tissue affinity
  • syndromes range from trivial superficial to life-threatening systemic; may involve any anatomical structure
  • ubiquitous normal flora: difficult for laboratory to diagnose as a pathogen
33
Q

Diaper rash

A

-dampness from wet diapers predisposes to overgrowth of Candidia

34
Q

Vaginitis

A
  • overgrowth of candidiasis leading to itching and curdlike discharge
  • cervix is normal on exam
  • predisposition by antibiotics, diabetes
  • may spread to male partner, who develops penile vesicles, white spots
35
Q

Thrush/Esophagitis

A
  • overgrowth of candidiasis leading to pseudomembrane formation in the mouth
  • predisposition by steroid inhalers for asthma
  • inevitable in HIV+ patients not on HAART
  • generally not dangerous, but can contribute to wasting cycle in AIDS
36
Q

What are the less common pathogenesis for Candidiasis?

A
  • skin with overgrowth becomes red and wet; may be seen on fingers in dishwashers, buttocks in diapered infants, nail beds in diabetics who soak their hands or feet; any skin fold that stays warm and wt (intertrigo)
  • folliculitis: forms a boil
  • infection of entire GI may occur with leukemia and lymphoma
37
Q

Chronic mucocutaneous candidiasis

A
  • arises with impaired CMI
  • genetic predisposition to low interferon gamma, interluekin 2, 17, and or 22
  • persistent refractory cutaneous infections, little dissemination
38
Q

Systemic and Disseminated Infections pathogenesis

A
  • candidas are the 4th most common isolate from blood cultures
  • incidence increasing with vulnerable population: ICU, complex surgeries, indwelling vascular devices, cancer survivors, immunosuppressed
  • about 50% Candida albicans, then C. glabrata (more drug resistant), C. krusei (intrinsic resistance to azoles and less susceptible to all antifungals), C. lusitaniae (intrinsic resistance to Amphotericin B), C. parapsilosis (common in infections of vascular catheters), C. tropicalis (often seen in leukemia patients)
39
Q

Candidemia

A
  • systemic candidiasis
  • usually nosocomial with underlying major illness
  • fever unresponsive to broad spectrum antibiotics
  • history of catheterization
  • endocarditis with large septic emboli to major organs
  • may see symptoms of Candida on skin or mouth
  • blood cultures positive
  • 30-40% mortality
40
Q

Disseminated candidiasis with organ invasion

A
  • one or more deep organs infected: eye, kidney, CNS, joints, muscles, heart/pericardium, peritonium, spleen
  • blood cultures often negative
  • fever unresponsive to broad-spectrum antibiotics
  • sepsis/septic shock
  • mortality even higher
41
Q

Candidiasis on Exam

A
  • Skin: red, wet, itchy surfaces, risk factors
  • GI: endoscopy
  • Liver/spleen: ultrasound, CT
  • Abdomen, kidney: CT
  • Endocarditis: echo (vegetations are often large, easy to detect)
  • Tissue biopsy- often helpful, use bronchoalveolar lavage for lungs
42
Q

How to identify Candidiasis on lab

A
  • Exudates and Biopsies- visualize mix of budding yeasts, pseudohyphae, and hyphae; gram-positive; visualized by KOH smear, calcofluor-white, methylene blue stain, H and E
  • culture- on agar, large colonies form, yeast colonies look similar to bacterial
  • in serum 37C- germ tubes form
  • positive culture results from sterile sites are diagnostic
  • culture from nonsterile sites (GI, respiratory, urinary) may still give evidence of increased colonization
  • in refractory cases, including all AIDS, antifungal susceptibility testing
  • Bloodwork: blood cultures for disseminated, urinalysis for colonization or kidney infection, liver/spleen- serum alkaline phosphatase, serum assays for several cell wall components (beta-glucan, mannan) are available, sensitivity and specificity vary widely
  • if disseminated disease is suspected- persistent leukocytosis, neutropenia, other risk factors, fever remaining despite antibiotic coverage
43
Q

Treatment for Candidiasis

A
  • many of them require fluconazole, or alternates
  • surgical care- drain abscesses, prosthetic joint infection requires joint removal, endocarditis requires valve replacement
  • supplement drug treatment by reducing predisposing factors

MSII Micro Unit 2 (7 decks)

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