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265 Cards in this Set
- Front
- Back
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What are fungi?
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Eukaryotic organisms that have membrane-bound nuclei, unlike viruses or bacteria, and are heterotrophic.
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What are heterotrophic organisms?
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Organisms that require preformed organic carbon sources for growth.
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What are the two morphoogic forms of fungi?
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Filamentous molds
Unicellular yeasts |
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What are three general structural components of filamentous moulds?
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Mycelium/hypha
Septa Thallus |
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What is the function of Mycelium/hypha?
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A mycelium is a mass of filamentous threads that resembles a 'cotton ball' composed of intercommunicating individual threads of tubular cells called hyphae.
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What is the function of Septa?
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Septa forms partitions between cells within a hypha.
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What is the function of Thallus?
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Thallus is the vegetative body; a simply fungus body.
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What is the morphology of yeast-like fungi?
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Single, unconnected spheroid cells
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What is the difference between yeasts and filamentous moulds?
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Yeasts reproduce by budding or fission.
Filamentous moulds grow by branching and tip elongation of hyphae. |
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What are dimorphic fungi?
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Fungi with the ability to grow in two forms, most commonly as yeast-like organisms in certain environments but can also grow as mold-like in others.
"Mold in the cold, yeast in the heat". Systemic mycoses are dimorphic fungi |
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What are the two mechanisms by which fungi reproduce?
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Asexual sporulation
Sexual sporulation |
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Which is more common among human pathogens?
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Asexual sporulation
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What is sporulation?
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Production of fungal spores
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What are fungal spores?
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Metabolically dormant, protected cells capable of germinating and establishing colonies.
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What is asexual sporulation?
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Asexual formation of spores through mitosis.
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What are asexually produced spores called?
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Conidia or spores;
Although spores are technically distinct from conidia, the term spore is often used to encompass both. |
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What is sexual sporulation?
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Sexual formation of spores through meiosis between two haploid nuclei of compatible strains.
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What are sexually produced spores called?
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Ascospores
Zygospores Balidiospores |
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What are two predominant components of fungal cell walls?
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Chitin
Glucans |
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What is chitin composed of?
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N-acetylglucosamine polymers
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What is glucan composed of?
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Polymers of glucose
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What is one difference between the cell wall of fungi and bacteria?
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Fungal cell wals are composed of N-acetylglucosamine and gluxose polymers instead of peptidoglycan.
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What is the clinical significance of the difference between cell wall of fungi and bacteria?
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Beta-Lactam antibiotics that interfere with bacterial cell wall production and subsequently have no effect on fungi
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What is a standard medium for fungal culture?
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Sabouraud dextrose agar
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What type of medium is sabouraud dextrose agar?
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A low pH beef-broth agar.
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How are human fungal diseases typically classified?
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Based on their level of involvement and depth of invasion.
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What are four classified cations of fungal disease?
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1) Superficial when limited to hair and stratum corneum
2) Cutaneous when limited to the epidermis. 3) Subcutaneous when the epidermis is breached 4) Systemic when there is significant penetration or dissemination to internal organs |
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What are three cutaneous fungal pathogens?
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Epidermophyton
Microsporum Trichophyton |
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What are four subcutaneous fungal pathogens?
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Sporothrix shenckii
Madurella grisea Cladophialophora Phialophora |
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What are four systemic fungal pathogens?
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Coccidioides immitis
Histoplasma capsulatum Blastomyces dermatitidis Paracoccidioides brasiliensis |
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How else are fungal infections classified?
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Based on their infectivity in regards to the host's immune status?
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What is one group of fungal infections based on this distinction of the host's immune status?
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Opportunistic fungal infections
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What property do opportunistic fungal infections have in common?
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Opportunistic organisms cause clinically significant disease in the immunocompromised, but rarely in the immunocompetent.
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What are six opportunistic fungal pathogens?
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1) Candida species (yeast)
2) Cryptococcus neoformans (yeast) 3) Aspergillus fumigatus (mold) 4) Rhizopus species (mold) 5) Fusarium species (mold) 6) Pneumocystis carinii (yeast), now called P. jiroveci. |
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How are pathogenic fungi classified?
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1) Superficial and cutaneous pathogens
2) Subcutaneous pathogens 3) Systemic pathogens 4) Opportunistic Pathogens |
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What are superficial and cutaneous fungi?
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Microsporum spp.
Epidermophyton spp. Trichophyton spp. |
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What are subcutaneous fungal pathogens?
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Sporothrix schenckii
Madurella grisea Cladophialophora spp. Phialophora spp. |
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What are systemic fungal pathogens?
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Coccidioides immitis
Histoplasma capsulatum Blastomyces dermatitidis Paracoccidioides brasiliensis |
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What are opportunistic fungal pathogens?
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Candida spp.
