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97 Cards in this Set
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1. How do fungi grow in tissues and what do they produce?
What do invasive fungi cause? What is this due to? (three things) What can engulf small fungi cells? |
Grow slowly producing granulomas
Cause tissue damage 1. Displacement or destruction of vital structures 2. Effect of low grade inflammatory response 3. Hyper-sensitivity reaction Macrophages or giant cells |
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2. Why are fungi and their extracellular products good antigens?
What is resistance to fungal disease mainly due to? How does this work? (three steps) |
Evoke both cellular and humoral responses
T lymphocyte-mediated immunity 1. T-cell receptors recognize fungal antigens 2. Secrete cytokines to activate macrophages 3. Macrophages kill invading fungi |
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3. What do saprophitic fungi live on?
What are four uses of saprohpitic? |
Live on dead organic matter
1. Food supplement 2. Industrial importance 3. Organic acids, enzymes, sterols 4. Baker's yeast |
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4. What are mycotoxins?
What can ingestion of mycotoxins in food leads to? What do common molds elaborate? |
Toxins elaborated by poisonous mushrooms and cause a disease known as mycetismus
Mycotoxicosis Very potent nephrotoxic and hepatotoxic metabolites |
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5. What are the characteristics of fungi in terms of cell structure?
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1. Membrane bound organelles
2. Rigid cell wall -provides rigidity and strength 3. Mannans -on surface and in structural matrix 4. Glucans -increase strength of cell wall 5. Chitin -inert, insoluble, rigid |
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6. What do the cell wall of fungi lack?
(three things) What two things do the cell wall of fungi have? |
1. Muramic acid
2. Teichoic acid 3. Peptidoglycan 1. Hexose polymers -glucaans and mannans 2. Chitin |
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7. What do the cell membranes contain?
What are the functions of the cell membrane? |
1. Phosphatidylethanolamine
2. Ergosterol and zymosterol **cholesterol is usually absent Osmotic barrier and facilitates synthesis of cell wall material |
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8. What does heterophilic metabolism require?
What is an example? Are most fungi aerobes or anaerobes? |
Exogenous organic compounds as energy source
Saprophytes which derive nutrients from decaying organic matter Most are strict aerobes **no strict anaerobes |
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9. What is the morphology of yeasts?
What is the morphology of molds? What is a mass of hyphae called? What does dipmorphism mean? |
Smooth colonies and single cells which reproduce by budding
Fuzzy colonies which extend by formation of tube-like extensions w/ thick parallel walls call hyphae Mycelium Some fungi can grow as either a yeast or a mold phase depending upon environmental conditions **example is candida albicans |
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10. When do dimorphic fungi grow as the mold form?
When do dimorphic fungi grow as the yeast form? What is the change in morphology directly related to? What is the most extensively studied dimorphic fungi? |
Mold form - room temp (28C)
Yeast form - body temp (37C) Adaptation from a saprophytic to a parasitic existence H. capsulatum |
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11. What are sexual spores derived from?
What are three types of sexual spores? |
Derived from a sexual process that involves a diploid state
*fusion of two nuclei that generally undergo mitosis 1. Zygospore 2. Ascospores 3. Basidiospores |
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12. What are four types of asexual spores?
How are most pathogenic fungi? |
1. Blastospore
-budding yeast 2. Chlamydospore -thick walled & produced under adverse conditions 3. Arthrospres 4. Sporangiospores Lack a known sexual spore stage |
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13. How are molds identified?
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1. Macroscopic characteristics
-morphological description -color descriptoin 2. Microscopic characteristics -type of spore produced and method of formation |
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14. How are yeast identified?
What three types of conditions do fungi elicit in humans? |
By sugar fermentation, sugar assimilation and some biochemical patterns
1. Allergy IgE - mold allergy Non-complicated Type I 2. Toxins -aflatoxins 3. Disease -mycosis |
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15. How do yeasts and molds grow?
What are hyphae? What are non-septate hyphae considered and why? What are septate hyphae less primitive? |
1. Yeasts - formation of bud
2. Molds - produce septate or non-septate hyphae which extend to form a mycelium Branching tubular structures that make up the mycelium More primitive b/c when hyphal strand is damage entire strand dies Pore between adjacent compartments can be plugged preventing death of entire strand |
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16. What is the grouping of medically important fungi often based on?
