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Micro > Mycology > Flashcards

Mycology Flashcards

1
Q

Describe the defining characteristics of Malassezia furfur.

A

It is a lipophilic yeast that has short hyphae. Normal part of skin flora.

“Spaghetti and meatballs” appearance in skin scrapings.

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2
Q

What superficial mycoses are associated with Malassezia furfur? What distinguishes these mycoses?

A

Pityriasis versicolor (tinea versicolor) - infection of stratum corneum, may be hypo- or hyperpigmented itchy macules; fluoresce under Wood’s lamp.

Seborrheic dermatitis - squamous disorder of sebum rich areas of scalp; dandruff

Follicular pityriasis - infected follicles show yeast at their openings

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3
Q

What stains or solutions are used to identify Malassezia furfur?

A

10% KOH, glycerol and Parker’s stain

20% KOH

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4
Q

What organisms cause the superficial mycoses?

A

Malassezia furfur

Trichosporon beigelii

Piedraia hortae

Hortae werneckii

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5
Q

Describe the characteristics of Trichosporon beigelii. What conditions are associated with it?

A

Mycelial and yeast like morphologies, normal flora of mouth and skin. Has hyaline, septate hyphae and oval arthroconidia.

It causes white piedra

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6
Q

Briefly describe Piedraia hortae. What conditions does it cause?

A

Filamentous mold with dark septate hyphae.

Causes black piedra.

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7
Q

Describe Hortae werneckii. What does it cause?

A

Filamentous mold with brown septate hyphae or dark brown budding cells in KOH.

Causes tinea nigra - hyperpigmented macula on palms and soles.

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8
Q

What is a dermatophytosis?

A

Dermatophytoses or cutaneous mycoses are infections of the skin where the stratum corneum is colonized. The causative organisms use keratinase to digest keratin and use it as nutrient.

They induce pathological changes and may involve cellular immune responses.

Cause ringworm lesions.

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9
Q

Which organisms cause the dermatophytoses?

A

Microsporum spp.

Trichophyton

Epidermophyton

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10
Q

Describe the Microsporum genus.

A

Spindle shaped, thick walled and rough macroconidia.

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11
Q

What defines a fungal infection as a dermatomycoses?

A

Limited to the outer keratinized layer of skin and hair, they do not elicit a cellular immune response and are not pathologic. Cause only cosmetic problems.

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12
Q

Describe the Epidermophyton genus.

A

Smooth, thin walled club shaped macroconidia

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13
Q

Describe the Trychophyton genus

A

They have thin walled, smooth, pencil shaped macroconidia.

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15
Q

What are the different manifestations of tinea capitis? What is the causative organism of each?

A

Ectothrix - development of arthroconidia outside hair shaft; fluoresces green; Microsporum canis and gypseum, Trichophyton verrucosum

Endothrix - arthroconidia within hair shaft; no fluorescence; Trichophyton tonsurans and violaceum

Favus - acute infection of hair follicle; produces crust and hair loss, green flourescence; Trichophyton schoenleinii

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16
Q

Whatbare the etiologic agents of tinea corporis?

A

Epidermophyton floccosum

Trichophyton rubrum and tonsurans

Microsporum canis and gypseum

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17
Q

What are the etiologic agents of onychomycosis?

A

Trichophyton rubrum

Trichophyton interdigitale

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18
Q

What are the etiologic agents of tinea cruris?

A

Trichophyton rubrum

Trichophyton interdigitale

Epidermophyton floccosum

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19
Q

What is a subcutaneous mycosis? What is the etiologic agent?

A

A subcutaneous mycosis is a fungal infection of the deeper layers of the dermis, the subcutaneous tissue, and deeper tissues like bone. They are followed by chronic and insidious growth. Saprophytes found in soil or decaying vegetation are the etiologic agents.

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20
Q

How does a subcutaneous mycosis generally start?

A

Usually begins with trauma. They are mycoses of implantation.

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21
Q

What is the causative agent of sporotrichosis? What are the characteristics of this organism?

A

Sporothrix schenkii. It is a thermally dimorphic fungus.

Sporotrichosis is known as the rose gardner’s disease

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22
Q

What determines the pathogenicity of sporotrichosis?

A

Dimorphism and thermotolerance.
Glycoprotein on cell wall mediates attachment.
Asteroid body deposits protect yeast from immune attack.

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23
Q

Describe the morphology of Sporothrix mold and yeast

A

Sporothrix mold has branching septate hyphae and conidiophores. Described as a flower like arrangement. (Floret or daisy cluster).

The yeast form appears as short round oval or cigar shaped.