Cryptococcus neoformans Aspergillus fumigatus Rhizopus spp. Mucorales spp. Pneumocystis carinii (P. jiroveci) |
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What is teh level of involvement of cutaneous mycoses?
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Cutaneous involvement is limited to the epidermis
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What is the general name given to cutaneous fungal pathogens?
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Cutaneous involvement is limited to the epidermis.
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What is the general name given to cutaneous fungal pathogens?
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Dermatophytes
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What do dermatophytes cause?
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Dermatophytosis
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What are three main genera of cutaneous fungal pathogens?
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Epidermophyton
Microsporum Trichophyton |
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Where are cutaneous fungi found?
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Human skin
Domestic animal skin Soil |
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What are the modes of ermatophytosis transmission?
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Contact with soil
Human-to-human Animal-to-human transmission by direct contact or inoculation with infected skin scales. |
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how do dermatophytoses present clinically?
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Depends on part of body infected.
The classic presentation is an annular, sharply marginated, raised lesion that may be erythematous and pruritic with a clear or scaly center. |
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How are dermatophytoses classified?
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According to the affected tissue or region.
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What are six common dermatophytoses?
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Tinea corporis (ringworm)
Tinea pedis (athletes foot) Tinea capitis (scalp ringworm) Tinea barbae (beard) Tinea cruris (jock itch) Tinea unguium (nails |
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Which genus of dermatophytes does not infect hair?
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Epidermophyton
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Which genus of dermatophytes does not usually infect nails?
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Microsporum
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What are two cutaneous manifestations of dermatophytoses?
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Microsporum
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What are two cutaneous manifestations of dermatophytoses?
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Kerion
Id reaction |
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What is kerion?
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Highly inflammatory pustular lesion secondary to scalp or beard dermatophytoses
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What is an id reaction?
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Sterile skin vesicles formation distant from primary dermatophytoses sites secondary to hypersensitivity response to circulating fungal antigens; it is commonly seen in tinea pedis with subsequent hand lesions.
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What are four ways in which a clinical diagnosis of dermatophytosis can be confirmed?
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1) Application of potassium hydroxide (KOH) to tissue sample with active fungal growth revealing fungal filaments by direct microscopy.
2) Green fluorescence visualization of dermatophyte hyphae invasion of hair shafts under long-wave UV light (Wood lamp) 3) Culture on Sabouraud agar at room temperature demonstrating characteristic hyphae adn conidia 4) Postiive skin test with fungal extracts, e.g., trichophytin. |
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How is dermatophytosis treated?
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1) Removal of infected hairs
2) Topical antifungals for most infections 3) Oral/systemic antifungal therapy for hair and nail infections 4) Keep skin cool and dry |
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What caused pityriasis tinea versicolor?
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Malassezia species
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How does pityriasis versicolor present clinically?
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Noninflamed patches of fine brown scaling, particularly on the trunk and upper arms.
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How does pityriasis lesions appear?
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The affected area may appear uniformly darker or unifermly lighter than the person's overall skin tone.
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What is the pathophysiology of pityriasis tinea versicolor?
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Melanocyte toxicity.
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What commonly predisposes one to pityriasis versicolor infection?
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Systemic steroid therapy, suntan lotions and other lipid-containing lotions.
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How is a clinical diagnosis of pityriasis versicolor confirmed?
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1) KOH treatment of skin scrapings revealing clusters of round, thick-walled yeast budding from a medium base with a collar, and fragmented thick-walled hyphae
2) Yellow fluorescence under long-wave UV light. |
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How is pityriasis versicolor treated?
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2.5% selenium sulfide
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What is the level of involvement of subcutaneous mycoses?
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Fungal infection in which the epidermis is breached.
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How are subcutaneous mycoses commonly acquired?
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Traumatic laceration or puncture wound
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What are four subcutaneous fungal pahtogens?
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Sporothri shenckii
Madurella grisea Cladophialophora Phialophora |
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What does S. shenckii cause?
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Sporotrichosis
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What is sporothrichosis also known as?
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Rose gardeners disease
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What is the natural habitat of S. schenckii?
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Soil and decaying or live vegtation, most commonly in tropical or subtropical areas.
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What is teh morphology of S. schenckii?
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Dimorphic, cigar-shaped yeasts, septate mold.
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How does sporotrichosis present clinically?
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1) Granulomatous ulcer with irregular, friable edges at a puncture site (primary lesion)
2) Nodular or ulcerative lesions can occur along draining lymphatics (seondary lesion), i.e., ascending, "cord-like" lymphangitis |
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What is the most reliable method used to confirm a clinical diagnosis of sporotrichosis?
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Culture of biopsy material on Sabouraud agar.
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What is the treatment for sporotrichosis?
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Most lesions heal spontaneously with scarring; otherwise, oral itraconazole or potassium iodide can be used.
