Mycoses (9) Flashcards
What are the cutaneous mycoses?
Dermatophytoses, Tinea vesicolor, tinea nigara
What causes dermatophytoses?
Dermatophytes
What do dermatopytes infect?
Superficial keratinized structures only!
skin, hair, nails
What is the virulence factor of dermatophytes?
Keritinase–> allows invasion of the cornified cell layer
What are the 3 major genera of dermatophytes? How are each spread?
Epidermophyton (direct contact)
Trichophyton (direct contact)
Microsporum (Direct contact, zoonosis from pets)
Describe how dermatophytosis presents?
Forms chronic infections in warm, humid areas of body surface
Inflammed circular border of papules and or vesicles (skin w/in can be normal)
Broken hairs, thickened/ broken nails
What can be found in some patietns with dermatophytosis that are hypersensitive?
They can form “id” reactions–> vesicles on fingers
They are caused by circulating fungal antigen.
Do “id” vesicles contain live fungus or spores?
No
What can happen due to prolonged dermatophytosis?
bacterial superinfection
How do you diagnose dermatophytosis?
PPD w/ trichophyton
Microskope exam of scraping and KOH mount–> you will see hyphae and spores
Culture on sabouraud’s ager at room temp
Microsporum under wood’s lamp
How is dermatophytosis treated?
Topical antifungal cream
(**need to treat all affected areas simultaneously)
Oral griseofulvin
Keep skin dry and cool
What causes tinea versicolor?
Malassezia furfur or Malessezia globosa
Importance of Tinea versicolor?
Superficial skin infection only of cosmetic importance. It is an overgrowth of normal flora.
How does tinea versicolor present?
Hypopigmented areas w/ slightly scaling/ itching
Seen in hot, humid weather
There is also an uncharacterized genetic component (seen in families)
How is tinea versicolor diagnosed?
Microscope exam: Skin scraping w/ KOH mount–> you will see yeast and hyphae
Wood lamp will show coppery-orange fluorescence
Treatment of tinea versicolor?
Topical selenium sulfide or azole used daily for 2 weeks
What causes tinea nigra?
Cladosporium weneckii
What is the pathogenesis of tinea nigra?
1- spores in soil enter injury
2- Germinate in the keratinized skin layers
3- Generate a brown pigment which appears as a brown spot
Who is tinea nigra mostly seen in?
Soutern coastal US and mostly in children.
Overall, it is not common
Diagnosis of tinea nigra?
Microscope: skin scraping and KOH mount will show tick septate branching hyphae with dark pigment on their walls
Culture: sabourd’s agaer–> yeast like shiny black colonies grow in 1 week
Treatment of tinea nigra?
Topical keratolytic agen (like salicylic acid)
Topical azole
What are the subcutaenous mycoses? And how are they contracted?
Sporotrichosis
Chromocycosis
Mycetoma
Introduced by trauma exposing subcutaenous tissue to soil or vegitation
What causes sporotrichosis?
What is special about the organism?
What is another name for this diease?
Sporothrix schenckii
It is thermally dimprophic.
“rose picker’s disease”
Pathogenesis of sporotrichosis?
Introduced into the skin by thorn puncture.
Yeasts grow at sites and form painless pustule or ulcer.
Draiing lymphatics form suppurating subcutaneous nodules
May progress to disseminated disease and meningitis if immunosuppressed
What happens in patients with COPD and those on corticosteroids with a sporotrichosis infection?
They may develop pulmonary symptoms from inhaling the spores (which is difficut to distiguish from TB or histoplasmosis)
How is sporotrichosis diagnosed in exam?
Painless pusule/ ulcer (usually on hand or arm)
History of gardening
History of ineffective antibiotic treatment
How is sporotrichosis diagnosed in the lab?
Tissue biopsy–> shows round or cigar-shaped budding yeasts
Culture of pus/ biopsy at room temp–> shows hyphae “daisy chains”
Treatment of sporotrichosis?
2- months of intraconazole or oral azoles
More serious need amphotericin B
Where is chromomycosis seen?
