Microbiology - Greenblatt - Superficial, Cutaneous, Subcutaneous Mycoses Flashcards Preview

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Flashcards in Microbiology - Greenblatt - Superficial, Cutaneous, Subcutaneous Mycoses Deck (43):

What are dermatophytoses? What are these cutaneous mucoses commonly referred to as?

superficial/cutaneous fungal infections (mycoses) caused by dermatophytes Ringworm, tinea


dermatophytoses are restricted to where? Why? How are they spread?

dermatophytes only infect the superficial keritinized structures (skin, hair, nails) lack virulance structures needed to penetrate skin spread is through direct contact with fomites or by auto-innoculation from other sites on the body **microsporum can be transferred via zoonosis (i.e. from animals to humans) usually from pets


What would direct contact to Epidermophyton result in?

dermatophytosis of the superficial keritinized structures (skin, hair, nails).


What would direct contact to Trichophyton result in?

dermatophytosis of the superficial keritinized structures (skin, hair, nails).


After playing with your dog you develop an inflamed circular boarder of papules and vesicles surrounding normal appearing skin in the groin region. Initially you suspected it was a reaction the peanut butter, but then you also noticed weird bumpy vesicles on your fingers. After weeks of it failing to respond to over the counter antibiotic ointment you shamefully called your dermatologist. What was the diagnosis? What type of organism was responsible? What type of reaction took place that caused the finger vesicles? What could you have done instead of going to the dermatologist? What woud be the worse side effect of not treating the infection?

Tinea cruris (jock itch) -- Dermatophytosis of the Jock region Microsporum fungi- only genera of cutaneous dermatophytes that exhibit zoonosis (transfer from animals) - form chronic infections Hypersensitivity reaction to circulating fungal antigen (vesicles do not contain live fungus or spores) Over the counter antifungal cream No morbidity results from primary infection, but progressive itching can lead to bacterial superinfection (infection occurring after or on top of an earlier infection)


After walking around the locker-room with bare feet you develop a rash with an inflamed cirular boarder of papules and vesicles surrounding normal appearing skin. The condition does not go away with over the counter antibiotic cream and eventually turns into dry flaky skin. What is the Dx? Mode of transmission? Virulance factor?

Dermatophytosis (tinea pedis - athletes foot) direct contact keratinases that allow invasion of the cornified cell layer


Can dermatophytes penetrate human skin?

No. Only keratinases that permit invasion of cornified cell layer of superficial keratinized structures (hair, skin, nails).


What are the most likely body regions you will find dermatophytosis? Why?

Warm humid areas (armpits, groin etc) Not fully resistant to cold and dry conditions


How is dermatophytosis diagnosed?

Take scraping from affected skin or nail, treat with 10% KOH, examine remains for hyphae (filamentous structure of a fungus) & spores Culture on sabourauds agar at room temp PPD with trichophytin Microsporum show fluorescence when examined under Wood's lamp


i. Superficial skin infection of only cosmetic importance ii. Hypopigmented areas with slight scaling/itching on trunk back or abdomen (may occur with immunocompromise and has an uncharacterized genetic predisposition) iii. Most frequent in hot, humid weather What is it, how is it diagnosed, how is it treated?

tinea versicolor caused overgrowth of normal flora (by Malassezia furfur or glabosa) Take skin scrapings and treat w/ 10% KOH Examine microscopically for mix of budding yeasts and "cigar butt" hyphae Selenium sulfide (selson blue) Topical or oral miconazole


Inflamed circular border of papules and/or vesicles on body with normal skin inside and broken hairs

Tinea corporis


Inflamed circular border of papules and/or vesicles on foot with normal skin inside and broken hairs. What if it was in groin region?

Tinea pedis (Athlete’s foot) Tinea cruris (Jock itch)


What is different about dermatophytosis and tinea versicolor

Dermatophytosis is aquired, versicolar is overgrowth of normal flora


i. Spores in soil enter injury ii. Germinate in the keratinized skin layers iii. Generate a brown pigment iv. seen in southern coastal US, mostly peds, not common v. resemblance to melanoma but benign and curable

Tinea Nigra - (from cladosporium weneckii)


What is diagnosis and treatment for Tinea Nigra?

c. Diagnosis i. Take skin scrapings ii. Culture on Sabouraud’s agar at room temp iii. Also treat w/ 10% KOH and examine microscopically for "Thick septate, branching hyphae with dark pigment in their walls" d. Treat with topical keratolytic agent (Salicyclic acid) plus topical azole


Tinea nigra, tinea vesicolor, and dermatophytosis are all what type of mycoses?



How are subcutaneous mycoses introduced?

trauma exposing subcutaneous tissue to soil or vegetation


Name this mycosis: Organism i. Thermally dimorphic ii. Found on vegetation iii. Often seen in gardeners, particularly of roses (thorns) Pathogenesis i. Introduced into skin by thorn puncture ii. Yeasts grow at site and form painless pustule or ulcer iii. Draining lymphatics form nodules iv. Symptoms wax and wane over years v. May progress to disseminated disease if immunosuppressed Diagnosis On Exam: i. Painless pustule or ulcer on hand or arm ii. History of gardening ii. Lab i. Tissue specimen: round or cigar-shaped budding yeasts ii. Culture at room temp: hyphae with oval conidia in culsters at tip of slender conidiophores (resembles a daisy) iii. Treatment: itraconazole (Sporanox) iv. Prevention: garden gloves



How does tinea nigra gain entry to body?