What do the superficial fungi cause? What are opportunistic fungi? What are systemic pathogens? |
The tissues they parasitize and the disease they produce
Indolent lesions of the skin and its appendages (ringworm and athlete's foot) Those found in the environment or in the normal flora that occasionally produce disease Most virulent fungi that may cause serious progressive systemic disease |
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17. What are yeasts able to colonize?'
What does adherence or ability to colonize require? What is invasion? In C. albicans what is invasion associated with? |
Mucosal surface of the GI and urogenital tract
Requires a surface adhesion on the microbe and a receptor on the epithelial cell Moving across surface barriers **may be through mechanical breaks in epithelium Formation of hyphae and pseudohyphase |
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18. What phagocyte interactions can occur between neutrophils/macrophages and fungi?
How is Coccidiodes immitis in its conidial (infective) phase? |
1. Neutrophils and macrophages are able to kill hyphae of most fungi
2. Dimorphic species are more resistant to killing by neutrophils Antiphagocytic due to a component in its wall **hyphae convert to a spherule phase in tissue and become resistant |
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19. Do the extracellular products of opportunistic fungi cause tissue damage?
What is injury by fungal infections due to? |
None have been shown to injure the host directly
Exotoxins/mycotoxins are produced in the environment by a number of fungi but not in vivo Due to inflammatory and immune responses stimulated by prolonged presence of fungi |
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20. How is humoral immunity involved in preventing infection by fungi and progression of disease?
How is cellular immunity involved? Progressive fungal disease occur in what type of patients? What happens to fungi that escape neutrophils? |
Opsonizing antibody effective in some yeast infections
T-cell mediated response of primary important Immunocompromised patients **systemic disease associated w/ deficiencies in neutrophils and T-cell mediated immunity Grow slowly in macrophages |
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21. What are some antimicrobial mechanisms of cell membranes?
(two) What are some antimicrobial mechanisms of nuclei acids? What are some antimicrobial mechanisms of cell walls? (two) |
1. Polyenes
2. Imidazoles Flucytosine & griseofulvin 1. Cilofungin -beta-glucan synthetase inhibitor 2. Nikkomycins & polyoxins -chitin synthetase inhibitors |
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22. What are polyenes?
What do they bind to? What do they cause? |
Lipophilic and fungicidal
Bind to ergosterol forming cylindrical channels that penetrate membrane Cause derangement of membrane integrity and leakage of cytoplasmic components |
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23. What are two examples of polyenes?
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1. Nystatin (mycostatin)
-treat tropical yeast or vaginal infections -too toxic & insoluble for systemic use 2. Amphotericin B (Fungizone) -most reliable and standard antifungal for systemic use |
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24. What are the indications for using amphotericin B?
What is its toxicity? |
Use limited to progressive, life-threatening fungal infections
1. Renal dysfunction 2. Cardiotoxic 3. GI tract 4. Bone marrow suppression 5. Thrombophlebitis (inflammation of vein) |
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25. What type of activity do imidazoles have?
What do imidazoles attach to? What do they interfere with? What does this lead to? |
Fungistatic activity
Attach to cytochrome p-450 of fungi Interfere w/ conversion of lanosterol to ergosterol Leads to defective cell membrane w/ altered permeability |
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26. What are some examples of imidazoles?
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1. Miconazole
2. Clotrimazole 3. Ketoconazole -highly lipophilic -treat systemic infections -second line drug for treatment of infections due to dimorphic fungi |
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27. What is itraconazole (sporonox)?
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Primary oral alternative to amphotericin B for treatment of systemic mycosis
**Broadest spectrum of activity against fungi |
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28. What is fluconazole (diflucan)?
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Primary alternative to amphotericin B for treatment of systemic mycosis
**Good CNS penetration |
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29. What do allylamines do?
What are two examples of allylamines? |
Inhibit ergosterol biosynthesis inhibits conversion of squalene
**squalene builds up and is toxic --> fungicidal 1. Naftifine -topical agent 2. Terbinafine (lamisil) -oral therapy for tinea pedis and onychomycosis |
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30. What type of activity does Griseoflvin have?
What does it act on? What does it interfere with then? |
Fungistatic activity
Acts on the microtubules and associate proteins that make up mitotic spindles Interferes w/ cell division and other functions associated w/ microtubules |
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31. What does flucytosine do?