Found in soil of the tropics
Pathogenesis of chromomycosis?
Introduced into legs or feet with injury by wood splinters or thorns
Gradually progressive dubcutaneous disease
Granulomas from as immune system attempts to contain the infection
Wartlike lesions gradualy spread from initial site
What will physical exam show for chromomycosis?
History or travel
Wartlike dark colored lesions
Crusting abscesses extending along lymphatics
How does lab diagnose chromomycosis?
KOH mount shows dark colored septate hyphae or condidia
Biopsy shows dark brown, round fungal cells inside leukocytes or giant cells
ELISA
How is chromomycosis treated?
Oral flucytosine and or itraconazole
Local surgery
Which two mycosis have dark colored hyphae?
tinea nigra and chromomycosis
What causes mycetoma? Where are the organisms found?
Petriellidum or Madurella
Found in soil but rare in the US
Pathogenesis of mycetoma?
Replicating fungi form abscesses
Pus containing compact colored granules forms and drains through the local sinuses
Granulomatoous inflammatory response in the deep dermis and subcutaenous tissue may extend to the bone
What can mycetoma resemble and how can it be differentiated?
Resembles actinomyces
Forms in foot, lower leg or hand, rather than the face
actinomyces are smaller and are gram +
mycetoma causing fungi are larger and appear in fugal stains
How is mycytoma diagnosed?
Needle biopsy for culture
H&E stain will show grains in pus
X ray to determine whether bone is involved
How is mycetoma treated?
First attempt antifungal/ antibiotic therapy
Surgical excision of abscess is sometime needed
Name a cutaenous and opportunistic mycosis?
Candisiasis
Describe candidia?
Yeastlike, oval w/ single bud
May also appear as psuedohyphae or hyphae when invading tissues
Virulence factors of candidia?
Adhesins for surface attachment
Acid proteases and phospholipases for tissue invasion
Phenotypic switching/ morphogenesis
Symptoms of candidiasis? Common conditions caused by candidia?
Range from trivial superficial to life-threatening systemic.
Diaper rash, vaginitis, thrush/ esophagitis
Pathogenesis of diaper rash?
dampness from wet diapers predisposing to overgrowth
Pathogenesis of vaginitis?
Overgrowth leading to itching and curdlike discharge
Pathogenesis of thrush?
Overgrowth leading to psuedomembrane formation in the mouth
Who is predisposed to thrush?
Steroid inhaler users
HIV + patients not on HAART
Name some less common presentations of candidasis?
Skin–> overgrowth becomes red and wet, may be seen on fingers in dishwasers, butt of infants, nail beds in diabetics
Folliculitis–> forms a boil
Chronic mucocutanous candidiasis–> seen in people with impaired CMI
GI infection–> may occur with leukemia/ lymphoma
T/F: systemic and disseminated infections of cancidiasis is rare
Once true, but they are now increasing
Pathogenesis of systemic candidiasis (candidemia)?
Usually nosocomial with underlying major illness
Fever unresponsive to broad-spetrum antibiotics
History of cathetarization
Endocarditis is seen, also symtoms on skin or moth
30-40% mortality
Pathogenesis of disseminated candidiasis (w/ organ invasion)?
One or more deep organs infected (eye, kidney, CNS, joints, muscles, heart/ pericardium, peritonium, spleen)
Blood cultures are often negative
Fever unresponsive to broad-spectrum antibiotics
Mortality is very high
How does the lab make the diagnosis of candidiasis?
Exudates and biopsies show: Mix of budding yeasts, psuedohyphae, and hyphae. Gram positive.
Visualized by KOH smear, calcoflour white and methylene blue stain
Cultures show: Colonies are large
Bloodwork: will sometimes be positive for disseminated infection
Can candidia develop drug resistance?
Yes, antifungal resistance is common
How are candida infections treated?
Treatment ramps up with severity:
Topical azoles and polyenes for superficial
Oral azoles for more serious but not life threatening
Add amphoteracin B for more life threatening
Add echinocandins and/ or voriconazole for life threatening drug resistant