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24
Q

What characterizes chromoblastomycosis/chromomycosis?

A

Nodular and verrucous lesions; thick walled pigmented sclerotic bodies in tissues

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25
Q

What determines the pathogenicity of chromomycosis?

A

Dimorphism.

Melanin.

Enzymes.

Platelet activating factor .

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26
Q

What are the etiologic agents of chromomycoses?

A

Melanized fungi associated with decaying wood, plants or soil.

Fonsacaea pedrosoi
Philarophora verrucosa
Cladophialophora carrionii

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27
Q

What characterizes Fonsacaea pedrosoi?

A

Filamentous mold with dark green color; intercalary or terminal conidiophores

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28
Q

What are the clinical manifestations of chromomycosis?

A

On the skin surface: crusted, verrucose, wart like lesions. Hyperplasia and hyperkeratosis of epithelium.

Microscopically: production of copper-colored spherical cells called sclerotic bodies or medlar bodies.

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29
Q

What characterizes a mycetoma?

A

Tumefaction of the affected area, draining sinus, discharging grains.

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30
Q

What are the etiologic agents of eumycetoma?

A

Madurella mycetomatis

Pseudoallescheria boydii

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31
Q

What determines the pathogenicity of mycetomatous fungi?

A

Melanin in some species

Translational controlled tumor protein

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32
Q

What is the morphology of mycetomatous fungi?

A

White, yellow, pink-red, brown or black granules in pus

Long septate hyphae around granules

Chlamydospores may be present

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34
Q

What are the dermatophytoses? Briefly describe each one.

A

Tinea pedis - athlete’s foot; chronic infection of toes; presents with desquamated infectious scales

Tinea capitis - dermatophyte infection of scalp and hair

Tinea corporis - superficial infection of non hairy skin

Tinea unguium (onychomycosis) - invasion of nail plate in hands or feet

Tinea cruris - dermatophyte infection of thighs and buttocks

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35
Q

What are the etiologic agents of tinea pedis?

A

Trychophyton interdigitale

Trychophyton rubrum

Epidermophyton floccosum

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36
Q

What are the principal characteristics of a systemic mycosis?

A

Endemic - definitive geographical area, usually self limited and subclinical

True pathogens - inherently virulent fungi, with primary focus at the lungs

Dimorphic - filamentous mold at 25 degrees Celcius, yeast at 37. (Mold is cold, yeast is heat).

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37
Q

What changes are involved in dimorphism process?

A

The transition is genetically determined. Activated in response to environmental conditions within host. Initiated by signal transduction. Modifications to cell wall to express antigenic molecules and virulence markers. Expression of adhesins. Activation of virulence and survival genes.

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38
Q

How do dimorphic fungi involved in systemic mycoses cause disease?

A

Eliciting inflammatory response.

Direct invasion of tissues.

Destruction of tissues and vital structures.

From toxic effect of inflammatory response.

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39
Q

Whichnare the endemic regions of histoplasmosis?

A

Ohio, Mississipi river valleys, Latin America, temperate subtropical and tropical areas.

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40
Q

What is the etiologic agents of histoplasmosis?

A

Histoplasma capsulatum

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41
Q

What are other names for histoplasmosis?

A

Cave disease, Ohio valley disease, Darling’s disease, Reticuloendotheliosis

42
Q

Describe the mold and yeast phases of Histoplasma capsulatum. What is the natural reservoir?

A

The mold phase displays septate hyphae with tuberculate macroconidia (with spiny projections) and microconidia (infectious).

The parasitic yeast can be found budding within macrophages.

The reservoir is soil with high nitrogen content - areas contaminated with bat and bird feces; bats are naturally infected.

43
Q

What determines the pathogenicity of Histoplasma capsulatum?

A

The mold to yeast dimorphism.

Alpha 1->3 glucan in cell wall gives strain specific virulence to evade phagocytosis.

Heat shock protein 60 acts as an adhesin that bind CD18 on monocytes.

Calcium binding protein to scavage calcium as a means to kill macrophages.

Ability to acquire iron affects macrophages.

pH modulation of phagosome inactivates phagocytotic mechanism.

44
Q

What is the mode of transmission of Histoplasma capsulatum

A

Inhalation of airborne microconidia or hyphal fragments

45
Q

What are the clinical syndromes associated with Histoplasma capsulatum?

A

In normal host - asymptomatic flu-like illness after light exposure; acute pulmonary histoplasmosis after heavy exposure (snowstorm pattern with scattered calcification on CXR)

Opportunistic - chronic pulmonary histoplasmosis; disseminated histoplasmosis (rapid course/fatal).