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What does Madurella grisea cause?
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Mycetoma
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What is mycetoma also known as?
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Madura
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How does Mycetoma present clinically?
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Localized abscess, usually on the feet
Madura foot, that discharges pus, serum, and blood through sinus tracts and is capable of spreading to bone. |
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What is the defining feature of mycetoma?
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Presence of white or colored grains composed of copacted hyphae in the exudates.
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What is the treatment for mycetoma?
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Surgical excision, which is more effective than antifungals.
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What do Phialophora and Cladophialophora cause?
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Chromoblastomycosis
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How does Chromoblastomycosis present clinicallly?
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Warty nodule that slowly infects the lymphatic system, resulting in crusty abscesses.
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How do fungal cells appear?
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As "copper pennies" i.e., fungal cells appear somewhat round and may have one to two transverse septa.
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What is the treatment for chromoblastomycosis?
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Surgical excision, which is more effective than antifungals.
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What is the level of involvement of systemic mycoses?
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Fungal infection in which there is significant penetration or dissemination to internal organs.
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What are four common systemic fungal pathogens affecting individuals?
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Coccidioides immitis
Histoplasma capsulatum Blastomyces dermatitidis Paracoccidioides brasiliensis |
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What are four fungal characteristics of systemic mycoses?
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1) Uniformly dimorphic
2) Exist as molds as lower temperatures (in soil) 3) Exist as yeasts or spherule at higher temps (in the host) 4) Geographical/regional distribution. |
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How do systemic mycoses begin?
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Inhaled fungal spores convert into yeasts or spherule in the lungs and initiate a lower respiratory tract infection with potential for dissemination within the host.
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What predisposes one to disseminated systemic mycoses?
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Defective cell-mediated immunity
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Which cells, when infected cause disseminated systemic mycoses?
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Cells of teh reticuloendothelial system, macrophages, become infected and disseminate throughout the body.
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Are systemic mycoses communicable?
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NO
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How are disseminated systemic mycoses treated?
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Amphotericin B (many side effects)
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How are localized systemic mycoses treated?
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Itraconazole or voriconazole
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What are the two species of Coccidioides?
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C. immitis
C. posadasii |
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What is the pathogenesis of coccidioides species?
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1) Coccidioides species generate spores in soil by hyphal filaments septation
2) Spores aerosolize and are inhaled, especially when the soil is disturbed and in dry environments 3) Spores swell in lungs and develop into endospores filled large spherules. 4) Spherules rupture releasing endospores 5) Endospore dissemination to the CNS, bone, or other tissues. |
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What are four symptoms of acute pulmonary coccidioidomycosis?
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Cough
Fever Arthralgia Rash |
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What is this quadrad of symptoms associated with pulmonary coccidioidomycosis called?
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San Joaquin Valley Fever or desert rheumatism.
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What is the characteristic chest x-ray finding?
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Infiltrates and hilar lymphadenopathy
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What type of rash is seen with C. immitis infection?
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Erythema multiforme, erythema nodosum, or toxic erythema.
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What is the prognostic value of developing erythema nodosum?
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Erythema nodosum is a good prognostic indicator because it represents a delayed, cell-mediated hypersensitivity response to fungal antigens.
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What is the most comon outcome of acute pulmonary coccidioidomycosis?
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Recovery within 10-21 days
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What are three uncommon outcomes of pulmonary coccidioidomycosis?
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1) Solig-lung granuloma formation
2) Cavitary coccidioidomycosis in apical or mid-lung fields 3) Dissemination |
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What are three sites of dissemination and their manifestations for coccidioidomycosis?
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1) CNS, resulting in meningitis
2) Skin, resulting in ulers or crusted granulomas 3) Bone, resulting in lytic lesions of long bones, skill, and joint cavities. |
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What percentage of patients infected with C. immitis develop disseminated disease?
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1%
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What population have a higher percentage of disseminated disease?
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Filipinos and African Americans have a roughly 10% chance of developing disseminated disease.
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What cerebrospinal fluid findings are consistent with coccidioidal meningitis?
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1) Lymphocytosis, eosinophilia
2) Increased protein 3) Decreased glucose 4) C. immitis can rarely be seen directly with microscopy of CSF |
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How can you tell if a person has produced adequate cell-mediated immunity to prevent disseminated C. immitis disease?
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A positive skin test to fungal extracts, i.e., 5mm induration developing within 48 hours; although false positives do occur because of cross reactivity and/or past exposure.
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Which serological tests suggest C. immitis infection?
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Immunoglobulin (IgM and IgG) precipitins within 2-4 weeks of infection.
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Which serological tests suggest C. immitis dissemination?
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Increasing complement fixing antibody titer.
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What are three treatment options for coccidioidomycosis?
