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33 Cards in this Set
- Front
- Back
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Define virulence. |
The degree of pathogenicity within a group or species of parasites as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. |
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What type of parasite are most pathogenic fungus? |
Most are faculative parasites (opportunistic) |
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What is the rise in fungal disease tied to recently? |
Tied to the rise in autoimmune diseases. |
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What is fugal dimorphism? |
Where funghi can exist as either single cells (yeasts) or in a mycelial form |
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What is typically the pathogenic form of fungus in the body? |
The yeast form. |
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What is dimorphism into the yeast form triggered by? |
1. Elevated temperatures 2. High CO2 and low O2 3. Levels of nutrients |
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How does being in a yeast form contribute to virulence? |
Increases the possiblity of the wider spread of the infection through the blood and lymph system. |
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What are infection types of a fungal infection? Briefly describe each. |
1. Superficial infection - colonisation of superficial layers of tissue such as hair and skin - Often cause little damage and are of minor important 2. Cutaneous infection - caused by Dermatophytes - colonsation of hair, nails and skin - can cause some damage 3. Subcutaneous infection - Tropical, enter by wounds - Form abscesses called mycetomas 4. Systemic - fungus spreads from one internal organ to another |
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What is athletes food also known as? What are the causative agents? |
Tinea pedis - caused by dermatophytes 1. Trichophyton rubrum 2. Trichophyton mentagrophytes 3. Epidermophyon floccosum |
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What are subcutaneous infection abscesses called? |
Mycetomas |
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Where do systemic infections commonly originate? |
Originate from inhaled spores in the lungs. |
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What can cause death from a fungal systemic infection? How is a fungal systemic infection diagnosed? |
1. Brain infection can cause death 2. Biopsies from as many sites as possible |
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What culture agar can you use to culture: 1. Pathogenic funghi 2. Non-Pathogenic funghi |
1. Brain Heart Infusion agar & Blood agar 2. Sabouraud's glucose agar & 4% malt extract agar |
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What is 'serology'? |
The study of serum. In practice, the term usually refers to the diagnostic identification of antibodies in the serum. |
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What are the critical techniques involved in serology? |
1. Immunodiffusion 2. Whole cell agglutination 3. Enzyme linked immunosorbent assay (ELISA) |
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What is the causative agent of Aspergillosis? |
Aspergillus fumigatus. |
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What are the risk groups for aspergillosis? |
1. Farmers / people handling decaying matter 2. Individuals suffering from immunosupressive disorders |
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What causes aspergillosis? |
Inhaled spores which germinate in the lungs. The hyphae penetrate the tissue and invade blood vessels where thrombosis can occur. |
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What is the hallmark structure of aspergillosis? Describe the process of formation. |
An aspergilloma - a 'fungus ball' Mycelium forms in previously existing cavities in the lung - The aspergilloma becomes surrounded by a dense fibrous wall. |
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What is the causitive agent of Candidiasis? How does it spread? |
1. Candida albicam 2. Lives as a saprotroph (decaying matter feeder) inside healthy hosts and then spreads to vulnerable groups to form grey/white lesions on mucous membranes as a faculative parasite. |
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What is Darling's disease otherwise known as? What is the causative agent? What is its mode of infection? Typically misdiagnosed as x? |
1. Histoplasmosis 2. Histoplasma capsulatum 3. Thermal dimorph - yeast @ body temp 4. Tuberculosis |
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What is San Joaquin Valley Fever otherwise known as? What is the causative agent? What are the risk groups? |
1. Coccidioidomycosis 2. Coccidiodes immitis - a deuteromycete 3. Those in South Western USA |
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What is the pathogenesis of San Joaquin Valley fever? |
1. Coccidioidomycosis is initiated by arthrospores produced by mycelium in the soil. 2. When inhaled they change into parasitic - yeast like cells called spherules. 3. The spherules fill up with endospores which further promotes spread of spherules to surrounding tissues. 4. If misdiagnosed / treatment delayed this can lead to a systemic infection with a high mortality rate |
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Why is treatment of fungal infections difficult? |
Both parasite and host are eukaryotic so targeting of the parasite without harming the surrounding eukaryotic host tissue is difficult. |
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What main treatment exists for fungal infections? What produces them? |
1. Antifungal antibiotics - polyene macrolides 2. Produced by Streptomyces species |
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What are the 3 polyene macrolides? What is a key feature of their structure? What molecule do they bind to have their effect? |
1. Amphotericin B Nystatin Pimaricin 2. All have a large ring structure 3. All bind to the fungal sterol - ergosterol |
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How do the polyene macrolides cause fungal cell lysis? |
Binding to ergosterol inhibits its maintaining functions thus increases the permeability of the plasmalemma which allows the leakage of ceullular constituents. Lysis and cell death follow. |
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Describe the clinical adminstration and use of amphotericin B. |
Intravenously administrates - suspended in bile salts. Used for the treatment of systemic infections - drug of choice for life threatening mycosis. |
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Describe the clinical adminstration and use of nystatin. Why is it used in this way? |
Applied topically with pimericin to treat superficial infections. Cannot be absorbed in the GI tract, too toxic to be intravenously administered |
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Describe the clinical adminstration and use of griseoflavin. What is a possible side effect? |
Administered to treat chronic dermatophytic infections in the skin, nails and hair. Mitosis arrest in human cells by altering microtubules. |
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Describe the clinical adminstration of ketoconizole and how it has its effect. |
Taken orally, absorbed by GI tract - non toxic to human cells as it inhibits synthesis of ergosterol. |
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What are the two distinct groups of allergic response? |
1. Immediate 2. Delayed |
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What does the immediate allergic response involve? |
1. Involves IgE antibodies developed in response to previous exposures.. |