What toxicity can it have? |
Inhibits fungal protein synthesis by replacing uracil w/ 5-fluorouracil in fungal RNA and inhibits thymidylate synthetase (enzyme essential for DNA synthesis)
**fungistatic Reversible bone marrow suppression that can lead to neutrophenia and thrombocytopenia |
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32. What are some oral antifungals?
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1. Griseoflumvin
2. Nystatin 3. Azole group 4. 5-fluorocytosine |
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33. Since fungi are eukaryotic what problems are posed when using anti-fungals?
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1. Lack of selective toxicity
2. Few drugs to treat life-threatening fungal infections 3. Amphotericin B is only drug against life-threatening fungal infections |
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34. What are five factors that may contribute to the emergence of anti-fungal resistance?
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1. Frequency and dosage
2. Intermittent dosage 3. Prophylaxis 4. Cumulative dose 5. Fungistatic nature of azoles |
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35. What are four cellular mechanisms of anti-fungal resistance?
Four things... |
1. Intrinsic resistance of endogenous strains
2. Replacement w/ a more resistance species 3. Genetic alteration that results in a more resistant strain 4. Transient gene expression that renders a cell temporarily resistant |
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36. What are some molecular mechanisms of anti-fungal resistance?
Three things... |
1. Change in sterol components of plasma membrane
2. Genetic change in ERG16 -point mutation -over expression -gene amplification 3. Alteration in other enzymes in ergosterol biosynthetic pathway |
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37. What are superficial mycoses limited to?
What are three types? Where do cutaneous mycoses grow? What are two examples of cutaneous mycoses? |
Limtied to outermost layers of the skin and hair
1. Tinea nigra 2. Tinea nodosa 3. Pityriasis versicolor Fungi grow only in or on the skin, hair and nails 1. Dermatophytomycoses 2. Candidiasis -candida albicans |
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38. What do subcutaneous mycoses infect?
What are four examples? |
Infect dermis, subcutaneous tissue, muscle, fascia and bone tissue
1. Sprortrichosis -most common type 2. Chromomycosis 3. Phycomycosis 4. Mycetome |
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39. What are some systemic mycoses that are pathogenic?
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1. Histoplasmosis
2. Blastomycosis 3. Paracoccidioidomycosis 4. Coccidioidomycosis |
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40. What are some systemic mycoses that are opportunistic?
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1. Aspergillosis
2. Mucomycosis 3. Candidiasis 4. Cryptococcosis 5. Sporotrichosis **affect compromised host |
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41. What si onychomycosis?
What are three tissue reactions to mycoses? What are three sources of infection? |
Infection of the nails
1. Chronic inflammatory 2. Pyogenic 3. Mixed pyogenic & granulomatous 1. Geophilic (soil) 2. Zoophilic (animals) 3. Anthropophilic (human to human) |
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42. What are four barriers to infection?
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1. FA content of skin
2. pH 3. Epithelial turnover of skin 4. Normal bacterial flora |
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43. What type of fungus is pityriasis (Tinea) nigra?
What is the causitive agent? What does it produce? Clinically how does it present? How does it appear clinically? |
Dimorphic fungi
Exophiala werneckii Produces melanin causing brown to black color organism Asymptomatic and on palm, sole, neck and/or thorax Brown to black non-scaly macular lesion that spreads peripherally **no inflammatory reaction |
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44. What is the etiology of piedra (tinea) nodosa?
Where does black piedra occur? Where does white piedra occur? What is the therapy? |
Piedraia hortai (black piedra)
Scalp hair, under cuticle, hair shaft Hair, beard, mustache Remove infected hair |
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45. What is the etiology of pityriasis (tinea) versicolor?
What is the distribution? How does the clinical disease present? |
Malazzezia furfur
Anthropophilic 1. Keratinized cells of epidermis -depigmented patches or continuous lesions 2. Chronic, mild, asymptomatic infection 3. Intense itching, macular patches, desquamation |
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46. What does dermatophytes (ringworm) infections cause infection of?
Are dermatophytes contagious? What does the fungi contain? |
Infection of keratinized tissues, epidermis, hair and nails
**non-invasive Yes! - only fungal infections which are contagious Keratinase - digest keratin |
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47. What do microsporum attack?