46
Q

What are the 4 fungi associated with systemic mycoses?

A

Histoplasma

Blastomyces

Coccidiodes

Paracoccidiodes

47
Q

What are the 6 fungi that display dimorphism?

A 
Sporothrix 
Histoplasma 
Blastomyces
Coccidiodes
Paracoccidiodes
Candida
48
Q

It is generally said that yeast forms exist in warmer temperatures (yeast is heat, mold is cold). What is the exception?

A

Candida

49
Q

Which are the endemic areas of blastomycosis?

A

Central and southeastern US, Canada, Africa, India, Israel, Saudi Arabia

50
Q

How is histoplasmosis diagnosed definitively?

A

Culture from sputum, blood, tissue or body fluids

Histopathology is suggestive with intracellular yeast.

51
Q

What are other names for blastomycosis?

A

North American blastomycosis, Gilchrist disease, Chicago disease

52
Q

What is the etiological agent of blastomycosis?

A

Blastomyces dermatiditis

53
Q

Describe the mode of transmission of blastomycosis

A

Conidia are inhaled from contaminated dust. Not spread person to person.

54
Q

Describe the morphology of Blastomyces epidermitidis mold and yeast.

A

The mold phase has septate hyphae and conidia.

The parasitic yeast has large, broad-base cells with thick cell wall.

55
Q

What is the hallmark of blastomycosis? What precedes this stage?

A

The chronic cutaneous disease presents with hallmark skin lesions - papular, nodular, or postular lesions which form on the face, neck and extremities.

It is preceded by a flu-like illness. Not every pt will develop systemic disease.

56
Q

What is the other form of blastomycosis?

A

Cutaneous inoculation blastomycosis presents with no evidence of systemic involvement. Skin lesions are characteristic.

57
Q

How is the blastomycosis diagnosis made?

A

Suggestive - histopathological demonstration of large cells with thick cell walls resembling the figure 8; 20% KOH

Definitive - culture, serology

58
Q

Which are the endemic regions of coccidiodomycosis?

A

Desert areas of the Western hemisphere.

59
Q

What are other names for coccidiodomycosis?

A

San Joaquin Valley fever, desert fever, desert rheumatism, coccidiodal granuloma

60
Q

What is the etiologic agent of coccidiodomycosis? What is the infective particle? What is the mode of transmission?

A

Coccidiodes immitis

The infective particle is the arthroconidia fragmented from mycelia

Transmission is by inhalation from soil; not zoonotic or person to person

61
Q

What are the clinical manifestation of coccidioidomycosis?

A

Acute pulmonary infection

“Desert rheumatism”

Extrapulmonary infection most often involves skin and meninges

62
Q

How is the coccidioidomycosis diagnosis made?

A

Suggestive - histopathological demonstration of spherules in tissue (remember spherules!!!)

Definitive - culture, serology

63
Q

What is the etiologic agent of paracoccidioidomycosis?

A

Paracoccidioides brasilensis

64
Q

What is the endemic areas for paracoccidioidomycosis?

A

Rural Central and South America

65
Q

What are the pathogenic determinants of paracoccidioides?

A

Dimorphism

Cell wall associated gp43 acts as an adhesin to bind to laminin in ECM

66
Q

What is the infectious particle in paracoccidioidomycosis?

A

The P. brasilensis conidia

67
Q

How to diagnose paracoccidioidomycosis?

A

Pilot wheel shape

Multipolar budding yeast in tissue

68
Q

What patients are most susceptible to opportunistic mycoses?

A

The immunocompromised, burn victims, trauma victims, those with long-term central IV lines, etc

69
Q

What are the major opportunistic mycoses?

A

Candidiasis, mucormycosis, aspergillosis, cryptococcosis, pneumocystosis.

70
Q

What is the etiologic agent of aspergillosis?

A

Aspergillus fumigatus, Aspergillus flavus

71
Q

Describe the characteristics of Aspergillus spp.

A

Thermotolerant, hyaline filamentous fungi with micellium of septate hyphae growing with V-shaped branches at 25 degree angles and conidiophores.

72
Q

What determines the pathogenicity of Aspergillus spp.

A

Production of catalase, superoxide dismutase, proteinases, and phospholipases.

73
Q

How do Aspergillus spp. invade the body?

A

Conidia are inhaled into URT and LRT. Spores germinate into hyphae which invade tissues.

It is an angioinvasive fungus - can cause infarction and necrosis.

74
Q

What are the clinical manifestations of aspergillosis?