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1) No treatment for asymptomatic or mild primary pulmonary infection.
2) Amphotericin B for persistent lung disease or disseminated disease 3) Fluconazole is the drug of choice for C. immitis meningitis |
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What does H. capsulatum cause?
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Histoplasmosis
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What is unique about the life cycle of H. capsulatum?
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It is an intracellular fungus
H. capsulatum has no capsule |
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What cells do H. capsulatum show tropism for?
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Reticular endothelial cells, e.g., macrophages.
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What are teh endemic areas for H. capsulatum?
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Ohio and Mississippi River Valleys
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Where is H. capsulatum most commonly found?
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Bird and bat droppings.
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What is the pathogenesis of H. capsulatum?
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1) Soil laden with bird or bat droppings rich in H. capsulatum microconidia aerosolize and are inhaled
2) Spores germinate in lungs into yeast-like cells 3) Yeast cells are engulfed by macrophages 4) Dissemination secondary to intracellular yeat cells division and macrophage movement throughout the body. |
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What is the characteristic chest x-ray finding?
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Infiltrates and hilar lymphadenopathy
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What are seven symptoms of acute epidemic histoplasmosis?
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Chills
Fever Cough Headache Pneumonia Arthralgia Rashes |
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What is the common clinical course of acute epidemic histoplasmosis in healthy individuals?
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Spontaneous resolution
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What are two uncommon clinical manifestations of histoplasmosis?
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Chronic pulmonary histoplasmosis
Disseminated histoplasmosis |
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What type of patient is at increased risk for chronic pulmonary histoplasmosis?
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Patients with preexisting lung disease, particularly emphysema.
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What are teh sites for disseminated histoplasmosis infection?
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Liver, spleen, lmph nodes, and bone marrow.
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What are four useful lab tests for diagnosing histoplasmosis?
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1) Tissue biopsy or bone marrow aspiration demonstrating oval yeast cells within macrophages
2) Culture on Sabouraud agar showing hyphae with macroconidia 3) Histoplasma antigen detection by radioimmunoassay, especially in urine. 4) Complement fixation assay |
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What tests are not diagnostically useful for histoplasmosis?
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Skin and serologic tests because they lack specificity.
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What are four treatment options for histoplasmosis?
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1) No treatment for asymptomati or mild primary pulmonary infection
2) Oral itraconazole in treating progressive lung lesions 3) Amphotericin B for disseminated disease |
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What is the treatment for chronic suppression of histoplasmosis in AIDS patients?
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Oral Itraconazole
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What does B. dermatitidis cause?
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Blastomycosis
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What is the classic histologic finding or B. dermatitidis?
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Broad-based bud
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What are the endemic areas for B. dermatitidis?
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Mississippi and Ohio River Valleys
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Where is B. dermatitidis most commonly found?
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Moist soil with decomposing wood.
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What is the pathogenesis of blastomycosis?
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1) Soil laden spores aerosolize and are inhaled
2) Spores germinate in lungs into thick-walled yeast cells, often with buds |
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What are six symptoms of acute blastomycosis?
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Headache
Cough Fever Chills Signs of pulmonary consolidation Possibly pleural effusion. |
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What is the charateristic chest x-ray finding?
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Infiltrates and hilar lymphadenopathy
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Does gender influence the presentation of systemic mycoses?
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YES
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How does gender influence presentation?
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Symptomatic infection is much more common in adut males than in adult females.
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What are sites for disseminated blastomycosis infection?
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Bone
Skin Genitourinary tract Blastomycosis causes granulomatous lesions. |
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How can a clinical diagnosis of blastomycosis be confirmed?
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1) Tissue biopsy specimens demonstrating thick-walled yeast cells with single broad-based buds
2) Cultures of hyphae with small pear-shaped conidia are diagnostic |
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What are three treatment options for blastomycoisis?
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1) No treatment for asymptomatic patients
2) Itraconazole for mild, primary pulmonary infection or progressive lung lesions. 3) Amphotericin B for disseminated disease or life-threatening disease. |
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What are teh endemic areas for P. brasiliensis?
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Latin America
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What is the morphology of P. brasiliensis?
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P. brasiliensis has a pilot-wheel appearance.
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What is the clinical manifestation of P. brasiliensis?
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Similar to histomycosis and blastomycosis with a distinct predilection to cause secondary oral and nasal mucosal painful lesions.
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What are oppoutunistic organisms?
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Organisms that caue clinically significant disease in the immunocompromised, but rarely in the immunocompetent.
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What are six opportunistic fungal pathogens?
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Candida species (yeast/mold)
Cryptococcus neoformans (yeast) Aspergillus fumigatus (mold) Rhizopus species (mold) Mucor (mold) Pneumocystis jiroveci (yeast-like) |
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What is the relationship between the morphology assumed by a fungus in tissue and the pathogenesis it causes?