What do trichophyton attack? What do epidermophyton attack? |
Attack hair and skin
**hairs will fluoresce green under a Wood's lamp Attack hair, skin and nails **hairs do not fluoresce Attack skin and nails |
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48. In order for symptomatic infections dermatophytes to develop what is need?
Six predisposing factors? |
1. Trauma
2. Occlusion 3. Maceration of the skin 4. Temperate stress 5. Moisture 6. Hyperhydrosis |
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49. What is the pathogenesis for dermatophytes?
What are the lesions like? What happens to the more inflammatory lesions? |
Typically round lesions spreading centrifugally (ringworm)
Patchy scaling to toxic eczema-like eruption Resolve after a short duration |
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50. What is the pathogenesis in nails?
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1. Distal subfungal onychomycosis
2. White superficial onychomycosis 3. Proximal subfungal onychomycosis |
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51. What type of reaction occurs with trichophytin?
How is the "Id" reaction manifested? |
Immediate and delayed reactions
**cutaneous hypersenstivity By the appearance of small, grouped vesicles usually on the hands |
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52. How are granulomatous lesions?
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Small, usually involved hair follicles in tinea corporis infections
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53. What is ringworm of the scalp?
What is the pathogenesis for an infected scalp? What is the pathogenesis for arthrospores? What is the pathogenesis with trichophyton species? What is the pathogenesis with microsporum species? |
Tinea capitis
Hyphae migrate to hair follicle Sheath formed or hair invaded Endothrix or ectothrix w/ mycelia extending into hair shaft Extothrix |
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54. What does tinea corporis invade?
How does it spread? What do hair follicles act as? Is hypersensitivity seen? |
Invasion of glabrous (smooth & bare) skin
Spread centrifugally **center heals, margin spread peripherally Follicles act as reservoirs "Id" hypersensitivity reactions |
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55. What happens to the lesions in tinea corporis?
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Lesions resolve spontaneously in 2 months
Annular, plaque and vesicular types require 2 weeks of topical therapy More severe lesions (granulomatous and verrucous) require oral therapy for up to 6 months |
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56. What is tinea cruris?
What are predisposing factors? How is it transmitted? |
Jock itch
1. Perspiration 2. Humidity 3. Irritation 4. Maceration of skin 5. Tight clothing 6. Obesity Via intimate contact and fomites |
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57. What are some skin infections?
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1. Tinea Barabe
2. Tinea Manuum 3. Tinea Pedis 4. Onychomycosis |
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58. What is tinea manuum almost always associated with and why?
What type of hypersensitivity can be seen with tinea manuum? Where does tinea pedis begin? How are the lesions of tinea pedis? Is tinea pedis highly contagious? |
Tinea pedis (athlete's foot) b/c both areas lack sebaceaous glands
Vesicles on hands that are itchy and sometimes painful Begins in cleft of 4th and 5th toes and spreads Mild, acute or chronic, scaling, exfoliative, or vesicular No b/c infection depends on host and environmental factors |
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59. What is onychomycosis?
How do fungus skin infections relate with nail infections? |
Toenail infection that may involve only one nail, some or all
30% of patients with fungus skin infections have nail infections **serves as a constant source of reinfection of the feet and body |
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60. How do subcutaneous mycoses fungi gain entry into the host?
What are the organisms normally inhabitants of? What are three subcutaneous mycoses? |
Entry into host by trauma
(minor wounds of skin) Normal soil inhabitants 1. Chromoblastomycoses 2. Sporotrichosis 3. Mycetome |
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61. What is the symptomatology of chromoblastomycoses?
What develops over months or years? After several years what develops? |
Wart-like growths along the lymphatics of the leg or feet
A mononuclear cellular infiltrate and satellite lesions develop Cauliflower-like nodules w/ crusting abscesses develop |
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62. Do patients experience discomfort w/ chromoblastomycoses?
What happens to the lymph channels? Is there systemic invasions? |
Minimal discomfort
Obstruction & fibrosis of lymph channels **elephantiasis results Systemic invasion is extremely rare **when it does occur CNS in involved |
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63. What is the treatment for chromoblastomycoses?
Three things... |
1. Flucytosine or thiabendazole
2. Surgical removal of lesions and skin grafting 3. Secondary bacterial infection may be more threatening than the fungal infection |
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64. What are some specific important properties of sporotrichosis?