A

Invasive pulmonary aspergillosis (aspergilloma)

Disseminated aspergillosis

75
Q

How is aspergillosis diagnosed?

A

Microscopy - look for septate, hyphae, culture on Sabouraud’s, serology

76
Q

What is the etiologic agent of Cadidiasis?

A

Candida spp.

Candida albicans is predominant

77
Q

In what sites is Candida considered to be part of the normal flora?

A

GI tract, skon, vagina

78
Q

What are the morphological features of Candida spp.?

A

Budding yeast, blastospore, pseudohyphae.

Germ tube (albicans, dublinensis)

Chlamidospore (albicans, dublinensis)

Macroscopic - creamy yeast colonies on SDA

79
Q

When/how does Candida spread to cause disease?

A

When it is allowed to proliferate on mucosa - usually due to disruption of normal flora.

When it is allowed to spread hematogenously fro, the gut - neutropenia, chemotherapy.

When it gains access to the bloodstream - thru central line.

80
Q

What determines the pathogenicity of Candida spp?

A

Attachment mediated by germ tube, adherence to plastic surfaces, proteases, phospholipases.

81
Q

What are the clinical manifestations of Candidiasis?

A

Cutaneous - intertriginous candidiasis, diaper rash, onychomycosis

Mucocutaneous - thrush

Chronic mucocutaneous - verrucous lesions

Systemic - candidemia and spread to organs

82
Q

How is candidiasis diagnosed?

A

Mucosal - scraping of lesions reveals budding yeast and pseudohyphae; culture is also suggestive

Invasive - biopsy and culture of invaded tissue

Germ tube grows Candida quite fast (hours)

83
Q

What is the etiologic agent of cryptococcosis?

A

Cryptococcus neoformans

84
Q

What is cryptococcosis usually associated with?

A

Meningitis (subacute or chronic)

85
Q

Describe reproduction of C. neoformans. What is its distribution?

A

Reproduces by budding; worldwide distribution in soil contaminated with bird feces (pigeons).

86
Q

What is the mechanism of infection with C. neoformans?

A

Yeast are inhaled into alveoli. Production of polysaccharide capsule by yeast inhibits phagocytosis and immune response.

Melanin also helps the yeast.

Shows neurotropism (infects CNS)

87
Q

Who is at risk for Cryptococcosis?

A

AIDS patients, transplant patients

88
Q

What are the clinical manifestations of cryptococcosis?

A

Primary pulmonary infection - asymptomatic, incidental finding on CXR with solitary pulmonary nodule

Symptomatic pneumonia

Cryptococcal meningitis

Other disseminated manifestations - skin and osteolytic bone lesions

89
Q

How is cryptococcosis diagnosed?

A

Lumbar puncture - look for encapsulated yeast in India ink

Latex agglutination test for antigen

90
Q

What is the etiologic agent of Pneumocystosis? How is acquired and how is it transmitted? Where is it most commonly found in an infected patient?

A

Pneumocystis jirovecii (P. carinii)

Transmitted person to person by inhalation of respiratory droplets.

Rarely found outside lungs.

91
Q

What is the most common risk factor for pneumocystosis?

A

T cell deficiency

92
Q

What is the principal virulence factor for P. jirovecii?

A

Major surface glycoprotein which allows binding to ECM

Trophic forms bind to type 1 pneumocytes.

93
Q

What are the clinical manifestations of pneumocystosis?

How is the diagnosis made?

A

PCP - pneumocystis carinii pneumonia

Diagnosis - organism is demonstrated by silver stain; PCR, biopsy, antibody fluorescence

94
Q

What are the etiologic agents of mucormycosis/zygomycosis?

What are the associated risk factors?

A

Rhizopus, Mucor, Absidia

Risk factors - uncontrolled diabetes, immunosuppression, prolonged neutropenia

Has an extremely high death rate

95
Q

What is the mechanism of infection of mucormycosis?

A

Sporangiospores are inhaled, alveolar macrophages bind to spores and inhibit germination.

The tissue invasive form displays broad and irregular coenocytic hyphae - can cause infarction when in blood vessels, etc.

96
Q

What syndromes are associated with mucormycosis?

A

Rhinocerebral infection (sinuses and brain)

Thoracic or pulmonary mucormycosis - pneumonia

Mucormycosis of GI tract, skin, kidneys

97
Q

How is mucormycosis diagnosed?

A

Microscopy of samples of sputum, paranasal sinuses, bronchoalveolar lavage - look for ceonocytic hyphae branched at right angles with sporangia

Cotton candy appearance on SDA

Micro (3 decks)

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