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Fungal morphology determines which coomponent of host defense is needed to fight infection.
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What five risk factors lead to systemic fungal infection?
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1) Infection with HIV
2) Endocrinopathies, e.g., diabetes 3) Neutropenia, e.g., secondary to chemotherapy 4) Systemic corticosteroids 5) Systemic broad-spectrum antibiotics |
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What are five species of candida?
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C. albicans
C. tropicalis C. parapsilosis C. krusei C. glabrata |
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What is the most clinically important species of Candida?
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C. albicans
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Do immunocompetent individuals typically develop candidiasis?
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YES
vaginal candidiasis or oral thrush in young children |
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Do immunocomptent individuals typically develop systemic candidiasis?
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NO
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How does candidiasis commonly present in immunocompromised, e.g., AIDS patients?
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Candida infection is almost exclusively mucosal in AIDS patients becase helper T-cell deficiency predisposes to mucosal infection.
Intact polymorphonuclear function in AIDS patients precludes disseminated, deepseated candidiasis. |
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How is a diagnosis for candida infection made on microscopy?
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Oval yeasts, single or multiple buds, and pseudohyphae in tissue.
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What two observations are used to distinguish C. albicans from other Candida species?
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1) Germ tube formation in serum at body temperature.
2) formation of dormant asexual spores, i.e., chlamydospores, at room temperature. |
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What is the role of skin tests in the diagnosis of candidiasis in immunocompetent versus immunosuppressed individuals?
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1) Skin tests with Candida antigens are uniformly positive among immunocompenent adults capable of mounting a cellular immune delayed type hypersensitivity response.
2) Patients who do not respond to Candida antigens have deficient cell-mediated immunity and are considered anergic. NOTE: Other skin tests, e.g., purified protein derivative (PPD), cannot be correctly interpreted in anergic patients. |
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What comorbidities are associated with C. albicans?
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Esophagitis, mucosal ulcerations, perforations, and abdominal surgery.
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What comorbidities are associated with C. tropicalis?
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Cancer and leukemic patients with prolonged granulocytopenia.
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What comorbidities are associated with C. parapsilosis?
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Prolonged total parenteral nutrition.
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Is C. albicans part of the normal flora?
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YES
It is commonly found in the upper respiratory, gastrointestinal, and female genital tracts. |
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What are six types of C. albicans infection
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1) Oral thrush
2) GU mucocutaneous candidiasis 3) GI mucocutaneous candidiasis 4) Pulmonary candidiasis 5) Endocarditis 6) Cutaneous candidiasis |
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What is the most common site for superficial candidiasis?
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Oral mucosa
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What is thrush?
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Inflammation of the oral mucosa and formation of superficial, white, elevated C. albicans plaques with possible ulceration.
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What are two common risk factors for thrush?
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HIV infection
Patients receiving chemotherapy. |
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How is thrush treated?
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Nystatin "swish and swallow" or an oral azole.
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What two GU sites are associated with candida?
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Urinary tract
Vagina |
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What could predispose someone to candidiasis in each site?
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1) Urinary tract candidiasis in the setting of a Foley catheter with superimposed antibiotic treatment.
2) Vaginal candidiasis in the setting of being immunocompromised, e.g., diabetics, chronic steroid use, and pregnancy |
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What are the clinical manifestations of vaginal candidiasis?
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Intense, burning, pruritic, erythematous vulva with abundant thick, white, and curd-like vaginal discharge.
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Which patient population is especially predisposed to hepatosplenic candidiasis?
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Leukemic patients recovering form remission-indication treatment.
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What are three situations associated with andidal peritonitis?
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1) Peritoneal dialysis complication
2) GI perforation secondary to ulcers, colitis, trauma, or neoplasia 3) Contamination during or after abdominal surgery. |
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How common is dissemination following candidal peritonitis?
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Rare
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What are two manifestations of cardiovascular candidiasis?
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1) Candidal blood infetion (fungemia)
2) Candidal endocarditis |
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What are four dissemination sites for candidal fungemia?
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1) Pulmonary
2) Renal 3) Ocular 4) Cardiac valves |
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What types of patients are likely to contract pulmonary candidiasis?
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Patients with phagocytic cell defects such as chronic granulomatous disease or myeloperoxidase deficiencies.
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How is candida endocarditis treated?
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Systemic antifungals and often surgery
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Which two cutaneous sites are associated with candidiasis?
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Skin folds-intertrigo(diaper rash)
Finger nails |
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How does intertrigo present clinically?
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Pruritic, erythematous vesicopustules between skin folds
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What activity predisposes to finger and nail candidiasis?
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Repeated immersion of hands in water, restaurant dishwasher.
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How is disseminated candidiasis treated?