(two things) What is the morphology of sporotrichosis? |
1. Found in soil, decaying organic matter, on plants
2. Exposure may be occupational and/or related to hobbies Dimorphic fungi |
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65. What type of infection can sporotrichosis cause?
What is the most common form of extracutaneous sporotrichosis? What is treatment? |
Lymphatic infection
Osteoarthritic 1. Amphotericin B for disseminated 2. Potassium iodide for localized cutaneous lesions |
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66. What is transmission of mycetoma associated with?
What causes it? What is the most common cause in the USA? What is mycetoma called? What is the treatment for it? |
Trauma of the foot
Cause by any of several fungal species Pseudallescheria boydii Madura foot Treatment is difficult but ketoconazole and itraconazole have been used with some success |
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67. What are the characteristics of all organisms that are systemic mycoses?
Four characteristics... |
1. Dimorphic fungi
2. Exist in soils as molds 3. Seen in a different form in invaded tissue 4. Primary respiratory pathogens |
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68. What are four true systemic (endemic) mycoses?
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1. Histoplasmosis
2. Blastomycosis 3. Paracoccidioidomycosis 4. Coccidioidomycosis |
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69. What are the general features of true systemic mycoses?
Four features... |
1. Thermally dimorphic fungi that exist in nature, soil
2. Inhalation leads to pulmonary infection and dissemination 3. No evidence of transmission among humans or animals 4. Otherwise healthy individuals are infected |
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70. What is the pathogenesis of histoplasmosis?
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1. Inhalation of microconidial/primary cutaneous inoculation
2. Conversion to budding yeast cells 3. Phagocytosis by alveolar macrophages 4. Restriction of growth or dissemination to RES by bloodstream 5. Suppression of cell-mediated immunity |
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71. How can histoplasmosis affect the oral cavity?
What is special about histoplasmosis? |
Oral lesions
Painful oropharyngeal indurated ulcers seen in oral mucosa, larynx, gingivae and tongue Only fungus that is an intracellular parasite |
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72. What are the symptoms associated with histoplasmosis?
What is useful in identifying this organism? |
Fever, night sweats, weight loss
**life-threatening in immunocompromised & AIDS patients Tuberculates (knobby) macroconidia |
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73. What are the epidemiologic factors for blastomycosis?
What is the pathogenesis for blastomycosis? |
Most often found in males in their 20's to 40's usually residing, working or spending time in a rural setting
1. Inhalation of infectious particles 2. Primary cutaneous inoculation 3. Infiltration of macrophages and neutrophils and granuloma formation 3. Oxidative killing mechanisms of neutrophils and fungicidal activity of macrophages |
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74. What are the clinical finding of blastomycosis?
Five things.... |
1. Asymptomatic infection
2. Pulmonary infection 3. Chronic cutaneous infection 4. Disseminated infection -skin, bone, gut, CNS, spleen 5. Primary cuntaneous infection |
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75. What is seen orally with blastomycosis?
What is the treatment? |
Ulcers at various sites w/ possible bone involvement
Lips, tongue and buccal mucosa plus facial and nasal areas are often affected 1. Amphotericin B 2. Itraconazole (drug of choice) 3. Fluconazole 4. Corrective surgery |
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76. What is paracoccidioidomycosis?
What is the pathogenic mechanism of paracoccidioidomycosis? |
Chronic granulomatous disease w/ pulmonary and/or lymph node involvement and lesions of the mucocutaneous areas and internal organs
Small fragments of the mold phase are inhaled into the lungs and convert to budding yeast once they are in tissue |
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77. What does paracoccidioidomycosis cause?
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Acute, self-limiting infection which in turn may proceed to local cavitation or dissemination
Followed by secondary dissemination via the blood stream and lymphatic system |
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78. What is the pathogenesis of coccidioidomycosis?
What is immunosuppression the result of? |
1. Inhalation of infectious particle, arthroconidia and spherule formation in vivo
2. Engulfment w/in phagosomes by alveolar macrophages 3. Immune complex formation -deposition leading to local inflammatory reactions Resulting from binding of complexes to cells bearing Fc receptors |
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79. What are the clinical findings in coccidioidomycosis?
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1. Primary infection
-asymptomatic in most -fever, chest pain, cough, weight loss -nodular lesions in lungs 2. Secondary infection (disseminated) -infection of lungs, meninges, bones and skin |
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80. What do opportunistic fungi cause?
