Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
34 Cards in this Set
- Front
- Back
|
What are the three categories of mycotic infection?
|
Superficial/cutaneous
Subcutaneous Systemic |
|
|
What are some example of superficial mycoses?
|
tinea versicolor
dermatophytosis |
|
|
What are some examples of subcutaneous mycoses?
|
sporotrichosis
chromoblastomycosis mycetoma |
|
|
What are the two categories of systemic mycoses?
|
Dimorphic fungi and opportunistic fungi
|
|
|
What are some pathogenic mechanisms of fungal infections?
|
morphological adaptation (dimorphic fungi adapt to temperature of env)
resistance to phagocytosis and modulation of host response virulence factors such as keratinase and adherence |
|
|
How does B. dermatidis modulate host immune response?
|
Shedding of WI-1 glycoprotein
|
|
|
HOw does C. immitus modulate host immune response?
|
Urease activity and extracellular protease
|
|
|
How does H. capsulatum modulate host immune response?
|
Modulates phagolysosome pH
|
|
|
How does C. neoformans modulate host immune response?
|
Polysaccharide capsule and melanin production
|
|
|
What innate or nonspecific barriers are important in immunity to fungal infections?
|
Skin barriers
Muco-ciliary clearance Alveolar macrophage Neutrophils |
|
|
What role does specific immunity play in fungal infections?
|
Humoral = minor role; Ab not protective
CMI = major; if depressed then become more susceptible to fungal infection |
|
|
What are some predisposing factors to fungal infection?
|
Immunosuppressive therapy
Broad-spectrum antibiotics Long-term catheters Radiation DM Hypoparathyroidism Blood disorders Neoplasm |
|
|
Name some miscellaneous agents used to treat superficial infections.
|
Desenex
Tinactin Selsen lotion Griseofulvin - toxic *many just increase skin turnover rate |
|
|
What is the MOA of 5-fluorocytosine?
|
Cystosine agonist = inhibits nucleic acid synthesis (esp. RNA)
|
|
|
Why is resistance to 5FC so common?
|
There are many enzymes involved in 5FC MOA that are mutated when resistance arises.
May involve permease (can't get into cell), deaminase, incorporation into RNA, etc. |
|
|
5FC is often combined with AmpB for treatment of ______.
|
Meningitis caused by C. neoformans
|
|
|
What toxicity is associated with 5FC?
|
Bone marrow suppression = leukopenia and thrombocytopenia
|
|
|
What are the polyenes?
|
Amphotericin B
Nystatin |
|
|
What is the MOA of polyenes?
|
They are amphipathic molecules that can insert into and disrupt membranes by binding ergosterol
*disruption of membrane permeability leads to dEATH |
|
|
Why is AmpB often the first choice for life-threatening fungal infections?
|
It has excellent broad-spectrum activity against many systemic pathogenic fungi.
|
|
|
What reduces the severe host toxicity seen with AmpB therapy?
|
Lipid-associated forms of AmpB can deliver AmpB in higher doses with reduced toxicity
|
|
|
What is the MOA of the azoles?
|
Prevent ergosterol synthesis by inhibiting P450 enzymes --> also disrupt membrane integrity
|
|
|
What was so great about the 2nd generation azoles?
|
They were the first non-toxic parenteral agents to approach the efficacy of AmpB
First generation azoles included topical agents and first azole for parenteral use |
|
|
Name some 2nd generation azoles?
|
Fluconazole
Intraconazole New: voriconazole, posaconazole |
|
|
What is the MOA of echinocandins?
|
These are lipopeptides that inhibit the syntesis of beta-1,3-glucan (an essential component of fungal cell walls)
|
|
|
Name some echinocandins used in Candida and Aspergillus infections:
|
caspofungin
micafungin anidulafungin |
|
|
What is the MOA of Terbinafine (Lamisil)?
|
allyamine deriviative that inhibits squalene epoxidase (an enzyme essential for ergosterol synthesis)
|
|
|
What is terninafine used for?
|
topical or oral therapy for dermatophytic infections
|
|
|
What are some ways anti-fungal susceptibility testing is useful?
|
1. Estimate activity against an org
2. Correlates with in vivo activity to predict likely outcomes 3. Monitor resistance to anti-fungals 4. Predict therapeutic potential of investigational agents |
|
|
Why has the need for immunodiagnostic methods increased for mycoses?
|
1. Rise in incidence of systemic fungal disease.
2. Increase in the # of individuals predisposed (AIDS, drug therapies, catheters) 3. Need for rapid information for high-risk patients |
|
|
What are some approaches to fungal immunodiagnostics?
|
Same as bacteria...
Specific Ab responses Changes in Ab titers Measure critical Ab titers Detect fungal Ag in body fluids Skin testing |
|
|
What are some problems with detection of serum antibody in fungal infections?
|
Lack of Ab production even in disseminated disease
Presence of Ab late in disease Presence of Ab in non-infected individuals (endogenous Candida) Cross-reactive Ab |
|
|
What are some problems with detection of fungal antigens?
|
Need to distinguish infection vs. colonization
Appearance of Ag late in disease Conservation of Ag within a species Paucity of std assays that can be performed in clinical laboratory |
|
|
What is the usefulness of skin tests?
|
Mostly used for histoplasmosis and coccidioidomycosis.
Mostly just give evidence of exposure - endemic areas Cross-reactions can occur May affect serologic testing by giving false positives |