Person falls and scrapes themselves spores in soil enter keratinized skin layers


What mycosis is 1) contracted after falling and coming in contact with soil and 2) has microscopically detectable "Thick septate, branching hyphae with dark pigment in their walls"?

tinea nigra


Which characteristic is useful for lab diagnosis of tinea nigra? 1) appearance in acid fast stain 2)lactose fermentation 3)colony morphology

3 acid fast stain is used for TB and mycobacteria lactose fermentation is used for nisseria (prefers maltose) and enteric bacteria, useful for differntiating E. coli


What is "rose picker's disease"?

sporotrichosis - often seen in gardeners or anyone exposed to vegitation **Thermally dimorphic - means it is adapted to survive inside a warm blooded host


What is characteristic of the pathogenesis of sporotrichosis? Is this a cutaneous or subcutaneous mycosis?

Subcutaneous mycosis 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


How does sporotrichosis present?

Painless pustule or ulcer on hand or arm: reddish, necrotic, nodular papules may extend along lymphatic from initial injury site


What does sporotrichosis look like in culture (at room temp from pus, biopsy)?

hyphae with oval conidia in clusters at tip of slender conidiophores (resembles a daisy)


Name the mycosis! hyphae with oval conidia in clusters at tip of slender conidiophores (resembles a daisy)



What is treatment for sporotrichosis?

3-6 months itraconazole (Sporanox) or other oral azoles for normal form of disease For more serious types, admit for Amphotericin B


Name the mycosis! Caused by a variety of dermatiaceous fungi: Fonsecaea, Phialophora, Cladosporium Found in soil in the tropics Conidia or hyphae are gray or black



Describe the transmission and pathogenesis/progression of Chromomycosis

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


Name the mycosis! ▪ History of farming, travel to tropical locations ▪ Wartlike dark colored lesions ▪ Crusting abscesses extending along lymphatics ▪ Black dots scattered among lesions ▪ Secondary infection with bacteria produces an ill odor and elephantiasis



How is Chromomycosis diagnosed? What is treatment? Prevention?

KOH mount from skin scraping: dark colored septate hypahe or conidia Biopsy: H&E stain for dark brown, round fungal cells inside leukocytes or giant cells ELISA is available for some species Treatment: 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


How can you differentiate from chromomycosis and tinia nigra?

Both have dark-colored hyphae but ONLY tinea nigra grows at room temp (25C)


On biopsy what cells are fungal cells associated with in chromomycosis?

fungal cells can be found INSIDE leukocytes or giant cells


Name the mycosis! Organism: Petriellidium or Madurella Found in soil Enters through wounds Rare in US 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 subcutaneous tissue may extend to bone ▪ After years of infection, initial painless nodule swells and bursts, becomes painful ▪ On exam, shit looks fucking hideous.



How can you differentiate mycetoma from actinomycosis?

Tissue Gram stain plus Gomori methenamine silver or periodic acid-Schiff stain Actinomyces demonstrates gram positive staining of branching fillaments whereas madurella/Petriellidium have larger hyphae


What is the shape of candida albicans? What does infection cause?

Oval with single bud **may also appear as pseudohyphae or hyphae when invading tissues Infection causes candidiasis


What are the virulance factors for C. albicans?

▪ Adhesins for surface attachment ▪ Acid proteases and phospholipases for tissue invasion ▪ Phenotypic switching/morphogenesis : changes antigen expression and tissue affinity


Where can candidiasis develop?

any anatomical structure!


Why is C. albicans difficult for laboratory diagnosis as a pathagen?

Because it's a ubiquitous normal flora


What are some common presentations of candidiasis?

Diaper rash: dampness from wet diapers predisposes to overgrowth Vaginitis: ▪ Overgrowth 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 Thrush/Esophagitis: ▪ Overgrowth 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


What are some less common presentations of candidiasis?

Chronic mucocutaneous candidiasis arises with impaired cell mediated immunity; Genetic predisposition to low Interferon-gamma, Interleukin 2, 17, and/or 22 Persistent refractory cutaneous infections, little dissemination Infection of entire GI may occur w/ leukemia/lymphoma


Systemic candidiasis

Systemic Candidiasis = Candidemia 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


What is the treatment for Candidiasis?

Depends on the presentation: Thrush: fluconazole, alts caspofungin, micafungin Skin infection: topical antifungals: clotrimazole, nystatin Chronic mucocutaneous: oral azoles Vaginitis: intravaginal azoles: clotrimazole, micoazole, or oral fluconazole Kidney, UTI: fluconazole, if catheter-associated, remove/switch catheter Liver/spleen: Amphotericin B Disseminated w/o neutropenia: fluconazole Disseminated w/ neutropenia: Echinocandin or amphotericin B (must be liposomal if any kidney issues) ; voriconazole if need more mold coverage Fluconazole-resistant infections: echinocandins Surgical Care → Drain abscesses → Prosthetic joint infection requires joint removal → Endocarditis requires valve replacement