Where are the organisms found? How do we acquire them? |
Secondary infections in immunocompromised individuals and otherwise debilitated individuals
**often cause death Ubiquitous in nature (soil) Breath them into our lungs daily |
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81. What is a notable exception to most opportunistic fungi?
Why? |
Candida albicans
Part of normal gastrointestinal flora so infection is endogenous in origin |
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82. What type of fungi is cryptococcosis?
What can cryptococcosis affect? |
Yeast infection where reproductive vegetative form is budding
**associated w/ pigeon droppings 1. CNS involvement - menigitis 2. Reticulendothelial defects 3. Chronic lymphoblastic leukemia |
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83. How is pulmonary cryptococcosis manifested?
What is cryptococcal menigitis associated with? How is cryptococcosis treated? |
1. Cryptococcoma = single lesion
2. Diffuse pneumonitis Most common clinical presentation and in patients with AIDS 1. Amphotericin B 2. Fluconzole **T-cell response are most important in containment and pathogen clearance |
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84. What is the pathogenicity of candidiasis associated with?'
What is the most common cause of candidiasis? Where is this species found? |
Transformation of yeast to hyphal form
Candida albicans In normal human gut flora and found in all women during pregnancy **by age 1 everyone has a positive skin test |
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85. What local factors influence the acquisition of candidiasis?
Three things... |
1. Disruption of skin
2. Common in people that keep their hands in water 3. People w/ poor fitting dentures |
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86. What intrinsic factors influence the acquisition of candidiasis?
(three things) What diseases promote candidiasis? (Three things) |
1. Age (young children)
2. Pregnancy 3. Physiological disturbances 1. Diabetes mellitus 2. Malignancies 3. Leukemias and lymphomas |
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87. What extrinsic factors influence the acquisition of candidiasis?
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1. Antibiotics
2. Corticosteroids (anti-inflammatory) 3. Surgically acquired 4. Transplantation 5. Oral contraceptives |
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88. What are some disease manifestations of candidiasis?
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1. Mucocutaneous
-mouth -esophagus -vagina -perianal 2. Cutaenous -skin and nail infections |
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89. What happens in thrush?
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Involves the mouth and formation of white plaques and red lesions under plaques
May spread to face and surrounding tissues |
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90. What are predisposing factors for candida vaginitis?
What is chronic mucocutaneous candidiasis (CMC)? |
1. Antibiotics for acne
2. Mild deficiencies of iron metabolism (chronic vaginitis) Generally begins in early life and is associated w/ polyendocrine disorders, defects of immune mechanisms or other malfunctions **all patients have defects in T-cell immunity **never develop life threatening Candida infections |
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91. What is systemic (disseminated) candidiasis?
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Organism can invade any organ system in patients whose immunity is impaired by disease, debilitation or iatrogenic measures
**Very serious and most often results in death of patient *life-threatening infections and acute leukemia |
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92. What is the mechanism of candida esophagitis?
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1. Organism absorbed from gut
2. Transported to liver via portal vein 3. Forms liver abscesses **may be origin in many cases of systemic candidiasis |
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93. Why is candidiasis more common today?
How is C. albicans in disease? |
Result of...
1. Antibiotic use 2. Organ transplantation 3. Cardiac surgery (heart valves) 4. Immunosuppression Found in both yeast and hyphal forms |
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94. What site is most commonly affected by aspergillosis?
In what three ways do aspergillus species act on lung? |
Respiratory site
1. Act as allergens 2. Saprophytes in lung cavities or dead ares of lung tissue 3. Actively invade the living lung parenchyma in patients w/ reticuloendothelial disease w/ resultant pulmonary aspergiollosis |
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95. What four types of acute disease can zygomycosis cause?
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1. Rhinocerebral
(in diabetics) 2. Pulmonary (leukemia and lymphoma patients) 3. Gastrointestinal 4. Disseminated *usually entering through skin infection |
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96. What do zygomycetes fungi show a strong predilection for?
What is the most common form? |
Brain and CNS
Cerebral disease **also like to invade blood vessels |
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97. What is pneumocystis pneumonia caused by?
Where is it commonly found? Does it respond to antifungal drugs? What does pathogenicity depend on? |
Cause by yeast-like fungi
Specific to humans and commonly found in lungs of healthy people Does not respond to anti-fungal drugs Pathogenicity depends on a host w/ depressed cellular immunity |