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IV amphotericin B
Recent evidence suggests that IV caspofungin may be effective |
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What does C. neoformans cause?
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Cryptococcosis
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How is cryptococcosis acquired?
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Inhalation of aerosolized soil enriched with pigeon droppings.
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Where is C. neoformans found?
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Worldwide distribution
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What five diseases predispose one to cryptococcosis?
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1) AIDS
2) Sarcoidosis 3) Lymphoma (mainly Hodgkin) 4) Systemic Lupus erythematosus 5) Diabetes |
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What four sites are commonly infected by C. neoformans?
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1) Meninges
2) Lungs 3) Skin 4) Bone |
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How does pulmonary cryptococcosis present?
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Usually asymptomatic
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What other clinical manifestations are possible pulmonary cryptococcosis?
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Fever
Moderately productive cough Blood-tinged sputum |
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What are five possible chest x-ray findings suggestive of pulmonary cryptococcosis?
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1) Hilar lymphadenopathy
2) Dense infiltrates in mid to lower lung fields 3) Single or multiple discrete nodules 4) Cavitation of upper lobes 5) Calcification |
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Waht is the treatment for pulmonary cryptococcosis?
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Most cases resolve without treatment, although amphotericin B and flucytosine can be used.
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What are the clinical manifestations of cryptococcal meningitis?
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Slow onset symptoms including frontal or temporal headache, mental status changes, nuchal rigidity, foccal neurological deficits, and mild fever
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What is a common complication of Cryptococcus-caused meningitis?
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Hydrocephalus
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Does cryptococcal meningitis only occur in the immunosuppressed?
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NO
Cryptococcal meningitis can occur in a small subset of immunocompetent individuals, but a throrough workup for an immunologic defect should still be performed. |
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What is used for prophylaxis in AIDS patients against cryptococcal meningitis?
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Indefinite prophylaxis with oral fluconazole.
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What is the mean survival for cryptococcal meningitis in AIDS patients?
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6 months from time of diagnosis
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What CSF findings are consistent with cryptococcal meningitis?
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High CSF opening pressure, high protein, low glucose, and lymphocytosis
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What are three tests are available for Cryptococcus diagnosis?
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1) India ink staining of CSF
2) Serologic testing for antigen, e.g., cryptococcal antigen latex particle agglutination testing. 3) Culture |
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What does India ink staining demonstrate?
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Thick, cear-appearing polysaccharide-encapsulated yeast cells resistant to India ink staining
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How is cryptococcal meningitis treated?
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IV amphotericin B and flucytosine for 4-6 weeks.
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What is the most reliable test for assessing remission from cryptococcosis?
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Negative cryptociccal antigen tests
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Hw commin is relapse in non-AIDS-related cases?
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Up to 30%
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How are non-AIDS-related patients monitored for cryptococcosis?
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Serial lumbar punctures
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Waht are three clinical manifestations of cutaneous cryptococcosis?
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1) Painless, soft, and fluctuant subcutaneous swellings
2) Hard, occasionally purpuric, dermal plaques or nodules 3) Raised granulomata that can be papular or pustular. |
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Which three studies are indicated in patients with cutaneous cryptococcus?
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1) Lumbar puncture to rule out cryptococcal meningitis
2) X-ray for bone involvement of overlyig cutaneous lesions 3) Serology to rule out disseminated cryptococcosis |
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What does A. fumigatus cause?
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Aspergillosis?
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What other organisms cause aspergillosis?
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A. flavus
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What is unique about A. flavus?
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A. flavus is carinogenic because it produces aflatoxin, which i implicated with hepatomas.
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What foods are associated with A. flavus?
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Moldy peanuts and grains.
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What three morphologic features of Aspergillus distinguish it from other opportunistic organisms?
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1) Aspergillus and Zygomycetes exist only as molds, whereas Candida, Cryptococcus, and P. carinii exist as yeast-like forms.
2) Aspergillus has septate hyphae with arallel walls and typically V-shaped dichotomous, 45-degree branching whereas Zygomycetes (Mucor spp) and Rhizopus spp have nonseptate hyphae with irregular walls and right-angle branching. 3) Aspergillus conidia form radiating chains, whereas Rhizopus and Zygomycetes conidia are enclosed within a sporangium |
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What is the pathogenesis of aspergillosis?
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1) Inhalation of airborne conidia/environmental spores
2) Primary pulmonary infection 3) Colonization of skin, wounds, burns, cornea, external ear, or paranasal sinuses secondary to epidermal invasion. |
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What is the most common cause of fungal sinusitis?
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Aspergillus
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What are four other clinical manifestations of aspergillosis?
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1) Pulmonary hypersensitivity syndromes, e.g., extrinsic asthma, extrinsic allergic alveolitis, or allergic broncho-pulmonary aspergillosis (ABPA)
2) Acute invasive and chronic necrotizing pulmonary aspergillosis 3) Aspergilloma (fungus ball) 4) Miscellaneous infections, e.g., CNS, cardiac, cutaneous, ocular, bone, GI, GU involvement. |
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Which two host defense mechanisms are responsible for combating aspergillosis?
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1) Pulmonary alveolar macrophages, which ingest inhaled spores and inhibit germination.
2) Neutrophils, which destroy hyphae |
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What conditions predispose one to developing invasive aspergillosis?
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High-dose corticosteroid treatment
Neutropenia |
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Would you expect Aspergillus to be a major opportunist in HIV infection?
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NO
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Why wouldn't you expect Aspergillus to be a major oppurtunist in HIV infection?
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Aspergillosis is not commonly associated with T-cell deficiencies such as in HIV.
HIV patients can effectively defect against aspergillus infection because alveolar macrophages and neutrophils are unaffected byt the virus |
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What are five common manifestations of pulmonary aspergillosis?
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Lobar pneumonia
Abscesses Hemorrhagic infarction Necrotizing Bronchopneumonia Aspergilloma |
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What is an aspergilloma?
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Aspergilloma, or fungus ball, is a noninvasive mass of hyphal tissue that forms in lung cavities from prior necrotizing lung disease, such as tuberculosis.
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What clinical features suggest invasive pulmonary aspergillosis?
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1) Persistent fever while on antibiotic therapy
2) Rales without fluid overload 3) Pleuritic chest pain |
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What is the chest x-ray finding seen with aspertilloma?
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Radiopaque structure that changes position when the patient is moved from an erect to a supine position.
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What is ABPA?
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Allergic reaction that arises form inhalation of Aspergillus spores without subsequent extensive spore germination or hyphal invasion
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What symptoms do ABPA patients present with?
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Asthmatic symptoms
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Waht lab test is diagnostic for ABPA?
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High IgE titer against aspergillus antigens.
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What are four manifestations of intracranial aspergillosis?
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1) Subcortical hemorrhagic infarction
2) Solitary or multiple abscesses 3) Meningitis 4) Granuloma |
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Why is pulmonary and cerebral infarctiona hallmark of aspergillus infection?
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Aspergillus is angioinvasive, leading to throombosis and infarction of distal tissue.
Rhizopus, Aspergillus and Mucor "RAM" are angioinvasive. |
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What CSF findings are associated with Aspergillus meningitis?
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Normal CSF is up to 50% of patients, i.e., isolation of Aspergillus form CSF is rare; however, may resut in a modestly elevated protein, monocytosis or neutrophilia, and normal glucose
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What is the most common manifestation of paranasal sinus aspergillosis?
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Aspergilloma
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How does paranasal aspergillosis present clinically?
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Headache or facial pain with periorbital swelling and visual disturbance.
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What is a complication of paranasal aspergillosis?
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Local extension of infection from the paranasal sinuses to the brain.
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What is the x-ray finding seen with paranasal aspergillosis?
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Opacification of the sinuses and, occasionally, local bone destruction
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What are two clinical manifestatins of cardiac aspergillosis?
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1) Endocarditis secondary to heart surgery
2) Myocarditis secondary to hematogenous dissemination |
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What patient population is particularly at risk for paranasal aspergillosis?
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IV drug users
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What is the clinical manifestation of cutaneous aspergillosis?
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Macule, nodule, or area of cellulitis that slowly develops into black necrotic eschars.
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What is the gold standard for diagnosis of aspergillosis?
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Histologic evidence of tissue invasion by fungus with Asprgillus morphology; however, diagnosis is often difficult
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What is the drug of choice for treatment of aspergillosis?
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Amphotericin B
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What are three genera of fungi cause mucomycosis?
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Rizopus
Absidia Rhizomucor |
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How is mucormycosis commonly acquired?
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1) Inhalatin of spores
2) Germination and invasion of mucosal membranes 3) Less commonly, infection can follow ingestion, direct inoculation through traumatic breaks in skin, or through IV injection. |
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What is one characteristic that the pathogens that cause mucormycosis, especially Rhizopus, share with Aspergillus?
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All are angioinvasive Rhizopus, Aspergillus, and Mucor.
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What is the pathogenesis of Rhizopus- and Mucor-mediated vasculopathy?
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1) Invade vessel walls
2) Form a tangled fibrin mesh inside the vessel lumen with rapid extension. 3) Thrombosis and resultant infarction of distal tissue follow. |
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What are five major clinical maniestations of mucormycosis?
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1) Rhinocerebral mucormycosis (most common)
2) Pulmonary mucormycosis 3) Disseminated mucormycosis 4) Cutaneous mucormycosis 5) GI mucormycosis (rare) |
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What is the major risk factor for rhinocerebral mucormycosis?
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Conditions associated with acidosis such as diabetes, renal failure, and diarrhea.
Rhinocerebral mucormycosis rarely occurs in normal hosts. |
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What other patient groups are at increased risk for mucormycosis?
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condidions associated with immunosuppression, e.g., leukemia, lymphoma, diabetics, and organ transplation.
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How does rhinocerebral mucormycosis evolve?
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1) Inhaled spores germinate and invade nasopharyngeal, palatal, or paranasal sinus mucosa.
2) Extension spreads from these primary sites along vessels to secondarily infect the frontal lobes of the brain. |
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How does rhinocerebral mucormycosis present clinically?
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In early stages, patients present with facial or sinus pain and stuffiness, headache, and serosanguinous discharge.
Most patients are not seen this early adn more than two thirds present in stupor or coma caused by spread to frontal lobes. Proptosis, eye pain, conjunctival and eyelid swelling, and injection, as well as gangrenous changes of hte skin of nose, eyelid, and face, suggest impending CNS involvement. |
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What clinical scenario raises the concern for possible rhinocerebral mucormycosis?
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Mental status changes in patients with acidosis secondary to uncontrolled diabetes who do not improve with correction of electroyte abnormalities.
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How is rhinocerebral mucormycosis diagnosed?
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Presence of nonseptate hyphae with right-angle branching in necrotic tissue.
However, swab cultures of nose and palate are usually negative. |
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How are imaging studies useful regarding rhinocerebral mucormycosis?
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To delineate the extent of infection and evaluate for therapeutic debridement.
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What is the characteristic pulmonary lesion associated with mucormycosis?
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Pulmonary infarction secondary to vessel invasion.
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Does the inflammatory reaction to Rhizopus and mucor result in granuloma formation?
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NO
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What are two methods used to diagnose pulmonary mucormycosis?
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1) V/Q scan demonstrating multiple segmental perfusion defects resembling multiple pulmonary emboli.
2) Biopsy of open long or metastatic skin lesions. |
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Who is at highest risk for cutaneous mucormycosis?
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Patients with extensive burn wounds?
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what is the treatment for mucormycosis?
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Acidosis correction
Debridement when possible Amphotericin B |
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What is the outcome of untreated mucormycosis?
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Death
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What type of organism auses pneumocystis pneumonia?
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Unicellular eukaryote
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How does P. jiroveci differ from fungi?
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Lacks essential components of fungi, e.g., ergosterol
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Why has deciphering the classification of P. jiroveci been difficult?
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P. jiroveci has not been successfully grown in culture.
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How is P. jiroveci transmitted?
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Respiratory route.
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By what age have most humans been exposed/become immune to P. jiroveci?
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3 years old
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How does P. jiroveci infection most commonly present?
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Pneumonia, Pneumocystis pneumonia.
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What is the triad of PCP symptoms?
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Fever
Exertional dyspnea Nonproductive cough |
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What is the pathogenesis of P. jiroveci?
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1) Attachment to type I alveolar cells
2) Proliferation 3) Formation of eosinophilic foamy exudates secondary to host inflammatory response 4) Occlusion of alveolar air spaces causing desaturation and respiratory distress 5) Interstitiall thickening and fibrosis. |
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What four factors predispose one to PCP?
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1) Defective T-cell immunity with CD4 count <200/mL
2) Previous PCP or another AIDS definig illness 3) Primary immunodeficiency disease, especially severe combined immunodeficiency disease 4) Protein malnutrition. |
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What is a life-threatening complication of PCP?
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Spontaneous pneumothorax
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How is PCP diagnosed?
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1) Silver stain of bronchial alveolar lavage revealing thick-walled cysts containing 6-8 intracystic sporozoites or extracystic trophozoites
2) Direct fluorescent antibody of sputum or bronchoalveolar lavage |
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What is the characteristic chest x-ray finding in PCP?
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NONE
PCP can mimic many disease processes including normal. |
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What is the treatment for PCP?
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TMP-SMX and corticosteroids
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Why are TMP-SMX and corticosteroids used for PCP?
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TMP-SMX is an antibiotic and kills the organism
Administration of corticosteroids within first 72 hours if initiating antipneumocystis treatment decreases respiratory failure and death by attenuating the inflammatory response in AIDS patients. |
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Should treatment be stopped if patients desturate more when TMP-SMX is initiated?
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NO
Desaturation is often secondary to inflammatory reaction to P jivireci. cell death and treatment shoud not be changes for 5-7 days |
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What is the mortality of patients treated for PCP?
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9-20% mortality despite full course of treatment
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What are the indications for PCP prophylaxis with TMP-SMX?
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1) Patients with a CD4 count <200/mL
2) Patients receiving aggressive immunosuppressive therapy |
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What other pathogens does TMP-SMX protect against?
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Toxoplasma gondii infection
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